In leucocytes

Aplastic anemia and leukemia are not the only health effects ascribed to benzene exposure. A number of recent studies have associated benzene exposure with chromosomal changes (aberrations) (118). Other studies have shown abnormalities in porphyrin metabolism and decrease in leucocyte alkaline phosphatase activity in apparendy healthy workers exposed to 10—20 ppm benzene (119,120). Increases in leukoagglutinins, as well as increases in blood fibrinolytic activity, have also been reported and are believed to be responsible for the persistent hemorrhages in chronic benzene poisoning (121,122). 

Konietzko H, Reill G. 1980. The effect of trichloroethylene on some serum enzymes and on the cytoenzymological activity in leucocytes and on the acid base equilibrium. Int Arch Occup Environ Health 47 61-67. 

Recently in a study of long-term Li+ patients, the levels of neutrophils, helper T-cells, -lymphocytes, and NK cells were all significantly higher than normal, indicating that these, generally favorable, quantitative changes in leucocyte populations persist with Li+ therapy [207]. 

In leucocytes of individuals suffering from myelocytic and lymphatic leukemia a significant decrease of G-6-PDH and 6-PGDH has been described (B3, B4, G4), the activity of the latter being noticeably more reduced than that of the former. 

Vadas, M. A., Lopez, A. F., Gamble, J. R., Elliot, M. J. (1991). Role of colony-stimulating factors in leucocyte responses to inflammation and infection. Curr. Opin. 

Serum lipase is synthesized and stored in the granules of pancreatic acinar cells and is excreted from the apical poles of the acinar cells into the duct system of the gland. Lipases are produced not only in the pancreas but also at various sites in the human digestive tract [126][127]. Lipases are also found in leucocytes, adipose tissue, lung, and milk. 

The fats also have a plastic function as they are included in cell membranes and other cell structures. The central and peripheral nervous systems are rich in lipids. PNFA are included in cell membranes, with their most significant function being the synthesis of cell hormones — prostaglandins. The properties of cell membranes as well as their interaction with external factors depend on the relation of PNFA concentration in cell components. In humans, prostaglandins are created not only in tissues but also in thrombocytes (thromboxanes) and in leucocytes (leukotrienes). The biological action of thrombocytes is extremely variant and depends on PNFA type which are the basis for fatty acid creation. 

Clinical improvement, especially the disappearance of fever or defervescence, is the best parameter to judge the response to therapy. However, clinical improvement can be difficult to monitor objectively in critically ill patients with multi-system disease. Also, clinical improvement can be very slow for certain infections, e.g. tuberculosis. The peripheral blood leukocyte count including the presence of early stages in leucocyte differention and the level of serum C-Reactive Protein (CRP, an acute phase protein) are parameters that can be sequentially determined to monitor improvement. For monitoring the effect of treatment of chronic infections such as endocarditis or osteomyelitis, weekly determination of the erythrocyte sedimentation rate has been proven useful. 

Unquenched endogenous alkaline phosphatase activity may be seen in leucocytes, kidney, liver, bone, ovary bladder, salivary glands, placenta and gastro-intestinal tissue. Add levamisole to the alkaline phosphatase chromogen reagent or use another enzyme label such as horseradish peroxidase. Intestinal alkaline phosphatase is not quenched by the addition of levamisole. Pretreat the tissue with 0.03 N HCI. 115-121... 

The interaction of the various aP integrin complexes with ICAMs results in firm attachment and spreading. Subsequent VCAM-1-integrin and PECAM-1-integrin interactions are involved in leucocyte transmigration through endothelial cell junctions into the extravascular space. Leucocytes can thence proceed to interact with target cells and initiate inflammatory processes. 

Disposition in the Body. Readily absorbed after oral administration the proportion of a dose absorbed tends to decrease with increasing dose it is widely distributed in the body tissues. The concentration of ascorbic acid is higher in leucocytes and platelets than in erythrocytes and plasma. Ascorbic acid is metabolised to dehydroascorbic acid, 2,3-diketogulonic acid, oxalate, and carbon dioxide some conjugation with sulphate occurs to form ascorbate-3-sulphate. Ascorbic acid in excess of the body s requirements is rapidly eliminated in the urine. About 85% of an intravenous dose, given to subjects previously saturated with the vitamin, is excreted in the urine in 24 hours, with about 70% of the dose excreted unchanged and 15% as dehydroascorbic acid and diketogulonic acid. The amount normally present in the body is in excess of 1.5 g. 

Blood Concentration. Concentrations in plasma and in leucocytes are normally about 5 to 12 pg/ml and 25 to 30 pg/lO cells respectively these concentrations exhibit circadian and seasonal rhythms. 

Finally, it should be remembered that a statistically significant decrease of coenzymatically active Be in plasma was found only in patients with nutritional anemia and various forms of leukemia. Moreover, Be values in leucocytes were consistently decreased in patients with various forms of leukemia [Wachstein et al. (W7) used a modification of the mano-metric method of Umbreit (Ul) for the determination of pyridoxine levels]. 

The complete DNA sequence has meanwhile been clarified. HCV binds to the cell surface structure CD 81 via its envelope protein E2 for this reason, HCV can also infect other cell types (apart from hepatocytes). (318) Virus replication can be detected very early (within the first week after exposure). The viral particle load is < 10 /ml serum, which is less than half of an HBV infection. The highest antibody titres are found in the preacute and early acute stages. HCV can replicate extra-hepatically, e. g. in leucocytes and B or T lymphocytes as well as, occasionally, in oral lichen tissue. (284) The spleen serves as a large extrahepatic reservoir for HCV. (280, 288, 313, 318, 334, 342, 355, 358, 377, 383, 404) (s. p. 115)... 

The diagnosis is established by determining the specific YF IgM antibodies and/or the virus RNA. Laboratory parameters reveal an elevation of the transaminases, GDH, y-GT and LDH as well as a reduction in leucocytes, Quick s value and cholinesterase. Albuminuria is also present. Mortality (5-10%) is generally due to renal insufficiency. After recovery, immunity is lifelong. 

The iron or haemoprotein catalysed oxidative reactions may mediate the responses associated with acute and chronic inflammation. In the post-ischaemic, reperfused heart the role of oxidant stress has been linked with increases in leucocyte adhesion and transendothelial cell migration from oxidant production within the microcirculation [115]. This is probably caused by an increased expression in adhesion molecules or the fixation of transiently expressed adhesion molecules by the peroxidation of membrane lipids which reduces membrane fluidity [117,118]. This oxidant stress may also lead to apoptosis induction, DNA damage, inflammatory mediator synthesis and regulate gene expression [119,120,121]. 

LEUKOTRIENE RECEPTOR AGONISTS act at receptors recognizing leukotrienes and analogues. The lipoxygenase system forms the leukotrienes, which are members of the eicosanoid family of phospholipid mediators. Their name derives from the fact that leukotrienes are found in leucocytes and contain a triene system of double bonds. The other members of the eicosanoid family are the prostanoids (thromboxanes and the prostaglandins), and these are formed by the cyclooxygenase system see cyclooxygenase INHIBITORS. All the eicosanoids are derived mainly from arachidonic acid. These mediators are synthesized on demand, and in some cases their half-lives are short. The... 

Stimulation of cultured endothelial cells with thrombin, histamine, or H202 results in a rapid (within minutes) translocation of P-selectin (CD62P) to the cell surface from secretory granules known as Weibel-Palade bodies. In contrast, induction of endothelial E-selectin (CD62E) expression is dependent upon de novo synthesis following stimulation with cytokines such as IL-1 a and TNF-a.57 58 P- and E-selectin are only transiently expressed on the cell surface, during which time they bind to the sialylated Lewis X antigens of neutrophils and monocytes.59-61 Both selectins are implicated in leucocyte extravasation associated with the acute inflammatory response.62-63... 

Maule, A.G. and C.B. Schreck. Glucorticoid receptors in leucocytes and gill of juvenile coho salmon (Oncorhynchus kisutch). Gen. Comp. Endocrinol. 77 448-455, 1990. 

Affinity studies were performed in leucocytes and in extracted membrane antigens. Isolated CD20 antigen membrane preparations were developed using a pool of concentrated leucocytes from a blood bank. After an initial centrifugation at 500g for 10 min at 4°C, the yellow layer containing the leucocytes was... 

PI. Patriarca, P., Cramer, R., Moncalvo, S., Rossi, F., and Romeo, D., Enzymatic basis of metabolic stimulation in leucocytes during phagocytosis. The role of activated NADPH oxidase. Arch. Biochem. Biophys. 145, 255-262 (1971). 

Since 1964, Victor has been in the Department of Pathology of NYU Medical School. Early interests were on the complement system where his main contributions were the discovery of complement receptors in leucocytes, the studies on control of activation of the cascade by C4 binding protein (C4BP) and decay accelerating factor (DAF), and the... 

C. N. Palmer (2002). Elevated expression of the genes encoding TNF-a and thromboxane synthase in leucocytes from patients with systemic sclerosis. Rheumatology 41, 869-875. 

Shiga, K., R. Fukuyama, S. Kiraura, K. Nakajima, and S. Fushiki (1999). Mutation of the sterol 27-hydroxylase gene (CYP27) results in truncation of mRNA expressed in leucocytes in a Japanese family with cerebrotendinous xanthomatosis. J. Neurol. Neurosurg. Psychiatr. 67, 675-677. 

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