Miracle-dz/UniFAR-FTUs huggingface dataset:
Differentiation of Transplanted Microencapsulated Fetal Pancreatic Cells

Background. Fetal &bgr; cells are a potential form of cell therapy for type 1 diabetes. To protect transplanted cells from cellular immune attack, microencapsulation using barium alginate can be employed. Whether microencapsulated fetal pancreatic cells will differentiate as occurs with nonencapsulated fetal pancreatic cells is presently unknown. It is suggested that such differentiation would occur in encapsulated cells, similar to previous experiments conducted using encapsulated embryonic stem cells. Methods. Streptozotocin-induced diabetic severe combined immunodeficient mice were transplanted with 5,000 to 38,000 fetal pig islet-like cell clusters (ICCs) within barium alginate microcapsules of diameter 300, 600, or 1000 &mgr;m. Viability, insulin secretion, and content of encapsulated cells were measured prior to transplantation. Blood glucose levels (BGL) were measured twice weekly and porcine C-peptide monthly. Encapsulated cells were recovered from mice at 6 months posttransplantation for analysis. Results. Encapsulated cells became glucose responsive and normalized BGL within 13 to 68 days posttransplantation, with 5,000 to 10,000 ICCs required. Microcapsule diameter did not affect the time required to achieve normoglycemia. BGL remained normal for the 6-month duration of the experiments. After removal of grafts at 25 weeks posttransplantation, glucose stimulated insulin secretion of the explants was enhanced 96-fold, insulin content was enhanced 34-fold, and the percentage of insulin and glucagon positive cells increased 10-fold and threefold, respectively, from the time of transplantation. Conclusions. This study demonstrates that fetal pancreatic cells differentiate and function normally when placed within barium alginate microcapsules and transplanted.
The Neurobiological Toll of Child Abuse and Neglect

Exposure to interpersonal violence or abuse affects the physical and emotional well-being of affected individuals. In particular, exposure to trauma during development increases the risk of psychiatric and other medical disorders beyond the risks associated with adult violence exposure. Alterations in the hypothalamic-pituitary-adrenal (HPA) axis, a major mediating pathway of the stress response, contribute to the long-standing effects of early life trauma. Although early life trauma elevates the risk of psychiatric and medical disease, not all exposed individuals demonstrate altered HPA axis physiology, suggesting that genetic variation influences the consequences of trauma exposure. In addition, the effects of abuse may extend beyond the immediate victim into subsequent generations as a consequence of epigenetic effects transmitted directly to offspring and/or behavioral changes in affected individuals. Recognition of the biological consequences and transgenerational impact of violence and abuse has critical importance for both disease research and public health policy.
Renal gangliosides are involved in lead intoxication

The biological effects of lead are well defined; however, neither the risk exposure level nor the subcellular mechanism of its action is completely clear. The present work was undertaken to investigate the effects of low level and long term lead exposure on the composition and expression of rat renal gangliosides. In order to identify ganglioside expression, frozen sections of kidneys were stained with monoclonal antibodies GMB16 (GM1 specific), GM28 (GM2 specific), AMR‐10 (GM4 specific) and CDW 60 (9‐O‐Ac‐GD3 specific). Strong reactivity was observed for GMB28, AMR‐10 and CDW 60, while GMB16 developed only weak labelling in treated kidney compared with the control. The alterations in the expression of renal gangliosides observed by immunohistochemistry were accompanied by quantitative and qualitative changes in the thin layer chromatography of total gangliosides isolated from kidney tissues. Lead treatment produced a significant increase in 9‐O‐Ac GD3, a ganglioside involved in apoptotic processes. In agreement with this result, a significant decrease in the number of apoptotic glomerular cells was observed with the TUNEL assay. These findings lead us to suggest that alterations in renal gangliosides produced by low level lead exposure are associated with the apoptotic processes that take place in the kidney.
Screening of six polymorphisms related with folate metabolism in parents of individuals with Down syndrome

Abstract Objective The study aim to investigate MTHFR C677T, MTHFR A1298C, RFC1 A80G, MTR A2756G, CBS 844ins68, MTRR A66G polymorphisms in Down syndrome (DS) parents. Methods Polymorphisms were evaluated in 35 mothers and 24 fathers of individuals with free trisomy of chromosome 21 confirmed by karyotype. The control group included 26 mothers and 26 fathers who had no children with DS. The molecular analysis was performed by polymerase chain reaction and restriction fragment length polymorphism (reaction chain polymerase restriction fragment length polymorphism) or polymerase chain reaction. The χ2 test (chi-square) was used to compare allele’s differences among the study and the control group. Hardy–Weinberg equilibrium model was performed by χ2 testing. Multiple logistic regression models and binary logistic regression used to determine the association between polymorphisms and parental DS risk. Results This study did not reveal any significant difference in frequencies of polymorphisms. The haplotype analysis did not reveal linkage disequilibrium. The logistic regression analysis did not demonstrate differences between the groups. However, the binary logistic regression showed a higher frequency of the polymorphic homozygote genotype in DS parent group to codominant and dominant model in the RFC1 A80G. Conclusion In conclusion, although the screening results were significant only to the RFC1 A80G polymorphism, the other determinations of the genetic factors associated with abnormal chromosome segregation could be helpful in future studies, including other polymorphisms involved in folate metabolism.
Crystalline silicon passivation with amorphous silicon carbide layers

Amorphous silicon enables the fabrication of very high-efficiency crystalline-silicon-based solar cells due to its combination of excellent passivation of the crystalline silicon surface and permeability to electrical charges. Yet, amongst other limitations, the passivation it provides degrades upon high-temperature processes, limiting possible post-deposition fabrication possibilities (e.g. forcing the use of low-temperature silver pastes). We previously evidenced the superior temperature stability of low-carbon-content intrinsic amorphous silicon carbide (a-SiCx:H) passivating layers to sidestep this issue, and investigate here in more details the reason for the improved temperature stability. The passivation from intrinsic a-SiCx:H layers is shown to first improved upon annealing, and then degrade past 350°C. The initial passivation can be improved and the degradation postponed by capping the a-SiCx:H layer by an a-Si:H film. We compare here the passivation provided by stacks of a-Si:H and a-SiCx:H, and investigate the hydrogen bonding and content of these films.
Purchasing Information to Reduce Uncertainty in Trajectory Prediction

Previous studies show people underestimate the amount of uncertainty in predictive states. This experiment tested an implication of such findings: that people will be less likely (than optimal) to acknowledge their uncertainty, and hence less likely to purchase information that reduces future uncertainty. In a trajectory prediction task, participants had the opportunity to reduce uncertainty by a constant amount by purchasing either an expensive (bad deal), neutral-cost, or cheap (bargain) sensor. Participants were biased, relative to expected value theory, in integrating cost with uncertainty reduction in their decisions to purchase. In contrast to our primary hypothesis that they would place more decision weighting on reducing the cost of the purchase, than on gaining information, our results revealed the opposite. The findings are interpreted in the context of models of attribute salience in decision-making.
Potassium carbonate as a potassium source and dietary buffer for lactating Holstein cows during hot weather.

Twenty-four lactating Holstein cows were offered diets containing . 93, 1.29, and 1.53% potassium during hot weather. Cows fed 1.53% potassium consumed more dry matter than cows fed either . 93 or 1.29% potassium. Milk production and composition were not different. Potassium intake and fractional excretion increased, and fecal output as a percentage of intake declined with diets containing 1.29 and 1.53% potassium. Magnesium fractional excretion was least and fecal output greatest in cows fed 1.29% potassium. Fecal sodium output and fecal output as a percentage of intake was reduced by 1.53% dietary potassium. During comparison period 2, potassium carbonate at 0, . 5, or 1.0% had no effect on feed consumption or milk yield, but buffered diets increased milk fat percentage and depressed milk protein percentage. No effects of buffers on ruminal pH, volatile fatty acids, or digestibility of dry matter or fiber were noted. Cows responded favorably during hot weather to potassium supplementation at 1.53% of the diet, but with high dietary potassium, effects on other minerals must be considered. Chloride, although present above requirements in all diets, was greater in the highest potassium diet.
Modeling H2 formation in the turbulent ISM: Solenoidal versus compressive turbulent forcing

We present results from high-resolution three-dimensional simulations of the turbulent interstellar medium that study the influence of the nature of the turbulence on the formation of molecular hydrogen. We have examined both solenoidal (divergence-free) and compressive (curl-free) turbulent driving, and show that compressive driving leads to faster H2 formation, owing to the higher peak densities produced in the gas. The difference in the H2 formation rate can be as much as an order of magnitude at early times, but declines at later times as the highest density regions become fully molecular and stop contributing to the total H2 formation rate. We have also used our results to test a simple prescription suggested by Gnedin et al. (2009) for modeling the influence of unresolved density fluctuations on the H2 formation rate in large-scale simulations of the ISM. We find that this approach works well when the H2 fraction is small, but breaks down once the highest density gas becomes fully molecular.
Kinetic analysis of plasma insulin disappearance in nonketotic diabetic patients and in normal subjects. A tracer study with 125I-insulin.

The studies so far reported on the metabolic clearance rate of insulin in human diabetes mellitus have given conflicting results, probably because they have been conducted on few patients and have used a variety of experimental techniques and data treatments. We investigated the kinetics of insulin distribution and degradation in 35 normal subjects and in 42 nonketotic, nonobese, overtly diabetic patients, of whom 26 were above 40 yr old and 16 were 40 yr old or less at diagnosis. The design of the study combined (a) the use of a tracer to perturb minimally the steady state and to avoid glucose infusion; (b) the preparation of purified [(125)I]-monoiodoinsulin, which has a metabolic behavior similar to that of native insulin; and (c) noncompartmental analysis of the plasma immunoprecipitable (125)I-insulin disappearance curves, which were recorded for 2 h after pulse i.v. injection of the tracer.Metabolic clearance rate was found to be similar in diabetics (404+/-18 ml/min.m(2), mean+/-SEM) and in normals (420+/-14), although the latter-onset patients had slightly, if not significantly, lower metabolic clearance rate values than the earlier-onset diabetics (385+/-19 and 443+/-36, respectively). The initial distribution volume of the hormone also did not significantly differ in diabetics and normals and was similar to plasma volume. The reentry rate into the initial distribution volume of the hormone and the total, plasma-equivalent distribution volume of insulin were both significantly raised in diabetics (251+/-12 ml/min.m(2) and 10.3+/-0.5 liters/m(2)) in comparison with normals (195+/-8 and 7.5+/-0.3). The posthepatic delivery rate of insulin was found to be slightly raised in later-onset diabetics (194+/-20 mU/h.m(2)), but somewhat reduced in earlier-onset diabetics (133+/-15) in comparison with normals (172+/-14); these differences reflected the different basal plasma insulin concentrations in these three groups. Chronic treatment with oral hypoglycemic drugs, age, duration of the disease, and degree of metabolic control appeared to have only little effect on the kinetics of insulin.On the basis of these results, we conclude that insulin-independent adult diabetics show, already in the fasting state, a combination of insulin resistance and insulin deficiency and a derangement in insulin distribution, the precise significance of which is uncertain.
Cocaine modulates HIV‐1 integration in primary CD4+ T cells: implications in HIV‐1 pathogenesis in drug‐abusing patients

Epidemiologic studies suggest that cocaine abuse worsens HIV‐1 disease progression. Increased viral load has been suggested to play a key role for the accelerated HIV disease among cocaine‐abusing patients. The goal of this study was to investigate whether cocaine enhances proviral DNA integration as a mechanism to increase viral load. We infected CD4+ T cells that are the primary targets of HIV‐1 in vivo and treated the cells with physiologically relevant concentrations of cocaine (1 µM–100 µM). Proviral DNA integration in the host genome was measured by nested qPCR. Our results illustrated that cocaine from 1 µM through 50 µM increased HIV‐1 integration in CD4+ T cells in a dose‐dependent manner. As integration can be modulated by several early postentry steps of HIV‐1 infection, we examined the direct effects of cocaine on viral integration by in vitro integration assays by use of HIV‐1 PICs. Our data illustrated that cocaine directly increases viral DNA integration. Furthermore, our MS analysis showed that cocaine is able to enter CD4+ T cells and localize to the nucleus‐. In summary, our data provide strong evidence that cocaine can increase HIV‐1 integration in CD4+ T cells. Therefore, we hypothesize that increased HIV‐1 integration is a novel mechanism by which cocaine enhances viral load and worsens disease progression in drug‐abusing HIV‐1 patients.
Bone turnover marker reference intervals in young females

Background The use of bone turnover markers in clinical practice and research in younger people is limited by the lack of normative data and understanding of common causes of variation in bone turnover marker values in this demographic. To appropriately interpret bone turnover markers, robust reference intervals specific to age, development and sex are necessary. This study aimed to determine reference intervals of bone turnover markers in females aged 16–25 years participating in the Safe-D study. Methods Participants were recruited through social networking site Facebook and were asked to complete an extensive, online questionnaire and attend a site visit. Participants were tested for serum carboxy-terminal cross-linking telopeptide of type 1 collagen and total procollagen type 1 N-propeptide using the Roche Elecsys automated analyser. Reference intervals were determined using the 2.5th to 97.5th percentiles of normalized bone turnover marker values. Results Of 406 participants, 149 were excluded due to medical conditions or medication use (except hormonal contraception) which may affect bone metabolism. In the remaining 257 participants, the reference interval was 230–1000 ng/L for serum carboxy-terminal cross-linking telopeptide of type 1 collagen and 27–131 µg/L for procollagen type 1 N-propeptide. Both marker concentrations were inversely correlated with age and oral contraceptive pill use. Therefore, intervals specific to these variables were calculated. Conclusions We defined robust reference intervals for cross-linking telopeptide of type 1 collagen and procollagen type 1 N-propeptide in young females grouped by age and contraceptive pill use. We examined bone turnover markers’ relationship with several lifestyle, clinical and demographic factors. Our normative intervals should aid interpretation of bone turnover markers in young females particularly in those aged 16 to 19 years where reference intervals are currently provisional.
Implementation of Behavior-Based Training Can Improve Food Service Employees’ Handwashing Frequencies, Duration, and Effectiveness

Personal hygiene is a significant risk factor that contributes to foodborne illness. Appropriate handwashing behaviors can significantly reduce this risk; however, knowledge-based training alone may be insufficient to prompt preventive food safety practices. An improved, more effective food safety training approach that can directly influence employees’ behavior is strongly recommended. The main objective of this study was to investigate the effectiveness of behavior-based food safety training on improving food handlers’ handwashing practices and frequency. Four of the nine critical behaviors that help effectively prevent the spread of pathogens and control food safety hazards were identified as target behaviors, and handwashing frequencies and durations were also included as measures of handwashing performance. A four-phase within-group experimental study with a behavioral motivation intervention was conducted. Employees’ handwashing behaviors were videotaped and coded by researchers. Results indicated that knowledge-based training alone failed to improve employees’ handwashing performance, especially when employees had multiple work tasks simultaneously during the busy meal service time. In comparison, the behavior-based training approach was effective in improving employees’ handwashing performance and frequency. More specifically, proper rates of all the critical behaviors measured were significantly increased during the motivational phase.
Clinical trials in jeopardy.

BACKGROUND The controlled clinical trial, the gold standard for clinical research, is in jeopardy. The pharmaceutical industry is rapidly expanding its command over clinical trials but scientific rigor requires independence and objectivity. Safeguarding such criteria is hard because industrial sponsors, benefit directly from favorable results and are virtually in complete control. OBJECTIVE To review flawed procedures jeopardizing the credibility of trials and to look for possible solutions to the conflict between sponsored industry and scientific independence. RESULTS Flawed procedures jeopardizing current clinical trials can be listed as follows. Industries, at least in Europe, are allowed to choose their own independent protocol review board prior for approval. The independent protocol review board approves protocols even when the research is beyond the scope of its expertise. Health institutions hosting multicenter trials are requested to refrain from scientific or ethic assessment of the trial. Trial monitors are often employees of industry. Data control is predominantly in the hands of the sponsor. Interim analyses are rarely performed by independent groups. The scientific committee of the trial consists largely of prominent but otherwise uninvolved physicians attached to the study. The analysis and report of the trial is generally provided by clinical associates of the pharmaceutical companies and, after a brief review, co-signed by prominent physicians attached to the study. POSSIBLE SOLUTIONS: Possible solutions to the conflict between sponsored industry and scientific independence could include the following. Surveillance by independent observers during each stage of the trial is desirable. In contrast, tight control of study data, analysis, and interpretation by the commercial sponsor is undesirable. If, instead, the pharmaceutical industry allows the profession to more actively participate in different stages of the trial, scientific research will be better served, reasonable biological questions will be better answered, and, because the profession will be more convinced of the objective character of the research, it will not be counterproductive to the sales.
Fatty aldehyde dehydrogenase is up‐regulated by polyunsaturated fatty acid via peroxisome proliferator‐activated receptor α and suppresses polyunsaturated fatty acid‐induced endoplasmic reticulum stress

Fatty aldehyde dehydrogenase (FALDH; also known as ALDH3A2 or ALDH10) oxidizes medium‐ or long‐chain aliphatic aldehydes. FALDH deficiency in humans is known to be the cause of Sjögren–Larsson syndrome, in which individuals display neurological symptoms and cutaneous abnormality. FALDH‐V, a splice isoform of FALDH, is localized in the peroxisome and contributes to the oxidization of pristanal, an intermediate of the α‐oxidation pathway. FALDH‐N, another splice isoform of FALDH, is induced by peroxisomal proliferator‐activated receptor α ligands, although its activation mechanism has not been clarified. In the present study, we show that transcriptional activation of FALDH is directly regulated by peroxisomal proliferator‐activated receptor α through a direct repeat‐1 site located in the FALDH promoter. In addition, FALDH is efficiently induced by linoleic acid in rat hepatoma Fao cells through transcriptional activation by peroxisomal proliferator‐activated receptor α. Furthermore, ectopic expression of endoplasmic reticulum‐localizing FALDH‐N, but not peroxisome‐localizing FALDH‐V, suppresses endoplasmic reticulum stress caused by linoleic acid in HEK293 cells. These results suggest the autocatalytic nature of the FALDH‐N system against endoplasmic reticulum stress that is induced by polyunsaturated fatty acid; polyunsaturated fatty acid binds to peroxisomal proliferator‐activated receptor α to activate the expression of FALDH‐N, which then detoxifies polyunsaturated fatty acid‐derived fatty aldehydes and protects cells from endoplasmic reticulum stress.
A predictive nutritional model for plant cells and hairy roots

A structured nutritional model is proposed to describe growth and nutritional behavior of Eschscholtzia californica suspension cells and Catharanthus roseus and Daucus carota hairy roots in in vitro culture. The model describes the cells specific growth rate from concentration of intracellular nutrients such as inorganic phosphate (Pi), nitrogen sources (NO 3− and NH 4+ ) and sugars. Two‐level Michaelis–Menten kinetics are used to describe Pi and NO 3− uptake and simple Michaelis–Menten kinetics for description of sugars uptake. Model parameters for each cell line were calibrated using data from batch cultures. The predictive capacity of the model was tested using data from medium exchange hairy root cultures. The model describes growth and nutritional behavior for the cell and hairy root lines. A sensitivity analysis was performed to identify critical model parameters and effect of initial conditions. The cell and hairy roots lines are also compared from their kinetic parameters. The kinetic model is efficient for describing and predicting growth and nutritional behaviors of suspension cells and hairy roots. Biotechnol. Bioeng. 2008;99: 189–200. © 2007 Wiley Periodicals, Inc.