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Biomedical subjects

Y X Chen

Publications and source records attributed to Y X Chen.

At least 55 records · Page 3Linked to original sources
PubMed1998

Atherosclerosis: coagulation and fibrinolysis.

Tissue factor (TF) protein was overexpressed by macrophages and smooth muscle cells (SMCs) and deposited in the extracellular matrix of atherosclerotic intimas, probably resulting in enhanced procoagulant activity and the intimate participation in either thrombus formation or intimal fibrin deposition after the exposure of flowing blood and permeated fibrinogen to TF in atherosclerotic lesions. On the other hand, APO(a) was localized both in the stroma and within some macrophages. Fibrin deposition, which was more frequently detected in the matrix of advanced lesions than in that of early lesions, occasionally colocated with cell- and matrix-associated TF and APO(a) deposited in the matrix. These findings further support the hypothesis that the coagulation and fibrinolysis systems can play an essential role in the initiation and progression of atherosclerosis through fibrin deposition both in atherosclerotic plaques and on the arterial surface by neointimal hypercoagulability and a hypofibrinolytic state, which can also participate in SMC proliferation due to the decreased activation of TGF-beta by embedded and deposited APO(a). The clinical implications of these phenomena may thus contribute to future investigations in the prevention and treatment of atherosclerotic diseases.

Animals↗
PubMed1996

Diagnostic criteria for hypocellular acute leukemia: a clinical entity distinct from overt acute leukemia and myelodysplastic syndrome.

In order to establish diagnostic criteria for hypocellular acute leukemia (HL), we have reviewed 32 cases selected on the basis of hypothetical 40% or less cellularity, by focusing on morphology, immunophenotype, karyotype and response to low dose Ara-C (LDAC) regimen and compared them with 40 cases of myelodysplastic syndrome (MDS) and 66 cases of overt acute myeloid leukemia (AML). The onset age ranged from 44 to 75 years (median 67 years). Bone marrow (BM) cellularity ranged from 12.4 to 39.8% (mean 29.8%) in HL, being significantly lower than in MDS (mean 80.7%) or AML (mean 86.4%) (P < 0.001). All reviewed cases characteristically showed smoldering clinical course, bi- or pancytopenia with rare leukemic blasts in the peripheral blood (PB), proliferation of type I leukemic blasts in the BM and markedly reduced background hematopoietic cells with some dysplastic changes in 12/32 cases (37.50/6). Blast percentage (blast %) in the BM ranged from 38.2 to 93.7% (mean 57.3%) in all nucleated cells (ANC). Although a considerable number of cases had blasts with negative or very low myeloperoxidase activity, immunophenotyping revealed that the leukemic blasts in HL had only myeloid markers. Karyotyping revealed non-random chromosome abnormalities in 30% of cases analyzed, which were considerably different from those seen in MDS. With LDAC regimen, a significantly higher CR rate (13/20 cases: 65.0%) was gained in HL than in RAEB/RAEB-t (0%) and overt AML in the elderly cases (27.3%) (P < 0.05). In CR, most cases showed recovery to normocellular BM with an apparent normalization of PB parameters. However, 12 CR cases relapsed 4-12 months later; most of which again showed hypocellular BM. These results indicate that HL is a distinct subtype of AML characterized by slow but distinct proliferation of immature myeloid blasts and by unique hematological features distinct from MDS or overt AML in the elderly. We propose the following diagnostic criteria: (1) pancytopenia with rare appearance of blasts in PB; (2) less than 40% BM hypocellularity; (3) more than 30% blasts in BM-ANC; and (4) myeloid phenotypes of leukemic blasts by MPO staining and/or immunophenotyping.

Acute Disease↗
PubMed1995

Molecular detection of pre-ATL state among healthy HTLV-1 carriers in an endemic area of Japan.

Adult T-cell leukemia/lymphoma (ATL) usually develops after age 40 in Japan, suggesting a long latency since HTLV-I is considered to be transmitted mainly from mothers to babies via breast milk. Our previous studies had suggested that HTLV-I carriers who have a monoclonal integration of HTLV-I proviral DNA in the peripheral blood cells, designated pre-ATL, account for about 2% of healthy carriers and are at high risk of developing ATL. Their ages ranged from 32 to 80 (median 57). Nevertheless, many cases of pre-ATL showed a long-lasting carrier state (10-year probability around 90%). In the present investigation we conducted a large-scale molecular detection of monoclonal integration in a population (481 cases) of healthy carriers with ages ranging from 16 to 82 (median 49) for the purpose of clarifying the earliest onset of this pre-ATL state. Southern-blot analysis of DNA extracted from peripheral blood mononuclear cells revealed 6 cases (1.2%) with a monoclonal band. All of these 6 were older than 40; no single positive case was found in 220 carriers under age 40. These results indicate that the molecularly detectable pre-ATL state also develops after a long latency. Thus the pre-ATL state seems to be a subtype of ATL showing an extremely indolent course of disease development, but not merely an early phase of all subtypes of ATL. We propose that, in order to reveal a promoter(s) responsible for the development of ATL from the pre-ATL state, intensive epidemiological investigation of life style, eating habits, occupation and exposure to carcinogens must be conducted on this unique group prone to ATL. It is also important to perform such an epidemiological study on the general population of carriers by paying special attention to the first 3-4 decades of each carrier's life in Japan and by comparing the data with those from carriers in different geographical areas of the world.

Adolescent↗
PubMed1995

Trichomonas vaginalis and cervical cancer. A prospective study in China.

The relationship between Trichomonas vaginalis infection and cervical cancer was investigated prospectively in a cohort of 16,797 women aged 25 years or more who were followed from 1974 to 1985 within the framework of a cervical screening program in Jingan, China. Personal interviews were conducted by trained interviewers when the women first entered the screening program. At initial screening, 421 (2.51%) women had a positive cytologic diagnosis of T. vaginalis infection. Ninety-nine incident cases of pathologically confirmed squamous cell carcinoma were identified from the cohort, with a total of 140,018 person-years of observation. T. vaginalis infection was found to contribute to the risk of cervical cancer, as determined by crude estimates and after adjustment for potential confounding effects. In a multiple proportional hazards model, the relative risk for cervical cancer was 3.3 (95% confidence interval: 1.5 to 7.4) among women with T. vaginalis infection. Furthermore, in the multivariate analysis, increased risk of cervical cancer was associated with the following factors: number of extramarital sexual partners of both the subjects and their spouses, cigarette smoking, and irregular menstruation. Having a large number of negative Pap smears was associated with lower risk. This study suggests that there might be an association between T. vaginalis infection and the risk of cervical cancer, but only 4 to 5% of cervical cancer in Chinese women may be attributable to T. vaginalis infection.

Adult↗
PubMed1995

Studies on the role of plasminogen activators and plasminogen activator inhibitor type-1 in rat corpus luteum of pregnancy.

Luteal development and demise are characterized by substantial tissue destruction and remodeling, which is associated with local production of plasminogen activation. Recently we reported involvement of tissue-type plasminogen activator (tPA) in luteolysis in rhesus monkeys. In this study, we further investigated changes in expression of both tPA and urokinase-type plasminogen activator (uPA) activity during various developmental stages of rat corpus luteum (CL) of pregnancy and their possible physiological roles in luteolysis. Rat CL or dispersed luteal cells in vitro are capable of producing both tPA and uPA, and a plasminogen activator inhibitor type-1, in a stage-dependent manner. However, only tPA activity significantly increases in late phases of CL development. Furthermore, the increase in tPA activity in the CL is well correlated with a sharp decrease in luteal progesterone production. Addition of exogenous tPA to the luteal culture considerably decreases progesterone production. In contrast, immunoneutralization of endogenously produced tPA activity by inclusion of tPA monoclonal antibody in the culture results in a significant increase in luteal progesterone production. It is therefore suggested that tPA may also be involved in suppression of rat luteal function. This hypothesis is further supported by the findings that interferon-gamma significantly inhibits luteal basal and hCG-stimulated progesterone production and also stimulates basal and hCG-induced tPA activity. On the basis of the data provided in this study and similar findings in monkeys, we conclude that endogenously produced tPA in late phase of CL development may regulate luteal regression through local autocrine or paracrine action.

Animals↗
PubMed1995

[Experimental study on anti-duck hepatitis B viral effect of Phyllanthus urinaria of different areas and combined therapy with other drugs].

The duck hepatitis B virus model was treated with phyllanthus urinaria of different area and combined with Sophora flavesceus as well as ciprofloxacin once a day for one month, the results indicated: Guangxi and Yunnan Phyllanthus could lower the serum DHBV DNA significantly (P < 0.05), but Chongqing Phyllanthus couldn't. And the amount of serum DHBV DNA rose a week after stopping of Yunnan Phyllanthus. The antiviral effect of Guangxi Phyllanthus combined with ciprofloxacin seems to be strengthened (P < 0.05).

Animals↗
PubMed1995

Effect of glucose on TGF-beta 1 expression in peritoneal mesothelial cells.

The peritoneum's response to peritoneal dialysis is a complex and poorly understood process that can result in fibrosis. The transforming growth factor beta(TGF-beta 1) plays a central role in regulating tissue repair and remodeling after injury. To determine the role of mesothelial cells during peritoneal dialysis in the alteration of the peritoneum, we studied the effect of glucose on TGF-beta 1 expression by mesothelial cells. Human mesothelial cells were cultured in serum-free DMEM with different glucose concentrations for 48 hours. TGF-beta 1 messenger (mRNA) was measured by slot-blot hybridization using a TGF-beta 1 cDNA probe. The result was that glucose stimulates TGF-beta 1 mRNA expression in a dose-dependent way. The expression was more profound in high glucose concentrations. This suggests that TGF-beta 1 mRNA may overexpress by mesothelial cells due to the procedure of dialysis, which may be the most important mechanism of alteration of the peritoneum during peritoneal dialysis.

Autoradiography↗
PubMed1993

[An experimental study of hearing loss caused by mumps virus in guinea pigs].

Guinea pigs were inoculated with mumps virus into the scala tympani to establish an experimental animal model of viral labyrinthitis. Electrophysiological reactions of the inner ears were assessed by ECoG and histopathological changes of the cochleas were investigated under light and electron microscopes. Viral lesions or/and proliferation were demonstrated in 19 out of 25 cochleas. Compound action potential (CAP)N1 thresholds for the nineteen cochleas showed very significant elevations (P < 0.001) after inoculation with mumps virus. This study revealed that viral labyrinthitis caused by mumps virus presented various lesions in the stria vascularis, Reissner's membrane, basilar membrane and Corti's organ. Viral particles were found in the marginal, intermediate and capillary endothelial cells of striae vascularis. Pathological changes of the hair cells of the experimental animals were closely associated with elevations of CAP thresholds, the more serious pathological changes, the higher the CAP thresholds.

Animals↗
PubMed1993

[Protective action of taurine on ischemia-reperfusion liver injury in rats and its mechanism].

The protective effect of taurine on ischemia-reperfusion damages of rat perfused liver and its possible mechanism were investigated. Reflow with 20 mmol/L taurine markedly ameliorated reperfusion injury of post-ischemic liver as evidenced by reduction of lipid peroxidation (LPO), mitochondrial calcium overload in hepatocytes, as well as leakage of intracellular LDH and protein. Furthermore, taurine could significantly suppress in vitro LPO formation of hepatocyte plasma membrane induced by generating system of free radicals, inhibit calcium uptake and promote calcium release by mitochondria in addition to a membrane stabilizing action on rat isolated hepatic lysosome. The results demonstrated that taurine possesses significant protective efficacy on ischemia-reperfusion liver damage, and that the mechanism of its anti-hepatic injury may be mainly related to inhibiting LPO formation, regulating cellular calcium homeostasis and stabilizing biological membrane.

Animals↗
PubMed1993

Plasma endothelin levels in cirrhotic patients and their correlation with atrial natriuretic peptide.

Plasma levels of endothelin (ET) were determined by radioimmunoassay in 11 healthy volunteers and 34 patients with liver cirrhosis. The results revealed that mean ET plasma level was significantly lower in 34 cirrhotic patients than in normal subjects (40.21 +/- 4.38 ng/L vs 84.55 +/- 7.88 ng/L, P < 0.01). Plasma ET was 32.17 +/- 3.98 ng/L in 23 cirrhosis patients with ascites compared with 57.0 +/- 9.0 ng/L in patients without ascites (P < 0.01). Moreover, it is apparent that plasma levels of ET decreased with the increase of ascites volume, and increased after the disappearance of ascites. But plasma levels of atrial natriuretic peptide (ANP) in cirrhotic patients were markedly higher than those in the controls (830.12 +/- 72.18 ng/L vs 439.45 +/- 50.18 ng/L, P < 0.01). In patients with ascites, ET plasma levels were inversely correlated to ANP. The results suggest that deficiency of circulating ET might be one of the important factors involved in sodium and water retention in cirrhosis.

Adult↗
PubMed1993

[Effects of maternal intravenous glucose administration at term or shortly before cesarean section on fetus].

In order to investigate the effects of maternal intravenous glucose administration on fetus, two groups of pregnant women were observed. In the first group, 33 cases in late pregnancy, who received 50% glucose 80ml by intravenously injection. The mean fetal heart rate and fetal movements were found to be increased, maternal and fetal blood glucose levels elevated; umbilical artery pH decreased after the administrations as compared with the control group. The results indicated that a single injection of glucose at term had no adverse effect on fetus. In the second group 23 cases who received glucose 10% 400ml by intravenous drops shortly before CS, subclinical fetal acidosis was mated. Therefore, glucose given in this way should be employed cautiously, and rapid intravenous infusion should be avoided.

Cesarean Section↗
PubMed1993

[Pathogenetic significance of endothelin in experimental liver necrosis].

The changes in rat plasma level of endothelin-ir (ET-ir) during CCl4-induced hepatic necrosis and the therapeutic action of ET-antiserum (ET-Ab) were observed. The plasma level of ET-ir in rats with liver necrosis was significantly elevated (17.7 +/- 2.6 ng/L vs control 9.5 +/- 1.6 ng/L, P < 0.05). The plasma level of ET was markedly decreased by using ET-Ab, simultaneously the calcium overload in liver attenuated, the formation of liver lipid peroxidation product decreased, and activities of plasma ALT and LDH were also reduced. The results indicate that ET-Ab effectively alleviated the CCl4-induced damage to liver, and suggest that ET might be one of important humoral factors involved in liver necrosis.

Alanine Transaminase↗
PubMed1991

Glomerular macrophage proliferation in experimental immune complex nephritis.

In immune complex nephritis, glomerular hypercellularity is known to result from the proliferation of intrinsic cells and from the infiltration of mononuclear cells, primarily macrophages. An immunohistochemical double-labeling procedure was used to determine whether macrophages were among the cells which may undergo mitosis within the glomerular tuft. The monoclonal antibody ED1 served as a macrophage marker; cells in the S-phase of mitosis were recognized by uptake of bromodeoxyuridine. Glomerular proliferation was studied in chronic serum sickness of LEW rats, an animal model of immune complex nephritis for which the relationship between immunopathology and pathophysiology has been well described. In normal glomeruli, resident mesangial macrophages accounted for an unexpectedly large proportion (greater than or equal to one-third) of the total mitotic activity. In immune complex glomerulonephritis, the rate of glomerular macrophage proliferation increased rapidly just at the onset of proteinuria and remained high throughout the remaining course of disease. Glomerular macrophages from rats with proliferative nephritis also divided more vigorously than normal in short term culture in vitro, while persistently expressing abnormal surface marker phenotypes. The proliferation of mesangial macrophages appears to be a prominent feature of the normal process of glomerular cell renewal. In hypercellular glomeruli, vigorous local proliferation could greatly amplify the potential of macrophages to cause damage.

Animals↗