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Biomedical subjects

X Yao

Publications and source records attributed to X Yao.

At least 91 records · Page 5Linked to original sources
PubMed1999

Studies on the callus cultures of Ginkgo biloba and its metabolites-ginkgolides.

The production of ginkgolides in callus culture of Ginkgo biloba was reported. The affection of some physical factors and chemical substances on the induction and growth of calli was also investigated. A biologically quantitative method (platelet aggregation induced by PAF) and HPLC were successfully used for the determination of Ginkgolides A and B in all kinds of callus cultures. The result showed that the content of Ginkgolides B in the callus cultures varies from 0.005% to 0.01%, which is one of the best results for the callus culture of G.biloba in the world.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1999

Significance of anti-neutrophil cytoplasmic antibodies in patients with pauci-immune crescentic glomerulonephritis.

OBJECTIVE: To evaluate the significance of serum antineutrophil cytoplasmic antibodies (ANCAs) and the effects of immune suppressive treatments on its activity in patients with pauci-immune crescentic glomerulonephritis (PICGN). METHODS: Serum ANCAs and myeloperoxidase (MPO)-ANCA were detected by indirect immunofluorescence and enzyme-linked immunosorbent assay (ELISA) methods respectively, and the renal tissues infiltrating cells including CD4+, CD8+, CD68+ and PCNA+ cells were determined by four-layer peroxidase-antiperoxidase (PAP) method. The clinical manifestations, pathologic features and immune pathologic changes in patients with positive ANCAs were compared with that in patients with negative ANCAs. The effects of immune suppressive therapy on clinic and pathologic changes as well as ANCAs activity were also investigated in ANCAs positive and ANCAs negative patients. RESULTS: Both of clinic active manifestations such as the degree of hematuria, rapidly progressive renal failure and pathologic active features including segmental capillary necrosis and vasculitis were much common in patients with positive ANCAs as compared with that in patients with negative ANCAs. The number of infiltrating cells in renal tissue, especially CD4+ cells, was markedly higher in ANCAs positive patients than that in ANCAs negative patients. The effects of immune suppressive therapy were also much better in patients with positive ANCAs than that in patients with negative ANCAs. CONCLUSION: Serum ANCAs is not only a marker for diagnosis of systemic vasculitis, but also a sensitive predictor for evaluation of diseases' activity and treatment in patients with PICGN. The good effect of immune suppressive treatments on patients with PICGN is partially associated with the degree of ANCAs activity.

Adolescent↗
PubMed1999

[Spontaneous renal rupture].

OBJECTIVE: To study clinical regularity of spontaneous renal rupture. METHODS: 16 cases of this disease were reviewed. Renal carcinoma was found in 4, angiomyolipoma in 2, undetermined etiology in 3, and invasive colic cancer, kidney cyst, nephrolithiasis, SLE with nephritis, polycythemia vera, renal tuberculosis, portal hypertension in 1 each. RESULTS: CT demonstrated a sensitivity of 87.5% in identifying the underlying kidney mass, which was higher than that (25%) of B-type ultrasound and (0) KUB + IVU. Radical nephrectomy was carried out in 6 cases, renal-reserved operation in 5, and conservative treatment in 5. CONCLUSIONS: 60% of spontaneous renal rupture are due to kidney neoplasia. CT scanning is the most valuable diagnostic procedure. If the primary cause has not been clarified, close follow-up with periodic CT scanning might be mandatory.

Adult↗
PubMed1999

[Expression of heat shock protein (HSP70) in normal endometrium and endometrial carcinomas].

Expression of heat shock protein 70 (HSP70) in normal endometrium tissue and endometrial carcinoma was analyzed by the present authors to determine the relationship between HSP70 expression and the prognosis of endometrial carcinomas. The immunohistochemical reactivity of monoclonal antibodies against HSP70 was examined in 44 endometrial carcinomas and 40 normal endometria HSP70 respectively. HSP70 was expressed stronger in carcinomas than in normal. Expression of HSP70 was found in 56.82% of endometrial carcinomas and was well correlated with histological grade (P < 0.05). These results suggest that HSP70 may play a role in the prognosis of endometrial carcinomas.

Endometrial Neoplasms↗
PubMed1998

HERG potassium channel activation is shifted by phorbol esters via protein kinase A-dependent pathways.

We investigated the effects of the phorbol ester phorbol 12-myristate 13-acetate (PMA) on the rapid component of the delayed rectifier potassium current, IKr, in guinea pig cardiomyocytes and found that the IKr current amplitude was reduced by 20% with 10 nM PMA and 44% with 100 nM PMA. The ether-a-go-go-related gene (HERG) encodes IKr in human heart. We expressed HERG heterologously in Xenopus oocytes and investigated the effects of PMA on the delayed rectifier potassium current. Upon application of PMA in a concentration of 100 nM, we found a similar reduction of HERG outward current amplitude by 59%. This reduction was due to a shift in the HERG activation curve by 37 mV. The ED50 for the PMA-induced shift was 9.0 nM. The inactive 4alpha-phorbol 12-myristate 13-acetate (4alpha-PMA) had no effect. PMA is known to act by stimulating distinct protein kinase cascades. Additional application of the specific protein kinase C inhibitors chelerythrine (10 microM) or bisindolylmaleimide (1 microM) could not attenuate the PMA-induced shift. In contrast, the shift by PMA was reduced significantly when the specific protein kinase A (PKA) inhibitors H89 (50 microM) or KT5720 (2.5 microM) were applied. Forskolin (400 microM), an activator of the adenylate cyclase that results in PKA activation, shifted the HERG activation curve by 14 mV. Moreover the specific protein kinase C activator 1-stearoyl-2-arachidonylglycerol (10 microM) showed no effect. Our data suggest that mainly PKA is mediating the shift of the HERG activation kinetics.

Alkaloids↗
PubMed1998

Characterization of a regulatory region in the N-terminus of rabbit kv1.3.

The N-terminus of rabbit Kv1.3 contains a signal sequence which regulates expression of Kv1.3 proteins in the plasma membrane. Removal of an N-terminal region (aa3-39) produced an increase in expressed K+ current. Progressive deletion at the N-terminus demonstrated that the shortest deletion required for the elevation of K current is D6-34. Since the functional signal sequence must include both ends of the peptide segment aa6-34 where charged residues are densely distributed, it is conceivable that this N-terminal signal sequence is related to charge or its associated hydrophilicity. Removal of two charged residues (31R, 33E) through amino acid substitution which converts deletion construct D3-27 to D3-27* effectively raises the amplitude of expressed current, further indicating the importance of charged residues. With the use of a mutated dynamin and a soluble N-terminal peptide, we also revealed that the N-terminal signal sequence may not act through the endocytotic pathway.

Amino Acid Sequence↗
PubMed1998

Differential effects of d, l-sotalol and d-sotalol on isoproterenol-increased delayed rectifier outward potassium current in guinea pig single ventricular myocytes.

The aim of this study was to compare the effects of d, l-sotalol and d-Sotalol on the delayed rectifier K+ outward current in the presence of isoproterenol at different concentrations. Time-dependent delayed rectifier K+ outward currents were measured in isolated guinea pig single myocytes using the whole-cell configuration of the patch-clamp technique. Currents were measured in response to 300 ms depolarizing pulses from a holding potential of -40 mV in three experimental protocols [control, isoproterenol (10(-9) mol/L-10(-6) mol/L), and isoproterenol (10(-9) mol/L-10(-6) mol/L) plus either d, l-Sotalol (10(-4) mol/L) or d-Sotalol (10(-4) mol/L)]. IK tail currents were measured upon repolarization to -40 mV. It was found that IK was significantly amplified in the presence of isoproterenol (10(-9) mol/L-10(-6) mol/L) plus d-Sotalol. At 10(-8) mol/L isoproterenol, IK was increased by 92.7% +/- 17.1% (P < 0.05) and 54.3% +/- 13.4% after d-Sotalol addition (P < 0.05). In contrast, d, l-Sotalol completely conteracted the increase of Ik by isoproterenol (< 10(-8) mol/L), and compared to control, IK was decreased by 35.6% +/- 8.1% at 10(-8) mol/L isoproterenol plus d, l-Sotalol (P < 0.05). It is concluded that the beta-adrenergic blocking property of d, l-Sotalol but not that of d-Sotalol maintains the delayed rectifier K+ outward current blockade in the presence of isoproterenol in guinea pig myocytes. This might contribute to a superior antiarrhythmic efficacy as compared to d-Sotalol.

Adrenergic beta-Agonists↗
PubMed1998

A K+ single channel and whole-cell clamp study on the effects of levocromakalim in guinea pig portal vein cells.

Single channel cell-attached patch and whole-cell clamp experiments on the mode of action of the K+ channel opener (KCO), levcromakalim, were performed in guinea pig isolated portal vein cells. At +20 mV (135/23 mM K+ in bath/pipette), 10 microM levcromakalim activated K+ channels with a chord conductance of 23.2 pS (K(KCO)), which were sensitive to the blocker of ATP-dependent K+ channels (K(ATP)), glibenclamide. Voltage steps from -80 mV to +20 mV activated 4-aminopyridine-sensitive K+ channels of 6.5 pS with properties of delayed rectifier K+ channels (Kv). In patches which upon a previous voltage step had revealed the existence of Kv, levcromakalim reduced the open-probability of Kv, but it did not concomitantly activate K(KCO). During the course of the experiments, but unrelated to the presence of levcromakalim, large conductance K+ channels (BK(Ca)) appeared which could be inhibited by iberiotoxin, a selective blocker of BK(Ca), and by the membrane-permeant calcium buffer, BAPTA/AM, but not by glibenclamide. Whole-cell current-voltage (i-V) relations were established in response to voltage ramps from +50 mV to -100 mV; on subtraction of control i-V curves from i-V curves obtained in the presence of 10 microM levcromakalim, the KCO-induced K+ current remained which was proportional to voltage. This is not compatible with the upward-bent curvature predicted by the GHK current equation for purely resistive channels at high [K+]i versus low [K+]o. In conclusion, in the guinea pig portal vein cells, no evidence could be established for the hypotheses that KCOs may act via conversion of Kv to K(ATP) (Beech and Bolton 1989; Edwards et al. 1993) or by activation of BK(Ca) (Balwierczak et al. 1995). In these cells, mild inward rectification of the levcromakalim-induced current was observed which underlines their relationship to K(ATP) in other tissues.

Animals↗
PubMed1998

Polyglutamine-expanded human huntingtin transgenes induce degeneration of Drosophila photoreceptor neurons.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder. Disease alleles contain a trinucleotide repeat expansion of variable length, which encodes polyglutamine tracts near the amino terminus of the HD protein, huntingtin. Polyglutamine-expanded huntingtin, but not normal huntingtin, forms nuclear inclusions. We describe a Drosophila model for HD. Amino-terminal fragments of human huntingtin containing tracts of 2, 75, and 120 glutamine residues were expressed in photoreceptor neurons in the compound eye. As in human neurons, polyglutamine-expanded huntingtin induced neuronal degeneration. The age of onset and severity of neuronal degeneration correlated with repeat length, and nuclear localization of huntingtin presaged neuronal degeneration. In contrast to other cell death paradigms in Drosophila, coexpression of the viral antiapoptotic protein, P35, did not rescue the cell death phenotype induced by polyglutamine-expanded huntingtin.

Animals↗
PubMed1998

Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair.

Germline mutations in the human MSH2, MLH1, PMS2 and PMS1 DNA mismatch repair (MMR) gene homologues appear to be responsible for most cases of hereditary non-polyposis colorectal cancer (HNPCC; refs 1-5). An important role for DNA replication errors in colorectal tumorigenesis has been suggested by the finding of frequent alterations in the length of specific mononucleotide tracts within genes controlling cell growth, including TGF-beta receptor type II (ref. 6), BAX (ref. 7) and APC (ref. 8). A broader role for MMR deficiency in human tumorigenesis is implicated by microsatellite instability in a fraction of sporadic tumours, including gastric, endometrial and colorectal malignancies. To better define the role of individual MMR genes in cancer susceptibility and MMR functions, we have generated mice deficient for the murine homologues of the human genes MLH1, PMS1 and PMS2. Surprisingly, we find that these mice show different tumour susceptibilities, most notably, to intestinal adenomas and adenocarcinomas, and different mutational spectra. Our results suggest that a general increase in replication errors may not be sufficient for intestinal tumour formation and that these genes share overlapping, but not identical functions.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Nociceptin (ORL-1) and mu-opioid receptors mediate mitogen-activated protein kinase activation in CHO cells through a Gi-coupled signaling pathway: evidence for distinct mechanisms of agonist-mediated desensitization.

The recently identified 17-amino acid peptide nociceptin (orphanin FQ) is the endogenous ligand for the opioid receptor-like-1 (ORL-1) receptor. A physiologic role for nociceptin (OFQ) activation of the ORL-1 receptor (OFQR) may be to modulate opioid-induced analgesia. The molecular mechanism by which nociceptin (OFQ) and ORL-1 (OFQR) modify opioid-stimulated effects, however, is unclear. Both ORL-1 (OFQR) and opioid receptors mediate pertussis toxin (PTX)-sensitive signal transduction, indicating these receptors are capable of coupling to Gi/Go proteins. This study determines that nociceptin stimulates an intracellular signaling pathway, leading to activation of mitogen-activated protein (MAP) kinase in CHO cells expressing ORL-1 receptor (OFQR). Nociceptin (OFQ)-stimulated MAP kinase activation was inhibited by PTX or by expression of the carboxyl terminus of beta-adrenergic receptor kinase (betaARKct), which specifically blocks Gbetagamma-mediated signaling. Expression of the proline-rich domain of SOS (SOS-PRO), which inhibits SOS interaction with p21ras, also attenuated nociceptin (OFQ)-stimulated MAP kinase activation. The phosphatidylinositol 3-kinase (PI-3K) inhibitors wortmannin and LY294002 reduced nociceptin (OFQ)-stimulated MAP kinase activation, whereas inhibition of protein kinase C (PKC) activity by bisindolylmaleimide I or cellular depletion of PKC had no effect. In a similar manner, in cells expressing mu-opioid receptor, [D-Ala2,N-Me-Phe4,Gly-ol]-enkephalin (DAMGO; a mu-opioid receptor-selective agonist) stimulated PTX-sensitive MAP kinase activation that was inhibited by wortmannin, LY294002, betaARKct expression, or SOS-PRO expression but not affected by inhibition of PKC activity. These results indicate that both ORL-1 (OFQR) and mu-opioid receptors mediate MAP kinase activation via a signaling pathway using the betagamma-subunit of Gi, a PI-3K, and SOS, independent of PKC activity. In cells expressing both ORL-1 (OFQR) and mu-opioid receptors, pretreatment with nociceptin decreased subsequent nociceptin (OFQ)- or DAMGO-stimulated MAP kinase activation. In contrast, pretreatment of cells with DAMGO decreased subsequent DAMGO-stimulated MAP kinase but had no effect on subsequent nociceptin (OFQ)-stimulated MAP kinase activation. These results demonstrate that nociceptin (OFQ) activation of ORL-1 (OFQR) can modulate mu-opioid receptor signaling in a cellular system.

Animals↗
PubMed1998

Role of endothelin in thrombolysis in rat abdominal aorta.

The endothelium of blood vessels is of great importance in maintaining blood fluidity and modulating thrombogenesis. Endothelin (ET) participates in thrombogenesis and its role in the pathogenesis of heart diseases such as acute myocardinal infarction has been proved, but little is known about the effect of ET on thrombolysis. Using a model of thrombosis in rat abdominal aorta induced by direct current-ferric trichloride, we found that the plasma ET level was 3.7 times the baseline after lysing the thrombus with urokinase (250,000 U/kg) while 5 micrograms/kg of exogenous ET prolonged the time of thrombolysis to 115% of baseline control. Plasma ET level was six times the baseline level. Incubation of a rat aortic strip in vitro with taurine (20 mmol/L) had no effect on baseline ET release, but taurine prohibited the stimulation of thrombin and A23187 of ET release in a dose-dependent way. Plasma ET decreased between 17 and 40% after injection of taurine, which also decreased by 45% the time of lysis of thrombus. From the above data it might be concluded that ET inhibits thrombolysis and that the abnormally increasing plasma ET can be attenuated by taurine, which is beneficial to thrombolysis.

Animals↗
PubMed1998

State of actin in gastric parietal cells.

Remodeling of the apical membrane-cytoskeleton has been suggested to occur when gastric parietal cells are stimulated to secrete HCl. The present experiments assayed the relative amounts of F-actin and G-actin in gastric glands and parietal cells, as well as the changes in the state of actin on stimulation. Glands and cells were treated with a Nonidet P-40 extraction buffer for separation into detergent-soluble (supernatant) and detergent-insoluble (pellet) pools. Two actin assays were used to quantitate actin the deoxyribonuclease I binding assay to measure G-actin and F-actin content in the two pools and a simple Western blot assay to quantitate the relative amount of actin in the pools. Functional secretory responsiveness was assayed by aminopyrine accumulation. About 5% of the total parietal cell protein is actin, with about 90% of the actin present as F-actin. Stimulation of acid secretion resulted in no measurable change in the relative amounts of G-actin and cytoskeletal F-actin. Treatment of gastric glands with cytochalasin D inhibited acid secretion and resulted in a decrease in F-actin and an increase in G-actin. No inhibition of parietal cell secretion was observed when phalloidin was used to stabilize actin filaments. These data are consistent with the hypothesis that microfilamentous actin is essential for membrane recruitment underlying parietal cell secretion. Although the experiments do not eliminate the importance of rapid exchange between G- and F-actin for the secretory process, the parietal cell maintains actin in a highly polymerized state, and no measurable changes in the steady-state ratio of G-actin to F-actin are associated with stimulation to secrete acid.

Actins↗
PubMed1998

[Myocardial function after fluid resuscitation with addition of anisodamine in severely burned rabbits].

OBJECTIVE: To evaluate the effect of fluid resuscitation with addition of anisodamine (Ani) on myocardial function in severely burned rabbits. METHODS: III degree burn injury covering 25% total body surface area (TBSA) was produced on rabbits. LVSP, LV +/- dp/dtmax were measured with fluid resuscitation alone, administration of Ani alone, and fluid resuscitation plus Ani before burn, immediately after burn and 1, 3, 5, 7 h after burn. RESULTS: It was showed that myocardial contractility and relaxation were depressed 1 h after burn. Fluid resuscitation alone and administration of Ani alone could significantly improve myocardial contractility and relaxation only within 3 h postburn. With fluid resuscitation plus Ani (5 mg.kg-1), myocardial contractility and relaxation were improved statistically significantly as compared with control group without treatment (P < 0.01), with the values approaching the normal level. CONCLUSION: Our data demonstrate that the administration of Ani (5 mg.kg-1) in addition to fluid resuscitation is beneficial to burn injury, especially to myocardial function, and it provides a promising approach for the future treatment of burns.

Animals↗
PubMed1998

[Expression of P62c-myc protein in breast cancer and its clinical significance].

The objective of this study was to determine the clinical significance of P62c-myc protein expression in breast cancer. P62c-myc protein was detected in 107 patients with breast cancer by immunohistochemical techniques (LSAB). The results showed that the positive rate of P62c-myc protein expression was 63.55% (68/107). The overexpression of P62c-myc protein related negatively with survival. 94.00% of the cases with overexpression of P62c-myc protein survived < or = 5 years, 65.00% survived > 5 years-< 10 years, and 21.62% survived > or = 10 years. There were significant associations of P62c-myc expression with advance clinical stage, high histological grade, and positive axillary node status in breast cancers. All of these findings suggested that overexpression of P62c-myc might be an important prognostic factor, and the detection of P62c-myc protein might be arranged as a regular pathological examination in the cases of breast cancer.

Adolescent↗
PubMed1998

[Ex vivo study of ultraviolet-B inactivating immunocompetence and hematopoietic potential of cord blood].

OBJECTIVE: To determine the differences of the effect of ultraviolet-B(UVB) on lymphocyte and hematopoietic progenitor cell in cord blood. METHODS: The viability, proliferative response and stimulatory activity in mixed lymphocyte culture (MLC), colony forming unit-granulo-monocyte (CFU-GM) colony growth and percentage of CD34+ cell of cord blood in Hanks medium after 0, 5, 10, 20, 50 mJ/cm2 UVB-irradiation were compared. RESULTS: Like the proliferative response and stimulatory activity, CFU-GM colony also showed UVB-irradiation dose dependent decrease. However, much less colonies were destroyed by UVB irradition less than 10 mJ/cm2. More obvious differences were found when 20%(vol/vol) bovine serum was added to the MNC medium. The percentage of CD34+ cell remained unchanged after UVB exposure. CONCLUSION: A lower dose of UVB exposure can slectively inactivate cord blood lymphocyte and antigen presenting cell while sparing hematopoietic progenitor cells. The data indicates the possibility of utility of UVB irradiation for graft-versus-host disease prophylaxis in cord blood transplantation.

Antigens, CD34↗