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B Gao

Publications and source records attributed to B Gao.

At least 73 records · Page 4Linked to original sources
PubMed2000

The cross-cultural generalizability of Axis-II constructs: an evaluation of two personality disorder assessment instruments in the People's Republic of China.

We examined the reliability, cross-instrument validity, and factor structure of Chinese adaptations of the Personality Diagnostic Questionnaire (PDQ-4+; N = 1,926) and Personality Disorders Interview (PDI-IV; N = 525) in psychiatric patients. Comparisons with data from Western countries suggest that the psychometric properties of these two instruments are comparable across cultures. Low to modest agreement between the PDQ-4+ and PDI-IV was observed for both dimensional and categorical personality disorder evaluations. When the PDI-IV was used as the diagnostic standard, the PDQ-4+ showed higher sensitivity than specificity, and higher negative predictive power than positive predictive power. Factor analyses of both instruments replicated the four-factor structure O'Connor and Dyce (1998) found in Western samples. Results suggested that conceptions and measures of DSM-IV personality disorders are cross-culturally generalizable to Chinese psychiatric populations.

Adult↗
PubMed2000

Organic anion-transporting polypeptides mediate transport of opioid peptides across blood-brain barrier.

Organic anion-transporting polypeptides (Oatps) are a rapidly growing gene family of polyspecific membrane transporters. In rat brain, Oatp1 (gene symbol Slc21a1) and Oatp2 (Slc21a5) are localized at the apical and basolateral domains, respectively, of the choroid plexus epithelium. Furthermore, Oatp2 is strongly expressed at the rat blood-brain barrier (BBB). This study localizes the human OATP (now called OATP-A; SLC21A3) at the BBB in humans. Furthermore, with the Xenopus laevis oocyte system the delta-opioid receptor agonists [D-penicillamine(2,5)]enkephalin (DPDPE) and deltorphin II were identified as new transport substrates of OATP-A. This OATP-A-mediated DPDPE and deltorphin II transport exhibited apparent K(m) values of approximately 202 and 330 microM, respectively, and OATP-A-mediated deltorphin II transport was inhibited by the mu-opioid receptor agonist Tyr-D-Ala-Gly-N-methyl-Phe-glycinol, the endogenous peptide Leu-enkephalin, and the opiate antagonists naloxone and naltrindole. DPDPE also was transported by rat Oatp1 (K(m) approximately 48 microM) and Oatp2 (K(m) approximately 19 microM), whereas deltorphin II was only transported by Oatp1 (K(m) approximately 137 microM). These results demonstrate that OATP-A can mediate transport of the analgesic opioid peptides DPDPE and deltorphin II across the human BBB. Furthermore, because rat Oatp1 and Oatp2 exhibit similar but not identical transport activities as OATP-A, the results generally indicate that members of the Oatp/OATP gene family of membrane transporters play an important role in carrier-mediated transport of opioid peptides across the BBB and blood-cerebrospinal fluid barrier of the mammalian brain.

Aged↗
PubMed2000

Detecting residual ischemia and identifying coronary artery disease after myocardial infarction using dobutamine technetium-99m-MIBI SPECT.

OBJECTIVE: To evaluate dobutamine technetium-99m methoxy isobutyl nitrile (sestamibi) single-photon emission computed tomography (Dobu-ECT) in detecting residual ischemia and identifying coronary vessel disease after myocardial infarction. METHODS: Sixty-two patients with confirmed myocardial infarction were studied with Dobu-ECT at the time of coronary artery angiography. Dobutamine was administered intravenously in incremental rates from 5 to 40 micrograms.kg-1.min-1 at 3-minute intervals. At the highest infusion rate, 7.4 x 10(8) Bq 99mTc-MIBI was injected intravenously, and tomographic imaging was performed after one hour. Resting images were taken after 24 hours, with a second dose of 99mTc-MIBI. RESULTS: The sensitivity of Dobu-ECT in detecting residual ischemia of myocardial infarction was 76%, which was higher than dobutamine electrocardiography (Dobu-ECG). Regardless of the single-, double- or triple-vessel diseases, Dobu-ECT was superior to Dobu-ECG in identifying residual ischemia (56% vs 4%, 86% vs 27%, 100% vs 47%, P < 0.01, respectively). The incidence of residual ischemia in patients receiving thrombolytic therapy was 67%, lower than patients without thrombolysis (72%) or those with an old myocardial infarction (94%). But the differences were not statistically significant. Dobu-ECT detected only 56% of ischemias in non-infarct related myocardium. Eighty-two percent of all significantly stenosed vessels were detected with Dobu-ECT, and 84% of patients with multivessel disease could be accurately identified. The sensitivity of Dobu-ECT was significantly greater for detecting severe stenosis over moderate stenosis. The sensitivity for detecting stenosis in the right coronary artery was greater than left anterior descending or left circumflex, but its specificity was lower. CONCLUSION: Dobu-ECT can identify residual ischemia, as well as its location and extent after myocardial infarction. Dobu-ECT can also accurately detect significantly stenosed vessels.

Adult↗
PubMed1999

Cross-talk between alpha(1B)-adrenergic receptor (alpha(1B)AR) and interleukin-6 (IL-6) signaling pathways. Activation of alpha(1b)AR inhibits il-6-activated STAT3 in hepatic cells by a p42/44 mitogen-activated protein kinase-dependent mechanism.

Treatment of primary rat hepatocytes or tranfected HepG2 cells with the alpha(1B)-adrenergic receptor (alpha(1B)AR) agonist phenylephrine (PE) significantly inhibited interleukin 6 (IL-6)-induced STAT3 binding, tyrosine phosphorylation, and IL-6-induced serum amyloid A mRNA expression. Western analyses and in vitro kinase assays indicate that this inhibition is not due to either down-regulation of STAT3 protein expression nor inactivation of upstream-located JAK1 and JAK2. Blocking the new RNA and protein syntheses antagonized the inhibitory effect of PE on IL-6-activated STAT3, suggesting synthesis of an inhibitory factor(s) is involved. The inhibitory effect of PE on IL-6 activation of STAT3 was also abolished by the tyrosine phosphatase inhibitor sodium vanadate, indicating involvement of protein tyrosine phosphatases. Furthermore, preincubation of the cells with the specific MEK1 inhibitor PD98059 or a dominant negative MEK1 reversed the inhibitory effect of PE, and expression of constitutively activated MEK1 alone abolished IL-6-activated STAT3. Taken together, these data indicate that PE inhibits IL-6 activation of STAT3 in hepatic cells by a p42/44 mitogen-activated protein kinase-dependent mechanism, and tyrosine phosphatases are involved. This inhibitory cross-talk between the alpha(1B)AR and IL-6 signaling pathways implicates the alpha(1B)AR involvement in regulating the IL-6-mediated inflammatory responses.

Animals↗
PubMed1999

Ethanol reduces neuronal excitability and excitatory synaptic transmission in the developing rat spinal cord.

Effects of acute ethanol (EtOH) exposure on motoneuron excitability and properties of synaptic transmission were examined in spinal cords of postnatal rats. Whole-cell patch clamp recordings and intracellular recordings with high-resistance electrodes were carried out in motoneurons of 1- to 4-day-old postnatal rats. To determine the effects of extracellular EtOH on action potential waveform, properties of current-evoked soma action potentials and motoneuron ability to generate repetitive action potential firing were examined. During a brief EtOH (70 mM) exposure, larger depolarizing current was required for action potential generation, the duration of the after hyperpolarizing potential increased, and fewer action potentials were produced during a prolonged intracellular current injection. These effects were reversed within 20 min of EtOH removal from the extracellular solution. To determine whether the reduced probability of action potential generation was associated with changes in synaptic transmission, properties of evoked synaptic potentials and spontaneous synaptic currents were investigated. In the presence of EtOH, the amplitude of dorsal root-evoked synaptic potentials was reduced, the frequency of spontaneous excitatory postsynaptic currents decreased, while the frequency of inhibitory postsynaptic currents increased. Our data suggested that acute EtOH exposure suppressed motoneuron electrical activity by decreasing motoneuron excitability and shifting the balance between excitatory and inhibitory synaptic transmission toward inhibition.

Action Potentials↗
PubMed1999

Ethanol rapidly inhibits IL-6-activated STAT3 and C/EBP mRNA expression in freshly isolated rat hepatocytes.

The ability of ethanol to inhibit regenerative processes in the liver is thought to play a key role in the development of alcoholic liver disease. To understand the underlying mechanisms, we investigated the effects of ethanol on the Janus kinasesignal transducer and activator transcription factor (JAK-STAT) signaling pathways in hepatocytes. Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression. Western analyses, in vitro kinase assays and in vivo cell labelling assays indicate that this inhibitory effect is not due to blocking the upstream-located JAK1, JAK2 or Tyk2 activation. On the contrary, acute ethanol exposure significantly potentiates IL-6-induced JAK1 autophosphorylation in vitro and in vivo. Pretreatment with sodium vanadate, a non-selective tyrosine phosphatase inhibitor, or with MG132 and lactacystin, proteasome inhibitors, does not abolish the ethanol inhibition of IL-6-induced STAT3 activation, suggesting that activation of protein tyrosine phosphatases or the ubiquitin-proteasome pathway is not involved. In view of the critical role of IL-6 signaling in liver regeneration, these findings suggest that the ability of biologically relevant concentrations of ethanol to markedly inhibit IL-6-induced STAT3 phosphorylation is one of the cellular mechanisms involved in the pathogenesis and progression of alcoholic liver diseases.

Animals↗
PubMed1999

Maturation of the response to bradykinin in resistance and conduit pulmonary arteries.

OBJECTIVE: Immaturity of the endothelial-dependent relaxation is thought to be characteristic of the newborn pulmonary elastic arteries. In adulthood, the reactivity of different pulmonary arterial segments varies. Therefore, we investigated the presence of endothelial heterogeneity in perinatal porcine pulmonary arteries and compared it with the adult by studying the bradykinin-, substance P- and acetylcholine-induced relaxations in different arteries. METHODS: Three types of pulmonary arteries (large conduit elastic, distal branching and resistance-sized; in situ diameters 0.7-1.7, 0.3-0.5 and 0.1-0.2 mm, respectively) were isolated from lungs of adult (nine months), young (60-84 h), newborn (4 min) and near-term foetal pigs. They were mounted for isometric force recording, contracted first with K+ = 125 mmol/l (reference contraction). Cumulative concentration-response curves to acetylcholine, substance P or bradykinin were obtained from prostaglandin F2 alpha (30 mumol/l) precontracted vessels. The effects of captopril and O2(95 or 8%) were also determined. Experiments were terminated by adding 100 mumol/l papaverine, obtaining maximal relaxation, which was used for normalising relaxations. RESULTS: (i) Acetylcholine: In resistance arteries, relaxations were absent in the newborn and the adult. In conduit arteries, they were present from 60-84 h onward. (ii) Substance P: In resistance arteries, relaxations were only present in the adult. In the other two types of arteries, rudimentary relaxations were present from the mature foetal stage onward. (iii) Bradykinin: In resistance arteries, identical relaxations were present at all ages which, in the foetus and the adult, were insensitive to changes in O2 levels (95 to 8%). In conduit arteries, concentration-dependent relaxations were present from birth, increasing in amplitude with age and these were potentiated by captopril. Foetal conduit arteries relaxed to the single application of 0.1 mumol/l bradykinin, indicating age-dependent tachyphylaxis. CONCLUSIONS: (i) Bradykinin is unique among endothelium-dependent vasodilators in being able to relax all vascular segments, at all ages, subject to tachyphylaxis and bradykinin-breakdown but independent of the prevailing O2 concentration. (ii) Heterogeneity of the relaxations between conduit and resistance arteries is evident from the mature foetal stage onward. (iii) The type of agonist, the type of vessel and the age each independently determine the presence or absence of endothelial relaxations. Therefore, the perinatal pulmonary circulation is not immature with respect to endothelial-dependent relaxation; rather, the nature of this process changes within the perinatal period and between birth and adulthood.

Acetylcholine↗
PubMed1999

Localization and function of the organic anion-transporting polypeptide Oatp2 in rat liver.

BACKGROUND & AIMS: Multispecific organic anion-transporting polypeptides (Oatps) are involved in the transcellular movement of amphipathic compounds in many tissues including the liver, kidney, and blood-brain barrier. Recently, a high-affinity digoxin transporter (Oatp2) was cloned from rat brain and shown to be also expressed in the liver. METHODS: We investigated the cellular and subcellular distribution of Oatp2 in rat liver by in situ hybridization technology and immunofluorescence microscopy and compared its substrate specificity with that of Oatp1 in complementary RNA-injected Xenopus laevis oocytes. RESULTS: The results show a selective basolateral (sinusoidal) expression of Oatp2 in midzonal to perivenous hepatocytes, but not in periportal or the innermost layer of perivenous hepatocytes. Common substrates of both Oatp1 and Oatp2 include bile salts, steroid conjugates, thyroid hormones (T3, T4), ouabain, and the endothelin receptor antagonist BQ-123 (Michaelis constants: Oatp1, approximately 600 micromol/L; Oatp2, approximately 30 micromol/L). Other organic anions including sulfolithotaurocholate, bilirubin monoglucuronide, and sulfobromophthalein were transported only by Oatp1. CONCLUSIONS: These results provide definite evidence for the partially overlapping and partially selective substrate specificities of Oatp1 and Oatp2. The unique acinar distribution of Oatp2 might indicate that it represents a high-affinity "backup" system for complete hepatocellular removal of certain cholephilic substances from portal blood plasma.

Animals↗
PubMed1999

Study on genital tract Chlamydia trachomatis and gonococcal infection in Han and minority (Naxi and Dai) women in China's two provinces.

OBJECTIVES: To estimate the prevalence of lower female genital tract chlamydial (GTC) and gonococcal infection in 3 different ethnic groups in China, and to analyze the risk factors influencing these infections. METHODS: A cross-sectional survey + physical and laboratory examinations. 1,800 married women aged 18-35 Han (600, from Dujiangyan city, Sichuan), Naxi (600, from Yanyuan county, Sichuan), and Dai (600, from Jinghong Prefecture, Yunnan) were investigated between March 1996 to March 1997. Information was obtained about their personal history, socioeconomic status, medical history, STDs, sexual history, contraceptive history, results of both examinations. Tabulation, t-test, Chi-square test, multiple-logistic models were used to analyze the data. RESULTS: 3.2% of Han, 12.8% of Naxi and 4.5% of Dai women tested positive for gonococci; and 9.1% of Han, 16.7% of Naxi and 27.5% of Dai women tested positive for GTC infection. The differences of GTC and gonococcal infections between Han and Naxi, and Han and Dai women were significant. CONCLUSIONS: STDs are common in China today; both GTC and gonoccocal infections are related to non-use of condom, having sexual partners other than husband, number of abortions, and low education; and condom has a function in prevention of STDs.

Adolescent↗
PubMed1999

Pulmonary prostacyclin synthase overexpression in transgenic mice protects against development of hypoxic pulmonary hypertension.

Prostacyclin synthase (PGIS) is the final committed enzyme in the metabolic pathway leading to prostacyclin (PGI2) production. Patients with severe pulmonary hypertension have a PGIS deficiency of their precapillary vessels, but the importance of this deficiency for lung vascular remodeling remains unclear. We hypothesized that selective pulmonary overexpression of PGIS may prevent the development of pulmonary hypertension. To study this hypothesis, transgenic mice were created with selective pulmonary PGIS overexpression using a construct of the 3.7-kb human surfactant protein-C (SP-C) promoter and the rat PGIS cDNA. Transgenic mice (Tg+) and nontransgenic littermates (Tg-) were subjected to a simulated altitude of 17,000 ft for 5 weeks, and right ventricular systolic pressure (RVSP) was measured. Histology was performed on the lungs. The Tg+ mice produced 2-fold more pulmonary 6-keto prostaglandin F1alpha (PGF1alpha) levels than did Tg- mice. After exposure to chronic hypobaric hypoxia, Tg+ mice have lower RVSP than do Tg- mice. Histologic examination of the lungs revealed nearly normal arteriolar vessels in the Tg+ mice in comparison with vessel wall hypertrophy in the Tg- mice. These studies demonstrate that Tg+ mice were protected from the development of pulmonary hypertension after exposure to chronic hypobaric hypoxia. We conclude that PGIS plays a major role in modifying the pulmonary vascular response to chronic hypoxia. This has important implications for the pathogenesis and treatment of severe pulmonary hypertension.

Animals↗
PubMed1999

Localization of the organic anion transporting polypeptide 2 (Oatp2) in capillary endothelium and choroid plexus epithelium of rat brain.

In this study we investigated the distribution of a recently cloned polyspecific organic anion transporting polypeptide (Oatp2) in rat brain by nonradioactive in situ hybridization histochemistry and immunofluorescence microscopy. The results demonstrate that Oatp2 is expressed in brain capillary and in plexus epithelial cells. At the blood-brain barrier (BBB), Oatp2 expression could be co-localized with the endothelial marker vWF (von Willebrand factor) but not with the astrocyte marker GFAP (glial fibrillary acidic protein). In choroid plexus epithelial cells, Oatp2 could be localized to the basolateral cell pole, whereas the first member of the Oatp gene family of membrane transporters to be cloned (Oatp1) co-localized with the alpha(1)-subunit of Na,K-ATPase at the apical plasma membrane domain. Because Oatp1 and Oatp2 have been previously shown to mediate transmembrane transport of a wide variety of amphipathic organic compounds, including many drugs and other xenobiotics, the histochemical localization of Oatp2 at the BBB and of Oatp1 and Oatp2 in the choroid plexus imply a role for these transporters in the active exchange of amphipathic solutes between the blood, brain, and cerebrospinal fluid compartments. (J Histochem Cytochem 47:1255-1263, 1999)

Animals↗
PubMed1999

[Comparison of sensitivity of artesunate-sensitive and artesunate-resistant Plasmodium falciparum to chloroquine and amodiaquine].

AIM: To explore the in vitro sensitivity of artesunate-sensitive and -resistant Plasmodium falciparum to chloroquine and amodiaquine and to observe the effect of artesunate combined with chloroquine and artesunate combined with amodiaquine on artesunate-resistant P. falciparum. METHODS: The sensitivity of the artesunate-sensitive and -resistant P. falciparum to chloroquine and amodiaquine and their combination with artesunate was compared by using Rieckmann's in vitro micro-technique. RESULTS: The ID50 and ID95 values of chloroquine, amodiaquine and artesunete were 90.9, 50.9, 9.6 nmol/L and 320.0, 320.0, 40.0 nmol/L to the artesunate-sensitive P. falciparum respectively and were 112.0, 133.5, 85.1 nmol/L and 320.0, 320.0, 400.0 nmol/L to artesunate-resistant P. falciparum, respectively. When artesunate was combined with chloroquine, the ID50 values of the 2 drugs were 3.2 and 20.0 nmol/L to the artesunate-resistant P. falciparum. When artesunate was combined with amodiaquine, the ID95 values of the 2 drugs were 3.2 and 5.0 nmol/L to the artesunate-resistant P. falciparum, respectively. CONCLUSION: The artesunate-resistant P. falciparum has no cross resistance to chloroquine and amodiaquine, however, artesunate combined with chloroquine or amodiaquine exhibit an apparent synergistic effect in vitro.

Amodiaquine↗
PubMed1998

The simian virus 40 core C enhancer-like element is a positive regulator in the rat alpha1B adrenergic receptor gene proximal promoter.

Transcription of the rat alpha1B adrenergic receptor (alpha1B AR) gene is controlled by three promoters (P1, P2, and P3), which generate 2.3-, 2.7-, and 3.3-kb transcripts, respectively. The expression of the 2.3-kb mRNA species is tissue-specific. To explore the underlying mechanism, the P1 promoter was analyzed. DNase I footprinting of the P1 promoter yielded three protected regions: Plfl(-49 to -62); P1f2 (-73 to -90), and P1f3 (-95 to -115). Sequence analysis of P1f3 revealed the presence of an SV40 core C enhancer-like element. In gel mobility shift assays, P1f3 was found to bind a sequence specific protein, which was competed away by a SV40 core C enhancer consensus oligonucleotide. Mutations of this enhancer-like core sequence within P1f3 significantly reduced specific protein binding to P1f3 and inhibited P1 promoter activity. The distribution of the protein which binds to P1f3 is restricted. These findings suggest that the P1 promoter is controlled by a cell-type-specific transcription factor, which may account for the tissue-specific expression of 2.3-kb rat alpha1B AR mRNA species.

Animals↗
PubMed1998

Cell type-specific transcriptional activation and suppression of the alpha1B adrenergic receptor gene middle promoter by nuclear factor 1.

Nuclear factor 1 (NF1) has been reported to be a transcriptional activator for some genes and a transcriptional silencer for others. Here we report that in Hep3B cells, cotransfection of NF1/L, NF1/Red1, or NF1/X with the alpha1B adrenergic receptor (alpha1BAR) gene middle (P2) promoter increases P2 activity to more or less the same degree, whereas in DDT1 MF-2 cells cotransfection of NF1/L or NF1/Red1 causes a small but statistically significant decrease in the P2 promoter activity, and NF1/X causes a greater, 70% inhibition. Further experiments using truncated NF1/X mutants indicate that NF1/X contains both positive and negative regulatory domains. The positive domain, located between amino acids 416 and 505, is active in Hep3B cells, whereas the negative domain, located between amino acids 243 and 416, is active in DDT1 MF-2 cells. These functional domains are also capable of regulating transcription when isolated from their natural context and fused into the GAL4 binding domain. Furthermore, NF1 affinity purified from rat liver nuclear extracts copurified with a non-DNA binding protein, which can bind to the P2 promoter of the alpha1BAR gene via interacting with NF1. Taken together, these findings indicate that NF1/X contains both activation and suppression domains that may be recognized and modulated by cell type-specific cofactors. This may be one of the mechanisms whereby NF1 can activate or suppress the expression of different genes, and it may also underlie the tissue-specific regulation of the alpha1B AR gene.

Animals↗