tbuckley/cabot-search huggingface dataset:
Low-dose albumin in the treatment of spontaneous bacterial peritonitis: should we change the standard treatment?: Table 1
Authors: Alexandre de Araujo, Antônio de Barros Lopes, Gabriela Rossi, Gabriel Veber da Silva, Patrícia Ananias, Sandro Ness, Mário Reis Álvares-da-Silva
Journal: Gut (2012)

We read with interest the recent paper published on the management of patients awaiting liver transplant.1 The authors carried out a comprehensive review of liver complications, including spontaneous bacterial peritonitis (SBP). They stated that intravenous albumin (IV-A) at a dose of 1.5 g/kg at diagnosis and 1 g/kg 48 h later has been shown to prevent renal impairment and reduces mortality. We would like to address this point as this benefit has only been demonstrated in one clinical trial in which an arbitrary dose of albumin was used.2 …
Arthritis development in patients with arthralgia is strongly associated with anti-citrullinated protein antibody status: a prospective cohort study
Authors: W H Bos, G J Wolbink, M Boers, G J Tijhuis, N de Vries, I E van der Horst-Bruinsma, P P Tak, R J van de Stadt, C J van der Laken, B A C Dijkmans, D van Schaardenburg
Journal: Annals of the Rheumatic Diseases (2009)

Background Anti-citrullinated protein antibodies (ACPA) are associated with increased risk for rheumatoid arthritis. Objective To investigate the effect of the presence and levels of ACPA on arthritis development in patients with arthralgia. Methods Patients with arthralgia positive for ACPA or IgM rheumatoid factor (IgM-RF) were tested for the shared epitope (SE) and were prospectively followed up for at least 12 months. Absence of clinical arthritis at inclusion and arthritis development during follow-up were independently confirmed by two investigators. Cox regression hazard analyses were used to calculate hazard ratios (HRs) for arthritis development. Results 147 patients with arthralgia were included (50 ACPA positive, 52 IgM-RF positive and 45 positive for both antibodies). After a median follow-up of 28 months (interquartile range (IQR) 19–39), 29 patients developed arthritis in a median of 4 (IQR 3–6) joints and 26 (90%) of these were ACPA positive. The presence of ACPA (HR = 6.0; 95% confidence interval (95% CI) 1.8 to 19.8; p = 0.004), but not of IgM-RF (HR = 1.4, 95% CI 0.6 to 3.1) nor the SE (HR = 1.5, 95% CI 0.7 to 3.0), was associated with arthritis development. Within the group of ACPA-positive patients, the risk for arthritis was enhanced by the presence of IgM-RF (HR = 3.0; 95% CI 1.4 to 6.9; p = 0.01) and high ACPA levels (HR = 1.7; 95% CI 1.1 to 2.5; p = 0.008), but not the SE (HR = 1.0; 95% CI 0.5 to 2.1; p = 1.0). Conclusion In patients with arthralgia the presence of ACPA (but not of IgM-RF or SE) predicts arthritis development. The risk in ACPA-positive patients may be further increased by the concomitant presence of IgM-RF or high levels of ACPA.
Endoscopic therapy for bleeding peptic ulcer; A randomised, controlled trial comparing heater probe plus human thrombin injection with heater probe plus placebo injection
Authors: NI Church, HJ Dallal, J Masson, Annemarie Fraser, Nag Mowat, DA Johnston, G Fullarton, E Radin, Marc Turner, Robin Prescott, John Plevris, KR Palmer
Journal: Gut (2002)
Radioimmunoassay of Prostaglandin A
Authors: AHMAD A. ATTALLAH, JAMES B. LEE
Journal: Circulation Research (1973)

A highly specific, sensitive (25 pg) radioimmunoassay for prostaglandin A is described; the assay is characterized by high reproducibility (coefficient of variation 1-2%) and low cross-reactivity with respect to PGE 1 and PGE 2 (10%), PGB 2 (15%), and PGF 2α (0.01%). High specificity for PGA was obtained by chromatographic separation of the prostaglandins. Since it has been suggested that PGA is a natriuretic "hormone," the concentration of PGA in the renal cortex, outer medulla, and papilla was determined in rabbits on low-sodium and high-sodium diets in the presence and the absence of the prostaglandin synthetase inhibitor indomethacin. In rabbits on the low-sodium diet (12 mEq/24 hours). PGA2 was 15 ± 4 pg/mg in the cortex, 502 ± 67 pg/mg in the outer medulla, and 3740 ± 640 pg/mg in the papilla. In rabbits on saline loading (56 mEq/24 hours), cortical and outer medullary PGA2 rose to 32 ± 6 pg/mg and 1275 ± 290 pg/mg, respectively, but papillary PGA decreased to 1842 ± 480 pg/mg. PGA concentration in the outer medulla and papilla was markedly inhibited by indomethacin (50 mg/day), and this inhibition was associated with sodium retention. The results indicated that sodium induced papillary synthesis of PGA and intrarenal circulation of the prostaglandin to the outer medulla and the cortex possibly via the long veins of the outer medulla occurred. The results are compatible with PGA 2 involvement in salineinduced natriuresis.
c-Kit Is Essential for Alveolar Maintenance and Protection from Emphysema-like Disease in Mice
Authors: James Y. Lindsey, Koustav Ganguly, David M. Brass, Zhuowei Li, Erin N. Potts, Simone Degan, Huaiyong Chen, Brian Brockway, Soman N. Abraham, Annerose Berndt, Barry R. Stripp, W. Michael Foster, George D. Leikauf, Holger Schulz, John W. Hollingsworth
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Previously, we demonstrated a candidate region for susceptibility to airspace enlargement on mouse chromosome 5. However, the specific candidate genes within this region accounting for emphysema-like changes remain unrecognized. c-Kit is a receptor tyrosine kinase within this candidate gene region that has previously been recognized to contribute to the survival, proliferation, and differentiation of hematopoietic stem cells. Increases in the percentage of cells expressing c-Kit have previously been associated with protection against injury-induced emphysema.Determine whether genetic variants of c-Kit are associated with spontaneous airspace enlargement.Perform single-nucleotide polymorphism association studies in the mouse strains at the extremes of airspace enlargement phenotype for variants in c-Kit tyrosine kinase. Characterize mice bearing functional variants of c-Kit compared with wild-type controls for the development of spontaneous airspace enlargement. Epithelial cell proliferation was measured in culture.Upstream regulatory single-nucleotide polymorphisms in the divergent mouse strains were associated with the lung compliance difference observed between the extreme strains. c-Kit mutant mice (Kit(W-sh)/(W-sh)), when compared with genetic controls, developed altered lung histology, increased total lung capacity, increased residual volume, and increased lung compliance that persist into adulthood. c-Kit inhibition with imatinib attenuated in vitro proliferation of cells expressing epithelial cell adhesion molecule.Our findings indicate that c-Kit sustains and/or maintains normal alveolar architecture in the lungs of mice. In vitro data suggest that c-Kit can regulate epithelial cell clonal expansion. The precise mechanisms that c-Kit contributes to the development of airspace enlargement and increased lung compliance remain unclear and warrants further investigation.
Association of k-ras, b-raf, and p53 Status With the Treatment Effect of Bevacizumab
Authors: William L. Ince, Adrian M. Jubb, Scott N. Holden, Eric B. Holmgren, Patti Tobin, Meera Sridhar, Herbert I. Hurwitz, Fairooz Kabbinavar, William F. Novotny, Kenneth J. Hillan, Hartmut Koeppen
Journal: JNCI Journal of the National Cancer Institute (2005)

A recent phase III trial showed that the addition of bevacizumab, a monoclonal antibody to vascular endothelial growth factor-A, to first-line irinotecan, 5-fluorouracil, and leucovorin (IFL) prolonged median survival in patients with metastatic colorectal cancer. We carried out a retrospective analysis of patients in the trial to evaluate whether mutation status of k-ras, b-raf, or p53 or P53 expression could predict which patients were more likely to respond to bevacizumab.Microdissected tumors from 295 patients (274 primary tumors, 21 metastases) were subject to DNA sequence analysis to identify mutations in k-ras, b-raf, and p53. Nuclear P53 expression was determined by immunohistochemistry. Hazard ratios and 95% confidence intervals (CI) for overall survival were estimated using Cox regression analysis.In all biomarker subgroups, estimated hazard ratios for risk of death were less than 1 for bevacizumab-treated patients as compared with those for placebo-treated patients. Mutations in k-ras and/or b-raf were observed in 88 of 213 patients (41%). Hazard ratios for death among patients with tumors with wild-type k-ras/b-raf status, as compared with those of patients with mutations in one or both genes, were 0.51 (95% CI = 0.28 to 0.95) among those treated with IFL plus bevacizumab and 0.66 (95% CI = 0.37 to 1.18) among those treated with IFL plus placebo. Mutations in p53 were found in 139 of 205 patients (68%), and P53 was overexpressed in 191 of 266 patients (72%); neither p53 mutation nor P53 overexpression was statistically significantly associated with survival.We did not find a statistically significant relationship between mutations of k-ras, b-raf, or p53 and the increase in median survival associated with the addition of bevacizumab to IFL in metastatic colorectal cancer.
Diabetes and hepatocellular cancer risk: Not only a matter of hyperglycemia
Authors: Giulio Marchesini, Gabriele Forlani, Roberto J. Groszmann, Yasuko Iwakiri, Tamar H. Taddei
Journal: Hepatology (2012)

Studies of diabetes and hepatocellular carcinoma (HCC) yielded inconsistent findings. This meta-analysis was conducted to examine the association between diabetes and risk of HCC. Studies were identified by searching PUBMED and MEDLINE database up to February 2011. Pooled risk estimates were calculated using the random-effects model. Potential sources of heterogeneity were explored by subgroup analyses. A total of 17 case-control studies and 32 cohort studies were included in the meta-analysis. The combined risk estimate of all studies showed a statistically significant increased risk of HCC prevalence among diabetic individuals (RR = 2.31, 95% CI: 1.87–2.84). The pooled risk estimate of 17 case-control studies (OR = 2.40, 95% CI: 1.85–3.11) was slightly higher than that from 25 cohort studies (RR = 2.23, 95% CI: 1.68–2.96). Metformin treatment was potentially protective. On the contrary, long duration of diabetes and sulfonylureas or insulin treatment could increase HCC risk. Also meta-analysis of 7 cohort studies found a statistically significant increased risk of HCC mortality (RR = 2.43, 95% CI: 1.66–3.55) for individuals with (versus without) diabetes. This meta-analysis shows that diabetes is associated with moderately increased risk of HCC incidence, as well as HCC mortality. Considering the rapidly increasing prevalence of diabetes mellitus, the study underlines the need for cancer prevention in diabetic individuals. Further investigation is needed to focus on the potential mechanism for the pathogenesis of HCC and the link between HCC and different types, severity, treatment and duration of diabetes.
Splenectomy for Prolapse of the Spleen through a Perforating Wound of the Abdomen: Recovery
Authors: E. H. Brown
Journal: BMJ (1897)

Pressure of an organ like the spleen on the uterus not only mechanically interferes with the uterus but seriously disturbs menstruation.DANGER TO LIFE.It will be gathered from what has been stated in the fore- going sections that a wandering spleen may, and occasionally
Interaction between Tie receptors modulates angiogenic activity of angiopoietin2 in endothelial progenitor cells
Authors: K KIM, I SHIN, J KIM, J CHOI, J BYUN, E JEON, W SUH, D KIM
Journal: Cardiovascular Research (2006)

Ischemia-dependent upregulation of angiopoietin2 (Ang2) led us to hypothesize the potentially proangiogenic Ang2-Tie2 signaling in endothelial progenitor cells (EPCs). Given the well-known vascular destabilizing action of Ang2 in mature endothelium, we investigated the yet unidentified mechanism behind cell-dependent differential activity of Ang2.Both in vitro and in vivo experiments showed that Ang2 promoted angiogenicity of human cord blood-derived EPCs, where Ang2 directly activated Tie2 and its related downstream signaling molecules. However, Ang2 had no such effect in fully differentiated human umbilical vein endothelial cells (HUVECs) under the same condition. Such a cell-dependent Tie2 activation by Ang2 was explained by comparing EPCs and HUVECs, where most Tie2 receptors in EPCs were found to be present unbound to Tie1, whereas those in HUVECs existed as heterocomplexes with Tie1. When Tie2 in HUVECs was prevented from forming heterocomplexes by silencing Tie1 expression, they underwent rapid phosphorylation upon Ang2 treatment, as shown in EPCs.In contrast with its roles in mature endothelial cells, Ang2 has proangiogenic activities in EPC directly through Tie2 signaling pathway. Such a cell-dependent differential reactivity of Ang2 was for the first time found to be modulated by physical association between Tie1 and Tie2, which inhibited Ang2-mediated Tie2 activation.
Tumor stage, human papillomavirus and smoking status affect the survival of patients with oropharyngeal cancer: an Italian validation study
Authors: R. Granata, R. Miceli, E. Orlandi, F. Perrone, B. Cortelazzi, M. Franceschini, L.D. Locati, P. Bossi, C. Bergamini, A. Mirabile, L. Mariani, P. Olmi, G. Scaramellini, P. Potepan, P. Quattrone, K.K. Ang, L. Licitra
Journal: Annals of Oncology (2011)
Letter by Montenegro and Lundberg Regarding Article, “Unexpected Effect of Proton Pump Inhibitors: Elevation of the Cardiovascular Risk Factor Asymmetric Dimethylarginine”
Authors: Marcelo F. Montenegro, Jon O. Lundberg
Journal: Circulation (2014)

We read with interest the article by Ghebremariam et al 1 demonstrating that proton pump inhibitors (PPIs) reduce endogenous formation of nitric oxide (NO) and impair vascular reactivity. 1 This deleterious effect of PPIs occurred through inhibition of the enzyme dimethylarginine dimethylaminohydrolase, which degrades asymmetrical diemethylarginine, an endogenous NO synthase inhibitor. 1he authors discuss this as a possible mechanism explaining the increased risk of adverse cardiovascular events with prolonged PPI treatment. 2We bring up another mechanism by which PPIs may alter vascular NO homeostasis, with possible added deleterious effects in the cardiovascular system.Although classic formation of NO is from l-arginine and mediated by NO synthases, an alternative pathway for NO formation has been described more recently.The major oxidation products of NO metabolism nitrite and nitrate are recycled in blood and tissues through reductive pathways to again form NO and other bioactive nitrogen oxides. 3Nitrate is also found in our everyday diet, and studies have shown robust NO-like effects of nitrate ingestion, including a reduction in blood pressure and improvements in vascular function. 2These beneficial cardiovascular effects of dietary nitrate involve an entero-salivary circulation in which nitrate is rapidly absorbed in the gastrointestinal tract and then actively taken up by the salivary glands and concentrated up to 20-fold in saliva. 3Oral commensal bacteria then reduce salivary nitrate to nitrite, and when saliva enters the acidic stomach, much of the nitrite is rapidly protonated to form nitrous acid, which decomposes further to form NO and other nitrogen oxides. 3In addition, some nitrite is also absorbed systemically and reduced to NO in blood and tissues.The use of PPIs increases the gastric pH, and this contributes to impairments of the nitrate-nitrite-NO pathway described above.Indeed, a recent study in rats showed that the increases in gastric pH caused by the PPI omeprazole completely blunted the beneficial antihypertensive effects of oral nitrite. 4ntriguingly, nitrate also interacts directly with the pathway studied by Ghebremariam et al, 1 as demonstrated by decreases in asymmetrical diemethylarginine levels in a rat model of chronic cardiovascular disease after treatment with dietary nitrate. 5In addition, PPI-induced inhibition of NO synthase will lead to a decrease in circulating levels of nitrate and nitrite, thereby affecting also the nitrate-nitrite-NO pathway.In aggregate, PPIs may disturb vascular NO homeostasis in 2 interconnected ways, both of which may contribute to the association between PPIs and cardiovascular risk.
CD160 is essential for NK-mediated IFN-γ production
Authors: Tony C. Tu, Nicholas K. Brown, Tae-Jin Kim, Joanna Wroblewska, Xuanming Yang, Xiaohuan Guo, Seoyun Hyunji Lee, Vinay Kumar, Kyung-Mi Lee, Yang-Xin Fu
Journal: The Journal of Experimental Medicine (2015)

NK-derived cytokines play important roles for natural killer (NK) function, but how the cytokines are regulated is poorly understood. CD160 is expressed on activated NK or T cells in humans but its function is unknown. We generated CD160-deficient mice to probe its function. Although CD160−/− mice showed no abnormalities in lymphocyte development, the control of NK-sensitive tumors was severely compromised in CD160−/− mice. Surprisingly, the cytotoxicity of NK cells was not impaired, but interferon-γ (IFN-γ) secretion by NK cells was markedly reduced in CD160−/− mice. Functionally targeting CD160 signaling with a soluble CD160-Ig also impaired tumor control and IFN-γ production, suggesting an active role of CD160 signaling. Using reciprocal bone marrow transfer and cell culture, we have identified the intrinsic role of CD160 on NK cells, as well as its receptor on non-NK cells, for regulating cytokine production. To demonstrate sufficiency of the CD160+ NK cell subset in controlling NK-dependent tumor growth, intratumoral transfer of the CD160+ NK fraction led to tumor regression in CD160−/− tumor-bearing mice, indicating demonstrable therapeutic potential for controlling early tumors. Therefore, CD160 is not only an important biomarker but also functionally controls cytokine production by NK cells.
Autopoiesis and <i>Lifelines: </i>The importance of origins
Authors: Evan Thompson, Francisco J. Varela
Journal: Behavioral and Brain Sciences (1999)

Lifelines provides a useful corrective to “ultra-Darwinism” but it is marred by its failure to cite its scientific predecessors. Rose's argument could have been strengthened by taking greater account of the theory of autopoiesis in biology and of enactive cognitive science.
The Importance of Identification of the Myocardial-Specific Isoenzyme of Creatine Phosphokinase (MB Form) in the Diagnosis of Acute Myocardial Infarction
Authors: GALEN S. WAGNER, CHARLES R. ROE, LEE E. LIMBIRD, ROBERT A. ROSATI, ANDREW G. WALLACE
Journal: Circulation (1973)

Serial plasma determinations of the isoenzymes of CPK were performed in all patients (376) admitted to a coronary care unit during a 12-month period with diagnosis of possible acute myocardial infarction. Results were compared with data from other enzyme studies and from the electrocardiogram. An attempt was made to determine the incidence of falsely positive CPK-MB (myocardial-specific form). "No acute infarction" was diagnosed in all patients in whom neither total CPK nor the isoenzymes of LDH indicated myocardial necrosis, and in whom there were no QRS changes on ECG. Incidence of falsely negative CPK isoenzyme data was also determined. All patients, in whom total CPK was transiently elevated, and LDH 1 exceeded LDH 2 , and new QRS changes occurred, were termed "definite" acute infarction. CPK-MB form was present in all 55 of these (0% false negative). Therefore, determination of the isoenzymes of CPK by this method provides both a sensitive and specific indication of acute myocardial infarction.
Effects of Low-Carbohydrate and Low-Fat Diets
Authors: Lydia A. Bazzano, Tian Hu, Kristi Reynolds, Lu Yao, Calynn Bunol, Yanxi Liu, Chung-Shiuan Chen, Michael J. Klag, Paul K. Whelton, Jiang He
Journal: Annals of Internal Medicine (2014)

Low-carbohydrate diets are popular for weight loss, but their cardiovascular effects have not been well-studied, particularly in diverse populations.To examine the effects of a low-carbohydrate diet compared with a low-fat diet on body weight and cardiovascular risk factors.A randomized, parallel-group trial. (ClinicalTrials.gov: NCT00609271).A large academic medical center.148 men and women without clinical cardiovascular disease and diabetes.A low-carbohydrate (<40 g/d) or low-fat (<30% of daily energy intake from total fat [<7% saturated fat]) diet. Both groups received dietary counseling at regular intervals throughout the trial.Data on weight, cardiovascular risk factors, and dietary composition were collected at 0, 3, 6, and 12 months.Sixty participants (82%) in the low-fat group and 59 (79%) in the low-carbohydrate group completed the intervention. At 12 months, participants on the low-carbohydrate diet had greater decreases in weight (mean difference in change, -3.5 kg [95% CI, -5.6 to -1.4 kg]; P = 0.002), fat mass (mean difference in change, -1.5% [CI, -2.6% to -0.4%]; P = 0.011), ratio of total-high-density lipoprotein (HDL) cholesterol (mean difference in change, -0.44 [CI, -0.71 to -0.16]; P = 0.002), and triglyceride level (mean difference in change, -0.16 mmol/L [-14.1 mg/dL] [CI, -0.31 to -0.01 mmol/L {-27.4 to -0.8 mg/dL}]; P = 0.038) and greater increases in HDL cholesterol level (mean difference in change, 0.18 mmol/L [7.0 mg/dL] [CI, 0.08 to 0.28 mmol/L {3.0 to 11.0 mg/dL}]; P < 0.001) than those on the low-fat diet.Lack of clinical cardiovascular disease end points.The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet. Restricting carbohydrate may be an option for persons seeking to lose weight and reduce cardiovascular risk factors.National Institutes of Health.
Clinical Predictors of the Respiratory Arousal Threshold in Patients with Obstructive Sleep Apnea
Authors: Bradley A. Edwards, Danny J. Eckert, David G. McSharry, Scott A. Sands, Amar Desai, Geoffrey Kehlmann, Jessie P. Bakker, Pedro R. Genta, Robert L. Owens, David P. White, Andrew Wellman, Atul Malhotra
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

A low respiratory arousal threshold (ArTH) is one of several traits involved in obstructive sleep apnea pathogenesis and may be a therapeutic target; however, there is no simple way to identify patients without invasive measurements.To determine the physiologic determinates of the ArTH and develop a clinical tool that can identify patients with low ArTH.Anthropometric data were collected in 146 participants who underwent overnight polysomnography with an epiglottic catheter to measure the ArTH (nadir epiglottic pressure before arousal). The ArTH was measured from up to 20 non-REM and REM respiratory events selected randomly. Multiple linear regression was used to determine the independent predictors of the ArTH. Logistic regression was used to develop a clinical scoring system.Nadir oxygen saturation as measured by pulse oximetry, apnea-hypopnea index, and the fraction of events that were hypopneas (Fhypopneas) were independent predictors of the ArTH (r(2) = 0.59; P < 0.001). Using this information, we used receiver operating characteristic analysis and logistic regression to develop a clinical score to predict a low ArTH, which allocated a score of 1 to each criterion that was satisfied: (apnea-hypopnea index, <30 events per hour) + (nadir oxygen saturation as measured by pulse oximetry >82.5%) + (Fhypopneas >58.3%). A score of 2 or above correctly predicted a low arousal threshold in 84.1% of participants with a sensitivity of 80.4% and a specificity of 88.0%, a finding that was confirmed using leave-one-out cross-validation analysis.Our results demonstrate that individuals with a low ArTH can be identified from standard, clinically available variables. This finding could facilitate larger interventional studies targeting the ArTH.