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Biomedical subjects

M Chen

Publications and source records attributed to M Chen.

At least 883 records · Page 49Linked to original sources

Interaction of frog virus 3 with the cytomatrix. IV. Phosphorylation of vimentin precedes the reorganization of intermediate filaments around the virus assembly sites.

Frog virus 3 (FV3) assembles in morphologically distinct assembly sites in the cytoplasm of infected cells. As the assembly sites form, the intermediate filaments (IF) aggregate, delimit the assembly sites, and remain so throughout infection. To determine the molecular basis of reorganization of IF, we analysed the vimentin of uninfected and FV3-infected cells by two-dimensional gel electrophoresis. The results showed that (i) the vimentin was more acidic in FV3-infected cells than in uninfected cells, (ii) the acidification of vimentin in FV3-infected cells was possibly due to a fourfold increase in phosphorylation, and (iii) the phosphorylation of vimentin preceded the reorganization of IF around virus assembly sites. A temperature-sensitive mutant of FV3 (ts9467), which at the non-permissive temperature neither reorganized IF nor formed assembly sites, failed to increase the phosphorylation of vimentin. Together, the above results suggest that changes in phosphorylation may modulate IF organization and that changes in IF organization are required for FV3 assembly site formation.

Animals↗

Elimination of overgrowth in delayed-incubation membrane filter test for total coliforms by m-ST holding medium.

Two holding media were compared for their effects on total coliform recovery by the delayed-incubation membrane filter procedure. LES-MF holding medium contains tryptone, m-Endo broth, dipotassium hydrogen phosphate, sodium benzoate, sulfanilamide, para-aminobenzoic acid, and cycloheximide (pH 7.0). m-ST holding medium contains ethanol, sodium monophosphate, dipotassium hydrogen phosphate, sulfanilamide, and Tris (pH 8.6). In tests with natural water and wastewater samples from various sources, recovery with LES-MF and m-ST were similar after a 1-day holding period. With LES-MF, however, after a 2- or 3-day holding period, coliform bacteria frequently were partially or totally overgrown by noncoliforms, causing significant reductions in coliform counts. No significant overgrowth was observed with m-ST. We propose that m-ST be used for all holding periods longer than 1 day.

Culture Media↗

Endurance exercise training reduces lactate production.

In situ muscle stimulation in trained and untrained rats was used to reevaluate whether adaptations induced by endurance exercise training result in decreased lactate production by contracting muscles. The gastrocnemius-plantaris-soleus muscle group was stimulated to perform isotonic contractions. After 3 min of stimulation with 100-ms trains at 50 Hz at 60/min, the increases in lactate concentration in the plantaris, soleus, and fast-twitch red muscle (deep portion of lateral head of gastrocnemius) were only approximately 50% as great in trained as in sedentary rats. In the predominantly fast-twitch white superficial portion of the medial head of the gastrocnemius the increase in lactate concentration was 28% less in the trained than in the sedentary group. The decreases in muscle glycogen concentration seen after 3 min of stimulation at 60 trains/min were smaller in the trained than in the untrained group. The reduction in lactate accumulation that occurred in the different muscles in response to training was roughly proportional to the degree of glycogen sparing. These results show that endurance training induces adaptations that result in a slower production of lactate by muscle during contractile activity.

Adaptation, Physiological↗

Presynaptic inhibition produced by an identified presynaptic inhibitory neuron. II. Presynaptic conductance changes caused by histamine.

We have examined the morphology and pharmacology of the L32 neurons, identified cells that mediate presynaptic inhibition in the Aplysia abdominal ganglion, to gain insight into the putative transmitter released by the L32 cells. We analyzed the fine structure of the synaptic release sites of L32 cells stained with horseradish peroxidase. Each varicosity of L32 was found to contain two general classes of vesicles. One class of vesicles is large (mean long diameter of 98 nm) and contains an electron-dense core that typically filled or nearly filled each vesicle profile. The second class of vesicles is smaller (mean long diameter of 67 nm) and relatively electron lucent. The size, distribution, and morphology of the vesicle population in L32's terminals was similar to that described at the synapses of the identified histaminergic neuron C2 in Aplysia (2). These morphological observations suggested that L32 cells might be histaminergic. Among the various putative transmitters tested, histamine was most effective in mimicking the postsynaptic effects of L32 cells onto L10, and onto other follower cells of L32 in the abdominal ganglion. Histamine also caused inhibition of transmitter output from L10. Both the IPSP produced by L32 in L10 and the response of L10 to histamine could be reversibly blocked by cimetidine, a histamine antagonist in Aplysia (14). These results support, but do not establish the identification of histamine as the putative transmitter of L32 cells. Histamine mimics the action of L32 in mediating presynaptic inhibition allowing us to examine in more detail the conductance changes in L10 underlying presynaptic inhibition. Voltage-clamp analysis revealed that histamine blocked the voltage-dependent Ca2+ current and increased a voltage-dependent K+ current in L10, much as did L32. Both of these changes are likely to act synergistically to inhibit transmitter release. Reduction of Ca2+ current in L10 would directly inhibit transmitter release from L10 directly by decreasing the amount of Ca2+ entering during spike depolarization. The increase in K+ current would act indirectly to reduce transmitter release from L10, by hyperpolarizing L10 and decreasing the amplitude and duration of spikes in L10, as well as reducing the steady-state Ca2+ influx. These results support the idea that in Aplysia presynaptic inhibition is caused primarily by a direct transmitter-mediated reduction in presynaptic Ca2+ current and secondarily by a hyperpolarization of the presynaptic neuron due to a transmitter-mediated increase in a K+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdomen↗

The plasma and red cell vitamin B levels of chronic hemodialysis patients: a longitudinal study.

Plasma B12, folate, B6 and thiamine, and red blood cell folate, thiamine and niacin levels were monitored for a period of 6 months in 15 clinically stable, chronic hemodialysis patients who were not supplemented with the water-soluble vitamins. Microbiological assays were used to determine the blood levels of the water-soluble vitamins. Over the period of 6 months, none of the patients had plasma or red cell vitamin levels below the normal range. No appreciable changes were observed in the plasma and red blood cell vitamin levels before and after dialysis in 5 patients. This study showed that chronic hemodialysis patients are able to maintain normal plasma and red cell levels of some water-soluble vitamins without daily supplementation.

Adult↗

A sociodemographic analysis of preventive dental behavior among white American families.

Data collected from a national family dental survey were used to study the relationships between the sociodemographic characteristics and the preventive dental behavior of wives, husbands, and children. A canonical correlational analysis showed that preventive dental behavior of family members including toothbrushing, flossing, and preventive dental visits, significantly correlated with sociodemographic characteristics (level of education, income, occupation, population density, age, family size, and presence of children). The relationships studied accounted for 11-15% of the variance in the preventive dental behavior of family members. However, the patterns of correlation for different family members varied. The extent of the effects of various sociodemographic variables on preventive dental behavior were not uniform and the degrees of responsiveness of toothbrushing, flossing, and dental visits to the influence of sociodemographic characteristics were also different. The results of the study are compared with those of previous studies. The implications of the findings are discussed.

Adolescent↗

Plasma catecholamines, dietary carbohydrate, and glucose intolerance: a comparison between young and old men.

Catecholamines play an important role in glucose homeostasis. This study was designed to determine whether circulating catecholamine changes in the elderly play a role in the glucose intolerance of aging and whether these changes are related to dietary carbohydrate intake. Plasma catecholamines (epinephrine and norepinephrine) and glucose were measured before and for 2 h after the administration of 100 g oral glucose in both 18 young (age, 18-39 yr) and 20 old (age, 60-82 yr) normal men during ad libitum home diet and after 3-day weight-maintaining, high or low carbohydrate formula diets in the Clinical Research Center. The elderly men had higher plasma norepinephrine levels before and after oral glucose than the young men even when eating matched formula diets. Plasma epinephrine levels were similar and decreased significantly after oral glucose in both groups. There was no relationship between catecholamine levels and degree of glucose tolerance. A high carbohydrate diet improved glucose tolerance in both old and young subjects. However, changes in dietary carbohydrates were not associated with consistent changes in plasma catecholamines. Therefore, we conclude that 1) glucose intolerance of aging cannot be explained by changes in plasma catecholamines, 2) the age-related increase in plasma norepinephrine is unrelated to dietary carbohydrate intake, and 3) there is no effect of age on suppression of plasma epinephrine after oral glucose administration.

Adolescent↗

Adjuvant chemotherapy for medulloblastoma.

The use of adjuvant chemotherapy for cerebellar medulloblastoma is controversial. Twenty-one children and adolescents were treated with adjuvant low-dose cyclophosphamide and vincristine following surgery and radiotherapy. With a mean observation period of 6 years, the disease-free survival is 81%.

Adolescent↗

Interaction of frog virus 3 with the cytomatrix. III. Role of microfilaments in virus release.

The role of microfilaments in the release of frog virus 3 (FV3) from the plasma membrane was studied. Scanning electron microscopic study of FV3-infected baby hamster kidney (BHK) cells showed that late in infection (15 hr), numerous microvillus-like projections containing virions and microfilaments occur on the cell surface. Two microfilament-disrupting drugs, cytochalasin B and cytochalasin D, inhibited both the formation of microvillus-like projections and virus release. In the drug-treated cells, the virions accumulated in large numbers beneath the plasma membrane (transmission electron microscopy), suggesting that both drugs affected the release of the virus at the level of plasma membrane rather than the traverse of the virus to the plasma membrane. Two-dimensional gel analysis of actin from FV3-infected and uninfected cells revealed the following. There was no difference in the synthesis of actin in infected versus uninfected cells. However, the actin of infected cells is more acidic than its counterpart in uninfected cells. Temporally, the change in actin preceded the formation of microvilli-like projections involved in virus release. The change in actin is virus induced and is linked to virus maturation since a ts mutant of FV3 (ts9467), which is deficient in virus production at the restrictive temperature (30 degrees), did not modify actin. The mutant, at the permissive temperature (25 degrees), produced virions and altered the actin. Together, the above results attribute an active role for microfilaments in virus release.

Actin Cytoskeleton↗

Superoxide dismutase and catalase in skeletal muscle: adaptive response to exercise.

Cellular damage caused by free radical reactions may play a role in the aging process. A bout of exercise can increase free radical concentration with damage to mitochondria in muscle (Davies et al., 1982). This study was undertaken to determine if muscle adapts to exercise training with an enhancement of enzymatic defenses against free radical damage. A program of running that induced two-fold increases in mitochondrial enzymes in leg muscles of rats resulted in no increase in catalase or cytoplasmic superoxide dismutase (SOD) activities. Mitochondrial SOD activity was increased 37% in fast-twitch red and slow-twitch red types of muscle and 14% in white muscle. Thus, despite an increase in mitochondrial SOD, the ratio of SOD to mitochondrial citrate cycle and respiratory chain enzymes was decreased. It seems unlikely that increased capacity for enzymatic scavenging of superoxide radical is a major protective adaptation against free radical damage in exercise-trained muscle.

Animals↗

Effect of catecholamines on glucose uptake and glycogenolysis in rat skeletal muscle.

The effect of catecholamines on glycogenolysis and sugar transport was evaluated in rat epitrochlearis (fast-twitch) and soleus (slow-twitch) muscles in vitro. When muscles were incubated with 0.1 microM epinephrine (both an alpha- and beta-agonist), the proportion of phosphorylase in the a form increased from 6.2 +/- 0.7 to 37.4 +/- 5.7% in epitrochlearis muscle and from 9.1 +/- 0.7 to 21.6 +/- 1.3% in soleus muscle. Both the activation of phosphorylase and the resulting glycogenolysis could be prevented by preincubation with the beta-blocker, propranolol. The effect of catecholamines on the rate of sugar transport was also examined in epitrochlearis muscle. The beta-agonist, isoproterenol, significantly depressed the rate of 3-O-methylglucose uptake, while the alpha-agonist, phenylephrine, had no effect. Inclusion of 0.1% albumin in the incubation medium increased the resting rate of sugar transport twofold. When isoproterenol + albumin were present, rather than exerting a depressive effect the catecholamine further increased the rate of sugar uptake. This increase was prevented by preincubation with propranolol. It was concluded that glycogenolysis and sugar transport in rat skeletal muscle are solely under beta-adrenergic control.

Animals↗

Pathogenesis of age-related glucose intolerance in man: insulin resistance and decreased beta-cell function.

To identify the pathogenic factors responsible for glucose intolerance of aging, we measured a variety of metabolic parameters, including insulin sensitivity and islet cell function, in 10 young (18-36 yr old) and 10 older (57-82 yr old) men of normal body weight. Subject groups had equivalent fasting plasma glucose and fat cell size values. Frequently sampled iv glucose tolerance tests were performed, and the data were analyzed by computer using the minimal model approach. This technique yields the following measures: SI, the insulin sensitivity index; phi 1 and phi 2, indices of first and second phase beta-cell responsiveness to glucose; n, fractional insulin clearance, and SG, a measure of dynamic glucose disappearance dependent on glucose per se. We also evaluated beta-cell responsiveness independently by measuring the plasma insulin response to arginine injections at three levels of glycemia and calculated potentiation slope from the relationship between the acute insulin response to arginine and the prestimulus glucose level. The older men were glucose intolerant (glucose disappearance rate, 1.32% min-1) compared to the younger men (glucose disappearance rate, 2.21% min-1; P less than 0.01). This intolerance was the result of both a beta-cell defect and insulin resistance. The potentiation slope (r = -0.67; P less than 0.02) and phi 2 (r = -0.47; P less than 0.05) both decreased with age. In addition, SI in the older group was diminished 63% (2.4 vs. 6.5; 10(-4) min-1/microU/ml; P less than 0.001) and was unrelated to differences in body fat. No differences were found in either n or SG. These studies suggest that the diminished glucose tolerance of aging in normal weight men has multifactorial causality. Both beta-cell dysfunction and insulin resistance are important. In contrast, we found little evidence for changes in insulin clearance or insulin-independent glucose disappearance contributing to age-related glucose intolerance.

Adipose Tissue↗