Miracle-dz/UniFAR-FTUs huggingface dataset:
Peritoneal Function and Assessment of Reference Values Using a 3.86% Glucose Solution

Background The most widely used peritoneal function test, the peritoneal equilibration test (PET), is performed with a 2.27% glucose solution. Recently, the International Society for Peritoneal Dialysis committee on ultrafiltration failure (UFF) advised performing the test with 3.86% glucose solution because it is more sensitive for detecting clinically significant UFF. Because no reference values for this test were available, we analyzed the results of standard peritoneal permeability analyses (SPAs) using 3.86% glucose. Methods The tests were performed in our center on 154 clinically stable peritoneal dialysis (PD) patients that were free of peritonitis for at least 4 weeks. For the assessment of reference values, we used two approaches. In approach A, patients with UFF, defined as net ultrafiltration (UF)< 400 mL/4 hours, were excluded. In approach B, only patients within their first 2 years of PD treatment were included, regardless of net UF. Means and 95% confidence intervals (95% CI) were calculated for the transport parameters of the PET and SPA. Results Means of normal distribution with 95% CI in approach A were as follows: for 2.0-L exchanges, mass transfer area coefficient (MTAC) for creatinine 8.8 mL/minute (4.7 – 12.7 mL/min), dialysate/plasma ratio (D/P) creatinine 0.70 (0.52 – 0.88), glucose absorption 58% (44% – 72%), dialysate240/initial dialysate ratio of glucose (D t /D0) 0.28 (0.18 – 0.38), net UF 675 mL (375 – 975 mL), and maximal dip in D/P sodium after correction for diffusion from the circulation 0.110 (0.050 – 0.164); for 1.5-L exchanges, MTAC creatinine 7.4 mL/min (3.8 – 11.0 mL/min), D/P creatinine 0.69 (0.52 – 0.86), glucose absorption 62% (52% – 72%), D t /D0 glucose 0.25 (0.17 – 0.32), net UF 551 mL (430 – 670 mL), and maximal dip D/P sodium 0.120 (0.048 – 0.166). In approach B, most of the transport values were similar; however, values for lymphatic absorption were significantly higher [1.52 mL/min (2-L) and 1.40 mL/min (1.5-L), p < 0.01] and values for the maximum dip in D/P sodium were lower [0.101 (2-L) and 0.112 (1.5-L), p > 0.05]. This was probably the result of including patients with UFF in approach B, since these parameters can be causative factors of UFF. Conclusions A peritoneal transport function test using 3.86% glucose provides data on various aspects of transport. This study gives normal reference values that can be used for analysis of causes of UFF.
A twin study of post-traumatic stress disorder symptoms and asthma.

RATIONALE Studies have suggested heightened anxiety among adults with asthma; the mechanism of this association is not known. OBJECTIVES To determine the association between post-traumatic stress disorder (PTSD) symptoms and asthma among adults, and to examine if this association is due to confounding by environmental and genetic factors. METHODS Data were obtained from twins in the Vietnam Era Twin Registry, which includes male veteran twin pairs born between 1939 and 1956 who served during the Vietnam era (1965-1975). Measurements included a symptom scale for PTSD, history of a doctor diagnosis of asthma, and sociodemographic and health confounding factors. Co-twin control analytic methods used mixed-effects logistic regression to account for the paired structure of the twin data and to examine the association between PTSD symptoms and asthma in all twins. Separate analyses were conducted within twin pairs and according to zygosity. MEASUREMENTS AND MAIN RESULTS PTSD symptoms were associated with a significantly increased likelihood of asthma (P(trend) < 0.001) even after adjustment for confounding factors. Among all twins, those in the highest quartile of PTSD symptoms were 2.3 times as likely (95% confidence interval, 1.4-3.7) to have asthma compared with those in the lowest quartile. These findings persist when examined within twin pairs and when stratified by zygosity. CONCLUSIONS Symptoms of PTSD were associated with an elevated prevalence of asthma. Even after careful adjustment for familial/genetic factors and other potential confounding factors, an association between PTSD symptoms and asthma remains. Efforts to understand this comorbidity may be useful in identifying modifiable environmental risk factors contributing to this pattern and therefore in developing more effective prevention and intervention strategies.
Flagellin-Independent Regulation of Chemokine Host Defense in Campylobacter jejuni-Infected Intestinal Epithelium

ABSTRACT Campylobacter jejuni is a leading cause of bacterial food-borne diarrheal disease throughout the world and the most frequent antecedent of autoimmune neuropathy Guillain-Barré syndrome. While infection is associated with immune memory, little is known regarding the role of the epithelium in targeting dendritic cells (DC) for initiating the appropriate adaptive immune response to C. jejuni. The objective of this study was to define the role for the intestinal epithelium in the induction of the adaptive immune response in C. jejuni infection by assessing the production of DC and T-cell chemoattractants. Human T84 epithelial cells were used as model intestinal epithelia. Infection of T84 cells with C. jejuni dose- and time-dependently up-regulated DC and T-cell chemokine gene transcription and secretion. Induction required live bacteria and was in the physiologically relevant direction for attraction of mucosal immunocytes. C. jejuni-activated NF-κB signaling was shown to be essential for proinflammatory chemokine secretion. Notably, C. jejuni secretion occurred independently of flagellin identification by Toll-like receptor 5. Secretion of a DC chemoattractant by differing clinical C. jejuni isolates suggested adherence/invasion were key virulence determinants of epithelial chemokine secretion. The regulated epithelial expression of DC and T-cell chemoattractants suggests a mechanism for the directed trafficking of immune cells required for the initiation of adaptive immunity in campylobacteriosis. Chemokine secretion occurs despite Campylobacter evasion of the flagellin pattern recognition receptor, suggesting that alternate host defense strategies limit disease pathogenesis.
Digital image analysis system for the quantification of infiltrates and cell adhesion molecules in inflammatory cardiomyopathy.

BACKGROUND We attempted to develop a digital image analysis (DIA) system for endomyocardial biopsies (EMBs) to reliably quantify a) biopsy quality, b) immunohistochemically-marked infiltrates, and c) cell adhesion molecules (CAMs) in relation to net heart area (HA) for the semi-automated diagnosis of inflammatory cardiomyopathy (InfCM). MATERIAL/METHODS 140 EMBs from dilated cardiomyopathy (DCM) patients and 14 autopsy heart samples (controls) were immunostained for T-lymphocytes (CD2, CD3, CD4, CD8), beta(2)-integrin+ infiltrates (CD18, LFA-1, Mac-1) and CAMs (immunoglobulin superfamily: ICAM-1, HLA class I, HLA DR, VCAM-1, CD58; selectins: CD62E and CD62P; and the beta(1)-integrin chain CD29). EMB quality was assessed visually on a three-point scale. Infiltrates were quantified visually (per hpf) and by DIA (per mm2 HA). CAM expression was evaluated semiquantitatively and by DIA (area fraction [AF]: stained area relative to HA). RESULTS DIA-evaluated HA correlated significantly with the visual assessment of EMB quality. The visual evaluation of both infiltrates and CAMs correlated significantly with the respective DIA-based quantification. DIA-quantified CAM-AF and infiltrates were discriminated by the CAM classification (CAMs+: n=87; 62%) compared to controls. DIA-quantified CAM immunoreactivity correlated significantly with the DIA-quantified counter-receptor+ infiltrates. DIA evaluation of biopsy quality, infiltrates, and CAMs was devoid of inter- and intraobserver variability. CONCLUSIONS The DIA system presented here enables standardized and observer-independent assessment of EMB quality and intramyocardial inflammation (density of infiltrates and CAM expression) in DCM biopsies related to HA. Our data confirm that endothelial CAM count and counter-receptor+ immunocompetent infiltration are interdependent pathogenic and diagnostic hallmarks of InfCM.
Mistreatment among undergraduate medical trainees: A case study of a Nigerian medical school.

BACKGROUND Several international studies have shown that abuse or mistreatment is a regular phenomenon faced by medical students. However, there is limited information on medical student abuse/mistreatment in Nigeria. The study was therefore conducted to assess the prevalence and patterns of mistreatment experienced by Medical Students in the University of Calabar. MATERIALS AND METHODS A descriptive cross-sectional study was conducted among 451 undergraduate medical trainees in the University of Calabar. Systematic sampling was used in recruiting participants into the study. A self-administered questionnaire was then employed to obtain information on patterns of mistreatment experienced by medical undergraduates. Data were analyzed using Statistical Package for Social Scientists version 19 and level of significance set at <0.05. RESULTS More than a third (35.5%) of all respondents interviewed had experienced one or more forms of mistreatment during their training, with 38.5% of them experiencing it weekly. The most common form of mistreatment experienced was verbal abuse (52.5%), and the main perpetrators of these incidents were medical consultants, (18.6%) other cadre of doctors (17.3%) and lecturers (14.4%). Being in the clinical level of study and aged above 25 years were significantly associated with experiencing mistreatment in this study (P < 0.05). However, only 8.8% reported these incidents. CONCLUSION With more than a third of undergraduate medical trainees experiencing mistreatment, development of appropriate strategies for the prevention and reduction of these incidents are strongly recommended.
Strong Upregulation of AIM2 and IFI16 Inflammasomes in the Mucosa of Patients with Active Inflammatory Bowel Disease

Background:Inflammatory bowel disease (IBD) is characterized by a chronic inflammation of the gut, partly driven by defects in the innate immune system. Considering the central role of inflammasome signaling in innate immunity, we studied inflammasome components in IBD mucosa. Methods:Expression of genes encoding inflammasome sensor subunits was investigated in colonic mucosal biopsies from 2 cohorts of patients with IBD and controls. Results:A significant upregulation (>2-fold change in expression, false discovery rate <0.05) of the PYHIN inflammasomes AIM2 and IFI16 in active IBD versus controls was found. Also IFI16 was significantly increased in inactive IBD versus controls. Moreover, responders to anti-tumor necrosis factor therapy showed decreased expression of these inflammasomes although IFI16 remained significantly increased in responders showing endoscopic healing versus controls. AIM2 was mainly expressed in epithelial cells, whereas IFI16 was expressed in both lymphocytes and epithelial cells. Functional activation of predominant AIM2/IFI16-mediated inflammasomes in active IBD colon was shown by the presence of the downstream effectors CASP1 and HMGB-1 in inflamed mucosa. Conclusions:Our results highlight the importance of PYHIN inflammasome signaling in IBD and also link anti-tumor necrosis factor responsiveness to inflammasome signaling. Together, this points to the potential value of the inflammasome pathway as a new therapeutic target for IBD treatment.
A novel multidrug resistance plasmid isolated from an Escherichia coli strain resistant to aminoglycosides.

OBJECTIVES Previous studies have reported several different plasmids that confer multidrug resistance (MDR) including resistance to aminoglycosides. In this study, we investigated the aminoglycoside resistance patterns for 224 Escherichia coli isolates from diseased chickens and ducks in China, characterized a novel MDR plasmid, and collected prevalence data on similar resistance plasmids. METHODS Antibiotic susceptibilities were determined using disc diffusion and the microdilution method. The plasmid pXZ was analysed by restriction fragment length polymorphism (RFLP) with EcoRI and SalI, and sequenced. The prevalence of similar resistance plasmids was assessed by multiplex PCR and by RFLP analysis. RESULTS Among the 224 E. coli isolates, 189 (84.4%) were resistant to streptomycin, 125 (55.8%) were resistant to kanamycin, 116 (51.8%) were resistant to gentamicin, 106 (47.3%) were resistant to neomycin and 98 (43.8%) were resistant to amikacin. Among the 224 E. coli isolates, 17 contained a plasmid with the MDR-encoding region of pXZ, which showed high-level resistance to aminoglycosides (MICs of gentamicin and amikacin ≥ 512 mg/L). The plasmid pXZ was digested into five fragments by EcoRI and six fragments by SalI. The plasmid pXZ was a circular DNA molecule of 76635 bp with a 51.65% guanine + cytosine content and included four resistance genes (rmtB, fosA3, bla(TEM-1) and bla(CTX-M-24)). CONCLUSIONS A novel MDR plasmid, pXZ, harbouring four resistance genes (rmtB, fosA3, bla(TEM-1) and bla(CTX-M)) was identified. To our knowledge, this is the first report of an aminoglycoside resistance plasmid harbouring the fosA3 gene.
Herbicides as Probes in Plant Biology

Abstract Herbicides are small molecules that inhibit specific molecular target sites within plant biochemical pathways and/or physiological processes. Inhibition of these sites often has catastrophic consequences that are lethal to plants. The affinity of these compounds for their respective target sites makes them useful tools to study and dissect the intricacies of plant biochemical and physiological processes. For instance, elucidation of the photosynthetic electron transport chain was achieved in part by the use of herbicides, such as terbutryn and paraquat, which act on photosystem II and I, respectively, as physiological probes. Work stemming from the discovery of the binding site of PS II–inhibiting herbicides was ultimately awarded the Nobel Prize in 1988. Although not as prestigious as the seminal work on photosynthesis, our knowledge of many other plant processes expanded significantly through the ingenious use of inhibitors as molecular probes. Examples highlight the critical role played by herbicides in expanding our understanding of the fundamental aspects of the synthesis of porphyrins and the nonmevalonate pathway, the evolution of acetyl-coenzyme A carboxylase, cell wall physiology, the functions of microtubules and the cell cycle, the role of auxin and cyanide, the importance of subcellular protein targeting, and the development of selectable markers.
Sodium‐dependent control of intracellular pH in Purkinje fibres of sheep heart.

Intracellular pH (pHi) of Purkinje fibres from sheep heart was recorded with pH‐sensitive glass micro‐electrodes. The cells were acidified by one of three methods: (1) exposure to and subsequent removal of NH4Cl, (2) exposure to solutions containing 5% CO2 or (3) exposure to an acidic Tyrode solution. The pHi recovery from these acidifications was studied. The time constant of recovery from an acidification induced by NH4Cl was almost twice as long as that from one induced by CO2 or acid extracellular pH. Following an acidification induced by exposure to CO2 the time constant of pHi recovery was not changed when the cell was depolarized to ‐40 mV (by replacement of some Na+ by K+). An intracellular acidification was produced when extracellular Na+ was removed and replaced by quaternary ammonium ions or K+. Such Na+‐free solutions also inhibited pHi recovery from an acidification. A 50% inhibition of the rate of recovery was produced by lowering the [Na+]o to 8 mM. When used as a Na+ substitute, Li+ could permit recovery. Tris (22 mM) changed pHi in the alkaline direction. Amiloride (1 mM) or a decrease in temperature slowed the recovery from an acidification (Q10 = 2.65). There was no effect of SITS (4‐acetamido‐4'‐isothiocyanatostilbene‐2,2'‐disulphonic acid disodium salt; 100 microM) on the recovery. Na+‐sensitive glass micro‐electrodes were used to measure the intracellular Na+ activity when [Na+]o was lowered to levels used in our pHi recovery experiments. From these data we have calculated the apparent Na+ electrochemical gradient at different values of [Na+]o. If this gradient is responsible for H+ efflux from the cell then, by applying thermodynamic considerations, it can be shown that only low concentrations (1‐2mM) of extracellular Na+ are required. Solutions containing a very low [Ca2+]o (less than 10(‐8) M, buffered with EGTA) were used to prevent large rises of [Ca2+]i which may occur on removal of external Na+. Under these conditions pHi recovery is still dependent upon [Na+]o, and the apparent inhibition of pHi recovery by removal of Na+ is not simply due to rises in [Ca2+]i. The intracellular acidification which occurs on removal of Na+ does not occur when [Ca2+]o is very low (less than 10(‐8) M). (ABSTRACT TRUNCATED AT 400 WORDS)
Interaction between Pseudorabies Virus and Heparin/Heparan Sulfate

Cell surface heparan sulfate serves as an initial receptor for a number of herpesviruses including pseudorabies virus (PrV). It has been demonstrated that the heparan sulfate-binding domain of PrV glycoprotein C is composed of three discrete clusters of basic residues corresponding to amino acids 76-RRKPPR-81, 96-HGRKR-100, and 133-RFYRRGRFR-141, respectively, and that these clusters are functionally redundant, i.e. each of them could independently support PrV attachment to cells (Flynn, S. J., and Ryan, P. (1996) J. Virol. 70, 1355–1364). To evaluate the functional significance of each of these clusters we have used PrV mutants in which, owing to specific alterations in glycoprotein C, the heparan sulfate-binding site is dominated by a single specific cluster. These mutants exhibited different patterns of susceptibility to selectively N-, 2-O-, and 6-O-desulfated heparin preparations in virus attachment/infectivity assay. Moreover PrV mutants differed as regard to efficiency of their attachment to and infection of cells pretreated with relatively low amounts of heparan sulfate-degrading enzymes. Furthermore glycoprotein C species, purified from respective mutants, bound heparin oligosaccharide fragments of different minimum size. These differences suggest that specific clusters of basic amino acids of the heparan sulfate-binding domain of glycoprotein C may support PrV binding to different structural features/stretches within the heparan sulfate chain.
MODE OF TRANSMISSION, HOST SWITCHING, AND ESCAPE FROM THE RED QUEEN BY VIVIPAROUS GYRODACTYLIDS (MONOGENOIDEA)

Compared to other monogenoidean groups, viviparous gyrodactylids exhibit extraordinary species diversity and broad host range. It has been suggested that this evolutionary success is associated with a suite of morphological and life-history traits that include, in part, continuous transmission (i.e., ability to infect new hosts throughout the gyrodactylid life cycle). Experiments were conducted to explore the putative adaptive advantage of continuous transmission within viviparous gyrodactylids during colonization of new host resources. Differences in infrapopulation growth, such as abundance, prevalence, and duration of the infection, of Gyrodactylus anisopharynx on 3 species of fish—Corydoras paleatus and Corydoras ehrhardti (both natural hosts) as well as Corydoras schwartzi (a host not known to harbor G. anisopharynx)—held under isolated and grouped conditions were determined. Results showed that infrapopulations of G. anisopharynx on C. paleatus and C. schwartzi had higher growth when the parasite had the opportunity for host transfer (grouped hosts). Infrapopulations of G. anisopharynx on isolated and grouped C. ehrhardti showed an opposite trend, although differences in mean duration and maximum abundance were not statistically different. Results obtained from experiments with C. paleatus and C. schwartzi support the hypothesis that continuous transmission in viviparous gyrodactylids enhances colonization success, probably by allowing initial avoidance of Red Queen dynamics. The absence of statistical differences between infrapopulations on isolated and grouped C. ehrhardti suggests that parasite dynamics may be influenced by factors other than continuous transmission in this host.
BcrC from Bacillus subtilis Acts as an Undecaprenyl Pyrophosphate Phosphatase in Bacitracin Resistance*

Overexpression of the BcrCBs protein, formerly called YwoA, in Escherichia coli or in Bacillus subtilis allows these bacteria to stand higher concentrations of bacitracin. It was suggested that BcrCBs was a membrane-spanning domain of an ATP binding cassette (ABC) transporter involved in bacitracin resistance. However, we hypothesized that this protein has an undecaprenyl pyrophosphate (UPP) phosphatase activity able to compete with bacitracin for UPP. We found that overexpression of a recombinant His6-BcrCBs protein in E. coli (i) increased the resistance of the cells to bacitracin and (ii) increased UPP phosphatase activity in membrane preparations by 600-fold. We solubilized and prepared an electrophoretically pure protein exhibiting a strong UPP phosphatase activity. BcrCBs, which belongs to the type 2 phosphatidic acid phosphatase (PAP2) phosphatase superfamily (PF01569), differs totally from the already known BacA UPP phosphatase from E. coli, a member of the PF02673 family of the Protein family (Pfam) database. Thus, BcrCBs and its orthologs form a new class of proteins within the PAP2 phosphatase superfamily, and likely all of them share a UPP phosphatase activity.
Plasma insulin and lipid levels in untreated obstructive sleep apnoea and snoring; their comparison with matched controls and response to treatment

SUMMARY Obstructive sleep apnoea (OSA), and snoring are associated with coronary heart disease. To assess whether OSA or snoring may contribute to this by raising fasting lipid or insulin levels, venous fasting total cholesterol, triglyceride, very‐low‐density lipoprotein, low‐density lipoprotein, high‐density lipoprotein, and insulin were measured in 15 untreated OSA patients and 18 snorers. Each of these subjects was individually matched to a control of the same sex, age ± 10%, body index ± 15%, smoking and drinking habits. This produced study groups which did not differ significantly by any of these criteria. Fasting venous blood samples were collected at 06.30 hours following polysomnography, and analysed blind of the subjects respiratory status. The OSA patients were then treated with nasal continuous positive airway pressure. In 10 of these subjects lipid and insulin levels were repeated after more than three months treatment. Lipid and insulin levels were also remeasured in the controls matched to these 10 subjects. The end points were compared with paired t‐tests.
Adipocytokine levels in children: effects of fatness and training.

To investigate the effects of obesity and exercise training on plasma adipocytokines a sample of 42 children (lean = 24, %BF = 17.8 ± 7.5%; obese = 18; %BF = 29.1 ± 9.3%; mean age = 12.4 ± 1.9 yrs), were divided into 4 age-matched for activity groups: lean inactive (n = 11), obese inactive (n = 9), lean active (n = 13) and obese active (n = 9). Active children participated in swimming training (≥1 year, ≥3 times/week, ≥1 h per session, covering a distance of 10,000-12,000 m per week). Obese individuals demonstrated greater visfatin levels (3.3 ± 1.3 ng/ml) than their lean counterparts (2.6 ± 1.1 ng/ml; p = .06) whereas adiponectin was significantly lower in obese children (3.8 ± 1.9) than their lean counterparts (5.9 ± 2.7; p £ .05). Insulin and HOMA values were significantly greater in obese compared with lean children (p £ .05). Within obese individuals, active individuals had significantly lower visfatin levels (2.8 ± 1.2 ng/ml) compared with their inactive counterparts (3.8 ± 1.2 ng/ml; p £ .05). Resistin levels were comparable between groups (p > .05). Childhood obesity elevates visfatin and lowers adiponectin levels whereas exercise training could reduce visfatin levels in obese children.