Miracle-dz/UniFAR-FTUs huggingface dataset:
Glucocorticoids Regulate the Synthesis of Glial Fibrillary Acidic Protein in Intact and Adrenalectomized Rats but Do Not Affect Its Expression Following Brain Injury

Short (5 days)‐to long‐term (4 months) corticosterone (CORT) administration by injection, pellet implantation, or in the drinking water decreased glial fibrillary acidic protein (GFAP) by 20–40% in hippocampus and cortex of intact rats. In contrast to CORT, adrenalectomy (ADX) caused elevations (50–125%) in hippocampus and cortex GFAP within 12 days of surgery that persisted for at least 4 months. CORT replacement of ADX rats decreased GFAP amount in hippocampus and cortex. The effects of long‐term CORT and ADX on GFAP in hippocampus and cortex were also seen in striatum, midbrain, and cerebellum, findings suggestive of brain‐wide adrenal steroid regulation of this astrocyte protein. The changes in GFAP amount due to CORT and ADX were paralleled by changes in GFAP mRNA, indicating a possible transcriptional or at least genomic effect of adrenal steroids. Glucocorticoid regulation of GFAP was relatively specific; it could not be generalized to other astrocyte proteins or other major structural proteins of neurons. The negative regulation of GFAP and GFAP mRNA by adrenal steroids suggested that increases in GFAP that result from brain injury may be attenuated by glucocorticoids. However, chronic CORT treatment of intact rats did not reverse or reduce the large increases in GFAP caused by trauma‐or toxicant‐induced brain damage. Thus, glucocorticoids and injury appear to regulate the expression of GFAP through different mechanisms. In contrast to the lack of effects of CORT on brain damage‐induced increases in GFAP, CORT treatment begun in 2‐week ADX rats, after an increase in GFAP had time to occur, did reverse the ADX‐induced increase in GFAP. These results suggest that the increase in GFAP resulting from ADX is not mediated through an injury‐linked mechanism.
Glycoxydation promotes vascular damage Via MAPK‐ERK/JNK pathways

Oxidation and glycation enhance foam cell formation via MAPK/JNK in euglycemic and diabetic subjects. Here, we investigated the effects of glycated and oxidized LDL (glc‐oxLDL) on MAPK‐ERK and JNK signaling pathways using human coronary smooth muscle cells. Glc‐oxLDL induced a broad cascade of MAPK/JNK‐dependent signaling transduction pathways and the AP‐1 complex. In glc‐oxLDL treated coronary arterioles, tumor necrosis factor (TNF) α increased JNK phosphorylation, whereas protein kinase inhibitor dimethylaminopurine (DMAP) prevented the TNF‐induced increase in JNK phosphorylation. The role of MKK4 and JNK were then investigated in vivo, using apolipoprotein E knockout (ApoE−/−) mice. Peritoneal macrophages, isolated from spontaneously hyperlipidemic but euglycemic mice showed increases in both proteins and phosphorylated proteins. Compared to streptozotocin‐treated diabetic C57BL6 and nondiabetic C57BL6 Wt mice, in streptozotocin‐diabetic ApoE−/− mice, the increment of foam cell formation corresponded to an increment of phosphorylation of JNK1, JNK2, and MMK4. Thus, we provide a first line of evidence that MAPK‐ERK/JNK pathways are involved in vascular damage induced by glycoxidation. J. Cell. Physiol. 227: 3639–3647, 2012. © 2012 Wiley Periodicals, Inc.
Glycosaminoglycans in the nonswelling corneal stroma of dogfish shark.

Qualitative and quantitative determinations of glycosaminoglycans in the nonswelling corneal stroma of the spiny dogfish shark, Squalus acanthias, were made with the use of a cetylpyridinium chloride-cellulose microfractionation technique. Dogfish stroma was found to contain predominantly highly sulfated galactosaminoglycans forming approximately 75 per cent of the total glycosaminoglycans when calculated on the basis of hexosamine content. The remaining portion of corneal glycosaminoglycans was identified as glucosaminoglycans with a molar ratio of sulfate to hexosamine higher than one. Quantitative differences were observed between the anterior and posterior parts of the dogfish corneal stroma both as to the concentration of hexosamine and the ratio of galactosamine to glucosamine.
Characterization of brain neurons that express enzymes mediating neurosteroid biosynthesis

Allopregnanolone (ALLO) and tetrahydrodeoxycorticosterone (THDOC) are potent positive allosteric modulators of GABA action at GABAA receptors. ALLO and THDOC are synthesized in the brain from progesterone or deoxycorticosterone, respectively, by the sequential action of two enzymes: 5α-reductase (5α-R) type I and 3α-hydroxysteroid dehydrogenase (3α-HSD). This study evaluates 5α-R type I and 3α-HSD mRNA expression level in mouse brain by using in situ hybridization combined with glutamic acid decarboxylase 67/65, vesicular glutamate transporter 2, glial fibrillary acidic protein, and S100β immunohistochemistry. We demonstrate that 5α-R type I and 3α-HSD colocalize in cortical, hippocampal, and olfactory bulb glutamatergic principal neurons and in some output neurons of the amygdala and thalamus. Neither 5α-R type I nor 3α-HSD mRNAs are expressed in S100β- or glial fibrillary acidic protein-positive glial cells. Using glutamic acid decarboxylase 67/65 antibodies to mark GABAergic neurons, we failed to detect 5α-R type I and 3α-HSD in cortical and hippocampal GABAergic interneurons. However, 5α-R type I and 3α-HSD are significantly expressed in principal GABAergic output neurons, such as striatal medium spiny, reticular thalamic nucleus, and cerebellar Purkinje neurons. A similar distribution and cellular location of neurosteroidogenic enzymes was observed in rat brain. Taken together, these data suggest that ALLO and THDOC, which can be synthesized in principal output neurons, modulate GABA action at GABAA receptors, either with an autocrine or a paracrine mechanism or by reaching GABAA receptor intracellular sites through lateral membrane diffusion.
Comparison of cardiopulmonary responses to forward and backward walking and running.

Backward running has long been used in sports conditioning programs and has recently been incorporated into rehabilitative settings as a method of increasing quadriceps strength while decreasing the joint compressive forces about the knee. Although backward locomotion has been studied kinetically, the metabolic cost of backward walking and/or running has not to our knowledge been previously characterized. Oxygen consumption and other cardiopulmonary variables were measured under constant speed exercise during backward and forward walking at 107.2 m.min-1 and during backward and forward running at 160.8 m.min-1. Peak oxygen consumption (VO2peak) was also measured during maximal incremental backward and forward running. VO2, HR, and blood lactate were significantly higher (P < 0.001) during backward walking and running than during forward walking and running. During backward walking and backward running, subjects exercised at 60% and 84% of their forward VO2peak, respectively. In conclusion, for a given speed, backward locomotion elicits a greater metabolic demand and cardiopulmonary response than forward locomotion. In general, these data suggest that while undergoing rehabilitation, an injured athlete may continue to exercise using backward walking/running at an intensity sufficient enough to maintain cardiovascular fitness levels.
Combination of suppository diclofenac and intravenous morphine infusion in post-caesarean section pain relief--a step towards balanced analgesia?

UNLABELLED Post-Caesarean section analgesia can be achieved by morphine infusion. NSAIDs are frequently administered to relieve uterine cramps. This study is aimed at assessing the efficacy of the combination of suppository diclofenac and morphine infusion in post-Caesarean section pain relief. General anaesthesia was given to 60 patients who were randomly allocated into two groups: group A received 100 mg suppository diclofenac before surgical incision and morphine infusion 1.5 mg per hour postoperatively while group B received only morphine infusion 1.5 mg/H postoperatively. Pain assessment was done by an unbiased observer on arrival of the patients in the recovery room, then 6 hours, 12 hours and 24 hours later. Pain relief was found to be better in group A, with group B requiring more supplemental analgesia. Apart from better analgesic effect for wound pain, group A also had more favourable scores for uterine cramping pain. The incidence of nausea or vomiting was similar in both groups. No respiratory depression was observed in both groups. Two cases of increased bleeding (one from each group) were observed, both receiving conservative treatment. THE CONCLUSION suppository diclofenac improved the analgesic efficacy of morphine infusion in post-Caesarean analgesia.
Sch 9 Is a Major Target of TORC 1 in Saccharomyces cerevisiae

Jörg Urban, Alexandre Soulard, Alexandre Huber, Soyeon Lippman, Debdyuti Mukhopadhyay, Olivier Deloche, Valeria Wanke, Dorothea Anrather, Gustav Ammerer, Howard Riezman, James R. Broach, Claudio De Virgilio, Michael N. Hall, and Robbie Loewith* Department of Molecular Biology Department of Biochemistry Department of Microbiology and Molecular Medicine, Centre Médical Universitaire University of Geneva, Geneva, CH-1211, Switzerland Department of Biochemistry, Biozentrum, University of Basel, Basel, CH-4056, Switzerland Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA Max F. Perutz Laboratories, Department of Biochemistry, University of Vienna, Dr. Bohrgasse 9, A1030 Vienna, Austria *Correspondence: robbie.loewith@molbio.unige. ch DOI 10.1016/j.molcel. 2007.04. 020
Indoor air risk factors for schoolchildren’s health in Portuguese homes: Results from a case-control survey

ABSTRACT Allergic diseases have been on the rise in many countries over the past few decades and indoor exposure may be a possible cause. An overall investigation of children’s health status and residential indoor air pollutants known or suspected to affect respiratory health was conducted in the homes of primary schoolchildren during winter in Porto, Portugal. In a case-control study (30 case children with asthma and 38 controls) and over a 1-wk monitoring period, air sample collection was conducted in children’s bedrooms for the analysis of 12 volatile organic compounds (VOC), aldehydes, particulate matter (PM)2.5, PM10, bacteria, and fungi. Home exposures to indoor pollutants are similar for children with and without asthma, except for d-limonene. For both groups, most VOC were present at low concentrations (median < 5 µg/m3) and below the respective World Health Organization (WHO) guidelines. Concentrations of PM2.5, PM10, and bacteria were frequently higher than WHO/reference values (80, 25, and 60% of all studied dwellings, respectively). Concentrations of carbon dioxide (CO2) exceeding 1000 ppm were encountered in 60% of the homes. Although this study does not provide evidence of causative factors for asthmatic status, the postulation that poor indoor air quality in homes heightens the risk of allergic symptoms development among children is conceivable.
Genes Required for Intrinsic Multidrug Resistance in Mycobacterium avium

ABSTRACT Genes required for intrinsic multidrug resistance by Mycobacterium avium were identified by screening a library of transposon insertion mutants for the inability to grow in the presence of ciprofloxacin, clarithromycin, and penicillin at subinhibitory concentrations. Two genes, pks12 and Maa2520, were disrupted in multiple drug-susceptible mutants. The pks12 gene (Maa1979), which may be cotranscribed with a downstream gene (Maa1980), is widely conserved in the actinomycetes. Its ortholog in Mycobacterium tuberculosis is a polyketide synthase required for the synthesis of dimycocerosyl phthiocerol, a major cell wall lipid. Mutants of M. avium with insertions into pks12 exhibited altered colony morphology and were drug susceptible, but they grew as well as the wild type did in vitro and intracellularly within THP-1 cells. A pks12 mutant of M. tuberculosis was moderately more susceptible to clarithromycin than was its parent strain; however, susceptibility to ciprofloxacin and penicillin was not altered. M. avium complex (MAC) and M. tuberculosis appear to have different genetic mechanisms for resisting the effects of these antibiotics, with pks12 playing a relatively more significant role in MAC. The second genetic locus identified in this study, Maa2520, is a conserved hypothetical gene with orthologs in M. tuberculosis and Mycobacterium leprae. It is immediately upstream of Maa2521, which may code for an exported protein. Mutants with insertions at this locus were susceptible to multiple antibiotics and slow growing in vitro and were unable to survive intracellularly within THP-1 cells. Like pks12 mutants, they exhibited increased Congo red binding, an indirect indication of cell wall modifications. Maa2520 and pks12 are the first genes to be linked by mutation to intrinsic drug resistance in MAC.
A performance evaluation of load frequency controller using discrete model predictive controller

Load frequency control becomes one of the important parts in a power system since frequency deviation is an important issue in power system stability. This paper has introduced model predictive controller to handle the frequency deviation when disturbance happen. Result of simulation in a three area power system shows that PI controllers have faster response than model predictive controllers, but calculation shows that model predictive controller will have decay faster than PI controllers. On the other hand, model predictive controllers showed better performance and signal processing time which are verified with disturbance variations in long time simulation; therefore it can be a good candidate for a load frequency control.
TATA-binding Protein (TBP)-like Protein Is Required for p53-dependent Transcriptional Activation of Upstream Promoter of p21Waf1/Cip1 Gene

Background: TLP and p21 are involved in growth inhibition. Results: TLP decreased cell growth and activated upstream promoter of p21 gene p53-dependently. TLP bound to p53. The promoter was associated with TLP and p53, and TLP enhanced recruitment of p53 to the promoter. Conclusion: TLP is required for p53-dependent transcriptional activation of p21 upstream promoter. Significance: A novel regulator for p53-p21 pathway was identified. TATA-binding protein-like protein (TLP) is involved in development, checkpoint, and apoptosis through potentiation of gene expression. TLP-overexpressing human cells, especially p53-containing cells, exhibited a decreased growth rate and increased proportion of G1 phase cells. TLP stimulated expression of several growth-related genes including p21 (p21Waf1/Cip1). TLP-mediated activation of the p21 upstream promoter in cells was shown by a promoter-luciferase reporter assay. The p53-binding sequence located in the p21 upstream promoter and p53 itself are required for TLP-mediated transcriptional activation. TLP and p53 bound to each other and synergistically enhanced activity of the upstream promoter. TLP specifically activated transcription from the endogenous upstream promoter, and p53 was required for this activation. Etoposide treatment also resulted in activation of the upstream promoter as well as nuclear accumulation of TLP and p53. Moreover, the upstream promoter was associated with endogenous p53 and TLP, and the p53 recruitment was enhanced by TLP. The results of the present study suggest that TLP mediates p53-governed transcriptional activation of the p21 upstream promoter.
Prevention of Malicious Attack on Smart Phones using Amendment Capture Service

Sensitive data and information is at a greater risk due to the exploitation of the smart phones by Malwares. Malwares that once targeted the computers are now fully designed to extract all the information possible from the mobile phones. This work focuses on preventing the malicious attack on the mobile phones by using Amendment capture service, which checks the smart phone periodically or when a change has taken place and executes the DtKFc algorithm to detect the malicious applications. General Terms Machine Learning, Decision tree Algorithm, K-fold Algorithm, Amendment Capture Algorithm.
Release of carbon nanoparticles of different size and shape from nanocomposite poly(lactic) acid film into food simulants

ABSTRACT Poly(lactic) acid (PLA) film with 2 wt% mixed carbon nanofillers of graphene nanoplates (GNPs) and multiwall carbon nanotubes (MWCNTs) in a weight ratio of 1:1 with impurities of fullerene and carbon black (CB) was produced by layer-to-layer deposition and hot pressing. The release of carbon nanoparticles from the film was studied at varying time–temperature conditions and simulants. Migrants in simulant solvents were examined with laser diffraction analysis and transmission electron microscopy (TEM). Film integrity and the presence of migrants on the film surfaces were visualised by scanning electron microscopy (SEM). The partial dissolution of PLA polymer in the solvents was confirmed by swelling tests and differential scanning calorimetry (DSC). Nanoparticle migrants were not detected in the simulants (at the LOD 0.020 μm of the laser diffraction analysis) after migration testing at 40°C for 10 days. However, high-temperature migration testing at 90°C for 4 h provoked a release of GNPs from the film into ethanol, acetic acid and oil-based food simulants. Short carbon nanotubes were observed rarely to release in the most aggressive acetic acid solvent. Obviously, the enhanced molecular mobility at temperatures above the glass transition and partial dissolution of PLA polymer by the food simulant facilitate the diffusion processes. Moreover, shape, size and concentration of nanoparticles play a significant role. Flexible naked GNPs (lateral size 100–1000 nm) easily migrate when the polymer molecules exhibit enhanced mobility, while fibrous MWCNTs (> 1 μm length) formed entangled networks on the film surfaces as the PLA polymer is partly dissolved, preventing their release into food simulants. The impurities of fullerenes and CB (5–30 nm) were of minor concentration in the polymer, therefore their migration is low or undetectable. The total amount of released migrants is below overall migration limits. Graphical Abstract
The potential adverse role of leptin resistance in nonalcoholic fatty liver disease: a hypothesis based on critical review of the literature.

BACKGROUND Leptin is an adipocyte-derived hormone that plays a crucial role in energy homeostasis and lipid metabolism. Most of the biological effects of leptin are exerted through activation of the Janus kinase-2/signal transducer and activator of transcription-3 pathway. Signal transducer and activator of transcription-3 activation ultimately leads to an increased transcription and expression of suppressors of cytokine signaling-3, which acts as a feedback inhibitor by attenuating leptin signaling. Apart from inhibiting leptin signaling, suppressor of cytokine signaling-3 inhibits insulin signaling. Leptin increases with increasing fatty mass as a compensatory mechanism to preserve insulin sensitivity, but persistent hyperleptinemia is implicated in liver fibrinogenesis and carcinogenesis. HYPOTHESIS Considering this dual role of leptin in the liver pathophysiology, we hypothesized that leptin resistance may vary according to the different types of liver cells and nonalcoholic fatty liver disease progression. CLINICAL CONSEQUENCES It is speculated that recombinant leptin, proposed to be used in common forms of obesity or nonalcoholic fatty liver disease, might have serious unfavorable therapeutical drawbacks, through promotion of insulin resistance, fibrosis, and hepatocellular carcinoma.
Mature cataracts increase risk of capsular complications in manual small-incision cataract surgery of pseudoexfoliative eyes.

BACKGROUND To evaluate rates of intraoperative posterior capsule complications in manual small-incision cataract surgery of eyes with and without pseudoexfoliation syndrome in terms of cataract maturity level. METHODS We identified patients who had undergone manual small-incision cataract surgery between January 1997 and October 2003 from a review of patient charts. Preoperative data collected were cataract maturity level, best corrected visual acuity, and intraoperative posterior capsule complications as documented in the surgical report, namely (1) posterior capsule rupture or zonulolysis, or both, and (2) vitreous loss. RESULTS Two hundred and twenty-five eyes of 187 patients met the study criteria, of which 99 eyes had pseudoexfoliation syndrome (group 1) and 126 did not (group 2). Intraoperative posterior capsule complications occurred in 18 eyes (18%) in group 1 and 7 eyes (5.5%) in group 2 (difference was significant at p=0.003). The rate of capsular complications was significantly higher in both groups for eyes with preoperative visual acuity worse than 20/200 than for eyes with 20/200 or better. The number of eyes with visual acuity worse than 20/200 (counting fingers, hand motion, or light perception) was 70 (70%) in group 1 and 63 (50%) in group 2. Mature or brunescent cataract occurred in 49.5% of group 1 eyes and 26% of group 2 eyes. INTERPRETATION In manual small-incision cataract surgery, pseudoexfoliation syndrome has an increased intraoperative posterior capsule complication rate that increases as the level of cataract maturity increases and the preoperative visual acuity decreases.
Field trial of end-to-end QoS control based on RACS

Quality of service (QoS) control is a challenge to today's telecommunication world. Guangdong Telecom has been conducting a field trial to demonstrate end-to-end QoS control, which is based on resource and admission control subsystem (RACS) standardized by ETSI. From the results of the field trial, we have confirmed that RACS architecture and the corresponding end-to-end QoS control trial solution will be of great benefit to operator's next generation network (NGN). The solution adds a service aware, policy based QoS control layer to NGN. It can assist network operators to recapture the missing role in the telecommunication value chain, give necessary QoS support for new services, and grow revenue as a value added service itself
evelopment of a lentiviral vector system to study the role of the Andes virus lycoproteins

To infect target cells, enveloped viruses use their virion surface proteins to direct cell attachment and subsequent entry via virus-cell membrane fusion. How hantaviruses enter cells has been largely unexplored. To study early steps of Andes virus (ANDV) cell infection, a lentiviral vector system was developed based on a Simian immunodeficiency virus (SIV) vector pseudotyped with the ANDV-Gn/Gc envelope glycoproteins. The incorporation of Gn and Gc onto SIV-derived vector particles was assessed using newly generated monoclonal antibodies against ANDV glycoproteins. In addition, sera of ANDV infected humans were able to block cell entry of the SIV vector pseudotyped with ANDV glycoproteins, suggesting that