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Biomedical subjects

M Yin

Publications and source records attributed to M Yin.

At least 37 records · Page 2Linked to original sources

[Inhibitory effect of gelsemium alkaloids extract on hepatic carcinoma HepG2 cells in vitro].

The inhibitory effect of gelsemium alkaloids exstract (GAA) on HepG2 cells in vitro were studied by crystal violet dyeing method. The morphological change of HepG2 cells were observed with optical microscope. The alterations of cell cycle induced by GAA were analyzed with flow cytometry. The results showed that HepG2 cells exposed to GAA 10 micrograms/ml was inhibited significantly (P < 0.05). The inhibitory effect appeared in a dose- and time-dependent manner. HepG2 cells showed nuclear chromosome segmentation and condensation after GAA treatment. There emerged obvious Sub-G1 peak in the DNA histogram of HepG2 cells. GAA has a significant inhibition on HepG2 cells in vitro. The mechanism of antitumor action may be related to their apoptosis inducing activity.

Alkaloids↗

[Improved retrosigmoid approach operation in the treatment of trigeminal neuralgia].

OBJECTIVE: To explore the surgical method which can raise the treatment effect and reduce the complication occurrence of cerebellopontine angle (CPA) operation by retrosigmoid approach. METHOD: Have improved the retrosigmoid approach in the skin incision, the hole position of bone, the intracranial operation skills and the duramatral suture, etc. By the improved retrosigmoid approach, we used partial sensory rhizotomy (PSR) to cure 54 cases with trigeminal neuralgia (TN). RESULT: 52 cases got satisfactory treatment effect and no complication appeared. In the other 2 cases, the trigeminal nerve was not found in CPA. CONCLUSION: The CPA operation by retrosigmoid approach is dangerous relatively, it usually can cause some serious complication. But improved retrosigmoid approach can expose CPA sufficiently and is convenient to operate. On the other hand, it can decrease intracranial unexpected hemorrhage and complication occurrence.

Adult↗

[Selective excitation spectra and energy level structure of Dy3+:ThO2 crystal].

Dy3+:ThO2 crystal was grown by the flux technique for the first time. The emission spectra, excitation spectra and fluorescence decay curves were measured and discussed. By using emission spectra obtained under selective dye laser excitation at 12 K, together with the crystal-field theory, the site symmetry of Dy3+ ions in ThO2 was determined as C3 nu and its energy level structure was tabulated. The lifetime of radiative level 4F9/2 was also determined as 0.40 ms.

Chemical Phenomena↗

[Luminescence dependence upon concentration and temperature in YPO4:Pr3+].

Under selective excitation 3P0 state of Pr3+ ion in YPO4, the emission spectra and fluorescence decay curves are measured at different concentrations and temperatures. The origin of the spectral line located at 613.2 nm has been discussed and assigned to be the 1D2 (gamma 3)-->3H4 (gamma 5) transition. The different concentration dependence of emission intensities of levels 3P0 and 1D2 has been studied. Using static model, the fluorescence decay curve of 1D2 level is fitted, and the result shows that the cross-relaxation caused by the interaction of dipole-quadrupole between adjacent Pr3+ ions results in the concentration quenching.

Attention↗

Inhibition of chronic rejection of aortic allografts by dietary glycine.

BACKGROUND: Chronic rejection is influenced by a variety of risk factors, including histoincompatibility and ischemia. Glycine, a cytoprotective agent, has been shown to protect against ischemia-reperfusion injury in the liver, inactivate hepatic resident macrophages, minimize cyclosporin A-induced nephrotoxicity, and exhibit immunosuppressive properties in vitro. The aim of this study was to investigate whether dietary glycine could reduce development of chronic rejection. METHODS: Lewis recipients of Fisher-344 abdominal aortic allografts received diets that contained either 5% glycine plus 15% casein or 20% casein as control for 10 weeks. Vascular lesions of aortic isografts and allografts were evaluated quantitatively with image analysis and cell counting. RESULTS: No significant vascular changes were observed in isografts (mean medial areas of 3.3 +/- 0.3x0(5) microm2). However, dramatic intimal thickening (neointimal area 2.1+/-0.3) and medial thinning (1.5+/-0.3) were observed in allografts from rats fed control diet. In contrast, glycine significantly reduced the neointima by 45% (1.2+/-0.3) and protected the media (3.5+/-0.2). This led to intima to media area ratios almost twice as large in the control group as in glycine-fed rats (2.2+/-0.4 vs. 1.1+/-0.3, P<0.05). Moreover, infiltrating leukocytes, especially macrophages, were reduced significantly in the adventitia by glycine. In addition, glycine inhibited proliferation and migration of rat aortic smooth muscle cells in culture by 45 and 60%, respectively. CONCLUSION: These results indicate that dietary glycine minimizes histopathological changes of chronic rejection by reducing the immune response and, in part, by minimizing proliferation and migration of smooth muscle cells.

Animals↗

Directed actin polymerization is the driving force for epithelial cell-cell adhesion.

We have found that epithelial cells engage in a process of cadherin-mediated intercellular adhesion that utilizes calcium and actin polymerization in unexpected ways. Calcium stimulates filopodia, which penetrate and embed into neighboring cells. E-cadherin complexes cluster at filopodia tips, generating a two-rowed zipper of embedded puncta. Opposing cell surfaces are clamped by desmosomes, while vinculin, zyxin, VASP, and Mena are recruited to adhesion zippers by a mechanism that requires alpha-catenin. Actin reorganizes and polymerizes to merge puncta into a single row and seal cell borders. In keratinocytes either null for alpha-catenin or blocked in VASP/Mena function, filopodia embed, but actin reorganization/polymerization is prevented, and membranes cannot seal. Taken together, a dynamic mechanism for intercellular adhesion is unveiled involving calcium-activated filopodia penetration and VASP/Mena-dependent actin reorganization/polymerization.

Actins↗

Estrogen is involved in early alcohol-induced liver injury in a rat enteral feeding model.

The aim of this study was to investigate whether reduction in blood estrogen by removal of the ovaries would decrease the sensitivity of female rats to early alcohol-induced liver injury using an enteral ethanol feeding model, and if so, whether estrogen replacement would compensate. Livers from ovariectomized rats with or without estrogen replacement after 4 weeks of continuous ethanol exposure were compared with nonovariectomized rats in the presence or absence of ethanol. Ethanol increased serum alanine transaminase (ALT) levels from 30 +/- 6 to 64 +/- 7 U/L. This effect was blocked by ovariectomy (31 +/- 7) and totally reversed by estrogen replacement (110 +/- 23). Ethanol increased liver weight and fat accumulation, an effect that was minimized by ovariectomy and reversed partially by estrogen replacement. Infiltrating leukocytes were increased 6. 7-fold by ethanol, an effect that was blunted significantly by ovariectomy and reversed by estrogen replacement. Likewise, a similar pattern of changes was observed in the number of necrotic hepatocytes. Blood endotoxin and hepatic levels of CD14 messenger RNA (mRNA) and protein were increased by ethanol. This effect was blocked in ovariectomized rats and elevated by estrogen replacement. Moreover, Kupffer cells isolated from ethanol-treated rats with estrogen replacement produced more tumor necrosis factor alpha (TNF-alpha) than those from control and ovariectomized rats. It is concluded, therefore, that the sensitivity of rat liver to alcohol-induced injury is directly related to estrogen, which increases endotoxin in the blood and CD14 expression in the liver, leading to increased TNF-alpha production.

Alanine Transaminase↗

Effects of cytomegalovirus infection and prolonged cold ischemia on chronic rejection of rat renal allografts.

Previous studies have demonstrated that both cytomegalovirus (CMV) infection and prolonged cold ischemia of the allograft (CI) are associated with chronic rejection of renal transplants. The purpose of this study is to investigate the effect of CMV infection, of CI and of the combination of both, on the progression of chronic rejection, and to obtain a more detailed insight in their effects on the expression of adhesion molecules. Therefore, a rat transplantation model was used. Lewis recipients of renal allografts (with and without CI) from MHC-incompatible Brown Norway rats were inoculated with rat CMV or left uninfected. CMV infection alone resulted in an increased influx of CD4+ cells and macrophages early after infection, and in an increase in glomerular sclerosis and intima proliferation. CI caused an increase in infiltrating NK cells and an effect on intimal proliferation, glomerular sclerosis, and tubular atrophy. When CMV infection and CI were combined, an additive effect could be measured. This was however not the case for the function of the kidney. The creatinin showed a synergistic effect of the two influencing factors. Due to the CMV infection, an increase in CD49d cells was detected. CI resulted in an increase in CD18 cells and an increase in the expression of CD62P on vessels, and CD54 and CD44 on tubules. When CMV infection and CI were combined, all the effects caused by CMV and CI alone were present in an additional way. The results of the present study suggest that special attention should be paid to the recipient of an ischemically injured graft when either the donor or the recipient is CMV-infected. The patterns seen in histology, the infiltration of leukocytes and the expression of adhesion molecules, suggest that CI and CMV infection both have an effect on rejection, but act by different mechanisms.

Animals↗

Development of an intragastric enteral model in the mouse: studies of alcohol-induced liver disease using knockout technology.

The establishment of a continuous intragastric enteral feeding protocol in the rat by Tsukamoto and French was a major development in research of alcohol-induced liver disease. Unlike other models which only produce fat, with this model, inflammation, necrosis, and fibrosis can now be studied. However, much of what has been learned to date involves inhibitors or nutritional manipulation which may not be specific. Knockout technology could avoid these potential problems. Therefore, we have adapted a rat long-term intragastric protocol to the mouse so that the knockout technology can be used to study the mechanism of alcohol-induced liver injury. Reactive free radicals are involved in the mechanisms of early alcohol-induced liver injury; however, the key source of these species remains unclear. Cytochrome P450 (CYP) 2E1 is induced predominantly in hepatocytes by ethanol and could be one source of reactive oxygen species leading to liver injury. On the other hand, NADPH oxidase or xanthine oxidase is also a potent source of free radicals. In studies using CYP2E1 and p47phox (NADPH oxidase-deficient) knockout mice with this enteral model, it was reported that oxidants from CYP2E1 play only a small role in the mechanisms of early alcohol-induced liver injury in the mouse. Further, free radicals from NADPH oxidase in Kupffer cells play an important role in early alcohol-induced liver injury. Thus, this new enteral mouse model using knockout technology will provide a powerful tool in alcohol research.

Animals↗

Individual and combined antioxidant effects of seven phenolic agents in human erythrocyte membrane ghosts and phosphatidylcholine liposome systems: importance of the partition coefficient.

Antioxidant activities of seven phenolic agents against Fe(2+)-induced lipid oxidation were compared with alpha-tocopherol, beta-carotene, and vitamin C in human erythrocyte membrane ghosts and liposome systems. The antioxidant activity of five test flavonoids followed the order catechin > epicatechin > rutin > quercetin > myricetin in both systems (p < 0.05), which was negatively correlated with their partition coefficients. The antioxidant interaction of these phenolic agents with alpha-tocopherol, beta-carotene, or vitamin C in inhibiting Fe(2+)-induced lipid oxidation was examined. Synergistic effects were present in the combinations of alpha-tocopherol plus caffeic acid, catechin, or epicatechin as well as in all combinations of vitamin C plus phenolic antioxidants. On the basis of the stronger individual and combined effects present in caffeic acid, catechin, and epicatechin, the application of these three phenolic agents with or without alpha-tocopherol, beta-carotene, and vitamin C may provide stronger protective benefits against lipid oxidation, which may be helpful for oxidation-related diseases prevention.

Antioxidants↗

NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease.

In North America, liver disease due to alcohol consumption is an important cause of death in adults, although its pathogenesis remains obscure. Despite the fact that resident hepatic macrophages are known to contribute to early alcohol-induced liver injury via oxidative stress, the exact source of free radicals has remained a mystery. To test the hypothesis that NADPH oxidase is the major source of oxidants due to ethanol, we used p47(phox) knockout mice, which lack a critical subunit of this major source of reactive oxygen species in activated phagocytes. Mice were treated with ethanol chronically, using a Tsukamoto-French protocol, for 4 weeks. In wild-type mice, ethanol caused severe liver injury via a mechanism involving gut-derived endotoxin, CD14 receptor, production of electron spin resonance-detectable free radicals, activation of the transcription factor NF-kappaB, and release of cytotoxic TNF-alpha from activated Kupffer cells. In NADPH oxidase-deficient mice, neither an increase in free radical production, activation of NF-kappaB, an increase in TNF-alpha mRNA, nor liver pathology was observed. These data strongly support the hypothesis that free radicals from NADPH oxidase in hepatic Kupffer cells play a predominant role in the pathogenesis of early alcohol-induced hepatitis by activating NF-kappaB, which activates production of cytotoxic TNF-alpha.

Alcohol Drinking↗

Effects of SSM (specific substance maruyama) on HBe antigen-positive chronic hepatitis B -clinical efficacy and modulation of cytokines.

Twenty-three patients with HBe antigen-positive chronic hepatitis B were treated with capitalite first letters Maruyama (SSM). HBe antigen turned negative in 15 patients. The levels of various cytokines in pre- and post-treatment frozen serum samples from six patients whose HBe antigen turned negative and from five whose HBe antigen did not were examined. Reduction of serum interleukin (IL) -10 level to below 20 pg/ml was observed after SSM treatment in four of the six patients whose HBe antigen turned negative. SSM was found to stimulate the production of interferon (IFN) -gamma in peripheral blood cells from two healthy volunteers. This stimulatory effect was confirmed in 12 out of 24 healthy volunteers. SSM augmented the production of IFN-gamma in eight out of 10 patients with chronic hepatitis B and nine of 10 with hepatitis C. These results demonstrate for the first time that SSM stimulates the production of IFN-gamma in human peripheral blood cells and also suggest that treatment of HBe antigen-positive chronic hepatitis B patients with SSM leads to the clearance of HBe antigen and normalization of serum aspartate aminotransferase levels through inhibition of IL-10 and stimulation of IFN-gamma.

Adult↗

[Studies on gene mutation and micronucleus formation induced by ethylnitrosourea (ENU) in transgenic mice in vivo].

OBJECTIVE: To determine the feasibility of using pUC 118NX plasmid-based transgenic mice in the study of induced mutation in vivo with known mutagen, ethylnitrosourea (ENU). METHODS: pUC 118NX plasmid was recovered from the spleen genomic DNA of ENU-treated and untreated xylE, C57BL/6J transgenic mice with enzyme digestion and circularizing. The recovered pUC 118NX plasmid was electroporated into DH10B host cells, which were incubated in LB solid medium containing proper ampicillin overnight and then sprayed with catechol solution. Mutant could be detected by difference in yellow and white color of the stains and its xylE target gene could be sequenced for further identifying its mutation type. In addition, peripheral blood and bone marrow cells were isolated from xylE, C57BL/6J transgenic mice and micronucleus frequency (MNF) induced by ENU was observed. RESULTS: The spontaneous mutant frequency for xylE gene in the spleen of xylE, C57BL/6J transgenic mice was less than 4.79 x 10(-5), significantly different from that treated with ENU (50 mg/kg), 19.83 x 10(-5). Types of gene mutation induced by ENU in the spleen of xylE, C57BL/6J transgenic mice included transversion (50%), one or two-base insertion (37.5%) and transition (12.5%). MNF in peripheral blood normochromatic erythrocyte (NCE) and in bone marrow polychromatic erythrocyte (PCE) of ENU-treated (50 mg/kg x 5) mice were 7.6 per thousand and 8.8 per thousand, respectively, both significantly different from the controls treated with solvent (P < 0.01). It indicated that chromosome aberration could be induced by ENU. CONCLUSION: The pUC118NX plasmid-based xylE, C57BL/6J transgenic mice, which could be used in detecting gene mutation and chromosome aberration in vivo simultaneously, provided a novel detection system for overall assessment of genetic toxicity of chemicals.

Animals↗

[A preliminary study on the incidence of cedar pollinosis in district of Wuhan].

OBJECTIVE: To investigate the incidence of cedar pollinosis in district of Wuhan. METHOD: A survey relative to cedar pollinosis was carried out in 309 students in Hubei Medical University in 1999, including questionnaire investigation, nasal inspection and scratch test. From February to April of 2000, a clinical investigation of cedar pollinosis was adopted among 205 patients of allergic rhinitis including scratch test and nasal mucosa test. RESULT: 1. The positive rate of cedar pollen scratch test of 309 students was 7.8%. 2. 59 cases (28.8%) was hypersensitive to cedar pollen clinically in allergen test. CONCLUSION: Cedar pollinosis is one kind of important pollinosis in district of Wuhan and should be paid high attention to.

Adolescent↗

Glycine: a new anti-inflammatory immunonutrient.

The mechanism of the immunosuppressive effects of glycine and its pathophysiological applications are discussed in this review. Glycine has been well characterized in spinal cord as an inhibitory neurotransmitter which activates a glycine-gated chloride channel (GlyR) expressed in postsynaptic membranes. Activation of the channel allows the influx of chloride, preventing depolarization of the plasma membrane and the potentiation of excitatory signals along the axon. Glycine has recently been shown to have similar inhibitory effects on several white blood cells, including hepatic and alveolar macrophages, neutrophils, and lymphocytes. Pharmacological analysis using a GlyR antagonist strychnine, chloride-free buffer, and radiolabeled chloride has provided convincing evidence to support the hypothesis that many white blood cells contain a glycine-gated chloride channel with properties similar to the spinal cord GlyR. Molecular analysis using reverse transcription-polymerase chain reaction and Western blotting has identified the mRNA and protein for the beta subunit of the GlyR in total RNA and purified membrane protein from rat Kupffer cells. Dietary glycine is protective in rat models against endotoxemia, liver ischemia-reperfusion, and liver transplantation, most likely by inactivating the Kupffer cell via this newly identified glycine-gated chloride channel. Glycine also prevents the growth of B 16 melanomas cell in vivo. Moreover, dietary glycine is protective in the kidney against cyclosporin A toxicity and ischemia-reperfusion injury. Glycine may be useful clinically for the treatment of sepsis, adult respiratory distress syndrome, arthritis, and other diseases with an inflammatory component.

Alcohols↗

Transforming growth factor beta1 enhances platelet aggregation through a non-transcriptional effect on the fibrinogen receptor.

Upon activation, platelets store and release large amounts of the peptide transforming growth factor beta1 (TGFbeta1). The released TGFbeta1 can then act on nearby vascular cells to mediate subsequent vessel repair. In addition, TGFbeta1 may circulate to bone marrow and regulate megakaryocyte activity. It is not known what effect, if any, TGFbeta1 has on platelets. Adult TGFbeta1-deficient mice exhibit thrombocythemia and a mild bleeding disorder that is shown to result from faulty platelet aggregation. TGFbeta1-deficient platelets are shown to contain functional receptors, and preincubation with recombinant TGFbeta1 improves aggregation, demonstrating that TGFbeta1 plays an active role in platelet aggregation. TGFbeta1-deficient platelets fail to retain bound fibrinogen in response to aggregation agonists, but they possess normal levels of the alpha(IIb)/beta(3) fibrinogen receptor. Signaling from agonist receptors is normal because the platelets change shape, produce thromboxane A(2), and present P-selectin in response to stimulation. Consequently, activation and maintenance of alpha(IIb)/beta(3) into a fibrinogen-binding conformation is impaired in the absence of TGFbeta1. 4-Phorbol 12-myristate 13-acetate treatment and protein kinase C activity measurements suggest a defect downstream of protein kinase C in its activation cascade. Because platelets lack nuclei, these data demonstrate for the first time a non-transcriptionally mediated TGFbeta1 signaling pathway that enhances the activation and maintenance of integrin function.

Adenosine Diphosphate↗

Essential role of tumor necrosis factor alpha in alcohol-induced liver injury in mice.

BACKGROUND & AIMS: Tumor necrosis factor (TNF)-alpha is associated with increased mortality in alcoholics, but its role in early alcohol-induced liver injury is not fully understood. Recently, it was shown that injury induced by the enteral alcohol delivery model of Tsukamoto and French was reduced by antibodies to TNF-alpha. To obtain clear evidence for or against the hypothesis that TNF-alpha is involved, we studied TNF receptor 1 (TNF-R1, p55) or 2 (TNF-R2, p75) knockout mice. METHODS: Long-term enteral alcohol delivery was modified for male gene-targeted mice lacking TNF-R1 and TNF-R2. Animals were given a high-fat liquid diet continuously with either ethanol or isocaloric maltose-dextrin as a control for 4 weeks. RESULTS: Ethanol elevated serum levels of alanine aminotransferase nearly 3-fold in wild-type and TNF-R2 knockout mice but not in TNF-R1 knockout mice. Likewise, ethanol caused severe liver injury in wild-type mice (pathology score, 5.5 +/- 0.6) and TNF-R2 knockout mice (pathology score, 5.0 +/- 0.4), but not in TNF-R1 knockout mice (pathology score, 0.8 +/- 0.4; P < 0.001). CONCLUSIONS: Long-term ethanol feeding caused liver injury in wild-type and TNF-R2 knockout mice but not in TNF-R1 knockout mice, providing solid evidence in support of the hypothesis that TNF-alpha plays an important role in the development of early alcohol-induced liver injury via the TNF-R1 pathway. Moreover, the long-term enteral ethanol feeding technique we described for the first time for knockout mice provides a useful new tool for alcohol research.

Alanine Transaminase↗

New techniques for DNA sequence classification.

DNA sequence classification is the activity of determining whether or not an unlabeled sequence S belongs to an existing class C. This paper proposes two new techniques for DNA sequence classification. The first technique works by comparing the unlabeled sequence S with a group of active motifs discovered from the elements of C and by distinction with elements outside of C. The second technique generates and matches gapped fingerprints of S with elements of C. Experimental results obtained by running these algorithms on long and well conserved Alu sequences demonstrate the good performance of the presented methods compared with FASTA. When applied to less conserved and relatively short functional sites such as splice-junctions, a variation of the second technique combining fingerprinting with consensus sequence analysis gives better results than the current classifiers employing text compression and machine learning algorithms.

Algorithms↗