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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In animals models, exposure of the brain, heart, or kidneys to sublethal ischemia induces tolerance for subsequent ischemia. However, the ability of human renal cells to undergo hypoxic preconditioning has not been evaluated. In addition, it is unclear if renal ischemic preconditioning induces resistance at the cellular level, or if preconditioning is a result of altered postischemic hemodynamics or the azotemic environment. In this study, we tested the ability of cultured human proximal tubular epithelial cells (PTEC) to undergo hypoxic preconditioning at the cellular level. Hypoxia was induced by incubating cells in an anaerobic incubator in glucose-free buffer (combined oxygen-glucose deprivation; COGD). Cell injury was assessed by lactate dehydrogenase (LDH) efflux, release of arachidonic acid metabolites, and light microscopy. PTEC preconditioned with 12 h of COGD and a 24-h recovery period had less LDH efflux than control PTEC after subsequent exposure to 20 h of COGD (15.0 +/- 2.5% vs. 44.0 +/- 3.4%, p < 0.05). Preconditioned PTEC also retained relatively normal morphology and had less release of arachidonic acid metabolites than control PTEC. Because renal ischemia is characterized predominately by tubular injury with relative sparing of the glomerulus, we determined if PTEC are more susceptible to hypoxic injury than glomerular cells. For further comparison, we also assessed the susceptibility to hypoxia of the porcine tubular epithelial cell line LLC-PK1. After exposure to 18 h of COGD, LDH efflux from PTEC (25.5 +/- 3.3%, mean +/- SEM) was lower than from LLC-PK1 cells (47.6 +/- 4.0%; p < 0.01), but not mesangial cells (22.7 +/- 5.0%) or glomerular endothelial cells (38.2 +/- 6.2%). In conclusion, we have demonstrated that cultured PTEC are as resistant to hypoxic injury as glomerular cells, and that PTEC attain cytoresistance after hypoxic preconditioning. Characterization of the molecular changes that occur in human PTEC after hypoxic preconditioning may reveal innate survival mechanisms that can be manipulated to promote protection from renal ischemia in patients.
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PMID:Susceptibility of human proximal tubular cells to hypoxia: effect of hypoxic preconditioning and comparison to glomerular cells. 904 51

Whole-body hyperthermia is currently under investigation as a method to treat systemic malignancies; however, available techniques induce a derangement in serum and urine chemistries. This study was done to determine whether veno-venous perfusion induced hyperthermia (vv-PISH) that incorporated a parallel dialysis system to control blood chemistries would eliminate these heat induced derangements. Adult female Yorkshire swine were divided into perfusion only (group P, n = 6, 62.8 +/- 2.5 kg), and perfusion with dialysis (group PD, n = 6, 63.8 +/- 4.3 kg). In both groups, hyperthermia was induced with a computer assisted jugular-to-femoral venovenous heat exchange/perfusion system primed with a balanced electrolyte solution, operating at 30 ml/min-1/kg-1, which used a thermal gradient induced by blood heated to a maximum of 48 degrees C and a perfusate-to-blood temperature gradient < 10 degrees C during heating. The target core temperature was 43 degrees C for 120 min as measured by the average of the rectal, bladder, esophageal, bilateral tympanic, and pulmonary artery temperatures. Including ramp-up and cool down, the total perfusion interval was 263 +/- 29 min in group P and 240 +/- 18 min in group PD (ns). Serum and urine chemistry values expressed as the mean value +/- SEM were compared before and after hyperthermia treatment. Variables include blood urea nitrogen, creatinine, sodium, potassium, chloride, calcium, magnesium, phosphorus, glucose, total protein, albumin, alkaline phosphatase (ALKP), creatinine kinase, aspartate aminotransferase, alanine aminotransferase (ALT), lactate dehydrogenase (LDH), plasma free hemoglobin, urine specific gravity, pH and urine creatinine. All variables remained within normal ranges for the PD group. In the P group, the following final values were outside the normal range: (normal range) creatinine 2.1 +/- 1 (0.4-1.4) mg/dl, Ca2+ 5.1 +/- 1 (6-13) mg/dl, Mg2+ .8 +/- 0.1 (1.2-10) mg/dl, ALKP 134 +/- 6 (34-122) U/L, ALT 69 +/- 3 (9-51) U/L, and LDH 1291 +/- 237 (300-600) U/L. We conclude that the significant changes in serum and urine chemistries associated with vv-PISH are normalized with the use of a parallel dialysis system and may decrease the incidence of electrolyte associated complications.
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PMID:Parallel dialysis normalizes serum chemistries during venovenous perfusion induced hyperthermia. 936 Jan 58

Epidemiologic studies have reported associations between fine particulate air pollution, especially particles less than 10 mm in diameter (PM10), and the development of exacerbations of asthma and chronic obstructive pulmonary disease. However, the mechanism is unknown. We tested our hypothesis that PM10 induces oxidant stress, causing inflammation and injury to airway epithelium. We assessed the effects of intratracheal instillation of PM10 in rat lungs. The influx of inflammatory cells was measured in bronchoalveolar lavage (BAL). Airspace epithelial permeability was assessed as total protein in bronchoalveolar lavage fluid (BALF) in vivo. The oxidant properties of PM10 were determined by their ability to cause changes in reduced glutathione (GSH) and oxidized glutathione (GSSG). We also compared the effects of PM10 with those of fine (CB) and ultrafine (ufCB) carbon black particles. Six hours after intratracheal instillation of PM10, we noted an influx of neutrophils (up to 15% of total BAL cells) in the alveolar space, increased epithelial permeability, an increase in total protein in BALF from 0.39 +/- 0.01 to 0.62 +/- 0.01 mg/ml (mean +/- SEM) and increased lactate dehydrogenase concentrations in BALF. An even greater inflammatory response was observed after intratracheal instillation of ufCB, but not after CB instillation. PM10 had oxidant activity in vivo, as shown by decreased GSH in BALF (from 0.36 +/- 0.05 to 0.25 +/- 0.01 nmol/ml) after instillation. BAL leukocytes from rats treated with PM10 produced greater amounts of nitric oxide, measured as nitrite (control 3.07 +/- 0.33, treated 4.45 +/- 0.23 mM/1 x 10(6) cells) and tumor necrosis factor alpha (control 21.0 +/- 3.1, treated 179.2 +/- 29.4 unit/1 x 10(6) cells) in culture than BAL leukocytes obtained from control animals. These studies provide evidence that PM10 has free radical activity and causes lung inflammation and epithelial injury. These data support our hypothesis concerning the mechanism for the adverse effects of particulate air pollution on patients with airway diseases.
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PMID:In vivo and in vitro proinflammatory effects of particulate air pollution (PM10). 940 Jul 38

In an unselected group of patients with high-grade non-Hodgkin's lymphoma (HG-NHL) treated at our institution during a 10-year period (1986-1995), we studied treatment outcome and influence of possible prognostic factors. 187 HG-NHL patients were analysed retrospectively with regard to personal, treatment and disease-specific characteristics. Median age was 65 years and the male:female ratio was 1.2:1. Over a median follow-up of 57 months the overall response rate was 87% (complete response 72%, partial response 15%). The 2- and 5-year cumulative disease-specific survival rates were 64+/-4% (mean +/- SEM) and 48+/-5%, respectively. In a univariate analysis, the following variables were associated with prognosis in terms of survival: Patient age, clinical stage, performance status, bone-marrow infiltration, haemoglobin, erythrocyte sedimentation rate, lactate dehydrogenase (LDH), and serum albumin. In multivariate analyses, patient age, performance status, LDH, and haemoglobin came out as independent prognostic factors for survival.
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PMID:High-grade non-Hodgkin's lymphoma treated in northern Norway--treatment, outcome, and prognostic factors. 1009 Jun 99

The activity of muscle metabolic enzymes depends on the amount and type of physical training. We examined muscle enzyme adaptation to prolonged training followed by a period of lowered activity in spinal-cord-injured individuals (SCI). Ten SCI [mean age 35 (SEM 2) years, mean body mass 78 (SEM 4) kg, mean time post-injury 12 (SEM 2) years and range of lesion C5-T4] were given 12 months of functional electrical stimulation of an upright cycling motion for 30 min a day, three times a week, followed by 6 months of training once a week. Activities of glycolytic (hexokinase HK, lactate dehydrogenase LDH) and oxidative (citrate synthase CS, 3-hydroxyacyl-CoA dehydrogenase HAD) enzymes were determined in biopsies of the vastus lateralis muscle taken at 0, 3, 6, 12, and 18 months of training. The degree of sympathoadrenergic activity was evaluated from arterial concentrations of catecholamines in response to acute exercise. Training three times a week induced increases (P < 0.05) in HK (150%), LDH (40%), CS (100%), and HAD (70%) activities that reached a plateau after 3 months. Peak oxygen uptake and power output during exercise by electrical stimulation rose continuously over the first 12 months. After reducing the amount of training by two-thirds, HK, LDH and CS activities remained elevated above basal levels (P < 0.05), whereas HAD, power output and maximal oxygen uptake returned to pretraining levels (P > 0.05). It is concluded that most improvements in glycolytic and mitochondrial oxidative enzyme activities induced by long-term training can be maintained in spinal-cord-injured individuals despite a marked reduction in training frequency unrelated to performance or to the degree of sympathoadrenergic impairment.
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PMID:Muscle enzyme adaptation to training and tapering-off in spinal-cord-injured humans. 1141 39

An in vivo sulfur mustard (HD) vapor exposure model followed by bronchoalveolar lavage was developed previously in this laboratory to study biochemical indicators of HD-induced lung injury. This model was used to test two treatment compounds--niacinamide (NIA) and N-acetyl cysteine (NAC)--for their ability to ameliorate HD-induced biochemical changes. Anesthetized rats were intratracheally intubated and exposed to 0.35 mg of HD in 0.1 ml of ethanol or ethanol alone for 50 min. At the beginning of the exposure (t = 0), the rats were treated with either NIA (750 mg kg(-1)) or NAC (816 mg kg(-1)), i.p. At 24 h post-exposure, rats were euthanized and the lungs were lavaged with saline (three 5-ml washes). One milliliter of the recovered lavage fluid was analyzed for cellular components. The remaining fluid was centrifuged (10 min at 300 g) and the supernatant was assayed on a Cobas FARA clinical analyzer for lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), albumin (ALB), total protein (TP) and glutathione peroxidase (GP). The HD alone and HD+NIA treatment caused significant increases in all of the biochemical parameters compared with control levels. The NAC treatment yielded LDH, ALB and TP values that, although elevated, were not significantly different from the control. The GP levels were significantly higher than the control but significantly lower than the HD alone levels, indicating some protection compared with the HD alone group. The GGT levels were unaffected by NAC compared with HD alone. Cytological analysis of lavage fluid showed that the percentages of neutrophils were 5.3 +/- 1.0 (mean +/- SEM) for control, 46.6 +/- 4.5 for HD, 31.4 +/- 4.7 for HD + NIA and 21.6 +/- 4.7 for HD + NAC, respectively. The neutrophil counts were significantly higher for the three HD-exposed groups vs controls; however, the NAC-treated group had neutrophil counts lower than HD alone, indicating decreased inflammatory response. These results show that NAC may be useful as a potential treatment compound for HD-induced lung injury.
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PMID:Treatment of sulfur mustard (HD)-induced lung injury. 1142 23

The aim of this study was to evaluate effect of a short-acting neuroleptic (acepromazine) on capture stress response in roe deer (Capreolus capreolus). Sixteen roe deer were captured by drive-nets in the winters of 1998, 1999, and 2001. Roe deer were divided into two groups: animals in the treatment group received an intramuscular injection of acepromazine (0.093 mg/kg +/- 0.003 SEM; n = 8) while animals in the control group (n = 8) did not receive tranquilizer. Heart rate and body temperature, as well as hematologic and biochemical indicators of stress, were used to evaluate effect of the neuroleptic over 3 hr. Heart rate decreased over time after capture in both groups (P < 0.05), but stabilized sooner in the treated roe deer (75 min after capture) than in the controls (105 min after capture). Body temperature decreased over 45 min and then stabilized in both groups (P < 0.05). Comparisons of blood parameters revealed significantly lower red blood cell count (RBC), lymphocyte count, hemoglobin concentration, packed cell volume (PCV), and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) activities in tranquilized animals compared with controls (at least P < 0.05). A reduction in PCV, lymphocyte count, and serum cortisol concentrations (at least P < 0.05) and an increase in serum creatinine levels (P < 0.05) were recorded over time in control animals, while a reduction in RBC and hemoglobin concentration (at least P < 0.05) and an increase in serum urea concentrations (P < 0.05) over time were observed in the treated group. Finally, a decrease in serum lactate and potassium levels and an increase in CK, AST, ALT, and LDH activities were recorded over time in both groups. Results obtained showed the suitability of using acepromazine in capture operations in order to reduce stress response and prevent its adverse effects in roe deer. The beneficial effect was not only due to the sedative effect of acepromazine, but also to peripheral vasodilatation.
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PMID:Effects of acepromazine on capture stress in roe deer (Capreolus capreolus). 1291 Jul 65

The biocompatibility of titania/hydroxyapatite (TiO(2)HA) composite coatings, at different ratio obtained by sol-gel process, was investigated studying the behavior of primary cultures of rat osteoblastic cells, isolated by femoral trabecular bone tissue. Moreover, the results have been compared with the response of human osteoblast-like MG63 cell line. Cytotoxicity of coatings was assessed by lactate dehydrogenase activity (LDH). The cellular behavior was analyzed by the cell proliferation (MTT test), cell morphology (SEM) and the biochemical markers evaluation of osteoblastic phenotype, such as alkaline phosphatase activity (ALP) and osteocalcin production. The results showed that TiO(2)/HA coatings have no toxic effects and seemed to be a good support for cell adhesion and proliferation. Moreover, these materials allowed the differentiation of osteoblasts, stimulating the expression of alkaline phosphatase activity. The responses of the primary rat osteoblasts and human osteoblast-like MG63 cell line grown onto these coatings were similar in terms of proliferation and ALP activity. Differences were found considering the osteocalcin production. The results show that these coatings, thanks to their chemical composition and the deposition technique, are very promising for the potential orthopedic and dental applications.
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PMID:In vitro response of primary rat osteoblasts to titania/hydroxyapatite coatings compared with transformed human osteoblast-like cells. 1534 68

Nitric oxide (NO) is the mediator of ischemic preconditioning against myocardial infarction. Desflurane produces anesthetic preconditioning to protect the myocardium against infarction. In the model of myocardial ischemia-reperfusion injury in rabbits, we evaluated desflurane-induced ischemic preconditioning and studied its mechanism of NO synthesis. Thirty-two male adult New Zealand white rabbits were anesthetized with intravenous (IV) 30 mg/kg pentobarbital followed by 5 mg/kg/hr infusion. All rabbits were subjected to 30 minutes (min) long lasting left anterior descending coronary artery (LAD) occlusion and three hours (hr) of subsequent reperfusion. Before LAD occlusion, the rabbits were randomly allocated into four groups for preconditioning treatment (eight for each group). The control group did not receive any preconditioning treatment. The desflurane group received inhaled desflurane 1.0 MAC (minimal end-tidal alveolar concentration) for 30 min that was followed by a 15 min washout period. The L-NAME-desflurane group received L-NAME (NG-nitro-L-arginine methyl ester; non-selective Nitric Oxide Synthetase (NOS) inhibitor) 1 mg/kg IV 15 min before 1.0 MAC inhaled desflurane for 30 min. The L-NAME group received L-NAME 1 mg/kg IV. Infarct volume, ventricular arrhythmia, plasma lactate dehydrogenase (LDH), creatine kinase (CK) activity and myocardial perfusion were recorded simultaneously. We have found that hemodynamic values of the coronary blood flow before, during, and after LAD occlusion were not significantly different among these four groups. For the myocardial ischemia-reperfusion injury animals, the infarction size (mean +/- SEM) in the desflurane group was significantly reduced to 18 +/- 3% in the area at risk as compared with 42 +/- 7% in the control group, 35 +/- 6 in the L-NAME group, and 34 +/- 4% in the L-NAME-desflurane group. The plasma LDH, CK levels, and duration of ventricular arrhythmia were also significantly decreased in the desflurane group during ischemia-reperfusion injury. Our results indicate that desflurane is an anesthetic preconditioning agent, which could protect the myocardium against the ischemia-reperfusion injury. This beneficial effect of desflurane on the ischemic preconditioning is probably through NO release since L-NAME abrogates the desflurane preconditioning effect.
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PMID:Effect of desflurane-induced preconditioning following ischemia-reperfusion on nitric oxide release in rabbits. 1556 90

Non-Hodgkin's lymphomas (nHL) is a heterogenous group of lymphoid malignancies with different patterns of behaviour and response to treatment. International Prognostic Index (IPI) is commonly used to predict outcome of treatment in nHL. There are several reports that vascular endothelial growth factor (VEGF), the most potent inducer of angiogenesis, may have prognostic significance in nHL. The aim of the study was to evaluate the serum level of VEGF as a marker of angiogenesis in 35 patients with B-cell nHL compared with control group of 14 healthy people. Moreover, in nHL group VEGF serum level was correlated with IPI risk factors. VEGF serum level was evaluated by ChemiKine sandwich ELISA kit (Chemicon International). VEGF serum level was significantly higher in nHL group than in the control, 193.78 pg/ml +/- 6.82 SEM and 31.51 +/- 1.67 SEM respectively. In nHL group a positive correlation was found between increased VEGF serum level and serum lactate dehydrogenase level. The levels of VEGF were not significantly different in agressive or indolent nHL patients. VEGF serum level is increased in active lymphoma. This observation may have prognostic and clinical significance and provides rationale for use antiangiogenic agents in nHL therapy.
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PMID:[Vascular endothelial growth factor (VEGF) serum concentration in non-Hodgkin's lymphoma patients]. 1567 66


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