Academic literature on the topic '832/.6'

Glucose homeostasis requires the proper expression and regulation of the catalytic subunit of glucose-6-phosphatase (G-6- Pase), which hydrolyzes glucose 6-phosphate to glucose in glucose-producing tissues. Glucose induces the expression of G-6- Pase at the transcriptional and posttranscriptional levels by unknown mechanisms. To better understand this metabolic regulation, we mapped the cis-regulatory elements conferring glucose responsiveness to the rat G-6- Pase gene promoter in glucose-responsive cell lines. The full-length (−4078/+64) promoter conferred a moderate glucose response to a reporter construct in HL1C rat hepatoma cells, which was dependent on coexpression of glucokinase. The same construct provided a robust glucose response in 832/13 INS-1 rat insulinoma cells, which are not glucogenic. Glucose also strongly increased endogenous G-6- Pase mRNA levels in 832/13 cells and in rat pancreatic islets, although the induced levels from islets were still markedly lower than in untreated primary hepatocytes. A distal promoter region was glucose responsive in 832/13 cells and contained a carbohydrate response element with two E-boxes separated by five base pairs. Carbohydrate response element-binding protein bound this region in a glucose-dependent manner in situ. A second, proximal promoter region was glucose responsive in both 832/13 and HL1C cells, with a hepatocyte nuclear factor 1 binding site and two cAMP response elements required for glucose responsiveness. Expression of dominant-negative versions of both cAMP response element-binding protein and CAAT/enhancer-binding protein blocked the glucose response of the proximal region in a dose-dependent manner. We conclude that multiple, distinct cis-regulatory promoter elements are involved in the glucose response of the rat G-6- Pase gene.

Abstract As models for β-cell metabolism, rat islets are, to some extent, a, heterogeneous cell population stressed by the islet isolation procedure, whereas rat-derived clonal β-cells exhibit a tumor-like phenotype. To describe to what extent either of these models reflect normal cellular metabolism, we compared metabolite profiles and gene expression in rat islets and the INS-1 832/13 line, a widely used clonal β-cell model. We found that insulin secretion and metabolic regulation provoked by glucose were qualitatively similar in these β-cell models. However, rat islets exhibited a more pronounced glucose-provoked increase of glutamate, glycerol-3-phosphate, succinate, and lactate levels, whereas INS-1 832/13 cells showed a higher glucose-elicited increase in glucose-6-phosphate, alanine, isocitrate, and α-ketoglutarate levels. Glucose induced a decrease in levels of γ-aminobutyrate (GABA) and aspartate in rat islets and INS-1 832/13 cells, respectively. Genes with cellular functions related to proliferation and the cell cycle were more highly expressed in the INS-1 832/13 cells. Most metabolic pathways that were differentially expressed included GABA metabolism, in line with altered glucose responsiveness of GABA. Also, lactate dehydrogenase A, which is normally expressed at low levels in mature β-cells, was more abundant in rat islets than in INS-1 832/13 cells, confirming the finding of elevated glucose-provoked lactate production in the rat islets. Overall, our results suggest that metabolism in rat islets and INS-1 832/13 cells is qualitatively similar, albeit with quantitative differences. Differences may be accounted for by cellular heterogeneity of islets and proliferation of the INS-1 832/13 cells.

1, 2, 9, 10-tetramethoxyaporphine phosphate (MDL-832) was once considered a potential human antitussive. MDL-832 was administered orally in the diets of Sprague-Dawley rats at dose levels of 0, 5, 10, 20, 40, 80 and 160 mg/kg/day for 3 and 6 months and in gelatin capsules to Beagle dogs at 0, 5, 10, 15, 30 and 60 mg/kg/day for 3, 6 and 12 months. Histopathologic examinations of hematoxylin and eosin-stained cerebellar sections revealed intracytoplasmic brown pigment accumulations in large fusiform neurons (presumably the motor type) of the pons. The pigment granules were found to be PAS-positive, non-acid fast, iron-free, Sudan B-positive and fuchsinophilic. Intraneuronal pigment accumulations were seen in rats after 3 months of treatment at 80 mg but not at 40 mg and after 6 months at 20 mg but not at 10 mg. For dogs the effect was observed after 3 months at 60 mg but not at 30 mg and after 12 months at 10 mg but not at 5 mg.

Summary: The authors have drawn the attention towards perhaps a common complication during intravascular techniques, and a novel use of ultrasound to aspirate the extravasated fluids / drugs to minimize the damaging effects. Abbreviations: GA: general anesthesia; MAC-age: Age-adjusted minimum alveolar concentration Key words: Patient Safety; Perioperative; Point-of-Care Ultrasound; Anesthetics Citation: Vankdavath L, Karim HMR, Arora P. Drug extravasation: can ultrasound-guided puncture and aspiration help? Anaesth. pain intensive care 2022;26(6):831−832; DOI: 10.35975/apic.v26i6.2073

Abstract Wolfram syndrome is a rare genetic disorder characterized by juvenile-onset diabetes mellitus, optic nerve atrophy, hearing loss, diabetes insipidus, and progressive neurodegeneration. Pathogenic variants in the WFS1 gene are the main causes of Wolfram syndrome. WFS1 encodes a transmembrane protein localized to the endoplasmic reticulum (ER) and regulates the unfolded protein response (UPR). Loss of function of WFS1 leads to dysregulation of insulin production and secretion, ER calcium depletion, and cytosolic calpains activation, resulting in the activation of apoptotic cascades. Although the terminal UPR is well known to yield an inflammatory response called "sterilized inflammation" that accelerates β-cell dysfunction and death in diabetes, the contribution of β-cell inflammation to the development of diabetes in Wolfram syndrome has not been fully understood. Here we show that WFS1-deficiency enhances the gene expression of pro-inflammatory cytokines and chemokines, leading to cytokine-induced ER-stress and cell death in pancreatic β-cells. Under thechronic[BL1] high-glucose condition, CRISPR/Cas9-mediated Wfs1-knockout (KO) INS-1 832/13 cells, the pancreatic β-cell model of Wolfram syndrome, showed enhanced gene expression levels of ER stress markers (Chop, sXbp1, Bip, and Txnip). Moreover, the gene expression levels of pro-inflammatory cytokines (Il-1β, Il-6), chemokine (Ccl2), and vascular endothelial growth factor A (VegfA) were higher in Wfs1- KO INS-1 832/13 cells when compared to Wfs1-wild type INS-1 832/13 cells. [BL2] The high glucose-induced pro-inflammatory cytokine genes in Wfs1-KO INS-1 832/13 cells were mediated by the PKR-like ER-resident kinase (PERK) and inositol-requiring enzyme 1α (IRE1α)pathways. Furthermore, the IFN-γ and IL-1β treatment enhanced ER stress-mediated cell death and upregulated the pro-inflammatory cytokine gene expression in Wfs1-KO INS-1 832/13 cells. To confirm these findings, we investigated whether inflammation occurs in a mouse model of Wolfram syndrome. Compared to wild-type mice, 10-month-old whole body Wfs1-KO mouse islets showed a significantly higher density of Iba1, which is a marker for macrophage expression. The islet-infiltrated macrophages in these Wfs1-KO mice expressed the M1-macrophage marker (CD68). There was also strong fibrosis and a high density of endothelial cell marker (CD31) in the Wfs1-KO mouse islets. These results demonstrate that WFS1 loss-of-function enhances the inflammatory responses in pancreatic β-cells. The results in our study identified sterile inflammation as a new pathological mechanism in the development of diabetes in Wolfram syndrome. In Wolfram syndrome model mice, islets are highly infiltrated with macrophages, suggesting that the vicious cycle of ER stress and sterile inflammation accelerates the progression of diabetes in a cell-autonomous and cell-nonautonomous manner. A deeper understanding of the pathophysiology of Wolfram syndrome is essential for developing novel therapeutic targets for the disease. Presentation: No date and time listed

Insulin secretion is coupled with changes in β-cell metabolism. To define this process, 195 putative metabolites, mitochondrial respiration, NADP+, NADPH and insulin secretion were measured within 15 min of stimulation of clonal INS-1 832/13 β-cells with glucose. Rapid responses in the major metabolic pathways of glucose occurred, involving several previously suggested metabolic coupling factors. The complexity of metabolite changes observed disagreed with the concept of one single metabolite controlling insulin secretion. The complex alterations in metabolite levels suggest that a coupling signal should reflect large parts of the β-cell metabolic response. This was fulfilled by the NADPH/NADP+ ratio, which was elevated (8-fold; P<0.01) at 6 min after glucose stimulation. The NADPH/NADP+ ratio paralleled an increase in ribose 5-phosphate (>2.5-fold; P<0.001). Inhibition of the pentose phosphate pathway by trans-dehydroepiandrosterone (DHEA) suppressed ribose 5-phosphate levels and production of reduced glutathione, as well as insulin secretion in INS-1 832/13 β-cells and rat islets without affecting ATP production. Metabolite profiling of rat islets confirmed the glucose-induced rise in ribose 5-phosphate, which was prevented by DHEA. These findings implicate the pentose phosphate pathway, and support a role for NADPH and glutathione, in β-cell stimulus-secretion coupling.

Neurotoxins such as rotenone, 1-methyl-4-phenylpyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) are well known for their high toxicity on dopaminergic neurons and are associated with Parkinson’s disease (PD) in murine models and humans. In addition, PD patients often have glucose intolerance and may develop type 2 diabetes (T2D), whereas T2D patients have higher risk of PD compared to general population. Based on these premises, we evaluated the toxicity of these three toxins on pancreatic β-cell lines (INS-1 832/13 and MIN6) and we showed that rotenone is the most potent for reducing β-cells viability and altering mitochondrial structure and bioenergetics in the low nanomolar range, similar to that found in dopaminergic cell lines. MPP+ and 6-OHDA show similar effects but at higher concentration. Importantly, rotenone-induced toxicity was counteracted by α-tocopherol and partially by metformin, which are endowed with strong antioxidative and cytoprotective properties. These data show similarities between dopaminergic neurons and β-cells in terms of vulnerability to toxins and pharmacological agents capable to protect both cell types.

Abstract The coffee variety 'Lempira', released in Honduras in 1998, was classified 100% resistant to races I and II of coffee rust identified by Portugal's Centre for Research into Coffee Rusts (Centro de Investigação das Ferrugens do Cafeeiro) (CIFC) in 1997. However, since 2007, the disease has been reported in seed foundation plots and producer farms, the most recent epidemic report being in April 2016 in Vegas de Jalan, Juticalpa Olancho, affecting 210 ha. Since this variety constitutes 45% of the cultivated area under coffee in the country, there is a need to identify the virulence genes of the new strain and to determine the resistance and susceptibility of other cultivated varieties. For these purposes, mass samples of rust were inoculated on leaf discs of the differential clones 1343/269, 110/5, 147/1, 152/3, 33/1, 419/20, 832/1 and 832/2, together with 87/1, 1006/10, 420/10 and 420/2 from the Federal University of Vicosa, as well as on the two main cultivated resistant varieties ('Parainema' and 'IHCAFE- 90'), and seven promising genotypes, under controlled temperature conditions and relative humidity. After 20-60 days of inoculation, seven virulence genes were identified (v1, v2, v4, v5, v6, v7, v9), of which v1, v4, v6, v7 and v9 had not been reported in Honduras previously. It is inferred that this rust population arose by recombination of race v5 with v6, v7 or v9. Races with 3, 4, 5, 6 or 7 virulence determinants were identified as the most complex and aggressive strains described but they lacked the v3 and v8 determinants. In addition, it was found that 'Parainema', 'H27', 'T5296-170', 'Central American', 'Pacamara yellow' and 'Anacafe-14' are resistant because they possess the SH8 gene, absent from 'Lempira'. 'IHCAFE-90' and 'Obatá' showed 20% susceptibility, and 'Ruiru 11' was susceptible. The results reveal the diversity of rust virulence genes in Honduras and emphasize the importance of the SH3 and SH8 genes as sources of resistance.

This new ASTM manual introduces the concept of the Master Curve Method so it can be understood and used by engineers who have had limited exposure to elastic-plastic fracture mechanics and/or advanced statistical methods. It addresses the practical design-related problem of defining the ductile-to-brittle fracture transition temperature of structural steels directly in terms of fracture mechanics data. 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The labour market has increasingly begun to impose, intensively and insistently, criteria for the competence profile of graduates. All the more important is its relationship with the university, providing, to the latter, anongoing and dynamic feedback on the job offer and demand for graduates with a certain profile and level of training. During July-December 2016, the Department of Professional Counselling from Vasile Alecsandri University of Bacău has implemented the project Professional Development and Employability – the convergence of university and labour market (DeProfAn) obtained in a CNFIS-FDI national competition (institutional development funds). It concerned the design, implementation and exploitation of a dedicated SharePoint platform to achieve its main objectives in relation to the labour market: monitoring the graduates’ insertion on the labour market; determining the degree of satisfaction of students and graduates in relation to the training and services offered by the university; identifying the point of view of employers regarding the quality of the graduates’ training. Realistically, platform implementation in monitoring the convergence of university with the labour market takes the form of an experiment. Its production period was 6 months (July-December 2016), the target group was 832 beneficiaries (500 students, 300 graduates, 32 employers).Through this study we aim: to illustrate how such an informatics tool may be achieved / may operate with relatively few funds; to highlight the main streams of data that we intend to collect; to globally interpret the main data sets obtained in terms of the efficiency of the achieved tool; to address the informatics tool and the results obtained through a SWOT analysis, having as a benchmark further development in the future.

e aim of the article is to grasp the mental division of mind of Russian intellectuals in solving the problem of organizing Orthodox school education. e organized schooling was largely absent in Muscovy and the practice of studying with a private teacher substituted for schools. e idea to create Orthodox schools, di erent from Latin ones of Western Europe, was set forth in the last quarter of the XVII century and led to the compilation of several handwritten teachers' collections, the compilers of which sought to present in them the content of school Orthodox education. at gives the ground for comparison between two of them: ABC for kids by Evfimy from Chudov monastery and School ABC by Prokhor Kolomniatin. Conclusions: two di erent compilers, who used di erent texts, show similar thematic composition in constructing a school curriculum. It includes: 1. Grammar as a main section; 2. Explanation the necessity of study and the meaning of “Wisdom”; 3. Norms of the pupils' conduct; 4. Instructions on piety as well as threats for ignoring them; 5. Catechisms and the texts of prayers; 6. Instructions for teachers. e two authorcompilers nearly exhausted the possibilities of the Muscovite repertoire of texts, which could be used for children's education. However, they added some new translations as well as their own compositions.