Nephrotic syndrome: a platelet hyperaggregability state

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.     

Suppressor activity of bovine Fc gamma positive cells during a persistent infection with Mycobacterium avium

The cell mediated immune response (CMI) was measured in calves after experimental infection with Mycobacterium avium. Using the tuberculin skin test a CMI response could be measured from four to 14 weeks after infection, and with a lymphocyte stimulation (LS) test from six to 40 weeks. One year after infection no CMI response was detected by either of the tests, in spite of the fact that in such calves M avium bacteria could be found in the intestinal lymph nodes at autopsy. After removal of mononuclear cells bearing receptors for the Fc part of IgG, the peripheral blood lymphocytes obtained from a calf infected one year earlier responded to M avium pure protein derivative in the LS test in contrast to lymphocytes obtained from uninfected calves.     

Toxicological effects of gamma-irradiated sewage solids fed as seven percent of diet to sheep for four years

Breeding ewes in drylot were fed pelleted complete diets with 3% cottonseed meal (CSM) or 7% dried, gamma-irradiated sewage solids (DGSS) for 4 yr. Cytochrome P-450 (P-450) content and enzyme activities for xenobiotics biotransformations were assayed in livers after 2 yr and in livers, kidneys and ileal tissue after 4 yr. Dietary DGSS caused no increase in P-450 and few changes in activities of oxidative, hydrolative and conjugative biotransformational enzymes. Consumption of DGSS for 4 yr caused slight enlargement of spleens (1.1-fold, P less than .10) and ovaries (1.3-fold, P less than .10), but no change in size of livers, kidneys, hearts, adrenals and thyroids (P greater than .10), nor liver vitamin A levels (P greater than .10). Of 22 refractory lipophilic residues assayed in abdominal adipose tissue, few were detected and of those detected DGSS caused none to exceed normal levels. Dietary DGSS increased (P less than .01) Fe in livers 1.5-fold and in spleens 5.6-fold, and increased Cu in livers 1.3-fold (P less than .01) and in kidneys 1.2-fold (P less than .05). Dietary DGSS increased Cd levels in livers (P less than .01) but not in kidneys or spleens (P greater than .10); yet all Cd levels were within ranges for livestock fed conventional feed. Dietary DGSS caused no increase (P greater than .10) in levels of Ag, Ca, Cr, Hg, K, Mg, Mn, Na, Ni, P, Pb or Zn in livers, kidneys or spleens. There were no histopathological lesions of toxicosis except mild hemosiderosis of spleens. Consumption of a diet with 7% DGSS throughout 4 yr caused no hazardous accumulation of toxic elements and little, if any, evidence of toxicosis.