Datasets:

proserve

/

FedML_PubMedQA_instruction_stf_dataset

like 0

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: In TNM staging system, lymph node staging is based on the number of metastatic lymph nodes in gastric cancer and micrometastasis is not considered. Several reports proposed the importance of lymph node micrometastasis as the causative factor for recurrence and poor survival, but it remains controversial among researchers. A total of 482 gastric cancer patients who underwent curative resection from 2004 to 2010 at Korea University Medical Center Ansan Hospital, South Korea were prospectively enrolled. For detecting lymph node micrometastasis, immunohistochemical staining with anti-cytokeratin antibody (CAM 5.2) was performed on negative lymph nodes by hematoxylin-eosin (H-E) staining. Survival differences were compared between conventional node staging and new node staging that took micrometastasis into consideration. Also, the prognostic value of lymph node micrometastasis was investigated in multivariate analysis. A total of 156 patients (32.4%) showed lymph node micrometastasis. Overall, the micrometastatic group had more advanced tumor and lymph node stage, lymphovascular cancer cell invasion, a higher rate of recurrence, and poor survival. Furthermore, when the cumulative numbers of macro- and micrometastatic lymph nodes were calculated together, the discriminative power of survival difference between each node stage became more stratified. Also, multivariate analysis using Cox's proportional hazards model demonstrated perineural invasion, pathologic T stage, dissected lymph nodes, macro- and micrometastatic lymph nodes are independent prognostic factors. Question: Should lymph node micrometastasis be considered in node staging for gastric cancer? <|endoftext|> <|assistant|> Lymph node micrometastasis was clinically significant as a risk factor for recurrent gastric cancer. Lymph node micrometastasis should be considered when estimating TNM stage for determining prognosis and the best treatment strategy.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Tumor tissue resembles chronically inflamed tissue. Since chronic inflammatory conditions are a strong stimulus for bone marrow-derived cells (BMDCs) it can be assumed that recruitment of BMDCs into cancer tissue should be a common phenomenon. Several data have outlined that BMDC can influence tumor growth and metastasis, e.g., by inducing a paracrine acting feedback loop in tumor cells. Likewise, cell fusion and horizontal gene transfer are further mechanisms how BMDCs can trigger tumor progression. Hygromycin resistant murine 67NR-Hyg mammary carcinoma cells were co-cultivated with puromycin resistant murine BMDCs from Tg(GFPU)5Nagy/J mice. Isolation of hygromycin/puromycin resistant mBMDC/67NR-Hyg cell clones was performed by a dual drug selection procedure. PCR analysis revealed an overlap of parental markers in mBMDC/67NR-Hyg cell clones, suggesting that dual resistant cells originated by cell fusion. By contrast, both STR and SNP data analysis indicated that only parental 67NR-Hyg alleles were found in mBMDC/67NR-Hyg cell clones favoring horizontal gene transfer as the mode of origin. RealTime-PCR-array analysis showed a marked up-regulation of Abcb1a and Abcb1b ABC multidrug transporters in mBMDC/67NR-Hyg clones, which was verified by Western Blot analysis. Moreover, the markedly increased Abcb1a/Abcb1b expression was correlated to an efficient Rhodamine 123 efflux, which was completely inhibited by verapamil, a well-known Abcb1a/Abcb1b inhibitor. Likewise, mBMDCs/67NR-Hyg clones revealed a marked resistance towards chemotherapeutic drugs including 17-DMAG, doxorubicin, etoposide and paclitaxel. In accordance to Rhodamine 123 efflux data, chemotherapeutic drug resistance of mBMDC/67NR-Hyg cells was impaired by verapamil mediated blockage of Abc1a/Abcb1b multidrug transporter function. Question: Do co-cultivation of murine BMDCs with 67NR mouse mammary carcinoma cells give rise to highly drug resistant cells? <|endoftext|> <|assistant|> Co-cultivation of mBMDCs and mouse 67NR-Hyg mammary carcinoma cells gave rise to highly drug resistant cells. Even though it remains unknown whether mBMDC/67NR-Hyg clones originated by cell fusion or horizontal gene transfer, our data indicate that the exchange of genetic information between two cellular entities is crucial for the origin of highly drug resistant cancer (hybrid) cells, which might be capable to survive chemotherapy.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Therapeutic proteins/peptides can produce immunogenic responses that may increase the risk of adverse events or reduce efficacy. The objectives were to measure and characterize antibody formation to liraglutide, a glucagon-like peptide-1 receptor agonist, to investigate the impact on glycemic control and safety, and to compare it with exenatide, an agent in the same class. Antibody data were collected during six Liraglutide Effect and Action in Diabetes (LEAD) trials (26-104 wk duration). Samples for determination of antibody formation were collected at LEAD trial sites and analyzed at central laboratories. Antibodies were measured in LEAD trial participants with type 2 diabetes. Interventions included once-daily liraglutide (1.2 or 1.8 mg) or twice-daily exenatide (10 μg). The main outcome measures included the proportion of patients positive for anti-liraglutide or anti-exenatide antibodies, a glucagon-like peptide-1 cross-reacting effect, and an in vitro liraglutide- or exenatide-neutralizing effect. Change in glycosylated hemoglobin A(1c) (HbA(1c)) by antibody status and magnitude [negative, positive (high or low level)]. After 26 wk, 32 of 369 (8.7%) and 49 of 587 (8.3%) patients had low-level antibodies to liraglutide 1.2 and 1.8 mg, respectively [mean 3.3% antibody-bound radioactivity out of total radioactivity (%B/T), range 1.6-10.7%B/T], which did not attenuate glycemic efficacy (HbA(1c) reductions 1.1-1.3% in antibody-positive vs. 1.2% in antibody-negative patients). In LEAD-6, 113 of 185 extension patients (61%) had anti-exenatide antibodies at wk 26 (range 2.4-60.2%B/T). High levels of anti-exenatide antibodies were correlated with significantly smaller HbA(1c) reductions (P = 0.0022). After switching from exenatide to liraglutide, anti-exenatide antibodies did not compromise a further glycemic response to liraglutide (additional 0.4% HbA(1c) reduction). Question: Is liraglutide treatment associated with a low frequency and magnitude of antibody formation with no apparent impact on glycemic response or increased frequency of adverse events : results from the Liraglutide Effect and Action in Diabetes ( LEAD ) trials? <|endoftext|> <|assistant|> Liraglutide was less immunogenic than exenatide; the frequency and levels of anti-liraglutide antibodies were low and did not impact glycemic efficacy or safety.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The aim of this experimental study was to investigate the early effects of interleukin-10 (IL-10) and interleukin-1beta antagonist (anti-IL-1beta) against cellular damage, inflammatory reactivity, lipid peroxidation (LPO), and myeloperoxidase (MPO) activity induced by spinal cord ischemia reperfusion injury (IRI). Thirty-two single strain female Albino rats were divided into four groups: control (sham-operated), IRI-alone, IL-10-treated (100 mug/kg), and anti-IL-1beta-treated (1 mg/kg) groups after IRI. IRI was induced by balloon occlusion of the aorta and simultaneous hypovolemia during occlusion. The animals were sacrificed at 24 h. Histopathological and ultrastructural analyses, biochemical studies for determination of LPO and MPO activity and Comet assays (single cell electrophoresis for detecting DNA single strand breaks) were performed in all study groups. Compared with the levels of control (sham-operated) animals, IRI produced a significant increase in the levels of LPO and MPO activity, and prominent tissue damage characterized by leukocyte infiltration, edema and neuronal and glial damage in the affected spinal cord in 24 h. The administration of IL-10 decreased LPO and MPO activity, and suppressed initial inflammatory response in the first 24 h. The effects of anti-IL-1beta were limited to decrease in LPO activity without considerable evidence of cellular preservation. Question: Does systemic administration of interleukin-10 attenuate early ischemic response following spinal cord ischemia reperfusion injury in rats? <|endoftext|> <|assistant|> These data suggest that systemic administration of IL-10 attenuates the early ischemic response, and may restrict the tissue damage in the first 24 h after spinal cord ischemia reperfusion injury. Anti-IL-1beta has no considerable effect in this time window. The results of this preliminary study promote further studies with longer time windows on the effects of anti-inflammatory cytokines in spinal cord IRI.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: In recent years a number of studies have examined subgroups within the smoking population. These studies have provided information which facilitate improved targeting of programs and interventions to help smokers quit. Despite this there have been few population studies which have described male and female heavy smokers and compared their characteristics. We used representative population data on 789 smokers to examine differences between light and heavy smokers of each gender and between male and female heavy smokers directly. Of those who smoked, 35% of males and 24% of females were classified as heavy smokers and represent a large target group within the smoking population. Whereas a light smoker was characterized as smoking a median of 12.5 cigarettes per day, the heavy smoker smoked a median of 32 cigarettes per day. Univariate comparison of heavy smokers and light smokers showed a number of statistically significant differences according to demographics, in smoking behaviors and knowledge, in beliefs about smoking, in smoking characteristics, and in other health indicators. Because of interactions between gender and work/leisure day smoking variation, separate logistic regression models based on gender were fitted to the data. Again, compared with light smokers, several significant differences emerged for both heavy female and heavy male smokers under the headings mentioned above. Further logistic regression analyses showed differences between male and female heavy smokers when compared directly. Question: Can we target smoking groups more effectively? <|endoftext|> <|assistant|> The smoking population of South Australia is not homogeneous and this segmentation study has shown the need for varying approaches to different segments when developing intervention programs.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: We use data from rural Nepal and South India to compare the prevalence of small-for-gestational-age (SGA) and neonatal mortality risk associated with SGA using different birth-weight-for-gestation reference populations. We identified 46 reference populations in low-, middle-, and high-income countries, of which 26 met the inclusion criteria of being commonly cited and having numeric 10th percentile cut points published. Those reference populations were then applied to populations from two community-based studies to determine SGA prevalence and its relative risk of neonatal mortality. The prevalence of SGA ranged from 10.5% to 72.5% in Nepal, and 12.0% to 78.4% in India, depending on the reference population. Females had higher rates of SGA than males using reference populations that were not sex specific. SGA prevalence was lowest when using reference populations from low-income countries. Infants who were both preterm and SGA had much higher mortality risk than those who were term and appropriate-for-gestational-age. Risk ratios for those who are both preterm and SGA ranged from 7.34-17.98 in Nepal and 5.29-11.98 in India, depending on the reference population. Question: Does prevalence of small-for-gestational-age and its mortality risk vary by choice of birth-weight-for-gestation reference population? <|endoftext|> <|assistant|> These results demonstrate the value of a common birth-weight-for-gestation reference population that will facilitate comparisons of SGA prevalence and mortality risk across research studies.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To ascertain whether initiation of protease inhibitors was associated with a change in depressive symptoms among persons infected with HIV. Study subjects included men and women who were enrolled in the HIV/AIDS Drug Treatment Program and who had completed an annual participant survey before and after initiating triple combination therapy with a protease inhibitor. Depressive symptoms were assessed using the Centre for Epidemiologic Studies-Depression scale (CES-D). Statistical analyses to determine the change in CES-D total and subscale scores before and after protease inhibitor use were conducted using parametric and multivariate methods. Our analysis was restricted to 453 participants. Of these 234 (52%) were depressed at baseline (CES-D score > or = 16). Compared with nondepressed participants, depressed participants were slightly younger (p = .048), less likely to be employed (p < .001) and more likely to have an annual income less than $10,000 per annum (p < .001). After adjusting for CD4 count, employment status, income, age, and CES-D total or subscale score at baseline, we found a significant improvement in total scale score (p = .001) and depressive mood (p = .002), positive affects (p = .005), and somatic symptoms (p = .011) subscale scores at follow-up. There was no significant change in the interpersonal relations score over the study period. Question: Do depressive symptoms decline among persons on HIV protease inhibitors? <|endoftext|> <|assistant|> Our findings indicate that in addition to conferring impressive clinical benefits, protease inhibitor use is associated with a significant improvement in HIV-positive individuals' mental health.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: DeltaNp73 is an isoform of the p53 homologue p73, which lacks an NH(2)-terminal transactivation domain and antagonizes the induction of gene expression by p53/p73. The aim of this study was to detect DeltaNp73 expression in lung cancer and to evaluate the relationship between the DeltaNp73 expression level and the prognosis of patients with resected lung cancer. We used immunohistochemistry to analyze the protein expression of DeltaNp73 in paraffin-embedded tumor samples from 132 well-characterized lung cancer patients and compared the expression level of DeltaNp73, clinical variables, and survival outcome. Positive expression of DeltaNp73 was detected mainly in the cytoplasm of tumor cells in 77 of 132 patients (58.3%) with lung cancer. The incidence of positive expression of DeltaNp73 was 52.2, 50.0, and 70.2% in patients with stage I, II, and III, respectively (P = 0.04). Positive expression of DeltaNp73 was associated with gender but not associated with age, histologic type, pathological stage, pathological T status, and pathological N status. Lung cancer patients with positive DeltaNp73 expression had a poorer prognosis than those with negative DeltaNp73 expression. In addition, multivariate analysis of the clinicopathological characteristics of lung cancer indicated that positive expression of DeltaNp73 was a significant independent factor for predicting poor prognosis (P < 0.0001, risk ratio = 3.39). Question: Does expression of deltaNp73 predict poor prognosis in lung cancer? <|endoftext|> <|assistant|> Expression of DeltaNp73 may be a useful marker for predicting poor prognosis of patients who underwent resection of lung cancer.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To examine longitudinal changes in mood and empathy over the course of the internal medicine residency. The authors conducted a cohort study of 61 residents who completed the Profile of Mood States (POMS) and the Interpersonal Reactivity Index (IRI) at six time points during their internal medicine residency at a university-based program. (POMS was administered five times, and IRI was administered six times.) The main outcomes measured were trends in mood disturbances and multiple domains of empathy over the three-year residency, and comparisons to norms. Response rates varied from Time 1 to Time 6 (98%, 72%, 79%, 79%, 94%, and 95%, respectively). Interns had better scores on four POMS subscales: Depression-Dejection (p = .0031), Anger-Hostility (p < .0001), Fatigue-Inertia (p < .0001), and Vigor-Activity (p < .0001) compared with later administrations, especially midinternship. By the end of residency all POMS scores were returning towards baseline (effects sizes in the .20 s), but only depression was no longer significantly different. IRI scores showed the decline in Empathic Concern remained over residency whereas Personal Distress peaked midinternship year but approached baseline at the end of residency. Compared with the general population, the graduating residents were less tense, depressed, and confused. Personal Distress was significantly lower than the norm group. Question: Do mood change and empathy decline persist during three years of internal medicine training? <|endoftext|> <|assistant|> Internal medicine residency presents challenges resulting in common mood disturbances. Although graduating residents appear to be better off than the population norms, some domains of their mood disturbances and empathy never fully recover from their internship year.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The present study aimed to explore the hypothesis that bile salt-stimulated lipase (BSSL), in addition to being a key enzyme in dietary fat digestion during early infancy, plays an important role in inflammation, notably arthritis. Collagen-induced arthritis (CIA) and pristane-induced arthritis (PIA) in rodents are commonly used experimental models that reproduce many of the pathogenic mechanisms of human rheumatoid arthritis, i.e. increased cellular infiltration, synovial hyperplasia, pannus formation, and erosion of cartilage and bone in the distal joints. We used the CIA model to compare the response in BSSL wild type (BSSL-WT) mice with BSSL-deficient 'knock-out' (BSSL-KO) and BSSL-heterozygous (BSSL-HET) littermates. We also investigated if intraperitoneal injection of BSSL-neutralizing antibodies affected the development or severity of CIA and PIA in mice and rats, respectively. In two consecutive studies, we found that BSSL-KO male mice, in contrast to BSSL-WT littermates, were significantly protected from developing arthritis. We also found that BSSL-HET mice were less prone to develop disease compared to BSSL-WT mice, but not as resistant as BSSL-KO mice, suggesting a gene-dose effect. Moreover, we found that BSSL-neutralizing antibody injection reduced both the incidence and severity of CIA and PIA in rodents. Question: Does bile salt-stimulated lipase play an unexpected role in arthritis development in rodents? <|endoftext|> <|assistant|> Our data strongly support BSSL as a key player in the inflammatory process, at least in rodents. It also suggests the possibility that BSSL-neutralizing agents could serve as a therapeutic model to reduce the inflammatory response in humans.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Severe acute pancreatitis leads to a systemic inflammatory response characterized by widespread leucocyte activation and, as a consequence, distant lung injury. In CC chemokines the first two cysteine residues are adjacent to each other. The aim of this study was to evaluate the effect of Met-RANTES, a CC chemokine receptor antagonist, on pancreatic inflammation and lung injury in caerulein-induced acute pancreatitis in mice. Acute pancreatitis was induced in mice by hourly intraperitoneal injection of caerulein. Met-RANTES was administered either 30 min before or 1 h after starting caerulein injections, and pancreatic inflammation and lung injury were assessed. There were five groups of eight mice each including controls. Treatment with Met-RANTES had little effect on caerulein-induced pancreatic damage. Met-RANTES, however, reduced lung injury when given either before administration of caerulein (mean(s.e.m.) lung myeloperoxidase (MPO) 1.47(0.19) versus 3.70(0.86)-fold increase over control, P = 0.024; mean(s.e.m.) microvascular permeability 1.15(0.05) versus 3.57(0.63) lavage to plasma fluorescein isothiocyanate-labelled albumin fluorescence ratio (L/P) per cent, P = 0.002) or after caerulein administration (lung MPO 1.96(0.27) versus 3.65(0.63)-fold increase over control, P = 0.029; microvascular permeability 0.94(0.04) versus 2.85(0.34) L/P per cent, P < 0.001). Question: Does treatment with Met-RANTES reduce lung injury in caerulein-induced pancreatitis? <|endoftext|> <|assistant|> Treatment with Met-RANTES reduces lung damage associated with caerulein-induced pancreatitis in mice. Chemokine receptor antagonists may be of use for the treatment of the systemic complications of acute pancreatitis.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: A simulator has been developed that enables previously recorded clinical oscillometric waveforms to be regenerated for testing oscillometric non-invasive blood pressure measurement devices. Two non-invasive blood pressure devices were evaluated using the simulator with its database of 243 waveforms, to assess the value of a simulator for such evaluations. Two oscillometric non-invasive blood pressure devices, both of which had previously been validated against auscultatory references, were selected. The Omron HEM-907 (Omron, Hoofddorp, The Netherlands) measures the pressure during linear cuff deflation and the GE ProCare 400 (GE Healthcare, Tampa, Florida, USA) measures during step deflation. Each non-invasive blood pressure device was attached to the simulator and pressures were recorded from all 243 waveforms. The differences between the systolic and diastolic pressures measured by each non-invasive blood pressure device and the auscultatory references for each waveform were calculated. These were assessed with the European and American validation standards and with the British Hypertension Society protocol. The paired pressure differences (non-invasive blood pressure device minus auscultatory reference) for each device complied partly, but not fully, with the standards or protocol. The means (+/-standard deviation) of the paired systolic and diastolic pressures differences for the Omron were -2.4 mmHg (+/-5.9 mmHg) and -8.9 mmHg (+/-6.5 mmHg), and for the ProCare were -6.5 mmHg (+/-10.4 mmHg) and -2.9 mmHg (+/-7.0 mmHg), respectively. The pressures recorded by the Omron device met the standards for systolic pressures but failed for diastolic pressures and conversely for the ProCare. Question: Can a simulator that regenerates physiological waveforms evaluate oscillometric non-invasive blood pressure devices? <|endoftext|> <|assistant|> This represents the first evaluation of non-invasive blood pressure devices with a simulator that generates previously recorded clinical oscillometric waveforms. It allowed data from over 100 study participants to be used. Both devices had been previously clinically validated, but their evaluation using the simulator with its regenerated waveforms only partly met the required criteria. Although the results did not fully match previous clinical validations, these initial results give encouragement that a simulator with sufficient stored waveforms might be able to replace the difficult and expensive clinical evaluation of non-invasive blood pressure devices that has prevented many devices from being fully evaluated.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The p300-CBP-associated factor (PCAF), other than its histone acetyltransferase (HAT) activity, possesses an intrinsic ubiquitination activity that is involved in various transcriptional regulators, including the transcription factor glioma-associated oncogene 1 (Gli1), a well-known regulator of epithelial-mesenchymal transition (EMT) in cancer. In present research, we detected that PCAF was down-regulated in hepatocellular carcinoma (HCC) tissues compared with the adjacent non-tumor tissues and significantly associated with malignant portal vein invasion (p < 0.05) and poor survival (p < 0.05) of HCC patients. Moreover, functional study demonstrated that downregulation of PCAF facilitated tumor cell migration, invasion via EMT. Further study found that Gli1 as a direct target of PCAF induced EMT and promoted tumor metastasis and invasion. Question: Does pCAF inhibit hepatocellular carcinoma metastasis by inhibition of epithelial-mesenchymal transition by targeting Gli-1? <|endoftext|> <|assistant|> PCAF is an anti-oncogene that plays an important role in the development of HCC by suppressing HCC cell metastasis and EMT by targeting Gli1, which indicates the potential therapeutic value of PCAF for suppression of metastasis of HCC.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Pressure-flow analysis allows assessing esophageal bolus transport in relation to esophageal pressures. This study aimed to characterize pressure-flow metrics in relation to dysphagia in paediatric patients. We analysed esophageal pressure-impedance recordings of 5 ml liquid and viscous swallows from 35 children (17 M, mean 10.5 ± 0.8 years). Primary indication for referral was gastroesophageal reflux disease (GERD) (9), post-fundoplication dysphagia (5), idiopathic dysphagia (16), trachea-esophageal fistula (2) and other (3). Peristaltic function was assessed using the 20 mmHg iso-contour defect and the timing between bolus pressure and flow was assessed using the Pressure Flow Index, a metric elevated in relation to dysphagia. Patients were stratified in relation to dysphagia and to peristaltic defect size. Dysphagia was characterized by a weaker peristalsis for liquids and higher Pressure Flow Index for viscous. When patients were stratified based on weak or normal peristalsis, dysphagia with weak peristalsis related to a larger iso-contour defect size and dysphagia with normal peristalsis related to higher Pressure Flow Index. Question: Does high-resolution manometry combined with impedance measurements discriminate the cause of dysphagia in children? <|endoftext|> <|assistant|> Pressure-flow analysis enables differentiation of patients with dysphagia due to weak peristalsis (poor bolus clearance) from abnormal bolus flow resistance (esophageal outflow obstruction). This new dichotomous categorization of esophageal function may help guide the selection of optimal treatment such as pharmacological or endoscopic therapy.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Three commonly used sutures were tested in a pig model of bile duct anastomosis to assess their relative contributions to inflammation and scarring. Thirty pigs were randomised to bile duct division and anastomosis with either polyglyconate (Maxon), polyglactin 910 (Vicryl) or polypropylene (Prolene). Half the animals were sacrificed at two weeks and the remainder at 23 weeks. Anastomoses were assessed by cholangiography, scanning electron microscopy and light microscopy. There was less short term histological reaction with the two monofilament materials, Prolene and Maxon, compared to the braided suture Vicryl. Maxon was associated with less long term inflammation than Prolene, was found to handle better, and has an advantage over Prolene by being absorbable. Question: Is maxon an optimal suture for bile duct anastomoses in pigs? <|endoftext|> <|assistant|> Maxon is an optimal suture for bile duct anastomoses. Its long term absorption characteristics make it suitable for situations where bile duct healing may be delayed.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Cancer antigen-125 is a high molecular weight glycoprotein used mainly for the diagnosis of ovarian carcinoma. However, elevation of cancer antigen-125 is observed in many benign conditions specially in liver cirrhosis but the reason behind the elevation remains unknown. Similarly intercellular adhesion molecule (ICAM-1) elevation is reported in liver cirrhosis but its role played in liver cirrhosis and ascites is unclear. A total of 76 patients were involved in the study diagnosed with liver cirrhosis, Budd-Chairi syndrome, and tuberculous peritonitis. The degree of ascites was graded according to standard criteria into mild, moderate and severe. Cancer antigen-125 levels and sICAM-1 levels of all the patients were measured along with other liver parameters to evaluate the association of CA-125 and sICAM-1 with ascites. When cancer antigen-125 levels of liver cirrhosis patients were correlated with ascites a strong correlation was observed with the degree of ascites but no association was seen with liver function parameters. A significant difference was shown when liver cirrhosis patients with ascites were compared with liver cirrhosis patients without ascites (p < 0.05). All the patients with ascites had elevated levels of CA-125 (mean: 261.11 U/mL +/- 118.15 U/mL) whereas most of the patients without ascites had CA-125 levels under the normal range. A strong correlation (p < 0.05) is seen between CA-125 level and the degree of ascites. Elevated levels of sICAM-1 were observed in liver cirrhosis patients with ascites as well as in patients with other benign diseases with ascites (mean sICAM-1: 7.23 +/- 4.12 ng/mL and 6.67 +/- 2.99 ng/mL, respectively). When sICAM levels of liver cirrhosis patients with and without ascites were compared a significant difference (p < 0.05) is observed. Question: Are cancer antigen-125 and ICAM-1 together responsible for ascites in liver cirrhosis? <|endoftext|> <|assistant|> The elevation of cancer antigen-125 in liver cirrhosis is specific to ascites. The mesothelial cells of the peritoneum chiefly contribute to the elevation of cancer antigen-125 along with the large surface area of the peritoneum. Therefore, CA-125 can be used as a good marker for early diagnosis of ascites and CA-125 has no relationship with the etiology of diseases in benign ascites. ICAM-1 plays a key role in the formation of ascites by influencing the endothelial-vascular permeability and therefore it along with CA-125 can be used as markers or alternative tools to diagnose ascites and to monitor the progression and severity of the disease.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To investigate the role of CD4(+)CD25(+) T cells (Tregs) in protecting fine particulate matter (PM-) induced inflammatory responses, and its potential mechanisms. Human umbilical vein endothelial cells (HUVECs) were treated with graded concentrations (2, 5, 10, 20, and 40 µg/cm(2)) of suspension of fine particles for 24h. For coculture experiment, HUVECs were incubated alone, with CD4(+)CD25(-) T cells (Teff), or with Tregs in the presence of anti-CD3 monoclonal antibodies for 48 hours, and then were stimulated with or without suspension of fine particles for 24 hours. The expression of adhesion molecules and inflammatory cytokines was examined. Adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), and inflammatory cytokines, such as interleukin (IL-) 6 and IL-8, were increased in a concentration-dependent manner. Moreover, the adhesion of human acute monocytic leukemia cells (THP-1) to endothelial cells was increased and NF- κ B activity was upregulated in HUVECs after treatment with fine particles. However, after Tregs treatment, fine particles-induced inflammatory responses and NF- κ B activation were significantly alleviated. Transwell experiments showed that Treg-mediated suppression of HUVECs inflammatory responses impaired by fine particles required cell contact and soluble factors. Question: Do regulatory T cells protect fine particulate matter-induced inflammatory responses in human umbilical vein endothelial cells? <|endoftext|> <|assistant|> Tregs could attenuate fine particles-induced inflammatory responses and NF- κ B activation in HUVECs.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Recent research demonstrated that bladder pain syndrome/interstitial cystitis (BPS/IC) is associated with many coexisting physical and psychiatric conditions. In this study, we explored the potential association between anxiety disorder (AD) and BPS/IC using a case-controlled population-based approach in Taiwan. Data on the sampled subjects analyzed in this study were retrieved from the Longitudinal Health Insurance Database 2000. Our study included 396 female cases with BPS/IC and 1,980 randomly selected female controls. We excluded subjects who had a history of major psychosis (except AD) or a substance-related disorder. A conditional logistic regression was performed to calculate the odds ratio (OR) for the association between a previous diagnosis of AD and IC/BPS. Of the 2,376 sampled subjects, 136 (5.72%) had received an AD diagnosis. AD was found in 64 (16.16%) cases and in 72 (3.64%) controls (P < 0.001). The conditional logistic regression analysis (conditioned on age group and the index year) suggested that compared to controls, the OR for prior AD among cases was 4.59 (95% confidence interval (CI) = 2.32-9.08, P < 0.001). After adjusting for chronic pelvic pain, irritable bowel syndrome, fibromyalgia, migraines, sicca syndrome, allergies, asthma, and an overactive bladder, the OR for prior AD among cases was 4.37 (95% CI = 2.16-8.85, P < 0.001) compared to the controls. Question: Is bladder pain syndrome/interstitial cystitis associated with anxiety disorder? <|endoftext|> <|assistant|> There was an association between AD and BPS/IC, even after taking demographic characteristics, medical co-morbidities, and substance-related disorders into consideration. Results of this study should alert clinicians to evaluate and monitor the presence of BPS/IC in patients with AD.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: This study was designed to investigate the presence of the secretory phospholipase A2 receptor in RPE, a protein closely related to the phagocytic mannose receptor. Proteins from cultured rat, pig, and human RPE were separated by SDS-PAGE and immunoblotted with a polyclonal guinea pig sPLA2 receptor antibody. RT-PCR was performed on rat and pig RPE samples using primers designed from published rat pancreatic sPLA2 receptor sequences. The sPLA2 receptor protein was not detected in rat, pig, or human RPE by immunoblots. Additionally, message for this receptor was not detected in rat or pig RPE. Question: Is another mannose receptor-like lectin present in retinal pigment epithelium? <|endoftext|> <|assistant|> With these techniques, these data demonstrate that the sPLA2 receptor is undetectable in the RPE.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Progressive hepatic fibrosis is common after the Fontan operation, but little is known about its onset. We sought to determine whether hepatic abnormalities before the Fontan operation, and whether further abnormalities can be identified soon afterward. Patients undergoing the Fontan operation at our institution were prospectively enrolled and underwent hepatic ultrasound with Doppler and serum testing immediately before and 3 to 6 months after the operation. Thirty patients were enrolled at a median age of 3.1 years (range, 2.2 to 8.1 years). Extracardiac Fontan was performed in 67%. Three patients (10%) had abnormal hepatic echotexture before the operation. At the post-Fontan study, mean liver length increased (9.9 versus 10.9 cm; p < 0.0001), and mean hepatic artery end-diastolic velocity decreased (18.8 versus 14.5 cm/s; p = 0.03). One patient showed new, abnormal hepatic echotexture after surgery. Mean aspartate aminotransferase (56.7 versus 60.7 U/L; p = 0.04), alanine transaminase (18.9 versus 33.9 U/L; p = 0.0002), and γ-glutamyl transferase (18.7 versus 46.1 U/L; p = 0.002) increased at the post-Fontan assessment compared with the preoperative values. By linear regression, hospital length of stay and duration with chest tube after Fontan operation were both significantly associated with an increase in γ-glutamyl transferase (p < 0.001 for both) and alanine transaminase (p = 0.008, p = 0.048). Question: Do hepatic Abnormalities Are Present Before and Early After the Fontan Operation? <|endoftext|> <|assistant|> In this cohort, hepatic abnormalities were observed in some patients before the Fontan operation and new abnormalities developed soon afterward. These findings suggest that liver insult may occur before or soon after the Fontan operation.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Chronic inflammation and subsequent tissutal alterations may play a key role in prostate carcinogenesis. In this way, molecular alterations of the suppressor of cytokine signaling 3 (SOCS3), one of the most important inhibitory molecule of inflammatory signal transduction circuitries, could contribute to explain the pleiotropic role of interleukin-6 (IL-6) in this type of cancer. We analyzed the methylation status and mRNA expression of SOCS3 in 20 benign prostate hyperplasias (BPH) and in 51 prostate cancer specimens. We analyzed the SOCS3 methylation status using methylation-specific PCR. Hypermethylation was confirmed by sequencing after subcloning. Epigenetic silencing of this gene was also demonstrated by real-time PCR and by immunohistochemistry. Results and correlation with clinical data were statistically analyzed. We found that the promoter of SOCS3 was methylated in 39.2% of prostate cancer. On the contrary, all BPH and normal controls had an unmethylated pattern. Real-time analysis showed that in methylated cases SOCS3 mRNA expression was reduced by three and four folds as compared to BPH and unmethylated cases, respectively. Interestingly, SOCS3 mRNA level was higher in unmethylated prostate cancer than in BPH. The immunohistochemical staining analysis for SOCS 3 confirmed mRNA results. Moreover, methylation of SOCS3 promoter significantly associated with intermediate-high grade Gleason score (P = 0.0007) and with an unfavorable clinical outcome (P = 0.0019). Question: Does epigenetic silencing of SOCS3 identify a subset of prostate cancer with an aggressive behavior? <|endoftext|> <|assistant|> Our data suggest that SOCS3 hypermethylation may be involved in the pathogenesis of prostate cancer and could identify a tumor subset with an aggressive behavior.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Recent reports have reopened discussion of the prognostic value of elevated pre-treatment carcinoembryonic antigen (CEA) levels in colorectal cancer. Due to the discrepancies in the published results, we aimed to analyze the possible predictive value of CEA, both overall and in different tumoral stages in our environment. We retrospectively studied 303 consecutive patients with colorectal cancer resected with curative intent by analysing tumor-related mortality. The frequency of patients with increased CEA levels (>5mg/l) was registered. Univariate and multivariate analyses of survival curves were performed, comparing patients with increased CEA levels and those with CEA levels within normal limits, both in the overall series and in the different pTNM tumoral stages. Frequency of patients with CEA>5mg/l was 31%. The median clinical follow-up was 83 months. A poor survival rate was registered in the multivariate analysis of the whole series in patients with high CEA levels: hazard ratio (HR)=1.81; 95% confidence interval (95% CI)=(1.15-3.10); P=.012. This predictive value was only maintained in stage II in the survival analysis of the distinct tumoral stages (n=104): HR=3.02; 95% CI=(1.22-7.45); P=.017. Question: Prognostic value of preoperative carcinoembryogenic antigen: Is it useful in all stages of colorectal cancer? <|endoftext|> <|assistant|> Before treatment, 31% of our patients with colorectal cancer resected with curative intent had pathological CEA values. In the overall series, a high pretreatment CEA level showed an independent prognostic value for poor survival. When pTNM tumoral stages were analyzed separately, CEA level had predictive value only in pTNM II tumors.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: We sought to determine whether tizanidine, an alpha2-agonist, relieved thermal hyperalgesia in rats with surgically induced neuropathic pain. We used a Sprague-Dawley rat model in which a chronic constriction of the sciatic nerve caused the rats to develop postural changes, mechanical allodynia, and thermal hyperalgesia. Thermal hyperalgesia was verified through paw withdrawal latency (PWL). PWL was tested before surgery, after surgery, and after injections with tizanidine (0.5, 1.0, or 2.0 mg/kg) or normal saline. Ambulatory and total movements were evaluated by placing the rats in activity cages. Thermal hyperalgesia was induced in all rats after surgery. Tizanidine, but not saline, caused a significant improvement in PWL (P < 0.05), with complete reversal of thermal hyperalgesia at all doses on postoperative Day 6. Rats who received tizanidine 2 mg/kg maintained complete reversal of thermal hyperalgesia through postoperative Day 9. Some sedation was observed with tizanidine 2 mg/kg, but not with smaller doses. We conclude that tizanidine effectively reversed thermal hyperalgesia in a rat model. Question: Does systemic tizanidine hydrochloride ( Zanaflex ) relieve thermal hyperalgesia in rats with an experimental mononeuropathy? <|endoftext|> <|assistant|> This study was conducted to determine whether tizanidine could attenuate the thermal hyperalgesia that occurs in rats with surgically induced chronic constriction of the sciatic nerve. Tizanidine was effective in reducing sensitivity to heat, as measured by paw withdrawal latency, and did not cause sedation at smaller doses.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To determine whether rheumatologists working in Canada's largest academic rheumatology center (University Health Network/Mount Sinai Hospital) adhere to the 2002 American College of Rheumatology (ACR) guidelines for the management of rheumatoid arthritis (RA). Ten patients with RA seen between January 1 and December 30, 2005, were randomly selected from each rheumatologist. A standardized form was used to verify whether the following items were collected at each visit: (1) degree of joint pain, (2) duration of morning stiffness, (3) degree of fatigue, (4) number of tender/swollen joints, and (5) assessment of function. Items recommended for periodic assessment were also collected and included: (1) examination for joint damage, (2) erythrocyte sedimentation rate and/or C-reactive protein, and (3) radiographic assessment of joint damage (radiograph/magnetic resonance imaging). One hundred thirty charts and 313 total visits met inclusion criteria. No rheumatologist consistently assessed each ACR item. Of the recommended items, tender and swollen joint counts and pain were most commonly assessed (95%, 95%, and 69%, respectively). Functional assessment, morning stiffness, and fatigue were least commonly reported (48%, 46%, and 33%, respectively). Items recommended for periodic assessment were not regularly recorded. There was a trend for the recommended items to be reported more regularly for new patients, patients taking a disease modifying antirheumatic drug (DMARD), and patients for whom a DMARD was added or increased in dosage. Question: Are the 2002 American College of Rheumatology guidelines for the management of rheumatoid arthritis being followed in Canada's largest academic rheumatology center? <|endoftext|> <|assistant|> Rheumatologists follow many but not all of the recommendations included in the revised ACR guidelines. The reasons underlying the noncompliance to some of the recommendations are not fully understood. In order to improve the adoption of future clinical practice guidelines, the ACR may have to plan specific dissemination and implementation strategies and fund studies to formally assess the effect of guideline use on clinical outcomes.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Cardiovascular disease provides the greatest mortality risk in patients with nonalcoholic fatty liver disease (NAFLD). Clinical practice guidelines recommend statins to treat dyslipidemia in patients with NAFLD; however, the extent to which such patients receive statins has not been studied. We conducted a structured medical record review to assess for appropriate statin use in patients in a Veterans Administration facility with dyslipidemia and NAFLD as well as a parallel cohort without NAFLD. Appropriate statin use was defined as receipt of statins without a clinically significant, unjustified dose change during the study period. Of 255 patients with NAFLD and dyslipidemia, 152 (59.6 %) patients received appropriate statin care. Primary care providers (PCPs) recognized the presence of NAFLD in 106 patients (41.6 %). Among the 63 of 106 (59.4 %) patients who were on a statin at the time of detection, 24 (38.1 %) received a clinically significant dose reduction or discontinuation. Patients whose PCPs recognized the presence of NAFLD (adjusted OR = 0.34, 95 % CI = 0.18-0.64) were less likely to receive appropriate statin care than patients with undetected NAFLD. Also, patients with detected NAFLD were less likely than dyslipidemic patients without NAFLD to receive appropriate statin care (OR = 0.45, 95 % CI = 0.25-0.79). Question: Do statins Are Underutilized in Patients with Nonalcoholic Fatty Liver Disease and Dyslipidemia? <|endoftext|> <|assistant|> Statins are underused in patients with NAFLD and dyslipidemia. The most important determinant for inappropriate statin use was PCP recognition of NAFLD. While these results need to be confirmed in non-VA healthcare systems, they highlight the need for efforts to enhance PCP knowledge of existing guidelines regarding statin use in NAFLD.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Insect-derived serine protease inhibitors (serpins) exhibit multiple inhibitory activities, but so far, no functional roles for serpins of Musca domestica have been identified. Here, the functional features of M. domestica serine protease inhibitor (MDSPI16) were characterized. Hundred forty seven differentially expressed genes including the MDSPI16 gene were screened by constructing the subtractive cDNA library. The 1154-bp full-length MDSPI16 gene was cloned, and the recombinant MDSPI16 serpin protein was expressed as a 42.6 kDa protein in an Escherichia coli expression system. The recombinant MDSPI16 protein was purified using Ni-NTA affinity chromatography, and the inhibitory activity of MDSPI16 was assessed. MDSPI16 did not inhibit trypsin, papain, or proteinase K but strongly inhibited elastase (Ki = 2.8 nM) and chymotrypsin (Ki = 28 nM). The inhibitory activity of MDSPI16 remained stable over from 37 to 100 °C and from pH 2 to 12. Question: Does a serine protease inhibitor from Musca domestica larva exhibit inhibitory activity against elastase and chymotrypsin? <|endoftext|> <|assistant|> The MDSPI16 exhibited inhibitory activity against elastase and chymotrypsin and the inhibitory activity remained stable.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: In laboratory animals, repeated administration of drugs of abuse causes sensitization to their stimulant and rewarding effects. Neuroadaptations underlying sensitization could be related to those that contribute to addictive behaviors. An increased understanding of the molecular mechanisms of sensitization could lead to improved treatments for addiction. Since baclofen (BCF) co-administration has been reported to block the development and the expression of motor sensitization to morphine (MOR), the present study examined the hypothesis that a chronic treatment with BCF alone might reverse and/or prevent MOR-induced sensitization. Rats were first sensitized to MOR (saline or 10 mg/kg MOR i.p.; days 1-10) and then chronically treated with BCF (saline or 2 mg/kg BCF i.p.; days 11-20). Finally, the motility effect of MOR (10 mg/kg i.p.) was assessed 3 and 30 days after the end of BCF treatment. The same rats were again challenged with MOR on day 70, after a further period of saline or MOR treatment (days 51-60). Behavioral sensitization to MOR was observed in control animals but not in rats chronically treated with BCF (days 23 and 50). Thus, BCF completely reversed MOR-induced sensitization, and its effect was long lasting. However, a previous repeated BCF treatment did not prevent the development of sensitization to MOR both in naive and desensitized rats. Question: Does a GABA ( B ) agonist reverse the behavioral sensitization to morphine in rats? <|endoftext|> <|assistant|> The present results confirm that gamma-aminobutyric acid (GABA)(B) receptors play an important role in the expression of motor sensitization to MOR and suggest that GABA(B) agonists could be useful for reversing the neuroadaptations related to drug addiction.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: There are conflicting data regarding the impact of breastfeeding on the development of asthma in late childhood. Our aim with this study was to investigate the relationship between breastfeeding and the prevalence of asthma in children at 14 years. The Mater-University of Queensland Study of Pregnancy is a birth cohort of 7223 women and their infants recruited from a public antenatal clinic in Brisbane, Australia, between 1981 and 1984. Data regarding breastfeeding and the duration of breastfeeding were collected through the use of a questionnaire completed by the mother 6 months postdelivery, and the prevalence of asthma was determined through the use of a questionnaire completed by the mother 14 years postdelivery. Data regarding both breastfeeding and asthma were available for 4964 children. The prevalence of asthma in children at 14 years was 28.4%. Breastfeeding for > or =4 months was not found to have a significant effect on the prevalence of asthma in 14-year-olds. The unadjusted odds ratio of developing asthma at 14 years if the child was breastfed for > or =4 months was 1.03. The odds ratio of developing asthma did not change appreciably when allowance was made for potential confounding factors. Question: Does breastfeeding increase the risk of asthma at 14 years? <|endoftext|> <|assistant|> Data from this study indicate that breastfeeding neither increases nor decreases the prevalence of asthma in children at 14 years.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Desmopressin (DDAVP) is a synthetic derivative of vasopressin with hemostatic and fibrinolytic properties that has been used during surgery in patients with bleeding disorders. Our aim was to investigate the effect of DDAVP on lung and lymph node metastatic cell colonization using a preclinical mouse mammary carcinoma model of subcutaneous tumor manipulation and surgical excision. Female BALB/c mice bearing the highly aggressive F3II mammary carcinoma were subjected to repeated manipulations of primary tumors (0.5 kg/cm(2) during 2 min), followed (or not) by surgical excision. DDAVP was administered intravenously 30 min before and 24 h after each manipulation or surgery, at a dose of 2 microg/kg. At the end of the experiment, mice were sacrificed and necropsied. Tumor manipulation induced dissemination to the axillary nodes and increased up to 6-fold the number of metastatic lung nodules. Perioperative treatment with DDAVP dramatically reduced regional metastasis. The incidence of lymph node involvement in manipulated animals was 12% with DDAVP and 87% without treatment (P < 0.02). Histopathological analysis of axillary nodes from DDAVP-treated animals showed sinusal histiocytosis and no evidence of cancer cells. Metastatic lung nodules were also reduced about 65% in animals treated with DDAVP (P = 0.026). Question: Does desmopressin inhibit lung and lymph node metastasis in a mouse mammary carcinoma model of surgical manipulation? <|endoftext|> <|assistant|> Our results suggest a potential clinical application of DDAVP in the management of breast cancer, as well as other aggressive solid tumors. DDAVP may be useful to reduce the risk of metastatic cell colonization both during and after surgical manipulation.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Bupleurum polysaccharides (BPs), isolated from Bupleurum smithii var. parvifolium, possesses immunomodulatory activity, particularly on inflammation. Bacterial endotoxin lipopolysaccharide (LPS) triggers innate immune responses through Toll-like receptor 4 (TLR4) on host cell membrane. The present study was performed to evaluate whether the therapeutic efficacy of BPs on suppression of LPS's pathogenecity could be associated with the modulating of TLR4 signaling pathway. LPS stimulated expression and activation of factors in the TLR4 signaling system, including TLR4, CD14, IRAK4, TRAF6, NF-κB, and JNK, determined using immunocytochemical and/or Western blot assays. BPs significantly inhibited these effects of LPS. LPS increased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-12p40, and IFN-β) and NO production, evaluated using ELISA and Griess reaction assays, respectively. BPs antagonized these effects of LPS. Interestingly, BPs alone augmented secretion of some pro-inflammatory cytokines of non-LPS stimulated macrophages and enhanced phagocytic activity towards fluorescent E.coli bioparticles. In a rat model of acute lung injury (ALI) with pulmonary hemorrhage and inflammation, BPs ameliorated lung injuries and suppressed TLR4 expression. Question: Does bupleurum polysaccharides attenuate lipopolysaccharide-induced inflammation via modulating Toll-like receptor 4 signaling? <|endoftext|> <|assistant|> The therapeutic properties of BPs in alleviating inflammatory diseases could be attributed to its inhibitory effect on LPS-mediated TLR4 signaling.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Platelet activation via the Fcγ receptor IIa (FcγRIIa) is implicated in the pathogenesis of immune complex (IC)-mediated thrombocytopenia and thrombosis (ITT). We previously showed that ICs composed of antigen and antibodies targeting CD40 ligand (CD40L) or β2 Glycoprotein I (β2GPI) induce ITT in mice transgenic for human FcγRIIa (hFcR) but not wild-type controls (which lack FcγRIIa). Here we evaluated the contribution of the guanine nucleotide exchange factor, CalDAG-GEFI, and P2Y12, key regulators of Rap1 signaling in platelets, to ITT induced by these clinically relevant ICs. Pre-formed anti-CD40L or anti-β2GPI ICs were injected into hFcR/Caldaggef1(+/+) or hFcR/Caldaggef1(-/-) mice, with or without clopidogrel pretreatment. Animals were observed for symptoms of shock for 30 min, during which time core body temperature was monitored. Platelet counts were obtained before and 30 min after IC injection. Lungs were assessed for thrombosis by histology or near-infrared imaging. Both CD40L and β2GPI ICs rapidly induced severe thrombocytopenia, shock and a reduction in body temperature in hFcR/Caldaggef1(+/+) mice. hFcR/Caldaggef1(-/-) mice were protected from CD40L and β2GPI IC-induced thrombocytopenia and shock, whereas P2Y12 inhibition had only a modest effect on IC-induced ITT. Consistent with these findings, IC-induced integrin activation in vitro and the accumulation of activated platelets in the lungs of IC-challenged mice was strongly dependent on CalDAG-GEFI. Question: Does calDAG-GEFI deficiency protect mice from FcγRIIa-mediated thrombotic thrombocytopenia induced by CD40L and β2GPI immune complexes? <|endoftext|> <|assistant|> Our studies demonstrate that CalDAG-GEFI plays a critical role in platelet activation, thrombocytopenia and thrombosis induced by clinically relevant ICs in mice. Thus, CalDAG-GEFI may be a promising target for the intervention of IC-associated, FcγRIIa-mediated thrombotic conditions.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Sulfasalazine (SSZ) is a commonly used drug in the treatment of inflammatory diseases such as rheumatoid arthritis and Crohn's disease. In both diseases, the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) plays a prominent role. In these studies, we investigated the mechanism by which SSZ inhibits TNFalpha expression in macrophages and macrophage-like cell lines. Monocyte-derived macrophages and several macrophage-like cell lines were exposed to SSZ in vitro, and the effect on TNFalpha expression was monitored by reverse transcriptase-polymerase chain reaction and Western blot analysis. In addition, the effects of SSZ in vivo were examined by intraperitoneally injecting mice with SSZ, after which peritoneal cells were harvested and examined using various staining methods. Preincubation of macrophages with SSZ, but not with methotrexate, inhibited lipopolysaccharide (LPS)-induced TNFalpha expression. Inhibition of TNFalpha expression by SSZ coincided with the induction of apoptosis, as judged by the appearance of morphologic changes typical of apoptosis, such as nuclear condensation and fragmentation. Induction of apoptosis by SSZ was confirmed by TUNEL analysis and by the detection of cleaved U1-70K, a substrate of caspase 3. Intraperitoneal injections of SSZ in mice resulted in the induction of apoptosis of peritoneal cells within a few hours. SSZ-induced cleavage of the U1-70K protein was inhibited by Zn2+ and by specific inhibitors of caspases 3 and 8, but not caspases 1 and 9. Interestingly, the reduced expression of LPS-induced TNFalpha in the presence of SSZ was restored by inhibition of caspase 8. Question: Does the antiinflammatory drug sulfasalazine inhibit tumor necrosis factor alpha expression in macrophages by inducing apoptosis? <|endoftext|> <|assistant|> Inhibition of TNFalpha expression in macrophages by SSZ is due to the induction of apoptosis and involves the activation of caspase 8.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The 2007 World Cancer Research Fund/American Institute for Cancer Research expert report concluded that foods containing vitamin C probably protect against esophageal cancer and fruits probably protect against gastric cancer. Most of the previous evidence was from case-control studies, which may be affected by recall and selection biases. More recently, several cohort studies have examined these associations. We conducted a systematic literature review of prospective studies on citrus fruits intake and risk of esophageal and gastric cancers. PubMed was searched for studies published until 1 March 2016. We calculated summary relative risks and 95 % confidence intervals (95 % CI) using random-effects models. With each 100 g/day increase of citrus fruits intake, a marginally significant decreased risk of esophageal cancer was observed (summary RR 0.86, 95 % CI 0.74-1.00, 1,057 cases, six studies). The associations were similar for squamous cell carcinoma (RR 0.87, 95 % CI 0.69-1.08, three studies) and esophageal adenocarcinoma (RR 0.93, 95 % CI 0.78-1.11, three studies). For gastric cancer, the nonsignificant inverse association was observed for gastric cardia cancer (RR 0.75, 95 % CI 0.55-1.01, three studies), but not for gastric non-cardia cancer (RR 1.02, 95 % CI 0.90-1.16, four studies). Consistent summary inverse associations were observed when comparing the highest with lowest intake, with statistically significant associations for esophageal (RR 0.77, 95 % CI 0.64-0.91, seven studies) and gastric cardia cancers (RR 0.62, 95 % CI 0.39-0.99, three studies). Question: Do an update of the WCRF/AICR systematic literature review on esophageal and gastric cancers and citrus fruits intake? <|endoftext|> <|assistant|> Citrus fruits may decrease the risk of esophageal and gastric cardia cancers, but further studies are needed.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: There is little direct evidence that fibroblasts are involved in the progression of the renal interstitial fibrosis in human glomerulonephritis. With the availability of a new specific marker for fibroblasts, we determined the presence of fibroblasts in kidneys with IgA nephropathy (IgAN) and correlated their numbers with various clinical parameters. In particular, we also prospectively asked if the number of fibroblasts in the renal interstitium correlates with prognosis. Cells positive for fibroblast-specific protein 1 (FSP1) were localized in renal biopsy specimens using immunohistochemistry with anti-FSP1 antibody. Clinical features were analyzed by one-way analysis of variance (ANOVA) with the Bonferroni correction. To assess the prognostic impact of the number of FSP1+ fibroblasts on renal survival in 142 patients with normal serum creatinine, the relationship between covariates to renal survival were evaluated univariately using the log-rank test and multivariately using Cox proportional hazards. Fibroblasts identified by their expression of FSP1 accumulate in areas showing severe interstitial fibrosis. Some tubular epithelial cells undergoing epithelial-mesenchymal transition (EMT) in fibrotic areas also express FSP1. Numbers of FSP1+ fibroblasts directly correlate with serum creatinine (r = 0.74, P < 0.0001) and inversely correlate with estimated creatinine clearance (r = -0.54, P < 0.0001), and by multivariate analysis, the clinical factors influencing renal survival are urinary protein excretion [> or = 1.0 g/day, relative risk (RR) = 4.20, P= 0.032], hypertension (RR 5.85, P = 0.0027), and > or = 20 FSP1+ fibroblasts per high power field (HPF) (RR 7.39, P = 0.0015). Staining for FSP1+ fibroblasts is largely nonoverlapping with alpha-smooth muscle actin+ (alpha-SMA) cells in the interstitium. Question: Is fibroblast-specific protein 1 a specific prognostic marker for renal survival in patients with IgAN? <|endoftext|> <|assistant|> The target protein FSP1 identifies human fibroblasts and tubular epithelium undergoing EMT, and distinguishes them from the diaspora of alpha-SMA+ vascular smooth muscle cells. FSP1+ fibroblasts are critically related to the progression of IgAN; consequently, staining FSP1 in renal biopsy specimens provides a valuable histologic index of progression.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Helicobacter pylori (H. pylori) is the major cause of chronic active gastritis and peptic ulcer disease. Recent studies have shown that H. pylori produces various cytokines that are related to neutrophil or mononuclear cell accumulation. Interleukin-17 (IL-17) is the founding member of an emerging family of inflammatory cytokines whose biological activities remain incompletely defined. In this study, the contributions of IL-17 to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using IL-17 gene-knockout (IL-17(-/-)) mice. IL-17(-/-)and wild-type C57BL/6 mice were challenged with H. pylori CPY2052 (2 x 10(8) CFU/mL) and the histological and microbiological evaluation were carried out at specified times. IL-17 and myeloperoxidase (MPO) protein levels in tissues were assayed in duplicate using ELISA kits. In wild-type mice, IL-17 was undetected at baseline; however, the protein expression of IL-17 was induced after infection with H. pylori. A severe infiltration of neutrophils appeared in the submucosa and the lamina propria in wild-type mice. In contrast, the degree of neutrophil infiltration in IL-17(-/-) mice was significantly lower than that in wild-type mice. Although wild-type mice infected with H. pylori showed drastically higher MPO activity compared with uninfected wild-type mice, any significant increase in the enzyme activity was not revealed in infected IL-17(-/-) mice. The number of H. pylori colonized in the stomach of IL-17(-/-) mice was significantly lower than that of wild-type mice from 1 to 6 months after infection. Question: Is iL-17 involved in Helicobacter pylori-induced gastric inflammatory responses in a mouse model? <|endoftext|> <|assistant|> These results suggest that IL-17 may play an important role in the inflammatory response to the H. pylori infection and ultimately influence the outcome of the H. pylori-associated disease.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The epidemiology and clinical course of candidaemia in patients with acute leukaemia, a population frequently exposed to antifungals, have not been extensively studied. In the present contemporary series of acute leukaemia patients, we describe patient characteristics, Candida species and MIC distributions and investigate the association between antifungal resistance and all-cause mortality. We performed a retrospective review of medical records and microbiological data of adult patients with acute leukaemia or high-risk myelodysplastic syndrome with at least one positive blood culture for Candida species at the MD Anderson Cancer Center between January 2008 and October 2012. Susceptibility was defined according to the 2012 epidemiological cut-off values and clinical breakpoints. We identified 67 episodes of candidaemia in 65 patients. Almost all episodes (94%) occurred in patients who were receiving antifungal agents, 71% in patients receiving an echinocandin. Almost all isolates (99%) were of non-albicans Candida species [most frequently Candida parapsilosis (32%), Candida tropicalis (23%) and Candida glabrata (20%)]. Caspofungin non-susceptibility was significantly associated with fluconazole resistance (P < 0.001). Non-susceptibility to caspofungin and multidrug resistance were associated with excess 14 day [adjusted HR (aHR) 3.02 (95% CI 1.28-7.09), P = 0.011 and aHR 3.02 (95% CI 1.27-7.14), P = 0.012, respectively] and 30 day [aHR 2.96 (95% CI 1.38-6.37), P = 0.005 and aHR 2.86 (95% CI 1.31-6.21), P = 0.008, respectively] all-cause mortality. Question: Are the ever-evolving landscape of candidaemia in patients with acute leukaemia : non-susceptibility to caspofungin and multidrug resistance associated with increased mortality? <|endoftext|> <|assistant|> In patients with acute leukaemia, a shift in candidaemia epidemiology was noted with a 99% predominance of non-albicans species. Non-susceptibility of Candida strains to caspofungin or multidrug resistance were independent markers of poor outcome in this patient population.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The aim of this study was to evaluate the usefulness of whole gut irrigation with a mannitol solution in the prevention of hepatic encephalopathy in patients with cirrhosis and bleeding oesophageal or gastric varices. The randomized prospective study included 40 patients with a mean age of 59.6 +/- 9.6 years. Bleeding was controlled by a Blakemore or Linton haemostatic tube, in all cases. The patients were divided into a "mannitol" group (n = 20) treated by whole gut irrigation with a 5 L solution containing 40 g/L of mannitol, and a "control" group (n = 20). The two groups did not differ for age, sex, aetiology of cirrhosis or gastrointestinal bleeding, Child-Pugh classification, delay of minimum fare or the number of transfused blood units. The onset of hepatic encephalopathy was investigated within the first 48 hours after the beginning of gastrointestinal bleeding. The grade of hepatic encephalopathy was established using an index with 4 criteria (mental status, asterixis, number connection test, arterial ammonia concentrations), each with 5 grades of severity. There were no adverse side-effects in the mannitol group. The incidence of hepatic encephalopathy (5 vs 30%) and the length of hospitalization (8.2 +/- 2.3 vs 13.6 +/- 3.1 days) were significantly decreased in the mannitol group (P<0.05). Mortality was not different between the 2 groups (P = 0.4). Question: Is the intestinal lavage with a solution of mannitol effective in the prevention of post-hemorrhagic hepatic encephalopathy in patients with liver cirrhosis? <|endoftext|> <|assistant|> Whole gut mannitol irrigation appears to be an effective, simple, inexpensive, well tolerated technique in the prevention of hepatic encephalopathy after variceal bleeding in patients with cirrhosis.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Detection of oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) is an important adjunct to the diagnosis of multiple sclerosis (MS) and clinically isolated syndromes (CIS). OCBs are considered present if two or more extra IgG bands are present in CSF in comparison to a simultaneously collected serum sample. However, using isoelectric focusing and immunofixation with anti-IgG, we observed two distinct banding patterns, one in which the bands were numerous and prominent (which we termed 'delta') and a much more subtle pattern, with fewer, more indistinct bands ('theta'). To perform a prospective study to determine the diagnostic implications of the two OCB patterns for multiple sclerosis. Over a 2-year period, 56 consecutive CSF samples with OCBs were identified. Clinical information and radiological data were collected and correlated with the two banding patterns. : Of the 56 positive CSF samples, 46 (82%) demonstrated a delta pattern, and 10 (18%), a theta pattern. The delta pattern was associated with MS/CIS in 34 of 46 (74%) samples, compared with zero of the 10 theta samples (0%, p < 0.001). Exclusion of the theta pattern samples increased the positive predictive value of OCB testing from 61% to 74% for MS/CIS. Question: Does differentiating patterns of oligoclonal banding in the cerebrospinal fluid improve diagnostic utility for multiple sclerosis? <|endoftext|> <|assistant|> The diagnostic significance of oligoclonal bands in CSF for MS/CIS can be improved by restricting interpretation to the delta banding pattern alone.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Teaching electrocardiogram (ECG) interpretation is a recommended component of the family practice residency curriculum. Published information concerning the ECG interpretation ability of residents is sparse. This study sought to ascertain the baseline knowledge of family practice residents' ECG interpretation skills and extent of improvement after one year of training. A 15 ECG examination was administered to 38 PG-1 and 14 upper level residents at 5 residency programs at the beginning of the academic year and to residents at the authors' program at the end of the academic year. Pre-test scores among the five programs were compared using an analysis of variance (ANOVA). Pre-test and post-test scores were compared using a paired randomization test. No difference was found between average scores from each site, or between the beginning and end of the academic year. Residents were more likely to misinterpret items such as myocardial infarction, myocardial ischemia, and atrial fibrillation. Question: Are family practice residents able to interpret electrocardiograms? <|endoftext|> <|assistant|> Residents in family practice have considerable deficiencies in ECG interpretation skills. Further studies are needed to determine effective ECG teaching curricula.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Possible transfusion-related acute lung injury (pTRALI) cases by definition have a clear temporal relationship to an alternative recipient risk factor for acute respiratory distress syndrome (ARDS). We questioned whether transfusion factors are important for the development of pTRALI. In this nested case-control study, we prospectively identified 145 consecutive patients with pTRALI and randomly selected 163 transfused controls over a 4-year period at the University of California at San Francisco and the Mayo Clinic (Rochester, Minnesota). For pTRALI, we found evidence against transfusion being important: receipt of plasma from female donors (odds ratio [OR], 0.82; 95% confidence interval [CI], 0.29-2.3; p = 0.70), total number of units transfused (OR, 0.99; 95% CI, 0.89-1.10; p = 0.86), and number of red blood cell and whole blood units transfused (OR, 0.78; 95% CI, 0.59-1.03; p = 0.079). In contrast, we found that risk for pTRALI was associated with additional recipient factors: chronic alcohol abuse (OR, 12.5; 95% CI, 2.8-55; p < 0.001), current smoker (OR, 4.2; 95% CI, 1.67-10.8; p = 0.0024), shock before transfusion (OR, 4.6; 95% CI, 2.0-10.7; p < 0.001), and positive fluid balance before transfusion (OR, 1.32/L; 95% CI, 1.20-1.44; p < 0.001). Question: Do recipient clinical risk factors predominate in possible transfusion-related acute lung injury? <|endoftext|> <|assistant|> Recipient risk factors for ARDS rather than transfusion risk factors predominate in pTRALI.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: In 2002, as part of a National Hospital Pharmaceutical Strategy, the New Zealand (NZ) government agency PHARMAC commenced a 3-year period of negotiating prices for 90% of hospital pharmaceuticals on behalf of all NZ public hospitals. The present study was undertaken to determine the effects of this first year of "pooled procurement." Using price changes and volume data for each of their top 150 pharmaceutical items, chief pharmacists at 11 public hospitals calculated projected cost savings for the financial year July 2003 to June 2004. Researchers calculated total projected savings for all 11 hospitals, and for three types of hospitals. Estimates of projected savings were made for all 29 major public hospitals by using savings per bed and savings per bed-day. A sensitivity analysis was undertaken. Items showing savings were categorized by using the Anatomical Therapeutic Chemical classification system. For the 11 hospitals, the top 150 items comprised 612 different items. Projected savings for 2003 to 2004 were NZ dollar 2,652,814, NZ dollar 658,984, and NZ dollar 127,952 for tertiary, secondary, and rural/special hospitals, respectively. Percentage savings as a median (range) of the total top 150 expenditure were: tertiary 5.28% (3.09-16.05%), secondary 7.41% (4.67-12.85%), and rural/special 9.55% (6.27-10.09%). For all 29 hospitals, estimated projected savings were NZ dollar 5,234,919 (NZ dollar 3,304,606-NZ dollar 8,044,482) by savings per bed, and NZ dollar 5,255,781 (NZ dollar 2,936,850-NZ dollar 8,693,239) by savings per bed-day. The main contributors to savings were: agents for infections, the nervous system, musculoskeletal system, and blood/blood-forming organs. Question: Managing prices for hospital pharmaceuticals: a successful strategy for New Zealand? <|endoftext|> <|assistant|> The first year of pooled procurement under the National Hospital Pharmaceutical Strategy (2002-2003) has resulted in moderate savings. For all 29 major public hospitals, savings of around NZ dollar 5.2 million (dollar 2.9 million-dollar 8.7 million) or 3.7% were projected for 2003 to 2004. Longer-term effects, however, on patient outcomes and availability of pharmaceuticals, as well as on pharmaceutical expenditure, have yet to be evaluated.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: A low body mass index (BMI) has been shown to be an independent indicator of poor prognosis in patients with COPD. However, some studies suggest that muscle mass depletion (MD) is the main factor responsible for the negative effects attributable to malnutrition. To evaluate the prognostic influence of MD estimated from anthropometric parameters. Mortality was studied in a prospective cohort of 96 male patients with COPD (average age, 69 +/- 9 years; FEV1 percentage of predicted, 44 +/- 18% [ +/- SD]) followed up for 3 years, with an evaluation of the prognostic influence of the following anthropometric parameters: BMI, mid-arm muscle area (MAMA), and fat-free mass index. Other risk factors were also analyzed, such as age, comorbidity (Charlson index), basal dyspnea index, the St. George's Respiratory Questionnaire score, the number of hospital admissions in the year prior to nutritional evaluation, the number of hospital admissions in the year immediately after nutritional evaluation (Hpost), spirometry, and blood gases. In the multivariate study, Pa(CO2) (p = 0.003; hazard ratio, 1.08), Hpost (p = 0.005, hazard ratio, 4.63), and a MAMA value less than or equal to percentile 25 of the reference value (p25) [p = 0.025; hazard ratio, 3.78] were found to be independent indicators of poor prognosis. Respiratory mortality after 12, 24, and 36 months in the patients with MAMA < or = p25 was 12.1%, 31.4%, and 39.2%, respectively, vs 5.9%, 7.9%, and 13% in the group of patients without MD (p = 0.006). In normal-weight or overweight patients, MAMA < or = p25 increased the risk of mortality 3.4-fold (p = 0.032). Question: Is mid-arm muscle area a better predictor of mortality than body mass index in COPD? <|endoftext|> <|assistant|> MD is a better predictor of mortality than BMI in patients with COPD, fundamentally in normal-weight or overweight patients. The prognostic influence of MD can be estimated indirectly by determining the MAMA, an inexpensive, simple, and rapidly obtained anthropometric measure.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Nearly all primary uveal melanoma (UM) that metastasize involve the liver. Hepatocyte growth factor (HGF) is proposed to be an important microenvironmental element in attracting/supporting UM metastasis through activation of MET. The majority (>85%) of UM express mutations in the G-alpha proteins, that drive the MEK-ERK1/2 pathway. Thus, we proposed that the combination of MET and MEK inhibition would inhibit the growth and migration of G-alpha protein mutant versus non-mutant UM cells. Western-blots demonstrated the relative protein levels of ERK1/2 and MET in UM cells. Cells were treated with the small molecule inhibitors AZD6244 (MEKi) and/or MK-8033 (METi) and downstream markers evaluated. Further studies determined the effect of combination MEKi and METi treatment on cell growth, apoptosis and migration. All G-alpha protein mutant UM cell lines express MET mRNA and protein. The level of mRNA expression correlates with protein expression. MEKi, but not METi treatment results in markedly reduced ERK1/2 phosphorylation. Either MEKi or METi treatment alone results in reduced cell proliferation, but only modest induction of apoptosis. The combination MEKi+METi results in significant reduction of proliferation in G-alpha protein mutant cells. UM cell migration was blocked by METi, but not MEKi treatment. Question: Do simultaneous inhibition of the HGF/MET and Erk1/2 pathways affect uveal melanoma cell growth and migration? <|endoftext|> <|assistant|> MET protein expression showed no correlation with G-alpha protein mutation status. Combining MEKi with METi treatment has added benefit to either treatment alone in reducing G-alpha protein mutant UM cell growth. Combining METi with MEKi treatment adds the effect of limiting uveal melanoma cell migration.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: American Joint Committee on Cancer (AJCC) staging for pancreatic adenocarcinoma is a validated predictor of prognosis but insufficiently discriminates postresection survival. We hypothesized that genetic analysis of resected cancers would correlate with tumor biology and postoperative survival. Resected pancreatic ductal and ampullary adenocarcinomas (n = 50) were analyzed for loss of heterozygosity (LOH) at 15 markers including 5q(APC), 6q(TBSP2), 9p(p16), 10q(PTEN), 12q(MDM2), 17p(TP53), and 18q(DCC/SMAD4). KRAS exon 1 mutations were detected by sequencing. The primary endpoint of this interim data analysis was survival at 18 month median follow-up. Negative margins were achieved in 43 (86%) cases. AJCC stage was: Ia/b (3), IIa (16), IIb (31). KRAS mutations were detected in 31 cases (62%) and LOH in 26 (52%) with mean fractional allelic loss score 23 +/- 16%. Median survival was significantly shorter with LOH (15.2 months versus not reached; p = 0.021) and KRAS mutations (19.6 months versus not reached; p = 0.038). Combining KRAS mutation with LOH was a powerful negative predictor in Cox regression (HR = 10.6, p = 0.006). Stage, nodal and margin status were not predictive of survival. Question: Does loss of heterozygosity predict poor survival after resection of pancreatic adenocarcinoma? <|endoftext|> <|assistant|> LOH and KRAS mutations indicate aggressive tumor biology and correlate strongly with survival in resected pancreatic ductal and ampullary carcinomas. Genetic analysis may improve risk stratification in future clinical trials.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Recent surgical reports on coarctation of the aorta have primarily focused on the relative merits of various operative techniques. However, appropriate timing for elective repair remains unclear. In a retrospective analysis we examined the surgical outcomes in 176 consecutive patients undergoing repair of coarctation of the aorta in our institution over a 25-year period. Ninety-nine percent of the patients had follow-up for a median of 7.5 years. A total of 13 patients have died (7.4% overall mortality). Nine of these patients had associated complex intracardiac anomalies. There was no mortality in the 113 patients with isolated coarctation. Residual or recurrent coarctation occurred in 27 patients (15.3%). The age at operation and the type of surgical repair did not have an effect on the incidence of recurrence. Persistent or late hypertension was identified in 18 of the 107 patients who have been followed up for more than 5 years (16.8%). A total of 48 patients operated on during infancy have been followed up for more than 5 years. Only 2 have developed late hypertension (4.2%). Both of these patients had recurrence. In contrast, 16 of the 59 patients operated on after a year of age had late hypertension (27.1%). Question: Does repair of coarctation of the aorta during infancy minimize the risk of late hypertension? <|endoftext|> <|assistant|> To minimize the risk of persistent hypertension, elective repair of coarctation should be performed within the first year of life.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Steatosis is the most common consequence of acute alcohol abuse and may predispose to more severe hepatic disease. Increased lipogenesis driven by the sterol response element binding protein (SREBP) transcription factors is essential for steatosis associated with chronic alcohol ingestion, but the mechanisms underlying steatosis following acute alcohol exposure are unknown. Zebrafish larvae represent an attractive vertebrate model for studying alcoholic liver disease (ALD), because they possess the pathways to metabolize alcohol, the liver is mature by 4 days post-fertilization (dpf), and alcohol can be simply added to their water. Exposing 4 dpf zebrafish larvae to 2% ethanol (EtOH) for 32 hours achieves approximately 80 mM intracellular EtOH and up-regulation of hepatic cyp2e1, sod, and bip, indicating that EtOH is metabolized and provokes oxidant stress. EtOH-treated larvae develop hepatomegaly and steatosis accompanied by changes in the expression of genes required for hepatic lipid metabolism. Based on the importance of SREBPs in chronic ALD, we explored the role of Srebps in this model of acute ALD. Srebp activation was prevented in gonzo larvae, which harbor a mutation in the membrane-bound transcription factor protease 1 (mbtps1) gene, and in embryos injected with a morpholino to knock down Srebp cleavage activating protein (scap). Both gonzo mutants and scap morphants were resistant to steatosis in response to 2% EtOH, and the expression of many Srebp target genes are down-regulated in gonzo mutant livers. Question: Does hepatic steatosis in response to acute alcohol exposure in zebrafish require sterol regulatory element binding protein activation? <|endoftext|> <|assistant|> Zebrafish larvae develop signs of acute ALD, including steatosis. Srebp activation is required for steatosis in this model. The tractability of zebrafish genetics provides a valuable tool for dissecting the molecular pathogenesis of acute ALD.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The power spectrum of the electroencephalogram (EEG) may be analyzed to provide quantitative measures of EEG activity (e.g., spectral edge, which defines the highest EEG frequency at which significant activity is found). The current study tested the hypothesis that spectral edge and similar measures distinguish different functional depths of anesthesia in humans. Three groups were studied. Group 1 consisted of 34 surgical patients (ASA physical status 1 or 2) who received 0.6, 1.0 and 1.4 MAC isoflurane anesthesia. A subgroup (group 2) of group 1 was tested during 1.0 MAC isoflurane anesthesia at surgical incision. Group 3 consisted of 16 volunteers who listened to an audiotape while receiving 0.15, 0.3, and 0.45 MAC isoflurane or 0.3, 0.45, and 0.6 MAC nitrous oxide in oxygen. The audiotape contained information designed to test implicit and explicit memory formation. We tested the ability of six EEG parameters (spectral-edge, 95th percentile power frequency, median power, and zero crossing frequencies and total power in the alpha- [8-13 Hz] and delta- [< 4 Hz] power ranges) to predict movement after surgical incision, purposeful response to command, or memory of information presented during anesthetic administration. Isoflurane decreased EEG activity in group 1 in a dose-related fashion. The 55% of group 2 who made purposeful movements in response to incision did not differ in their EEG from nonresponders (e.g., spectral edge 19.8 +/- 3.1 vs. 19.3 +/- 2.6 Hz, mean +/- SD). In group 3, memory of the information presented did not correlate with values of any EEG parameter. Response to verbal command was associated with lower anesthetic concentrations and with smaller alpha- and delta-band power (298 +/- 66 vs. 401 +/- 80 watts; and 75 +/- 20 vs. 121 +/- 49 watts, mean +/- SD), but there was no difference in values for other parameters. Question: Does the electroencephalogram predict depth of isoflurane anesthesia? <|endoftext|> <|assistant|> We conclude that our EEG measures do not predict depth of anesthesia as defined by the response to surgical incision, the response to verbal command or the development of memory.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: It is recommended that patients with impending abdominal compartment syndrome (ACS) should be volume loaded to insure the adequate preload. We evaluated our prospective resuscitation database to determine how patients who developed ACS differ from non-ACS patients in response to early volume loading. Over 36 months, 152 consecutive high-risk patients were resuscitated by a standard intensive care unit (ICU) protocol that escalates interventions in nonresponders. Interventions, responses, and outcomes are prospectively collected and the characteristics of ACS and non-ACS patients were compared. Twenty-three patients (15%) developed ACS and were decompressed 8 +/- 1 hours after ICU admission. The ACS and non-ACS patients had similar demographics and injury severity. The severity of pre-ICU shock tended to be greater in the ACS patients. During the first 8 hours of ICU resuscitation, patients who developed ACS received more blood transfusions (11 +/- 2 versus 2 +/- 0.2 units; P<0.05) and crystalloids (13 +/- 2 versus 4 +/- 0.3 L; P<0.05). As a result, pulmonary capillary wedge pressure increased more in the ACS patients (20 +/- 1.5 versus 15 +/- 0.5 mm Hg; P<0.05), but comparatively the cardiac index did not (3.2 +/- 0.2 versus 4.2 +/- 0.1 L/min/m(2); P<0.05) and the ACS patients developed pathologic elevations of gastric regional CO(2) pressures (70 +/- 7 versus 48 +/- 1 mm Hg P<0.05). Question: Do patients with impending abdominal compartment syndrome respond to early volume loading? <|endoftext|> <|assistant|> Conventional preload directed resuscitation to enhance cardiac function is not effective in patients with impending ACS, and this traditional resuscitation strategy is detrimental in this subgroup of patients.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Health is an important aspect of individuals' lives as they age. The aim of this study was to examine the relationship of sociodemographic factors, diagnosed chronic health conditions, and current depression with attitudes to aging in midlife. A cross-sectional baseline analysis was conducted on the first 300 participants from the Canterbury Health, Ageing and Life Course study in New Zealand, a stratified randomized community longitudinal study of adults recruited between 49 and 51 years. Attitudes were measured using the Attitudes to Aging Questionnaire (AAQ) and analyzed with a range of prevalent diagnosed chronic conditions, current depression, and sociodemographic variables. Individuals perceived their physical aging more negatively after a diagnosis of hypertension, arthritis or asthma. Diagnosed lifetime depression and anxiety, and current depression, showed strong relationships with attitudes to aging across domains. After controlling for sociodemographic factors and current depression, individuals with diagnosed hypertension, arthritis, asthma, lifetime depression or anxiety continued to report significantly more negative attitudes to aging. Current depression showed the strongest associations with attitudes to aging and mediated relationships of health on attitudes to aging. Question: Are attitudes to aging in midlife related to health conditions and mood? <|endoftext|> <|assistant|> Physical and mental health are related to attitudes to aging. Most chronic conditions examined are significantly associated with attitudes toward aging in the physical change domain. Diagnosed lifetime depression and anxiety, and current depression, are negatively related across attitudinal domains. Individuals can feel positive about aging while experiencing poorer health, but this is more difficult in the presence of low mood.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Allergic and nonallergic rhinitis with eosinophilia syndrome are characterized by tissue eosinophilia and nasal mucosal injury. Recently, it has been shown that the adherence of eosinophils and other leukocytes to epithelial cells is mediated by intercellular adhesion molecule-1 (ICAM-1) and related adherence-promoting glycoproteins. In this study we examined the constitutive expression of ICAM-1 on human nasal epithelial cells (HNECs), and the effects of interferon-gamma, tumor necrosis factor-gamma eosinophil major basic protein, and eosinophil cationic protein on the regulation of ICAM-1 expression on these cells. Similar studies were performed with A549 pneumocytes as comparative epithelial cells. Constitutive expression of ICAM-1 was significantly higher on cultured HNECs than on A549 cells, although nasal epithelial cells in tissue specimens did not demonstrate detectable levels of ICAM-1. This spontaneous expression of ICAM-1 on cultured HNECs may explain the unique susceptibility of the nasal mucosa to rhinovirus infection, because ICAM-1 is the epithelial cell receptor for most rhinoviruses. Physiologic concentrations of major basic protein and eosinophil cationic protein stimulated significant upregulation of ICAM-1 on HNECs, which was comparable to that produced by interferon-gamma and tumor necrosis factor-alpha. In contrast, these eosinophil constituents did not stimulate ICAM-1 upregulation on A549 alveolar epithelial cells, although A549 cells did respond to interferon-gamma and tumor necrosis factor-alpha. Question: Do cytokines and eosinophil-derived cationic proteins upregulate intercellular adhesion molecule-1 on human nasal epithelial cells? <|endoftext|> <|assistant|> The observation that eosinophil products upregulate ICAM-1 on HNECs suggests a positive feedback mechanism, in which the products released from migrating eosinophils might promote additional HNEC-leukocyte adherence by enhancing interactions between leukocyte beta 2 integrins (CD11/18) and nasal epithelial ICAM-1.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Glutamate transporters are responsible for removing glutamate from the extracellular space and have the potential to protect neurons from excitotoxicity. In the present study, the effects of ceftriaxone and (2R, 4R)-APDC (APDC) on the protein expression of GLAST and GLT-1, the rate of glutamate uptake, and neuroprotection were evaluated in a cell culture model of glutamate excitotoxicity. Mixed neuron/astrocyte cultures were prepared from 1 day old rat pups. Protein levels of GLAST and GLT-1 glutamate transporters were quantified using In-Cell Western techniques after acute or 5-day treatment with either ceftriaxone or APDC. Glutamate uptake was measured using Michaelis-Menten kinetics to evaluate the effects of 5-day treatment with ceftriaxone or APDC. Neuronal cell death in response to a 10-minute 1 mM glutamate challenge was measured following 5-day treatment with either ceftriaxone or APDC. Five-day treatment with 100 μM ceftriaxone significantly increased both GLAST and GLT-1 protein levels 31.3% and 47.5% above control, respectively, increased the Vmax 29.3%, increased the Km of glutamate uptake 117.9%, and reduced neuronal death 22.0% after a 1 mM glutamate challenge. Five-day treatment with 1 mM APDC significantly increased GLAST protein levels 27.6%, increased the Vmax 92.4%, increased the Km of glutamate transport 118.9%, and decreased neuronal death 36.8% after a 1 mM glutamate challenge. Question: Does pharmacological enhancement of glutamate transport reduce excitotoxicity in vitro? <|endoftext|> <|assistant|> Chronic treatment with ceftriaxone or APDC provided neuroprotection from glutamate excitotoxicity while increasing GLAST and GLT-1 protein levels and increasing glutamate uptake. These compounds may have therapeutic potential in chronic excitotoxic neurodegenerative diseases.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Since maternal diabetes may affect fetal development and the umbilical cord provides an extension of the fetal vasculature, we decided to investigate cords' biological responses to maternal diabetic milieu. Using microarray analysis, we determined the gene expression profiles in the umbilical cords of six neonates born to type 1 diabetic mothers and in six control cords. Umbilical cord tissue was collected immediately after elective cesarean section. Expression data were confirmed by real-time polymerase chain reaction (11 genes). Additionally, the same umbilical cords were analyzed histologically. Two hundred eighty six genes were differentially expressed in the umbilical cords from diabetic pregnancies compared to the controls (fold change ±1.5 and P < 0.01). Maternal diabetes had a major effect on the expression of genes involved in vascular development (Bone morphogenetic protein 4, Delta-like 1, and Notch homolog 4), vessel wall integrity (Collagen type VIII alpha 1, Myocyte enhancer factor 2C, and Matrix metalloproteinase 2), and vascular function (Natriuretic peptide precursor B, Endothelin 1, Endothelin receptor B, Cyclooxygenase 1, and Phosphodiesterase 5A). Maternal diabetes was associated with thicker umbilical vein intima-media layers and larger umbilical vein and artery intima-media areas compared to the controls. Question: Does maternal diabetes induce changes in the umbilical cord gene expression? <|endoftext|> <|assistant|> Maternal diabetic environment seems to alter umbilical cord expression of genes involved in the regulation of vascular development and function with simultaneous umbilical vessel muscle layer thickening. These alterations suggest vascular phenotypic modifications, which in turn may lead to long-term vascular consequences in various tissues in infants of diabetic mothers.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Many cancers show aberrant silencing of gene expression and overexpression of histone methyltransferases. The histone methyltransferases (HKMT) EZH2 and EHMT2 maintain the repressive chromatin histone methylation marks H3K27me and H3K9me, respectively, which are associated with transcriptional silencing. Although selective HKMT inhibitors reduce levels of individual repressive marks, removal of H3K27me3 by specific EZH2 inhibitors, for instance, may not be sufficient for inducing the expression of genes with multiple repressive marks. We report that gene expression and inhibition of triple negative breast cancer cell growth (MDA-MB-231) are markedly increased when targeting both EZH2 and EHMT2, either by siRNA knockdown or pharmacological inhibition, rather than either enzyme independently. Indeed, expression of certain genes is only induced upon dual inhibition. We sought to identify compounds which showed evidence of dual EZH2 and EHMT2 inhibition. Using a cell-based assay, based on the substrate competitive EHMT2 inhibitor BIX01294, we have identified proof-of-concept compounds that induce re-expression of a subset of genes consistent with dual HKMT inhibition. Chromatin immunoprecipitation verified a decrease in silencing marks and an increase in permissive marks at the promoter and transcription start site of re-expressed genes, while Western analysis showed reduction in global levels of H3K27me3 and H3K9me3. The compounds inhibit growth in a panel of breast cancer and lymphoma cell lines with low to sub-micromolar IC50s. Biochemically, the compounds are substrate competitive inhibitors against both EZH2 and EHMT1/2. Question: Does dual EZH2 and EHMT2 histone methyltransferase inhibition increase biological efficacy in breast cancer cells? <|endoftext|> <|assistant|> We have demonstrated that dual inhibition of EZH2 and EHMT2 is more effective at eliciting biological responses of gene transcription and cancer cell growth inhibition compared to inhibition of single HKMTs, and we report the first dual EZH2-EHMT1/2 substrate competitive inhibitors that are functional in cells.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: High protein diets are the most effective to stimulate cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1) release; however, which proteins are the most potent is not known. Here, the effects of specific dietary proteins on intestinal CCK and GLP-1 release were examined. Duodenal biopsies of 10 healthy male subjects and 10 male rats were taken and placed in an Ussing chamber system. The biopsies were exposed on the luminal side to buffer, egg protein, codfish protein, ovomucoid, pea protein, and wheat protein. After an exposure time of 2 h, samples were taken from the serosal side. Pea protein and wheat protein increased CCK and GLP-1 release in human duodenal tissue, while codfish protein only increased CCK release. No elevated levels of CCK and GLP-1 were found after exposure of rat tissue to different proteins. Question: Is release of satiety hormones in response to specific dietary proteins different between human and murine small intestinal mucosa? <|endoftext|> <|assistant|> Pea and wheat protein are the most potent stimulators of CCK and GLP-1 release in human duodenal tissue, and may therefore be good dietary additives in weight management.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Low incidence of adrenal cortical carcinoma in the general adult population has prompted a reevaluation of current protocol for the assessment of adrenal incidentalomas. To determine whether follow-up imaging for small (≤ 4 cm) incidental adrenal nodules is necessary for patients without known cancer. We performed a retrospective analysis of all patients found to have an incidental adrenal nodule on abdominal computed tomography (CT) scan during a 27-month period. The electronic medical record was reviewed to determine clinical outcomes in all patients with a minimum of 3 years of follow-up (mean follow-up = 6.7 years). Patients with a known primary cancer were excluded from the analysis unless they had a prior CT scan that documented an incidental adrenal nodule. Unenhanced CT attenuation was measured for all nodules, if available. A total of 392 patients with an incidental adrenal nodule had a mean (standard deviation [SD]) clinical follow-up of 6.7 (2.7) years. There were 200 men and 192 women with a mean (SD) age of 66.0 (13.2) years. None of these patients developed primary adrenocortical carcinoma during the follow-up period.Two hundred forty of these patients also had a minimum 3 years of imaging follow-up (mean [SD], 6.4 [2.4] years; range, 3.1-13.6 years). There were 173 left-sided and 91 right-sided nodules on index CT scan. There was no significant difference in the mean (SD) rate of growth between left- and right-sided nodules (0.1 [0.8]mm/year vs 0.1 [0.8] mm/year,p = 0.58). Mean unenhanced CT attenuation of adrenal nodules did not affect the likelihood of adrenal malignancy during follow-up. Question: Evaluation of Small Adrenal Incidental Nodules: Is Imaging Follow-Up Necessary? <|endoftext|> <|assistant|> Patients with small incidental adrenal nodules do not require additional imaging to exclude the possibility of adrenocortical carcinoma.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Discerning cardiac myocyte cell cycle behavior is challenging owing to commingled cell types with higher proliferative activity. To investigate cardiac myocyte cell cycle activity in development and the early postnatal period. To facilitate studies of cell type-specific proliferation, we have generated tissue-specific cell cycle indicator BAC transgenic mouse lines. Experiments using embryonic fibroblasts from CyclinA2-LacZ-floxed-EGFP, or CyclinA2-EGFP mice, demonstrated that CyclinA2-βgal and CyclinA2-EGFP were expressed from mid-G1 to mid-M phase. Using Troponin T-Cre;CyclinA2-LacZ-EGFP mice, we examined cardiac myocyte cell cycle activity during embryogenesis and in the early postnatal period. Our data demonstrated that right ventricular cardiac myocytes exhibited reduced cell cycle activity relative to left ventricular cardiac myocytes in the immediate perinatal period. Additionally, in contrast to a recent report, we could find no evidence to support a burst of cardiac myocyte cell cycle activity at postnatal day 15. Question: Does tissue-Specific Cell Cycle Indicator reveal Unexpected Findings for Cardiac Myocyte Proliferation? <|endoftext|> <|assistant|> Our data highlight advantages of a cardiac myocyte-specific cell cycle reporter for studies of cardiac myocyte cell cycle regulation.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The observation of a voluntary movement executed by another person is associated with an alpha and beta EEG desynchronization over the motor cortex, thought to reflect activity from the human "mirror neuron" system. The aim of our work was to study the changes in local field potentials (LFP) recorded from the subthalamic nucleus (STN) and their relationship with cortical activity, during movement observation. Bilateral EEG and STN LFP recordings were acquired in 18 patients with Parkinson's disease, through surgically implanted electrodes for deep brain stimulation. Oscillatory changes during movement execution and movement observation were compared with two different control conditions (simple stimulus and rotating stimulus observation), in "off" and "on" motor states. Time-frequency transforms and event-related coherence were used for the analysis. Movement observation was accompanied by bilateral beta reduction in subthalamic power and cortico-STN coherence, which was smaller than the decrease observed during movement execution, but significant when compared with the two control conditions. Question: Changes in subthalamic activity during movement observation in Parkinson's disease: is the mirror system mirrored in the basal ganglia? <|endoftext|> <|assistant|> Movement observation is accompanied by changes in the beta oscillatory activity of the STN, similar to those observed in the EEG.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Glutathione S-transferase P1 (GSTP1) has been reported to function as a tumor suppressor gene in various types of human cancers. Aberrant methylation of tumor-related genes at the promoter regions can inactivate genes, which is important in the carcinogenesis of breast cancer. However, the role of GSTP1 promoter methylation in the occurrence of breast cancer and its relationship with tumor stage and histological grade has not been fully elucidated. Thus, we carried out a meta-analysis to yield a more accurate association. A systematically literature search was made on PubMed, EMBASE and Web of Science databases for eligible studies. The odds ratio (OR) and 95 % confidence interval (95 % CI) were calculated by RevMan 5.2 software. Subgroup and sensitivity analyses were conducted to explore the source of heterogeneity. Eventually, 17 articles involving 19 case-control studies were included in the present meta-analysis. Overall, the pooled results indicated that aberrant GSTP1 promoter methylation was significantly associated with the risk of breast cancer (OR = 7.85, 95 % CI = 5.12-12.01; Caucasians OR = 7.23, 95 % CI = 3.76-13.90 and Asians OR = 11.71, 95 % CI = 5.69-24.07). Furthermore, our results revealed that GSTP1 promoter methylation was more often observed in late-stage breast cancer patients compared with early-stage ones (OR = 1.84, 95 % CI = 1.32-2.58). However, no significant association was identified between GSTP1 promoter methylation and histological grade (OR = 0.74, 95 % CI = 0.43-1.26). Question: Is aberrant GSTP1 promoter methylation associated with increased risk and advanced stage of breast cancer : a meta-analysis of 19 case-control studies? <|endoftext|> <|assistant|> The results indicated that GSTP1 promoter methylation probably plays an important role in breast carcinogenesis, which could serve as an effective biomarker for the diagnosis and monitor of breast cancer.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The aim of the study was to determine whether final year medical students in medical schools of south-east Nigeria were satisfied with rural community posting. A cross-sectional descriptive study design was used. All final year medical students in the six medical schools in south-east Nigeria who had completed their rural community posting and were willing to participate were included in the study. The students were interviewed using a pretested, self-administered questionnaire. A total of 457 medical students participated in the study, representing a response rate of 86.7%. Only a minor proportion of the students (22.5%) were satisfied with rural community posting. The most common reason for dissatisfaction among the students was lack of interest in rural communities. Most students (68.7%) were of the opinion that a good rural community posting could influence the students to practise in a rural area after graduation. Factors associated with satisfaction with rural community posting included being a student in a federal institution (adjusted odds ratio (AOR)=0.6, 95% confidence interval (CI)=0.4-0.9), being a male student (AOR=2.4, 95%CI=1.5-3.9) and intention to specialize in community medicine after graduation (AOR=2.7, 95%CI=1.2-6.0). Question: Are medical students satisfied with rural community posting? <|endoftext|> <|assistant|> Most students were dissatisfied with rural community postings and the major reason for dissatisfaction was lack of interest in rural communities. A properly organized rural community posting is capable of changing the negative attitude of the students towards life and medical practice in the rural area. Adequate orientation of the students on the relevance of the posting, good community exposure and enhanced student lecturer interactions during the posting period could ensure satisfaction of the students. There should be a targeted evaluation of the rural community posting at the various medical schools in the country with the aim of strengthening and modifying the posting where necessary so as to ensure its purpose is realized.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Increased production of Th2 cytokines characterizes Sezary syndrome, the leukemic form of cutaneous T-cell lymphomas (CTCL). To identify the molecular background and to study whether shared by the most common CTCL subtype, mycosis fungoides, we analyzed the gene expression profiles in both subtypes. Freshly isolated cells from 30 samples, representing skin, blood, and enriched CD4(+) cell populations of mycosis fungoides and Sezary syndrome, were analyzed with Affymetrix (Santa Clara, CA) oligonucleotide microarrays, quantitative PCR, or immunohistochemistry. The gene expression profiles were combined with findings of comparative genomic hybridization of the same samples to identify chromosomal changes affecting the aberrant gene expression. We identified a set of Th1-specific genes [e.g., TBX21 (T-bet), NKG7, and SCYA5 (RANTES)] to be down-regulated in Sezary syndrome as well as in a proportion of mycosis fungoides samples. In both Sezary syndrome and mycosis fungoides blood samples, the S100P and LIR9 gene expression was up-regulated. In lesional skin, IL7R and CD52 were up-regulated. Integration of comparative genomic hybridization and transcriptomic data identified chromosome arms 1q, 3p, 3q, 4q, 12q, 16p, and 16q as likely targets for new CTCL-associated gene aberrations. Question: Are th1 response and cytotoxicity genes down-regulated in cutaneous T-cell lymphoma? <|endoftext|> <|assistant|> Our findings revealed several new genes involved in CTCL pathogenesis and potential therapeutic targets. Down-regulation of a set of genes involved in Th1 polarization, including the major Th1-polarizing factor, TBX21, was for the first time associated with CTCL. In addition, a plausible explanation for the proliferative response of CTCL cells to locally produced interleukin-7 was revealed.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: We assessed regulation of volume-sensitive Cl(-) current (I(Cl,swell)) by endothelin-1 (ET-1) and characterized the signalling pathway responsible for its activation in rabbit atrial and ventricular myocytes. ET-1 elicited I(Cl,swell) under isosmotic conditions. Outwardly rectified Cl(-) current was blocked by the I(Cl,swell)-selective inhibitor DCPIB or osmotic shrinkage and involved ET(A) but not ET(B) receptors. ET-1-induced current was abolished by inhibiting epidermal growth factor receptor (EGFR) kinase or phosphoinositide-3-kinase (PI-3K), indicating that these kinases were downstream. Regarding upstream events, activation of I(Cl,swell) by osmotic swelling or angiotensin II (AngII) was suppressed by ET(A) blockade, whereas AngII AT(1) receptor blockade failed to alter ET-1-induced current. Reactive oxygen species (ROS) produced by NADPH oxidase (NOX) stimulate I(Cl,swell). As expected, blockade of NOX suppressed ET-1-induced I(Cl,swell), but blockade of mitochondrial ROS production with rotenone also suppressed I(Cl,swell). I(Cl,swell) was activated by augmenting complex III ROS production with antimycin A or diazoxide; in this case, I(Cl,swell) was insensitive to NOX inhibitors, indicating that mitochondria were downstream from NOX. ROS generation in HL-1 cardiomyocytes measured by flow cytometry confirmed the electrophysiological findings. ET-1-induced ROS production was inhibited by blocking either NOX or mitochondrial complex I, whereas complex III-induced ROS production was insensitive to NOX blockade. Question: Does endothelin signalling regulate volume-sensitive Cl- current via NADPH oxidase and mitochondrial reactive oxygen species? <|endoftext|> <|assistant|> ET-1-ET(A) signalling activated I(Cl,swell) via EGFR kinase, PI-3K, and NOX ROS production, which triggered mitochondrial ROS production. ET(A) receptors were downstream effectors when I(Cl,swell) was elicited by osmotic swelling or AngII. These data suggest that ET-1-induced ROS-dependent I(Cl,swell) is likely to participate in multiple physiological and pathophysiological processes.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Reactive oxygen species contribute to steatosis and inflammation in alcoholic liver disease (ALD). Here, we evaluated the selective contribution of p47phox, a critical subunit of nicotinamide adenine dinucleotide phosphate oxidase (NADPH) oxidase complex, in liver parenchymal cells and in bone marrow (BM)-derived cells. Female C57Bl/6 wild type [WT], total body p47phox-deficient knockout [KO] or p47phox chimera mice generated by BM transplantation of p47phox-KO-BM into irradiated WT mice (WT/p47phox-KO-BM mice) received 5% Lieber-DeCarli alcohol or control (pair feeding) diet for 4 weeks. Alcohol-induced liver steatosis as measured by Oil Red O staining and serum triglyceride up-regulation were prevented in p47phox-KO mice but not in WT/p47phox-KO-BM chimeras compared to WT controls. Serum alanine aminotransferase (ALT) was significantly increased in alcohol-fed WT mice but not in p47phox-KO mice compared to pair-fed controls. There was no protection from alcohol-induced increase in ALT and liver damage in the WT/p47phox-KO-BM mice. Alcohol-induced liver steatosis was accompanied by up-regulation of the lipid droplet-stabilizing protein, adipocyte differentiation-related protein (ADRP), and the fatty acid synthesis-associated genes, fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACACA). Total body deficiency in p47phox but not selective absence of p47phox in BM-derived cells prevented alcohol-induced up-regulation of ADRP, FASN, and ACACA in the liver. Finally, alcohol-induced activation and DNA binding of nuclear factor κB (NF-κB), a master regulator of inflammation, were significantly increased after alcohol feeding in WT but not in p47phox-KO mice. Selective deficiency of p47phox in BM-derived cells (WT/p47phox-KO-BM chimera) failed to prevent NF-κB induction after alcohol feeding. Question: Is the presence of p47phox in liver parenchymal cells a key mediator in the pathogenesis of alcoholic liver steatosis? <|endoftext|> <|assistant|> Total body deficiency in p47phox subunit of NADPH oxidase complex protects mice from alcohol-induced liver steatosis via mechanisms involving ADRP, FASN, and ACACA as well as from alcohol-induced NF-κB activation. In contrast, selective absence of p47phox in BM-derived cells fails to provide protection via these mechanisms. These results suggest that p47phox in parenchymal cells plays a critical role in the pathogenesis of ALD.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: After the demonstration that one-third of male patients with type 2 diabetes have hypogonadotrophic hypogonadism, we have shown that patients with hypogonadotrophic hypogonadism also have markedly elevated C-reactive protein (CRP) concentrations. We have now hypothesized that type 2 diabetic subjects with hypogonadotrophic hypogonadism may have a lower hematocrit because testosterone stimulates, whereas chronic inflammation suppresses, erythropoiesis. Seventy patients with type 2 diabetes at a tertiary referral center were included in this study. The mean hematocrit in patients with hypogonadotrophic hypogonadism (n = 37), defined as calculated free testosterone (cFT) of <6.5 ng/dl, was 40.6 +/- 1.1%, whereas that in eugonadal patients (n = 33) was 43.3 +/- 0.7% (P = 0.011). The hematocrit was related to cFT concentration (r = 0.46; P < 0.0001); it was inversely related to plasma CRP concentration (r = 0.41; P < 0.0004). Patients with CRP <3 mg/l had a higher hematocrit (42.7 +/- 0.7%) than those with CRP >3 mg/l (39.9 +/- 1.1%; P < 0.05). The prevalence of normocytic normochromic anemia (hemoglobin <13 g/dl) was 23% in the entire group, whereas it was 37.8% in the men with hypogonadotrophic hypogonadism and 3% in the eugonadal men (P < 0.01). Erythropoietin concentration was elevated or high normal in all 11 patients with anemia in whom it was tested. Question: Do low testosterone and high C-reactive protein concentrations predict low hematocrit in type 2 diabetes? <|endoftext|> <|assistant|> We conclude that hypogonadotrophic hypogonadism in male type 2 diabetic subjects is associated with a lower hematocrit and a frequent occurrence of mild normocytic normochromic anemia with normal or high erythropoietin concentrations. In these patients, hematocrit is also inversely related to CRP concentration. Thus, low testosterone and chronic inflammatory mechanisms may contribute to mild anemia. Such patients may also have a high risk of atherosclerotic cardiovascular events in view of their markedly elevated CRP concentrations.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Pain management is limited by inability to match a patient's condition-and pain mechanisms-to optimal treatment(s). Much is known about pain treatment from animal investigations, but antinociceptive mechanisms cannot be readily explored in clinical studies. Evidence suggests that self-report verbal pain descriptors characterize important pain dimensions and may reflect diverse underlying mechanisms. This exploratory analysis of data from a trial of a gabapentin-morphine combination evaluated effects of treatment on short-form McGill Pain Questionnaire sensory and affective descriptor profiles and prediction of treatment response by these descriptors. Severity of "throbbing," "shooting," and "aching" improved preferentially with morphine over gabapentin, whereas "tiring-exhausting" and "sickening" improved preferentially with gabapentin over morphine. Improvement in descriptor severity with gabapentin-morphine combination was superior to active placebo for 12 of 15 short-form McGill Pain Questionnaire descriptors, whereas morphine and gabapentin were superior to active placebo for only 7 and 6 descriptors, respectively. Baseline moderate-severe "throbbing" and "hot-burning" predicted poor outcomes with gabapentin, whereas moderate-severe "aching" and "punishing-cruel" predicted favorable outcomes with gabapentin. Baseline "throbbing" severity also predicted poor outcomes with morphine. Baseline allodynia predicted superior reduction of "stabbing" with morphine but not with gabapentin alone. Question: Do sensory and affective pain descriptors respond differentially to pharmacological interventions in neuropathic conditions? <|endoftext|> <|assistant|> These results point to the hypothesis that sensory and affective pain descriptor profiles exhibit a treatment-specific response. Larger, more definitive, investigations to evaluate treatment-specific effects on multiple sensory and affective pain descriptors, and prediction of treatment response by these descriptors, will advance efforts toward developing and implementing more effective individualized pain therapies.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The availability of pigs homozygous for alpha1,3-galactosyltransferase gene-knockout (GT-KO) has enabled study of the incidence and cytotoxicity of primate antibodies directed to antigens other than Galalpha1,3Gal (Gal), termed non-Gal antigens. Sera from 27 healthy humans and 31 patients awaiting renal allotransplantation, who were either unsensitized [panel reactive antibodies (PRA) < 10%] or allosensitized (PRA > 70%), were tested by flow cytometry for binding of immunoglobulin M (IgM) and IgG to peripheral blood mononuclear cells (PBMC) from both wild-type (WT) and GT-KO pigs. Complement-dependent cytotoxicity to WT and GT-KO PBMC was also measured. IgM and IgG from all 27 (100%) healthy human sera bound to WT PBMC, while 78% and 63% of these sera had IgM and IgG that bound to GT-KO PBMC, respectively. Mean binding to WT PBMC was significantly greater than GT-KO PBMC. Whereas 100% of sera were cytotoxic to WT PBMC, only 61% were cytotoxic to GT-KO PBMC, and the extent of lysis was significantly less. Neither mean binding of IgM and IgG nor cytotoxicity of unsensitized and allosensitized sera to WT and GT-KO PBMC was significantly different to that of healthy sera. Question: Are allosensitized humans at no greater risk of humoral rejection of GT-KO pig organs than other humans? <|endoftext|> <|assistant|> More than half of the healthy humans tested had cytotoxic antibodies to GT-KO PBMC, but allosensitized patients will be at no greater risk of rejecting a pig xenograft by a humoral mechanism.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Microvascular endothelial barrier breakdown in sepsis precedes organ failure and death in patients. We tested the hypothesis that the formation of endothelium-derived soluble vascular endothelial (VE)-cadherin fragments (sVE-cadherin) is involved in inflammation-induced endothelial barrier disruption. Incubation of human dermal microvascular endothelial cells (HDMEC) with tumour necrosis factor-α (TNF-α) and bacterial lipopolysaccharide (LPS) led to endothelial barrier disruption which correlated with significantly increased sVE-cadherin at a size of ∼90 kDa in cell culture supernatants. Inhibition of the VE-cadherin-cleaving disintegrin and metalloproteinase ADAM10 using GI254023X attenuated inflammation-induced formation of sVE-cadherin and endothelial barrier disruption, suggesting ADAM10-mediated shedding as a mechanism underlying sVE-cadherin release. Formation of VE-cadherin fragments at 90 and 110 kDa was observed when recombinant VE-cadherin (rVE-cadherin) was digested with recombinant ADAM10. Mass spectrometry of the VE-cadherin fragments showed that they originated from cleavage of the extracelluar domain and thereby several cleavage sites of ADAM10 were identified. Atomic force microscopy measurements demonstrated that cell culture supernatants containing sVE-cadherin and application of rVE-cadherin blocked VE-cadherin binding. Accordingly rVE-cadherin dose-dependently led to loss of endothelial barrier functions in HDMEC monolayers. Finally, in patients suffering from severe sepsis or septic shock with clinical signs of a microvascular leackage, serum levels of sVE-cadherin were significantly increased. Question: Is soluble VE-cadherin involved in endothelial barrier breakdown in systemic inflammation and sepsis? <|endoftext|> <|assistant|> Taken together, formation of sVE-cadherin is associated and contributes to inflammation-induced breakdown of endothelial barrier functions by inhibition of VE-cadherin binding. The underlying mechanism of VE-cadherin cleavage involves ADAM10 and appears to be of clinical relevance since sVE-cadherin was augmented in patients with severe sepsis.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Efferent ductules reabsorb more than 90% of the rete testis fluid, a process that involves ion transporters and AQP (aquaporin) water channels. Oestrogen has been shown to modulate the expression of the ion transporters involved in this activity, but reports of AQP regulation in the male tract have been confounding. To understand better the regulation of AQP1 and AQP9, we investigated their expression in rat efferent ductules and initial segment of the epididymis after treatment with the pure antioestrogen ICI 182,780 or bilateral efferent duct ligation, or castration, followed by hormone replacement. Results show that AQP9 is modulated by oestrogen in the efferent ductule epithelium, but not in the initial segment of the epididymis. DHT (5alpha-dihydrotestosterone) also modulated AQP9 in efferent ductules. AQP9 was down-regulated by the antioestrogen in efferent ductules on day 45 post-treatment, which occurred before the non-ciliated cells had shown significant loss of microvilli. DHT, but not oestradiol, modulated AQP9 expression in the initial segment of the epididymis. In contrast, testosterone, DHT, oestrogen or the antioestrogen did not alter AQP1 staining, indicating constitutive expression of AQP1 in the efferent ductule epithelium. AQP1 expression was induced in peritubular cells of efferent ductules and in the initial segment of the epididymis after castration and long-term treatment with the antioestrogen. Although peritubular AQP1 staining in efferent ductules was partially reversed by the androgens, it was not reversed after any treatment in the initial segment of the epididymis. Question: Are aquaporin-1 and -9 differentially regulated by oestrogen in the efferent ductule epithelium and initial segment of the epididymis? <|endoftext|> <|assistant|> These results demonstrate that efferent ductules are unique in requiring both oestrogen and androgen to regulate an important mediator of fluid reabsorption, whereas the initial segment is dependent only on androgen stimulation.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Hypoalbuminemia in patients with decompensated cirrhosis has traditionally been assumed to be a result of to impaired liver synthesis; however, protein-losing enteropathy (PLE) may also contribute. The aim of this study was to assess whether hypoalbuminemic cirrhotic patients with portal hypertension had evidence of PLE. Sixteen patients with alcoholic cirrhosis, hypoalbuminemia and portal hypertension underwent whole gut lavage with polyethylene glycol solution. The effluent obtained was analyzed for albumin, immunoglobulin (Ig)G and alpha1-antitrypsin (alpha1-AT). Serum C-reactive protein (CRP) was also measured to assess the systemic inflammatory response. Twelve of the 16 enrolled patients had a persistently low albumin concentration at the time of lavage. Only one patient (who was subsequently found to have celiac disease) had elevated concentrations of lavage albumin, alpha1-AT and IgG levels. There was a significant correlation between lavage albumin and alpha1-AT (r = 0.671, P = 0.024), and between lavage albumin and IgG (r = 0.614, P = 0.045). There was no correlation between serum albumin and lavage proteins. Six patients had elevated serum CRP levels, but serum albumin or lavage protein concentrations did not correlate with serum CRP. Question: Is portal hypertension associated with protein-losing enteropathy? <|endoftext|> <|assistant|> There is no evidence of a significant PLE in patients with alcoholic cirrhosis, hypoalbuminemia and portal hypertension.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To determine whether racial and ethnic disparities in publicly funded alcohol treatment completion are due to racial differences in attending outpatient and residential treatment. Statistical analysis of alcohol treatment completion rates using alcohol treatment patients' discharge records from all publicly funded treatment facilities in Los Angeles County from 1998 to 2000 (n = 10,591). Among these patients, African American (OR = 0.52; 95% CI 0.47, 0.57) and Hispanic (OR = 0.89; 95% CI 0.81, 0.99) patients were significantly less likely to complete treatment as compared with White patients. We found that the odds of being in outpatient versus residential care were 1.42 (95% CI 1.29, 1.55) and 2.05 (95% CI 1.85, 2.26) for African American and Hispanic alcohol treatment patients, respectively, compared with White patients. Adjusting for addiction characteristics, employment, other patient-level factors that might influence treatment enrollment, and unobserved facility-level differences through a random effects regression model, these odds increased to 1.89 (95% CI 1.22, 2.94) for African American and to 2.12 (95% CI 1.40, 3.21) for Hispanics. We developed a conditional probability model to assess the contribution of racial differences in treatment modality to racial disparities in treatment completion. Estimates from this model indicate that were African American and Hispanic patients observed in outpatient care in this population to have the same probability of receiving residential care as White patients with otherwise similar characteristics, the White-African American difference in completion rates would be reduced from 13.64% (95% CI 11.58%, 15.71%) to 11.09% (95% CI 8.77%, 13.23%) and the White-Hispanic difference would disappear, changing from 2.63% (95% CI 0.29%, 4.95%) to -0.45% (-3.52%, 2.43%). Question: Are racial disparities in alcohol treatment completion associated with racial differences in treatment modality entry? <|endoftext|> <|assistant|> It appears that reductions in racial disparities in treatment completion could be gained by increasing enrollment in residential alcohol treatment for African American and Hispanic alcohol abusers in Los Angeles County. Further research addressing why minority alcohol abusers are less likely to receive residential alcohol treatment should be conducted, as well as research that examines why African American alcohol treatment patients have lower completion rates as compared with White patients regardless of treatment modality.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: We previously showed that ultrasound altered position of biopsy in 15% of cases by demonstrating intervening structures. This study was designed to test whether one could predict in which cases ultrasound would be useful. A standard percussion technique was used. The site chosen was marked. Criteria were established to indicate whether a move might be predicted to be likely. If 10 or more points were assigned, then it was predicted that ultrasound would change position. A difficult percussion was assigned 10 points; obesity, 5 points; and chest deformity, 5 points. The ultrasound was then applied to the marked spot in every case. If an intervening structure was present within 6 cm, the biopsy site was moved. Otherwise, the biopsy was taken from the marked site. One hundred seventeen consecutive liver biopsies were included between January 1999 and January 2000. The criteria predicted the desirability of nine moves. No moves were made, however, in these cases. In 17 cases (14.5%), moves were made because of intervening structures. None of the cases were predicted. A move was made in 1 of 23 obese patients. There was no statistical difference in moves made between obese and nonobese patients. Question: Can one predict when ultrasound will be useful with percutaneous liver biopsy? <|endoftext|> <|assistant|> Using criteria of difficult percussion, obesity, and unusual chest shape, we could not predict when ultrasound would be useful. This is in contrast to the belief that ultrasound can be applied to selected liver biopsies considered in advance to be more difficult, as in the obese patients, and instead suggests that to avoid intervening structures, one should apply ultrasound to all cases.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To investigate the impact of operator experience on amniocentesis-related adverse outcomes. Retrospective study of mid-trimester amniocenteses performed by the same operator on singleton pregnancies in a single private institution during 1994-2007. Outcomes were hemorrhagic or dark amniotic fluid aspiration, insufficient volume aspiration, repeated puncture and fetal loss. Rates were estimated annually, as well as for every 10% of procedures up to the total number. The association of each outcome with epidemiological aspects was also examined. In total, 5913 amniocenteses were performed. The overall rate of adverse outcomes was 5.4%. The total adverse outcome rate reduced from 10.2% in the first 10% of cases to 3.0% in the last 10% (P=.001). The rate of hemorrhagic fluid gradually decreased from 4.4% to 1.5% (P=.05) over the same intervals. The fetal loss rate was also reduced from 0.5% during the first half to 0.3% in the second half of the study period (P=NS). Logistic regression analysis indicated no significant correlations between adverse outcomes with any of epidemiological parameters of women undergoing amniocentesis. Question: Does operator experience reduce the risk of second trimester amniocentesis-related adverse outcomes? <|endoftext|> <|assistant|> Operator experience has a beneficial impact on preventing procedure-related adverse outcomes.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Autism is a neurodevelopmental disorder which is known to have a strong genetic component and is most likely oligogenic. However, the necessary role of environmental factors has been well documented. Prior research suggests that parental characteristics, such as age and level of education, may be associated with a risk of autism. Parental age has been shown to be associated with many disorders, such as schizophrenia, childhood cancer and fetal death. However, results from studies of parental age and autism are inconsistent. In the present study, we investigated the association of autism with parental age in 179 autism cases and 1611 matched cohort children from Iran. Each case was matched with nine cohort controls on parental education, sex, order of birth, consanguineous marriage, urbanism and province of residence. The Cox regression model was used to carry out conditional logistic regression on the matched data. There was a significant association between higher paternal age, but not maternal age, and an increasing risk of autism. An analysis of the combined effect of parental age and education also revealed that parents with higher education had an increased risk of having autistic children, with a dose-response effect of parental age. Question: Does paternal age increase the risk for autism in an Iranian population sample? <|endoftext|> <|assistant|> This study, which is the first epidemiological study of autism in Iran, provides evidence of the association of paternal age and risk of autism.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The value of lymph node dissection (LND) in the treatment of bladder urothelial carcinoma is well established. However, standards for the quality of LND remain controversial. We compared the distribution of lymph node (LN) metastases in a two-institution cohort of patients undergoing radical cystectomy (RC) using a uniformly applied extended LND template. Patients undergoing RC at the University of Southern California (USC) Institute of Urology and at Oregon Health Sciences University (OHSU) were included if they met the following criteria: (1) no prior pelvic radiotherapy or LND; (2) lymphatic tissue submitted from all nine predesignated regions, including the paracaval and para-aortic LNs; (3) bladder primary; and (4) category M0 disease. The number and location of LN metastases were prospectively entered into corresponding databases. LN maps were constructed and correlated with preoperative and pathologic characteristics. Kaplan-Meier curves were constructed to estimate overall survival (OS) and recurrence free survival (RFS) among LN-positive (LN+) patients. Question: Is lymph node dissection technique more important than lymph node count in identifying nodal metastases in radical cystectomy patients : a comparative mapping study? <|endoftext|> <|assistant|> Inclusion criteria were met by 646 patients (439 USC, 207 OHSU), and 23% had LN metastases at time of cystectomy. Although there was a difference in the median per-patient LN count between institutions, there were no significant interinstitutional differences in the incidence or distribution of positive LNs, which were found in 11% of patients with ≤pT2b and in 44% of patients with ≥pT3a tumors. Among LN+ patients, 41% had positive LNs above the common iliac bifurcation. Estimated 5-yr RFS and OS rates for LN+ patients were 45% and 33%, respectively, and did not differ significantly between institutions.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The objective of this study was to determine whether 16 weeks of resistance training (RT) can reduce the blood pressure response and improve the cardiovascular function of men aged 70-80 years during submaximum aerobic exercise. Twenty-four men aged between 70 and 80 years were randomly assigned to an RT group (n = 12) and control group (n = 12). Training consisted of three sets of six to 10 repetitions at 70-90% of one repetition maximum, three times per week, on an incline squat machine for 16 weeks. Blood pressure and cardiovascular function were assessed during submaximum cycle exercise at 40 W, and 50 and 70% of maximum oxygen consumption (VO2max) before training and after 16 weeks of training. Leg strength and VO2max were assessed every 4 weeks of the 16-week study. At 40 W, heart rate, systolic blood pressure, and rate pressure product were lower and stroke volume was significantly higher after 16 weeks of training. At 50% VO2max, heart rate and rate pressure product were lower after 16 weeks of training and at 70% VO2max, cycle ergometry power, VO2, and arterio-venous oxygen difference were higher after 16 weeks of training. Leg strength significantly increased after 16 weeks of training. Question: Does resistance training reduce the blood pressure response of older men during submaximum aerobic exercise? <|endoftext|> <|assistant|> Sixteen weeks of RT significantly reduces the blood pressure response and improves the cardiovascular function of older men during submaximum aerobic exercise. Therefore, RT not only increases muscular strength and hypertrophy but also provides significant cardiovascular benefits for older individuals.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), are ubiquitous toxic environmental pollutants capable of inducing cell death. Intracellular pH plays a key role in the regulation of cell survival and death. Our previous works have demonstrated that intracellular alkalinization mediated by Na(+)/H(+) exchanger 1 (NHE-1) is a critical event involved in B[a]P-induced apoptosis. The aim of this study was to further elucidate the mechanisms of NHE-1 activation upon B[a]P exposure. We tested the effects of plasma membrane cholesterol enrichment or depletion on B[a]P-induced NHE-1 activation related to apoptosis. We isolated cholesterol-rich plasma membrane microdomains to assess NHE-1 submembrane location and immunoprecipitated NHE-1 from the different sub-membrane fractions obtained to examine NHE-1 protein interactions during B[a]P-induced apoptosis. We found that NHE-1 is preferentially located in cholesterol-rich microdomains and that B[a]P activates NHE-1 via its relocation and binding of calmodulin outside these specialized plasma membrane microstructures; these events are necessary for the execution of the apoptosis-related intracellular alkalinization. Question: Is nHE-1 relocation outside cholesterol-rich membrane microdomains associated with its benzo [ a ] pyrene-related apoptotic function? <|endoftext|> <|assistant|> Plasma membrane location of NHE-1 affects its protein interactions and apoptotic function.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: A healthy gingival condition after endodontic surgery may depend on adequate soft tissue management. The aim of this study was to compare 2 incision techniques, papilla base incision (PBI) and intrasulcular flap (IS), which are currently used in endodontic surgery. In the present nonrandomized controlled clinical trial, patients requiring endodontic surgery on a single tooth were enrolled. PBI was used in 1 group and IS was used in the other group. The primary outcomes were changes in periodontal probing depth, gingival recession, and height of the interproximal mesial and distal papillae. Outcome variables were assessed preoperatively and 6 months after surgery. Between-group differences were evaluated through appropriate statistical analysis, with significance set at a P value equal to .05. Each group was composed of 12 patients and the 2 groups were comparable at baseline. Two weeks after surgery, papilla height decreased significantly in the IS group (2.05 and 1.80 mm at the mesial and distal aspects, respectively), whereas no significant decrease in papilla height was observed in the PBI group (0.10 and 0.20 mm). No statistically significant difference between groups was observed after 6 months. No significant difference between groups was found for gingival recession or probing depth at any follow-up time. Question: Do gingival soft tissues benefit from the application of a papilla preservation flap technique in endodontic surgery? <|endoftext|> <|assistant|> Better soft tissue preservation in the early postoperative period was achieved using the PBI approach compared with the IS approach. The PBI can be recommended for endodontic surgical procedures involving esthetic regions.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Metabolic Syndrome (MetS) is a phenotype cluster predisposing to type 2 diabetes and cardiovascular disease. We conducted a study to elucidate the genetic basis underlying linkage signals for multiple representative traits of MetS that we had previously identified at two significant QTLs on chromosomes 3q27 and 17p12. We performed QTL-specific genomic and transcriptomic analyses in 1,137 individuals from 85 extended families that contributed to the original linkage. We tested in SOLAR association of MetS phenotypes with QTL-specific haplotype-tagging SNPs as well as transcriptional profiles of peripheral blood mononuclear cells (PBMCs). SNPs significantly associated with MetS phenotypes under the prior hypothesis of linkage mapped to seven genes at 3q27 and seven at 17p12. Prioritization based on biologic relevance, SNP association, and expression analyses identified two genes: insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) at 3q27 and tumor necrosis factor receptor 13B (TNFRSF13B) at 17p12. Prioritized genes could influence cell-cell adhesion and adipocyte differentiation, insulin/glucose responsiveness, cytokine effectiveness, plasma lipid levels, and lipoprotein densities. Question: Do qTL-based association analyses reveal novel genes influencing pleiotropy of metabolic syndrome ( MetS )? <|endoftext|> <|assistant|> Using an approach combining genomic, transcriptomic, and bioinformatic data we identified novel candidate genes for MetS.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Despite increasing use of assistive devices (ADs) by physically disabled (PD) children, the use rate, number, effects and related services have seldom been studied. Understanding AD utilization is helpful in improving the related services. This study describes the usage of ADs by children with physical disabilities (PDs). This regional survey enrolled children with PDs. The children's parents or primary caregivers filled out structured questionnaires regarding the children's use of and need for ADs, the benefits and problems associated with the ADs and related services. In total, 224 ADs were used by 124 children (1.79 ADs per child). The most commonly used ADs were orthoses (n = 77, 62.10%), mobility aids (n = 51, 41.13%), and aids for therapy and training (n = 21, 16.94%). The degree of disability, age, gender, diagnosis and rehabilitation training location were not associated with the number of ADs used. Most children (n = 103, 83.06%) benefited from ADs, and 93 (75%) children had been evaluated prior to buying ADs. Eighty three (66.94%) parents paid for the Ads, and 108 (87.10%) parents acquired information from rehabilitation professionals. Forty one (40.20%) parents were satisfied with the services of local suppliers; 119 (95.97%) parents had applied to their local government for financial support; 82 (68.91%) parents were not satisfied with the application procedures or the amount of support they received. Question: Do regional survey of assistive devices use by children with physical disabilities in southern Taiwan? <|endoftext|> <|assistant|> Although parents of PD children favored the usage of ADs, they needed additional information. We suggest that policies and strategies are needed to reduce barriers to ADs utilization, enhance insurance coverage and improve ease of using the services.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The reported frequency of recovery of fungi from infected nails varies according to the geographical area. To establish the nature of the causal agents in a sample of the Libyan population presenting with suspected onychomycosis. Samples were taken from the infected fingernails of 648 patients attending the Tripoli Medical Centre. Samples from 500 patients proved positive for fungi following culturing, while 476 were potassium hydroxide and culture positive. Of the culture-positive samples, yeasts of the genus Candida (C. albicans, C. parapsilosis, C. glabrata, C. guillermondii and C. tropicalis) were the dominant cause of this condition in women (417 of 434, 96%) but were responsible for only a minority of cases in men (three of 66, 5%). In contrast, dermatophytes (Trichophyton violaceum, T. rubrum, T. mentagrophytes and Microsporum canis) were responsible for this condition in the majority of cases in men (53 of 66, 80%) but only 3% (15 of 434) of cases in women. The mould Aspergillus nidulans was isolated from the nails of 10 (15%) men and two (0.5%) women. Question: Are yeasts of the genus Candida the dominant cause of onychomycosis in Libyan women but not men : results of a 2-year surveillance study? <|endoftext|> <|assistant|> The data obtained in this study reveal an almost total separation of the aetiological agents responsible for onychomycosis based on gender.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Restless legs syndrome (RLS) is a distressing sleep disorder to which individuals appear to be genetically predisposed. In the present study, we assumed that antipsychotic-induced RLS symptoms were attributable to differences in individual genetic susceptibility, and investigated whether MEIS1, a promising candidate gene, was associated with antipsychotic-induced RLS symptoms in schizophrenia patients. All subjects were diagnosed with schizophrenia by board-certified psychiatrists using the Korean version of the Structured Clinical Interview for DSM-IV. We assessed antipsychotic-induced RLS symptoms in 190 Korean schizophrenic patients using the diagnostic criteria of the International Restless Legs Syndrome Study Group. Genotyping was performed for the rs2300478 and rs6710341 polymorphisms of the MEIS1 gene. We divided subjects into RLS symptom (n=96) and non-symptom (n=94) groups. There was no significant between-group difference in the genotype or allele frequencies of the two polymorphisms investigated, nor in the frequency of the rs2300478-rs6710341 haplotype. Question: Is mEIS1 , a Promising Candidate Gene , Associated with the Core Symptoms of Antipsychotic-Induced Restless Legs Syndrome in Korean Schizophrenia Patients? <|endoftext|> <|assistant|> Our data do not suggest that the rs2300478 and rs6710341 polymorphisms of the MEIS1 gene are associated with the core symptoms of antipsychotic-induced RLS in schizophrenia; different genetic mechanisms may underlie antipsychotic-induced vs. primary RLS.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: In response to changes in wall shear stress (WSS) the vascular endothelium releases several factors, among others nitric oxide. On the basis of studies of endothelial cells in culture, suggesting that platelet endothelial cell adhesion molecule-1 (PECAM-1) is specifically involved in sensing and coupling high temporal gradients of fluid shear stress with activation of eNOS, we hypothesized that dilations of isolated skeletal muscle arterioles from PECAM-1 knockout mice (PECAM-KO) will be reduced to rapid increases in WSS elicited by increases in perfusate flow. Small and large step increases in flow resulted in substantial dilations in arterioles of WT mice (45+/-4%), but they were markedly reduced in arterioles of PECAM-KO mice (22+/-5%). The initial slope of dilations, when WSS increased rapidly, was greater in vessels of WT than those of PECAM-KO mice (slopes: 0.378 and 0.094, respectively), whereas the second phase of dilations, when flow/shear stress was steady, was similar in the 2 groups (slopes: 0.085 and 0.094, respectively). Inhibition of eNOS significantly reduced the initial phase of dilations in arterioles from WT, but not from those of PECAM-KO mice. The calcium ionophore A23187 elicited similar NO-mediated dilation in both WT and PECAM-KO mice. Question: Does pECAM-1 mediate NO-dependent dilation of arterioles to high temporal gradients of shear stress? <|endoftext|> <|assistant|> In isolated arterioles of PECAM-KO mice activation of eNOS and consequent dilation by agonists is maintained, but the dilation to high temporal gradients of wall shear stress elicited by increases in perfusate flow is reduced. Thus, we propose that PECAM-1 plays an important role in the ability of the endothelium to sense and couple high temporal gradients of wall shear stress to NO-mediated arteriolar dilation during sudden changes in blood flow in vivo.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To report a novel method of establishing a stable shock model of swine. A total of 12 Guangxi BA-MA female miniature swines (aged 4-6 months) into A and B groups according to a random number table. Total body surface area (TBSA) was calculated according to the Meeb-Rubner formula. After intravenous anesthesia and other steps, solidified gasoline was used as burns material to establish TBSA 40% skin burn (Group A: 45 s, Group B: 50 s). Burn depth by was judged by visual and histopathological examination. Fluid resuscitation was instituted at 2 h post injury. At the same time, the hourly and pre-injury data of heart rate (HR), blood pressure (BP), urinary volume, central venous pressure (CVP) and pulmonary arterial wedge pressure (PAWP) were recorded. The actual input quantities of fluid resuscitation were assessed at the 1st and 2nd 24 h post injury. And shock condition was estimated by shock index at 2 h post injury. All miniature swines were successfully modeled without any mortality. The burn wound observed by visual examination and light microscope showed that Group A was of deep II burn and Group B III burn. Compared with the pre-injury data, HR (111 ± 6 vs 74 ± 9, 119 ± 13 vs 75 ± 13 beats/min) increased, urinary volume (0.99 ± 0.06 vs 1.45 ± 0.05, 0.82 ± 0.04 vs 1.47 ± 0.06 ml×kg(-1)×h(-1)), CVP and PAWP decreased at 2nd 24 h post-injury in two groups (P < 0.01, P < 0.05). But the changes of BP (120 ± 6/93 ± 9 vs 120 ± 6/94 ± 6, 121 ± 15/90 ± 11 vs 124 ± 10/91 ± 8 mm Hg) had no statistical significance (P > 0.05). The average value of HP in 48 h post-injury had no statistical significance in two groups (P > 0.05). The recovery liquid quantity in the first 24 h of Group B (1.66 ± 0.10 ml×kg(-1)×1%(-1) TBSA) was significantly more than Group A (1.53 ± 0.05 ml×kg(-1)×1%(-1) TBSA) (P < 0.05). The ratio between liquid input and output of Groups A and B showed that the comparison had no statistical significance (P > 0.05). In the second 24 h post-injury, the recovery liquid quantity (0.69 ± 0.17, 0.65 ± 0.16 ml×kg(-1)×1%(-1) TBSA) and the ratio between liquid in and out (1.48 ± 0.28, 1.52 ± 0.27)% between Groups A and B had no statistical significance (P > 0.05). The shock index at 2 h post-injury showed that Groups A and B were in shock compensatory period (0.92 ± 0.07) and mild shock state (1.00 ± 0.16) respectively (P > 0.05). Question: Do [ Shock modeling of large area third-degree burn in miniature swine ]? <|endoftext|> <|assistant|> Such a shock model is stable and dependable.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Atrial fibrillation is the most common postoperative complication in patients undergoing coronary artery bypass grafting (CABG) with advancing age having been shown to have a significant association with its incidence. This study aims to assess whether off-pump coronary artery bypass (OPCAB) reduces the incidence of atrial fibrillation in elderly patients. A meta-analysis of all observational studies reporting a comparison between the two techniques in elderly patients (>70 years) between 1999-2003 was performed. The primary outcome of interest was the incidence of postoperative atrial fibrillation. The quality of each study was evaluated by examining three items: patient selection, matching of the off-pump and cardiopulmonary bypass patient groups, and assessment of outcome. Meta-regression analysis was undertaken to see the effects of study size and quality on the calculated odds ratio. Eight studies fulfilled our inclusion criteria, all of which were nonrandomized. In total the studies identified 3017 subjects, of which 764 had off-pump surgery (25%) and 2253 underwent cardiopulmonary bypass (75%). Meta-analysis showed that after off-pump surgery there was a significantly lower incidence of postoperative atrial fibrillation in these patients (odds ratio 0.70, 95% confidence interval [CI] 0.56-0.89). Meta-regression analysis including study characteristics did not show any associations affecting the calculated odds ratio of atrial fibrillation. Question: Do off-pump techniques reduce the incidence of postoperative atrial fibrillation in elderly patients undergoing coronary artery bypass grafting? <|endoftext|> <|assistant|> Our study demonstrates a reduced incidence of postoperative atrial fibrillation in an elderly population with off-pump as compared with cardiopulmonary bypass techniques. We appreciate, however, that our statistical analysis uses nonrandomized published data and that the results must be treated with caution. If this finding is confirmed by a large-scale randomized trial, it has significant implications on the operative strategy employed for this patient group.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The rates for traumatic brain injury (TBI) have risen in the last decade. Studies in animal models and clinical trials have not yet resulted in an effective treatment for TBI. Leptin, a 16kDa peptidic hormone is mainly known as a regulator of energy balance and has been shown to exert neuroprotective effects in different models of brain pathology. In this study, we have assessed whether leptin exerts protective actions in a TBI mouse model. In addition, the possible implication of CB2 cannabinoid receptor in leptin actions has been explored, since it is known that the endocannabinoid system interacts with leptin and actively participates in brain recovery after lesions. Swiss (CD1) male mice were subjected to weigh-drop model for TBI. Prior to the lesion, mice were injected with an antagonist of CB2 receptor (AM630) or the vehicle and immediately after TBI, they received leptin or vehicle treatment. Data were analyzed using a two-way ANOVA or the non-parametric test Kruskal-Wallis when appropriate. For correlation analyses, Spearman's rho test, followed by linear regression test, was used. TBI induced a neurological deficit, which was improved by leptin treatment. Leptin recovered several parameters affected by TBI, including the expression of cannabinoid receptors, axonal injury marker and neuroinflammatory components. The effects of leptin were prevented or reduced when it was administered in combination with the CB2 receptor antagonist, AM630. Question: Is cB2 cannabinoid receptor involved in the anti-inflammatory effects of leptin in a model of traumatic brain injury? <|endoftext|> <|assistant|> Since some of the beneficial effects of leptin were not evident in the presence of AM630, our results suggest that CB2 receptor might be involved in the full expression of the neuroprotective effects of the hormone. These findings open new avenues for the study of leptin as a therapeutic treatment for TBI and enhance the importance of CB2 receptor in TBI pathophysiology and recovery.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The oral contraceptive pill (OCP) is widely prescribed throughout the world. Although it is associated with a small but significant increase in blood pressure, the influence of the OCP on large artery stiffness and wave reflection is unclear. The aim of this study was to determine the relationship between use of the OCP and aortic stiffness and wave reflections in a young, healthy cohort of women. Participants were drawn from the ENIGMA study, which examines the natural history of blood pressure in young adults. A detailed medical history and lifestyle questionnaire, including OCP details were taken. Blood pressure was measured according to the British Hypertension Society guidelines. Aortic pulse wave velocity (aPWV) was measured together with augmentation index (AIx). Stroke volume (SV) and cardiac output (CO) were also assessed. Women taking the OCP (n = 225) had a higher SBP and pulse pressure compared with nonusers (n = 660; 112 ± 12 vs. 110 ± 11 and 43 ± 8 vs. 42 ± 8 mmHg, respectively, P < 0.05 for both). CO and SV were also higher (6.6 ± 1.5 vs. 6.3 ± 1.5 l/min, P < 0.01 and 81 ± 16 vs. 78 ± 19 ml, P < 0.05) as was aPWV (5.5 ± 0.7 vs. 5.4 ± 0.7 m/s, P < 0.05). However, there was no difference in DBP (68 ± 9 vs. 69 ± 9 mmHg), mean arterial pressure (81 ± 10 vs. 81 ± 10 mmHg) or AIx (2 ± 12 vs. 3 ± 13%) between the groups. Question: Is use of the oral contraceptive pill associated with increased large artery stiffness in young women : the ENIGMA study? <|endoftext|> <|assistant|> Use of the OCP is associated with elevated pulse pressure and SV and a small increase in aPWV in young women. The longer term implications of these effects require further investigation.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: This study aimed to evaluate the possibility of predicting radiologically the scalar localization of a 31.5-mm-long, free-fitting electrode carrier for cochlear implantation, using conventional planar computed tomography. A cross-sectional human temporal bone study was conducted. Twenty human temporal bones were acquired postmortem and implanted with 31.5-mm-long electrode carriers. Ten of these were implanted into the scala tympani using the round window approach, whereas the other 10 electrodes were inserted into the scala vestibuli by cochleostomy. Computed tomography was then performed, and 2 experienced blinded radiologists evaluated the intracochlear position of the array. The estimated position of the electrode carrier was described using a 5-point scale. After sectioning and histologic investigation, the results of the radiologic and histologic investigations were compared. In 17 of 20 cases, it was possible to estimate the correct position of the electrode carrier within the basal turn of the cochlea by means of computed tomography. As the insertion angles widened beyond 360 degrees, it became increasing difficult for the radiologists to correctly determine the position of the electrode carrier. Question: Do scalar localization by computed tomography of cochlear implant electrode carriers designed for deep insertion? <|endoftext|> <|assistant|> The comparison of our temporal bone experiment results with the computed tomography results revealed the difficulty of assessing the correct position of intracochlear electrodes. Scalar localization of deeply inserted electrode carriers cannot be precisely determined by means of computed tomography.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The presently available pharmaceutical aids in smoking cessation possess a rather limited effectiveness. Therefore, we have synthesized a series of immunoconjugates that stimulate the induction of antibodies which may bind nicotine in the blood, thereby preventing it from passing the blood-brain barrier. Thus, the reinforcing action of nicotine in the brain, which is the driving force in tobacco smoking, should be abolished. The present study was undertaken to test this notion in a long-term relapse model in rats, measuring the reinstatement of nicotine-seeking behavior, following active immunization with IP18-KLH, one of our immunoconjugates. Male Wistar rats were immunized with a nicotine-KLH conjugate (nicotine immunogen) and Freund's adjuvant after having been trained to meet the criteria of stable nicotine self-administration on a fixed ratio (FR3) schedule. The rats were subsequently extinguished from nicotine self-administration behavior and finally, as extinction was completed, they were exposed to small, priming doses of nicotine, which previously have been shown to reinstate the nicotine-seeking behavior. The antibody titers were measured by ELISA. It was found that rats with high titers (>1:10,000) of antibodies against nicotine, in contrast to those with low/no nicotine selective antibodies, do not reinstate nicotine self-administration behavior when they are exposed to nicotine. Question: Does active immunization against nicotine prevent reinstatement of nicotine-seeking behavior in rats? <|endoftext|> <|assistant|> Our findings indicate that active immunization against nicotine may effectively abolish the reinforcing action of nicotine in brain, an effect which is critical for relapse in nicotine dependence. These data suggest the potential utility of active immunization in smoking cessation programs.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: International and national bodies promote interdisciplinary care in the management of people with chronic conditions. We examine one facilitative factor in this team-based approach - the co-location of non-physician disciplines within the primary care practice. We used survey data from 330 General Practices in Ontario, Canada and New Zealand, as a part of a multinational study using The Quality and Costs of Primary Care in Europe (QUALICOPC) surveys. Logistic and linear multivariable regression models were employed to examine the association between the number of disciplines working within the practice, and the capacity of the practice to offer specialized and preventive care for patients with chronic conditions. We found that as the number of non-physicians increased, so did the availability of special sessions/clinics for patients with diabetes (odds ratio 1.43, 1.25-1.65), hypertension (1.20, 1.03-1.39), and the elderly (1.22, 1.05-1.42). Co-location was also associated with the provision of disease management programs for chronic obstructive pulmonary disease, diabetes, and asthma; the equipment available in the centre; and the extent of nursing services. Question: Is under the same roof : co-location of practitioners within primary care associated with specialized chronic care management? <|endoftext|> <|assistant|> The care of people with chronic disease is the 'challenge of the century'. Co-location of practitioners may improve access to services and equipment that aid chronic disease management.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Rad (Ras associated with diabetes) GTPase is a prototypic member of a new subfamily of Ras-related GTPases with unique structural features, although its physiological role remains largely unknown. In the present study, we characterized the Rad function in vascular smooth muscle cells (VSMCs) and the influence of adenovirus-mediated Rad (Ad-Rad) gene delivery on vascular remodeling after experimental angioplasty. We documented for the first time that neointimal formation using balloon-injured rat carotid arteries was associated with a significant increase in Rad expression as determined by immunohistochemistry and quantitative real-time reverse-transcriptase polymerase chain reaction. The levels of Rad expression in VSMCs were highly induced by platelet-derived growth factor and tumor necrosis factor-alpha. Morphometric analyses 14 days after injury revealed significantly diminished neointimal formation in the Ad-Rad-treated carotid arteries compared with Ad-GFP or PBS controls, whereas the mutated form of Rad GTPase, which can bind GDP but not GTP, increased neointimal formation. Overexpression of Rad significantly inhibited the attachment and migration of VSMCs. In addition, Rad expression dramatically reduced the formation of focal contacts and stress fibers in VSMCs by blocking the Rho/ROK signaling pathway. Question: Does rad GTPase attenuate vascular lesion formation by inhibition of vascular smooth muscle cell migration? <|endoftext|> <|assistant|> Our data clearly identified Rad GTPase as a novel and critical mediator that inhibits vascular lesion formation. Manipulation of the Rad signaling pathway may provide new therapeutic approaches that will limit vascular pathological remodeling.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: We have previously showed that endothelial progenitor cells (EPCs) through uptake of hepatitis B virus (HBV) may play a critical role in mediating extrahepatic HBV diseases. However, it remains to be elucidated whether mesenchymal stem cells (MSCs) are capable of mediating HBV trans-infection into extrahepatic tissues. In this study, we showed that HBV antigens, HBV DNA and the viral particles were detected in MSCs after 3 days virus challenge. Neither HBV covalently closed circular DNA nor pregenomic RNA were detected in MSCs. Intravenously transplantation of HBV-exposed MSCs into myocardial infarction mouse model resulted in incorporation of HBV into injured heart and other damaged tissues. Question: Are bone marrow-derived mesenchymal stem cells capable of mediating hepatitis B virus infection in injured tissues? <|endoftext|> <|assistant|> These results indicate that MSCs could serve as an additional extrahepatic virus reservoir, which may play a role at least in part in mediating HBV trans-infection into the injured tissues through the process of MSCs recruitment.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To investigate whether Helicobacter pylori causes inflammation in the normal middle ear and in the middle ear with effusion. Sixteen adult New Zealand white rabbits were divided into two gropus equally. Group I was representing histamine-induced middle ear inflammation and Group II was representing normal middle ear. While H. pylori was inoculated in the right ears, physiologic saline was inoculated in the left ears of the rabbits in both groups. Results were evaluated clinically, histopathologically and microbiologically. Fisher's exact test was used for statistical analysis. In Group I, clinical scores of the inflammation in the right ears were higher than the left ears scores at the 7th day. Histopathological scores of the inflammation in the right ears were higher than the left ears scores at the 7th day. Also, H. pylori was isolated in 6 of the 8 right ears of the rabbits. In Group II, while clinical scores of the inflammation in the right ears scores were higher than the left ears scores at the 7th day, histopathological scores were not significantly different between both ears. Also, no H. pylori was isolated in right ears of the rabbits. Question: Can Helicobacter pylori cause inflammation in the middle ear? <|endoftext|> <|assistant|> Effusion in the middle ear induced by histamine is an appropriate medium for H. pylori reproduction and it also aggravates the inflammation process. In contrary, H. pylori did not cause inflammation in the normal middle ear. We suggest that H. pylori does not play a role in the etiology of otitis media with effusion alone, but it contributes to the inflammation process in the presence of an effusion.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: The aim of this study was to investigate the relationship between pterygium and a decrease in the corneal endothelial cell density (ECD) in patients with unilateral primary pterygium. In this retrospective cross-sectional study, 90 consecutive patients with unilateral primary pterygium were enrolled from January 2010 to June 2012. Corneal ECD was measured in both eyes, and the fellow eyes were considered as controls. The relationship between the percentage of pterygium to cornea and a decrease in the ECD was analyzed. An increase in astigmatism in eyes with pterygium was evaluated for association with decreased ECD using the Pearson correlation test. The percentage of pterygium to cornea ranged from 3.5% to 65.2%, with a median of 12.35%. The difference in the corneal ECD between eyes with pterygium and control eyes ranged from +9.6% to -37.7%, with a median of -9.75%. The results of the Pearson correlation statistical test showed a strong logarithmic correlation between a decrease in the corneal ECD and the percentage of pterygium to cornea (R = 0.688, P < 0.001). An increase in astigmatism was correlated with a decrease in the ECD in eyes with pterygium. Question: Is pterygium related to a decrease in corneal endothelial cell density? <|endoftext|> <|assistant|> Pterygium is related to a decrease in corneal ECD. Surgical intervention should be considered in patients with extensive pterygium involvement in the cornea or a significant increase in astigmatism.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Early stage lung cancer has a variable prognosis, and there are currently no markers that predict which patients will recur. This study examined the relation between tumor-regulatory T (Treg) cells and total tumor-infiltrating T-cell lymphocytes (TIL) to determine whether they correlated with recurrence. The authors reviewed all patients in our tissue databank from 1996 to 2001 and identified 64 consecutive pathologic stage I non-small cell lung cancer (NSCLC) patients who had surgical resection and at least a 2.5 years disease-free follow-up or documented recurrence within 2 years. Immunohistochemical analyses were performed on paraffin-embedded lung cancer tissue and the relation between Treg cells, TIL, and disease-specific survival was determined. A risk index was devised deductively for various possible combinations of Treg cells and TIL. Treg cells and TIL were detected in 33 of 64 (51%) and 53 of 64 (83%) patients, respectively. When data were analyzed by using a Treg/TIL Combination Risk Index, patients with high-risk and intermediate-risk indices had hazard ratios of 8.2 (P = .007) and 3.3 (P = .109), respectively. Question: Do tumor infiltrating Foxp3+ regulatory T-cells are associated with recurrence in pathologic stage I NSCLC patients? <|endoftext|> <|assistant|> Patients with stage I NSCLC who have a higher proportion of tumor Treg cells relative to TIL had a significantly higher risk of recurrence. These data may be useful, particularly if combined with a panel of tumor markers, to suggest at the time of diagnosis which patients with seemingly early-stage NSCLC will relapse.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: This study investigated whether substance P potentiates the muscular and cardiac pain caused by the intraarterial infusion of adenosine, an autocoid known to induce muscular and cardiac ischemic-like pain in humans. Substance P is involved in the generation of neurogenic inflammation and causes cutaneous hyperalgesia. Because substance P is present in perivascular nerves it might also cause muscular and cardiac hyperalgesia. To test this hypothesis its effects on adenosine-induced muscular and cardiac pain were investigated in humans. A randomized, crossover study of the algogenic effects of the intrailiac infusion of increasing scalar doses (from 125 to 2,000 micrograms/min) of adenosine or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, was carried out in nine patients with no evidence of peripheral vascular disease. A similar protocol was carried out by infusing increasing scalar doses of adenosine (from 50 to 800 micrograms/min) or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, into the left coronary artery of eight patients with angina. Pain severity, assessed by a visual analog scale, is presented as median. The remaining data are presented as mean value +/- 1 SD. All patients experienced pain during both adenosine and substance P plus adenosine infusion; no patient experienced pain during the infusion of substance P alone. During intrailiac infusion, all patients experienced pain in the right leg that occurred earlier (207 +/- 152 vs. 321 +/- 154 s, p < 0.05) and was greater (47 vs. 30 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during the infusion of adenosine. Similarly, during intracoronary infusion, all patients experienced chest pain that occurred earlier (409 +/- 242 vs. 596 +/- 210 s, p < 0.05) and was greater (51 vs. 33 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during infusion of adenosine. No patient exhibited electrocardiographic signs of ischemia. Question: Does substance P potentiate the algogenic effects of intraarterial infusion of adenosine? <|endoftext|> <|assistant|> Substance P does not cause muscular or cardiac pain, but it provokes muscular and cardiac hyperalgesia.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To determine if mortality is increased in individuals with human immunodeficiency virus type 1 (HIV-1)-associated neurocognitive disorders less severe than frank dementia. A prospective cohort study; median duration of follow-up was 2.4 years. Kaplan-Meier analysis and Cox proportional hazards models were used to compare survival times according to neurocognitive classification. University-based research unit. A volunteer sample of 414 individuals seropositive for HIV-1. Subjects were classified at their baseline evaluation as neuropsychologically (NP) normal or abnormal (impaired in > or = 2 NP test domains). A subgroup of NP abnormal subjects met operational criteria for HIV-associated minor cognitive motor disorder; the remaining subjects were designated NP impaired. Subjects with frank dementia were excluded. Mortality. At the baseline evaluation, 256 (62%) of 414 subjects were designated normal; 109 (26%). NP impaired; and 49 (12%), minor cognitive motor disorder. One hundred six participants (26%) died during follow-up. Compared with the NP normal group, the unadjusted relative risk (RR) of death for all NP abnormal subjects (minor cognitive motor disorder and NP impaired) was significantly increased (RR, 1.7; 95% confidence interval [CI], 1.2-2.6; P < .005). After adjusting for concurrently measured predictors of survival (CD4 lymphocyte counts, Centers for Disease Control and Prevention HIV disease classification, hemoglobin concentration, and serum beta 2-microglobulin) in proportional hazards models, mortality for all NP abnormal subjects remained elevated (RR, 1.8; 95% CI, 1.2-2.8; P < .01). The elevation in mortality risk for subjects with minor cognitive motor disorder was statistically significant (RR, 2.2; 95% CI, 1.2-3.8; P < .01); for NP impaired subjects it was marginally significant (RR, 1.6; 95% CI, 1.0-2.8; P = .06). Question: Is neurocognitive impairment an independent risk factor for death in HIV infection . San Diego HIV Neurobehavioral Research Center Group? <|endoftext|> <|assistant|> The HIV-infected individuals with NP impairment had a higher risk of dying than those without impairment. This was particularly true for those meeting syndromic diagnostic criteria.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Epithelial-mesenchymal transition (EMT) is a crucial process in cancer progression that provides cancer cells with the ability to escape from the primary focus, invade stromal tissues and migrate to distant regions. Cell lines that lack E-cadherin show increased tumorigenesis and metastasis, and the expression levels of E-cadherin and Snail correlate inversely with the prognosis of patients suffering from breast cancer or oral squamous cell carcinoma (OSCC). Moreover, recent studies have shown that most EMT cases are regulated by soluble growth factors or cytokines. Among these factors, fibroblast growth factors (FGFs) execute diverse functions by binding to and activating members of the FGF receptor (FGFR) family, including FGFR1-4. Fibroblast growth factor receptor 1 is an oncoprotein that is involved in tumorigenesis, and PD173074 is known to be a selective inhibitor of FGFR1. However, the roles of FGFR1 and FGFR1 inhibitors have not yet been examined in detail. Here, we investigated the expression of FGFR1 in head and neck squamous cell carcinoma (HNSCC) and the role of the FGFR1 inhibitor PD173074 in carcinogenesis and the EMT process. Fibroblast growth factor receptor 1 was highly expressed in 54% of HNSCC cases and was significantly correlated with malignant behaviours. Nuclear FGFR1 expression was also observed and correlated well with histological differentiation, the pattern of invasion and abundant nuclear polymorphism. Fibroblast growth factor receptor 1 was also overexpressed in EMT cell lines compared with non-EMT cell lines. Furthermore, treatment of HOC313 cells with PD173074 suppressed cellular proliferation and invasion and reduced ERK1/2 and p38 activation. These cells also demonstrated morphological changes, transforming from spindle- to cobble stone-like in shape. In addition, the expression levels of certain matrix metalloproteinases (MMPs), whose genes contain activator protein-1 (AP-1) promoter sites, as well as Snail1 and Snail2 were reduced following PD173074 treatment. Question: Does the FGFR1 inhibitor PD173074 induce mesenchymal-epithelial transition through the transcription factor AP-1? <|endoftext|> <|assistant|> Taken together, these data suggest that PD173074 inhibits the MAPK pathway, which regulates the activity of AP-1 and induces MET. Furthermore, this induction of MET likely suppresses cancer cell growth and invasion.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: To describe a more limited and less malignant form of Rasmussen encephalitis (RE). Three subjects (all women; 37, 31, and 32 years of age) developed childhood or late onset chronic focal encephalitis, with a relatively nonprogressive form of the disorder. In our patients, clinical features were dominated by partial seizures without marked focal motor deficit and in two with choreo-dystonic movements. The diagnosis of RE was supported by histologic examination and anatomic and functional MRI. Question: Limited chronic focal encephalitis: another variant of Rasmussen syndrome? <|endoftext|> <|assistant|> These cases extend the phenotypic presentations of Rasmussen encephalitis and confirm Theodore Rasmussen's suggestion that there may be mild and nonprogressive forms of the disease.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Reducing central line-associated bloodstream infections (CLABSIs) poses a set of unique challenges in long-term acute care hospitals (LTACHS). Patients are often admitted to LTACHs with central lines in place from the previous hospitalization; thus, LTACHs lack control over insertion techniques and respective central line care and maintenance. This study aimed to demonstrate the impact of a methodical bathing approach with 2% chlorhexidine gluconate (CHG) cloths and a correlation with a reduced prevalence of CLABSIs in our LTACH population. This retrospective observational quality initiative conducted in a 105-bed LTACH used plan-do-study-act methodology to assess the effects of a revised bathing approach using 2% CHG. Statistical significance demonstrated a 65% reduction in CLABSI on the pilot unit after the 6-month initial trial. The results of the quality initiative were evaluated through the end of 2012. Question: Does quality improvement intervention reduce episodes of long-term acute care hospital central line-associated infections? <|endoftext|> <|assistant|> The decision was made to implement the revised bathing protocol throughout the entire LTACH hospital stay.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: NO produced by endothelial NOS is needed for normal vascular function. During diabetes, aging and hypertension, elevated levels of arginase can compete with NOS for available l-arginine, reducing NO and increasing superoxide (O(2) (.-)) production via NOS uncoupling. Elevated O(2) (.-) combines with NO to form peroxynitrite (ONOO(-)), further reducing NO. Oxidative species increase arginase activity, but the mechanism(s) involved are not known. Our study determined the mechanism involved in peroxynitrite and hydrogen peroxide-induced enhancement in endothelial arginase activity. We hypothesized that oxidative species increase arginase activity through PKC-activated RhoA/Rho kinase (ROCK) pathway. Arginase activity/expression was analysed in bovine aortic endothelial cells (BAEC) treated with an ONOO(-) generator (SIN-1) or H(2) O(2). Pretreatment with inhibitors of Rho kinase (Y-27632) or PKC (Gö6976) was used to investigate the mechanism involved in arginase activation. Exposure to SIN-1 (25 µM, 24 h) or H(2) O(2) (25 µM, 8 h) increased arginase I expression and arginase activity (35% and 50%, respectively), which was prevented by ROCK inhibitor, Y-27632, PKC inhibitor, Gö6976 or siRNA to p115-Rho GEF. There was an early activation of p115-Rho GEF (SIN-1, 2 h; H(2) O(2), 1 h) and Rho A (SIN-1, 4 h; H(2) O(2), 1 h) that was prevented by using the PKC inhibitor. Exposure to SIN-1 and H(2) O(2 ) also reduced NOS activity, which was blocked by pretreatment with p115-RhoGEF siRNA. Question: Do oxidative species increase arginase activity in endothelial cells through the RhoA/Rho kinase pathway? <|endoftext|> <|assistant|> Our data indicate that the oxidative species ONOO(-) and H(2) O(2) increase arginase activity/expression through PKC-mediated activation of RhoA/Rho kinase pathway.

<|system|> You are an biomedical AI assistant that follows instruction extremely well, Your task is to answer biomedical questions precisely and truthfully using the given abstract <|endoftext|> <|prompter|> Abstract: Airway smooth muscle (ASM) hyperplasia is a hallmark of asthma that is associated with disease severity and persistent airflow obstruction. We sought to investigate whether fibrocytes, a population of peripheral blood mesenchymal progenitors, are recruited to the ASM compartment in asthma. We assessed the number of fibrocytes in bronchial biopsy specimens and peripheral blood from subjects with mild-to-severe refractory asthma versus healthy control subjects. In vitro we investigated potential mechanisms controlling fibrocyte migration toward the ASM bundle. Fifty-one subjects with asthma and 33 control subjects were studied. In bronchial biopsy specimens, the number of fibrocytes was increased in the lamina propria of subjects with severe refractory asthma (median [interquartile range] number, 1.9/mm(2) [1.7/mm(2)]) versus healthy control subjects (median [interquartile range] number, 0/mm(2) [0.3/mm(2)], P < .0001) and in the ASM bundle of subjects with asthma of all severities (subjects with severe asthma, median [interquartile range] number, 3.8/mm(2) [9.4/mm(2)]; subjects with mild-to-moderate asthma, median [interquartile range] number, 1.1/mm(2) [2.4/mm(2)]); healthy control subjects, (median [interquartile range] number, 0/mm(2) [0/mm(2)]); P = .0004). In the peripheral blood the fibrocyte number was also increased in subjects with severe refractory asthma (median [interquartile range] number, 1.4 x 10(4)/mL [2.6 x 10(4)/mL]) versus healthy control subjects (median [interquartile range] number, 0.4 x 10(4)/mL [1.0 x 10(4)/mL], P = .002). We identified that in vitro ASM promotes fibrocyte chemotaxis and chemokinesis (distance of migration after 4.5 hours, 31 microm [2.9 microm] vs 17 microm [2.4 microm], P = .0001), which was in part mediated by platelet-derived growth factor (mean inhibition by neutralizing antibody, 16% [95% CI, 2% to 32%], P = .03) but not by activation of chemokine receptors. Question: Is fibrocyte localization to the airway smooth muscle a feature of asthma? <|endoftext|> <|assistant|> This study provides the first evidence that fibrocytes are present in the ASM compartment in asthma and that ASM can augment fibrocyte migration. The importance of fibrocytes in the development of ASM hyperplasia and airway dysfunction in asthma remains to be determined.