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Biomedical subjects

M Chen

Publications and source records attributed to M Chen.

At least 865 records · Page 48Linked to original sources
PubMed1987

Combined total body electron beam irradiation and chemotherapy for mycosis fungoides.

Since 1979 a protocol of total body electron beam therapy (3,600 rads; 6 MeV), followed by six monthly cycles of chemotherapy (doxorubicin, 30 mg/M2 given intravenously once monthly, and cyclophosphamide, 100 mg/M2 given orally each day for 14 days), has been used to treat fifty patients with mycosis fungoides (primarily Stages I and II). A group of twenty-four patients, treated by identical high-dose electron beam therapy alone, served as control subjects. Actuarial analysis by the Kaplan-Meier method and statistical analysis by the generalized Wilcoxon test of Gehan demonstrated a significant difference (p = 0.008) in the probability of Stages I and II patients' remaining in complete clinical remission when combination therapy was compared with high-dose electron beam therapy alone. No statistically significant difference was demonstrated in patients in Stages III and IV mycosis fungoides. Although 60% of patients were in "complete clinical remission," the longest follow-up being 75 months, all continued to show karyotypic abnormalities of circulating lymphocytes, and 70% had intermittently and abnormally elevated blood levels of Sézary cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1987

Molecular epidemiology of adenovirus type 35 infections in immunocompromised hosts.

Adenovirus type 35 (Ad35) is an uncommon group B adenovirus that has been isolated nearly exclusively from immunosuppressed hosts. In our series of 46 patients with Ad35 isolates, 36 had AIDS or AIDS-related complex (ARC), seven patients were immunocompromised because of other diseases, and three patients were "normal." Neither patients with AIDS or ARC made specific antibody to Ad35, whereas antibody was present in one immunocompetent host and one renal transplant recipient. All isolates were identified as Ad35 by using genomic analysis with the restriction endonuclease SmaI, but many viruses exhibited other group B hemagglutinins, a property of the fiber protein. Further analysis of DNAs from 40 of these isolates, mapped by using the enzymes BamHI, HpaI, and PstI, revealed a total of 14 genomic variants from the Ad35 prototype. Seven of these genomic types, with either Ad7 or Ad11 hemagglutinin, had corresponding restriction site differences within the fiber gene, a result consistent with recombination events with other group B adenoviruses.

AIDS-Related Complex↗
PubMed1987

The role of dietary carbohydrate in the decreased glucose tolerance of the elderly.

In this study we have attempted to evaluate the role of dietary carbohydrate (CHO) in the decreased glucose tolerance of aging. Eighteen healthy young (mean age, 27 +/- 1 standard error of the mean) (SEM) and 18 old (71 +/- 1 SEM) subjects matched for relative weight and socioeconomic group were studied. Oral glucose tolerance tests were performed while eating ad lib diet and after being given high (85%), medium (45%), and low (20% to 30%) CHO formula diets for at least three days. A three- to seven-day food record was used to determine the major nutrients including CHO and fiber intake in the ad lib diet at home. Our older subjects consumed significantly less total calories and slightly less carbohydrate but there was no difference in dietary fiber, protein, and fat intake. When studies were performed on matched CHO diets, decreased glucose tolerance was present in the older group. However, the mechanism(s) involved may vary with dietary CHO and with age. During the low CHO formula diet and the medium CHO ad lib diet, impaired insulin secretion was prominent in the elderly but was not present in the young. During the high CHO formula diet, insulin response was adequate in both old and young, but decreased glucose tolerance persisted in the older group, suggesting that insulin resistance may be the major contributing factor. We conclude that decreased glucose tolerance in the elderly is modified by CHO intake, but is present even when dietary CHO variability is acutely controlled.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1987

Difference in sporogenous bacterial populations in thermophilic (55 degrees C) and mesophilic (35 degrees C) anaerobic sewage digestion.

Spores, sporeforming vegetative cells, and asporogenous populations were enumerated in two semicontinuous anaerobic fermentors digesting municipal primary sludge at 35 and 55 degrees C for more than 87 days. In the 35 degrees C fermentor, the anaerobic total population was 312.5 X 10(6)/ml, with 25.0 X 10(6)/ml being sporogenous. The populations that digest casein, starch, pectin, and cellulose were 23.1 X 10(6), 59.2 X 10(6), 26.2 X 10(6), and 7.3 X 10(6)/ml, respectively, with 2.8 X 10(6), 6.7 X 10(6), 3.4 X 10(6), and 1.5 X 10(6)/ml being sporogenous, respectively. The sporeformers accounted for 8.0 to 20.0% of each of the respective populations. In the 55 degrees C fermentor, the anaerobic total population was 512.5 X 10(6)/ml, with 336.6 X 10(6)/ml being sporogenous. The populations that digest casein, starch, pectin, and cellulose were 97.7 X 10(6), 190.7 X 10(6), 75.8 X 10(6), and 11.2 X 10(6)/ml, respectively, with 47.8 X 10(6), 110.6 X 10(6), 43.3 X 10(6), and 5.1 X 10(6)/ml, respectively, being sporogenous. The sporeformers represented 45.5 to 65.7% of each of the respective populations. The numbers of thermophilic sporeforming vegetative cells in the 55 degrees C fermentor were 9.0 to 19.8 times higher than their counterparts in the 35 degrees C fermentor. Most sporeformers were in the vegetative state in the 35 and 55 degrees C fermentors. After 18 days of fermentation at 55 degrees C, sporeformers carried out most of the digestion; however, the digestion was shared by both sporeformers and asporogenous bacteria after 87 days of fermentation. In the 35 degrees C fermentor, asporogenous bacteria digested most of the sludge. During the 18- and 87-day experimental periods, sporeformers were never predominant.

Bacteria, Anaerobic↗
PubMed1987

Characterization of a major histocompatibility complex class I antigen-binding glycoprotein from adenovirus type 35, a type associated with immunocompromised hosts.

Adenovirus type 35 (Ad35) is a group B adenovirus that has been isolated primarily from patients with acquired immunodeficiency syndrome and other immunodeficiency disorders. We have studied the interaction of this unique adenovirus with the immune system by analyzing Ad35 early viral proteins in infected HeLa cells. We have identified a 29,000-Mr Ad35 early glycoprotein, E29, which associates with class I antigens of the major histocompatibility complex (MHC) in the endoplasmic reticulum. Ad35 E29 is analogous to the group C Ad2 early glycoprotein E3-19K (E19), which has been shown to interfere with the expression of class I antigens on the cell surface (H. Burgert and S. Kvist, Cell 41:987-997, 1985). In contrast to the Ad2 glycoprotein, Ad35 E29 was synthesized in much smaller amounts, was more extensively glycosylated, and did not cross-react with polyclonal antibody against the Ad2 protein. As a control, a class I antigen-binding glycoprotein from another group B adenovirus, Ad7, was also characterized and was found to have properties similar to those of Ad35 E29. Therefore, the differences in the glycosylation and quantity of class I antigen-binding glycoproteins between Ad35 and Ad2 are group related. Inhibition of the expression of MHC class I antigens, which are needed for cytotoxic-T-lymphocyte recognition of virus-infected cells, appears to play a vital role in the adenovirus life cycle in vivo. Our data indicate that this function has been conserved despite significant differences in the MHC class I antigen-binding glycoprotein and in the pathogenicity between serotypes.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Energy metabolism in contracting rat skeletal muscle: adaptation to exercise training.

Rats were trained by means of a program of treadmill running. Hindlimb muscles were stimulated to contract in anesthetized rats. Measurements were made on the plantaris and the deep, predominantly fast-twitch red portion of the gastrocnemius. The concentration of ATP plus phosphocreatine (approximately P) decreased less and stabilized at a higher level, whereas inorganic phosphate (Pi) and AMP concentrations increased less and attained lower steady-state levels in trained than in untrained muscles at the same work rate. Similarly, when muscles were stimulated to contract in the perfused rat hindquarter preparation, phosphocreatine (PC) concentration decreased less in trained plantaris muscle during contractile activity that resulted in the same rate of oxygen uptake by trained and untrained muscles. In both preparations, glycogen concentration decreased less and lactate increased less in the trained muscle. From the changes that occurred in the PC-to-creatine ratio during contractile activity and from ATP concentration, it could be estimated that free ADP concentration increased less than one-half as much in trained as in untrained muscles. We conclude that, as a consequence of the adaptive increase in muscle mitochondria, approximately P concentration is higher and Pi, ADP, and AMP concentrations are lower in muscles of exercise-trained compared with untrained rats during the same contractile activity.

Adaptation, Physiological↗
PubMed1987

Induction of an increase in mitochondrial matrix enzymes in muscle of iron-deficient rats.

Young rats maintained on an iron-deficient diet developed severe anemia and had large decreases in the levels of the iron-containing flavoproteins and cytochromes of the mitochondrial respiratory chain in skeletal muscle. In contrast, the levels of a number of mitochondrial matrix marker enzymes, including citrate synthase, isocitrate dehydrogenase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and aspartate aminotransferase, increased in red skeletal muscle but not in white muscle. Phosphocreatine concentration was decreased and inorganic phosphate concentration was increased in soleus muscle frozen in situ. We hypothesize that the increase in mitochondrial matrix enzymes reflects a stimulus to mitochondrial biogenesis in posture-maintaining and weight-bearing red muscle fibers in severely iron-deficient rats. It is our working hypothesis that this stimulus to mitochondrial biogenesis arises from mild activity of the red fibers and is due to the same perturbation in cellular homeostasis that is normally caused by vigorous exercise or hypoxia. In iron deficiency, the stimulus to mitochondrial biogenesis can induce an increase in only those enzymes not prevented from increasing by iron deficiency, resulting in formation of mitochondria of grossly abnormal composition.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1987

Age-related changes in the neuroendocrine (endocrine-paracrine) cell population and the serotonin content of the guinea pig prostate.

Neuroendocrine (endocrine-paracrine, APUD) cells of the guinea pig prostatic complex (prostate and coagulating gland) were studied at three age points (9-day-old weanlings, 11 to 12 week mature pre-breeders, and retired breeders) using serotonin immunocytochemistry for detection and subsequent morphometric analysis. Prostatic complex serotonin levels were determined for the same age groups using high performance liquid chromatography with electrochemical detection. The numbers of neuroendocrine (NE) cells in the prostatic complex of retired breeders was 1.42 +/- 0.29 NE cells/mm gland length (mean +/- SEM) and was increased nearly 24-fold when compared with mature pre-breeders with 0.06 +/- 0.03 NE cells/mm gland length and nearly 16-fold when compared with the weanlings with 0.09 +/- 0.04 NE cells/mm gland length. The increase in cell number in the retired breeders versus each of the other age groups was highly significant (p less than 0.001). The increase in NE cells appeared to take place exclusively in the prostate, whereas the number of NE cells in the coagulating gland were few and not significantly different in the three age groups. The number of urethral NE cells also appeared similar in all three age groups. The number of prostatic epithelial cells/gland length increased with age. The number of NE cells/100 prostatic epithelial cells was examined in the three age groups and the increase in retired breeders over the other two groups was still highly significant (p less than 0.001). Serotonin levels, which were measured for the whole prostatic complex, indicated a nearly 6-fold increase with age: retired breeders had 97.72 +/- 21.26 ng/g of wet tissue (mean +/- SEM) whereas mature pre-breeders had 17.1 +/- 2.88 ng/g of wet tissue (p less than 0.01). Weanling serotonin levels were not detectable. This dramatic age-related increase in prostatic NE cells and serotonin content could reflect a compensation for a decreased effectiveness of NE cell hormones, a nonfunctional primary hyperplasia, a hyperplasia secondary to endogenous hormonal or involutional changes or exogenous factors. Whatever the mechanism, this increase in prostatic NE cells with age is of great interest since human prostatic carcinoma and benign nodular hyperplasia are both strongly correlated with advanced age. Prostatic NE cells may, therefore, directly or indirectly be in the pathogenesis and/or evolution of these important pathologic processes.

Aging↗
PubMed1986

Perturbation of mitochondrial composition in muscle by iron deficiency. Implications regarding regulation of mitochondrial assembly.

It has been reported that the mitochondrial cytochromes and citrate cycle enzymes occur in constant proportions to each other and increase or decrease roughly in parallel in response to various stimuli. The purpose of this study was to determine whether this proportionality is an obligatory consequence of the way in which mitochondria are assembled. Severe iron deficiency was used to bring about decreases of the iron-containing constituents of the mitochondrial respiratory chain in skeletal muscle. Cytochrome c concentration and cytochrome oxidase activity were decreased approximately 50%, while succinate dehydrogenase and NADH dehydrogenase activities were decreased by 78% in iron-deficient muscle. On electron microscopic examination, mitochondria in iron-deficient muscles had relatively sparse numbers of cristae. The iron deficiency had little or no effect on the levels of a range of mitochondrial matrix enzymes, including citrate synthase, isocitrate dehydrogenase, fumarase, aspartate aminotransferase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and acetoacetyl-CoA thiolase. These results show that the usual constant proportions between the constituents of the mitochondrial respiratory chain and matrix enzymes are not obligatory; they provide evidence that mitochondrial matrix enzymes and respiratory chain constituents can be incorporated into mitochondria independently and that the ratios between them can vary within wide limits.

Adenosine Triphosphatases↗
PubMed1986

Rapid redox equilibrium between the mitochondrial Q pool and cytochrome b during triphasic reduction of cytochrome b by succinate.

The reliability of monitoring the redox reactions of cytochrome b using the different wavelengths employed by different authors has been reexamined. It was found that 562-575 nm is suitable in succinate: cytochrome c reductase but not in mitochondria, in which case 562-540 nm is a better pair. Direct optical measurements of the redox reaction kinetics of the mitochondrial Q pool using a commercial dual-wavelength spectrophotometer are possible when succinate is used as the electron donor. Using the correct wavelength pair, and with malonate to slow down the electron input, the reduction course of cytochrome b was still triphasic but a plateau or a turn replaced the oxidation phase previously reported by several authors. At the same time, the reduction course of the Q pool was also triphasic, and in perfect match with that of cytochrome b. Destruction of the Rieske iron-sulfur cluster by British anti-Lewisite (BAL) + O2 treatment or prereduction of the high-potential components made the reduction of both Q and b monophasic. The plot of log (Q/QH2) against log (b3+/b2+) gave a straight line with an n value of 1.7 for cytochrome b at pH 7.4. This n value rose to 2.0 at pH 6.5 and dropped to 1.4 at pH 8.5. On the other hand, the mid-point potential of cytochrome b relative to that of the Q pool remained essentially unchanged between pH 6.5 and 8.4. BAL treatment had a small effect on the midpoint potential of cytochrome b relative to that of the Q pool and had no effect on the n value. Addition of quinone homologues and analogues extended the plateau phase in the reduction of cytochrome b, but exogenous quinones did not equilibrate rapidly with cytochrome b. It was concluded that the appearance of the plateau between the two reduction phases of Q and b is caused by the rapid delivery of electrons to the high-potential components of the respiratory chain as envisaged in the Q cycle; the unexpected n value for cytochrome b suggests a concerted reduction by QH2 of two species of cytochromes b-562.

Animals↗
PubMed1986

The effect of ring substituents on the mechanism of interaction of exogenous quinones with the mitochondrial respiratory chain.

In uncoupled pig-heart mitochondria the rate of the reduction of duroquinone by succinate in the presence of cyanide is inhibited by about 50% by antimycin. This inhibition approaches completion when myxothiazol is also added or British anti-Lewisite-treated (BAL-treated) mitochondria are used. If mitochondria are replaced by isolated succinate:cytochrome c oxidoreductase, the inhibition by antimycin alone is complete. The reduction of a plastoquinone homologue with an isoprenoid side chain (plastoquinone-2) is strongly inhibited by antimycin with either mitochondria or succinate:cytochrome c reductase. The reduction by succinate of plastoquinone analogues with an n-alkyl side chain in the presence of mitochondria is inhibited neither by antimycin nor by myxothiazol, but is sensitive to the combined use of these two inhibitors. On the other hand, the reduction of the ubiquinone homologues Q2, Q4, Q6 and Q10 and an analogue, 2,3-dimethoxyl-5-n-decyl-6-methyl-1,4-benzoquinone, is not sensitive to any inhibitor of QH2:cytochrome c reductase tested or their combined use, either in normal or BAL-treated mitochondria or in isolated succinate:cytochrome c reductase. It is concluded that quinones with a ubiquinone ring can be reduced directly by succinate:Q reductase, whereas those with a plastoquinone ring can not. Reduction of the latter compounds requires participation of either center i or center o (Mitchell, P. (1975) FEBS Lett. 56, 1-6) or both, of QH2:cytochrome c oxidoreductase. It is proposed that a saturated side chain promotes, while an isoprenoid side chain prevents reduction of these compounds at center o.

Animals↗
PubMed1986

Longitudinal follow-up of chronic hemodialysis patients without vitamin supplementation.

Vitamin supplementation for dialysis patients is still controversial. In our study, we followed longitudinally over a period of a year, 15 patients on chronic hemodialysis who were deprived of vitamin supplementation. Microbiological assays were used to determine the levels of five vitamins of the B group (folate, niacin, B12, B6, and thiamine). Vitamin C was measured chemically. During the observation period when vitamins were not supplemented, a marked drop of many of these vitamins in blood levels were encountered. For vitamins B12 and C, the plasma levels remained within the normal range in all the subjects studied. For the other vitamins, the blood levels were found to be low in a few patients. Our data suggest that vitamin supplementation is probably not needed in most stable hemodialysis patients as it is recommended now, and that perhaps, if supplementation is indicated, less should be given than is presently prescribed. Further research is needed in this area.

Adult↗