Biomedical subjects

Hongyu Zhang

Publications and source records attributed to Hongyu Zhang.

24 records · Page 2Linked to original sources

PubMed2003

Sequential non-invasive mechanical ventilation following short-term invasive mechanical ventilation in COPD induced hypercapnic respiratory failure.

OBJECTIVE: To estimate the feasibility and the efficacy of early extubation and sequential non-invasive mechanical ventilation (MV) in chronic obstructive pulmonary disease (COPD) with exacerbated hypercapnic respiratory failure. METHODS: Twenty-two intubated COPD patients with severe hypercapnic respiratory failure due to pulmonary infection (pneumonia or purulent bronchitis) were involved in the study. At the time of pulmonary infection control window (PIC window) appeared, when pulmonary infection had been significantly controlled (resolution of fever and decrease in purulent sputum, radiographic infiltrations, and leukocytosis) after the antibiotic and the comprehensive therapy, the early extubation was conducted and followed by non-invasive MV via facial mask immediately in 11 cases (study group). Other 11 COPD cases with similar clinical characteristics who continuously received invasive MV after PIC window were recruited as control group. RESULTS: All patients had similar clinical characteristics and gas exchange before treatment, as well as the initiating time and all indices at the time of the PIC window. For study group and control group, the duration of invasive MV was (7.1 +/- 2.9) vs (23.0 +/- 14.0) days, respectively, P < 0.01. The total duration of ventilatory support was (13 +/- 7) vs (23 +/- 14) days, respectively, P < 0.05. The incidence of ventilator associated pneumonia (VAP) were 0/11 vs 6/11, respectively, P < 0.01. The duration of intensive care unit (ICU) stay was (13 +/- 7) vs (26 +/- 14) days, respectively, P < 0.05. CONCLUSIONS: In COPD patients requiring intubation and MV for pulmonary infection and hypercapnic respiratory failure, early extubation followed by non-invasive MV initiated at the point of PIC window significantly decreases the invasive and total durations of ventilatory support, the risk of VAP, and the duration of ICU stay.

Adult↗

PubMed2003

Beta-carotene protects rats against bronchitis induced by cigarette smoking.

OBJECTIVE: To investigate the protective effects of beta-carotene in rats against the development of chronic bronchitis induced by cigarette smoking. METHODS: Forty-two Male Wistar rats were randomly divided into three study groups: (1) control (n = 15), animals underwent no treatment; (2) cigarette smoking (n = 15), animals developed chronic bronchitis through long-term cigarette smoking twice a day for 75 d; (3) beta-carotene plus cigarette smoking animals (n = 12) were given 1 ml or 15 mg/kg beta-carotene orally every day just before cigarette smoking. The levels of IL-6, IL-8, NO, superoxide dismutase (SOD) and lipoperoxide (LPO) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were measured and the pathological changes to lung tissue were analyzed using light microscopy. RESULTS: Long-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. beta-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis. CONCLUSIONS: Quantitative oral intake of beta-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

Animals↗

PubMed2002

Methylation profiling of twenty promoter-CpG islands of genes which may contribute to hepatocellular carcinogenesis.

BACKGROUND: Hepatocellular carcinoma (HCC) presents one of the major health threats in China today. A better understanding of the molecular genetics underlying malignant transformation of hepatocytes is critical to success in the battle against this disease. The methylation state of C5 of the cytosine in the CpG di-nucleotide that is enriched within or near the promoter region of over 50 % of the polymerase II genes has a drastic effect on transcription of these genes. Changes in the methylation profile of the promoters represent an alternative to genetic lesions as causative factors for the tumor-specific aberrant expression of the genes. METHODS: We have used the methylation specific PCR method in conjunction with DNA sequencing to assess the methylation state of the promoter CpG islands of twenty genes. Aberrant expression of these genes have been attributed to the abnormal methylation profile of the corresponding promoter CpG islands in human tumors. RESULTS: While the following sixteen genes remained the unmethylated in all tumor and normal tissues: CDH1, APAF1, hMLH1, BRCA1, hTERC, VHL, RARbeta, TIMP3, DAPK1, SURVIVIN, p14ARF, RB1, p15INK4b, APC, RASSF1c and PTEN, varying degrees of tumor specific hypermethylation were associated with the p16INK4a, RASSF1a, CASP8 and CDH13 genes. For instance, the p16INK4a was highly methylated in HCC (17/29, 58.6%) and less significantly methylated in non-cancerous tissue (4/29. 13.79%). The RASSF1a was fully methylated in all tumor tissues (29/29, 100%), and less frequently methylated in corresponding non-cancerous tissue (24/29, 82.75%). CONCLUSIONS: Furthermore, co-existence of methylated with unmethylated DNA in some cases suggested that both genetic and epigenetic (CpG methylation) mechanisms may act in concert to inactivate the p16INK4a and RASSF1a in HCC. Finally, we found a significant association of cirrhosis with hypermethylation of the p16INK4a and hypomethylation of the CDH13 genes. For the first time, the survey was carried out on such an extent that it would not only provide new insights into the molecular mechanisms underscoring the aberrant expression of the genes in this study in HCC, but also offer essential information required for a good methylation-based diagnosis of HCC.

Adult↗

PubMed2002

The genome sequence of the malaria mosquito Anopheles gambiae.

Anopheles gambiae is the principal vector of malaria, a disease that afflicts more than 500 million people and causes more than 1 million deaths each year. Tenfold shotgun sequence coverage was obtained from the PEST strain of A. gambiae and assembled into scaffolds that span 278 million base pairs. A total of 91% of the genome was organized in 303 scaffolds; the largest scaffold was 23.1 million base pairs. There was substantial genetic variation within this strain, and the apparent existence of two haplotypes of approximately equal frequency ("dual haplotypes") in a substantial fraction of the genome likely reflects the outbred nature of the PEST strain. The sequence produced a conservative inference of more than 400,000 single-nucleotide polymorphisms that showed a markedly bimodal density distribution. Analysis of the genome sequence revealed strong evidence for about 14,000 protein-encoding transcripts. Prominent expansions in specific families of proteins likely involved in cell adhesion and immunity were noted. An expressed sequence tag analysis of genes regulated by blood feeding provided insights into the physiological adaptations of a hematophagous insect.

Animals↗

PubMed2002

[Prophylactic effect of retinoic acid on chronic obstructive pulmonary emphysema in rats].

OBJECTIVE: To evaluate the effect and molecular mechanism of retinoic acid (RA) in preventing experimental pulmonary emphysema in rats. METHODS: Thirty-six Wistar rats were randomly divided into three groups, the normal group(A), the model group (B) and the RA treated group (C). Rats in group B group were exposed to cigarette smoke, and group C was treated with RA. Pulmonary function indices and histopathological changes were evaluated. The enzymatic activity of gelatinases was measured by ELISA, and the expression of gelatinases and the proliferating cell nuclear antigen (PCNA) was examined by immunohistochemical method. RESULTS: Compared with group A, group B presented significant differences in FEV(0.3),FEV(0.3)/FVC and FRC [(5.1 +/- 0.4) ml vs (6.0 +/- 0.3) ml, (71 +/- 10) ml/s vs (87 +/- 3) ml/s, (7.2 +/- 2.2) ml vs (2.9 +/- 1.1) ml (P < 0.01)];the enzymatic activity [(1.06 +/- 0.23)ng/ml vs (0.53 +/- 0.17)ng/ml, (0.960 +/- 0.230)ng/ml vs (0.300 +/- 0.090)ng/ml] and the expression of gelatinases were also markedly elevated(P < 0.01). In comparison with group B, the pulmonary function indices in group C [(5.2 +/- 0.4)ml, (81 +/- 5) ml/s, (6.1 +/- 2.7)ml/s] were improved (P < 0.05); the enzymatic activity [(0.83 +/- 0.23)ng/ml, (0.570 +/- 0.010)ng/ml] and the expression of gelatinases were decreased, while the PCNA index staining (93 +/- 4 vs 53 +/- 6) was increased (P < 0.01). CONCLUSION: RA can prevent the development of pulmonary emphysema in rats.

Animals↗

PubMed2002

[The pathology of and the cardio-pulmonary functional changes in acute multiple pulmonary microthromboembolism in a canine model].

OBJECTIVE: To evaluate the effect of acute multiple pulmonary microthromboembolism on circulation, ventilation, lung histology, and the coagulatory and fibrinolytic functions. METHODS: Thirteen dogs were studied, 7 in the embolism group and 6 in the control group. 10 ml of blood was withdrawn from each animal. Thrombi were formed and cut into pieces of 1 mm to 2 mm in size. The thrombi were counted, and 300 thrombi were infused at one time back to the same animal. PAP, PAWP, VO(2), DO(2), D-dimer, protein C, protein S were measured before and immediately, 30 min, 1 hour, 2 hour after embolism. RESULTS: PAP was increased immediately after embolisation, and then decreased at 1 hour. The level of D-dimer was elevated at an early stage. Pulmonary hemorrhage, consolidation and microembolism were observed. CONCLUSIONS: Multiple microthromboembolism caused lung injury and thrombosis. PAP was increased at the early stage, but ventilation was not affected. The level of D-dimer changed at the early stage of thromboembolism.

Acute Disease↗