Search PubMed⌕ Search

Biomedical subjects

H Wang

Publications and source records attributed to H Wang.

At least 1,189 records · Page 66Linked to original sources

Intraventricular vascular endothelial growth factor antibody increases infarct volume following transient cerebral ischemia.

AIM: To clarify the role of vascular endothelial growth factor (VEGF) in neuronal damage induced by cerebral ischemia. METHODS: Expression of VEGF in adult rat brain was measured by immunohistochemistry. Transient middle cerebral artery occlusion (MCAO) model was induced by placing a nylon thread in the lumen of the internal carotid artery. The infarct volume was shown with 2,3,5-triphenyltetrazolium chloride (TTC) staining and quantitated by computer image analyzer with and without VEGF antibody treatment. RESULTS: VEGF expression was widely distributed in neuronal cells besides vascular endothelial cells, and the neuronal distribution of VEGF was specific. After intraventricular treatment with VEGF antibody (0.1 g.L-1 daily, for 7 d following the ischemia), infarct volume in the antibody treatment was increased versus vehicle-treated rats [(21.6 +/- 2.7 vs 16 +/- 6) mm3, P < 0.05] respectively. CONCLUSION: Intraventricular injection of VEGF antibody increased the infarct volume after focal cerebral ischemia in rats, suggesting that expression of neuronal VEGF may be one of neuronal protective mechanisms.

Animals↗

Demethylation capacity of human fetal adrenal mitochondrial cytochrome P-450 in vitro.

AIM: To explore the capacity and characteristics of adrenal mitochondria to metabolize xenobiotics in vitro in human fetus. METHODS: Subcellular fractions of fetal adrenal were prepared by differential centrifugation. Mitochondrial P-450 system was proved by spectral analyses and SDS-PAGE. The formaldehyde formation contents were measured with Nash reagent. RESULTS: The erythromycin N-demethylation linearly increased in the protein concentration (1-4 mg)- and incubation time (10-30 min)-dependent manners. A typical concentration-effect relationship appeared with erythromycin 0.067-1 mmol.L-1 and a positive correlation (r = 0.641, P < 0.05) existed between erythromycin N-demethylation and gestation months. The N-demethylation values (nmol.s-1/g protein) of erythromycin (2.7 +/- 0.8), benzfetamine (1.1 +/- 0.5), and aminophenazone (0.9 +/- 0.4) in mitochondria were 89% (P > 0.05), 162% (P < 0.01), and 62% (P < 0.01), respectively, of those in microsomes. There was correlation between mitochondria and microsomes in the N-demethylation of erythromycin (r = 0.708, P < 0.05) and benzfetamine (r = 0.707, P < 0.05). Troleandomycin stimulated erythromycin N-demethylation in adrenal mitochondria as well as in adrenal and liver microsomes in vitro. CONCLUSION: Fetal adrenal mitochondria, with multiple P-450 isoforms and greater capacity of demethylation, play a role in drug-metabolism during fetal development.

Adrenal Glands↗

Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes.

BACKGROUND: Cytokines mediate the metabolic and physiologic responses to injury and infection. Anterior pituitary cells express receptors for tumor necrosis factor (TNF) and interleukin 1 (IL-1), which can signal these cells to release corticotropin, growth hormone, and cytokines such as IL-1 and macrophage migration inhibitory factor. This interaction provides an important link between the immune system and the neuroendocrine system. We reasoned that pituicytes activated with TNF or IL-1 might release previously unrecognized factors that could participate in this signaling from the neuroendocrine to the immune system. METHODS: Proteins released from rat pituicytes (GH3) after stimulation with proinflammatory cytokines were identified by N-terminal amino acid sequencing. Polyclonal antibodies against a peptide corresponding to the N-terminal amino acid sequence were generated and used to determine the kinetics of protein release. RESULTS: Cytokine stimulation induced the release of a 30-kd protein from rat pituicytes. After the protein was isolated and the N-terminal amino acid sequence determined, a protein database analysis revealed that it is high mobility group-1 (HMG-1) protein. TNF and IL-1 induced the release of HMG-1 from pituicytes in a time- and dose-dependent manner. Interferon gamma alone did not induce the release of HMG-1, but it enhanced TNF-induced HMG-1 release. CONCLUSION: Stimulation of pituicytes by TNF or IL-1 induces the release of HMG-1, which may participate in the regulation of neuroendocrine and immune responses to infection or injury.

Amino Acid Sequence↗

[Apoptosis of peripheral blood lymphocytes of patients with chronic hepatitis B and clinical significance].

OBJECTIVE: To explore the effects of apoptosis of peripheral blood lymphocytes (PBLs) of patients with chronic hepatitis B (CHB) on the persistent infection of hepatitis B virus (HBV). METHODS: The PBLs of 15 patients with CHB were isolated and cultured with or without Staphylococcus aureus enterotoxin B (SEB; 0.2 mg/L), or in the presence or absence of recombinant HBcAg (rHBcAg; 1.0 mg/L) for 48 hours in vitro. After incubations, the cells were harvested by centrifugation and then apoptosis of the PBLs was studied by staining with fluorescent dyes YOPRO-1 and Hoechst33342. RESULTS: The percentage of apoptotic cells of PBLs of patients with CHB was significantly higher than in normal controls (P < 0.01) in the presence or absence of SEB or rHBcAg, but the ratio of apoptotic cells in rHBcAg-stimulated PBLs of the patients was the highest, reaching (24.6 +/- 6.1)%. The patients with seropositive for HBeAg had higher percentage of apoptotic cells in their cultured PBLs than those with seronegative for HBeAg had, but the ratio of apoptotic cells in cultured PBLs of the patients with chronic heavy and severe hepatitis B was lower than that of the patients with chronic mild and moderate hepatitis B (P < 0.01). CONCLUSION: Activation-induced cell death of PBLs of the patients with CHB may be related to persistent infection of HBV, and assay of apoptosis of PBLs of patients with CHB may provide valuable information about pathogenesis of CHB.

Adolescent↗

MDM2 oncogene as a target for cancer therapy: An antisense approach.

The MDM2 oncogene is amplified or overexpressed in human cancers. It has also been suggested that MDM2 levels are associated with poor prognosis of several human cancers. The MDM2 oncoprotein binds to the p53 tumor suppressor protein and serves as a negative regulator of p53. The p53 tumor suppressor also has an important role in cancer therapy, with p53-mediated apoptosis being a major mechanism of action for many clinically used cancer chemotherapeutic agents and radiation therapy. Therefore, the negative regulation of p53 by MDM2 may limit the magnitude of p53 activation by DNA damaging agents, thereby limiting their therapeutic effectiveness. The investigators hypothesize that, by inhibiting MDM2 expression, the MDM2 oncoprotein level will be reduced and the MDM2 negative feedback inhibition of p53 will be diminished, resulting in a significant increase of functional p53 levels that will modulate p53-mediated therapeutic effects. The overall objective of the present study was to investigate the functions of MDM2 oncogene in tumor growth and the potential value of MDM2 as a drug target for cancer therapy. The role of MDM2 in tumor growth is determined by inhibiting MDM2 expression in in vivo models of human cancers. The in vivo synergistically therapeutic effects of MDM2 inhibition and DNA damaging agents were also evaluated. Significant in vitro antitumor activities were found in cell lines, human osteosarcoma SJSA and choriocarcinoma JAR, in a time-, concentration-, and sequence-dependent manner. Following i.p. administration of anti-MDM2 antisense oligonucleotides, in vivo antitumor activity was observed in nude mice bearing SJSA and JAR xenografts in a dose-dependent manner. Moreover, in vivo synergistically therapeutic effects of MDM2 inhibition and DNA damaging agents adriamycin and 10-hydroxycamptothecin were observed. This study should provide the basis for future development of anti-MDM2 antisense oligonucleotides as cancer therapeutic agents used alone or in combination with conventional chemotherapeutics.

Animals↗

Physiological and anatomical correlates of the human dentate gyrus: consequences or causes of epilepsy.

The presence of paroxysmal discharges in the epileptic human dentate gyrus provides a physiologic basis for hyperexcitability that may initiate seizure discharges during the development of epilepsy. Although these responses can occur with single orthodromic stimulation, data obtained under conditions that weaken synaptic inhibition (e.g., 1 Hz stimulation or bicuculline disinhibition) suggest that paroxysmal discharges may be a more common feature of tissue from temporal lobe epileptic patients than has been reported previously. Hilar cell loss and weakened synaptic inhibition may provide conditions favorable for the activation of N-methyl-D-aspartate acid (NMDA) receptors that would allow triggering of paroxysmal discharges that normally never are evoked in dentate granule cells in nonepileptic humans. As the dentate gyrus in normal animal tissue is not susceptible to intrinsic bursting behavior and is characterized by a relatively short duration excitatory postsynaptic potential even under pharmacologic disinhibition, paroxysmal discharges in the epileptic human dentate gyrus may provide an important clue to understanding the prerequisite conditions for seizure discharge.

Animals↗

Spermine inhibition of monocyte activation and inflammation.

The innate immune system functions as a defensive front line against pathogenic invasion, but the proinflammatory products of activated monocytes and macrophages (e.g., TNF and NO) can also injure normal cells. Anti-inflammatory mediators restrain the innate immune response and prevent excessive collateral tissue damage. Spermine, a ubiquitous biogenic polyamine, specifically and reversibly suppresses the synthesis of monocyte proinflammatory cytokines. This may provide a counterregulatory mechanism to restrain monocyte activation in injured or infected tissues and in tumors where spermine levels are significantly increased. Here we show that monocyte spermine uptake was significantly increased following lipopolysaccharide stimulation. The polyamine analogue 1, 4-bis(3-aminopropyl)-piperazine (BAP) inhibited LPS-stimulated monocyte spermine uptake via the "nonselective" polyamine transporter. BAP fully restored macrophage TNF synthesis despite the presence of spermine, indicating that the mechanism of monocyte deactivation by spermine is dependent on spermine uptake. Administration of BAP in vivo significantly augmented the development of carrageenan-induced paw edema and nitric oxide release. Thus, endogenous spermine normally inhibits the innate inflammatory response by restraining macrophages.

Animals↗

Effects of oxidative damage of membrane protein thiol groups on erythrocyte membrane viscoelasticities.

In three oxidative damaging systems: the diamide-mercaptoethanol redox modification system (DM), the pyrogallol oxygen free radicals system (PG) and the hypoxanthine-xanthine oxidase oxygen free radical system (HXO), the effect of erythrocyte membrane oxidative damage on membrane viscoelasticities was investigated with micropipette aspiration method. The experimental results indicated that erythrocyte membrane oxidative damage has a great influence upon the membrane mechanical properties. The oxidative damage led to decrease of contents of membrane protein thiol radical. The scanning of SDS-PAGE presented that membrane proteins form the higher molecular weight component (HMP) by the cross-linking of membrane protein thiol radicals that might hinder the conformational change of membrane protein. This might be the reason for the increased membrane elastic modulus and viscous coefficient upon treating erythrocytes with the oxidative damaging systems. A significant negative logarithm regression relation was found between the membrane elastic modulus, mu, or viscoefficient, eta, and the contents of membrane protein thiol radicals. These experimental results suggested that thiol radicals oxidative damage reaction due to the superoxides anions (*O2-) may be an important molecular mechanism inducing changes of membrane viscoelasticities or whole cell deformability of erythrocyte under physiological and pathological oxidative stress.

Blood Viscosity↗

Apoptosis induced by zinc deficiency in rat osteoblast: possible involvement of protein kinase C.

Rat osteoblasts were isolated from the 21-day fetal rat calvarias. The cells were grown in DMEM plus 10% FBS, and were treated for 24 h. with 10 mumol/L TPEN or 10 mumol/L TPEN supplemented with 10 mumol/L Zn2+. Apoptosis of osteoblasts were measured by flow cytometry, electron microscopy and DNA fragmentation analyzed by gel electrophoresis. In addition, IP3 production and PKC activity were measured in order to show whether they are involved in apoptosis in osteoblast induced by zinc deficiency. The results showed that 10 mumol/L TPEN could induce apoptosis in osteoblast in 24 h. But cells treated with 10 mumol/L TPEN supplemented with 10 mumol/L Zn2+ showed no apoptotic changes in 24 h. TPEN significantly reduced the formation of IP3 and PKC activity after 24 h incubation. No differences were observed between the cells treated with TPEN supplemented with Zn2+ simultaneously and the untreated cells. It can be inferred that apoptosis induced by zinc deficiency may be due to the decreased activity of PKC which is impaired by reduced formation of IP3.

Animals↗

[Interleukin 10(IL-10) levels in serums and in culture supernatants of peripheral blood mononuclear cells from patients with chronic hepatitis B].

OBJECTIVE: To understand the impacts of interleukin 10(IL-10) in serums and in culture supernatants of peripheral blood mononuclear cells (PBMCs) from patients with chronic hepatitis B (CHB) on the persistent infection of hepatitis B virus (HBV). METHODS: The levels of IL-10 in serums and in culture supernatants of PBMCs from 15 patients with CHB and 6 normal controls were measured by ELISA method. PBMCs were cultured with or without Staphylococcus aureus enterotoxin B(SEB; 0.2 microgram/ml) or recombinant HBcAg(rHBcAg; 1.0 microgram/ml) for 48 hours in vitro. RESULTS: The levels of IL-10 in serums was greater in patients with CHB (123.11 +/- 13.89 ng/L) than in controls (95.97 +/- 11.68 ng/L, P < 0.01). Spontaneous, SEB-induced and rHBcAg-induced IL-10 production by PBMCs after culturing in vitro for 48 hours was also higher in patients with CHB (280.82 +/- 50.56 ng/L, 321.69 +/- 37.04 ng/L and 369.58 +/- 30.52 ng/L) than in controls (100.2 +/- 8.54 ng/L, 203.41 +/- 12.02 ng/L and 202.38 +/- 15.79 ng/L; P < 0.01). In addition, IL-10 production by rHBcAg-stimulated PBMCs was significantly greater than by SEB-stimulated PBMCs in patients with CHB. Patients with seropositive for HBV DNA had higher levels of IL-10 in serums and in culture supernatants of PBMCs than patients with seronegative for HBV DNA. But the levels of IL-10 were lower in patients with chronic heavy and severe hepatitis B than in patients with chronic mild and moderate hepatitis B. CONCLUSION: IL-10 may have an important role in persistent infection of HBV in patient with CHB.

Adolescent↗

[WAF1/CIP1 gene expression in human hepatocellular carcinoma and its relationship with p53 mutation].

OBJECTIVE: To study the WAF1 gene expression in human hepatocellular carcinoma(HCC) and its relationship with p53 mutation. METHODS: Using semiquantitative reverse transcriptase-polymerase chain reaction(RT-PCR) and immunohistochemistry, the expression of WAF1 and p53 in 32 HCC samples and their surrounding liver tissues and 5 normal liver tissues was detected respectively. RESULTS: The expression level of WAF1 mRNA in HCC samples was lower than that in paratumor liver tissues(1.06 U +/- 0.37 U vs 1.30 U +/- 0.37 U, P < 0.01) and its positive rate of p21WAF1 was also lower than that in paratumor liver tissues(53.1% vs 100%, P < 0.01). The expression level of WAF1 mRNA in HCC samples with intra-hepatic metastatic lesions was lower than that without intra-hepatic metastatic lesions(0.92 U +/- 0.33 U vs 1.24 U +/- 0.35 U, P < 0.01) and its positive rate of p21WAF1 was also lower than that without intra-hepatic metastatic lesions(33.3% vs 78.6%, P < 0.05). The expression level of WAF1 mRNA in HCC samples with p53 mutation was lower than that without p53 mutation (0.92 U +/- 0.28 U vs 1.16 U +/- 0.40 U, P < 0.05) and its positive rate of p21WAF1 was also lower than that without p53 mutation(15.4% vs 78.9%, P < 0.01). The percentage of cells in S-phase in p21WAF1-positive HCC samples was lower than that in p21WAF1-negative HCC samples(44.57% +/- 7.56% vs 51.83% +/- 8.51%, P < 0.01). However, no significant difference in expression of WAF1 mRNA and p21WAF1 in HCC samples was found in other clinical pathological parameters such as the degree of differentiation, the histological pattern, the size of tumors, the status of capsule in tumors and the formation of tumor thrombus of portal vein. The expression level of WAF1 mRNA in normal liver tissues was strikingly lower(0.17 U +/- 0.06 U), and the immunohistochemical staining of p21WAF1 in all normal liver tissues was positive(100%). CONCLUSION: The expression of WAF1 gene in HCC is predominantly regulated by dependence on p53 and the reduced WAF1 expression may participate in the carcingenesis and progression of HCC and the mechanisms of infiltration and metastasis of HCC.

Carcinoma, Hepatocellular↗

An experimental investigation of osseointegration and stability of implants used as orthodontic anchorage in dogs.

OBJECTIVE: To investigate osseointegration and stability of three kinds of implants used as orthodontic anchorage in dogs. METHODS: HA-coated, titanium plasma-coated, and uncoated titanium implants were inserted into each femur of two dogs. After a healing period of three months, orthodontic force of 200 g was applied by means of Ni-Ti springs which were connected to the two adjacent implants for two months. Position change of the implant was first measured and then calculated. The shear bond strength of the interface between implant and bone was measured with a push test. After the test, the fracture surface at the interface was observed with a scanning electronic microscope. RESULTS: All implants were stable, without mobility. The highest bond strength and mature bone compactness were found at the interface between HA-coated implant and bone. The other two showed no significant difference in bond strength. However, osseointegration existed at the interface between all three kinds of implants and bone. CONCLUSION: HA-coated, titanium plasma-coated, and uncoated titanium implants can each serve as orthodontic anchorage as well as prosthodontic abutment.

Animals↗

[Clinical study on pathologic changes of umbilical cord vessels in pregnancy induced hypertension].

OBJECTIVE: To evaluate the relationship between the pathologic features of umbilical cord vessels and the severity of disease in pregnancy induced hypertension (PIH). METHODS: The umbilical cord vessels of forty-five women with PIH and thirty normal term-pregnant women (control group) were observed under light microscopy; the three parts of cord i.e. near placenta, near fetus and middle section of twenty women with PIH selected randomly were observed as well. RESULTS: There were no different pathologic changes in the 3 parts of umbilical cord in PIH; Forty-five women with PIH were categorized into three groups according to the degree of lesions: no lesion (n = 6), mild (n = 13) and severe (n = 26). The pathologic changes of umbilical vessels in moderate and severe PIH were more severe than those in mild PIH (P < 0.05, P < 0.01). However, there were no apparent pathologic changes in the control. The pathologic changes of umbilical vessels in PIH had significant relationship with mean arterial pressure (MAP), neonatal outcome and urinary protein. CONCLUSIONS: The pathologic changes of umbilical vessels can reflect the characteristic lesion of PIH and are parallel with the severity of disease; and there is a homogeneity in pathomorphology of umbilical cord.

Adult↗

[Rehabilitation of 269 fingers with electrical burns].

OBJECTIVE: To summarize the clinical feature of the fingers with electrical burns. METHODS: 269 fingers with electrical burns were analysed in the characteristics of injury and the types of repair. RESULTS: Fingers with electrical burns were often multiple, characterizing the complexity of the wound repair. Operation time should be determined by different conditions. Usually the fingers with electrical burns should be operated early but the circumferential wound surface should be depressed or eschar excised during early stage in order to avoid ischemia of distal segment. When the circulation of the finger distal to the injury is improved, operation should be done to repair wound surface. CONCLUSION: Many kinds of flaps might be used for repair of fingers with electrical burns. The flaps from the same finger should be the first choice, followed by flaps from the same hand and distant flaps.

Adolescent↗

[Modulation of the secretion of active renin in human decidual cells by progesterone].

Uterine decidua is a major source of renin, both active and inactive. Active renin cleaves angiotensinogen to produce angiotensin I and exerts its effect on the expression of angiotensin II in the local tissue. Our experiments showed that (1) in the decidua of early pregnancy the contents of active renin increased gradually with advancing pregnancy, and at 8th week of gestation the level of active renin reached to a maximum (63.37 +/- 12.84) AI ng/gww.h(-1); (2) active renin accounted for about 1/4 of the total renin; and (3) the synthesis and secretion of active renin were regulated by progesterone in incubated decidual cells. These data indicate that a high level of active renin in decidual tissue at early pregnancy plays an important role in the uterine renin-angiotensin system during pregnancy.

Cells, Cultured↗