Human ; Female ; Aged ; Brain Diseases ; Calcium Metabolism Disorders ; Spasm ; Angiotensins ; Hypocalcemia

We characterized and compared the characteristics of Ca2+ movements through the sarcoplasmic reticulum of inferior oblique muscles in the various conditions including primary inferior oblique overaction (IOOA), secondary IOOA, and controls, so as to further understand the pathogenesis of primary IOOA. Of 15 specimens obtained through inferior oblique myectomy, six were from primary IOOA, 6 from secondary IOOA, and the remaining 3 were controls from enucleated eyes. Ryanodine binding assays were performed, and Ca2+ uptake rates, calsequestrins and SERCA levels were determined. Ryanodine bindings and sarcoplasmic reticulum Ca2+ uptake rates were significantly decreased in primary IOOA (p < 0.05). Western blot analysis conducted to quantify calsequestrins and SERCA, found no significant difference between primary IOOA, secondary IOOA, and the controls. Increased intracellular Ca2+ concentration due to reduced sarcoplasmic reticulum Ca2+ uptake may play a role in primary IOOA.
Sarcoplasmic Reticulum Calcium-Transporting ATPases ; Sarcoplasmic Reticulum/*metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Ryanodine/metabolism ; Oxalates/metabolism ; Oculomotor Muscles ; Ocular Motility Disorders/*metabolism/*pathology ; Muscles/*pathology ; Models, Statistical ; Middle Aged ; Male ; Humans ; Female ; Child, Preschool ; Child ; Calsequestrin/metabolism ; Calcium-Transporting ATPases/metabolism ; Calcium/metabolism/*pharmacokinetics ; Blotting, Western ; Aged ; Adult ; Adolescent

OBJECTIVETo study the protection of stress protein calreticulin (CRT) in rat skeletal muscle during the adaptation mechanism of calmodulin in the course of heat treatment.

METHODSIncreased heat treatment program would be applied, 40 SD rats were randomly divided into the quiet control group C (n = 8) and heat-treated group H (n = 32), then the heat treatment group would be divided into immediately group (H1), 24-hour post-heat treatment group (H2), 48 -hour post-heat treatment group (H3) and six days post-heat treatment group (H4) (n = 8).

RESULTSAfter heat treatment, the Ca(2+)-ATP activity in rat skeletal muscle sarcoplasmic reticulum in H2 group reached the highest value compared with that in the quiet control group C (P < 0.01), and the value in H1 group showed significant differences compared with control group C (P < 0.05); The Ca(2+)-ATP activity in mitochondrial had the highest value in H1 group, compared with the quiet control group C (P < 0.05), while the Ca2+ concentration in rat skeletal muscle sarcoplasmic reticulum had the highest in group H2, followed by H1 group, both showing significant difference compared with the quiet control group (P < 0.05); The Ca2+ concentration in mitochondrial was high in H1 and H2 group than that of the quiet control group C, and the value in H3 and H4 group was lower than that of the quiet control group C, which had no difference; After heat treatment, the expression of stress proteins of CRT from H1, H2 and H3 group in rat skeletal muscle increased significantly compared with quiet group C.

CONCLUSIONIn the process of increased heat treatment, calreticulin played the regulatory role on the imbalance of calcium homeostasis in skeletal muscle cells, and the adaptation protection from the thermal stimulation could have the very good effect on muscle.

Adaptation, Physiological ; Animals ; Calcium ; metabolism ; Calreticulin ; physiology ; Heat Stress Disorders ; metabolism ; physiopathology ; Male ; Mitochondria ; metabolism ; Muscle, Skeletal ; metabolism ; physiology ; Rats ; Rats, Sprague-Dawley ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; metabolism

Primary hyperparathyroidism (PHPT) is imbalance of calcium, phosphate, and bone metabolism attributed to an increased secretion of parathyroid hormone (PTH). Although PHPT is mainly associated with musculoskeletal and kidney dysfunction, variable symptoms can be presented in the elderly patients. A 75-year-old man presented with rapidly progressive dementia (RPD). Through etiological work-up of hypercalcemia and increased PTH, parathyroid adenoma was found. Subtotal parathyroidectomy resulted in recovery of cognitive impairment. Primary hyperparathyroidism should be considered in a differential diagnosis of RPD.
Aged ; Calcium ; Cognition Disorders ; Dementia* ; Diagnosis, Differential ; Humans ; Hypercalcemia ; Hyperparathyroidism ; Hyperparathyroidism, Primary* ; Kidney ; Metabolism ; Parathyroid Hormone ; Parathyroid Neoplasms ; Parathyroidectomy

PURPOSE: Bilateral high signal intensity in basal ganglia on Tl-weighted images is unusual. the purpose of this study is to describe the pattern of high signal intensity and underlying disease. METHODS AND MATERIALS: During the last three years, 8 patients showed bilateral high signal intensity in basal ganglia on Tl-weighted image, as compared with cerebral white matter. Authors analized the images and underlying causes retrospectively. Of 8 patients, 5 were male and 3 were female. The age ranged from 15 days to 79 years. All patient were examined by a 0.5T superconductive MRI. Images were obtained by spin echo multislice technique. RESULTS: Underlying causes were 4 cases of hepatopathy, 2 cases of calcium metabolism disorder, and one case each of neurofibromatosis and hypoxic brain injury. These process were bilateral in all cases and usually symmetric. In all cases the hyperintense areas were generally homogenous without mass effect or edema, although somewhat nodular appearence was seen in neurofibromatosis. Lesions were located in the globus pallidus and internal capsule in hepatopathy and neurofibromatosis, head of the caudate nucleus in disorder of calcum metabolism, and the globus pallidus in hypoxic brain injury. CONCLUSION: Although this study is limited by its patient population, bilateral hyperintense basal ganglia is associated with various disease entities. On analysis of hyperintense basal ganglia lesion, the knowledge of clinical information improved diagnostic accuracy.
Basal Ganglia* ; Brain ; Brain Injuries ; Calcium Metabolism Disorders ; Caudate Nucleus ; Edema ; Female ; Ganglia ; Globus Pallidus ; Head ; Humans ; Internal Capsule ; Magnetic Resonance Imaging ; Male ; Metabolism ; Neurofibromatoses ; Retrospective Studies

The present study was aimed at determining the effects of Tongqiao Huoxue Decoction (TQHXD) on the Ca(2+)-CaMKII-CREB pathway and the memory and learning capacities of rats with vascular dementia (VD). The rat VD model was established by using an improved bilateral carotid artery ligation method. The Morris water maze experiment was used to evaluate the ethology of the VD rats following treatments with TQHXD at 3.01, 6.02, and 12.04 g·kg(-1) per day for 31 days. At the end of experiment, the hippocampus were harvested and analyzed. Western blotting and RT-PCR were used to measure the expression levels of calmodulin-binding protein kinase II(CaMKII), protein kinase A(PKA), cAMP-response element binding protein(CREB), and three N-methyl-D-aspartic acid receptor subunits (NR1, NR2A, and NR2B). Our results revealed that TQHXD could alleviate the loss of learning abilities and increase the memory capacity (P < 0.05 and P < 0.01 vs the model group, respectively). The treatment with 6.02 and 12.04 g·kg(-1) of TQHXD significantly up-regulated the Ca(2+)-CaMKII-CREB pathway in the hippocampus. In conclusion, TQHXD showed therapeutic effects on a bilateral carotid artery ligation-induced vascular dementia model, through the up-regulation of calcium signalling pathways.
Animals ; Calcium ; metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; metabolism ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Dementia, Vascular ; complications ; drug therapy ; metabolism ; psychology ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Hippocampus ; drug effects ; metabolism ; Learning Disabilities ; drug therapy ; etiology ; metabolism ; Male ; Maze Learning ; drug effects ; Memory ; drug effects ; Memory Disorders ; drug therapy ; etiology ; metabolism ; Phytotherapy ; Rats, Sprague-Dawley ; Signal Transduction ; Up-Regulation

OBJECTIVE: Serum parameters of calcium homeostasis were measured based on previously published evidence linking osteoporotic fractures and/or bone/mineral loss with antipsychotics. METHODS: Prospective, four-week, time-series trial was conducted and study population consisted of patients of both genders, aged 35-85 years, admitted within the routine practice, with acute psychotic symptoms, to whom an antipsychotic drug was either introduced or substituted. Serial measurements of serum calcium, phosphorous, magnesium, 25(OH)D, parathyroid hormone, calcitonin, osteocalcin and C-telopeptide were made from patient venous blood samples. RESULTS: Calcium serum concentrations significantly decreased from baseline to the fourth week (2.42+/-0.12 vs. 2.33+/-0.16 mmol/L, p=0.022, n=25). The mean of all calcemia changes from the baseline was -2.6+/-5.7% (-24.1 to 7.7) with more decreases than increases (78 vs. 49, p=0.010) and more patents having negative sum of calcemia changes from baseline (n=28) than positive ones (n=10) (p=0.004). There were simultaneous falls of calcium and magnesium from baseline (63/15 vs. 23/26, p<0.001; OR=4.75, 95% CI 2.14-10.51), phosphorous (45/33 vs. 9/40, p<0.001; 6.06, 2.59-14.20) and 25(OH)D concentrations (57/21 vs. 13/35, p<0.001; 7.31, 3.25-16.42), respectively. Calcemia positively correlated with magnesemia, phosphatemia and 25(OH)D values. Parathyroid hormone and C-telopeptide showed only subtle oscillations of their absolute concentrations or changes from baseline; calcitonin and osteocalcin did not change. Adjustment of final calcemia trend (depletion/accumulation) for relevant risk factors, generally, did not change the results. CONCLUSION: In patients with psychotic disorders and several risks for bone metabolism disturbances antipsychotic treatment was associated with the decrease of calcemia and changes in levels of the associated ions.
Antipsychotic Agents* ; Blood Chemical Analysis ; Bone and Bones ; Calcitonin ; Calcium* ; Homeostasis ; Humans ; Ions ; Magnesium ; Metabolism* ; Minerals ; Osteocalcin ; Osteoporotic Fractures ; Parathyroid Hormone ; Prospective Studies ; Psychotic Disorders ; Risk Factors

OBJECTIVETo examine the effects of Pb2+ on N-methyl-D-aspartate (NMDA)-, K(+)- and quisqualate(QA)/kainite(KA)-induced increases in intracellular free calcium concentration ([Ca2+]i) in cultured fetal rat hippocampal neurons in order to explain the cognitive and learning deficits produced by this heavy metal.

METHODSLaser scanning confocal microscopy was used.

RESULTSThe results clearly demonstrated that adding Pb2+ before or after NMDA/glycine stimulation selectively inhibited the stimulated increases in [Ca2+]i in a concentration-dependent manner. In contrast, Pb2+ treatment did not markedly affect increases in [Ca2+]i induced by an admixture of QA and KA. The minimal inhibitory effect of Pb2+ occurred at 1 mumol/L, and more than seventy percent abolition of the NMDA-stimulated increase in [Ca2+]i was observed at 100 mumol/L Pb2+. Evaluation of Pb(2+)-induced increase in [Ca2+]i response to elevating extracellular concentrations of NMDA, glycine or calcium revealed that Pb2+ was a noncompetitive antagonist of both NMDA and glycine, and a competitive antagonist of Ca2+ at NMDA receptor channels. In addition, Pb2+ inhibited depolarization-evoked increases in [Ca2+]i mediated by K+ stimulation (30 mumol/L), indicating that Pb2+ also depressed the voltage-dependent calcium channels. Also, the results showed that Pb2+ appeared to be able to elevate the resting levels of [Ca2+]i in cultured neurons, implying a reason for Pb(2+)-enhanced spontaneous release of several neurotransmitters reported in several previous studies.

CONCLUSIONLead can inhibit NMDA-, K(+)-, QA/KA-induced increases in intracellular [Ca2+]i in cultured hippocampal neurons.

Animals ; Calcium ; metabolism ; Cognition Disorders ; chemically induced ; Disease Models, Animal ; Hippocampus ; physiology ; Kainic Acid ; pharmacology ; Lead ; adverse effects ; Learning Disorders ; chemically induced ; Microscopy, Confocal ; N-Methylaspartate ; pharmacology ; Neurons ; physiology ; Potassium ; pharmacology ; Quisqualic Acid ; pharmacology ; Rats ; Rats, Wistar

OBJECTIVES: Phencyclidine(PCP) or PCP-like substances such as ketamine have been know to rekindle the cognitive dysfunction in schizophrenia. The aims of this study were to identify whether PCP-like substances can produce cognitive deficit in schizophrenia, to discuss relation with aging process, and finally to speculate underlying neurochemical mecha-nisms by various drug responses. METHODS: In experiment I, radial maze tests were done in 24 Sprague-Dawley rats for 3 days to get baseline data. Being divided into 4 groups(6 rats respectively) of normal aged, normal adult controls, atropine-treated and ketamine-treated, the radial maze tests were repeated on every week for 6 weeks, and then the rats were sacrificed by intracardiac perfusion with phosphate-buffered 10% formaldehyde solution for histology. The brain specimen was stained with hematoxylin-eosin to count cells in the prefrontal cortex and hippocampus. In experiment II, radial maze tests were done for 48 rats before any drug treatment and only after ketamine administration. Thereafter, haloperidol, bromocriptine, clonidine, nimodipine, tacrine, valproic acid, naloxone and fluoxetine were intramuscularly injected on every other day in addition to ketamine. Radial maze tests were repeated on every week for 6 weeks, and then rats were prepared by the same procedure for histology. RESULTS: 1) Reaction times of radial maze tests of atropine-treated rats were significantly prolonged than those of normal aged(p<0.05) or normal adult controls(p<0.05). Cell numbers of prefrontal cortex & hippocampus in ketamine-treated rats were significantly reduced than those in normal aged(p<0.05) or normal adult controls(p<0.005). 2) Reduced cell numbers by ketamine became significantly raised by tacrine administration in prefrontal cortex $ hippocampus(p<0.05), while there were no significant changes on radial maze test. Cell numbers also tended to be raised by nimodipine, fluoxetine and haloperidol administration. CONCLUSIONS: In conclusion, the visuospatial memory disorders in ketamine-induced psychotic rats might be partly associated with aging process. Furthermore, the responses to the various drugs suggested cholinergic system might have an important role in the neurochemical mechanism of the cognitive dysfunction in ketamine-induced psychosis. Otherwise, calcium metabolism as well as serotonergic and dopaminergic systems seemed to be possibly related.
Acetylcholine ; Adult ; Aging* ; Animals* ; Brain ; Bromocriptine ; Calcium ; Cell Count ; Clonidine ; Fluoxetine ; Formaldehyde ; Haloperidol ; Hippocampus ; Humans ; Ketamine ; Memory Disorders ; Metabolism ; Models, Animal* ; Naloxone ; Nimodipine ; Perfusion ; Prefrontal Cortex ; Psychotic Disorders ; Rats ; Rats, Sprague-Dawley ; Reaction Time ; Schizophrenia* ; Tacrine ; Valproic Acid

Child ; Child Behavior Disorders ; etiology ; Child, Preschool ; Encephalitis ; complications ; metabolism ; virology ; Enterovirus ; Female ; Humans ; Infant ; Male ; Nerve Growth Factors ; metabolism ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins ; metabolism