Proteins tubular

Occupational exposure to Hg vapors Tamm-Horsfall protein, tubular antigen Cardenas et al. 1993 ... 

In subsequent studies attempting to find a correlation of physicochemical properties and antimicrobial activity, other parameters have been employed, such as Hammett O values, electronic distribution calculated by molecular orbital methods, spectral characteristics, and hydrophobicity constants. No new insight on the role of physiochemical properties of the sulfonamides has resulted. Acid dissociation appears to play a predominant role, since it affects aqueous solubiUty, partition coefficient and transport across membranes, protein binding, tubular secretion, and reabsorption in the kidneys. An exhaustive discussion of these studies has been provided (10). 

Cadmium is effectively accumulated in the kidneys. When the cadmium concentration exceeds 200 gg/g in the kidney cortex, tubular damage will occur in 10% of the population, and proteins begin to leak into urine (proteinuria). When the concentration of cadmium in the kidney cortex exceeds 300 pg/g, the effect is seen in 50% of the exposed population. Typically, excretion of low-molecular weight proteins, such as beta-microglobulin, is increased, due to dysfunction of proximal tubular cells of the kidney. The existence of albumin or other high-molecular weight proteins in the urine indicates that a glomerular injury has also taken place. The excretion of protein-bound cadmium will also be increased. 

An ultrafiltration plant is required to treat 50m3/day of protein-containing waste stream. The waste contains 0.05% by weight of protein which has to be concentrated to 2% to allow recycling to the main process stream. The tubular membranes to be used are... 

The kidney contains the major site of renin synthesis, the juxtaglomerular cells in the wall of the afferent arteriole. From these cells, renin is secreted not only into the circulation but also into the renal interstitium. Moreover, the enzyme is produced albeit in low amounts by proximal tubular cells. These cells also synthesize angiotensinogen and ACE. The RAS proteins interact in the renal interstitium and in the proximal tubular lumen to synthesize angiotensin II. In the proximal tubule, angiotensin II activates the sodium/hydrogen exchanger (NHE) that increases sodium reabsorption. Aldosterone elicits the same effect in the distal tubule by activating epithelial sodium channels (ENaC) and the sodium-potassium-ATPase. Thereby, it also induces water reabsotption and potassium secretion. 

Four different localizations of fatigue can be identified (a) decreased central command (b) decreased activation of the muscle membrane and the T-tubular system (c) decreased Ca release from the SR and (d) decreased response to the Ca release by the contractile proteins. The first two are partly extra-muscular while c and d are intramuscular responses to the excitation of the muscle membrane and often defined as excitation-contraction coupling. 

The general picture of muscle contraction in the heart resembles that of skeletal muscle. Cardiac muscle, like skeletal muscle, is striated and uses the actin-myosin-tropomyosin-troponin system described above. Unlike skeletal muscle, cardiac muscle exhibits intrinsic rhyth-micity, and individual myocytes communicate with each other because of its syncytial nature. The T tubular system is more developed in cardiac muscle, whereas the sarcoplasmic reticulum is less extensive and consequently the intracellular supply of Ca for contraction is less. Cardiac muscle thus relies on extracellular Ca for contraction if isolated cardiac muscle is deprived of Ca, it ceases to beat within approximately 1 minute, whereas skeletal muscle can continue to contract without an extraceUular source of Ca +. Cyclic AMP plays a more prominent role in cardiac than in skeletal muscle. It modulates intracellular levels of Ca through the activation of protein kinases these enzymes phosphorylate various transport proteins in the sarcolemma and sarcoplasmic reticulum and also in the troponin-tropomyosin regulatory complex, affecting intracellular levels of Ca or responses to it. There is a rough correlation between the phosphorylation of Tpl and the increased contraction of cardiac muscle induced by catecholamines. This may account for the inotropic effects (increased contractility) of P-adrenergic compounds on the heart. Some differences among skeletal, cardiac, and smooth muscle are summarized in... 

Possible causes of increased ratio of Cgm/Ccr pancreatitis can be liberation of a more readily excretable form of amylase, a protein with a molecular weight of 55,000 or less which can be easily filtered via the glomerulus and undergoes no appreciable tubular reabsorption. 

Monitoring of Cd exposure can take place by the determination of Cd in whole blood (reflects recent exposure) or urine (reflects body burden) by GF-AAS. Early effects can be monitored by the determination of a tubular protein (e.g. 132-microglobulin, retinol binding protein, a2-microglobulin) or the activity of an enzyme (e.g. N-acetyl 3-D-glucosaminidase) in urine. 

Figure 8.41 Separation of the enantiomers of the common protein amino acids (N-perfluoropropionylamide isopropyl esters) on a 20 m X 0.25 mm I.D. open tubular column coated with Chirasil-Val. (Reproduced with permission from ref. 764. Copyright Elsevier Scientific Publishing Co.)...

Gebauer, P. and Thormann, W., Isotachophoresis of proteins in uncoated open-tubular fused-silica capillaries with a simple approach for column conditioning, J. Chromatogr., 558, 423, 1991. 

CF patients have larger volumes of distribution of many antibiotics due to an increased ratio of lean body mass to total body mass and lower fat stores. CF patients also have an enhanced total body clearance, although the exact mechanism has not been determined. Increased renal clearance, increased glomerular filtration rate, decreased protein binding, increased tubular secretion, decreased tubular reabsorption, extrarenal elimination, and increased metabolism have all been proposed as possible reasons for the increased clearance. 

The presence of protein in the urine is a marker of glomerular and tubular dysfunction and is recognized as an independent risk factor for the progression of CKD.8 Furthermore, the degree of proteinuria correlates with the risk for progression of CKD. An increase of 1 g of protein excretion per day is associated with a five-fold increase in the risk of progression of CKD, regardless of the cause of CKD.9 The mechanisms by which proteinuria potentiates CKD are discussed later. Microalbuminuria is also linked with vascular injury and increased cardiovascular mortality.10... 

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