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Biomedical subjects

Hong Zhang

Publications and source records attributed to Hong Zhang.

At least 325 records · Page 18Linked to original sources
PubMed2004

Neutrophil protein kinase Cdelta as a mediator of stroke-reperfusion injury.

Thrombolysis is widely used to intervene in acute ischemic stroke, but reestablishment of circulation may paradoxically initiate a reperfusion injury. Here we describe studies with mice lacking protein kinase Cdelta (PKCdelta) showing that absence of this enzyme markedly reduces reperfusion injury following transient ischemia. This was associated with reduced infiltration of peripheral blood neutrophils into infarcted tissue and with impaired neutrophil adhesion, migration, respiratory burst, and degranulation in vitro. Total body irradiation followed by transplantation with bone marrow from PKCdelta-null mice donors reduced infarct size and improved neurological outcome in WT mice, whereas marrow transplantation from WT donors increased infarction and worsened neurological scores in PKCdelta-null mice. These results indicate an important role for neutrophil PKCdelta in reperfusion injury and strongly suggest that PKCdelta inhibitors could prove useful in the treatment of stroke.

Animals↗
PubMed2004

Recombinant human bone morphogenetic protein-2 enhances anterior spinal fusion in a thoracoscopically instrumented animal model.

BACKGROUND: Thoracoscopically assisted anterior spinal arthrodesis and instrumentation is being used more widely to treat idiopathic scoliosis. However, harvesting autologous bone increases operative time and morbidity. The purpose of this study was to compare autologous iliac crest and rib graft with recombinant human bone morphogenetic protein-2 (rhBMP-2) in thoracoscopically assisted anterior spinal arthrodesis and instrumentation in an animal model. METHODS: Twenty-two pigs underwent thoracoscopically assisted anterior spinal arthrodesis. Each animal had five contiguous thoracic discectomies followed by anterior instrumentation. The animals were randomly assigned to five treatment groups. Group I consisted of control animals that received no graft material; group II, animals treated with autologous rib graft; group III, animals treated with autologous iliac crest graft; group IV, animals treated with an rhBMP-2-composite sponge (collagen-hydroxyapatite-tricalcium phosphate carrier); and group V, animals treated with a composite sponge carrier alone. The animals were killed four months after the procedure, and the spines were harvested. The fusion mass was assessed with use of axial and sagittal computed tomography scans. The spines were tested biomechanically with incremental loads applied in the frontal and axial planes to achieve bending moments of up to 6.0 N-m. Angular motion at each segment was recorded with use of a three-dimensional motion analysis system. Histomorphometric analysis of each undecalcified disc segment was also performed. RESULTS: The fusion grades, according to computed tomography analysis with use of a 4-point grading system in which scores of 3 and 4 indicated a solid fusion, were 0.6 point for group I, 2.1 points for group II, 2.3 points for group III, 3.8 points for group IV, and 0.4 point for group V. Group IV (the rhBMP-2-treated animals) had a higher grade than all of the other groups. Group II (rib graft) and group III (iliac crest) had similar grades, and both were greater than group I (the untreated controls) and group V (composite sponge alone) (p < 0.05). In axial rotation, lateral bending, and flexion-extension, the spines in group IV were stiffer than those in the four other groups (p < 0.05); the spines in groups II and III were similar, and the spines in both of those groups were stiffer than those in groups I and V (the control groups). Histologic analysis demonstrated that the total new-bone area, expressed as a percentage of the total disc space area, was 23.2% in group I, 37.1% in group II, 37.2% in group III, 48.5% in group IV, and 5.9% in group V. Group IV had significantly greater bone formation than all of the other groups (p < 0.001). The animals treated with rib graft (group II) and iliac crest (group III) had a similar amount of bone formation, and it was greater than that in both control groups (p < 0.001). CONCLUSIONS: The rhBMP-2 significantly increased the prevalence and quality of the spinal fusion after thoracoscopically assisted anterior arthrodesis and instrumentation in an animal model compared with that in the other treatment groups and in the controls.

Animals↗
PubMed2004

Deletion in p16INK4a and loss of p16 expression in human skin primary and metastatic melanoma cells.

p16INK4a gene mapped at chromosome 9p21 region encodes a tumor suppressor protein p16 which is frequently inactivated in human cancers, including skin melanoma. In order to clarify the importance of p16 alterations in melanoma, we examined the deletions of p16INK4a and expression of p16 protein in eight unselected primary and metastatic melanoma cell lines from human skin melanomas. Normal skin melanocytes were used as controls. Deletions of entire exons in the p16INK4a gene were detected by PCR technique and expression of the p16 protein was examined by Western blotting and immunocytochemistry. Results showed that the fragments from exons 2A, 2C and 3 in p16INK4a gene were totally deleted in the metastatic melanoma cell line, FM28.7 and the fragment from exon 3 was deleted in the metastatic melanoma cell line, FM55M2. P16 protein was strongly expressed in two of the primary melanomas cell lines (FM55P and RaH3). The p16 protein was weakly expressed in one of the metastatic melanoma cell lines (FM55M1) and negative in the other metastasis (FM55M2) as compared to their matched primary melanoma cells (FM55P). The p16 protein was strongly expressed in normal skin melanocytes. Immunocytochemistry showed that p16 protein was mainly localized in the nuclei of the melanoma cells and normal melanocytes, if it was expressed. Deletions of p16INK4a gene was uncommon and loss of p16 protein expression was common event in melanoma, especially in the later stages of melanoma.

Blotting, Western↗
PubMed2004

[Uteroglobin G38A polymorphism is associated with the progression of IgA nephropathy in Chinese patients].

OBJECTIVE: Uteroglobin is a multifunctional protein. Both uteroglobin gene knockout and antisense transgenic mouse models developed the pathological and clinical features of IgA nephropathy. Uteroglobin G38A polymorphism has been reported to be associated with the progression of IgA nephropathy in some Caucasian and Asian populations, but there are no documents on Chinese population. The present report was to investigate the associations of uteroglobin G38A polymorphism with the development and progression of IgA nephropathy in Chinese patients. METHODS: Three hundred patients with biopsy proven IgA nephropathy were identified from Renal Disease database. Ninety-three patients had been followed-up for 2-6 years. 145 healthy donors served as normal controls. Genomic DNAs were extracted from peripheral blood leucocytes. The uteroglobin G38A polymorphism was determined by PCR-RFLP. Uteroglobin G38A genotype and allele frequency were compared between patients with IgA nephropathy and normal controls. In addition, associations of G38A polymorphism with blood pressure, hematuria, proteinuria, pathological lesions and prognosis of renal function were analyzed in patients with IgA nephropathy. RESULTS: Distribution of uteroglobin G38A polymorphism in patients with IgA nephropathy (38AA: 13.2%; 38AG: 57.6%; 38GG: 30.2%) and normal controls (38AA: 18.2%; 38AG: 60%; 38GG: 21.8%; P > 0.05) showed no difference. But patients with the 38AA genotype showed a higher odds ratio for progression of renal function (OR = 2.37, 95% CI = 1.12-5.01) as compared to patients with the 38AG/GG genotype. CONCLUSION: Uteroglobin G38A polymorphism had no association with the development of IgA nephropathy, but the homogeneous 38AA genotype maybe one of the genetic markers for disease progression in Chinese IgA nephropathy.

Adult↗
PubMed2004

[An experiment to study the treatment of sarcomas by electroporation].

In this paper is reported a new approach for the treatment of sarcoma--electroporation therapy. Electroporation can accelerate pharmacal molecules into cytoplasm by transient electromagnetic pulses. We have utilized the phenomenon of electroporation treating the S-180 sarcomas in the hind legs of the Kunming mice by intratumoral injection of anti-tumor agent at low dose. From the experiment, we learned that this approach can bring about remarkable effect. The technical procedure is easy to do and easy to control. Especially, it is useful in curing the flat tumor and has little untoward side effect. It deserves to be recommended as a new approach to treating the tumor in clinics.

Animals↗
PubMed2004

[Exploration of the pathogenesis and the management of hypernatremia in burn patients].

OBJECTIVE: To explore the pathogenesis and the management of hypernatremia in burn patients. METHODS: Twenty eight burn patients with hypernatremia were enrolled in the study and were divided into infection and non-infection groups. The pathogenesis, clinical features, biochemical indices in blood, the therapeutic results and the prognosis were compared between the two groups. RESULTS: In non-infection group, the hypernatremia was mainly induced by improper fluid resuscitation and occurred on the 3.1 postburn day (PBD), while that in the infected group, on 7.2 PBD. The patients in non-infected group exhibited much more excited and the blood levels of glucose and urea nitrogen (BUN) were obviously decreased when compared with those in the infected group (P < 0.01). The survival rate in non-infected and infected group were 94.12% and 9.09%, respectively. CONCLUSION: The mortality rate of the patients with hypernatremia could be lowered by means of taking optimal measures according to the different patterns of hypernatremia.

Adult↗
PubMed2004

[Construction of sense and antisense eukaryotic expression vector of novel gene Collectrin and its function in cell growth].

OBJECTIVE: To construct sense and antisense eukaryotic expression vector of novel gene Collectrin and identify its function in cell growth. METHODS: The open reading frame of Collectrin was amplified by PCR and inserted into pcDNA3.1/V5-His plasmid. The recombinant plasmid was identified by restriction enzyme analysis and sequencing analysis. The recombinant plasmid was transfected into M-1 cell by using lipofectin mediation after being identified by restriction enzyme analysis and sequencing analysis. RT-PCR and Western blot were performed to identify the expression of Collectrin. Beta-Gal staining was used to define the effect of transfection. The growth of M-1 cells was examined by MTT and cell counting. RESULTS: Compared with control group, the expression of Collectrin was decreased significantly at both nucleotide and protein levels transfected by antisense vector, but elevated in sense group. The cell growth was blocked after being transfected by antisense plasmid. CONCLUSION: The sense and antisense eukaryotic expression vector of novel gene Collectrin was successfully constructed. Collectrin was one of basic factors in cell growth.

Animals↗
PubMed2004

Expression of CD44 in cultured human trabecular meshwork cells.

PURPOSE: To determine whether cultured human trabecular meshwork cells express CD44 and to discuss their possible relationship with primary open angle glaucoma. METHODS: Human trabecular meshwork cells were cultured in DMEM/F12 media. Total RNAs from the cells were extracted with Trizol reagent. Messenger RNA expression of CD44 in human trabecular meshwork cells was examined by using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Expression of CD44 was confirmed by Western-blotting and immunofluorescent microscopy. Effect of CD44-specific antisense oligonucleotide on adhesion of trabecular meshwork cells to hyaluronate was determined by MTT assay. RESULTS: A single RT-PCR product whose size was 471 bp was obtained. A band about 80kD was stained by Western-blot. Immunofluorescent examination of expression of CD44 on the cell surface was positive and reactions were mainly localized in cell membranes. Adhesion of trabecular meshwork cells to hyaluronate was inhibited by CD44-specific antisense oligonucleotide. CONCLUSIONS: Cultured human trabecular meshwork cells express CD44. CD44 may play a role in pathogenesis of primary open angle glaucoma.

Cell Adhesion↗
PubMed2004

Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells.

We have previously shown that all-trans-retinoic acid (atRA) induces apoptosis in melanoma cells and primary melanoma cells are more sensitive to the exposure of atRA than the matched metastases. However, mechanisms behind the atRA-induced apoptosis have not been studied. In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis. The primary and metastatic melanoma cells were exposed to 0.1 and 10 micro M atRA in serum-free RPMI 1640 cell culture medium in the dark for up to 96 h. The protein expression of p53, p21, bax and bcl-2 were examined by Western blotting and immunocytochemistry. Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. The changes of p53, p21, bax, and bcl-2 protein levels were dose- and time-dependent. The primary melanoma cells were more sensitive to the atRA treatments than cells from matched metastatic melanoma. These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Modification of these protein levels in the tumour cells might be beneficial for early treatment of melanoma.

Apoptosis↗
PubMed2004

[Effect of dexamethasone on adhesion and phagocytosis of bovine trebacular meshwork cells].

PURPOSE: To study the effect of dexamethasone on adhesion and phagocyosis of bovine trebacular cells (BTC). METHODS: After treated with different concentrations of dexamethasone (10(-7) M, 10(-6) M, 10(-5) M) for three days, BTC were added to 96-well plates coated with various extracellular matrix (ECM) and incubated for 90 minutes at 37 degrees C, Methyl thiazolyl tetrazolium (MTT) assay were used to evaluate the amount of the cells attach to ECM; In addition, using latex micropheries 0.8 microm in diameter as markers,we investigated the effect of dexamethasone on phagocytosis of BTC. RESULTS: All groups of Dexamethasone can inhibit BTC attach to various ECM and in a dose-depend manner; the phagocytosis of BTC were also inhibited by three concentrations of dexamethasone and in a dose-depend manner. CONCLUSIONS: Dexamethasone can inhibit adhesion and phagocytosis of BTC, it may be related with pathogenasis of glucocorticoid induced glaucoma.

Animals↗
PubMed2004

[Protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia and reperfusion-injury of rat retina].

OBJECTIVE: To study the protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia-reperfusion-injury of rat retina. METHODS: Rats were divided randomly into group of ischemia-reperfusion, group of electrical-stimulation-treated and group of sham-operated. The duration ischemia was 1 hour except sham-operated. In treated group, harvests of retinas followed electrical stimulation of cerebellar fastigial nucleus for 60 min after reperfusion for 6 hours; in reperfusion group, retinas were harvested only after 6 hours reperfusion. Retinal ischemia was produced in rats by ligating vessels and the optic nerve for 1 hour. Expression of inducible nitric oxide synthase (iNOS) in retina was measured by NADPH-NDP histochemistry; Apoptosis was measured by Tdt-dUTP terminal nick-end labeling (TUNEL) method. Morphology change was observed with the help of HPIAS-1000 auto-medical-imagined computer analyzer. RESULTS: (1) The thickness of inner retinal (including outer plexiform layer, inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrane) and the inner plexiform layer were increased significantly in ischemia-reperfusion group than those in treated group. (2) The morphological changes of the scattered and condensed nucleus were observed more slightly under light microscopy in treated group than those in ischemia-reperfusion group. (3) Expression of inducible nitric oxide synthase (iNOS) in retinal ganglion cell in treated group is more significant than in ischemia-reperfusion group. (4) The amount of apoptosis cells in retina in treated group is significantly less than thatin ischemia-reperfusion group. CONCLUSIONS: (1) The results indicated that ischemia-reperfusion injury can induce retinal apoptosis. Retinal apoptosis can be inhibited by electrical stimulation cerebellar fastigial nucleus. (2) iNOS maybe involved in the mechanism of apoptosis. (3) Cerebellar fastigial nucleus electrical stimulation can protect ischemia-reperfused retina.

Animals↗
PubMed2004

[Influence of N-acetylcysteine on the cytokines and matrix metalloproteinases in chronic obstructive pulmonary disease rat models].

OBJECTIVE: To investigate the changes of interferon-gamma (IFNgamma), interleukin (IL)-4, matrix metalloproteinase (MMP)-9, MMP-12 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in smoke-induced chronic obstructive pulmonary disease (COPD) rat models and the therapeutic effect of N-acetylcysteine (NAC). METHODS: Male Wistar rats were exposed to cigarette smoke for 3.5 months. NAC was given in the last month. Lung function was measured at the end of the study. The levels of IL-4 and IFNgamma in broncho-alveolar lavage fluid (BALF) and lung tissues were determined by ELISA. The expression of MMP-9, MMP-12 and TIMP-1 mRNA in lung tissues were determined by RT-PCR. RESULTS: (1) In comparison with the control group, smoke exposed group presented a significant decrease in forced expiratory volume in 0.3 second (FEV(0.3))/forced vital capacity (FVC), dynamic lung compliance (Cdyn), mean alveolar numbers (MAN) and a significant increase in expiratory resistance (Re), pulmonary mean linear intercept (Lm) (P < 0.05). After treatment with NAC, FEV(0.3)/FVC, Re and Cdyn were improved significantly (P < 0.05). No significant changes were found in Lm and MAN (P > 0.05). (2) In the lung tissues of smoke exposed group, IL-4 level was 10.00 pg/ml, IFNgamma level was 19.37 pg/ml, and the IL-4/IFNgamma ratio was 0.49. In the lung tissues of the control group, they were 4.38 pg/ml, 54.94 pg/ml and 0.10, respectively. There were significant differences in these indexes between the smoke exposed group and the control group (P < 0.05). IL-4 level in the NAC group was 7.99 pg/ml which was similar to that in the smoke exposed group (P > 0.05). IFNgamma and IL-4/IFNgamma ratio were 43.40 pg/ml and 0.15, the former being significantly higher and the latter being significantly lower than those in the smoke exposed group (P < 0.05). (3) The expression of MMP-12 mRNA and MMP-12/TIMP-1 ratio in the smoke exposed group (0.36, 1.21) were significantly higher than those in the control group (0.24, 0.88) (P < 0.05). There was no difference in TIMP-1 (P > 0.05). The expression of MMP-12, TIMP-1 mRNA and the MMP-12/TIMP-1 ratio in NAC group were similar to those in the smoke exposed group (P > 0.05). CONCLUSIONS: (1) Cigarette smoke exposure increased IL-4 and decreased IFNgamma. This may contribute to smoke-induced changes in lung function. NAC had no effect on IL-4, but increased IFNgamma, and the IL-4/IFNgamma ratio returned to normal. This might be one of the mechanisms of NAC in improving lung function. (2) Cigarette smoke promoted MMP-12 gene expression and increased the MMP-12/TIMP-1 ratio. This may play a role in smoke-induced emphysema. NAC did not alter MMP-12/TIMP-1 ratio when given in the late phase of smoke exposure. This result could explain the emphysematous changes in the NAC group.

Acetylcysteine↗
PubMed2004

[Approach to the maxillary sinus, the peterygopalatofossa for resecting maxillary nerve under the endoscopy].

OBJECTIVE: This paper presents a method for treating maxillary neuralgia, the second division of trigeminal nerve, in the weak aged. METHOD: Thirty-nine cases with forty trigeminal neuralgia were treated from 1996 to 2001. All patients were treated through the maxillary sinus, the peterygopalatofossa for resecting maxillary nerve with endoscopic surgery. RESULT: The pain of all patients was relieved after operation and no recurrence of neuralgia was occurred in more than 2-years follow-up. CONCLUSION: This method had the advantages of avoiding to operate craniotomy, no complications, performing easily and the ideal treatments remained.

Aged↗
PubMed2004

[Combining of TNP-470 and 5-Fu in inhibition of adenoid cystic carcinoma in nude mice model].

OBJECTIVE: To study the effect of angiogenesis inhibitor and its combine with chemical drug in suppressing the growth of adenoid cystic carcinoma (ACC). METHODS: Acc-M cells were inoculated subcutaneous into BABL/C nu/nu mice. The mice were divided into control, different dose of TNP-470 treatment groups, 5-Fu treatment group and TNP-470 plus 5-Fu treatment group. Treatments were given 48 hours after inoculation. The mice were sacrificed on the 22nd day and excised tumors were weighted. Tumors were also investigated by immunohistochemistry and ultrastructural observations. RESULTS: TNP-470 100 mg/kg/qod efficiently inhibited the growth of Acc-M tumors. TNP-470 30 mg/kg/qod combined with 50 mg/kg/week 5-Fu also resulted in significant growth inhibit of the tumors. TNP-470 suppressed tumor growth by inhibiting neovascularization, therefore inducing apoptosis of Acc-M cells. All experimental groups had different degrees of VEGF and bFGF express. CONCLUSION: Since ACC is a slow developing tumor, blood supply is not so sufficient as sarcomas. Angiogensis inhibitor may inhibit its growth in high dosage. Combining medium dosage of angiogensis inhibitor with chemical drug may have synergistic result in inhibiting ACC growth.

Angiogenesis Inhibitors↗
PubMed2004

[Inflammatory injurious effect of angiotensin II on pulmonary microvascular endothelium in rat].

OBJECTIVE: To investigate the effects of angiotensin II (AngII) and its receptors on monolayer permeability of pulmonary microvascular endothelial cells in rat. METHODS: The following examinations were done on cultured rat pulmonary microvascular endothelial cells (RPMVECs). 1. Micro-filter was used to assay the variations of lipopolysaccharide (LPS)-induced increased RPMVECs monolayer permeability coefficient (Kf) in different periods. 2. Effect of angiotensin II on LPS-induced permeability injury to the endothelium, and preventive effects of angiotensin II type 1 receptor antagonist (Sar1, Ile8)-Ang II. RESULTS: LPS increased RPMVECs monolayer permeability compared with normal control, and AngII exacerbated LPS-induced RPMVECs monolayer permeability significantly. This synergistic effect was significantly prevented by the addition of (Sar1, Ile8 )-Ang II. CONCLUSION: AngII and LPS have synergistic injurious effects to the pulmonary microvascular endothelium in rat, and AngII exacerbates increase in LPS-induced RPMVECs monolayer permeability. This synergistic effect is significantly prevented by the addition of (Sar1, Ile8)-Ang II.

Angiotensin II↗