Antimicrobial sensitivity pattern and detection of antimicrobial resistance genes of E. coli isolated from respiratory tract infections in poultry

The present study was conducted at College of Veterinary Science, Guru Angad Dev Veterinary and Animal Sciences University with the objective to determine the antimicrobial sensitivity pattern and anti-microbial resistance genes on E. coli isolates obtained from respiratory infection samples of poultry. A total of 115 samples were collected from different respiratory disease outbreaks from various poultry farms of Ludhiana district of Punjab. Various bacteria related to respiratory infections were isolated and E. coli was found to be in highest number among the isolated bacteria. The isolates of E. coli were confirmed by MALDI-TOF and were subjected to Kirby Bauer’s disc diffusion method to study the antimicrobial sensitivity pattern phenotypically. The isolates were also screened for the presence of six antimicrobial resistance genes associated with certain antibiotics by Polymerase Chain Reaction (PCR). All the isolates showed 100% resistance towards the antibiotics, viz. tetracycline, chlortetracycline, enrofloxacin, erythromycin, ofloxacin, tylosin, amikacin, and ciprofloxacin. This demonstrates the multidrug-resistance of the isolates. The antimicrobial resistance gene strA (60%) was found to be expressed more among the isolates followed by ere (50%), tetA (47.5%), aac-(3)-(IV) (37.5%) and blaTEM (32.5%). None of the isolate was found to have tetC gene

Sistema Solar: Planetas Clássicos

O conhecimento curricular de Astronomia para surdos, não pode ser empobrecido, subtraído, fragmentado, mas sim formulado para corresponder a sua identidade de cognição, sem distanciar-se, porém, do direito inalienável a tudo que devem conhecer. Métodos de ensino não podem ser únicos para todos e, um sistema educacional que não revela estas diferenças está fadado em provocar a exclusão destes educandos por considerá-los inaptos, intelectualmente. Sendo assim, ao organizar o conteúdo que será trabalhado em sala de aula, o professor terá sempre em mente o tema Sistema Solar /Planetas Clássicos. Este tema está diretamente ligado a outros temas, permitindo ao aluno surdo fazer parte desse todo tão complexo que é o Universo em que vivemo

[pt] ORGANIZAÇÃO E CLIMA ESCOLAR DE UMA ESCOLA DE TEMPO INTEGRAL VOCACIONADA PARA O ESPORTE: O GINÁSIO EXPERIMENTAL OLÍMPICO NO RIO DE JANEIRO

Alterations in the podocyte actin cytoskeleton have been implicated in the development of proteinuric kidney diseases. In the present study, we evaluated the effect of HIV on the podocyte actin cytoskeleton and the mechanism involved. We hypothesized that HIV may be compromising the actin cytoskeleton via downregulation of the vitamin D receptor (VDR) of conditionally immortalized differentiated human podocytes (CIDHPs). HIV-transduced podocytes (HIV/CIDHPs) not only displayed downregulation of VDR but also showed activation of the renin-angiotensin system (RAS) in the form of enhanced expression of renin and increased production of ANG II. Moreover, CIDHPs lacking VDR displayed enhanced ANG II production, and treatment of HIV/CIDHPs with EB1089 (vitamin D3; VD) attenuated ANG II production. HIV/CIDHPs as well as ANG II-treated CIDHPs exhibited enhanced expression of cathepsin (CTS) L. Additionally, losartan (an ANG II type I receptor blocker) inhibited both HIV- and ANG II-induced podocyte cathepsin L expression. Furthermore, VD down-regulated HIV-induced podocyte CTSL expression. Both losartan and free radical scavengers attenuated HIV- and ANG II-induced podo-cyte reactive oxygen species (ROS) generation. HIV also led to cytosolic CTSL accumulation through enhancement of podocyte lys-osomal membrane permeabilization; on the other hand, VD, losartan, and superoxide dismutase (SOD) attenuated HIV-induced enhanced podocyte cytosolic CTSL accumulation. Morphological evaluation of HIV/CIDHPs revealed sparse actin filaments and attenuated expression of dynamin. Interestingly, podocytes lacking CTSL displayed enhanced dynamin expression, and HIV/CIDHPs expressing CTSL exhibited downregulation of dynamin. These findings indicate that HIV-induced downregulation of podocyte VDR and associated RAS activation and cytosolic CTSL accumulation compromised the actin cytoskeleton. © 2013 the American Physiological Society.link_to_subscribed_fulltex

Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors

In the present study, we evaluated the effect of short term hyperglycemia on renal lesions in a mouse model (Tg26) of HIV-associated nephropathy (HIVAN). Control and Tg26 mice in groups (n=6) were administered either normal saline (FVBN or Tg) or streptozotocin (FVBN+STZ or Tg26 + STZ). After two weeks, biomarkers were collected and kidneys were harvested. FVBN+ STZ and Tg26 + STZ displayed elevated serum glucose levels when compared to FVBN and Tg26 respectively. Tg26 +STZ displayed elevated (P<0.05) blood urea nitrogen (BUN) levels (P<0.05) and enhanced (P<0.01) proteinuria when compared to Tg26. Tg26 + STZ displayed enhanced (P<0.001) number of sclerotic glomeruli and microcysts vs. Tg26. Renal tissues of Tg26 displayed down regulation of vitamin D receptor (VDR) expression and enhanced Ang II production when compared to FVBN mice. Hyperglycemia exacerbated down regulation of VDR and production of Ang II in FVBN and Tg mice. Hyperglycemia increased kidney cell reactive oxygen species (ROS) production and oxidative DNA damage in both FVBN and Tg26 mice. In in vitro studies, HIV down regulated podocyte VDR expression and also enhanced renin angiotensin system activation. In addition, both glucose and HIV stimulated kidney cell ROS generation and DNA damage and compromised DNA repair; however, tempol (superoxide dismutase mimetic), losartan (Ang II blocker) and EB1089 (VDR agonist) provided protection against DNA damaging effects of glucose and HIV. These findings indicated that glucose activated the RAS and inflicted oxidative stress-mediated DNA damage via down regulation of kidney cell VDR expression in HIV milieu both in vivo and in vitro

AT1R blockade in adverse milieus:role of SMRT and corepressor complexes

ANG II type 1 receptor blockade (AT(1)R-BLK) is used extensively to slow down the progression of proteinuric kidney diseases. We hypothesized that AT(1)R-BLK provides podocyte protection through regulation of silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) and vitamin D receptor (VDR) expression under adverse milieus such as high glucose and human immunodeficiency virus infection. Both AT(1)R-BLK and VDR agonists (VDAs) stimulated VDR complex formation that differed not only in their composition but also in their functionality. AT(1)R-BLK-induced VDR complexes contained predominantly unliganded VDR, SMRT, and phosphorylated histone deacetylase 3, whereas VDA-VDR complexes were constituted by liganded VDR and CREB-binding protein/p300. AT(1)R-BLK-induced complexes attenuated podocyte acetyl-histone 3 levels as well as cytochrome P-450 family 24A1 expression, thus indicating their deacetylating and repressive properties. On the other hand, VDA-VDR complexes not only increased podocyte acetyl-histone 3 levels but also enhanced cytochrome P-450 family 24A1 expression, thus suggesting their acetylating and gene activation properties. AT(1)R-BLK- induced podocyte SMRT inhibited expression of the proapoptotic gene BAX through downregulation of Wip1 and phosphorylation of checkpoint kinase 2 in high-glucose milieu. Since SMRT-depleted podocytes lacked AT(1)R-BLK-mediated protection against DNA damage, it appears that SMRT is necessary for DNA repairs during AT(1)R-BLK. We conclude that AT(1)R-BLK provides podocyte protection in adverse milieus predominantly through SMRT expression and partly through unliganded VDR expression in 1,25(OH)(2)D-deficient states; on the other hand, AT(1)R-BLK contributes to liganded VDR expression in 1,25(OH)(2)D-sufficient states