Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the effects of parenteral nutrition on the immunocompetence, we administrated parenteral nutritional support to the malnourished gastric cancer patients during perioperative periods. Changes of peripheral blood natural killer cytotoxicity (NKC) activity (LDH enzyme-release assay) and T lymphocyte subsets (OKT series monoclone antibody indirect fluorescent assay) were monitored before and after nutritional support. The results showed that one week of pre or postoperative parenteral nutrition significantly increased the NKC activity, T-helper, and T-helper/T-suppressor ratio. The total T lymphocytes count may also increase. T-suppressors remained unchanged no matter whether nutritional support was given or not. The authors believe that perioperative nutritional support could improve the immunocompetence of gastric cancer patients to some extent, and promote the restoration of immune depression caused by operation, but it could not eliminate the effects of immune depressing factor produced by the tumor. Intralipid can be used properly as non protein energy source without immunodepressing effects.
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PMID:[Effects of perioperative parenteral nutrition on immunocompetence in patients with gastric cancer]. 212 63

Whether there is preferential loss of certain types of nerve cells or specific cellular functions after hypoxic or ischemic insults remains unclear. To evaluate this phenomenon in vitro, the vulnerability of GABAergic neurons to hypoxia was investigated both quantitatively and with autoradiography. Immature neuronal cortical cultures obtained from fetal mice were subjected to chronic hypoxia (5% O2) for 24 h or 48 h and then returned to the normoxic condition for 48 h. The shorter hypoxic exposure resulted in significantly reduced numbers of neurons in comparison to the longer exposure and also to controls (29% and 26%, respectively; p less than 0.001). LDH efflux, a reliable indicator of cell damage, also was higher after the shorter exposure insult. Nevertheless, in these same 24 h hypoxic cultures there was prominent sparing of those neurons which accumulate GABA: by 48 h of recovery GABAergic neurons constituted 29.3 +/- 2.0% of the remaining neuronal population in comparison to 11.6 +/- 0.6 and 14.4 +/- 0.8% for controls and 48 h hypoxia, respectively; (p less than 0.001). Although total GABA uptake per neuron was significantly decreased after both types of insult, there was a concomitant increase in glial GABA uptake (i.e., that which could be displaced by beta-alanine). These observations suggest that certain GABAergic cortical neurons are relatively more resistant to chronic hypoxia than the general neuronal population and that depression of overall neuronal GABA uptake may be associated with enhanced glial GABA uptake.
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PMID:GABA accumulating neurons are relatively resistant to chronic hypoxia in vitro: an autoradiographic study. 228 58

It is well known that excessive calcium entry into the myocardial cells may contribute considerably to damage of the heart caused by postischemic reperfusion. The effect of increased calcium entry on hemodynamics, energy metabolism and histochemically estimated enzyme activities in isolated, perfused (Langendorff) rat heart preparation was investigated using calcium paradox (CaPX) as a model. After a 15 min period of stabilized perfusion of the heart, CaPX was induced at 37 degrees C by 2.5 min lasting calcium depletion (calcium-free perfusion) and subsequent calcium repletion (10 min). Changes induced by CaPX concerned loss of electrical and mechanical activities of the heart, significant decreases in coronary flow and ATP, ADP and the total content of adenine nucleotides in tissue as well as considerable depression in ATPases, SDH, beta-HBDH, LDH and glycogen phosphorylase activities in the myocardium. Diltiazem in concentration of 4.0 mumol.l-1 applied prior to calcium depletion and during calcium repletion prevented partially the deterioration of cardiac function by improving contractility and electrical activity of the heart as well as the coronary flow. The effect of diltiazem in concentration of 0.4 mumol.l-1 was less expressed. After both concentrations of diltiazem used, a better preserved ultrastructure, higher activities of the enzymes investigated, significantly higher ATP and total adenine nucleotide levels were seen in the myocardium as compared to the untreated controls.
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PMID:Partial prevention of calcium paradox in isolated perfused rat hearts by diltiazem. 252 34

The effects of i.v. nitroglycerin were studied by ECG and enzymatically in 16 patients (mean age 57.9 +/- 1.4 years) (NTG) in comparison with a control lot (c) of 17 patients (mean age 62.7 +/- 2.1 years) treated with dipyridamole and/or nifedipine (N), admitted in the first 4-10 hours after the onset of the first symptoms. The patients with heart failure and those with Q waves and CPK or LDH values greater than 2 x n were not admitted. NTG was administered in doses of 20 micrograms--60 microgram/hour for 24-96 hours and systolic AT (s) was kept under 10% of the basic values but not under 100 mmHg. Myocardial infarction appeared in 9 N-treated patients (54.86%) and 11 controls (58.25%) (p = 0.07). The size of myocardial necrosis was reduced in the N-treated patients. Peak serum CPK levels had considerably less increases in N (from 72.9 U to 73.4 U) (p greater than 00.5) versus C from 34.2 U to 364.5 U) (p less than 0.001). The sum of segmentary depression failed from 9.13 mm to 3.19 mm (p less than 0.05) in N, whereas in C the decrease was not significant (6.12 mm as against 9.38 mm; p greater than 0.05). The evolution was severe in C, as the angina crises (14 cases versus 2 cases, p less than 0.01) and the extension of the infarction (8 cases versus, 0; p 0.05) less than 0.05) appeared more frequently than in N. Only two patients in C died (p less than 0.05). Therefore, i.v. NTG administration in small doses in acute myocardial infarction leads to immediate disappearance of the anginal pain, lowers the extent of the myocardial necrosis and improves the clinical evolution.
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PMID:[The effects of nitroglycerin administered intravenously in acute myocardial ischemia]. 257 23

The changes of the serum biochemical features induced by cyanamide, a drug used in the pharmacological treatment of alcoholism, were studied in Wistar rats. Sixty five Wistar rats were divided into 6 groups, 4 experimental and 2 control. Two experimental groups received cyanamide intraperitoneally, at a dose of 1 and 16 mg per kg of body weight, for 8 weeks. One experimental group received CCl4 and the other one CCl4 and cyanamide for 13 weeks. In addition to a delay in the increase of body weight as compared with the control group, the rats receiving cyanamide underwent a marked dispersion of the transaminase and LDH values. This could be explained by the double effect of cyanamide: its capacity to depress the cellular activity (lowered synthesis of proteins, transaminase and LDH among them) and cellular damage. Therefore, some animals showed a marked depression of protein synthesis, causing low enzyme values while cytolysis prevailed in the rest as seen in higher enzyme values. When cyanamide and CCl4 were employed simultaneously, the cyanamide tended to diminish the higher enzyme values caused by CCl4 when used alone. These findings can explain why patients on cyanamide may develop severe liver damage without serious alterations in tests for liver function.
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PMID:Effect of cyanamide on transaminases and other serum proteins in the rat. 264 31

Effects of ulinastatin on operative stress in upper abdominal surgery were investigated. The operation caused damages to the body functions such as enhancement of protein catabolism, hepatic dysfunction and pancreatic dysfunction, followed by elevation of GOT, GPT, LDH and serum amylase. The operative stress also decreased the total lymphocyte and T cell counts in the peripheral blood, and attenuated the lymphocyte transformation induced by phytohaemagglutinin (PHA) and concanavalin A (Con A). Ulinastatin 7500 u.kg-1 failed to decrease the elevation of plasma enzyme levels and the depression of immune function. But ulinastatin had no immunosuppressive effect like glucocorticoid and attenuated the decrease in plasma levels of protein and albumin. The results suggest that ulinastatin has an effect in modulating the enhancement of protein catabolism by operative stress.
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PMID:[Effects of ulinastatin on operative stress in major surgery]. 272 19

The effect of iron loading on membrane potential and cellular contractility was examined in cultured heart cells obtained from newborn rat ventricles exposed to ferric ammonium citrate at iron concentrations of 20, 40, and 80 micrograms/ml for 24 hours. The main functional effect of iron loading was depression of the overshoot potential. Severe arrhythmias were encountered in two of eight studies with 40 micrograms/ml iron and in two of seven studies with 80 micrograms/ml iron, but they were not found in any of the 29 control studies (p less than 0.01). Iron loading also resulted in a significant enhancement of cellular LDH release, indicating a loss of cell membrane integrity. In vitro treatment of iron-loaded cells with deferoxamine, a selective iron-chelating compound, resulted in a striking reversal of the iron-induced depression in the plateau phase of action potential, the disappearance of arrhythmias, and a reduction in LDH leakage. These favorable effects of deferoxamine lend support to the contention that the observed abnormalities following iron-loading were specific expressions of iron toxicity. Although these observations are consistent with iron-induced peroxidative damage to membrane lipid components, further studies are required in order to elucidate the nature of such a putative membrane effect of excess iron.
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PMID:Effect of iron loading on transmembrane potential, contraction, and automaticity of rat ventricular muscle cells in culture. 290 44

In order to evaluate the enzymes CPK and LDH as potential biochemical markers of tricyclic antidepressant (TCA) cardiotoxicity, we prospectively followed 29 patients with TCA overdose. Serum CPK and LDH were obtained on all patients at admission. Population characteristics included a mean age of 33 y, a mean peak serum TCA concentration of 1190 ng/ml and mean maximal QRS interval of 0.10 sec. Seven patients (23%) had admission hypotension, 7 (23%) had severe respiratory depression, 6 (20%) had seizures and 4 (13%) had cardiac arrhythmias. One patient died. Mean admission CPK was 301 IU/L (nl less than 230 IU/L) while mean LDH was 221 IU/L (nl less than 250 IU/L). In 17 patients (57%), CPK remained in the normal range. There was no correlation between blood pressure, maximal QRS interval, serum TCA concentration, arrhythmias or seizures and CPK or LDH by regression analysis. CPK isoenzymes were obtained in 6 patients (both with and without severe myocardial dysfunction). One patient had an MB fraction of 10%; the remaining 5 had no measurable enzymes of myocardial origin. We conclude that modest elevations in CPK or LDH may occur after TCA overdose. These enzymes do not appear to originate from the myocardium and are of no utility in the assessment of antidepressant cardiotoxicity or prediction of clinical course.
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PMID:Serum enzyme disturbances after tricyclic antidepressant overdose. 292 29

The effects of phenol, guaiacol and m-cresol on erythrocytes, hepatocytes, dipalmitoyl phosphatidylcholine (DPPC)-liposomes and surface tension were studied at various concentrations. Phenol at 10 mM caused a slight inhibition of hypotonic hemolysis in rat erythrocytes. Guaiacol at 4 and 10 mM and m-cresol at 0.6 to 10 mM caused a significant inhibition of hypotonic hemolysis. In the enzyme leakage from isolated rat hepatocytes, phenol at 0.001 to 0.4 mM and 2 to 10 mM, guaiacol at 2 to 10 mM and m-cresol at 0.001 to 4 mM caused an inhibition in GOT leakage. The leakage of GPT from hepatocytes was inhibited by phenol at 0.4 to 10 mM, guaiacol at 2 to 10 mM, and m-cresol at 0.001 to 4 mM. m-Cresol at 10 mM caused increases in GOT and GPT leakage. The inhibition of phenol and m-cresol on the LDH leakage in hepatocytes were observed at a concentration of 0.001 mM and 0.1 to 1 mM, respectively. Guaiacol or m-cresol at 10 mM caused an increase in LDH leakage. Phase-transition temperature of DPPC-liposomes was depressed by phenol and m-cresol at 1 to 10 mM and by guaiacol at 5 and 10 mM. Guaiacol at 1 and 10 mM and m-cresol at 10 mM caused a depression of surface tension, but phenol caused no change in surface tension. The order of effects on erythrocyte, hepatocyte and DPPC-liposome membranes was m-cresol greater than phenol greater than or equal to guaiacol. In the present study, phenol and its related compound showed a positive correlation between their effects on various membranes and germicidal effects as evaluated by the phenol coefficient, but the effects were not related to a depression of surface tension.
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PMID:[Effects of phenol and related compounds on erythrocytes and hepatocytes from rats and dipalmitoyl phosphatidylcholine-liposomes]. 360 69

The effect of essential oils, eugenol, thymol and menthol, on erythrocytes, hepatocytes, dipalmitoyl phosphatidylcholine (DPPC)-liposomes and surface tension were studied at various concentrations. Maximal inhibition of eugenol, thymol and menthol on the hypotonic hemolysis in rat erythrocytes were observed at a concentration of 2 mM, 1 mM and 1 mM, respectively. Eugenol at 4 mM and thymol at 2 mM caused an acceleration of hypotonic hemolysis. In isolated rat hepatocytes, thymol caused an increase in GOT leakage, but eugenol at 4 mM and menthol at 0.1 and 0.4 mM inhibited the GOT leakage. The leakage of GPT from hepatocytes was inhibited by eugenol at 0.1 mM and 0.4 to 4 mM and menthol at 0.1 to 0.6 mM. The inhibition of eugenol and menthol on the LDH leakage in hepatocytes were observed at a concentration of 0.001 to 4 mM and 0.1, 0.4 and 0.6 mM, respectively. Thymol caused no change in GPT and LDH leakage. Eugenol, thymol and menthol indicated a depression of surface tension at a concentration of 0.1 mM. The rank by order of surface activity was eugenol greater than thymol. Eugenol, thymol and menthol depressed the phase-transition temperature of DPPC-liposomes. The depression of phase-transition temperature by thymol was greater than that by eugenol and menthol. These results suggest the periapical tissue damage produced by essential oils may be related to membrane lysis and surface activity and that their tissue penetration may be related to membrane affinity and lipid solubility.
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PMID:Effects of essential oils on erythrocytes and hepatocytes from rats and dipalmitoyl phosphatidylcholine-liposomes. 362 86


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