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Biomedical subjects

Ping Wang

Publications and source records attributed to Ping Wang.

At least 307 records · Page 17Linked to original sources
PubMed2003

[Age-dependent alternations in beta-adrenoceptor function in human detrusor and possible mechanism].

OBJECTIVE: To study the age-dependent alternations in beta-adrenergic response and possible mechanism. METHODS: The response to beta-adrenergic agonists isoprenaline and BRL37344, forskolin and dibutyryl cyclic AMP (DBcAMP) of samples from senile people in 10 cases were examined by cellular functional test. Radioligand binding assay was also performed using non-selective beta-adrenergic receptors ligand [(3)H]-dihydroalprenolol ([(3)H]-DHA), the specimens of young men in 10 cases as the control group. RESULTS: There was no age-dependent change in the contractile response to potassium chloride. The relaxing responses to isoprenaline, BRL37344 and forskolin decreased by 15.0%, 17.6% and 12.6% respectively (P < 0.01). The pD(2) values of the isoprenaline and BRL37344 also declined significantly. There was no difference in the responses to DBcAMP between the two groups. The maximum binding site decreased significantly with increasing age, but the equilibrium-dissociation constant did not change. CONCLUSIONS: There is an age-related decline in beta-adrenergic responsiveness, which might be one of the causative factors of the reduced bladder compliance of the elderly. The decrease of cAMP level caused by the reduced receptor density and adenyl cyclase activity might be the molecular mechanisms underlying the changes of beta-adrenergic responsiveness.

Adult↗
PubMed2003

Role of thrombosis in osteonecrosis.

We think that osteonecrosis, to a large degree, develops because of familial and acquired thrombophilia and hypofibrinolysis causing venous thrombosis in the femoral head. We postulate that venous thrombosis leads to increased intraosseus venous pressure, reduced arterial flow, and hypoxic bone death. Many studies suggest that familial and acquired thrombophilia and hypofibrinolysis may play an important etiologic role in adults with osteonecrosis of the hip and jaw and in children with Legg-Perthes disease (pediatric osteonecrosis). We have limited pilot data in adults with osteonecrosis associated with familial thrombophilia and hypofibrinolysis that suggest that 12 weeks of therapy with enoxaparin, if started early (Ficat stages I/II) before femoral head collapse (Ficat stages III/IV), may interrupt the progression of osteonecrosis of the hip. Placebo-controlled trials with a 2-year follow-up or longer in adults will be required to assess the promise of the pilot anticoagulant studies in osteonecrosis.

Adult↗
PubMed2003

Ghrelin clearance is reduced at the late stage of polymicrobial sepsis.

The cardiovascular response to sepsis is characterized by an early, hyperdynamic phase followed by a late, hypodynamic phase. Ghrelin, a newly-identified endogenous ligand for growth hormone secretagogue receptor (i.e., ghrelin receptor), was recently demonstrated to be a potent vasoactive peptide in addition to its effects on growth hormone release and energy homeostasis. We have shown that ghrelin (via its receptor) may play an important role in regulating cardiovascular responses in the progression of polymicrobial sepsis. However, it remains unknown whether the clearance of this peptide is altered in sepsis. To determine this, male adult rats were injected with 125I-ghrelin through the jugular vein at 5 or 20 h after cecal ligation and puncture (CLP, i.e., sepsis model) or sham operation. The blood sample was collected every 2 min for 30 min for determining half-life (t1/2). Tissue samples (i.e., kidneys, liver, brain, heart, lungs, spleen, stomach, small intestine, large intestine, skin and muscle) were then harvested. The radioactivities of samples were counted. The results indicate that 125I-ghrelin's t1/2 and its distribution were not significantly altered in early sepsis (5 h after CLP). However, the t1/2 increased significantly in late sepsis (20 h after CLP). Tissue distribution of 125I-ghrelin was far greater in the kidneys than in any other tissues tested in both sham and septic animals. Moreover, the kidneys and liver had significantly less radioactive uptake at 20 h after CLP, but the radioactivity in blood was much higher at the same time point. There were no significant changes in 125I-ghrelin distribution in other organs at the late stage of sepsis. These results indicate that the kidneys are the primary site of ghrelin clearance, which is significantly diminished in late sepsis. In addition, the liver also plays a role in the clearance of ghrelin, which was also reduced in late sepsis. The decreased clearance of ghrelin by the kidneys and liver may be due to renal and hepatic dysfunctions under such conditions.

Aging↗
PubMed2003

Age-dependent changes in beta-adrenoceptor function in human detrusors and possible mechanisms.

OBJECTIVE: To study age-dependent changes in beta-adrenergic responsiveness and their possible mechanisms. METHODS: Responsiveness to the beta-adrenergic agonists isoprenaline, BRL37344, forskolin, and dibutyryl cyclic AMP (DBcAMP) was examined in samples from 10 older patients by using a cellular function test. A radioligand binding assay was performed using the non-selective beta-adrenergic receptor ligand [3H]-dihydroalprenolol ([3H]-DHA). Specimens from 10 young men were used as controls. RESULTS: There were no age-dependent changes in contractile response to KCl. The relaxation responses to isoprenaline, BRL37344, and forskolin decreased in the aged group by 15.0%, 17.6%, and 12.6%, respectively (P < 0.001). The pD2 values for isoprenaline and BRL37344 also declined significantly. There was no difference in the responsiveness to dibutyryl cyclic AMP (DBcAMP) between the two groups; the maximum binding site decreased significantly with increasing age, but the equilibrium-dissociation constant did not change. CONCLUSIONS: There is an age-related decline in beta-adrenergic responsiveness which might be one of the causative factors of reduced bladder compliance in the elderly. A decrease in cAMP level caused by reduced receptor density and adenylyl cyclase activity might be the underlying molecular mechanism of the changes in beta-adrenergic responsiveness.

Adrenergic beta-Agonists↗
PubMed2003

Endoscopic biliary drainage for biliary obstruction.

OBJECTIVE: To improve the successful rate of endoscopic biliary drainage. METHODS: Three hundred and fifty-two patients with biliary obstruction were given biliary drainage via duodenoscope from January 1998 to December 2002. 258 patients received endoscopic naso-biliary drainage (ENBD), 51 endoscopic retrograde biliary drainage (ERBD), and 43 endoscopic metal biliary endoprothesis (EMBE). RESULTS: Of the 352 patients with biliary obstruction, 337 succeeded in drainage by endoscopy and 15 failed. Ten ENBD failed patients were handled successfully by readjustment of the site of the naso-biliary tube. In 3 ERBD failed patients, 2 were given plastic stents with appropriate length and got a fluent drainage. Percutaneous transhepatic biliary drainage (PTBD) was performed in one patient after failure of endoscopic management. In 2 patients with failed EMBE, one stent could not exceed the site of tumor stricture and one was obstructed by tumor implantation only one month after EMBE. Placement of another metallic stent and a plastic stent through the previous prothesis for each patient ensured a successful drainage. CONCLUSIONS: The effect of endoscopic biliary drainage for biliary obstruction is definite. Drainage failure can be avoided or remedied as early as possible by taking some active measures.

Adolescent↗
PubMed2003

[Change of T lymphocyte and its activated subsets in SARS patients].

OBJECTIVE: To study abnormal changes of T lymphocyte and its activated subsets in severe acute respiratory syndrome (SARS) patients. METHODS: Flow cytometer with multi-color flouroscence and hematology analyzer were used to detect the expression of T lymphocyte and its activated a subsets in 240 SARS patients including 50 cases of critical type and 190 cases of common type. RESULTS: Statistical analysis by means of SAS software showed that there was significant decrease in absolute counts (AC) of T lymphocyte and its subsets in SARS patients when compared with normal people, while percentages (PC) of CD3+CD25+ and CD3+ HLA-DR+ subsets were increased markedly. Compared with common type, there was significant decrease in absolute counts of critical type of T lymphocyte, CD4+, CD25+CD3+, CD28+CD4+, and CD95+CD4+subsets. The ACs of T lymphocytes including CD4 and CD8 subsets in different phases were as below: III > II > I. The ACs of subsets involved in activation such as CD3+ HLA-DR+/lym, CD3+CD25+/lym, CD28+CD4+/CD4, CD28+CD8+/CD8, and CD38+CD4+/CD4 all were highest in group III. In addition, the AC and PC of CD95+CD4+/CD4 and CD95+CD8/CD8 subset in group III were highest while group I was lowest. CONCLUSIONS: With depressing cellular immunity, the activation of T lymphocytes were suppressed obviously in SARS patients, especially for critical patients.

Adult↗
PubMed2003

[Cephalometric study of Holdaway analytical method by computer on 58 adults with normal occlusion in Chongqing].

OBJECTIVE: In order to establish the normal value of Holdaway analytical method of Chongqing and to reveal the regular patterns and characteristics concerning the craniofacial morphology. METHODS: 58 students, with permanent dentition were selected as the samples. The cephalometric images were scanned into a computer and the images were imported into the program. The cephalometric analysis were automated by the computer. The cephalometric analytical method of Holdaway was used in this study. Correlational analysis were calculated. RESULTS: The normal values of Holdaway analytical method for permanent denition on normal occlusal adults of Chongqing were established and compared with that of Pekingman, Japanese and White man. CONCLUSIONS: We found that soft cephalometric measurement values are various in sex and races and regional population. There were correlations between hard and soft tissues.

Adolescent↗
PubMed2003

[Preparation and identification of phage-displayed ICAM-1-mimic peptide].

AIM: To obtain bioactive ICAM-1 mimetic peptide. METHODS: Phages displaying P1 and P2 were prepared by phage amplication and PEG precipitation. The binding between phage-displayed peptides and anti-ICAM-1 mAb 15.2 was evaluated by sandwich ELISA and competitive ELISA. Bioactivities of P1 and P2 was detected by immunohistochemical staining. RESULTS: Phage-displayed peptides P1 and P2 could specifically bind to mAb 15.2, and the binding could be competitively inhibited by ICAM-1. Immunohistochemical staining showed that P1 and P2 could mimic the binding of ICAM-1 to its receptor LFA-1. CONCLUSION: Phage-displayed peptides P1 and P2 are bioactive just as native ICAM-1.

Antibodies, Monoclonal↗
PubMed2002

Beta-arrestin 2 functions as a G-protein-coupled receptor-activated regulator of oncoprotein Mdm2.

Oncoprotein Mdm2 is a master negative regulator of the tumor suppressor p53 and has been recently shown to regulate the ubiquitination of beta-arrestin 2, an important adapter and scaffold in signaling of G-protein-coupled receptors (GPCRs). However, whether beta-arrestin 2 has any effect on the function of Mdm2 is still unclear. Our current results demonstrated that the binding of Mdm2 to beta-arrestin 2 was significantly enhanced by stimulation of GPCRs. Activation of GPCRs led to formation of a ternary complex of Mdm2, beta-arrestin 2, and GPCRs and thus recruited Mdm2 to GPCRs at plasma membrane. Moreover, the binding of beta-arrestin 2 to Mdm2 suppressed the self-ubiquitination of Mdm2 and consequently reduced the Mdm2-mediated p53 degradation and ubiquitination. Further experiments revealed that overexpression of beta-arrestin 2 enhanced the p53-mediated apoptosis while suppression of endogenous beta-arrestin 2 expression by RNA interference technology considerably attenuated the p53-mediated apoptosis. Our study thus suggests that beta-arrestin 2 may serve as a cross-talk linker between GPCR and p53 signaling pathways.

Animals↗
PubMed2002

A novel one-dimensional coordination polymer, catena-poly[[diaquacobalt(II)]-mu-(2,2'-bipyridyl-3,3'-dicarboxylato-kappa4N,N':O,O')].

The title compound, [Co(C(12)H(6)N(2)O(4))(H(2)O)(2)](n), has been hydrothermally synthesized and structurally characterized. It consists of polymeric chains of [Co(mu-(2,2'-bipyridyl-3,3'-dicarboxylato-kappa(4)N,N':O,O'))(H(2)O)(2)] units, in which each Co(II) cation is octahedrally coordinated by two chelating pyridyl N atoms, two chelating carboxyl O atoms from different carboxylate groups of another bipyridyl ligand, and two water molecules as terminal ligands. A crystallographic twofold axis parallel to the chain axis, passes through the Co atom.

Journal Article↗
PubMed2002

Hemorrhage induces the rapid development of hepatic insulin resistance.

Hyperglycemia is an early metabolic response to trauma and hemorrhage. The role of hepatic insulin resistance to the development of this hyperglycemia is not well understood. The aim of this study was to determine whether the liver becomes insulin resistant and to identify the particular hepatic insulin signaling pathways that may be compromised following trauma and hemorrhage. Male adult rats were bled to a mean arterial pressure of 40 mmHg and maintained at that pressure for 90 min followed by resuscitation with Ringer lactate. Data showed that trauma and hemorrhage rapidly induced profound hyperinsulinemia in combination with significant hyperglycemia, suggesting the development of insulin resistance. After trauma and hemorrhage, hepatic insulin signaling via the insulin-induced phosphatidylinositol 3 (PI3)-kinase-Akt pathway was abolished, whereas ERK1/2 signaling was relatively normal. The regulation (inhibition) of a hepatic-, insulin-, and the PI3-kinase-dependent gene, IGF binding protein-1, was also lost. The present study provides convincing evidence of a rapid onset hepatic insulin resistance following a combination of trauma and hemorrhage.

Abdominal Injuries↗
PubMed2002

Rapid positive selection of stable integrants following transfection of Plasmodium falciparum.

With the near-completion of the genome sequence of Plasmodium falciparum, further understanding of this major human pathogen urgently requires more effective genetic tools. These must include faster and more reliable gene replacement or gene knockout techniques, essential for the analysis of gene function. We describe a serial system which uses the blasticidin S deaminase (bsd) gene of Aspergillus and the neomycin phosphotransferase II (neo) gene from transposon Tn5 as selectable markers for, respectively, transient transfection of malaria parasites and the selection of stable integrants. Challenge with blasticidin S (BS) enriches the parasite population transiently expressing the bsd gene, laying the foundation for the subsequent, much less frequent, integration event. Positive selection for this rare event is enormously facilitated by fusing the neo gene in frame to the replacement or knockout targeting gene. The sequence employed for the targeting (the polymorphic pppk-dhps gene of P. falciparum, as a model system) is truncated at the 5' end with no promoter located upstream, therefore neo cannot be expressed without specifically integrating within the genomic copy of the target gene. After BS selection, the culture is immediately exposed to geneticin (G418), leading to an apparently homogenous population of mutant parasites. As well as excluding spurious integrants at non-targeted sequences, this system greatly reduces the lengthy selection period for obtaining the desired mutants by eliminating the drug-on and drug-off cycles for the production of stable integrants, which are normally required by the single marker systems currently in use for transfection of malaria parasites.

Aminohydrolases↗
PubMed2002

Modulation of alternative pre-mRNA splicing in vivo by pinin.

Pre-mRNA splicing occurs in a large macromolecular RNA-protein complex called the spliceosome. The major components of the spliceosome include snRNP and SR proteins. We have previously identified an SR-like protein, pinin (pnn), which is localized not only in nuclear speckles but also at desmosomes. The nuclear localization of pnn is a dynamic process because pnn can be found not only with SR proteins in nuclear speckles but also in enlarged speckles following treatment of cells with RNA polymerase II inhibitors, DRB, and alpha-amanitin. Using adenovirus E1A and chimeric calcitonin/dhfr construct as a splicing reporter minigene in combination with cellular cotransfection, we found that pnn regulates alternative 5(') and 3(') splicing by decreasing the use of distal splice sites. Regulation of 5(') splice site choice was also observed for RNPS1, a general splicing activator that interacts with pnn in nuclear speckles. The regulatory ability of pnn in alternative 5(') splicing, however, was not dependent on RNPS1 and a pnn mutant, lacking the N-terminal 167 amino acids, behaved like a dominant negative species, inhibiting E1A splicing when applied in splicing assays. These results provide direct evidence that pnn functions as a splicing regulator which participates itself directly in splicing reaction or indirectly via other components of splicing machinery.

5' Untranslated Regions↗
PubMed2002

The blockage of the high-affinity lysine binding sites of plasminogen by EACA significantly inhibits prourokinase-induced plasminogen activation.

Prourokinase-induced plasminogen activation is complex and involves three distinct reactions: (1) plasminogen activation by the intrinsic activity of prourokinase; (2) prourokinase activation by plasmin; (3) plasminogen activation by urokinase. To further understand some of the mechanisms involved, the effects of epsilon-aminocaproic acid (EACA), a lysine analogue, on these reactions were studied. At a low range of concentrations (10-50 microM), EACA significantly inhibited prourokinase-induced (Glu-/Lys-) plasminogen activation, prourokinase activation by Lys-plasmin, and (Glu-/Lys-) plasminogen activation by urokinase. However, no inhibition of plasminogen activation by Ala158-prourokinase (a plasmin-resistant mutant) occurred. Therefore, the overall inhibition of EACA on prourokinase-induced plasminogen activation was mainly due to inhibition of reactions 2 and 3, by blocking the high-affinity lysine binding interaction between plasmin and prourokinase, as well as between plasminogen and urokinase. These findings were consistent with kinetic studies which suggested that binding of kringle 1-4 of plasmin to the N-terminal region of prourokinase significantly promotes prourokinase activation, and that binding of kringle 1-4 of plasminogen to the C-terminal lysine158 of urokinase significantly promotes plasminogen activation. In conclusion, EACA was found to inhibit, rather than promote, prourokinase-induced plasminogen activation due to its blocking of the high-affinity lysine binding sites on plasmin(ogen).

Aminocaproates↗
PubMed2002

Translocation of pleckstrin requires its phosphorylation and newly formed ligands.

Pleckstrin is the major substrate of protein kinase C (PKC) in platelets. We sought to determine whether pleckstrin phosphorylation is sufficient to target the soluble protein to binding sites. Permeabilization of platelets by streptolysin O (SLO) was used to separate bound and soluble pleckstrin. Platelets were incubated with phorbol 12-myristate 13-acetate (PMA) and/or guanosine 5'-[gamma-thio]triphosphate (GTP[S]) in the presence of [gamma-(32)P]ATP and SLO. PMA stimulated pleckstrin phosphorylation, but this pleckstrin diffused from permeabilized platelets. Addition of GTP[S] with PMA caused up to 40-50% of pleckstrin to be retained within platelets and enhanced secretion of platelet 5-hydroxytryptamine. PKC alpha pseudosubstrate peptide inhibited pleckstrin phosphorylation, the binding of pleckstrin and secretion. After extraction of permeabilized platelets containing bound pleckstrin with Triton X-100, the protein was solubilized. Thus, phosphorylated pleckstrin was retained in platelets only after activation of GTP-binding proteins that stimulate the formation of membrane-bound pleckstrin ligands. Translocation of pleckstrin may facilitate the associated secretion.

Blood Platelets↗
PubMed2002

Saturation of adrenomedullin receptors plays an important role in reducing pulmonary clearance of adrenomedullin during the late stage of sepsis.

Adrenomedullin (AM) is a potent vasodilator that plays a major role in the cardiovascular response during the progression of sepsis. Although pulmonary clearance of AM (i.e., the primary site of AM clearance) is reduced during the late, hypodynamic stage of sepsis, the role of AM receptors under such conditions remains unclear. This study was carried out to test the hypothesis that saturation of AM receptors is responsible for the decreased clearance of AM in the lungs during sepsis. Polymicrobial sepsis was induced in male adult rats by cecal ligation and puncture (CLP). At 20 h after CLP (i.e., the late phase), 125I-labeled rat AM was administered through the jugular vein, both with (+) and without (-) pre-injection of the human AM fragment AM(22-52) (an AM receptor antagonist). Pulmonary tissue samples were harvested after 30 min and the radioactivity was determined. In addition, lung levels of AM were determined at 5 and 20 h after CLP by radioimmunoassay. Alterations in gene expression of the recently identified AM receptor subunits calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein-2 and -3 (RAMP-2 and -3) were assessed in the lungs by reverse transcription-polymerase chain reaction (RT-PCR) at 5 and 20 h after CLP. The results indicate that there was a significant decrease in pulmonary [125I]AM clearance at 20 h in -AM(22-52) CLP animals. Lung clearance in +AM(22-52) sham animals was significantly lower than in -AM(22-52) sham animals and was not statistically different from the -AM(22-52) CLP group. There was no statistical difference between +AM(22-52) and -AM(22-52) CLP groups. However, there was a significant increase in lung AM levels at 20 but not 5 h after CLP. In addition, RAMP-3 expression was significantly upregulated at 5 but not 20 h after CLP. There were no alterations in the expression of CRLR or RAMP-2 at either time point. These results suggest that pulmonary AM receptors become saturated as more AM enters the bloodstream, thereby reducing the ability of the lungs to clear this peptide during late sepsis. Early upregulation of RAMP-3 may be a compensatory mechanism to help clear the upregulated AM from the bloodstream. The lack of upregulation of RAMP-3 during late sepsis could also contribute to the decreased clearance observed during this phase.

Adrenomedullin↗