Miracle-dz/UniFAR-FTUs huggingface dataset:
Global cardiometabolic risk profile in patients with hypertension: results from the Turkish arm of the pan-European GOOD survey.

OBJECTIVES We evaluated the results of the Turkish arm of the GOOD survey which investigated the cardiometabolic risk profile and the control of blood pressure (BP) of adult hypertensive outpatients in 12 countries across Europe. STUDY DESIGN A total of 218 hypertensive patients (139 females, 79 males; mean age 57.2±10.9 years) from Turkey were included in this pan-European survey. Blood pressure control (defined as BP <140/90 mmHg for nondiabetics and <130/80 mmHg for diabetics) and cardiometabolic risk factors such as diabetes mellitus, metabolic syndrome, obesity, sedentary lifestyle, and atherogenic dyslipidemia were evaluated in accordance with the 2003 ESH/ESC guidelines on management of hypertension. RESULTS Control of BP was achieved in only 21.6% of the patients diagnosed with hypertension for a mean duration of 7.7±5.4 years. The mean systolic and diastolic BPs were 144±21 mmHg and 88±14 mmHg, respectively. The most frequent concomitant disease was type 2 diabetes mellitus (66 patients, 30.3%). Patients with diabetes had a higher prevalence of metabolic syndrome compared to nondiabetics (78.8% vs. 48%, p<0.01). The absence of BP control was more pronounced among diabetics than in nondiabetics for systolic (77.3% vs. 63.8%) and diastolic (84.9% vs. 57.2%) pressures. Nearly half of the hypertensive patients had atherogenic dyslipidemia, but only 35.8% of them were treated with lipid lowering drugs. CONCLUSION Despite appropriate treatment, poor BP control in Turkish hypertensive patients was associated with metabolic syndrome, diabetes, and undertreatment of atherogenic dyslipidemia. Therefore, more effective measures must be taken in the management of cardiovascular risk factors to improve BP control.
Citalopram as Treatment of Depression in Patients With Epilepsy

Objectives:To assess the safety of citalopram as a treatment of depression in patients with epilepsy. Methods:This is an open, multicentered, uncontrolled study. Depressed epileptic patients on antiepileptic drugs (AEDs) took part in the study. Patients who had a mild frequency of seizures in the 4 previous months underwent treatment with citalopram (20 mg/d) for 4 consecutive months. A change in seizure frequency from the baseline was chosen as the primary measure for the safety of citalopram and efficacy against depressive symptoms was taken as secondary measure. Depression was rated using the Montgomery–Åsberg and Zung depression rating scales. Clinical assessments were performed at baseline, and at 2 and 4 months of citalopram therapy. Results:Forty-five patients were enrolled. Six patients dropped out of the study early: none of them because of a deterioration of seizure frequency. An overall improvement in seizure frequency was observed in the 39 patients who completed the study. Plasma AED concentrations were unchanged during therapy, and depressive symptoms improved markedly. Twenty-two patients complained of adverse effects, mainly headache, nausea, dizziness, somnolence, and fatigue. Conclusions:In this open, multicentered, uncontrolled study, 4 months’ of treatment with citalopram (20 mg/d) were associated with an improvement in depressive symptoms and reduction in seizure frequency.
Functionally distinct groups of X‐cells in the lateral geniculate nucleus of the cat

The latencies and visual response properties of 202 X‐cells in the A‐laminae of the cat dorsal lateral geniculate nucleus (LGN) were examined to investigate the recent claim (Mastronarde, '85,'87a) that functionally different groups of X‐cells reside there. Two groups of X‐cells were found, which differed in their extracellularly recorded responses to spots of light flashed within their receptive fields. One group, constituting one‐third of the sample, responded to spot onset with a profound and often long‐lasting dip in discharge rate, such that cell discharge usually did not reach half maximum until ≥ 100 msec after spot onset. About 70% of these cells also displayed a transient discharge at spot offset. These cells correspond to Mastronarde's lagged X‐cells, and we similarly refer to them as XL‐cells. The second group, constituting the remainder of the X‐cell population, generally responded to spot onset with a short latency (≤ 60 msec) brisk discharge, no detectable XL‐type dip, and a rapid reduction in firing at spot offset. We refer to these neurons as nonlagged (XN) X‐cells; this group probably encompasses all of Mastronarde's non‐XL‐cells.
Engraftment potential of human placenta-derived mesenchymal stem cells after in utero transplantation in rats.

BACKGROUND Human placental mesenchymal stem cells (hPMCs) are thought to be multipotent, but their fate after in utero transplantation is not known. METHODS hPMCs isolated from term placenta were assessed for their phenotype markers, mutilineage capacity, and immunomodulatory properties. Their engraftment potential was analyzed in a pregnant rat model after in utero transplantation at embryonic day 17. Immunohistochemistry, tracing of labeled cells, fluorescence in situ hybridization and real-time PCR were used to assess post-transplant chimerism. RESULTS In vitro, lineage-negative, CD34-negative hPMCs differentiated into osteocytes, adipocytes, hepatocytes and endothelial cells with tube formation, and actively suppressed the rat lymphocyte proliferative response to allogeneic lymphocyte stimulation (P < 0.0001). After in utero transplantation into pregnant rats, a low level of engraftment was achieved in various fetal tissues. Engraftment occurred in more than 60% of the fetal rats. Cells persisted for at least 12 weeks after delivery and evidence was obtained to suggest differentiation into specific lineages, including hepatocytes and hematopoietic cells. However, a greater number of hPMCs migrated to the placenta than to the fetus, thus limiting the degree of cell engraftment in fetal organs. CONCLUSIONS We conclude that hPMCs are mutipotent cells that can be engrafted long-term in immunocompetent rats after in utero transplantation.
Elevated concentrations of exhaled hydrogen peroxide in asthmatic patients.

BACKGROUND Airway inflammation is important in the development and progression of asthma. Activation of inflammatory cells induces a respiratory burst resulting in the production of reactive oxygen species, such as H(2)O(2). The aim of this study was to measure the concentration of H(2)O(2) in exhaled breath condensate and its correlation with airway obstruction, airway hyperresponsiveness, and concentration of eosinophil cationic protein (ECP) in serum in 70 steroid-naive, atopic patients with unstable asthma (20 men; age range, 18 to 62 years) and 17 normal subjects (7 men; age range, 19 to 34 years). METHODS Exhaled H(2)O(2) was measured using a colorimetric assay, and the concentration of ECP in serum was measured using radioimmunoassay. Airway hyperresponsiveness was expressed as the provocative concentration of inhaled histamine causing a 20% fall in FEV(1) (PC(20)). RESULTS In patients with asthma, the mean H(2)O(2) concentration was significantly elevated compared to values in normal subjects: 0.127 +/- 0.083 mol/L vs 0.024 +/- 0.016 mol/L (p < 0.001). There was a significant correlation among H(2)O(2) concentration, FEV(1), PC(20), and ECP in serum. CONCLUSION We conclude that exhaled H(2)O(2) is significantly elevated in asthmatic patients. This is correlated with disease severity and indirect markers of airway inflammation. Measurement of exhaled H(2)O(2) may be useful to assess airway inflammation and oxidative stress in asthmatic patients.
Mannheimia Species Associated with Ovine Mastitis

ABSTRACT Mannheimia glucosida, M. haemolytica, and M. ruminalis were isolated from cases of acute mastitis in ewes. M. glucosida was found to be a common cause of clinical mastitis in sheep. Selected phenotypic tests in addition to genotyping were needed to definitively identify Mannheimia species causing ovine mastitis.
Exercise and tachycardia increase NADPH oxidase and ryanodine receptor-2 activity: possible role in cardioprotection.

AIM Our objective was to investigate in cardiac muscle the contribution of NADPH oxidase to (a) ryanodine receptor-2 (RyR2) S-glutathionylation and (b) the preconditioning effects of exercise and tachycardia on infarct size following coronary artery occlusion. METHODS AND RESULTS We measured NADPH oxidase activity, RyR2 S-glutathionylation, and calcium release kinetics in sarcoplasmic reticulum (SR) vesicles isolated from dog ventricular muscle after exercise and tachycardia, plus or minus prior administration of the NADPH oxidase inhibitor apocynin. In ventricular muscle sections, we studied the colocalization of NADPH oxidase and RyR2 by confocal microscopy using fluorescent antibodies. We determined the effect of apocynin on the infarct size produced by occlusion of the descendent anterior coronary artery in animals preconditioned by exercise or tachycardia. Exercise and tachycardia increased NADPH oxidase activity, RyR2 S-glutathionylation, and calcium release rates in isolated SR vesicles. Cardiac muscle sections displayed significant colocalization of NADPH oxidase and RyR2, suggesting direct and specific effects of reactive oxygen species (ROS) produced by NADPH oxidase on RyR2 activation. The NADPH oxidase inhibitor apocynin prevented the increase in RyR2 S-glutathionylation, reduced calcium release activity, and completely prevented the protective effects of exercise and tachycardia on infarct size. CONCLUSIONS The loss of cardioprotection induced by the NADPH oxidase inhibitor suggests that ROS generated by this enzyme are important mediators of the preconditioning response, which presumably involves NADPH oxidase-induced RyR2 S-glutathionylation.
Roles of the Na,K-ATPase alpha4 isoform and the Na+/H+ exchanger in sperm motility.

The Na,K-ATPase generates electrochemical gradients that are used to drive the coupled transport of many ions and nutrients across the plasma membrane. The functional enzyme is comprised of an alpha and beta subunit and families of isoforms for both subunits exist. Recent studies in this laboratory have identified a biological role for the Na,K-ATPase alpha4 isoform in sperm motility. Here we further investigate the role of the Na,K-ATPase carrying the alpha4 isoform, showing again that ouabain eliminates sperm motility, and in addition, that nigericin, a H+/K+ ionophore, and monensin, a H+/Na+ ionophore, reinitiate motility. These data, along with the observation that the K+ ionophore valinomycin has no effect on the motility of ouabain-inhibited sperm, suggest that ouabain may change intracellular H+ levels in a manner that is incompatible with sperm motility. We have also localized NHE1 and NHE5, known regulators of intracellular H+ content, to the same region of the sperm as the Na,K-ATPase alpha4 isoform. These data highlight the important role of the Na,K-ATPase alpha4 isoform in regulating intracellular H(+) levels, and provide evidence suggesting the involvement of the Na+/H+ exchanger, which is critical for maintaining normal sperm motility.
Changes in rates of autopsy-detected diagnostic errors over time: a systematic review.

CONTEXT Substantial discrepanies exist between clinical diagnoses and findings at autopsy. Autopsy may be used as a tool for quality management to analyze diagnostic discrepanies. OBJECTIVE To determine the rate at which autopsies detect important, clinically missed diagnoses, and the extent to which this rate has changed over time. DATA SOURCES A systematic literature search for English-language articles available on MEDLINE from 1966 to April 2002, using the search terms autopsy, postmortem changes, post-mortem, postmortem, necropsy, and posthumous, identified 45 studies reporting 53 distinct autopsy series meeting prospectively defined criteria. Reference lists were reviewed to identify additional studies, and the final bibliography was distributed to experts in the field to identify missing or unpublished studies. STUDY SELECTION Included studies reported clinically missed diagnoses involving a primary cause of death (major errors), with the most serious being those likely to have affected patient outcome (class I errors). DATA EXTRACTION Logistic regression was performed using data from 53 distinct autopsy series over a 40-year period and adjusting for the effects of changes in autopsy rates, country, case mix (general autopsies; adult medical; adult intensive care; adult or pediatric surgery; general pediatrics or pediatric inpatients; neonatal or pediatric intensive care; and other autopsy), and important methodological features of the primary studies. DATA SYNTHESIS Of 53 autopsy series identified, 42 reported major errors and 37 reported class I errors. Twenty-six autopsy series reported both major and class I error rates. The median error rate was 23.5% (range, 4.1%-49.8%) for major errors and 9.0% (range, 0%-20.7%) for class I errors. Analyses of diagnostic error rates adjusting for the effects of case mix, country, and autopsy rate yielded relative decreases per decade of 19.4% (95% confidence interval [CI], 1.8%-33.8%) for major errors and 33.4% (95% [CI], 8.4%-51.6%) for class I errors. Despite these decreases, we estimated that a contemporary US institution (based on autopsy rates ranging from 100% [the extrapolated extreme at which clinical selection is eliminated] to 5% [roughly the national average]), could observe a major error rate from 8.4% to 24.4% and a class I error rate from 4.1% to 6.7%. CONCLUSION The possibility that a given autopsy will reveal important unsuspected diagnoses has decreased over time, but remains sufficiently high that encouraging ongoing use of the autopsy appears warranted.
Design and measurements of low power multichannel chip for recording and stimulation of neural activity

A 64-channel Neuro-Stimulation-Recording chip named NRS64 for neural activity measurements has been designed and tested. The NRS64 occupies 5×5 mm2 of silicon area and consumes only 25 μW/channel. A low cut-off frequency can be tuned in the 60 mHz - 100 Hz range while a high cut-off frequency can be set to 4.7 kHz or 12 kHz. A voltage gain can be set to 139 V/V or 1100 V/V. A measured input referenced noise is 3.7 μV rms in 100 Hz - 12 kHz band and 7.6 μV rms in 3 Hz - 12 kHz band. A digital correction is used in each channel to tune the low cut-off frequency and offset voltage. Each channel is equipped additionally with a stimulation circuit with an artifact cancellation circuit. The stimulation circuit can be set with 8-bit resolution in six different ranges from 500 nA - 512 μA range.
Pleiotropic Constraint Hampers the Resolution of Sexual Antagonism in Vertebrate Gene Expression

The numerous physiological and phenotypic differences between the sexes, as well as the disparity between male and female reproductive interests, result in sexual conflicts, which are often manifested at the genomic level. Sexually antagonistic genes benefit one sex at the expense of the other and experience strong pressure to evolve male‐ and female‐specific expression patterns to resolve sexual conflicts and maximize fitness for both sexes. Sex‐biased gene expression has recently been demonstrated for much of the metazoan transcriptome, suggesting that many loci are sexually antagonistic. However, many coding regions function in multiple processes throughout the organism. This pleiotropy increases the complexity of selection for any given gene, which in turn may obscure sex‐specific selective pressures and hamper the evolution of sex‐biased gene expression. Here we use microarray gene expression data, in conjunction with data on transcript abundance from expressed sequence tag libraries, to demonstrate that loci with sex‐biased gene expression are significantly less pleiotropic than unbiased genes. This relationship was independent of sex chromosome gene dosage effects, and the results were concordant across two study organisms, chicken and mouse. These results suggest that the resolution of sexually antagonistic gene expression is determined by the evolutionary constraints acting on any given antagonistic locus.
Joggobot: jogging with a flying robot

Joggobot illustrates a novel approach towards a more social use of robots, where the robot acts as exercise companion to make physical activity more enjoyable. Joggobot is the first autonomous flying robot companion for joggers. Joggobot makes the solo running experience more enjoyable by flying next to you when jogging, offering a coach mode to motivate you to run faster and further, and a "looking after" mode that is similar to jogging with a dog. The results are more enjoyable runs, furthering the many physical health benefits of exercise.
Ethnic processes in post-communist Europe during the 1990s

In this paper, the author assesses and explains changes in ethnic composition that occurred in the postcommunist countries of Europe and the Caucasus during the 1990s. Quantitative as well as qualitative aspects of ethno-demographic changes are emphasized. Points of departure are the censuses of 1989/1992 and 1999/2004, and alternatively, the estimates of international organizations. Assessment is carried out at the state and regional levels. The current ethnic composition of post-communist Europe is the result of three ethnic processes. Homogenization concerns those states with a lower initial degree of ethnic homogeneity. Polarization (the formation of two or more ethnically dissimilar entities within one state) was also a prevalent outcome. Those processes were more powerful in war-stricken areas due to forced migrations and ethnic cleansing. Natural increase, governmental ethnic policies and the social atmosphere played an important role in the establishment of peaceful conditions. Conversely, countries that are ethnically homogeneous to a high degree recorded a decrease in their level of ethnic homogeneity. This was caused not only by immigration, but also by subjective factors.
Kinetics and dose-response of residual 53BP1/γ-H2AX foci: Co-localization, relationship with DSB repair and clonogenic survival

Purpose: Recent studies revealed that some foci produced by phosphorylated histone 2A family member X (γ-H2AX) and tumor suppressor p53 binding protein 1 (53BP1) that co-localize with radiation-induced DNA double-strand breaks (DSB) remain in cells at relatively long times after irradiation and indicated a possible correlation between cellular radiosensitivity and residual foci. In this study, we investigated dose-responses and kinetics for radiation-induced 53BP1/γ-H2AX foci formation in relation to their co-localization, DSB repair and cell survival. Materials and methods: Cell survival, DSB and foci were analyzed by clonogenic assay, pulsed field gel electrophoresis (PFGE), and confocal laser microscopy, respectively, in normal human fibroblasts (VH-10) and in a cancer cell line (HeLa). Computer analysis was used to determine both the number and the area of foci. Results: We show that even at doses down to 1 cGy a statistically significant induction of 53BP1 foci is observed. While the number of foci was found to constantly decrease with post-irradiation time, the per-cell normalized area of foci does not change within a time window of approximately 4 h post-irradiation. Co-localization of γ-H2AX and 53BP1 foci is shown to depend on dose and post-irradiation time. No clear correlations were established between radiosensitivity and foci formation because the dose response for 53BP1/γ-H2AX foci may depend on time after irradiation and duration of the cell cycle. We show that the kinetics of foci disappearance within 24 h post-irradiation do not coincide with those of DSB repair. Conclusions: The data suggest that the post-irradiation time used for estimation of radiosensitivity at therapeutically relevant low doses (e.g., <3 Gy) in proliferating cells by scoring residual foci should be limited by the duration of the cell cycle, and that direct comparison of the kinetics of DSB repair and disappearance of DSB-co-localizing foci is not possible. Therefore, results obtained from the counting of foci should be interpreted with caution in terms of DSB repair.
Responses to Scenarios That May Provoke Acts of Conflict and Aggression Among the General Public: An Exploratory Study

The purpose of this article is to use empirical research and theory to investigate the context that may provoke individuals to engage in acts of conflict and aggression. A random sample of the general public from a midsouthern state was surveyed to explore this inquiry. Respondents were asked to indicate their level of reaction to a number of situations that often lead people to engage in conflict and/or aggression with other people. Several sociodemographic factors served as control variables in the study. The findings of the Pearson product—moment correlations suggest that respondents were more likely to report that they would respond more aggressively as the situations presented to them were perceived as being more physically threatening to them and/or their loved ones. Also, gender and age were the most significant predictors of engagement in acts of conflict and aggression in the multiple ordinal least squares regression analyses. Strengths and drawbacks of the study and direction of future research are also discussed.
Methylation matters

DNA methylation is not just for basic scientists any more. There is a growing awareness in the medical field that having the correct pattern of genomic methylation is essential for healthy cells and organs. If methylation patterns are not properly established or maintained, disorders as diverse as mental retardation, immune deficiency, and sporadic or inherited cancers may follow. Through inappropriate silencing of growth regulating genes and simultaneous destabilisation of whole chromosomes, methylation defects help create a chaotic state from which cancer cells evolve. Methylation defects are present in cells before the onset of obvious malignancy and therefore cannot be explained simply as a consequence of a deregulated cancer cell. Researchers are now able to detect with exquisite sensitivity the cells harbouring methylation defects, sometimes months or years before the time when cancer is clinically detectable. Furthermore, aberrant methylation of specific genes has been directly linked with the tumour response to chemotherapy and patient survival. Advances in our ability to observe the methylation status of the entire cancer cell genome have led us to the unmistakable conclusion that methylation abnormalities are far more prevalent than expected. This methylomics approach permits the integration of an ever growing repertoire of methylation defects with the genetic alterations catalogued from tumours over the past two decades. Here we discuss the current knowledge of DNA methylation in normal cells and disease states, and how this relates directly to our current understanding of the mechanisms by which tumours arise.