Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149958 (complex partial seizures)
 2,563 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal hyperviscosity syndrome is known to affect multiple organ systems. The effects of polycythemic hyperviscosity on cutaneous blood flow and transcutaneous PO2 and PCO2 were compared in ten term infants prior to and following correction of the hyperviscous state. Cutaneous blood flow was measured by the heat clearance method; transcutaneous PO2 and PCO2 were detected by a polarographic O2 cathode and a potentiometric pH-sensitive glass electrode, respectively. Whole blood viscosity was measured at five shear rates from 11.25/s to 225/s using a Wells-Brookfield viscometer. Following partial exchange transfusion with fresh frozen plasma, there was a significant decrease in arterial blood hematocrit from 62.7% +/- 5.9% to 48.4% +/- 4.8% (P less than .001) and in whole blood viscosity from 13.9 +/- 2.9 cps to 8.5 +/- 1.8 cps (P less than .001) at a shear rate of 11.25/s. The arterial and transcutaneous O2 and CO2 tensions were in the normal range in the hyperviscous state and remained unchanged following exchange transfusion. The static measure of cutaneous blood flow increased 36% from 208 +/- 54 mW to 283 +/- 75 mW (P less than .01) while the dynamic measure of cutaneous blood flow increased 38% to 41% (P less than .01). The lack of demonstrable cutaneous hypoxia and hypercapnia, despite a significant decrease in blood flow in the hyperviscous state, may be due to one or more factors.
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PMID:Effects of polycythemia and hyperviscosity on cutaneous blood flow and transcutaneous PO2 and PCO2 in the neonate. 643 20

In this study, the factors in overnight dwell fluid (8 to 10 hr dwell) depressing granulocyte (GC) NAD(P)H-oxidase dependent radical species production are characterized. At present, most studies have essentially focused on fresh, unspent dialysate and on peritoneal macrophages. The response to Staphylococcus aureus (Staph A) was dose-dependently depressed for both GC CO2 production (from 91.3 +/- 8.4 to 9.0 +/- 1.5 dpm/10(3) GC, P < 0.01) and chemiluminescence (CL) (peak from 7.3 +/- 0.8 to 1.6 +/- 0.8 cps x 10(3)/GC, P < 0.01). Stimulation with formyl-methionine-leucine-phenylalanine (f-MLP), phorbol myristic acid (PMA), Staphylococcus epidermidis (Staph Epi), E. coli, latex and zymosan revealed a parallel depression, pointing to an intrinsic metabolic defect, rather than failure of particle ingestion. The addition of glucose to the normal cell medium to obtain the same concentration as in the CAPD effluent (2.9 +/- 0.3 mg/dl) depressed function but not to the same extent as the genuine PD effluent. Opsonization of Staph A and E. coli induced a partial correction. No effect of pH or osmolality was observed. HPLC fractionation of CAPD effluent on a polarity based gradient revealed an elution of depressive factors in hydrophobic fractions with a nadir in F7 and F12. Analysis of the elution pattern of various uremic solutes revealed elution in F12 of p-cresol, a solute with known inhibitory effect on GC function. These events may be related to recent peritonitis (CL in response to Staph A 0.3 +/- 0.1 in effluent of 6 patients with recent peritonitis versus 2.6 +/- 0.8 cps x 10(3)/GC in 12 patients without recent peritonitis (P < 0.01). We conclude that the GC response is depressed in the presence of CAPD effluent due to excess glucose, lack of opsonization, and uremic solutes of which p-cresol is one of the responsible compounds.
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PMID:Disturbed host defense in peritoneal cavity during CAPD: characterization of responsible factors in dwell fluid. 884 Feb 97