Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Voltage-activated high- and low-threshold Ca2+ currents were studied using whole-cell voltage-clamp techniques and fura-2 fluorescence measurements of intracellular Ca2+ in neurons acutely isolated from rat neostriatum. High-threshold Ca2+ currents activated around -40 mV and were present in at least 95% of neostriatal neurons. The maximum current, 736 +/- 44 pA (mean +/- SEM, n = 141), was observed around 0 mV. In 70% of neurons, high-threshold Ca2+ currents exhibited both inactivating and noninactivating components. The majority of the high-threshold Ca2+ currents appeared to belong neither to the "L-type" nor the "N-type" classification, since omega-conotoxin (5 microM) decreased this current by only 29% and nimodipine (10 microM) decreased the noninactivating component of this current by only 17%. A low-threshold transient (T-type) Ca2+ current was observed in 40% of neurons. When both T-type and high-threshold Ca2+ currents were present, their maximum amplitudes were 78 +/- 7 pA and 800 +/- 57 pA, respectively (mean +/- SEM, n = 58). At a holding potential of -100 mV, the T-type Ca2+ current activated around -60 mV, with maximum current near -40 mV. Steady-state inactivation of the T-type Ca2+ current was observed at holding potentials positive to -125 mV, and the current was half-inactivated at -88 mV. Recovery from inactivation to 90% of maximum occurred within 800 msec. Mn2+ or Co2+ (3 mM) blocked both high-threshold and T-type Ca2+ currents, whereas Cd2+ (25 microM) or verapamil (50 microM and 150 microM) preferentially blocked high-threshold over T-type Ca2+ currents. In response to depolarization by 50 mM K+, fura-2 fluorescence measurements showed increased intracellular Ca2+ in both the soma and the proximal dendrites of neostriatal neurons that was markedly reduced by 25 microM Cd2+. These findings suggest that high-threshold Ca channels are present in both the soma and proximal dendrites of neostriatal neurons.
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PMID:Multiple types of calcium channels in acutely isolated rat neostriatal neurons. 838 36

The cobalt model of epilepsy, in combination with the C-14 2-deoxyglucose (2-DG) autoradiographic technique, was used to assess the effects of phenytoin (PHT) and ethosuximide (ESM), two antiepileptic drugs, and ketamine (KET), a drug with anticonvulsant properties, on brain activity. Nine days after the unilateral insertion of a cobalt rod into visual cortex, the nondrugged control rats showed the usual hypermetabolic regions of putative epileptogenic tissue both adjacent to the necrotic cortical cobalt rod implant zone and more distally in the connecting thalamus. PHT and ESM, given a single injections immediately before the 2-DG uptake and clearing period, diminished glucose uptake in the cobalt-induced hypermetabolic "patches" as well as in normal tissue. However, both drugs decreased 2-DG uptake more in the thalamic patches, than in the less hypermetabolic cortical patches, where the drug-induced depression in glucose metabolism was the same as for normal tissue. These findings suggest that PHT and ESM, regardless of their actions on cell receptors and membrane conductances, are ultimately of therapeutic value because more active nervous tissue (such as epileptic tissue) is more vulnerable to the depressing effects of these drugs than is less active tissue. KET, in contrast to PHT and ESM, did not depress metabolic activity throughout the brain generally and even clearly increased it in limbic system structures. Also in contrast to PHT and SEM, KET diminished activity in the cobalt-induced patches without reducing it in the normal tissue of the homotopic control regions. The more selective depressing action of KET, an N-methyl-D-aspartate (NMDA) antagonist, may be related to the role NMDA receptors play in supporting strong nervous activity. The discussion emphasizes the usefulness of a combined cobalt/2-DG approach to antiepileptic drug assessment.
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PMID:A combined cobalt and C-14 2-deoxyglucose approach to antiepileptic drug assessment. 882 60

Most reports of excellent long-term results of cemented total hip arthroplasty originate from studies of Charnley prostheses. A radiographic and clinical study was performed on 126 patients who underwent a cemented total hip arthroplasty from 1983 to 1985 with the Harris Design 2 prosthesis (Howmedica, Rutherford, NJ). The femoral component was cobalt-chromium and it had a broad, rounded medial border and a collar. The head diameter was 26 mm. A cemented all-polyethylene socket was used in all cases. At the last follow-up examination, 71% of the patients were completely free of pain and no patient had severe pain or pain at rest. Kaplan-Meier survival analysis estimated the revision rate at 10 years after operation to be 5 +/- 2% (mean +/- SEM) (including planned revisions). The rate of complete acetabular demarcation was 20% at 10 years, and femoral demarcation involving more than 50% of the bone-implant surface or endosteal cavitation was noted in only three cases. These results are as good as the best reported after total hip arthroplasty with the Charnley prosthesis.
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PMID:Outcome of total hip arthroplasties with cement. Results after implantation of the Harris Design 2 prosthesis, 1983-1985. 893 18

The uptake of 59Fe ascorbate by suspensions of human enterocytes prepared from endoscopically derived duodenal biopsies was studied, with each subject's serum ferritin concentration determined at the time of endoscopy. Iron uptake was greatest at 37 degrees C. Uptake increased from pH 5.5 to 7.3, before being totally inhibited at pH 9.0. However, ferrous ion concentration, determined by 3-(2-Pyridyl)-5,6-bis(4-phenyl sulfonic acid)-1,2,4-triazine, was greatest at pH 5.5 and fell over this pH range. The rate of uptake was significantly greater by enterocytes isolated from individuals with a low serum ferritin (< 22 ng/L) compared with those with normal serum ferritin (> 22 ng/L). Vmax +/- (SEM) was 78.7 +/- 8.5 pmol Fe/(micrograms DNA.min) in the normal group (n = 12) and 141 +/- 17.2 pmol Fe/(micrograms DNA.min) in the low ferritin group (n = 4, P < 0.008). Corresponding Km values were 52.5 +/- 11.7 and 66.7 +/- 5.1 mumol/L, respectively (P < 0.91). Zinc, lead, cobalt and manganese added to the incubation buffer significantly lowered iron uptake into cells (unselected patients). The concentrations of each metal required to halve the uptake rate from 50 mumol/L iron (IC50) were 85 +/- 5 mumol/L (Zn), 570 +/- 170 mumol/L (Pb), 1.1 +/- 0.1 mmol/L (Co), and 3.8 +/- 0.7 mmol/L (Mn). The results demonstrate that enterocytes isolated by this method show the characteristics of iron uptake seen in animal studies. We suggest that these cells will be useful in the study of iron uptake in humans.
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PMID:Iron uptake by isolated human enterocyte suspensions in vitro is dependent on body iron stores and inhibited by other metal cations. 904 May 63

Cobalt-chromium alloy porous coatings have become increasingly popular as a means of achieving a stable, longer lasting fixation on orthopedic implants. However, sintering heat treatments cause changes in the microstructure that result in changes in the corrosion behavior of the porous coatings. Experiments were conducted to examine the effects of microstructure on the corrosion of CoCr porous coatings. Four distinct microstructures were characterized. Light microscopy revealed microstructures A and B had relatively fewer carbides and a large-grain structure, microstructures C and D displayed a finer grain size with significant carbide formation, predominantly within grains and fusion zones. Accelerated anodic corrosion experiments were conducted to study the localized attack of each microstructure. Experiments were conducted using metallographically polished porous-coated disks for durations of 1, 4, 16, 24, and 72 h. The disks were examined with SEM and EDS to observe preferential attack and element depletion. Results showed a progressive dissolution of the matrix, with preferential attack of the grain boundaries and regions adjacent to the carbides due to sensitization. A precipitation layer was found to be Cr-rich and possibly composed of chromium hydroxide or a chromium orthophosphate. In addition, the solution became yellow in color with longer exposure times, possibly due to the presence of chromate ions, as indicated by an increased chromium level detected by AAS.
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PMID:Effects of microstructure on the corrosion behavior of CoCr porous coatings on orthopedic implants. 945 60

Adhesion of cells to a biomaterial surface can be a major factor mediating its biocompatibility. In this investigation, jet impingement techniques were used to quantify strength of cellular adhesion to various material surfaces. The metals tested: HS25 (a cobalt-based alloy similar to F75), 316L stainless steel, Ti-6Al-4V, and commercially pure tantalum, exhibited nearly a fivefold increase in adhesion strength above that characteristic of the polymeric materials tested (PTFE, silicone rubber, and HDPE). The present study examines physical and biological factors that might influence fibroblast adhesion to the biomaterial surface. The relation between surface charge and cellular adhesion was investigated in a controlled manner by measuring adhesion strength over a range of charge densities. The cells showed charge and electrical potential-dependent adhesion maxima, suggesting that surface alloying for optimum adherence may be possible. In a preliminary series of experiments adsorbed serum protein layers on a series of materials of differing adherence were investigated using gel electrophoresis to assess protein composition. Analysis of adsorbed proteins revealed little difference in relative abundance or total adsorption quantity. SEM micrographs of cells on Ti-6Al-4V and silicone rubber (high and low adhesion materials, respectively) demonstrated differences in cell morphology and cell density.
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PMID:Cell adhesion to biomaterials: correlations between surface charge, surface roughness, adsorbed protein, and cell morphology. 1017 29

Chronic beryllium disease (CBD) results from exposure to the light-weight metal beryllium (Be). In vitro stimulation of bronchoalveolar lavage cells from CBD subjects causes the production of high levels of TNF-alpha, IFN-gamma and IL-6. We tested the hypothesis that Be-stimulation might induce the production of TNF-alpha by macrophage cell lines. We observed that H36.12j cells (12j), a mouse hybrid macrophage cell line, but not other mouse and human macrophage cell lines, produced TNF-alpha upon Be-stimulation. The response was maximal at 100 microM BeSO4 and did not occur when 12j cells were stimulated with either aluminum sulfate or cobalt sulfate. Beryllium-stimulated the production of 725+/-25 pg/ml (mean +/- SEM) TNF-alpha protein by 12j cells as measured by ELISA of culture supernatants after 24 h. As measured by RT-PCR, Be-stimulated 12j cell TNF-alpha protein production was accompanied by an increased intracellular TNF-alpha mRNA at 3 and 24 h. The addition of 10U or 100U of rMu-IFN-gamma to Be-stimulated 12j cells further increased TNF-alpha production 1.5-4 fold (1.6+/-0.1 ng/ml) respectively. Bacterial lipopolysaccharide (LPS, 1 microg/ml) stimulated production of TNF-alpha in 12j culture supernatants after 6 h (515+/-151 pg/ml). This early versus late TNF-alpha production suggests that LPS and Be both stimulate 12j cell TNF-alpha synthesis, but through different pathways. We report for the first time, the direct effects of Be stimulation on the ability of 12j cells to produce TNF-alpha. The 12j cell line, contrasted with other macrophage hybrids that do not respond to Be-stimulation, may provide a useful tool to evaluate the mechanisms by which Be stimulates macrophage cytokine production, and by which T cell derived IFN-gamma amplifies TNF-alpha production in granulomatous diseases.
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PMID:Beryllium-stimulated production of tumor necrosis factor-alpha by a mouse hybrid macrophage cell line. 1075 10

Brain irradiation in prepubertal children with malignomas can cause precocious puberty. A selective cranial cobalt (Co(60))-irradiation technique has been developed in rats. In two experiments early juvenile (13-15 days old) female rats received a single dose of 5 Gy or sham irradiation. At pubertal age (post-natal days 33-34) irradiated rats had higher serum estradiol and luteinizing hormone levels. In experiment 1 irradiated rats had higher gonadotropin releasing-hormone (GnRH) mRNA levels in the preoptic area compared to controls (P<0.05). In experiment 2 the release rates of gamma-aminobutyric acid (GABA) in vitro from preoptic mediobasal hypothalamic areas of irradiated rats were significantly reduced after stimulation with the GABA(A) receptor agonist muscimol (maximum values 4607+/-804 vs. 7399+/-1048 pM in controls, mean+/-SEM, P<0.05). Radiation induced central precocious puberty might be caused by damage to inhibitory GABAergic neurons leading to premature activation of the GnRH-pulse generator.
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PMID:Reduction of gamma-aminobutyric acid-ergic neurotransmission as a putative mechanism of radiation induced activation of the gonadotropin releasing-hormone-pulse generator leading to precocious puberty in female rats. 1111 81

Hypoxia in the tubulointerstitium has been thought to play pivotal roles in the pathophysiology of acute renal failure and the progression of chronic kidney disease. Pre-induction of hypoxia-inducible and renoprotective gene expression may protect subsequent ischemic injury. This study evaluated the efficacy of cobalt, which inhibits HIF-1 degradation and increases the expression level of hypoxia-related genes, in an acute ischemic tubulointerstitial injury model of rats. Ischemic renal injury was induced by 45-min clamping of renal pedicles with contralateral nephrectomy. Elevation of serum creatinine and morphologic injury after the ischemic insult was observed. Administration of cobalt chloride afforded striking functional improvement (mean +/- SEM creatinine in mg/dl: Co treatment group, 2.14 +/- 1.21; control, 3.69 +/- 1.43; P < 0.05) associated with amelioration of tubulointerstitial damage. Cobalt treatment also reduced macrophage infiltration significantly. In the kidney of rats treated with cobalt, mRNA levels of several genes that serve for tissue protection, such as HO-1, EPO, Glut-1, and VEGF, were increased before ischemic injury. Upregulation of HO-1 by cobalt was confirmed at the protein level. Subcutaneous injection of cobalt also ameliorated ischemic injury, which was associated with upregulation of renal HIF-1alpha protein expression. These results suggest that protection against hypoxic tubulointerstitial injury by cobalt administration is mediated by induction of renoprotective gene expression. HIF induction is one possible and attractive explanation for the observed effects.
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PMID:Induction of renoprotective gene expression by cobalt ameliorates ischemic injury of the kidney in rats. 1281 42

The intercalation of Co(2+), [Co(NH(3))(6)](3+), and [Co(NH(3))(5)Cl](2+) ions into layered manganese oxide (birnessite) was studied by chemical, XRD, SEM, IR, and DTA-TG analyses. The intercalation reaction progressed by a 2:1 or 3:1 ion-exchange mechanism depending on the valence of the starting ions. The oxidation state of cobalt did not change with the intercalation reaction. The intercalation of [Co(NH(3))(6)](3+) ions resulted in an increase of basal spacing from 0.716 to 0.956 nm, giving a layered structure material consisting mainly of platelike particles. The chemical analysis results showed that the structure of [Co(NH(3))(6)](3+) ions was maintained in the interlayer. On the other hand, an H(2)O/NH(3) ligand exchange reaction progressed for the intercalation of [Co(NH(3))(5)Cl](2+) ions, resulting in an increase in the basal spacing from 0.716 to 0.956 nm.
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PMID:Intercalation of cobaltammine complex ions into layered manganese oxide. 1292 72


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