Charlie Norwood VA Medical Center

About: Charlie Norwood VA Medical Center is a healthcare organization based out in Augusta, Georgia, United States. It is known for research contribution in the topics: Autophagy & Kidney. The organization has 349 authors who have published 490 publications receiving 16360 citations. The organization is also known as: Augusta VA Medical Center.

Deletion of p75NTR prevents vaso-obliteration and retinal neovascularization via activation of Trk- A receptor in ischemic retinopathy model.

Abstract: Ischemic retinopathy is characterized by ischemia followed by retinal neovascularization (RNV) resulting in visual impairment. Given the role of neuron-secreted growth factors in regulating angiogenesis, we examined how genetic deletion of the neurotrophin receptor; p75NTR can overcome retinal ischemia using oxygen-induced retinopathy (OIR) mouse model. Wildtype (WT) or p75NTR−/− mice pups were subjected to hyperoxia (70% O2, p7-p12) then returned to normal air (relative hypoxia, p12-p17). Vascular alterations were assessed at p12 and p17 time-points. Deletion of p75NTR prevented hyperoxia-associated central vascular cell death (p12) and hypoxia-associated RNV and enhanced central vascular repair (p17). Decreased expression of apoptotic markers; preserved Akt survival signal decreased proNGF were also observed at p12. During hypoxia, deletion of p75NTR maintained VEGF and VEGFR2 activation and restored NGF/proNGF and BDNF/proBDNF levels. Deletion of p75NTR coincided with significant increases in expression and activation of NGF survival receptor, TrkA at basal and hyperoxic condition. Pharmacological inhibition of TrkA using compound K-252a (0.5 μg 1 μl−1/eye) resulted in 2-fold increase in pathological RNV and 1.34-fold increase in central vascular cell death in p75NTR−/− pups. In conclusion, deletion of p75NTR protected against retinal ischemia and prevented RNV, in part, through restoring neurotrophic support and activating TrkA receptor.

The Ubuntu concept, sexual behaviours and stigmatisation of persons living with HIV in Africa: A review article.

Abstract: Stigma and discrimination and risky sexual behaviours have been major stumbling blocks to the efforts by implementers to mitigate the effects of HIV amongst communities in Africa. A key cultural resource, based on evolving South African cultural traditions, is the notion of Ubuntu, which is grounded in respect, ethics, humanity and the interconnectedness of beings. This concept can be a useful resource in upholding confidentiality, a central requirement in research ethics and the deliverance of health promotion interventions regarding HIV/AIDS. This article explored the applicability of the Ubuntu concept in enhancing safe sexual practices and positive attitudes towards persons living with HIV, with the view of achieving Zero new infections, Zero discrimination against persons living with HIV (PLHIV), and Zero AIDS-related deaths. A review of literature was undertaken. Electronic databases, academic journals and books from various sources were accessed. Several key search terms relating to the tenets of Ubuntu, stigma and discrimination towards PLHIV, and sexual behaviours were used. Only references deemed useful from relevant texts and journal articles were included. Going therefore by the Ubuntu tradition of basic respect and compassion for others, one will expect positive attitudes towards PLHIV. This review therefore advocates positive attitudes towards PLHIV. Also, according to the Ubuntu tradition that prescribes a rule of conduct and social ethics, one would expect the sexual behaviours of youths in Africa to be good. This review article also advocates safe sexual behaviours of adolescents in Africa. With this in mind, from a critical Ubuntu-centric philosophical perspective, this article breaks new ground by advocating the use of the Ubuntu concepts in enhancing safe sexual practices and positive attitudes towards PLHIV in Africa. This could in turn bring about safe sexual practices among youths, and curb the discrimination and stigmatization against PLHIV in Africa.

Phospholipase D Activity Underlies Very-Low-Density Lipoprotein (VLDL)-induced Aldosterone Production in Adrenal Glomerulosa Cells

Abstract: Aldosterone is the mineralocorticoid responsible for sodium retention, thus increased blood volume and pressure. Excessive production of aldosterone results in high blood pressure as well as renal disease, stroke, and visual loss via both direct effects and effects on blood pressure. Weight gain is often associated with increased blood pressure, but it remains unclear how obesity increases blood pressure. Obese patients typically have higher lipoprotein levels; moreover, some studies have suggested that aldosterone levels are also elevated and represent a link between obesity and hypertension. Very-low-density lipoprotein (VLDL) functions to transport triglycerides from the liver to peripheral tissues. Although previous studies have demonstrated that VLDL can stimulate aldosterone production, the mechanisms underlying this effect are largely unclear. Here we show for the first time that phospholipase D (PLD) is involved in VLDL-induced aldosterone production in both a human adrenocortical cell line (HAC15) and primary cultures of bovine zona glomerulosa cells. Our data also reveal that PLD mediates steroidogenic acute regulatory (StAR) protein and aldosterone synthase (CYP11B2) expression via increasing the phosphorylation (activation) of their regulatory transcription factors. Finally, by using selective PLD inhibitors, our studies suggest that both PLD1 and PLD2 isoforms play an important role in VLDL-induced aldosterone production.