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B Luo

Publications and source records attributed to B Luo.

At least 19 recordsLinked to original sources
PubMed1999

Age-related variation in the interstitial tissues of the cardiac conduction system; and autopsy study of 230 Han Chinese.

The amount of fatty and fibrous tissues in 230 Han Chinese who died of noncardio-vascular diseases has been studied by a semi-quantitative method and analysed by chi-square test. The results have shown some consistency. Generally, in the sino-atrial node (SAN), fibrosis and fatty influtratin appear only after 40 years of age and increase one grade with every 20 years. The atrio-ventricular node (AVN) showed fatty change after 30 years of age and fibrosis appeared after 60. In the His bundle (HB), fatty infiltration and fibrosis appear after 40 years. The left bundle branch (LBB) showed similar changes. The appearance of fibrosis in the AVN seems to be later than that reported by Lev.

Adolescent↗
PubMed1999

Endothelin-1 stimulation of endothelial nitric oxide synthase in the pathogenesis of hepatopulmonary syndrome.

Biliary cirrhosis in the rat triggers intrapulmonary vasodilatation and gas exchange abnormalities that characterize the hepatopulmonary syndrome. This vasodilatation correlates with increased levels of pulmonary microcirculatory endothelial nitric oxide synthase (eNOS) and hepatic and plasma endothelin-1 (ET-1). Prehepatic portal hypertension induced by portal vein ligation (PVL) does not cause similar changes, suggesting that ET-1 in cirrhosis may modulate pulmonary eNOS and vascular tone. We assessed whether ET-1 altered eNOS expression and nitric oxide production in bovine pulmonary artery endothelial cells (BPAECs) and if a 2-wk low-level intravenous ET-1 infusion in PVL animals modulated pulmonary eNOS levels, microcirculatory tone, and gas exchange. ET-1 caused a 2.5-fold increase in eNOS protein in BPAECs, inhibitable with an endothelin B receptor antagonist, and an increase in eNOS mRNA and nitrite production. ET-1 infusion in PVL animals caused increased pulmonary eNOS levels, intrapulmonary vasodilatation, and gas exchange abnormalities without increasing pulmonary arterial pressure. ET-1 produced during hepatic injury may contribute to the hepatopulmonary syndrome by modulating eNOS and inducing pulmonary microcicrulatory vasodilatation.

Animals↗
PubMed1998

Cholecystokinin B receptors in the periaqueductal gray potentiate defensive rage behavior elicited from the medial hypothalamus of the cat.

Defensive rage behavior is mediated over a descending pathway from the medial hypothalamus to the dorsolateral midbrain periaqueductal gray (PAG) where further integration of this response takes place. The present study sought to determine the roles of CCK-A and CCK-B receptor activation in the PAG in modulating defensive rage behavior. The 'hissing' component of the defensive rage response was used throughout the experiment as the measure of defensive rage behavior. The basic design of the experiment involved placement of monopolar electrodes into the medial hypothalamus from which defensive rage could be elicited and cannula electrodes into the dorsal PAG for purposes of identifying defensive rage sites in this region and for microinjections of CCK compounds into these sites at a later time. Microinjections of the selective CCK-B receptor antagonist, LY288513 (1.05, 4.2, 17.0 nmol/0.25 microliter), into the PAG suppressed the hissing response in a dose- and time-dependent manner. Microinjections of the CCK-B agonist, pentagastrin, (0.5 and 1.0 nmol/0.25 microliter) facilitated the occurrence of defensive rage behavior. Moreover, administration of LY288513 (17 nmol/0.25 microliter) 55 min prior to pentagastrin (1.0 nmol/0.25 microliter) delivery blocked the facilitatory effects of pentagastrin. Administration of the CCK-A antagonist, PD140548 (34 nmol/0.25 microliter), into the PAG failed to alter response latencies for defensive rage behavior. In contrast, microinjections of the CCK-B antagonist, LY288513 (4.2, 17.0 nmol/0.25 microliter), facilitated the occurrence of predatory attack behavior elicited from the lateral hypothalamus. This finding demonstrates the specificity of the effects of CCK-B receptor blockade upon hissing. A combination of immunocytochemical and retrograde tracing procedures using microinjections of Fluoro-Gold (8%, 6 microliters) into the PAG were employed to identify the possible loci of CCK neurons that project to the PAG. The data revealed that neurons labeled for both CCK and Fluoro-Gold were located in the dorsolateral aspect of the midbrain tegmentum, identifying this region as a source of CCK inputs to the PAG. Overall, the findings demonstrate that CCK-B receptors in the PAG potentiate defensive rage behavior and likely suppress predatory attack.

Animals↗
PubMed1998

Endothelin-1 in the rat bile duct ligation model of hepatopulmonary syndrome: correlation with pulmonary dysfunction.

BACKGROUND/AIMS: Models of hepatopulmonary syndrome require both hepatic injury and portal hypertension to develop pulmonary microvascular and gas exchange abnormalities. Recently, increased endothelin-1 levels associated with vasodilatation, have been observed in cirrhosis. We investigated endothelin-1 production in common bile duct ligated animals with hepatopulmonary syndrome in comparison to partial portal vein ligated animals that do not develop hepatopulmonary syndrome. METHODS: Organ and plasma endothelin-1 were measured in sham, bile duct ligated and portal vein ligated rats, and Northern analysis and immunohistochemistry were performed in liver. Plasma endothelin-1 levels were correlated with pulmonary endothelial nitric oxide synthase levels and alveolar-arterial oxygen gradients. RESULTS: Hepatic and plasma endothelin-1 increased only after bile duct ligation, and were accompanied by increased hepatic endothelin-1 mRNA and increased endothelin-1 protein in biliary epithelium. Plasma endothelin-1 levels correlated directly with both pulmonary endothelial nitric oxide synthase levels and alveolar-arterial gradients. CONCLUSIONS: Enhanced hepatic production and increased plasma levels of endothelin-1 occur after bile duct ligation, but not after portal vein ligation, and correlate with associated molecular and gas exchange alterations in the lung. Endothelin-1 may contribute to the pathogenesis of hepatopulmonary syndrome.

Animals↗
PubMed1998

Garlic prevents hypoxic pulmonary hypertension in rats.

Hypoxic pulmonary vasoconstriction underlies the development of high-altitude pulmonary edema. Anecdotal observations suggest a beneficial effect of garlic in preventing high-altitude symptoms. To determine whether garlic influences pulmonary vasoconstriction, we assessed the effect of garlic on pulmonary pressures in rats subjected to alveolar hypoxia and on vasoconstriction in isolated pulmonary arterial rings. Garlic gavage (100 mg/kg body wt) for 5 days resulted in complete inhibition of acute hypoxic pulmonary vasoconstriction compared with the control group. No difference in mean arterial pressure or heart rate response to hypoxia was seen between the groups. Garlic solution resulted in a significant dose-dependent vasorelaxation in both endothelium-intact and mechanically endothelium-disrupted pulmonary arterial rings. The administration of NG-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor) inhibited the vasodilatory effect of garlic by 80%. These studies document that garlic blocks hypoxic pulmonary hypertension in vivo and demonstrate a combination of endothelium-dependent and -independent mechanisms for the effect in pulmonary arterial rings.

Acetylcholine↗
PubMed1997

Mapping sequence specific DNA-protein interactions: a versatile, quantitative method and its application to transcription factor XF1.

We have developed a method for the quantitative, exhaustive sequence specificity determination of DNA-binding proteins. The QuESSD method overcomes the limitations inherent in other published in vitro selection methods, not only defining the consensus sequence, but also quantifying the effect on DNA-protein affinity of replacing each base in the recognition domain with every other base. The features distinguishing this method from other in vitro selection approaches are: (1) instead of synthesizing one target oligonucleotide population containing a long randomized domain, we synthesize several oligonucleotide populations, each randomized at two positions. (2) Instead of carrying out several cycles of selection and amplification, we carry out a single cycle. (3) We have developed data collection and analysis procedures that eliminate artifacts and allow generation of quantitative results. The QuESSD method yields accurate measures of: (a) the selectivity of the protein for each base at each position within the recognition domain (normalized relative selectivity), (b) the contributions of individual sites within the recognition domain to the binding affinity (selectivity variance), (c) the relative binding affinity of any given sequence (global selectivity). We confirmed results by (1) tabulating directly the frequency of appearance of individual species in the pool of protein-bound oligonucleotides by cloning and sequencing individual oligonucleotides, and (2) competition EMSA analysis of oligonucleotides designed on the basis of QuESSD data. We have used this method to map the sequence specificity of the nuclear protein XF1 and to distinguish the sequence specificities of XF1 and the AH receptor complex, both of which bind to XRE1, a xenobiotic responsive element (XRE) located upstream of the CYP1A1 gene. Using data obtained by the QuESSD method, we designed oligonucleotides specific for XF1 or for the AH receptor, and prepared CAT reporter gene constructs carrying these oligonucleotides, or wild-type XRE1, upstream of a minimal promoter. Transfection studies using these constructs indicated that XF1 can function as a weak activator of basal transcription, and can, under some circumstances, compete with the AH receptor for binding to XRE1.

Animals↗
PubMed1997

The role of endothelial nitric oxide synthase in the pathogenesis of a rat model of hepatopulmonary syndrome.

BACKGROUND & AIMS: The hepatopulmonary syndrome occurs when intrapulmonary vasodilatation causes impaired arterial gas exchange in liver disease. The pathogenesis is poorly understood, although nitric oxide may be involved. Common bile duct ligation in the rat is a model of the hepatopulmonary syndrome, but no studies have evaluated NO in pulmonary vasodilatation in this model. The aim of this study was to determine whether NO contributes to intrapulmonary vasodilatation after bile duct ligation. METHODS: Endothelial and inducible NO synthase (NOS) levels and localization and NO activity in pulmonary artery rings were assessed after bile duct ligation. RESULTS: Pulmonary endothelial NOS levels increased and alveolar vascular staining was enhanced after bile duct ligation. No change in pulmonary inducible NOS levels or localization was detected. Increased endothelial NOS levels correlated with alterations in gas exchange and were accompanied by enhanced NO activity and a blunted response to phenylephrine, reversible by NOS inhibition, in pulmonary artery rings. Portal-vein-ligated animals, which do not develop intrapulmonary vasodilatation, had no changes in pulmonary NOS production or in NO activity in pulmonary artery rings. CONCLUSIONS: NO, derived from pulmonary vascular endothelial NOS, contributes to intrapulmonary vasodilation in animal hepatopulmonary syndrome.

Acetylcholine↗
PubMed1997

Isolation and functional analysis of a cDNA for human Jagged2, a gene encoding a ligand for the Notch1 receptor.

Signaling through Notch receptors has been implicated in the control of cellular differentiation in animals ranging from nematodes to humans. Starting from a human expressed sequence tag-containing sequence resembling that of Serrate, the gene for a ligand of Drosophila melanogaster Notch, we assembled a full-length cDNA, now called human Jagged2, from overlapping cDNA clones. The full-length cDNA encodes a polypeptide having extensive sequence homology to Serrate (40.6% identity and 58.7% similarity) and even greater homology to several putative mammalian Notch ligands that have subsequently been described. When in situ hybridization was performed, expression of the murine Jagged2 homolog was found to be highest in fetal thymus, epidermis, foregut, dorsal root ganglia, and inner ear. In Northern blot analysis of RNA from tissues of 2-week-old mice, the 5.0-kb Jagged2 transcript was most abundant in heart, lung, thymus, skeletal muscle, brain, and testis. Immunohistochemistry revealed coexpression of Jagged2 and Notch1 within thymus and other fetal murine tissues, consistent with interaction of the two proteins in vivo. Coculture of fibroblasts expressing human Jagged2 with murine C2C12 myoblasts inhibited myogenic differentiation, accompanied by increased Notch1 and the appearance of a novel 115-kDa Notch1 fragment. Exposure of C2C12 cells to Jagged2 led to increased amounts of Notch mRNA as well as mRNAs for a second Notch receptor, Notch3, and a second Notch ligand, Jagged1. Constitutively active forms of Notchl in C2C12 cells also induced increased levels of the same set of mRNAs, suggesting positive feedback control of these genes initiated by binding of Jagged2 to Notch1. This feedback control may function in vivo to coordinate differentiation across certain groups of progenitor cells adopting identical cell fates.

Amino Acid Sequence↗
PubMed1997

Common bile duct ligation in the rat: a model of intrapulmonary vasodilatation and hepatopulmonary syndrome.

Hepatopulmonary syndrome (HPS) causes impaired oxygenation due to intrapulmonary vasodilatation in patients with cirrhosis. Chronic common bile duct ligation (CBDL) in the rat results in gas-exchange abnormalities similar to HPS, but intrapulmonary vasodilatation has not been evaluated. We assess intrapulmonary vasodilatation, measured in vivo, after CBDL. Sham, 2- and 5-wk CBDL, and 3-wk partial portal vein ligated (PVL) rats had hepatic and lung injury, portal pressure, and arterial blood gases assessed. The pulmonary microcirculation was evaluated by injecting microspheres (size range 5.5-10 microm) intravenously and measuring the size and number of microspheres bypassing the lungs in arterial blood. CBDL animals developed progressive hepatic injury and portal hypertension accompanied by gas-exchange abnormalities and intrapulmonary vasodilatation. PVL animals, with a similar degree of portal hypertension, did not develop intrapulmonary vasodilatation or abnormal gas exchange. No lung injury was observed. CBDL, but not PVL, causes progressive intrapulmonary vasodilatation, which accompanies worsening arterial gas exchange. These findings validate CBDL as a model to study HPS.

Animals↗
PubMed1997

[Immunohistochemical study on SMDS using anti-actin monoclonal antibody].

For elucidating the relationship between the causes of sudden manhood death syndrome (SMDS) and cardiac sudden death, the cardiac conducting system-(CCS) and myocardium of 23 cases including SMDS group, coronary heart disease group and normal control group were studied using anti-actin monoclonal antibody (HHF35) S-P immunohistochemical method. The results showed that some areas of CCS and myocardium were stained negatively by HHF35 in SMDS group but no infarction area can be found with H.E staining. The negative staining by HHF35 can be also observed in all cases of coronary heart disease group. In control group, the CCS and myocardium stained positively. It indicated that there were pathological changes such as early ischemia or infarction of myocardium in SMDS, which related closely to cardiac sudden death.

Actins↗
PubMed1996

The diabetic state increases the activity but not the number of peritoneal macrophages in the GK rat promoting the tube formation of cultured endothelial cells in rat aorta.

The influence of the diabetic state on the number and activity of intraperitoneal macrophages was investigated in the GK rat. This rat is a model of non-insulin-dependent diabetes mellitus and was established from the normal Wistar rat. The cell number of a macrophages preparation in diabetic GK rats (10-15 weeks of age) did not differ from that in normal Wistar rats (9-10 weeks of age). The co-cultured macrophages in diabetic GK rats (9-12 weeks of age) significantly increased the tube formation of aortic endothelial cells (EC) compared with that in age-matched Wistar rats. The conditioned medium obtained from a culture of macrophages from GK rats also increased tube formation more than that from a culture of macrophages from Wistar rats. The effect of macrophages in the GK rat was not influenced by interferon-gamma (160 and 460 pM), but macrophages in normal rats were activated by these concentrations of interferon-gamma. In conclusion, the diabetic state increased the activity but not the number of macrophages in the GK rat, to stimulate tube formation of EC. The tube-forming effect of macrophages in the diabetic state may depend on released factors which differ from that of normal macrophages.

Animals↗
PubMed1996

[Color Doppler in evaluating the effects of octreotide on portal hemodynamics].

OBJECTIVE: To study the effects of octreotide on portal pressure and the relationship between the portal pressure and portal hemodynamics measured by color Doppler. METHODS: A high portal resistance model by injecting bletilla hyacinthina was established in 6 dogs. The portal pressure and portal hemodynamics studied by color Doppler were measured respectively by two investigators before and after injecting octreotide into the peripheral vein. RESULTS: Portal hypertension was caused by injecting bletilla hyacinthina into the portal vein. The portal pressure was reduced and portal venous velocity increased after injecting octreotide into the peripheral vein. There was a significant negative correlation between the portal pressure and portal venous velocity. CONCLUSION: Color Doppler is helpful in evaluating the effects of octreotide on the portal pressure.

Animals↗
PubMed1995

Computerized microimage analysis of age-related changes of the human sinoatrial node.

This paper reports the age-related changes in the histological features of the sinoatrial node (SAN). The hearts of 106 persons dying at different ages (2 days-83 years), without clinical or pathological evidence of cardiac disease, were taken and divided into seven age-groups. Serial sections with a thickness of 2 microns, parallel to the long axis of the SAN, were prepared. Sections with the maximal area of the SAN were stained with hematoxylin/eosin (H & E) and Betty's method. The largest area of SAN were calculated by a computerized microimage analysis system. The age-related changes of the human SAN were discussed.

Adolescent↗
PubMed1995

[Surgical treatment of 165 cases of stage III small cell lung carcinoma].

The author analysed the effect of surgical therapy in 165 cases with stage III SCLC from 1979 to the end of 1991, and compared with 87 cases of combined therapy and 78 cases in simple operative therapy. The author also makes an observation of cases with pre-operative and (or) post-operative chemo- and radiation therapy. Their over-all 5 year survival rate was 16.6%. Stage among 5 year survival cases in TNM stage. IIIa was 20.4% and no for Stage IIIb. The 5 year survival of combined therapy was 22.8% and that of simple operative group was 7.9%. The result shows that in the Stage III SCLC combined therapy is superior to that of simple operative group. It seems that postoperative radiation and chemotherapy is better than pre-operative in combined therapy group. The author's opinion is that surgical indication of SCLC is limited to stage IIIa.

Adult↗