Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growing male rats were fed purified diets that contained either 0.6% or 0.1% calcium to investigate the relationship of calcium intake to the uptake, tissue distribution, and excretion of 109Cd. An equal number of rats were fed either the 0.6 or 0.1% calcium diets for 4 wk before they were used for experiments. In the first experiment 11 rats from each dietary group were administered 5 muCi 109Cd by stomach tube and were then maintained in metabolism cages for 72 hr. Animals fed the low-calcium diet took up more 109Cd, as significantly higher levels of radioactivity were found in the intestinal mucosa, serum, lungs, liver, kidneys, and urine and a significantly lower level was found in the feces. Higher levels of 109Cd, associated with low-molecular-weight proteins that may be related to the absorption process, were found in the intestinal mucosa of the low-calcium group. In the second experiment 10 rats from each dietary group were administered 5 muCi 109Cd by subcutaneous injection and then maintained in a metabolism cage for 72 hr. No significant differences were found in the distribution or excretion of 109Cd except for the lungs where radioactivity was greater in the low-calcium group. The results of the study indicate that the enhanced cadmium toxicity observed in calcium-deficient animals exposed to the heavy metal is the result of an increased uptake from the small intestine.
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PMID:Metabolism of 109Cd in rats fed normal and low-calcium diets. 96 16

Isolated protein kinase C (PKC) was irreversibly inactivated by a brief (min) incubation with calphostin C in the presence of light. This inactivation required Ca2+ either in a millimolar range in the absence of lipid activators or in a submicromolar range in the presence of lipid activators. In addition, an oxygen atmosphere was required suggesting the involvement of oxidation(s) in this inactivation process. Furthermore, PKC inactivation might involve a site-specific oxidative modification of the enzyme at the Ca(2+)-induced hydrophobic region. Physical quenchers of singlet oxygen such as lycopene, beta-carotene, and alpha-tocopherol all reduced the calphostin C-induced inactivation of PKC. In intact cells treated with calphostin C, the inactivation of PKC was rapid in the membrane fraction compared to cytosol. This intracellular PKC inactivation was also found to be irreversible. Therefore, calphostin C can bring prolonged effects for several hours in cells treated for a short time. Taken together these results suggest that the calphostin C-mediated inactivation of PKC involves a site-specific and a 'cage' type oxidative modification of PKC.
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PMID:Irreversible oxidative inactivation of protein kinase C by photosensitive inhibitor calphostin C. 128 Nov 16

Eight 6-week-old piglets were inoculated with a strain of encephalomyocarditis virus (EMCV) isolated from an outbreak which occurred naturally in the Po Valley in 1988. Two non-infected animals, kept in the same cage, were used as controls. Out of the eight inoculated piglets, two died and two were suppressed on the 2nd post infection day (PID), the four remaining were killed on the 5th, 7th, 11th and 15th PIDs. Control animals were killed at the end of the experiment. The pathogenesis of myocarditis has been studied using routine methods (Alcian-PAS, Masson's trichrome, Gomori's for reticulin and Mallory's stain), histochemical techniques (ATPase and NADH-TR reactions) and ultrastructural observations (TEM). All the inoculated piglets showed macro and/or microscopic lesions of lymphocytic myocarditis, only in one case associated with fibrinous exudation. One control piglet also showed myocarditic lesions, probably due to a contact infection. An early myocardial fibrosis was already present on the 5th PID. Ultrastructurally the cardiac muscle cells showed severe myofibrillar losses and other regressive alterations. Only on the 15th PID did we observe calcification of the degenerating myocytes, while ultrastructurally we detected needle-like calcium deposits in the mitochondria from the 5th PID. From the 5th PID in the areas of myocarditis the myocytes showed a reduction and/or absence of ATPase and NADH-TR reactions. On TEM, one or more aggregates of viral particles in crystalline array were detected in the cytoplasm of many endothelial cells.
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PMID:Ultrastructural study of experimental myocarditis induced by cardiovirus (EMCV-M) in swine. 132 99

The purpose of this study was to test the hypothesis that exercise training induces enhanced intracellular free Ca2+ (Cai) availability to the contractile elements of cardiac cells. Cai transients were directly measured in single isolated contracting ventricular myocytes from exercise-trained (EX) and sedentary control (SED) rats. Male Sprague-Dawley rats underwent 16 wk of progressive treadmill exercise (32 m/min, 8% grade, 1.5 h/day) (EX) or were cage confined (SED). EX rats had lower resting heart rate and elevated skeletal muscle oxidative capacity. Cai was measured with the fluorescent Cai indicator fura-2. Simultaneous video monitoring indicated that myocytes suspended in physiological salt solution were quiescent until stimulated electrically at a frequency of 0.2 Hz (12-36 V, 2-ms duration). Stimulated Cai transients, measured from changes in fura-2 fluorescence, were similar in cells from EX and SED groups. Peak shortening, time to peak shortening, velocity of shortening, contraction duration, and time to half-relaxation were also similar in cells from EX and SED rats. Ryanodine (10 microM) was applied to eliminate the contribution of Ca2+ release from sarcoplasmic reticulum to the Cai transient. Verapamil was applied to eliminate the contribution of voltage-gated Ca2+ channels to Cai transients. Cai transients were also similar in cells from EX and SED groups after these pharmacological interventions. These results suggest that treadmill training of rats does not alter Cai availability to the contractile elements in isolated ventricular myocytes.
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PMID:Effect of exercise training on intracellular free Ca2+ transients in ventricular myocytes of rats. 133 32

Paraneoplastic neurological syndromes are mostly associated with small cell lung cancer. Lambert-Eaton myasthenic syndrome appears to be caused by anti-presynaptic calcium channel antibodies. Calcium channels are also present in the cell membrane of small cell lung cancer, which may trigger the formation of anti-calcium channel antibodies. It is the most convincing argument in support of the auto-immune paraneoplastic theory, which refers to cross-antigenicity. Serum of patients with small cell carcinoma and cancer-associated retinopathy contains immunoglobulins against several antigens in the retinal and tumor cells. Patients with chronic intestinal pseudoobstruction (gastrointestinal neuropathy) associated with small cell lung cancer displayed circulating IgG antibodies reactive with neurons of myenteric plexus (anti-enteric neuronal antibodies). On the other hand, high levels of anti-neuronal antibodies (anti-Hu) have been found in the serum and cerebrospinal fluid of patients suffering from subacute encephalomyelitis (limbic encephalitis, cerebellar degeneration, sensory neuronopathy) associated with small cell lung cancer. The pathogenic role of the anti-neuronal antibody is not well established. Nevertheless, the finding of high titer antineuronal antibody in patients with a suggestive clinical syndrome is of great interest since it confirms the paraneoplastic syndrome and suggests the location of the primary tumor when the cancer is unknown.
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PMID:[Autoimmunity and cancer: paraneoplastic neurological syndromes associated with small cell cancer]. 133 87

The 23 kDa protein was localized by immunocytochemistry to photoreceptor cells of the mouse retina, and bovine and mouse cDNA clones were isolated and sequenced. The deduced amino acid sequences showed that the mouse 23 kDa protein is 91% identical to the bovine protein, and is the same as S-modulin, the CAR (cancer-associated retinopathy) protein and recoverin, the Ca(2+)-dependent activator of photoreceptor guanylate cyclase. The amino acid sequence reveals two Ca2+ binding sites, no internal repeats, 59% homology to the chicken visinin protein and 40% homology to calmodulin while Northern analysis demonstrated a single 1.0 kb mRNA species in bovine and mouse retina.
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PMID:Cloning and sequencing of the 23 kDa mouse photoreceptor cell-specific protein. 138 25

Pamidronate (aminopropylidene diphosphonate, APD) is known to be an effective agent in lowering plasma calcium in cancer associated hypercalcaemia and in primary hyperparathyroidism. Combined therapy with pamidronate and calcitonin has proved efficient in the treatment of severe cancer-associated hypercalcaemia. A 66-year-old woman in hypercalcaemic crisis caused by primary hypreparathyroidism was successfully treated with this combined therapy. Albumin corrected plasma calcium was 5.26 mmol/l on arrival and the PTH level was very high. The combined therapy lowered the plasma calcium to normal and made it possible to perform elective parathyreoidectomy. A 5.8 g parathyroid adenoma was removed. It is recommended to consider combined therapy with pamidronate and calcitonin in the emergency management of hypercalcaemic crisis.
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PMID:[Combination therapy with pamidronate and calcitonin in hypercalcemic crisis caused by primary hyperparathyroidism]. 146 41

Circulating N-terminal PTH-related protein (PTHrP), N-terminal PTH, and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in normal dogs and dogs with cancer-associated hypercalcemia (CAH), parathyroid adenomas, and miscellaneous tumors. PTHrP was undetectable (less than 1.8 pM) in normal dogs and increased in dogs with CAH due to adenocarcinomas derived from apocrine glands of the anal sac (44.9 +/- 27 pM), lymphoma (8.3 +/- 4.4 pM), and miscellaneous carcinomas (13.3 +/- 11.4 pM). The PTHrP concentration decreased in dogs with lymphoma and anal sac adenocarcinomas after successful treatment of CAH. The PTHrP concentration had a significant linear correlation with total serum calcium in dogs with anal sac adenocarcinomas and hypercalcemia, but not in dogs with lymphoma and hypercalcemia. Serum N-terminal PTH concentrations were usually in the normal range (12-34 pg/ml) for all groups of dogs except dogs with parathyroid adenomas (83 +/- 38 pg/ml). The serum PTH concentration increased after successful treatment of CAH. Serum 1,25-(OH)2D concentrations were decreased, normal, or increased in dogs with CAH, and 1,25-(OH)2D levels decreased after treatment of CAH. In summary, circulating concentrations of PTHrP are consistently increased in dogs with CAH, and PTHrP appears to play an important role in the induction of hypercalcemia.
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PMID:Parathyroid hormone (PTH)-related protein, PTH, and 1,25-dihydroxyvitamin D in dogs with cancer-associated hypercalcemia. 150 57

Parathyroid hormone and calcitonin, two major calcium-regulating hormones, were measured in the plasma of five experimental groups of rats to evaluate postflight calcium homeostasis after the 14-day COSMOS 2044 flight. Parathyroid hormone values were slightly higher in the flight animals (F) than in the appropriate cage and diet controls (S) (44 +/- 21 vs. 21 +/- 4 pg/ml, P less than 0.05), but they were the same as in the vivarium controls (V), which had different housing and feeding schedules. Neither V nor S showed the increase in plasma creatinine phosphorus and magnesium found in F, features of early renal insufficiency. F showed the lowest mean plasma calcitonin that was statistically different from V only. This difference in F and V (22 +/- 11 vs. 49 +/- 16 pg/ml, P less than 0.05) was most likely due to failure of circulating calcitonin in F to show the normal age-dependent increase we demonstrated in age-matched controls in a separate experiment. Basal values for parathyroid hormone and calcitonin were unchanged after 2 wk of hindlimb suspension, a flight simulation model, in age-matched and younger rats. From a time course experiment serum calcium was higher and parathyroid hormone lower after 4 wk than in ambulatory controls. Postflight circulating levels of parathyroid hormone appear to reflect disturbances in calcium homeostasis from impaired renal function of undetermined cause, whereas levels of calcitonin reflect depression of a normal growth process.
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PMID:Circulating parathyroid hormone and calcitonin in rats after spaceflight. 152 47

In single cells obtained by enzymic treatment of rabbit small-intestinal smooth muscle, and held under voltage clamp by patch pipette in the whole-cell recording mode, release of inositol trisphosphate (InsP3) from its caged precursor by flash photolysis caused complete inhibition of the voltage-dependent calcium current. No inhibition was seen in control experiments where the cage (2-nitrosoacetophenone) was released by flash photolysis from caged ATP. The inhibition by InsP3 of the calcium current was prevented if 10 mM EGTA or 2 mg/ml heparin was included in the pipette solution. Heparin is known to block InsP3 receptors. These results suggest that release of calcium stores by InsP3 raises Cai and that calcium ions inhibit the calcium current by acting either directly or otherwise on the internal mouth of the calcium channel.
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PMID:Inositol trisphosphate releases stored calcium to block voltage-dependent calcium channels in single smooth muscle cells. 165 41


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