Miracle-dz/UniFAR-FTUs huggingface dataset:
Exercise training reduces the sympathetic component of the blood pressure-heart rate baroreflex in man.

1. Exercise training reduces resting sympathetic activity, but the effects on sympathetic activation or withdrawal during baroreflex responses to blood pressure perturbations are controversial. The purpose of this study was to investigate the effects of training on both the vagal and sympathetic reflex heart rate responses to blood pressure changes. 2. Using 10 healthy males in a randomized cross-over design, we examined the effects of three 30 min cycling sessions at 70% of maximal capacity for 4 weeks on the steady-state reflex heart rate responses to perturbations in mean arterial pressure induced with injections of nitroprusside and phenylephrine. The method provides a sigmoidal relationship between changes in heart rate and blood pressure. The upper plateau (maximum tachycardia in response to blood pressure reduction) and lower plateau (maximum bradycardia in response to blood pressure elevation) are mainly mediated by the cardiac sympathetics and vagus, respectively. The slope of the relationship is a measure of reflex gain. 3. Training, which increased maximal oxygen consumption by 13 +/- 2% (mean +/- standard error of the difference), reduced supine and standing blood pressures by 3 +/- 1/3 +/- 1 mmHg (P less than 0.05) and 4 +/- 1/2 +/- 2 mmHg (P less than 0.05 for systolic), respectively, whereas resting heart rate was lowered by 6 +/- 1 beats/min (P less than 0.05). Reflex sensitivity in the presence of functioning vagus and sympathetics was not altered with training, but the vagal component of sensitivity, as assessed after sympathetic blockade with propranolol, was significantly reduced. (ABSTRACT TRUNCATED AT 250 WORDS)
Diagnostic value of plasma chromogranin A in neuroendocrine tumours

Aim The aim of this study was to assess the value of plasma chromogranin A (CgA), a protein produced by neuroendocrine cells, in the diagnosis of neuroendocrine tumours. Methods Eighty subjects with neuroendocrine tumours were studied. Thirty-four had carcinoids, 21 nonfunctioning endocrine pancreatic tumours, 17 multiple endocrine neoplasia type 1 (MEN 1) (six of these also had gastrinomas), and eight had functioning pancreatic tumours (four gastrinomas, two glucagonomas, two somatostatinomas). Twenty-eight healthy subjects were studied as controls. A fasting plasma sample was obtained from each subject, and CgA plasma levels were measured by the ELISA method using a kit (Dako A/S, Denmark). Results In control subjects, plasma CgA values were below 5 U/l. Among the patients, 20 of the 34 with carcinoid tumours, 12 of the 21 with nonfunctioning pancreatic tumours, nine of the 17 with MEN 1 (including the six with gastrinomas), and the four gastrinomas of the eight functioning pancreatic tumours, i.e. overall, 45 of the 80 patients (56.3%) had abnormally high CgA values (22–961 U/l). Most of the patients with elevated CgA values, except nine of the 10 with gastrinomas, had multiple liver metastasis. Conclusions The results show that the diagnostic value of plasma CgA in neuroendocrine tumours is relatively low; it may be of some interest only in patients with advanced disease and liver metastasis. Gastrinoma seems to be an exception, because in this tumour high CgA values are generally found even in the absence of liver metastasis.
Eating disorders in the general practice: a case-control study on the utilization of primary care.

OBJECTIVE To investigate primary care utilization between patients with an eating disorder (ED) and other patient groups, and between the ED subgroups anorexia nervosa (AN) and bulimia nervosa (BN). METHOD The present study was an observational case-control study. In total, 167 patients with ED were matched with two control groups (with and without mental disorders). General practitioners (GPs) kept electronic records and provided all patient contacts, prescriptions and referrals with a diagnostic code. RESULTS Although patients with BN have the highest number of face-to-face contacts compared with all other groups, these patients less often seek help for eating problems compared with patients with AN, even when the ED diagnosis is known to the GP. Overall, patients with mental disorders showed a comparable rate of GP care, which was elevated compared with patients without mental disorders. DISCUSSION Patients with BN might need more active encouragement by the GP to talk about their eating problems because there are indications that point at an unmet need for GP care.
Patients with Borderline Personality Disorder Not Participating in an RCT: Are They Different?

Background: Despite the notion that randomized controlled trials are regarded as the gold standard in psychotherapy research, questions about their generalizability have been raised. This paper focuses on the differences between participants and eligible nonparticipants of a randomized controlled trial for patients with borderline personality disorder (BPD). Sampling and Methods: One hundred forty-two patients were screened, and 122 were found eligible for study participation. Out of these, 64 patients (52.5%) gave informed consent and were included in the study. Results: The 58 eligible nonparticipants showed a lower level of functioning (global assessment of functioning score), had a history of more outpatient treatment attempts and were living alone more often. Regarding acute symptoms and severity of BPD as indexed by suicide attempts, inpatient treatments, substance abuse and history of trauma, no differences between the groups could be detected. Moreover, participants showed significantly more eating disorders, whereas nonparticipants presented more affective and anxiety disorders. Conclusions: The results indicate that lower psychosocial functioning and comorbid affective and anxiety disorders decrease BPD patients’ willingness to participate in an RCT.
The Association Between Maternal Obesity, Glucose Intolerance and Hypertensive Disorders of Pregnancy in Nondiabetic Pregnant Women

Objective. The aim of this study is to evaluate whether pregnancy-induced hypertension (PIH) among nondiabetic patients is associated with glucose intolerance. Materials and Methods. A retrospective case-control study was designed including a study group who had pregnancy-induced hypertension or preeclampsia. Patients with normal pregnancy were used as a control group matched to cases by parity. Diabetic patients, nonsingleton pregnancies, and women without prenatal care were excluded. Data concerning fasting glucose levels, glucose challenge test (GCT), and oral glucose tolerance test (OGTT) were collected from patients' files. Results. There were 131 patients in each study group. The study group had significantly higher mean maternal age, mean GCT levels, and mean pregestational body mass index (BMI) (28.0 ± 5.8 vs. 26.5 ± 5.3, p = 0.02; 5.8 ± 1.4 vs. 5.1 ± 1.1 p = 0.0018; 26 ± 5.1 vs. 23 ± 4.0 p < 0.001, respectively) than the control group. Mean gestational age and birthweight were also significantly lower in the study group (38.5 ± 2.1 vs. 39.4 ± 1.7 p < 0.001; 2929 g ± 614.7 vs. 3225 ± 461.1 p < 0.001, respectively). Stratified analysis according to parity demonstrated that pregestational BMI, weight gain during pregnancy, and cesarean section (CS) were significantly higher in women with pregnancy-induced hypertension than in controls in all parity groups. Maternal age and mean GCT levels of women with pregnancy-induced hypertension were higher in all parity groups but statistically significant only among multiparous patients. Multiple logistic regression demonstrated that BMI, weight gain, and maternal age were independently associated with pregnancy-induced hypertension, while GCT level was not. Conclusions. Elevated pregestational BMI is an independent risk factor for development of pregnancy-induced hypertension (PIH). Its association with elevated GCT levels implies that even without overt diabetes, glucose intolerance may play a role in the pathogenesis of preeclampsia in obese patients.
Interacting Regions in Stat3 and c-Jun That Participate in Cooperative Transcriptional Activation

ABSTRACT Independent but closely spaced DNA binding sites for Stat3 and c-Jun are required for maximal enhancer function in a number of genes, including the gene encoding the interleukin-6 (IL-6)-induced acute-phase response protein, α2-macroglobulin. In addition, a physical interaction of Stat3 with c-Jun, based on yeast two-hybrid interaction experiments, has been reported. Here we confirm the existence of an interaction between Stat3 and c-Jun both in vitro, with recombinant proteins, and in vivo, during transient transfection. Using fragments of both proteins, we mapped the interactive sites to the C-terminal region of c-Jun and to two regions in Stat3, within the coiled-coil domain and in a portion of the DNA binding domain distant from DNA contact sites. In transient-transfection experiments with the α2-macroglobulin enhancer, Stat3 and c-Jun cooperated to yield maximal enhancer function. Point mutations of Stat3 within the interacting domains blocked both physical interaction of Stat3 with c-Jun and their cooperation in IL-6-induced transcription directed by the α2-macroglobulin enhancer. While the amino acid sequences and the three-dimensional structures of Stat3 and Stat1 cores are very similar, fragments of Stat1 failed to bind c-Jun in vitro. Although Stat1 binds in vitro to the gamma interferon gene response (GAS) element in the α2-macroglobulin enhancer, Stat1 did not stimulate transcription, nor did Stat1 and c-Jun cooperate in driving transcription controlled by the α2-macroglobulin enhancer.
Sodium bicarbonate and hydrogen peroxide: the effect on the growth of Streptococcus mutans.

PURPOSE This in vitro experiment studied the effects of sodium bicarbonate and hydrogen peroxide on the cariogenic bacteria Streptococcus mutans through analysis with a spectrophotometer. METHODS The growth of S. mutans was analyzed using seven different environments. Twelve wells in each of the seven rows of a multi-well plate were used to incubate the test materials. In combinations of 10 microl distilled water, 100 microl broth, 10 microl 10% sucrose, 10 microl S. mutans, 10 microl 10% sodium bicarbonate, and 10 microl 3% hydrogen peroxide, seven different environments were created for testing. Environments had either sodium bicarbonate or hydrogen peroxide with S. mutans, or a combination of sodium bicarbonate and hydrogen peroxide with S. mutans. The plate was incubated at 37 degrees C and measured at 0, 18, 20, 22, 24, 26, 28, 30, and 42 hours by optical density with a spectrophotometer. RESULTS Results showed bacterial growth was prevented by sodium bicarbonate, hydrogen peroxide, and the combination of sodium bicarbonate and hydrogen peroxide. Although hydrogen peroxide is bacteriocidal and sodium bicarbonate is bacteriostatic, there were no significant differences among the three treatment groups in spectrophotometer readings at any of the nine readings over 42 hours. CONCLUSION There was no significant difference among the effects of hydrogen peroxide, sodium bicarbonate, or the sodium bicarbonate and hydrogen peroxide combination, as measured by optical density. The hydrogen peroxide, sodium bicarbonate, and the sodium bicarbonate and hydrogen peroxide combination prevented bacterial growth of S. mutans. The results show that products containing these agents have the ability to stop the growth of S. mutans. Products containing sodium bicarbonate and/or hydrogen peroxide may be useful to caries-prone patients. More studies are needed to confirm these results on patients.
The high susceptibility of heterozygous p53(+/-) mice to malformation after foetal irradiation is related to sub-competent apoptosis.

PURPOSE To investigate the relationship between the incidence of radiation-induced malformations and the extent of p53-dependent apoptosis. MATERIALS AND METHODS Wild-type p53(+ / +) and heterozygous p53(+ / -) mice were exposed to X-rays at the mid-gestational period. The incidence of anomalies and prenatal deaths, the extent of apoptosis, and the levels of p53 protein were assessed. RESULTS After X-irradiation with 2 Gy, the incidence of malformation (corrected for control levels) was 0 and 30%, respectively, for p53(+ / +) and p53(+ / -). After irradiation of p53(+ / +) foetuses with 3 Gy, the frequency (F) of apoptotic cells rapidly peaked at 80% at 4 h and fell close to the control level at 48 h. The relationship between F 4h after irradiation and dose (D) (1-3Gy) is accurately expressed by a single-hit equation, F= 1 -exp ( -(a + bD)¿, where the radiation-induced apoptosis rate, b, is 0.47 for the wild type and 0.22 for the heterozygous mice. The X-irradiated foetuses showed no increase in the levels of p53 protein. CONCLUSION The higher susceptibility of irradiated p53(+ / -) foetuses to malformation is related to a twofold lower rate of apoptosis; competent removal by apoptosis of damaged cells from irradiated tissues is impaired dramatically if one of two wild-type p53 alleles is lost. The frequency of apoptotic cells in the wild type reached a maximum 4h after foetal irradiation with no measurable increase in the level of p53 protein, indicating that radiation-induced p53-mediated foetal apoptosis depends on non-transcriptional events.
The association between maternal parity and birth defects.

BACKGROUND Previous studies observed that first birth is associated with an increased risk of some categories of birth defects. However, multiple statistical tests were conducted and it was unclear which of these associations would be replicated in a larger study. We used a large database to assess the association between maternal parity and 65 birth defects including birth defects that have not been previously studied. METHODS Using data from the Texas Birth Defects Registry for years 1999-2009, the risk of a birth defect occurring in a first, third, or fourth or higher birth was compared to the risk of a birth defect occurring in a second birth. RESULTS Women having their first birth had significantly increased odds of having an infant with 24 of 65 categories of birth defects when compared to women having their second birth. We also observed associations between first birth and an increased risk of five birth defects not previously reported (small penis, preaxial polydactyly, anomalies of the thoracic vertebrae, anomalies of the lumbar vertebrae, and sacroccygeal anomalies). Women having their third or fourth or higher birth had significantly increased odds of giving birth to infants with five of 65 birth defects when compared to second births. CONCLUSIONS Our observations regarding the categories of birth defects that were associated with first births were highly consistent with observations from two previous studies. Research into biological, behavioral, and environmental factors that may increase the risk of specific birth defects among first births is needed to further explore these associations.
Combination of p16INK4a/Ki67 immunocytology and hpv polymerase chain reaction for the noninvasive analysis of HPV involvement in head and neck cancer

High‐risk human papillomavirus (HPV) infection has been identified as a relevant risk for the development of head and neck squamous cell carcinomas (HNSCCs). As HPV status has also gained a role as a prognostic and predictive biomarker for this entity, there is a growing demand for valid HPV testing in HNSCC patients
Relapses in multiple sclerosis are age- and time-dependent

Objectives: To examine the relative relapse-rate patterns over time in a relapsing multiple sclerosis (MS) cohort and to investigate potential predictors of relapse rates and periods of low-relapse activity. Methods: This retrospective cohort study followed 2477 relapsing-remitting (RR) MS patients from onset to 1 July 2003. Annualised relapse rates were examined according to sex, age at onset, the patient’s current age and disease duration. The relationship between relapse rates and baseline characteristics (sex, onset age and onset symptoms) were examined using Poisson regression. Time to the first 5 years relapse-free was examined using Kaplan–Meier survival analysis. Results: The mean follow-up time (from onset of MS symptoms) was 20.6 years, during which time 11,722 post-onset relapses were recorded. The relapse rate decreased by 17% every 5 years (between years 5 to 30 post-onset), but this decline increased in magnitude with increasing onset age. Women and those with onset sensory symptoms exhibited a higher relapse rate (p⩽0.001). More than three-quarters of patients (1692/2189) experienced a 5-year relapse-free period during the RR phase. Conclusion: Relapse rates were age- and time-dependent. Our observations have clinical implications: 1) any drug able to modify relapse rates has the greatest potential for a population impact in patients <40 years old and within the first few demi-decades of disease; 2) continuation of drug beyond these times may be of limited value; 3) long-term follow-up studies must consider that relapse rates probably decline at different rates over time according to the patient’s onset age; 4) a relapse-quiescent period in MS is not uncommon.
Acid exposure activates the mitogen-activated protein kinase pathways in Barrett's esophagus.

BACKGROUND & AIMS To explore mechanisms whereby acid reflux might contribute to carcinogenesis in Barrett's esophagus (BE) we studied: (1) the effects of acid on the mitogen-activated protein kinase (MAPK) pathways, cell proliferation, and apoptosis in a Barrett's adenocarcinoma cell line (SEG-1); and (2) the ability of acid to activate the MAPK pathways in vivo in patients with BE. METHODS SEG-1 cells were exposed to acidic media for 3 minutes, and the activities of 3 MAPKs (ERK, p38, and JNK) were determined. Proliferation was assessed using flow cytometry; cell growth and apoptosis were assessed using cell counts and an apoptosis ELISA assay. MAPK activation was studied in biopsy specimens taken from patients with BE before and after esophageal perfusion for 3 minutes with 0.1N HCl. RESULTS Acid-exposed SEG-1 cells exhibited a significant increase in proliferation and total cell numbers, and a significant decrease in apoptosis. These effects were preceded by a rapid increase in the activities of ERK and p38, and a delayed increase in JNK activity. PD 98059 abolished the acid-induced increase in G0/G1 and decrease in subG0 phases of the cell cycle. Both SB 203580 and DN-JNK 1/2 inhibited the acid-induced progression from G0/G1 to G2/M. The acid-induced decrease in apoptosis was abolished by inhibition of either ERK or p38. In the patients, acid exposure significantly increased the activity of p38 in the metaplastic epithelium. CONCLUSIONS Acid increases proliferation and survival, and decreases apoptosis in SEG-1 cells by activating the MAPK pathways. Acid also activates the MAPK pathways in BE in vivo. These findings suggest that acid might contribute to carcinogenesis in BE through activation of MAPK pathways.
Effects of Saccharomyces boulardii on fecal short-chain fatty acids and microflora in patients on long-term total enteral nutrition.

AIM Diarrhea is a significant problem in patients on total enteral nutrition (TEN) and may involve changes in intestinal short chain fatty acids or microflora. Recent studies suggest that the probiotic yeast Saccharomyces boulardii (Sb) may decrease its incidence. The aim of this study was to assess the effects of Sb on fecal flora and short-chain fatty acids (SCFA) in patients on long-term TEN. METHODS Ten patients (3 females, 7 males, 59+/-5.5 years), on TEN for a median of 13 mo (1-125), and 15 healthy volunteers (4 females, 11 males, 32+/-2.0 years) received Sb (0.5 g bid PO) for 6 d. Two stool samples were taken before, on the last 2 d and 9-10 d after treatment, for SCFA measurement and for culture and bacterial identification. Values (mean+/-SE) were compared using sign tests and ANOVA. RESULTS Fecal butyrate levels were lower in patients (10.1+/-2.9 mmol/kg) than in controls (19.2+/-3.9, P = 0.02). Treatment with Sb increased total fecal SCFA levels in patients (150.2+/-27.2 vs 107.5+/-18.2 mmol/kg, P = 0.02) but not in controls (129.0+/-28.6 vs 113.0+/-15.2 mmol/kg, NS). At the end of treatment with Sb, patients had higher fecal butyrate (16.0+/-4.4 vs 10.1 [2.9] mmol/kg, P = 0.004). Total SCFAs remained high 9 d after treatment was discontinued. Before the treatment, the anaerobe to aerobe ratio was lower in patients compared to controls (2.4+/-2.3 vs 69.8+/-1.8, P = 0.003). There were no significant changes in the fecal flora of TEN patients. CONCLUSION Sb-induced increase of fecal SCFA concentrations (especially butyrate) may explain the preventive effects of this yeast on TEN-induced diarrhea.
Increased Response to Subcutaneous Erythropoietin on Type I Diabetic Patients on Capd: Is There a Synergistic Effect with Insulin?

Objective To evaluate the effect of subcutaneous erythropoietin (SC EPO) on the treatment of anemia in diabetic and nondiabetic continuous ambulatory peritoneal dialysis (CAPD) patients. Design A resistance index was designed for measuring the relative EPO response, dividing EPO dose (U/kg/ week) by the hemoglobin (Hb) increment with respect to the basallevel. Patients Eleven nonselected type I diabetic patients using subcutaneous insulin compared with 16 nondiabetic controls, all on CAPD therapy. Results The two groups showed similar mean baseline hemoglobin levels (7.4 D- l and 7.7 non-D, g/dL). There was a statistically significant lower resistance index for diabetics (13.8±9.7 U/kg/g Hb increment) compared to nondiabetic (55.8±128, p < 0.001). Multivariate analysis confirmed an independent association between diabetes and resistance index. The response to EPO was slightly better among those diabetic patients with lower levels of serum parathyroid hormone (iPTH) (PTH-resistance index, correlation coefficient, r = 0.7, p < 0.05). No other differences, apart from the use of subcutaneous insulin, were found between diabetics and controls. Although diabetic patients had an increased response to EPO, they had no more frequent side effects than nondiabetics. Conclusions According to our results, we suggest that factors related to insulin-dependent diabetes seem to be involved in a favorable response to SC EPO. Hyperinsulinemia derived from subcutaneous use of insulin might act as a comitogen with the induced increments of serum erythropoietin.