Biomedical subjects

M Zeng

Publications and source records attributed to M Zeng.

At least 37 records · Page 2Linked to original sources

PubMed2000

Role of denervation in modulating IIb MHC gene expression in response to T(3) plus unloading state.

Previously, we have reported that the combination of hindlimb suspension (HS) and thyroid hormone [triiodothyronine (T(3))] treatment induces the de novo expression of the fast IIb myosin heavy chain (MHC) gene in the soleus. Thus we tested the hypotheses that the induction of IIb MHC expression with HS + T(3) is prevented with denervation and that this IIb induction is regulated by transcriptional processes. Adult female rats were subjected to 2 wk of combined HS + T(3) in which one side of the lower leg was simultaneously denervated. HS + T(3) caused decreased expression of the slow type I MHC and concomitant increases in both the fast type IIx and IIb MHC isoforms in the intact soleus muscle. Denervation prevented the endogenous expression of the IIb MHC gene at both the protein and mRNA levels. Although HS + T(3) intervention was able to markedly increase the expression of the 2.6-kb IIb MHC promoter-reporter construct using direct gene transfer, this induction, however, was not inhibited by denervation. These findings collectively suggest that normal innervation is essential for inducing the unique expression of the IIb MHC in a slow muscle in response to HS + T(3); however, in the denervated muscle, there is a discordance between the regulation of the endogenous IIb MHC gene relative to the exogenous IIb MHC promoter-reporter construct.

Animals↗

PubMed2000

Effects of spaceflight and thyroid deficiency on hindlimb development. I. Muscle mass and IGF-I expression.

Thyroid deficiency (TD) in neonatal rats causes reduced growth of skeletal muscle that is disproportionately greater than that for other tissues (G. R. Adams, S. A. McCue, M. Zeng, and K. M. Baldwin. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 276: R954-R961, 1999). TD depresses plasma insulin-like growth factor I (IGF-I) levels, suggesting a mechanism for this effect. We hypothesized that TD and exposure to spaceflight (SF) would interact to reduce skeletal muscle growth via a reduction in IGF-I levels. Neonatal rats were flown in space for 16 days. There was a similar, nonadditive reduction in the growth of the body ( approximately 50%) and muscle weight (fast muscles, approximately 60%) with either TD or SF. In the soleus muscle, either SF or TD alone resulted in growth reductions that were augmented by SF-TD interactions. There were strong correlations between 1) muscle mass and muscle IGF-I levels and 2) circulating IGF-I and body weight. These results indicate that either hypothyroidism or exposure to SF will limit the somatic and muscle-specific growth of neonatal rats. The impact of these perturbations on skeletal muscle growth is relatively greater than the effect on somatic growth. The mechanisms by which either TD or SF impact growth appear to have a common pathway involving the control of plasma and muscle IGF-I concentrations.

Animals↗

PubMed2000

Effects of spaceflight and thyroid deficiency on rat hindlimb development. II. Expression of MHC isoforms.

Both slow-twitch and fast-twitch muscles are undifferentiated after birth as to their contractile protein phenotype. Thus we examined the separate and combined effects of spaceflight (SF) and thyroid deficiency (TD) on myosin heavy chain (MHC) gene expression (protein and mRNA) in muscles of neonatal rats (7 and 14 days of age at launch) exposed to SF for 16 days. Spaceflight markedly reduced expression of the slow, type I MHC gene by approximately 55%, whereas it augmented expression of the fast IIx and IIb MHCs in antigravity skeletal muscles. In fast muscles, SF caused subtle increases in the fast IIb MHC relative to the other adult MHCs. In contrast, TD prevented the normal expression of the fast MHC phenotype, particularly the IIb MHC, whereas TD maintained expression of the embryonic/neonatal MHC isoforms; this response occurred independently of gravity. Collectively, these results suggest that normal expression of the type I MHC gene requires signals associated with weight-bearing activity, whereas normal expression of the IIb MHC requires an intact thyroid state acting independently of the weight-bearing activities typically encountered during neonatal development of laboratory rodents. Finally, MHC expression in developing muscles is chiefly regulated by pretranslational processes based on the tight relationship between the MHC protein and mRNA data.

Animals↗

PubMed2000

[Effects of pravastatin on hepatic plasminogen activator inhibitor 1 mRNA expression in rabbits with fatty liver].

OBJECTIVE: To explore the effects of Pravastatin on the changes of plasminogen activator inhibitor 1 (PAI-1) gene expression of hepatic tissue in rabbit with fatty liver. METHODS: We observed the influences of Pravastatin on the rabbit model of hyperlipidemia and fatty liver induced by high fat diet for 12 weeks, and the plasma PAI-1 activity and the hepatic PAI-1 mRNA expression in therapeutic group (n=10); and meanwhile, designed the model group (n=10) and normal group (n=7) as control. RESULTS: Severe hepatocellular steatosis was found in model group compared with normal group. Plasma lipids and PAI-1 activity increased in model group in 6 and 12 weeks, and was significantly higher than normal group in 12 weeks. PAI-1 mRNA relative values in hepatic tissue in model group were higher than those in normal group. Compared with model group, hepatic pathological manifestation with the respect of steatosis had no obvious changes in therapeutic group, but the lipid content and PAI-1 activity in the plasma and the expression of PAI-1 mRNA in the liver were significantly reduced. The activity of PAI was (14.0A2. 5)X10(-3)U/L in model group, and (8.6A2.0)X10(-3)U/L in therapeutic group in 12 weeks. CONCLUSION: Pravastatin could inhibit over-expression of PAI-1 mRNA in the rabbit liver with hyperlipidemia and fatty liver, and reduce its plasma PAI-1 activity.

Animals↗

PubMed2000

[Effect of lipids on I and III procollagen mRNA expression of hepatic stellate cells].

OBJECTIVE: To study the effect of lipids on I and III procollagen mRNA expression of hepatic stellate cells (HSC). METHODS: HSC were isolated and cultured from the liver of Wistar rats by in situ perfusion with pronase and collagenase and the density gradient centrifugation with Nycodenz. HSC were incubated with triglyceride (25mg/L) and very low-density lipid (VLDL, 25 mg/L) for 10d, respectively. I and III procollagen mRNA expression of HSC was detected by Northern blot hybridization. RESULTS: After HSC was stimulated with triglyceride and VLDL, the expression of I and III procollagen mRNA increased obviously. CONCLUSION: Lipids may promote the expression of I and III procollagen mRNA, and may be associated with fatty liver and hepatic fibrogenesis.

Animals↗

PubMed2000

Effects of lipid on low-density and high-density lipoprotein receptors in hepatic stellate cell from rat liver.

OBJECTIVE: To study the effects of lipid (triglyceride and very low-density lipoprotein) on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) receptors in the hepatic stellate cell (HSC) from the rat liver. METHODS: HSC were isolated and cultured from the liver of Wistar rats by in situ perfusion with pronase and collagenase and density gradient centrifugation with Nycodenz. Radioligand conjugation assay with (125)I-LDL and (125)I-HDL(3) was detected for the effects of lipid on LDL and HDL receptor of HSC. RESULTS: LDL and HDL receptors were found on the membrane of the rat HSC. The lipid might increase the binding of LDL to LDL receptor, but decrease the binding of HDL(3) to HDL receptor. CONCLUSION: LDL and HDL receptors on the HSC membrane may have an important role in the metabolism of lipoprotein and the regulation of cholesterol. These results provided the basis of theory and experimentation for the genesis of fatty liver and liver fibrosis.

Animals↗

PubMed2000

[Experimental study on inhibitory effect of Chinese herbal compound on hepatocyte cytochrome P450 II E1 expression in rat model of nonalcoholic fatty liver].

OBJECTIVE: To study the effect of Chinese herbal compound (CHC) on hepatocyte cytochrome P450 II E1 expression in rat model of nonalcoholic fatty liver (NFL). METHODS: CHC was given to the models of NFL formed by high fat diet, and changes on pathology of liver and hepatocyte cytochrome P450 II E1 expression, as well as the contents of malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), vitamin E (VitE) and triglyceride (TG) in liver were observed and compared with those in the control group. RESULTS: The fatty degeneration of liver recovered to normal basically in the CHC group. Immunohistochemical examination showed that CHC could inhibit the hepatocyte cytochrome P450 II E1 expression markedly, and restore the liver contents of MDA, SOD, GSH, VitE and TG to near normal range. CONCLUSION: CHC could inhibit the hepatocyte cytochrome P450 II E1 expression markedly in rats with fatty liver, therefore, has the effect of preventing fatty liver.

Animals↗

PubMed2000

[Multiple patterns of angle closure mechanisms in primary angle closure glaucoma in Chinese].

OBJECTIVE: The mechanism of primary angle closure glaucoma (PACG) in Chinese is studied to establish a new classification system based on the etiology and mechanism of angle closure. METHODS: The anterior chamber angle's configuration and the anatomic structures related to the angle in 126 cases with PACG were observed with ultrasound biomicroscope (UBM), and the mechanisms of angle closure were analyzed by diagnostic treatment. RESULTS: Based on the configuration of the angle and anatomic structures related to the angle as well as the mechanisms of angle closure, PACG could be divided into following subtypes: pure pupillary block angle closure glaucoma [PPB, 48 cases (38.1%)]; pure non-pupillary angle closure glaucoma [PNP, 9 cases (7.1%)]; multiple mechanism angle closure glaucoma [MM, 69 cases (54.8%)]. PPB manifested that the relative position of pupillary margin was located anteriorly, the peripheral iris bombé was due to the pupillary block, and the angle closure was not related to the location and shape of the peripheral iris and ciliary body. PNP showed that the relative position of pupil margin was located posteriorly, the angle closure was not caused by the pupillary block, but caused by anterior located ciliary body and/or thick and anterior located peripheral iris. MM pattern was caused by both pupillary block and non-pupilary block, and most of the cases manifested creeping angle closure. CONCLUSIONS: The angle closure mechanisms of PACG in Chinese are of multiple patterns. Based on the different mechanisms of angle closure in PACG, a new classification system should be established to improve the diagnosis and treatment of PACG.

Adult↗

PubMed2000

[Herbological investigation on traditional Chinese medicine gegen].

In this paper, herbological investigation was carried out into a large of Ben-Cao literature that concerned the origin, clinical use and other relevant aspects of Gegen, from which we can judge that Gegen used in ancient times match to that specified in the present Chinese Pharmacopoeia.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1999

Hemoglobin induction in mouse macrophages.

The common perception that hemoglobin is involved solely in the transport of oxygen and carbon dioxide has been challenged by recent studies with nitric oxide (NO). These studies have shown that the primordial bacterial flavohemoglobin functions to consume NO enzymatically (to protect from nitrosative stress), whereas mammalian hemoglobin functions to deliver NO (thus maximizing oxygen delivery in the respiratory cycle). Here we report that murine macrophages stimulated to produce NO with lipopolysaccharide and interferon-gamma express the betaminor hemoglobin subunit. Consumption of NO, however, was not increased by cytokines or by hemoglobin expression. These data suggest alternative functions for globins in mammalian cells, and they challenge the prevailing view that the expression of alpha- and beta-globin genes is always balanced and coordinated.

Amino Acid Sequence↗

PubMed1999

Fas-induced caspase denitrosylation.

Only a few intracellular S-nitrosylated proteins have been identified, and it is unknown if protein S-nitrosylation/denitrosylation is a component of signal transduction cascades. Caspase-3 zymogens were found to be S-nitrosylated on their catalytic-site cysteine in unstimulated human cell lines and denitrosylated upon activation of the Fas apoptotic pathway. Decreased caspase-3 S-nitrosylation was associated with an increase in intracellular caspase activity. Fas therefore activates caspase-3 not only by inducing the cleavage of the caspase zymogen to its active subunits, but also by stimulating the denitrosylation of its active-site thiol. Protein S-nitrosylation/denitrosylation can thus serve as a regulatory process in signal transduction pathways.

Animals↗

PubMed1999

Post-radiotherapy myelitis observed in an AIDS patient with a meningioma: case report and review of the literature.

Radiation myelitis is an uncommon but serious complication of radiation therapy. Although the definitive threshold to cause myelitis is unknown, it is believed that less than 50 Gy when given in 25 or more fractions is highly unlikely to cause myelopathy. This report describes a case of myelitis within the radiotherapy portal in an HIV infected patient who received radiation therapy for an atypical meningioma located in the cervical spine. A complete resolution of the meningioma was also noted in this case. The possible contributing roles of HIV infection and concomitant administration of antiviral drugs are discussed.

Acquired Immunodeficiency Syndrome↗

PubMed1999

Time course of myosin heavy chain transitions in neonatal rats: importance of innervation and thyroid state.

During the postnatal period, rat limb muscles adapt to weight bearing via the replacement of embryonic (Emb) and neonatal (Neo) myosin heavy chains (MHCs) by the adult isoforms. Our aim was to characterize this transition in terms of the six MHC isoforms expressed in skeletal muscle and to determine the importance of innervation and thyroid hormone status on the attainment of the adult MHC phenotype. Neonatal rats were made hypothyroid via propylthiouracil (PTU) injection. In normal and PTU subgroups, leg muscles were unilaterally denervated at 15 days of age. The MHC profiles of plantaris (PLN) and soleus (Sol) muscles were determined at 7, 14, 23, and 30 days postpartum. At day 7, the Sol MHC profile was 55% type I, 30% Emb, and 10% Neo; in the PLN, the pattern was 60% Neo and 25% Emb. By day 30 the Sol and PLN had essentially attained an adult MHC profile in the controls. PTU augmented slow MHC expression in the Sol, whereas in the PLN it markedly repressed IIb MHC by retaining neonatal MHC expression. Denervation blunted the upregulation of IIb in the PLN and of Type I in the Sol and shifted the pattern to greater expression of IIa and IIx MHCs in both muscles. In contrast to previous observations, these findings collectively suggest that both an intact thyroid and innervation state are obligatory for the attainment of the adult MHC phenotype, particularly in fast-twitch muscles.

Aging↗

PubMed1999

Radiation-induced recombination is dependent on Ku80.

We have recently shown that irradiating cells prior to transfection induces recombination, as manifested by increased stable transduction of both plasmid and adenoviral vectors. We hypothesized that Ku proteins, which have previously been shown to be involved in both recombination and the repair of DNA damage after irradiation, would likely be important mediators of radiation-induced recombination. The present work demonstrates that Ku80 is essential for radiation-induced recombination. While human and hamster Ku80 are equally effective at restoring the transfection efficiency and radiation resistance of xrs-5 cells, human Ku80 is much more effective at radiation-induced recombination than hamster Ku80. This difference is not due to differences in Ku80 expression or DNA end-binding activity, but it may be due to structural differences between human and hamster Ku80.

Animals↗

PubMed1999

[Correlation between hepatocyte cytochrome P450IIE1 expression and oxidation, antioxidation in rat nonalcoholic steatosis model].

OBJECTIVE: To study the correlation between hepatocyte cytochrome P450 II E1(CYP II E1) expression and oxidation, antioxidation in rat nonalcoholic steatosis model. METHODS: The expression of hepatocyte CYP II E1 antigen in rat steatosis model induced by high fat diet was detected with immnohistochemistry. Meanwhile, MDA, SOD, GSH and VitE contents in the liver were measured by biochemical analysis. RESULTS: Expression of CYP II E1 in rat nonalcoholic steatosis by high fat diet was prominent in hepatic acinar zone 3, and had a more extensive acinar distribution from zone 3 to zone 2, MDA contents in fatty liver was significantly increased than in normal, SOD, GSH and VitE contents were significantly decreased than in normal. There were significant positive correlation between CYP II E1 and MDA (P < 0.01), and negative correlation between CYP II E1 and SOD, GSH, VitE (P < 0.05, P < 0.05, P < 0.01). CONCLUSIONS: Hepatocyte CYP II E1 expression in nonalcoholic steatosis is prominent in hepatic acinar zone 3. Its expression resembles alcoholic fatty liver. There is significant correlation between CYP II E1 and lipid peroxidation.

Animals↗

PubMed1999

A randomized double-blind placebo-controlled study of lamivudine in the treatment of patients with chronic hepatitis B virus infection.

OBJECTIVE: To evaluate the effect of lamivudine on the loss of serum hepatitis B virus (HBV) DNA, HBeAg/antiHBe seroconversion and ALT levels in chronic hepatitis B patients and its safety profile and tolerance compared with placebo. METHODS: Four hundred and twenty-nine patients with chronic HBV infection as defined by positive HBsAg, HBeAg and HBV DNA were enrolled and randomized into lamivudine and placebo groups. Three hundred and twenty-two patients received lamivudine 100 mg daily and 107 patients received placebo treatment for 12 weeks. Then, all patients were offered a further 9-month open label lamivudine treatment. The efficacy and safety were evaluated with clinical, biochemical, hematological and virological parameters. RESULTS: During the 12-week treatment period, 92.2% of lamivudine treated patients became HBV DNA negative (below 1.6 pg/ml) compared with only 14.1% of those receiving placebo (P < 0.01). At the end of 12 week, the sustained negative rate for HBV DNA in the lamivudine treated group was 78.5% compared with the placebo group (11.1%; P < 0.01). There was a trend to a high proportion of patients treated with lamivudine to lose HBeAg (8.1%) and develop antiHBe (10.2%) than treated with placebo (5.3% and 6.4% respectively), but this difference was not statistically significant. Patients with elevated ALT levels at baseline became normal in 60. 3% of the lamivudine treated group compared with the placebo group where only 27.5% were normal (P < 0.01). Lamivudine was well tolerated in a dose of (100 mg daily) and the overall incidence of adverse events was similar to that of the placebo. CONCLUSIONS: Lamivudine (100 mg daily) is very effective in the inhibition of HBV replication, indicated by the rapid loss of serum HBV DNA, and often accompanied by a decrease of serum ALT levels. Lamivudine is well tolerated without severe adverse events during treatment.

Adolescent↗

PubMed1999

Effects of Kupffer cells stimulated by triglyceride and very low-density lipoprotein on proliferation of rat hepatic stellate cells.

OBJECTIVE: To study the effects of triglyceride, very low-density lipoprotein (VLDL), and Kupffer cell-conditioned medium (KCCM) derived from triglyceride and VLDL treatment on proliferation of rat hepatic stellate cells (HSC). METHODS: HSC and Kupffer cells were isolated and cultured from liver of Wistar rats by in situ perfusion with proteinase and collagenase, and density gradient centrifugation with Nycodenz; HSC and Kupffer cells were identified by immunohistochemistry, endocytosis, and ultrastructure, etc. Kupffer cells were incubated with triglyceride (25 micrograms/ml) and VLDL (25 micrograms/ml) for 24 hours, KCCM were prepared, and MTT colorimetric assay was detected for HSC proliferation. RESULTS: HSC proliferation was 0.1894 +/- 0.0316 (12.5 micrograms/ml), 0.1637 +/- 0.0243 (25 micrograms/ml), 0.1450 +/- 0.0264 (50 micrograms/ml), 0.1212 +/- 0.0275 (100 micrograms/ml), 0.1226 +/- 0.0138 (200 micrograms/ml) and 0.0990 +/- 0.0163 (400 micrograms/ml) in the presence of triglyceride and was 0.1583 +/- 0.0314 (6.25 micrograms/ml), 0.1642 +/- 0.0269 (12.5 micrograms/ml), 0.1834 +/- 0.0498 (25 micrograms/ml), 0.1964 +/- 0.0287 (50 micrograms/ml) and 0.2202 +/- 0.0284 (100 micrograms/ml) in presence of VLDL, respectively. Compared with the control, HSC proliferation at 400 micrograms/ml of triglyceride was lower (P < 0.01), but at 12.5 micrograms/ml of triglyceride and 25, 50, 100 micrograms/ml of VLDL higher (P < 0.05 or 0.01); HSC proliferation was 0.1569 +/- 0.0144, 0.1924 +/- 0.0113 and 0.1871 +/- 0.0116 in the presence of KCCM, KCCM + triglyceride and KCCM + VLDL, respectively. Compared with the control and KCCM, KCCM + triglyceride and KCCM + VLDL might promote HSC proliferation (P < 0.01); there was no statistical significance between KCCM + triglyceride and KCCM + VLDL (P > 0.05); KCCM was greater in HSC proliferation than the control, but there was no significant change (P > 0.05). CONCLUSIONS: Triglyceride, VLDL, and KCCM stimulated by triglyceride and VLDL might promote HSC proliferation and be associated with fatty liver and hepatic fibrogenesis.

Animals↗

PubMed1999

[Effect of pneumothorax on membrane diffusing capacity and pulmonary capillary blood volume].

OBJECTIVE: Investigating the effect of pulmonary membrane diffusing capacity(Dm) and pulmonary capillary blood volume(Vc) on carbon monoxide diffusing capacity (DLCO) in patients with pneumothorax before and after treatment, and clarifying the mechanism of hypoxemia due to pulmonary reexpansion. METHODS: Pulmonary function test, DLCO, Dm, Vc and arterial blood gas analysis were determined in 21 cases of pneumothorax before treatment and one week after pulmonary reexpansion. RESULTS: DLCO, Dm, Vc, partial pressure of arterial oxygen (PaO2), alveolar ventilation volume (VA), percentage of forced expiratory volume in one second to predicted value, and the ratio of dead space ventilation (VD) to tidal volume (VT) [VD/VT] were (64 +/- 4)%, (66 +/- 5)%, (70 +/- 5)%, (83.7 +/- 2.3) mm Hg, (4.4 +/- 0.2) L, (59 +/- 4)%, 0.340 +/- 0.020 respectively before treatment. After pulmonary reexpansion, they respectively were (71 +/- 4)%, (74 +/- 4)%, (80 +/- 6)%, (89.4 +/- 1.5) mm Hg, (5.40 +/- 0.20) L, (79 +/- 4)%, 0.210 +/- 0.010. They were significantly improved after treatment. Except for Dm, they were statistically different. Between Dm, Vc and DLCO, significant positive correlations were found during pneumothorax and one week after pulmonary reexpansion, especially correlation between Dm and DLCO was more apparent. Between Dm and DLCO significant positive correlations (r2 = 0.862, P < 0.0001; r2 = 0.728, P < 0.001) were found in study patients before and after treatment. So were Vc and DLCO (r1 = 0.643, P < 0.01; r2 = 0.52, P < 0.05). The correlation coefficient of Dm was markedly larger than Vc. CONCLUSIONS: The decrease in pulmonary diffusing function is related to Dm and Vc during pneumothorax, while decrease of Dm plays a major role. The hypoxemia is still presented in a period of time after pulmonary reexpansion, which is not related to VA and abnormality of ventilation-perfusion ratio (V/Q). It is chiefly due to unrecovery of Dm.

Adolescent↗