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Biomedical subjects

W Liu

Publications and source records attributed to W Liu.

At least 487 records · Page 27Linked to original sources
PubMed1999

beta-adrenergic modulation of L-type Ca2+-channel currents in early-stage embryonic mouse heart.

Little information is available concerning the modulation of cardiac function by beta-adrenergic agonists in early-stage embryonic mammalian heart. We have examined the effects of isoproterenol (Iso) on the spontaneous beating rate and action potential (AP) configuration in embryonic mouse hearts at 9.5 days postcoitum (dpc), just 1 day after they started to beat. Iso (3 microM) increased the spontaneous beating rate in whole hearts, dissected ventricles, and isolated ventricular myocytes. In ventricular myocytes, Iso also increased the slope of the pacemaker potential and the action potential duration but decreased the maximum upstroke velocity. In whole cell voltage-clamp experiments, the Ca2+-channel currents were measured as Ba2+ currents (IBa). In 9.5-dpc myocytes, IBa was enhanced significantly from -4.7 +/- 0.9 to -6.7 +/- 1.2 pA/pF (by 52.4 +/- 14.8%, n = 10) after the application of Iso. Propranolol (3 microM) reversed the effect of Iso. Forskolin (For, 10 microM) produced an increase in IBa by 95.5 +/- 18.8% (n = 8). In ventricular myocytes at a late embryonic stage (18 dpc), 3 microM Iso caused an appreciably greater increase in IBa from -6.2 +/- 0.5 to -14.5 +/- 2.2 pA/pF (by 137.8 +/- 33.0%, n = 8), whereas the increase in IBa by 10 microM For (by 120.0 +/- 23.0%, n = 7) was comparable to that observed in the early stage (9.5 dpc). These results indicate that the L-type Ca2+-channel currents are modulated by beta-adrenergic receptors in the embryonic mouse heart as early as 9.5 dpc, probably via a cAMP-dependent pathway.

Action Potentials↗
PubMed1999

Effect of chromosome 19 transfer on blood pressure in the spontaneously hypertensive rat.

Linkage studies in the spontaneously hypertensive rat (SHR) have suggested that a gene or genes regulating blood pressure may exist on rat chromosome 19 in the vicinity of the angiotensinogen gene. To test this hypothesis, we measured blood pressure in SHR progenitor and congenic strains that are genetically identical except for a segment of chromosome 19 containing the angiotensinogen gene transferred from the normotensive Brown Norway (BN) strain. Transfer of this segment of chromosome 19 from the BN strain onto the genetic background of the SHR induced significant decreases in systolic and diastolic blood pressures in the recipient SHR chromosome 19 congenic strain. To test for differences in angiotensinogen gene expression between the congenic and progenitor strains, we measured angiotensinogen mRNA levels in a variety of tissues, including aorta, brain, kidney, and liver. We found no differences between the progenitor and congenic strains in the angiotensinogen coding sequence or in angiotensinogen expression that would account for the blood pressure differences between the strains. In addition, no significant differences in plasma levels of angiotensinogen or plasma renin activity were detected between the 2 strains. Thus, transfer of a segment of chromosome 19 containing angiotensinogen from the BN rat into the SHR induces a decrease in blood pressure without inducing any major changes in plasma angiotensinogen levels or plasma renin activity. These results indicate that the differential chromosome segment trapped in the SHR chromosome 19 congenic strain contains a quantitative trait locus that influences blood pressure in the SHR but that this blood pressure effect is not explained by differences in plasma angiotensinogen levels or angiotensinogen expression.

Angiotensinogen↗
PubMed1999

Genetic isolation of a chromosome 1 region affecting susceptibility to hypertension-induced renal damage in the spontaneously hypertensive rat.

Linkage studies in the fawn-hooded hypertensive rat have suggested that genes influencing susceptibility to hypertension-associated renal failure may exist on rat chromosome 1q. To investigate this possibility in a widely used model of hypertension, the spontaneously hypertensive rat (SHR), we compared susceptibility to hypertension-induced renal damage between an SHR progenitor strain and an SHR congenic strain that is genetically identical except for a defined region of chromosome 1q. Backcross breeding with selection for the markers D1Mit3 and Igf2 on chromosome 1 was used to create the congenic strain (designated SHR.BN-D1Mit3/Igf2) that carries a 22 cM segment of chromosome 1 transferred from the normotensive Brown Norway rat onto the SHR background. Systolic blood pressure (by radiotelemetry) and urine protein excretion were measured in the SHR progenitor and congenic strains before and after the induction of accelerated hypertension by administration of DOCA-salt. At the same level of DOCA-salt hypertension, the SHR.BN-D1Mit3/Igf2 congenic strain showed significantly greater proteinuria and histologically assessed renal vascular and glomerular injury than the SHR progenitor strain. These findings demonstrate that a gene or genes that influence susceptibility to hypertension-induced renal damage have been trapped in the differential chromosome segment of the SHR.BN-D1Mit3/Igf2 congenic strain. This congenic strain represents an important new model for the fine mapping of gene(s) on chromosome 1 that affect susceptibility to hypertension-induced renal injury in the rat.

Animals↗
PubMed1999

4-hydroxynonenal triggers an epidermal growth factor receptor-linked signal pathway for growth inhibition.

Lipid peroxidation has been implicated in the pathogenesis of various diseases. As a major product of membrane lipid peroxidation, 4-hydroxynonenal (HNE) appears after various kinds of oxidative stress, and is known to induce cell growth inhibition. We here analysed the HNE-mediated signal transduction cascade for the growth inhibition of human epidermoid carcinoma A431 cells. HNE dose-dependently induced phosphorylation of multiple cellular proteins including epidermal growth factor receptor (EGFR) in A431 cells, and rapidly upregulated the catalytic actions of EGFR for autophosphorylation and for phosphorylation of casein as an exogenous substrate. Immunoblot analysis by use of HNE-specific antibody demonstrated the binding of HNE to EGFR along with its activation. This binding, which did not induce cross-linking of EGFR, caused a capping of the receptor on the cell surface which mimicked the capping induced by EGF. Phosphorylation and activation of EGFR were followed by phosphorylation of adaptor protein Shc and activation of MAP kinase. Both genistein as a wide spectrum protein tyrosine kinase inhibitor and AG1478 as a specific EGFR tyrosine phosphorylation blocker inhibited activation of EGFR and MAP kinase by HNE. The same inhibitors prevented HNE-mediated growth inhibition, suggesting a close linkage between EGFR/MAP kinase activation and growth inhibition after exposure to HNE. Our results suggest that EGFR may be one of the primary targets of HNE for an oxidative stress-linked cell growth inhibition.

Aldehydes↗
PubMed1999

Vitamin D and retinoids in parathyroid glands (review).

Vitamin D and retinoids are important regulators of differentiation and proliferation in a number of tissues, and have been implicated as chemopreventive agents in several different tumors. While vitamin D is known to be important for regulation of parathyroid function and proliferation, it has recently been established that parathyroid cells also are targets for retinoids. Hyperparathyroidism (HPT) is a common disorder, and evaluation of the disease has indicated high prevalence of subclinical disease, as well as clear benefits of offering treatment for the disease. This review summarizes the data so far gathered concerning parathyroid cells, vitamin D and retinoids, with clear implication on prospects of possible medical treatment of hyperparathyroidism.

Animals↗
PubMed1999

Thrombopoietin has a differentiative effect on late-stage human erythropoiesis.

To further explore the mechanism of the effect of thrombopoietin (TPO) on erythropoiesis, we used a two-phase culture system to investigate the effect of TPO on late-stage human erythroid lineage differentiation. In serum-free suspension and semisolid cultures of human peripheral blood derived erythroid progenitors, TPO alone did not produce benzidine-positive cells. However, in serum-containing culture, TPO alone stimulated erythroid cell proliferation and differentiation, demonstrated by erythroid colony formation, production of benzidine-positive cells and haemoglobin (Hb) synthesis. Monoclonal anti-human erythropoietin antibody and anti-human erythropoietin receptor antibody completely abrogated the erythroid differentiative ability of TPO in the serum-containing systems. This implied that binding of EPO and EPO-R was essential for erythropoiesis and the resultant signal transduction may be augmented by the signals emanating from TPO-c-Mpl interaction. Experiment of withdrawal of TPO further demonstrated the involvement of TPO in late-stage erythropoiesis. RT-PCR results showed that there was EPO-R but not c-Mpl expression on developing erythroblasts induced by TPO in serum-containing system. Our results establish that TPO affects not only the proliferation of erythroid progenitors but also the differentiation of erythroid progenitors to mature erythroid cells.

Cell Differentiation↗
PubMed1999

The cytotoxic effects of a novel IH636 grape seed proanthocyanidin extract on cultured human cancer cells.

Grape seed proanthocyanidins are natural antioxidants which possess a broad spectrum of chemoprotective properties against free radicals and oxidative stress. In this study, we have assessed the cytotoxicity of a novel IH636 grape seed proanthocyanidin extract (GSPE) against MCF-7 human breast cancer cells, A-427 human lung cancer cells, CRL-1739 human gastric adenocarcinoma cells and K562 chronic myelogenous leukemic cells at 25 and 50 mg/lit concentrations for 0-72 h using cytomorphology and MTT cytotoxicity assay. In addition, we compared the effects on normal human gastric mucosal cells and normal J774A.1 murine macrophage cells with the effects on the cancer cell lines. Concentration- and time-dependent cytotoxic effects of GSPE were observed on the MCF-7 breast cancer, A-427 lung cancer and gastric adenocarcinoma cells. Following incubation of the MCF-7 cells with 25 mg/lit of the GSPE approximately 6.5, 30 and 43% inhibitions in cell growth were observed at 24, 48 and 72 h of incubation, respectively, while incubation of the MCF-7 cells with 50 mg/lit of the GSPE resulted in 11, 35 and 47% inhibition in cell growth at these same points, respectively. Similar results were observed in the A-427 and gastric adenocarcinoma cells. GSPE exhibited no cytotoxicity toward the neoplastic K562 myelogenous leukemic cells. However, GSPE enhanced the growth and viability of the normal human gastric mucosal cells and J774A.1 murine macrophage cells. These data demonstrate that GSPE exhibited cytotoxicity towards some cancer cells, while enhancing the growth and viability of the normal cells which were examined.

Adenocarcinoma↗
PubMed1999

Antisense knockdown of glutamate transporters alters the subfield selectivity of kainate-induced cell death in rat hippocampal slice cultures.

Organotypic rat hippocampal slice cultures were used to study the role of excitatory amino acid transporters (EAATs) in kainate-induced cell death. Expression of the neuronal (EAAT3) or glial (EAAT2) transporters was inhibited with antisense phosphothioate oligonucleotides, and cytotoxicity was assessed with propidium iodide uptake. In control cultures, a concentration of 10 microM kainate was more cytotoxic in CA3 than in CA1. Treatment for 24 h with EAAT3 antisense oligonucleotide decreased kainate toxicity in CA1 but had an opposite effect in CA3. Neither antisense oligonucleotide to EAAT2 nor mismatch oligonucleotide to EAAT3 decreased kainate toxicity in CA1. Immunoblotting with affinity-purified antibodies showed that EAAT3 antisense oligonucleotide decreased selectively EAAT3 but not EAAT2 protein levels, and vice versa. NMDA was more cytotoxic in CA1 than in CA3, and antisense oligonucleotides to either EAAT3 or EAAT2 did not decrease the NMDA effect in CA1 or CA3. Dihydrokainate and DL-threo-beta-hydroxyaspartic acid were more cytotoxic in CA1 than in CA3, suggesting that the higher vulnerability of CA3 to kainate was not the result of its activity as transporter blocker. We conclude that glutamate transporters differentially regulate excitotoxicity in different hippocampal subfields.

ATP-Binding Cassette Transporters↗
PubMed1999

Vascular endothelial growth factor levels and induction of permeability in malignant pleural effusions.

Vascular endothelial growth factor (VEGF) is an important mediator of angiogenesis and vascular permeability. We hypothesized that malignant pleural effusions may contain high levels of VEGF protein as well as other cytokines implicated in these processes. Pleural effusions cytologically proven to be malignant were collected from 39 patients with various types of cancer, and VEGF, interleukin-8, and angiogenin levels in the effusions were determined by immunoassay. Negative controls were nonmalignant ascites and serum samples from healthy individuals. VEGF levels were significantly higher than those of control samples in pleural effusions secondary to breast, mesothelioma, and non-small cell lung cancer and when all malignant pleural effusion samples were pooled. Neither interleukin-8 nor angiogenin levels were elevated in malignant pleural effusions relative to the control samples. Vascular permeability, which was measured by using the Miles assay in nude mice, was increased proportionately with VEGF levels in the malignant pleural effusions; this increase in permeability induced by injection of recombinant VEGF or the malignant effusions was reduced by pretreating the mice with a VEGF receptor antibody.

Angiogenesis Inducing Agents↗
PubMed1999

Inhibitory effects of sodium quercetin monosulfate on pig platelet aggregation induced by thrombin.

AIM: To study the inhibitory effects of sodium quercetin monosulfate (SQMS) on pig platelet aggregation induced by thrombin. METHODS: Platelet aggregation was analyzed by turbidimetry. Cytosolic free calcium concentration ([Ca2+]i) was determined by Fura-2 fluorescence. Activity of protein kinase C (PKC) was assayed by incubating PKC with histone III S and [gamma-32 P] ATP. The cytoskeletal proteins were precipitated by Triton X-100 and separated by SDS-PAGE. RESULTS: SQMS inhibited the platelet aggregation induced by thrombin 500 U.L-1 with IC50 132 (50-347) mumol.L-1. SQMS inhibited Ca2+ influx in blood platelets induced by thrombin 500 U.L-1 in the presence of extracellular Ca2+ 1 mmol.L-1 with IC50 20 (9-46) mumol.L-1; SQMS inhibited the internal Ca2+ release in the absence of extracellular Ca2+. SQMS also decreased [Ca2+]i level in quiescent blood platelets. SQMS (10-160 mumol.L-1) inhibited the activity of cytosolic PKC from blood platelets in a concentration-dependent manner, but had no effect on membrane PKC. SQMS (20-80 mumol.L-1) inhibited the actin polymerization induced by thrombin 500 U.L-1 inblood platelets in a concentration-dependent manner. CONCLUSION: SQMS inhibited pig platelet aggregation induced by thrombin and its mechanism might be due to its inhibitions of Ca2+ influx, internal Ca2- release, PKC activity, and actin polymerization.

Actins↗
PubMed1999

[Molecular-epidemiological analysis of HIV-1 initial prevalence in Guangxi, China].

OBJECTIVE: In April 1996, HIV-1 infection was first found among both commercial blood donors and IDUs in Guangxi. In order to identify the source of HIV-1 transmission and analyze the trend of HIV-1 epidemic, the study was carried out. METHODS: HIV-1 genetic subtypes were determined by peptide enzyme immunoassays (PEIA), RT-PCR and DNA sequencing. RESULTS: Four subtypes of Group M HIV-1 were found in Guangxi:subtype B' (Thai B), C,D and E. Subtype E and C (1 person) were circulating among IDUs and hetrosexual, while subtype B' and D (1 person) were among commercial blood donors. Subtype B' infections were discovered among a group of commercial blood donors and one of them was infected by subtype D. CONCLUSION: It is the first report of subtype D infection and subtype E that were identified in China. This observation indicated that subtype E HIV-1 was spread into China from Southeast Asia, and a new epidemic region with subtype E HIV-1 would emerge in southern China. Serotyping might be a useful screening method for HIV-1 molecular epidemiological analysis.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Tentative association of the serotonin transporter with schizophrenia and unipolar depression but not with bipolar disorder in Han Chinese.

The serotonin transporter gene (SERT) plays an important role in the serotonin uptake into neurons. Recently, several polymorphisms including a variable-number-tandem-repeat (VNTR) in the second intron and an insertion/deletion polymorphism (5-HTT linked polymorphic region, 5-HTTLPR) were identified and reported to be associated with a variety of mental illnesses, including major depression, bipolar disorder, anxiety-related traits, and autism. In our study, we performed an association study between the SERT VNTR polymorphism and schizophrenia (n = 260), bipolar disorder (n = 137), and unipolar depression (n = 33) in the Han Chinese. A large group of ethnically matched control individuals (n = 362) were also genotyped. Allele 12 of the VNTR polymorphism was associated with schizophrenia (P = 0.007) and unipolar depression (P = 0.011). Bipolar disorder was not associated with the VNTR (P = 0.93). Thus, we conclude that the SERT VNTR polymorphism may be a risk factor for both schizophrenia and unipolar depression, but not for bipolar disorder, in the Han Chinese.

Alleles↗
PubMed1999

[The clinical application of triamcinolone to accelerate soft tissue expansion].

OBJECTIVE: To speed up the expansion procedure. METHODS: Triamcinolone was injected during tissue expansion in 26 cases. RESULTS: The study proved that triamcinolone shortened the injection interval to 32 +/- 6 hours. The mean time of full expansion was shortened to 20 +/- 5 days in the experimental group. The injection interval and mean time of full expansion were 6 +/- 2 days and 42 +/- 8 days respectively in the control group (P < 0.01). The immediate retraction ratios of expanded skin of the two groups were 17% and 26% respectively. CONCLUSION: This new method is feasible in clinical application.

Adolescent↗
PubMed1999

[Study on the effect of ligustrazine on adherent molecule expression of bone marrow cells in immune-mediated aplastic anemia mice].

OBJECTIVE: To explore the effect of ligustrazine on the expression of adherent molecule of bone marrow cells in immune-mediated aplastic anemia(AA) mice. METHODS: Each immune-mediated AA mouse was intraperitoneally injected with 5 mg ligustrazine twice a day. On the 14th day, expressions of CD49d and CD49c in bone marrow mononuclear cells(MNC) were detected by flow cytometry, and VCAM-1 on stromal cells by immunohistochemistry SABC. RESULTS: Expressions of CD49d, CD49e and VCAM-1 were significantly lower in AA group than in normal group(t = 11.96, 17.18 and 7.09 respectively, P < 0.001), and were much higher in ligustrazine treated group than in non-treated group(t = 9.05, 14.61 and 6.91 respctively, P < 0.001). Expressions of CD49d and VCAM-1 were in the normal range in ligustrazine group. CONCLUSIONS: Ligustrazine can increase the expression of adherent molecule of bone marrow cells in immune-mediated AA mice, thus promote the growth of hematopoietic cells.

Anemia, Aplastic↗
PubMed1999

Selection and determination of specific and protective antigens of Mycobacterium tuberculosis.

OBJECTIVE: To select and identify the specific and protective antigens of Mycobacterium tuberculosis (M. tuberculosis) for searching a new approach to diagnose and treat tuberculosis. METHODS: Extract and culture filtrates of M. tuberculosis were obtained by ultrasonic treatment and millipore membrane filtration, respectively. The protein samples were tested with monoclonal antibody (MAb) and patient sera. The proteins showing positive reaction were sequenced on Beckman/LF 3200/peptide amino acid sequencer. RESULTS: Proteins of M. tuberculosis with molecular weight of 31 ku and 30 ku showed positive results when reacted with anti-M. tuberculosis MAb and sera of tuberculosis patients, but not with normal mouse serum and healthy human sera. N-terminal sequences of the 31 ku and 30 ku antigen were Ala Glu Val Asp Trp Leu Val Phe Ala Val and Phe Ser Arg Pro Gly Leu Pro Val Glu Try respectively. CONCLUSION: 31 ku and 30 ku proteins of M. tuberculosis are immune protective proteins. They play important or dominant roles in determination of immunorecognization.

Amino Acid Sequence↗
PubMed1999

[Effect of composite blood-activating decoction on expression of adherent molecule and cyclin in bone marrow hematopoietic cells in mice of immune-induced aplastic anemia].

OBJECTIVE: To study the effect of composite blood-activating decoction (CBAD) on expression of adherent molecule CD49 d and cyclin D2 in bone marrow hematopoietic cells in experimental immune-mediated aplastic anemia (AA) mice. METHODS: After the model of AA was established, the animals were fed with 0.2 ml of 100% CBAD, twice a day for 12 days. Te CD49 d and cyclin D2 expression level of bone marrow hematopoietic cells in model mice were measured by flow cytometor analysis system at the 13th day of experiment. RESULTS: CD49 d expression level in CBAD group was significantly higher than that in the AA group (P < 0.05), and was similar to that in the normal group (P > 0.05). The expression of cyclin D2 in CBAD group was significantly higher than that in the AA group (P < 0.01), but the cell count of G0 + G1 phase was significantly lower in the CBAD group, as compared with the AA group, P < 0.01. CONCLUSION: CBAD can increase the expression of adherent molecule CD49 d and cyclin D2 in bone marrow hematopoietic cells, and promote the growth of hematopoietic cells.

Anemia, Aplastic↗
PubMed1999

[The effects of levothyroxine replacement therapy on bone and mineral metabolism in patients with hypothyroidism].

OBJECTIVE: To investigate the effects of short-term thyroid hormone replacement therapy on bone and mineral metabolism in patients with hypothyroidism. METHODS: Enzyme linked immunosorbent assay (ELISA) was used to measure urinary deoxypyridinoline (DPD) and radioimmunoassay (RIA) to measure serum calcitonin (CT), parathyroid hormone (PTH-M), bone GLA protein (BGP), free T(3) (FT(3)), free T(4) (FT(4)) and thyroid-stimulating hormone (TSH) in 29 patients with hypothyroidism before and after treatment with levothyroxine for (11.5 +/- 2.5) months. Dual energy X-ray absorptiometry was used to measure bone mineral density (BMD) of their spine (L(2 - 4)) and femur neck, trochanter and Ward's triangle. The results were compared with those in 37 healthy controls. RESULTS: In hypothyroidism patients before treatment, serum BGP level was significantly lower (P < 0.05) than but urinary DPD was similar with those of control. BMD was significantly lower in postmenopausal patients (P < 0.01 - 0.001) than that in control group, but there was no change in premenopausal patients. After replacement therapy serum BGP and urinary DPD elevated significantly (P < 0.05), whereas BMD decreased slightly both in the premenopausal and postmenopausal patients when compared with that before treatment, with no statistical significance (P > 0.05). BMD decreased by 0.7% and 1.7% - 5.1% in premenopausal and postmenopausal patients respectively, but there was no significant difference between these two groups (P > 0.05). FT(3) was positively correlated with BGP. FT(4) and FT(3) were positively correlated with DPD. BMD of femur neck and trochanter sites was negatively correlated with FT(4). CONCLUSION: Short-term physiological dose levothyroxine replacement therapy causes increase of bone turnover and leads to bone mass loss to various extent on hypothyroidism patients.

Adult↗