Miracle-dz/UniFAR-FTUs huggingface dataset:
The Use of Vitamin E in Type 2 Diabetes Mellitus

Diabetes mellitus has assumed epidemic proportions in most parts of the world, and it is a major source of morbidity in developed countries. In addition, in several instances, diabetes is associated with a variety of metabolic abnormalities, including abdominal obesity, insulin resistance, hypertension, dyslipidemia, and hyperglycemia. There is considerable evidence that hyperglycemia causes the generation of reactive oxygen species (ROS), ultimately leading to increased oxidative stress in a variety of tissues. In the absence of an appropriate compensatory response by the endogenous antioxidants, such as vitamins C and E, catalase, glutathione, and superoxide dismutase, oxidative stress dominates, resulting in the activation of stress-sensitive intracellular signaling pathways. One of the major consequences is the generation of gene products that cause cellular damage and are ultimately responsible for the late complications of diabetes. The ability of antioxidants to protect against the effects of hyperglycemia in vitro, along with the clinical benefits often reported following antioxidant therapy, supports a causative role of oxidative stress in mediating and/or worsening these abnormalities. This review will focus on the critical assessment of the literature as it relates to the association between oxidative stress and diabetes, followed by the role of oxidative stress in the complications of type 2 diabetes mellitus. Finally, a review of the use of the antioxidant vitamin E will be provided in diabetic patients by assessing and evaluating some of the clinical trials in the literature.
The effect of recombinant IGF‐I on anterior pituitary function in healthy volunteers

OBJECTIVE Insulin‐like growth factor‐I is the mediator of many of the actions of GH and is a potent metabolic regulator. Recombinant IGF‐I (rhIGF‐I) is of potential value in the treatment of syndromes associated with either GH or insulin resistance. This study was designed to assess the effects of subcutaneous (s.c.) rhIGF‐I on anterior pituitary function.
Inhibition of the Dephosphorylation of Eukaryotic Initiation Factor 2E Ameliorates Murine Experimental Colitis

Background/Aims: Endoplasmic reticulum (ER) stress in the intestine is closely associated with the development of inflammatory bowel disease (IBD). However, the role of the protein kinase RNA-like ER kinase in this disease is not fully known. We studied whether an inhibitor of the dephosphorylation of eukaryotic initiation factor 2E, salubrinal, improves murine experimental colitis through the amelioration of ER stress. Methods: Colitis was induced by the administration of 3% dextran sulfate sodium (DSS) for 5 days. Mice were injected salubrinal intraperitoneally from the commencement of DSS treatment and were sacrificed on day 10. The severity of colitis was evaluated histologically using a scoring system. Myeloperoxidase activity and the expression of proinflammatory cytokine genes in the colon were analyzed. The expression levels of ER stress-related proteins were evaluated by Western blotting. Results: The administration of salubrinal significantly attenuated body weight loss and improved colitis, as assessed histologically. The elevation of myeloperoxidase activity and the expression of proinflammatory cytokine genes were suppressed in salubrinal-treated mice. The expression of glucose-regulated protein 78, activating translation factor 4, and heat-shock protein 70 was elevated in mice treated with salubrinal. Conclusion: The amelioration of ER stress may be a therapeutic target for the treatment of IBD. i 2014 S. Karger AG, Basel
IFN-γ Production by CD8+ T Cells Depends on NFAT1 Transcription Factor and Regulates Th Differentiation1

CD8+ T lymphocytes are excellent sources of IFN-γ; however, the molecular mechanisms that dictate IFN-γ expression upon TCR stimulation in these cells are not completely understood. In this study, we evaluated the involvement of NFAT1 in the regulation of IFN-γ gene expression in murine CD8+ T cells and its relevance during Th differentiation. We show that CD8+, but not CD4+, T cells, represent the very first source of IFN-γ upon primary T cell activation, and also that the IFN-γ produced by naive CD8+ T cells may enhance CD4+ Th1 differentiation in vitro. TCR stimulation rapidly induced IFN-γ expression in CD8+ T lymphocytes in a cyclosporin A-sensitive manner. Evaluation of CD8+ T cells showed that calcium influx alone was sufficient to activate NFAT1 protein, transactivate IFN-γ gene promoter, and induce IFN-γ production. In fact, NFAT1-deficient mice demonstrated highly impaired IFN-γ production by naive CD8+ T lymphocytes, which were totally rescued after retroviral transduction with NFAT1-encoding vectors. Moreover, NFAT1-dependent IFN-γ production by the CD8+ T cell compartment was crucial to control a Th2-related response in vivo, such as allergic inflammation. Consistently, CD8α- as well as IFN-γ-deficient mice did not mount a Th1 immune response and also developed in vivo allergic inflammation. Our results clearly indicate that IFN-γ production by CD8+ T cells is dependent of NFAT1 transcription factor and may be an essential regulator of Th immune responses in vivo.
AIDS events among individuals initiating HAART: do some patients experience a greater benefit from HAART than others?

Objective:To describe the rate of new AIDS events over the first year of HAART in patients with different characteristics and to describe the decrease in incidence of AIDS between the first and second 6 months of the year in these patients. Design:Collaboration of cohort studies from Europe and North America. Methods:AIDS rates in the first year of HAART were calculated for 22 217 antiretroviral-naive individuals. Event rates were compared in the periods 0–6 and 7–12 months after starting HAART. Results:The number of events and person-years of follow-up (PYFU) in the two time periods were 1185 (9601) and 336 (8690), respectively (event rates: 12.3 and 3.9 per 100 PYFU, relative decline in incidence: 68%). Whereas rates decreased in all groups, tests for interaction suggested that relative declines in incidence were more rapid in homosexual men (P = 0.002), in those starting HAART from 2001 in comparison with earlier years (P = 0.03), in those with lower CD4 cell counts (P-values of 0.001, 0.002 and 0.11 for those with cell counts < 50, 50–199 and 200–349 cells/μl compared to those with cell counts ≥ 350 cells/μl) and HIV RNA levels ≥ 5 log10 copies/ml (P = 0.0008). Those with AIDS at the time of starting HAART had a less rapid relative decline in incidence (P = 0.0007). Conclusions:Our results suggest that some groups may experience less rapid relative declines in AIDS incidence than others over the first year on HAART.
Ectopic expression of Fgf3 leads to aberrant lineage segregation in the mouse parthenote preimplantation embryos

Background: Parthenogenetic mammalian embryos were reported to die in utero no later than the 25‐somite stage due to abnormal development of both embryonic and extraembryonic lineages. Interestingly, it has been shown that parthenogenetic ICM cells tend to differentiate more into primitive endoderm cells and less into epiblast and ES cells. Hence we are interested in studying the molecular mechanisms underlying lineage defects of parthenotes. Results: We found that parthenote inner cell masses (ICMs) contained decreased numbers of Sox2+/Nanog+ epiblast cells but increased numbers of Gata4+ primitive endoderm cells, indicating an unusual lineage segregation. We demonstrate for the first time that the increased Gata4 level in parthenotes may be explained by the strong up‐regulation of Fgf3 and Fgfr2 phosphorylation. Inhibition of Fgfr2 activation by SU5402 in parthenotes restored normal Nanog and Gata4 levels without affecting Fgf3, indicating that Fgf3 is upstream of Fgfr2 activation. In parthenote trophectoderm, we detected normal Cdx2 but ectopic Gata4 expression and reduced Elf5 and Tbr2(Eomes) levels. Conclusions: Taken together, our work provides for the first time the insight into the molecular mechanisms of the developmental defects of parthenogenetic embryos in both the trophectoderm and ICM. Developmental Dynamics 241:1651–1664, 2012. © 2012 Wiley Periodicals,Inc.
Typing early Australian healthcare-associated MRSA: confirmation of major clones and emergence of ST1-MRSA-IV and novel ST2249-MRSA-III

Aims: To investigate the evolutionary origins of Australian healthcare-associated (HCA) methicillin-resistant Staphylococcus aureus (MRSA) strains from a panel of historical isolates typed using current genotyping techniques. Methods: Nineteen MRSA isolates from 1965 to 1981 were examined and antibiotic susceptibility profiles determined. Genetic characterisation included real-time (RT) polymerase chain reaction (PCR) assays to identify single nucleotide polymorhpism (SNP) clonal complexes (SNP CC) and sequence type (SNP ST), multi locus sequence typing (MLST) and staphylococcal chromosomal cassette mec typing. Results: All SNP CC30 isolates belonged to a novel sequence type, ST2249. All SNP CC239 isolates were confirmed as ST239-MRSA-III, except for a new single locus variant of ST239, ST2275. A further new type, ST2276, was identified. Conclusions: The earliest MRSA examined from 1965 was confirmed as ST250-MRSA-I, consistent with archaic European types. Identification of ST1-MRSA-IV in 1981 is the earliest appearance of this clinically important lineage which manifested in Australia and the United States in the 1990s. A previously unknown multi-resistant clone, ST2249-MRSA-III, was identified from 1973. Gentamicin resistance first appeared in this novel strain from 1976 and not ST239 as previously suspected. Thus, ST2249 was present in the earliest phase of the HCA MRSA epidemic in eastern Australia and was perhaps related to the emergence of the globally epidemic strain ST239.
Persistence of virus and viral genome in myocardium after Coxsackievirus B3‐induced murine myocarditis

Following infection with Coxsackievirus B3 (CVB3). A‐strain mice develop ongoing myocarditis that persists after the virus ceases to be cultivatable from heart tissue. We studied the natural history of this virus‐induced but apparently autoimmune inflammation by means of in situ hybridization (ISH) and by polymerase chain reaction (PCR). Both ISH and culture allowed detection of virus up to 2 weeks post‐infection in virtually all heart tissues. In contrast, PCR revealed the presence of viral genome for a substantially longer period of time, i.e. at least 34 days after CVB3 infection. Similarly, the majority of mice showed myocardial inflammation at this time point. However, the persistence of virus did not correlate with ongoing myocarditis, and vice versa. Most mice with ongoing myocarditis produced heart myosin autoantibodies, most probably as a result of tissue damage. The lack of correlation between presence of ongoing inflammation and persistence of virus supports our previous view that the late phase of CVB3‐induced myocarditis is mediated by auto immunological mechanisms.
Growth, IGF System, and Cortisol in Children with Intrauterine Growth Retardation: Is Catch-up Growth Affected by Reprogramming of the Hypothalamic-Pituitary-Adrenal Axis?

Intrauterine growth retardation (IUGR) is one of the major causes of short stature in childhood. Although postnatal catch-up growth occurs in the majority of IUGR children, approximately 20% of them remain permanently short. The mechanisms that allow catch-up growth or, on the contrary, prevent IUGR children from achieving a normal height are still unknown. Our aim was to investigate whether intrauterine reprogramming of hypothalamic-pituitary-adrenal axis may be involved in postnatal growth retardation of IUGR children through a modulation of the function of the IGF system. Anthropometry, IGF system assessment, cortisol measurement, and lipid profile evaluation were performed in 49 IUGR children. Children were subdivided into two groups according to their actual height corrected for midparental height: CG (catch-up growth) group, 19 children with corrected height ≥0 z-score; and NCG (noncatch-up growth) group, 30 subjects with corrected height <0 z-score. CG children showed significantly higher birth weight (p < 0.005) and body mass index (p < 0.05). No significant differences in IGF-I, IGF-II, IGF binding protein (IGFBP)-1, IGFBP-3, soluble IGF-II receptor levels (IGF2R), IGF-II/IGF2R ratio, and relative amounts of IGFBP-3 circulating forms were found between CG and NCG children. None of the IGF system-related variables correlated with anthropometric indices. NCG children showed significantly higher concentrations of cortisol (p < 0.005) and cortisol levels resulted inversely to birth weigh (r = −0.34, p < 0.05), birth length (r = −0.36, p < 0.05), and corrected height (r = −0.44, p < 0.01). Whereas total and HDL cholesterol concentrations were not significantly different in the two groups, LDL cholesterol levels were significantly higher in NCG children (p < 0.05), and five of 49 showed LDL cholesterol concentrations >3.4 mM (130 mg/dL). LDL cholesterol was inversely related to birth weight (r = −0.31, p < 0.05), corrected stature (r = −0.32, p < 0.05), and actual height (r = −0.31, p < 0.05) and directly related to the levels of IGF2R (r = 0.44, p < 0.01). Reanalysis of 15 of 30 IUGR newborns in whom we previously reported an inverse relationship between cord blood cortisol levels and first trimester length gain (r = −0.54, p < 0.005) showed that the relative amount of the IGFBP-3 18-kD fragment was related inversely to cortisol (r = −0.67, p < 0.01) and directly to early postnatal growth (r = 0.65, p < 0.05). Our results suggest that catch-up growth in IUGR children might be affected by intrauterine reprogramming of hypothalamic-pituitary-adrenal axis, which may result in a permanent modification of the neuroendocrine response to stress: children with increased cortisol secretion may be at higher risk of growth failure. During the neonatal period cortisol might act by limiting IGFBP-3 proteolysis and, therefore, reducing IGF bioavailability.
Craniofacial Morphology in Children with Complete Bilateral Cleft Lip and Palate: Does Infantile Size of the Premaxilla Predetermine Outcome?

Objective To evaluate the possible association between the size of the premaxilla in infants and craniofacial morphology in children with complete bilateral cleft lip and palate (CBCLP) and identify the characteristics of craniofacial morphology in children with CBCLP with median facial dysplasia (MFD). Design Retrospective study. Setting A university hospital craniofacial center. Subjects Thirty-four patients with nonsyndromic CBCLP, 24 boys and 10 girls, had large premaxilla (LP group). Thirty-six patients with nonsyndromic CBCLP, 16 boys and 20 girls, had small premaxilla (SP group). Thirteen CBCLP patients with MFD, five boys and eight girls (MFD group). Main Outcome Measures Infant maxillary dental cast at the age of 1 year was used to measure the size of the premaxilla. Cephalometric analysis was used to determine craniofacial morphology in children at the age of 5 years. Results The size of the premaxilla in infants with CBCLP varied greatly. The LP group tended to have a longer maxilla and a more protruded maxilla, producing a better interjaw relation. The opposite phenomena were observed in the MFD group; the SP group yielded results between those of the LP and the MFD groups. Conclusion The size of the premaxilla in infants with CBCLP can be used to predetermine subsequent craniofacial morphology at the age of 5 years. Children with nonsyndromic CBCLP had craniofacial characteristics that differed significantly from those of children with CBCLP with median facial dysplasia.
An Empirical Analysis of Effect of Exchange Rate on Sesame Subsectors Output in Nigeria: 1980-2016

Abstract: This study made use of Vector error correction model to analyse effect of exchange rate on sesame output in Nigeria from 1980-2016. Secondary data consisting of annual times covering a period of 37 years (1980-2016) were obtained from World Bank development indicators data base, food and agriculture organization. United Nations conference trade and development (UNCTAD), Impulse response and Variance decomposition. The result of direction of growth showed that the coefficient of exchange rate (-0.005) was negative and significant at 5% level and this implies that exchange rate decelerated over the period The result also showed that the direction of growth of sesame (0.000) was positive and significant at 1% level. This means that the direction of growth of sesame accelerated over the period under review. The result of coefficient of determinant (R) was 0.3726 indicating that 37.26% variation in sesame output was explained by exchange rate in the previous year, labour in the previous year, sesame output in the previous year, and public agriculture spending in the previous year. The study showed that a unit increase in public agriculture spending will decrease sesame output by 0.345% and 0.01% respectively. Further, the showed that sesame output responded positively to itself, labour and public agriculture spending in both long and short run. The result also showed that sesame output responded negatively to exchange rate in both long and short run over the period under review. The result further showed that in the long run sesame output contributed to itself by 75.57 %, exchange rate contributed to sesame output by 0.26 %, labour contributed by 10.045 and public agriculture spending by 14.12 % over the period under review. The result also showed that in the short run sesame output contributed to itself by 78.26 %, exchange rate contributed to sesame output by 0.45 %, labour contributed by 8.68 % and public agriculture spending by 12.59 %.
Genetic requirements for the survival of tubercle bacilli in primates.

BACKGROUND Tuberculosis (TB) leads to the death of 1.7 million people annually. The failure of the bacille Calmette-Guérin vaccine, synergy between AIDS and TB, and the emergence of drug resistance have worsened this situation. It is imperative to delineate the mechanisms employed by Mycobacterium tuberculosis to successfully infect and persist in mammalian lungs. METHODS Nonhuman primates (NHPs) are arguably the best animal system to model critical aspects of human TB. We studied genes essential for growth and survival of M. tuberculosis in the lungs of NHPs experimentally exposed to aerosols of an M. tuberculosis transposon mutant library. RESULTS Mutants in 108 M. tuberculosis genes (33.13% of all genes tested) were attenuated for in vivo growth. Comparable studies have reported the attenuation of only approximately 6% of mutants in mice. The M. tuberculosis mutants attenuated for in vivo survival in primates were involved in the transport of various biomolecules, including lipid virulence factors; biosynthesis of cell-wall arabinan and peptidoglycan; DNA repair; sterol metabolism; and mammalian cell entry. CONCLUSIONS Our study highlights the various virulence mechanisms employed by M. tuberculosis to overcome the hostile environment encountered during infection of primates. Prophylactic approaches aimed against bacterial factors that respond to such in vivo stressors have the potential to prevent infection at an early stage, thus likely reducing the extent of transmission of M. tuberculosis.
Playing-Related Health Problems Among Instrumental Music Students at a University in Malaysia.

UNLABELLED Musicians from a wide range of backgrounds experience playing-related health problems including musculoskeletal disorders, hearing loss, and performance anxiety. Few studies have focused specifically on the health concerns of musicians in Malaysia. AIMS This study aimed to investigate playing-related health problems among student musicians at a university in Malaysia as well as their knowledge and awareness of playing-related health problems. METHODS Instrumental music students enrolled in undergraduate and post-graduate university music courses (n=98) participated in a self-report online survey which addressed aspects such as educational background, playing experience, knowledge and awareness of musicians' health issues, history of physical problems, lifestyle factors, and prevention and management strategies. RESULTS Of the total participants, 28.9% reported that they were currently experiencing playing-related pain in a body part, and 46.4% had experienced playing-related pain at some time. More than half (56.7%) felt that they have not received enough information or advice on playing-related health during their current studies. Musicians who experienced playing-related pain, tension, and discomfort reported the main problem sites to be the fingers and hands, arms, neck, and shoulders. CONCLUSIONS The study results demonstrate that Malaysian university music students are affected by similar types of playing-related physical problems as their counterparts around the world. A greater awareness and knowledge of injury prevention and management strategies is needed so that these music students can sustain healthy playing careers.
Genomic differences between Candida glabrata and Saccharomyces cerevisiae around the MRPL28 and GCN3 loci

We report the sequences of two genomic regions from the pathogenic yeast Candida glabrata and their comparison to Saccharomyces cerevisiae. A 3 kb region from C. glabrata was sequenced that contains homologues of the S. cerevisiae genes TFB3, MRPL28 and STP1. The equivalent region in S. cerevisiae includes a fourth gene, MFA1, coding for mating factor a. The absence of MFA1 is consistent with C. glabrata's asexual life cycle, although we cannot exclude the possibility that a‐factor gene(s) are located somewhere else in its genome. We also report the sequence of a 16 kb region from C. glabrata that contains a five‐gene cluster similar to S. cerevisiae chromosome XI (including GCN3) followed by a four‐gene cluster similar to chromosome XV (including HIS3). A small‐scale rearrangement of gene order has occurred in the chromosome XI‐like section. The sequences have been deposited in the GenBank database with Accession Nos AY083606 and AY083607. Copyright © 2002 John Wiley & Sons, Ltd.
Characteristics of FDG-PET findings in the diagnosis of systemic juvenile idiopathic arthritis

Abstract Objective: To examine and delineate inflammatory focus in patients with juvenile idiopathic arthritis (JIA), 18F-Fluoro-deoxy-glucose (FDG)-positron emission tomography (PET) (18F-FDG-PET) was applied to patients with JIA, and the images of these patients were compared. Methods: Sixty-eight children (59 with systemic JIA (s-JIA) and 9 with polyarticular JIA) were included. The diagnosis of JIA was done to meet the International League of Associations for Rheumatology (ILAR) criteria. After 6-h fasting, whole-body positron emission tomography (PET) scans were acquired 60 min after intravenous injection of 3–5 MBq/kg 18F-FDG. The interpretation of 18F-FDG uptake was based on visual characteristics. Results: Two types of PET images were outstanding in s-JIA; one was 18F-FDG uptake in red bone marrow, such as the spine, pelvis, and long bones as well as spleen (12 cases), and other type was the uptake in the major joints, such as hips, elbows, wrists, knees, and ankles (8 cases). The former findings were correlated with elevated levels of inflammatory markers, while the latter were with significantly increased levels of MMP-3 (p < 0.05). Conclusion: There was a noticeable accumulation of 18F-FDG uptake in bone marrow of s-JIA patients which may indicate the inflammatory focus of this disease and play an important role in the pathogenic basis of arthritis and systemic inflammation of s-JIA.