Miracle-dz/UniFAR-FTUs huggingface dataset:
Is Type 1 Diabetes “Going Viral”?

Although genetic predisposition to type 1 diabetes (T1D) is a key risk factor, it does not explain the recent and rapid rise in incidence of the disease, particularly among children under the age of 5 (1). Changes in the environment and/or how individuals respond to these changes are now widely believed to be responsible for the recent increases in T1D. While viruses have been hypothesized to have an etiological role in T1D for more than five decades, definitive proof has not yet materialized. Nonetheless, a number of candidate viruses have been proposed, including enteroviruses, rotaviruses, herpesviruses, cytomegalovirus, and endogenous retroviruses (2). The strongest and most clinically significant associations point to enterovirus infection. A recent meta-analysis of 26 studies that assessed enteroviral infection using both molecular and immunological assays showed that compared with nondiabetic control subjects, the likelihood of finding evidence of enterovirus is 10-fold higher in T1D patients and fourfold higher in individuals with diabetes-related autoimmunity (3). Despite this evidence, important questions remain. These include whether a viral infection is causal in the development of T1D, whether it acts to accelerate the onset of disease in individuals in whom the process of β-cell destruction has already been initiated, or whether it is simply present because individuals with diabetes are more susceptible to infection. Two articles published in this issue of Diabetes help to address these questions. Ferreira et al. (4) and Kallionpaa et al. (5) used peripheral blood samples from two longitudinal birth cohorts—the BABYDIET cohort (6) and the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study (7), respectively. Both studies monitored development of diabetes-related autoantibodies as well as the onset of T1D in “at-risk” populations, thereby enabling access to samples …
Erythropoietin enhances recovery after cisplatin-induced acute renal failure in the rat.

BACKGROUND Erythropoietin (Epo) is a growth factor whose synthesis mainly takes place in the kidney. Epo has been shown to support the growth not only of erythroid progenitor cells but also of certain other cell types. We attempted to establish whether Epo enhances the recovery from acute renal failure induced by cisplatin. METHODS Sprague-Dawley rats were randomized into three groups. In the cisplatin group, animals received one intraperitoneal injection of cisplatin (6 mg/kg) and a daily injection of placebo for 9 days. In the cisplatin+Epo group, animals received intrapertoneal cisplatin and a daily injection of Epo (100 IU/kg) for 9 days. In the control group, animals received both placebo preparations alone. Para-aminohippuric acid and inulin clearances were determined after 4 and 9 days to evaluate renal blood flow and glomerular filtration rate. In addition, light microscopy and immunohistochemistry examinations were performed, and in situ proliferating cell nuclear antigen (PCNA) staining was done to estimate the degree of renal tubular cell regenerative activity. The potential role of epithelial growth factor (EGF) was evaluated by semi-quantitative assessment of EGF immunostaining. RESULTS Renal blood flow and glomerular filtration rate decreased significantly in cisplatin and cisplatin+Epo groups versus control group at day 4. However, at day 9, they both were significantly greater in cisplatin+Epo-treated animals than in rats that had received cisplatin alone. Tubular cell regeneration was significantly enhanced at day 4 in cisplatin+Epo group, compared with cisplatin and control groups respectively. EGF immunostaining was not significantly different between the three groups. CONCLUSION Epo significantly enhanced the rate of recovery from acute renal failure induced by cisplatin. PCNA staining indicated that Epo might act directly via stimulation of tubular cell regeneration.
Ovarian histopathology in breast cancer patients receiving tamoxifen.

OBJECTIVE The purpose of this study was to examine ovarian histopathology in tamoxifen-treated breast cancer patients undergoing oophorectomy. METHODS We reviewed the records and ovarian histopathology of 152 breast cancer patients who underwent oophorectomy at a single institution between January 1980 and October 1996. At the time of oophorectomy, 99 patients had never received tamoxifen, 44 patients were currently receiving tamoxifen, and 9 patients had previously received tamoxifen. Patient demographic and medical data and indication for oophorectomy were examined. Ovarian histopathology was classified as normal, functional ovarian cyst, benign ovarian tumor, endometriosis, ovarian cancer, and metastatic cancer. RESULTS Patient characteristics and indication for oophorectomy did not differ significantly based on tamoxifen exposure. There was no difference in the occurrence of benign ovarian tumors, functional ovarian cysts, or metastatic breast cancer based on tamoxifen exposure. Tamoxifen-treated patients were less likely to have ovarian cancer, 0 of 53 patients (95% confidence interval (CI): 0.0%, 6.7%) compared with 10 of 99 patients (95% CI: 5.0%, 17.8%) patients not receiving tamoxifen (P = 0.015). Endometriosis was slightly more common in patients currently receiving tamoxifen, but the difference was not statistically significant. CONCLUSIONS In women undergoing oophorectomy, there was no evidence that tamoxifen exposure was associated with an increase in benign or malignant primary or metastatic ovarian neoplasm or in functional ovarian cysts. Further study is necessary to better define any association between tamoxifen and endometriosis and the effect of tamoxifen on ovarian cancer risk.
Does Imidacloprid Seed-Treated Maize Have an Impact on Honey Bee Mortality?

ABSTRACT Beekeepers suspected maize, Zea mays L. , treated with imidacloprid to result in substantial loss of honey bee (Hymenoptera: Apidae) colonies in Belgium. The objective of this study was to investigate the potential impact of maize grown from imidacloprid-treated seeds on honey bee mortality. A survey of 16 apiaries was carried out, and all maize fields treated or not with imidacloprid were located within a radius of 3,000 m around the observed apiaries. Samples of honey, beeswax, and bees were collected in three colonies per apiary and analyzed for pesticide contain by liquid chromatography-tandem mass spectrometry and gas chromatography-tandem mass spectrometry. We first found a significant correlation between the number of colonies per apiary and the mortality rates in an apiary. In addition, this mortality rate was inversely correlated with the surface of maize fields treated and not with imidacloprid, suggesting that this pesticide do not interact with bees' fitness. Moreover, a very large number of our samples contained acaricides either prohibited or ineffective against Varroa destructor (Anderson & Trueman) (Acari: Varroidae), suggesting that the treatment methods used by the beekeepers to be inadequate for mite control. Our results support the hypothesis that imidacloprid seed-treated maize has no negative impact on honey bees.
Propofol Anesthesia Does Not Inhibit Stimulation of Cortisol Synthesis

Recent data suggest a negative effect of propofol anesthesia on cortisol secretion.The present study was designed to evaluate the effect of propofol anesthesia on the steroidogenic potential of the adrenal glands. The response of cortisol secretion to stimulation with an adrenocorticotropic hormone (ACTH) analog during intravenous anesthesia with propofol has not been reported before. The response of the secretion of cortisol, 11-deoxycortisol, and 17 alpha-hydroxyprogesterone to tetracosactide stimulation was compared in patients anesthetized with propofol-nitrous oxide (n = 10) or thiopental-isoflurane-nitrous oxide (n = 10) and in normal volunteers (n = 10). The response to tetracosactide was similar in all three groups. An adequate increase in cortisol plasma concentration (more than 7.25 micro gram/dL) was obtained in all subjects except one volunteer. The increase in the plasma concentration of the cortisol precursors was also similar. We were unable to detect any influence of propofol anesthesia on the synthesis of cortisol in response to tetracosactide stimulation. (Anesth Analg 1995;80:573-6)
Infant feeding and blood cholesterol: a study in adolescents and a systematic review.

OBJECTIVE To examine the influence of infant feeding method on serum total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol. METHODS A cross-sectional study of 13- to 16-year-olds and a systematic review of studies (all observational) on the effects of infant feeding on cholesterol in infancy (<1 year), childhood or adolescence (1-16 years), and adulthood (> or =17 years) were conducted using random effects models. Differences are presented as breastfed-bottle-fed. A total of 1532 individuals (92% white; 55% male; mean age: 15.1 years) in 10 British towns were studied, and 37 studies with 52 observations on TC (26 in infancy, 17 in childhood or adolescence, and 9 in adulthood; corresponding figures for LDL were 7, 4, and 6) were reviewed. RESULTS Mean TC in childhood or adolescence (including the new study) was not related to infant feeding pattern (mean TC difference = 0.00; 95% confidence interval [CI]: -0.07 to 0.07 mmol/L). However, in infancy, mean TC was higher among those breastfed (mean TC difference = 0.64; 95% CI: 0.50-0.79 mmol/L), whereas in adults, mean TC was lower among those breastfed (mean TC difference = -0.18; 95% CI: -0.30 to -0.06 mmol/L). Patterns for LDL were similar to those for TC throughout. CONCLUSIONS Breastfeeding is associated with increased mean TC and LDL levels in infancy but lower levels in adulthood/adult life. These results suggest that breastfeeding may have long-term benefits for cardiovascular health and may have implications for the content of formula feed milks.
Polycyclic aromatic hydrocarbons in soils of an industrial area of China: multivariate analyses and geostatistics

Tianjin Bin Hai New Area (BHNA) is the third largest economic zone in China. This is an older industrial area that has been developing rapidly but with many historic sources of contamination. The concentrations of 16 individual polycyclic aromatic hydrocarbons (PAHs) listed for priority control by the US EPA were quantified in 105 surface soil samples by the use of gas chromatography mass spectrometry (GC/MS). Multivariate statistical methods were used to characterise the mixtures and make comparisons in the patterns among areas. Concentrations varied among areas, ranging from moderate to relatively high. The coefficients of determination between concentrations of individual PAHs and total concentration of PAH (∑ PAH) increased with the number of rings. The first three factors from the principal component analysis (PCA) explained 81.6% of the total variation, while ten higher molecular weight (HMW) PAHs’ loadings for factor 1 accounted for 51.0%. Based on the patterns of relative loading proportions of individual PAHs calculated by PCA, the primary sources were coal combustion, traffic emissions including gasoline, diesel oil, and the burning of natural gas. The spatial distribution of concentrations of fluorene had a poor spatial autocorrelation in the study area. The sites with the greatest potential risk due to exposure to PAHs were mainly distributed around the chemical industry parks.
Vitamin K dependent actions of Gas 6

GAS6 (growth arrest-specific gene 6) is the last addition to the family of plasma vitamin Kdependent proteins. Gas6 was cloned and characterized in 1993 and found to be similar to the plasma anticoagulant protein S. Soon after it was recognized as a growth factor-like molecule, as it interacted with receptor tyrosine kinases of the TAM family; Tyro3, Axl and MerTK. Since then, the role of Gas6, protein S and the TAM receptors has been found to be important in inflammation, hemostasis and cancer, making this system an interesting target in biomedicine. Gas6 employs a unique mechanism of action, interacting through its vitamin Kdependent Gla module with phosphatidylserine-containing membranes and through its carboxy-terminal LG domains with the TAM membrane receptors. The fact that these proteins are affected by anti-vitamin K therapy is discussed in detail.
Cerebrospinal fluid corticotropin-releasing hormone in healthy humans: effects of yohimbine and naloxone.

CRH neurons projecting from the paraventricular nucleus (PVN) of the hypothalamus to the median eminence control hypothalamic-pituitary-adrenal (HPA) axis activity. However, CRH neurons outside the PVN as well as PVN neurons projecting to sites other than the median eminence also contribute to the stress response and may play a role in mood and anxiety disorders. We have attempted to investigate possible noradrenergic and opioid regulation of these non-HPA CRH neurons. We hypothesized that yohimbine (an alpha2-adrenergic antagonist) would have stimulatory action on non-HPA CRH neurons, whereas naloxone (a mu-opioid receptor antagonist) would not have this effect. Adult normal volunteers received i.v. yohimbine (n = 5; 0.4 microg/kg), naloxone (n = 4; 125 microg/kg), or placebo (n = 3; 0.9% saline). Cerebrospinal fluid (CSF) was collected continuously, and concentrations of CSF CRH, CSF norepinephrine (NE), and plasma cortisol were measured. Administration of either yohimbine or naloxone caused significant increases in plasma cortisol concentrations over time. Although yohimbine robustly increased CSF NE levels and appeared to increase CSF CRH levels, these effects were not seen after naloxone or placebo administration. Intraindividual correlations were not observed between the measured concentrations of plasma cortisol and CSF CRH for any of the subjects. The results support the idea that CSF CRH concentrations reflect the activity of non-HPA CRH neurons. Although both yohimbine and naloxone stimulated the HPA axis, only yohimbine appeared to have stimulatory effects on central NE and non-HPA CRH.
Whooping cough and whooping cough vaccine: the risks and benefits debate.

There has been extensive debate in Great Britain regarding the risks and benefits of routine infant immunization against whooping cough. As a result of highly publicized cases of brain damage alleged to have been caused by the vaccine, immunization acceptance rates have dropped dramatically and epidemics of the disease have recurred. On the basis of a review of the current state of knowledge on whooping cough, the vaccine, and vaccine safety, the authors conclude that the dangers of the disease outweigh any known hazards of the vaccine. Although whooping cough is less important a cause of death and disability at present, it remains a potentially lethal disease that should be controlled. The safety of the vaccine is an especially critical question, however, since it is being advocated for use on a mass scale in previously healthy children. The results of studies such as the National Childhood Encephalopathy Study suggest DPT vaccination is associated with a greater frequency of acute neurological illnesses than would be expected by chance. On the other hand, most cases of such complications were not time-associated with DPT vaccination and may have resulted from the less purified vaccines used in the past. The most critical element in decision making is the readiness of parents and doctors to accept the fact that active preventive measures such as pertussis immunization sometimes carry unavoidable risks that have to be weighed against the risk of nonintervention.
Reliability of Assessing Indices of Isokinetic Leg Strength in Pubertal Soccer Players

Using 95% limits of agreement (LOA), this study examined the reproducibility of indices of isokinetic leg strength in pubertal soccer players. Following familiarization, 23 boys performed isokinetic assessments of the knee joint muscles at 1.08, 2.16, and 4.32 rad/s during concentric exercise and at 2.16 rad/s during eccentric actions on two separate occasions. Peak torque values were recorded and reciprocal and bilateral muscle group ratios were calculated. As random error was heteroscedastic, 95% ratio LOA were employed. Systematic bias for the various measurements ranged from 0.97 to 1.07 for all data. Random variation associated with eccentric assessments of the hamstrings, concentric H:Q ratio calculated at 1.08 rad/s, and HECC:QCON ratios appeared narrow enough to be of practical use (×/÷ 1.05 to 1.20). Random errors associated with H:Q ratios calculated at high concentric velocities (4.32 rad/s) and during eccentric exercise (×/÷ 1.10 to1.37), and in all bilateral muscle group ratios (×/÷ 1.15 to 1.43) were too broad, rendering them prone to misinterpretation
Biological Treatment of Oil Field Wastewater in a Sequencing Batch Reactor

This work reports the results of experiments carried out in a sequencing batch reactor (SBR) operated under 24 hour cycles, treating an effluent containing a mixture of oil field wastewater and sewage, in different percentages. The removal of phenols, ammonium and COD was monitored in several experimental runs, varying the dilution degree of the oilfield wastewater (10 to 45% v/v). The volatile suspended solids (VSS) content in the reactor was also monitored and the protein (PTN) and polysaccharide (PS) contents of the suspended biomass were determined. The removal of ammonium and phenols did not vary significantly in the experimental runs, attaining average values of 95% and 65%, respectively. COD removal efficiencies in the range of 30 to 50% were attained in the experiments carried out with dilution percentages of 45 and 35% (v/v) respectively. An experiment carried out with a lower proportion of produced water (15% v/v), keeping the salinity level corresponding to a higher proportion of industrial effluent (45% v/v), led to an improvement in the COD removal, indicating that the recalcitrance of the organic compounds found in the effluent is the main cause of the moderate COD removal efficiencies attained in the SBR system. With regard to the composition of the microbial flocs, no significant variation was observed in the PS/PTN, PS/VSS and PTN/VSS ratios when the effluent composition changed (increased salinity and levels of organic material).
Inhibition of rat liver gap junction intercellular communication by tumor-promoting agents in vivo. Association with aberrant localization of connexin proteins.

BACKGROUND Gap junctional intercellular communication is believed to play an important role in the maintenance of tissue homeostasis, and disruption of it has been proposed to be involved in carcinogenesis. A number of tumor-promoting agents have been shown to inhibit capacity for intercellular communication in cell culture studies. Recently, we developed a simple dye-transfer technique to evaluate cell-coupling function in fresh liver slices, and we used it to show that inhibition of intercellular communication is associated with rat liver tumor progression. Using this method with analysis of gap junction protein connexin expression, we have examined whether and how different liver-specific tumor-promoting agents inhibit dye-coupling in rat liver in vivo. EXPERIMENTAL DESIGN Groups of Fischer 344 rats received repeated chronic treatment of phenobarbital (PB), polychlorinated biphenyls (PCB), dichlorodiphenyltrichloroethane (DDT), and clofibrate (CF) for 5 weeks. After 1, 2, and 5 weeks of treatment, intercellular communication via gap junctions was evaluated by the dye-transfer assay in liver slices taken immediately after killing the rats. In parallel, the expression of connexins (cx) 32, 26, and 43 (gap junction proteins expressed in the liver) was studied at the mRNA and protein levels. RESULTS All four tumor-promoting agents decreased dye-coupling in rat liver. This decrease was associated with a reduced number of gap junctions and aberrant localization of some amount of cx 32 proteins in hepatocytes; cx 32 often was observed in the cytoplasm of hepatocytes instead of at gap junctions in the plasma membrane. Western blot analysis showed only slight changes in the level of cx 32 proteins. Although cx 26 proteins at gap junctions were usually decreased by tumor promoters in rat liver, local induction of cx 26 protein expression in centrolobular groups of hepatocytes after PCB and DDT treatment was observed. The expression of cx 43 was induced in hepatocytes after PCB, DDT, and CF exposure, but this protein was also localized intracytoplasmically, suggesting no functional role. All four tested tumor-promoting agents also increased cell proliferation, as revealed by staining with an anti-Ki 67 antibody. CONCLUSION The results demonstrate that different types of liver tumor-promoting agents inhibit dye-coupling in rat liver in vivo. This inhibition may be due to aberrant localization of the major liver gap junction protein cx 32, rather than its transcriptional or translational disregulation.
A game theory simulator for assessing the performances of competitive electricity markets

Electricity markets have different structures in different nations. Market structure, market rules, load level, market concentration and energy sources used to produce electricity influence the performances of the market. Modifications on those aspects may significantly affect market outcomes. Market simulators are developed to study the market behavior both from the point of view of the regulator and of the market players. The goal of regulators are monitoring the system, testing the rules or detecting market deficiencies, while the goal of each player is to find the optimal strategy to bid in the market. In this paper a medium run electricity market simulator (MREMS) based on game theory is presented. This simulator aims at capturing the strategic behavior of the producers resorting to the Forchheimer or Bertrand models, the kind of model being chosen according to the market concentration. A Residual Demand Curve (RDC) approach is proposed for the best bid exploration. Real input data from the Italian market are considered with some simplifying hypotheses related mainly to the hydropower allocation. These hypotheses ensure that the level of complexity of the modelization stays within reasonable limits. To illustrate the main features of the simulator and its usefulness in analyzing the electricity markets we present the results of the simulations on the Italian market.
Sodium and calcium currents shape action potentials in immature mouse inner hair cells

Before the onset of hearing at postnatal day 12, mouse inner hair cells (IHCs) produce spontaneous and evoked action potentials. These spikes are likely to induce neurotransmitter release onto auditory nerve fibres. Since immature IHCs express both α1D (Cav1.3) Ca2+ and Na+ currents that activate near the resting potential, we examined whether these two conductances are involved in shaping the action potentials. Both had extremely rapid activation kinetics, followed by fast and complete voltage‐dependent inactivation for the Na+ current, and slower, partially Ca2+‐dependent inactivation for the Ca2+ current. Only the Ca2+ current is necessary for spontaneous and induced action potentials, and 29 % of cells lacked a Na+ current. The Na+ current does, however, shorten the time to reach the action‐potential threshold, whereas the Ca2+ current is mainly involved, together with the K+ currents, in determining the speed and size of the spikes. Both currents increased in size up to the end of the first postnatal week. After this, the Ca2+ current reduced to about 30 % of its maximum size and persisted in mature IHCs. The Na+ current was downregulated around the onset of hearing, when the spiking is also known to disappear. Although the Na+ current was observed as early as embryonic day 16.5, its role in action‐potential generation was only evident from just after birth, when the resting membrane potential became sufficiently negative to remove a sizeable fraction of the inactivation (half inactivation was at −71 mV). The size of both currents was positively correlated with the developmental change in action‐potential frequency.