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Biomedical subjects

M Chou

Publications and source records attributed to M Chou.

33 records · Page 2Linked to original sources
PubMed1996

A receptor in pituitary and hypothalamus that functions in growth hormone release.

Small synthetic molecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to stimulate and amplify pulsatile growth hormone (GH) release. A heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPC-R) of the pituitary and arcuate ventro-medial and infundibular hypothalamus of swine and humans was cloned and was shown to be the target of the GHSs. On the basis of its pharmacological and molecular characterization, this GPC-R defines a neuroendocrine pathway for the control of pulsatile GH release and supports the notion that the GHSs mimic an undiscovered hormone.

Amino Acid Sequence↗
PubMed1995

Interferon-alpha 2 variants in the human genome.

Variants of human leukocyte interferon alpha 2 (IFN-alpha 2a, alpha 2b, and alpha 2c) differ from each other by changes in their coding regions at nucleotide positions 137 and 170. As a result of these nucleotide variations, the DNA sequences of the three variants can be distinguished by selective restriction enzyme analysis. Human genomic DNA obtained from over 28,000 normal healthy individuals was used as templates in the polymerase chain reaction (PCR) to amplify the human IFN-alpha 2 gene sequence. The resulting PCR products were analyzed with restriction nucleases to identify the specific IFN-alpha 2 variant sequences present in the genomic DNA of the population examined. The results show that IFN-alpha 2b was detected as the predominant species and IFN-alpha 2c as a very minor species (< 0.1%). The IFN-alpha 2a gene was not detected in this population.

Alleles↗
PubMed1992

Modulation of chemical toxicity by modification of caloric intake.

Caloric restriction increases maximum achievable lifespan and offsets the time to development of degenerative disease. Part of these desirable effects may result from positive modulation of toxic events. We have shown that when rodents are placed on a diet that is reduced in total calories by 40%, several beneficial changes on biochemical systems which impact on toxicologic processes are positively enhanced. Lipid metabolism is reduced and, therefore, the potential for lipoperoxidation is reduced. Additionally, activity of enzymes that produce free radicals as byproducts (cytochrome P4502C11) are also reduced. Concurrently, we have shown that the "effective" activity of catalase and the activity of superoxide dismutase (which are required for the detoxification of toxic oxygen radicals) are significantly increased by caloric restriction. The activities of enzymes of drug and xenobiotic metabolism are also altered by caloric restriction. The effect upon activity may be to either decrease or increase activity, dependent upon whether the enzyme activates compounds to intermediates which may be more toxic or whether the enzyme acts to reduce toxicity. We have also shown that caloric restriction may affect the initiation stage of carcinogenesis. Aflatoxin B1 binding to hepatic nuclear DNA was reduced by caloric restriction (caloric restriction reduced both major adducts that are formed upon exposure to aflatoxin B1). caloric restriction also reduced cytochrome P4502C11 which converts aflatoxin B1 to its toxic epoxide, and may partly explain the reduction in binding. These results suggest that caloric restriction may, in part, extend the time to development of degenerative disease by altering basic biochemical mechanisms of toxicity.

Animals↗
PubMed1991

The scoring system for early technetium-99m pyrophosphate scintigraphy as a method of evaluation of limiting the myocardial infarct size by thrombolysis.

The usefulness of a scoring system with early technetium-99m pyrophosphate scintigraphy as a method for evaluating the efficacy of myocardial preservation after thrombolysis was studied. The mean time from the onset of acute myocardial infarction to injection of the tracer was 5.6 +/- 1.5 h (range 2.8 to 11.9 h). All 36 patients underwent successful recanalization. Patients with strongly positive technetium-99m pyrophosphate uptake in anterior acute myocardial infarction had a significantly lower regional ejection fraction and a significantly larger thallium-201 defect score than those with 2+ positive results in chronic stage. Similarly, in inferior acute myocardial infarction, the thallium-201 defect score was significantly larger in patients with strongly positive uptake than in those with 2+ and negative uptake scores. In conclusion, strongly positive results in early technetium-99m pyrophosphate scintigraphy within 12h after the onset of acute myocardial infarction may indicate failure in limiting the infarct size by coronary thrombolysis.

Aged↗
PubMed1989

Stereospecific effects of a kappa-opiate antagonist on the actions of morphine in morphine-tolerant rats.

The effects of kappa-opiate receptor antagonist, MR 2266 and its dextro isomer, MR 2267 on morphine-induced analgesia and changes in colonic temperature were determined in morphine-naive and morphine-tolerant male Sprague-Dawley rats. Intraperitoneal administration of morphine (8 mg/kg) produced analgesia and hyperthermia in morphine-naive rats. MR 2266 (0.3-3.0 mg/kg) antagonized morphine-induced analgesia and hyperthermia in morphine-naive rates but MR 2267 was inactive. Subcutaneous implantation of six morphine pellets during a 7 day period induced tolerance to the analgesic and hyperthermic effects of morphine in the rat. MR 2266 also antagonized morphine analgesia and hyperthermia in morphine-tolerant rats, however, MR 2267 had no effect. A high dose (3 mg/kg) of MR 2266 produced an intense hypothermic response in morphine-tolerant rats. Previously we have shown that kappa-opiate receptor agonists antagonize morphine analgesia in morphine-naive rats but potentiate it in morphine-tolerant rats. The results of the present studies indicate that the antagonist of kappa-opiate receptors, on the other hand, antagonize morphine effects in both morphine-naive and morphine-tolerant rats in a stereospecific manner.

Analgesia↗
PubMed1989

Plant cells contain calsequestrin.

Calsequestrin is a high capacity low affinity Ca2+-binding protein thought to be essential for the function of the intracellular rapid releasable Ca2+ pool of a variety of animal cells. Here we show that two types of plant tissues, cultured Streptanthus tortuosus cells and spinach leaves, contain a form of calsequestrin. In subcellular fractions of S. tortuosus cells, Stains-all staining reveals a metachromatically blue-staining 56,000-Da protein enriched in the microsomal fraction. This protein shares several biochemical characteristics with animal calsequestrin: 1) it changes its apparent molecular weight with the pH; 2) it is able to bind 45Ca2+ on nitrocellulose transfers; and 3) it is recognized by antibodies against canine cardiac calsequestrin. Calsequestrin was also identified in spinach leaves using a direct extraction procedure that was developed for muscle calsequestrin. Thus, our results demonstrate that plant cells contain calsequestrin within a subcellular membrane fraction. These results also suggest that calsequestrin is an ubiquitous protein rather than being limited only to animal cells.

Animals↗
PubMed1989

Thermotolerance of isolated mitochondria associated with heat shock proteins.

Mitochondria isolated from 2-day-old etiolated soybean (Glycine max) seedlings which had been subjected to various heat shock treatments, i.e. (A) 28 degrees C (2 h), (B) 38 degrees C (2 h), (C) 38 degrees C (2 h)-42.5 degrees C (0.5 h), and (D) 38 degrees C (2 h)-42.5 degrees C (0.5 h)-28 degrees C (4 h), were monitored for O(2) uptake using an oxygen electrode. Mitochondria isolated after all four heat shock treatments were active in O(2) consumption at 28 degrees C in response to succinate and ADP (derived P/O ratios were 1.6, 1.7, 1.3, and 1.3, respectively.) The mitochondria from all four treatments were also active in O(2) uptake at 42.5 degrees C. However, only mitochondria isolated after treatment (C) were tightly coupling at 42.5 degrees C (derived ADP/O ratio was about 1.4). Combined with our earlier findings on the subcellular localization of heat shock proteins, our present data demonstrate that association of heat shock proteins with mitochondria by treatment (C) enables them to phosphorylate at 42.5 degrees C (i.e. they become thermotolerant). Isolated mitochondria from treatment (C) and treatment (A) were compared by electron microscopy. They appeared to be very similar and no significant ultrastructural differences were noted.

Journal Article↗
PubMed1989

Antibodies against the Calcium-Binding Protein: Calsequestrin from Streptanthus tortuosus (Brassicaceae).

Plant microsomes contain a protein clearly related to a calcium-binding protein, calsequestrin, originally found in the sarcoplasmic reticulum of muscle cells, responsible for the rapid release and uptake of Ca(2+) within the cells. The location and role of calsequestrin in plant cells is unknown. To generate monoclonal antibodies specific to plant calsequestrin, mice were immunized with a microsomal fraction from cultured cells of Streptanthus tortuosus (Brassicaceae). Two clones cross-reacted with one protein band with a molecular weight equal to that of calsequestrin (57 kilodaltons) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. This band is able to bind (45)Ca(2+) and can be recognized by a polyclonal antibody against the canine cardiac muscle calsequestrin. Rabbit skeletal muscle calsequestrin cross-reacted with the plant monoclonal antibodies. The plant monoclonal antibodies generated here are specific to calsequestrin protein.

Journal Article↗
PubMed1983

Actin-stimulated myosin Mg2+-ATPase inhibition by brain protein.

A low-molecular-weight protein, isolated from bovine brain, inhibits the actin-stimulated Mg-ATPase activity of myosin from striated muscle. This inhibition is probably related to its ability to cause actin to revert from its polymerized to its depolymerized state and to prevent the polymerization of actin. Its effect on the polymeric state of the actin has been demonstrated by viscosity studies. DNase inhibition assay, and electron microscopy. Heavy meromyosin can overcome the effect of the brain protein and stimulate the polymerization of actin. The inhibition of ATPase activity is in part dependent upon the relative amounts of brain protein, actin, and myosin. The apparent molecular weight of the brain protein is approximately 20,000 daltons. It appears to be a heat-labile glycoprotein containing 5-6% carbohydrate.

Actins↗
PubMed1981

Effects of interferon on the cAMP-adenylate cyclase system of human, mouse, and bovine thyroid tissue.

This report studied the action of interferon on the thyroidal adenylate cyclase-cAMP system. It was found that human interferon did not increase cAMP levels in human or bovine thyroid slices during a 60-min incubation. Mouse interferon also had no effect on cAMP levels in mouse thyroidal lobes over the 60-min incubation, nor did it increase adenylate cyclase activity in mouse homogenates.

Adenylyl Cyclases↗
PubMed1980

Effects of thyrotropin and cholera toxin on the thyroidal adenylate cyclase-adenosine 3',5'-monophosphate system.

The present experiments examined the relationship between cholera toxin and TSH stimulation of the adenylate cyclase system in bovine thyroid tissue. Preincubation of thyroid slices for 20 min at 4 C with a maximal concentration of cholera toxin (100 microgram/ml) did not impair the subsequent stimulation of cAMP by submaximal amounts of TSH (1 mU/ml) during a 5-min incubation at 37 C. Incubation of cholera toxin or TSH with mixed gangliosides, followed by the addition of thyroid slices resulted in inhibition of the cholera toxin but not the TSH stimulation of cAMP formation. Previous exposure of thyroid slices to TSH induced refractoriness to subsequent stimulation of cAMP formation by TSH, but the response to cholera toxin was unchanged. NAD is necessary for cholera toxin, but not TSH, stimulation of adenylate cyclase. In the absence of NAD, cholera toxin inhibited the effect of maximal concentrations of TSH and prostaglandin E1 on adenylate cyclase activity but had no effect on NaF stimulation. In the presence of NAD, the stimulation of adenylate cyclase activity of bovine thyroid plasma membranes by a maximal amount of TSH was not influeced by maximal amounts of cholera toxin. Cholera toxin had a biphasic action on the binding of [125I]iodo-TSH, with low concentrations enhancing and high concentrations inhibiting binding. TSH augmented the binding of [125I]iodo-cholera toxin over the range of 1-100 mU/tube. Cholera toxin at 10 microgram/ml maximally inhibited binding. In addition to the requirement for ribosylation of adenylate cyclase, the present results indicate that the mechanisms of action of TSH and cholera toxin on cAMP formation are different.

Adenylyl Cyclases↗
PubMed1975

Persistent pancreatic glucagon but not insulin response to arginine in pancreatectomized dogs.

Effects of total pancreatectomy on plasma glucagon, insulin and glucose responses to arginine were determined in 5 dogs. Portal vein and femoral artery samples were obtained in response to an arginine infusion (10 g/30 min) prior to, 1 h, 1 day and 1 week after pancreatectomy. Glucagon was measured using pancreatic-specific antiserum 30K (Unger, Dallas). Before pancreatectomy arginine significantly increased portal vein glucagon from 373 plus or minus 36 to 595 plus or minus 31 pg/ml and femoral artery levels from 233 plus or minus 28 to 342 plus or minus 74 pg/ml. Portal vein and femoral artery insulin concentrations of 74 plus or minus 21 and 17 plus or minus 3 muU/ml increased significantly to 173 plus or minus 64 and 31 plus or minus 7 muU/ml. Glucose levels did not change. One h after pancreatectomy, portal vein glucagon decreased to 121 plus or minus 15 pg/ml but increased to 230 plus or minus 42 pg/ml after arginine. Elevated blood glucose and the necessity for insulin treatment established the adequacy of pancreatectomy. Furthermore portal vein insulin levels were undetectable and unresponsive to arginine or a combination of glucose, glucagon, and tolbutamide 1 week after pancreatectomy. One day after pancreatectomy arginine significantly increased portal vein glucagon from 343 plus or minus 42 to 776 plus or minus 152 pg/ml. One week after pancreatectomy basal glucagon values were 374 plus or minus 30 in the portal vein and 360 plus or minus 49 in the femoral artery and responded to 1226 plus or minus 641 and 825 plus or minus 270 pg/ml, respectively, with arginine. Chromatography of plasma from one pancreatectomized dog on Sephadex G-50 after arginine stimulation revealed that much of the material cross-reacting with antibody 30K was eluted from the column earlier than either 125I-insulin or 125I-glucagon. In contrast, peak glucagon activity in plasma obtained from a normal human given arginine eluted from the column between the peak of 125I-insulin and 125I-glucagon; glucagon added to human plasma also was recovered in this same area between the 125I-insulin and 125I-glucagon peaks. These results suggest that some of the material that reacted with 30K antibody and which increased after pancreatectomy in response to arginine has a molecular weight greater than pancreatic glucagon. At autopsy no pancreatic tissue could be identified. Thus, after pancreatectomy, validated by absent insulin responses, the glucagon response to arginine was normal or increased. Since arginine is not thought to increase intestinal glucagon-like immunoreactive material, the source and nature of the material measured as glucagon after pancreatectomy is unknown, but may be important to any understanding of plasma glucagon measurements.

Animals↗
PubMedDate not supplied

Analysis of orthodontic anomalies in mentally retarded developmentally disabled (MRDD) persons.

For this epidemiologic study, 458 individuals with mental retardation and developmental disability (MRDD), from 6 to 87 years old, from the Lower Hudson Valley region of New York, were evaluated for the occurrence of orthodontic anomalies. High occurrence of both anomalies of intermaxillary relation, as determined by Angle's classification, and the anomalies of occlusion were found in these individuals when compared with the general population. An increased incidence of both acquired (i.e., open bite) as well as hereditary (i.e., prognathia) orthodontic anomalies correlated with the severity of mental retardation. In addition, an increased incidence of Angle class II malocclusion was found in persons with cerebral palsy and autism, and an increase of Angle class III malocclusion in persons with autism and Down syndrome. Moreover, it was found that 74% of MRDD persons had definitive malocclusion, while only 37% of the US general population of comparable age has definitive malocclusion. High incidence of malocclusion in this population remained present into old age, mainly due to a lack of treatment and the need to employ non-conventional orthodontic treatment in this population.

Adolescent↗