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[en] Eight modifications of the ''universal'' medium are proposed, differing one from another by the method of preparing glucose. Thioglycolane and Saburo media were used as controls. All experiments were conducted in Petri dishes. It has been found that the ''universal'' medium can be improved by increasing glucose up to 1% and lowering sterilization temperature to 1080C (for glucose-enriched media). The ''universal'' medium was then compared with other media by calculating ID50 (50% infectivity dose). The results obtained for S.faecium A2I,B.pumilus E601, Bsphaericus C1A, B.subtilis 6633, S.aureus 209P, C.albicans L-45, and Cl.sporogenes 477 have confirmed the suitability of the ''universal'' medium for use in radiosterilization studies.(author)
[en] In diabetic retinopathy, prolonged high-level blood glucose induced significant impairments among various retinal tissues, including retinal pigment epithelial (RPE) cells. In an in vitro model of human RPE cells, we evaluated whether 7,8-Dihydroxyflavone (DHF) may effectively prevent high glucose-induced diabetic apoptosis among human RPE cells.
[en] The feasibility of glycosylation post-purification has been demonstrated by introducing glucose into the model protein lysozyme via a novel reaction that is compatible with biological samples. The crystallization of glycoproteins is one of the challenges to be confronted by the crystallographic community in the frame of what is known as glycobiology. The state of the art for the crystallization of glycoproteins is not promising and removal of the carbohydrate chains is generally suggested since they are flexible and a source of heterogeneity. In this paper, the feasibility of introducing glucose into the model protein hen egg-white lysozyme via a post-purification glycosylation reaction that may turn any protein into a model glycoprotein whose carbohydrate fraction can be manipulated is demonstrated
[en] Oxidation of glucose oxidase by ferrocenecarboxylic acid in the presence of glucose was examined by comparing experimental catalytic efficiencies from cyclic voltammetry with those digitally simulated by the general program ELEC. The program permitted consideration of individual diffusion coefficients of enzyme and mediator, the second-order nature of the initial electron-transfer event and the follow-up reaction of oxidized enzyme with glucose. A rate constant of 1.06x105 1 mol-1 s-1 was found by analysis with such simulations for the accepted two-electron EC'C pathway. This was nearly half the approximate value found by a previously used pseudo-first-order EC' model assuming equal diffusion coefficients. (author). 15 refs.; 3 figs.; 1 tab
[en] Highlights: • HG did not induce endothelial cell injury directly, but increased cell viability after 72 h. • HG triggered upregulation of survivin expression as well as key components of autophagy pathway. • Survivin regulated HG-induced vascular endothelial cell dysfunction mediated by autophagy pathway. Diabetic vascular complications are often defined by vascular endothelial lesions. However, as a plastic cell type, whether endothelial cells could transit from quiescence to hyper-active status and hamper vascular stability upon hyperglycemia stimulation and whether this process is involved in diabetic vascular complications remain obscure. Survivin has been identified as an anti-apoptotic protein in tumor or epithelial cells by either promoting proliferation or inhibiting apoptosis. Therefore, this study aims at investigating the effects of hyperglycemia on endothelial cell status and the potential involvement of survivin. We found that high glucose (25 mM) did not cause endothelial injuries, instead, it evidently promotes endothelial proliferation and tube formation capacity indicating endothelial cell dysfunction upon hyperglycemia characterized by its preference to hyper-active status. Concomitantly, an upregulation of survivin was detected accompanied by the key component elevations of autophagy pathway including LC3, Beclin1, and p62. YM155, a specific inhibitor of survivin, could abrogate hyperglycemia-induced endothelial hyper-activation. Application of the autophagy inhibitor (3MA) and agonist (rapamycin) supported that survivin could be as a downstream effect or of autophagy. Thus, our results suggested that survivin/autophagy axis a potential therapeutic target in treatment of diabetic vascular complications.
[en] Highlights: • Liver-X-receptors are nuclear receptors comprising two popular subtypes: LXRα & -β. • LXRα loss inhibited LXR-mediated cardiomyocyte protection from high-glucose stress. • Nuclear receptor corepressor signals marred LXR-mediated cardiomyocyte protection. • LXRα, not -β, protects cardiomyocytes against high-glucose oxidative stress. Liver-X-receptors (LXRs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily. The two popular homologous receptor subtypes, LXRα and LXRβ, exhibit differential expression patterns, thereby probably playing different roles in different contexts. This study aimed to evaluate the different roles of the two LXR subtypes and the mechanisms underlying their protection of cardiomyocytes against high-glucose stress. Silencing of LXRα, but not LXRβ impaired normal LXR-mediated cardioprotective effects against high glucose-induced oxidative stress, apoptosis, and inflammation. Mechanistically, silencing of small ubiquitin-like modifier (SUMO)1 or SUMO2/3 did not affect LXR-mediated cardioprotective effects; however, these were impaired in response to nuclear receptor corepressor (NCoR) silencing. Together, these findings indicate that LXRα, but not LXRβ, protects against high glucose-induced cardiomyocyte injury, probably via the NCoR-dependent transrepression of downstream target genes.
[en] Highlights: • CircHIPK3 downregulation in HG-treated HUVECs and diabetic patients' HAECs. • CircHIPK3 overexpression inhibits HG-induced endothelial cell death and apoptosis. • CircHIPK3 silencing exacerbates HG-induced endothelial cell death and apoptosis. • CircHIPK3 downregulation by HG induces miR-124 accumulation in endothelial cells. • MiR-124 inhibition protects endothelial cells from HG-induced cytotoxicity. High glucose (HG) induces vascular endothelial cell injury. However, the underlying mechanisms are poorly understood. Circular RNA HIPK3 (circHIPK3) is a highly conserved non-coding RNA. Here we show that circHIPK3 is downregulated in HG-treated human umbilical vein endothelial cells (HUVECs) and in primary aortic endothelial cells (HAECs) from diabetic patients. In both HUVECs and HAECs, lentivirus-mediated circHIPK3 overexpression inhibited HG-induced cell death and apoptosis. Contrarily, circHIPK3 silencing by targeted siRNA exacerbated HG-induced endothelial cell death and apoptosis. Further, circHIPK3 downregulation by HG caused microRNA-124 (miR-124) accumulation in HUVECs and HAECs. On the contrary, miR-124 inhibition by the adeno-associated virus (AAV)-packed miR-124 inhibitor protected endothelial cells from HG. Together, circHIPK3 downregulation mediates HG-induced endothelial cell injury. Targeting circHIPK3-miR-124 pathway could potentially be a novel approach for the treatment of diabetic-associated vascular injury.
[en] Highlights: • Ocimum tenuiflorum leaf extract and silver nitrate were used to prepare Ag NPs. • Structural, optical and morphological properties of Ag NPs were studied. • The GCE modified with Ag NPs showed a sensitivity of 895.8 μAmM−1cm−2. • Bio-mediated synthesized NPs showed sustainable glucose sensing properties.
[en] Natural killer/T-cell (NK/T-cell) lymphoma is a rare condition, which presents as necrotic, granulomatous lesions involving the nose and the upper respiratory tract. The condition usually has an aggressive clinical course. The predominant subtype of NK/T-cell lymphoma noted in Asian population is the nasal type. We describe a case of biopsy-proven NK/T-cell lymphoma with bilateral adrenal involvement. Adrenal involvement by lymphoma is usually of B-cell type and occurs in disseminated disease and often unilateral. Bilateral adrenal involvement by T-cell lymphoma is extremely rare
[en] GLUT4 is unique among specialized glucose transporters in being exclusively expressed in muscle and adipocytes. In the absence of insulin the distribution of GLUT4 is preferentially intracellular and insulin stimulation results in the movement of GLUT4 containing vesicles to the plasma membrane. This process is responsible for the insulin stimulation of glucose uptake in muscle and fat. While signalling pathways triggering the translocation of GLUT4 are well understood, the mechanisms regulating the intracellular retention of GLUT4 are less well understood. Here we report a role for β-catenin in this process. In 3T3-L1 adipocytes in which β-catenin is depleted, the levels of GLUT4 at and near the plasma membrane rise in unstimulated cells while the subsequent increase in GLUT4 at the plasma membrane upon insulin stimulation is reduced. Small molecule approaches to acutely activate or inhibit β-catenin give results that support the results obtained with siRNA and these changes are accompanied by matching changes in glucose transport into these cells. Together these results indicate that β-catenin is a previously unrecognized regulator of the mechanisms that control the insulin sensitive pool of GLUT4 transporters inside these adipocyte cells.