China 
Africa 
Explore chapters and articles related to this topic
Screening Tests for HIV-1 Infection
Published in Niel T. Constantine, Johnny D. Callahan, Douglas M. Watts, Retroviral Testing, 2020
Niel T. Constantine, Johnny D. Callahan, Douglas M. Watts
The development of tests to detect antibodies in urine has not been attempted in the past, probably because antibodies were considered too large (molecular weight) to pass through the kidney glomerulus, unless significant kidney damage had occurred. In addition, the pH of the urine was thought to interfere with pH-dependent immunological assays. Recently, serological assays have detected HIV antibodies in urine. However, the sensitivities of the tests have thus far proved to be less than optimal. In general, the tests can only detect antibodies in about 92 to 95% of infected individuals, with similar levels of specificity. Both ELISA and Western blot (WB) assays have been used on unconcentrated urine. Many commercial companies are actively pursuing the development of these assays, and it may not be long before they are used routinely in laboratories. Some recent publications have indicated that the performance of tests using urine is approaching that of tests using serum samples. They have also indicated that the antibodies detected in urine are intact IgG molecules, not just antibody fragments.
Getting a drug into the body: absorption
Published in Hugh McGavock, How Drugs Work, 2017
Although the cells lining many blood capillaries, particularly the kidney glomerulus, have pores between them allowing relatively free passage of drug molecules, most other tissues, including the intestine, have few intercellular pores large enough to permit drug absorption.
The Twentieth Century
Published in Arturo Castiglioni, A History of Medicine, 2019
Special functions have been suggested by finer differences in structure, such as the alpha and beta cells of the islands of Langerhans in the pancreas, their individuality brought out by the use of special stains by R. R. bensley (b. 1867). The carotid body (known since 1743) and aortic body are small structures lying in the bifurcation of the carotid arteries and touching the innominate artery and the arch of the aorta (A. biedl, 1902). Their function long remained unknown, but they have now been shown to be important sense organs regulating arterial blood supply through their sensitivity to chemical changes, producing the opposite effect of that of nerve endings in the vessel walls, which react to pressor stimuli (F. decastro, 1928; C. heymans, 1930; and C. schmidt and J. comroe, 1939). Similarly in the kidneys the juxta-glomerular apparatus described by N. goormaghtigh in 1932 appears to control, in some species at least, the amount of blood flowing to the kidney glomerulus. Cells in the intestinal wall with chrome-salt affinities and in intimate connection with nerve fibrils were demonstrated (1897, 1906) by W. kultczycki and A. ciaccio (1906). Such cells, by the use of silver impregnation studies, have been considerably explored by Masson. Further understanding of the finer anatomy of the brain followed the introduction of special stains — at first by Golgi, later by Ramon y Cajal (gold sublimate, 1913) and his pupil Pio delriohortega (silver carbonate, 1919) — which disclose the intimate details of the apparently structureless mass of the interstitial tissue. Instead of a dual system of the large astrocytes and a separate syncytium of supporting interlacing fibres, these investigators showed that there were three types of cells, each with ramifying dendrites connected with the cell body: the astrocytes (macroglia, spider cell), the oligodendroglia, numerous but apparently unimportant smaller cells with, as the name implies, fewer shorter processes, and the microglia, which have, surprisingly, been shown by the Spaniards to be of mesodermal origin — angular cells with many short branches.
Transient receptor potential canonical 6 knockdown ameliorated diabetic kidney disease by inhibiting nuclear factor of activated T cells 2 expression in glomerular mesangial cells
Published in Renal Failure, 2022
Jian Yu, Chunchun Li, Lisha Ma, Bin Zhai, Aiping Xu, Decui Shao
In our study, we focused on GMCs. GMCs in the interstitial cells in the kidney glomerulus are involved in the processes of DKD. In the priming of DKD, GMC activation leads to cell proliferation, overproduction of ECM proteins and thickening of the glomerular basement membrane [36,37]. Therefore, GMC activation is an indispensable factor in the initial pathophysiological changes of early DKD, but those changes will ultimately lead to glomerular sclerosis and kidney failure [38]. In our study, we observed that knockdown of TRPC6 by siRNA reduced ECM overproduction induced by HG. In neonatal pig GMCs, hyperforin-induced activation of the TRPC6 channel inhibited GMC proliferation and triggered apoptotic pathways [39]. We hypothesize that the intracellular signal transduction mediated by the TRPC6 channel might vary depending on the cell types or different pathological stimuli.
ANGPTL3: a novel biomarker and promising therapeutic target
Published in Journal of Drug Targeting, 2019
Shuang Jiang, Guo-Hui Qiu, Neng Zhu, Zhe-Yu Hu, Duan-Fang Liao, Li Qin
Podocyte is an integral member of the filtration barrier in kidney glomerulus. And podocyte detachment and apoptosis are two risk factors for podocyte loss, eventually, lead to glomerular disease and proteinuria [69]. ANGPTL3 expression is up-regulated in glomerular podocytes of patients with nephrotic syndrome [70]. Overexpression of ANGPTL3 expression increased the motility of podocytes by inducing actin filament (F-actin) rearrangement, mainly in lamellipodia formation. Definitely, F-actin rearrangement is involved in the podocyte detachment and apoptosis. This process is mediated by FAK and PI3K/PKB phosphorylation and small GTPases Rac1 activation. The enhanced movement of podocyte leads to podocyte foot process fusion, a typical form of podocyte injury [69]. In addition, ANGPTL3 modulates barrier properties of human glomerular endothelial cells (GEnCs) through a possible signalling pathway involving PI3K/PKB and αvβ3 [71]. ANGPTL3 increases the permeability of GEnCs and increase phosphorylation of PKB in cultured GenCs in vitro. LY294002, a phosphatidylinositol-3 kinase inhibitor, can prevent the increase of permeability of GEnCs induced by ANGPTL3. And, the integrin αvβ3 antibody (LM609) can block the ANGPTL3-induced PKB phosphorylation [71].
Effect of Simvastatin on Lipid Accumulation and the Expression of CXCL16 and Nephrin in Podocyte Induced by Oxidized LDL
Published in Journal of Investigative Surgery, 2018
Li Wang, Xiujun Yao, Qian Li, Shuzhen Sun
Podocyte plays a crucial role as an integral member of the filtration barrier for the integrity of kidney glomerulus. Podocyte foot processes (FP) surround the outstretched glomerular basement membrane (GBM), forming slit diaphragm (SD) complex which establishes selective permeability of glomerular filtration barrier [1]. Dysfunction of glomerular podocytes was found to be the driving forces behind the formation of nephrotic proteinuria [2]. Lipid and lipoprotein metabolism abnormalities are often observed in patients with nephrotic syndrome and chronic renal diseases [3]. Lipid deposition in the glomerular podocyte is an important risk factor for glomerulosclerosis [4, 5]. In particular, OxLDL plays a major role in the pathogenesis of atherosclerosis and in the development of various glomerular diseases [6]. The present study showed that the uptake and endocytosis of OxLDL through scavenger receptor CXCL16 on podocyte lead to intracellular lipid accumulation, in addition, OxLDL induced loss of nephrin expression and synthesis of ROS, leading foot processes fusion [7, 8]. Nephrin is the first found transmembrane protein in glomerular SD which plays a key role in maintaining the integrity and normal function of glomerular filtration barrier. Abnormal expression of nephrin can result in SD dysfunction and then foot process fusion and proteinuria.