6 results on '"Zhen-Yu Ke"'
Search Results
2. Metastasis-Associated Protein 1 Deficiency Results in Compromised Pulmonary Alveolar Capillary Angiogenesis in Mice
- Author
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Qiang Zhou, Jing Ye, Xing Gao, Li Wang, Junhui Qin, Yingmei Wang, Zhen-Yu Ke, Rui-An Wang, Yuan Liang, Tong Yang, and Rekesh Kumar
- Subjects
0301 basic medicine ,Transcriptional Activation ,Vascular Endothelial Growth Factor A ,medicine.medical_specialty ,Pathology ,Angiogenesis ,CD34 ,Neovascularization, Physiologic ,Antigens, CD34 ,Persistent Fetal Circulation Syndrome ,Neovascularization ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,Lab/In Vitro Research ,Internal medicine ,medicine ,Myocyte ,Animals ,Myocytes, Cardiac ,Mice, Knockout ,Lung ,business.industry ,General Medicine ,Hypoxia-Inducible Factor 1, alpha Subunit ,Immunohistochemistry ,Actins ,Capillaries ,Vascular endothelial growth factor ,Pulmonary Alveoli ,Repressor Proteins ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Trans-Activators ,medicine.symptom ,business ,Transcription Factors - Abstract
BACKGROUND The aim of this study was to investigate the effects of metastasis-associated protein 1 (MTA1) deficiency during angiogenesis of pulmonary alveolar capillaries in mice and to determine the molecular mechanisms involved. MATERIAL AND METHODS The expressions of MTA1, CD34, vascular endothelial growth factor (VEGF), alpha smooth muscle actin (α-SMA), and HIF-1α were analyzed in the lungs of MTA1-knockout (KO) and wild-type mice at embryonic day 18.5 and 2 months by quantitative PCR, immunoblotting, and immunohistochemistry. The morphological changes were investigated during pulmonary alveolar capillary formation. The heart weight/body weight (HW/BW) ratio and the size of the right ventricular wall cardiomyocytes were also measured. Regulation of MTA1 on HIF-1α was determined in vitro. RESULTS MTA1 deficiency reduced the number of pulmonary alveolar capillaries compared to the wild-type mice. MTA1-KO mice exhibited a decreased expression of HIF-1α and VEGF in the lungs. The retarded growth of the MTA1-KO mice was also noticed during the first week after birth. Accordingly, MTA1 deficiency resulted in increased infant mortality. In surviving adult mice, MTA1 deficiency induced myocardial hypertrophy, highlighted by an increased heart weight/body weight ratio and larger cardiomyocytes. In cultured cells, HIF-1α and VEGF levels were significantly upregulated upon MTA1 overexpression, suggesting a close relationship between all 3 molecules. CONCLUSIONS MTA1 participates in the formation of pulmonary capillaries via stabilization of HIF-1α. This finding sheds new light on the function of MTA1 in lung development, opening new avenues for the diagnosis/treatment of related pulmonary diseases.
- Published
- 2017
3. Why is Mycobacterium Tuberculosis Hard to Grow? The Principle of Biorelativity Explains
- Author
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Yuan Liang, Tong Yang, Jun-Hui Qin, Rui-An Wang, Li Wang, and Zhen-Yu Ke
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biology ,business.industry ,Tuberculosis Meningitis ,biology.organism_classification ,medicine.disease ,Bioinformatics ,Virology ,Mycobacterium tuberculosis ,Gene duplication ,Medicine ,Leprosy ,business ,Mycobacterium leprae ,Bacteria - Abstract
Comparing the lifespan and the proliferative potential of E. coli and MTB, we see a reverse relationship. E. coli live short, and grow fast. It just takes 18-20 minutes for them to duplicate. Conversely, MTBs live long, are quite tolerant to different environments, and grow so slowly that their duplication time exceeds 18 hrs. The duplication time of mycobacterium leprae is even longer, so that all the cultivation efforts have failed. Although nobody knows exactly how long these bacteria can live since they cannot be cultivated, it can be postulated that they live very long. That explains why leprosy is so difficult to cure.
- Published
- 2014
4. Metastasis-Associated Protein 1 Deficiency Results in Compromised Pulmonary Alveolar Capillary Angiogenesis in Mice.
- Author
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Jun-Hui Qin, Zhen-Yu Ke, Qiang Zhou, Li Wang, Yuan Liang, Ying-Mei Wang, Tong Yang, Xing Gao, Jing Ye, Kumar, Rakesh, and Rui-An Wang
- Published
- 2017
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5. Epithelial-mesenchymal transition as strategic microenvironment mimicry for cancer cell survival and immune escape?
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Yuan Liang, Li Wang, Zhen-Yu Ke, Qinlong Li, Jun-Hui Qin, and Rui-An Wang
- Subjects
0301 basic medicine ,lcsh:QH426-470 ,Cell ,Biology ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Antigen ,medicine ,Mimicry ,Epithelial–mesenchymal transition ,Molecular Biology ,Genetics (clinical) ,Cancer ,lcsh:R5-920 ,Immune escape ,Mesenchymal stem cell ,EMT ,Cell Biology ,medicine.disease ,Phenotype ,Epithelium ,lcsh:Genetics ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Immunology ,Cancer cell ,Cancer research ,lcsh:Medicine (General) - Abstract
Epithelial-mesenchymal transition (EMT) is the phenotypic transition of epithelial cells to mesenchymal cells characterized by loss of epithelial markers, loss of intercellular adherence and acquirement of mesenchymal cell markers and increased locomotive ability. EMT is widely considered to be a gene regulated process necessary for cancer metastasis. Yet it is a highly controversial issue. We here propose that EMT is an environmentally induced cell behavior. It is the mimicry of their living environment. It is a survival strategy, a way of immune escape. We also propose here that the epithelial cell markers may functionally act as tumor antigens since in the mesenchymal surroundings there are no other structures bearing the same antigens as epithelial cells.
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6. Prognosis of patients with gastric cancer and solitary lymph node metastasis.
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Chen CQ, Wu XJ, Yu Z, Bu ZD, Zuo KQ, Li ZY, and Ji JF
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- Adult, Age Factors, Aged, Aged, 80 and over, Chemotherapy, Adjuvant, Chi-Square Distribution, China, Female, Gastrectomy, Humans, Kaplan-Meier Estimate, Lymph Node Excision, Lymphatic Metastasis, Male, Middle Aged, Retrospective Studies, Risk Factors, Stomach Neoplasms mortality, Stomach Neoplasms therapy, Survival Rate, Time Factors, Treatment Outcome, Lymph Nodes pathology, Stomach Neoplasms pathology
- Abstract
Aim: To investigate the relationship of solitary lymph node metastasis (SLNM) and age with patient survival in gastric cancer (GC)., Methods: The medical records databases of China's Beijing Cancer Hospital at the Peking University School of Oncology and Shanghai Tenth People's Hospital affiliated to Tongji University were searched retrospectively to identify patients with histologically proven GC and SLNM who underwent surgical resection between October 2003 and December 2012. Patients with distant metastasis or gastric stump carcinoma following resection for benign disease were excluded from the analysis. In total, 936 patients with GC + SLNM were selected for analysis and the recorded parameters of clinicopathological disease and follow-up (range: 13-2925 d) were collected. The Kaplan-Meier method was used to stratify patients by age (≤ 50 years-old, n = 198; 50-64 years-old, n = 321; ≥ 65 years-old, n = 446) and by metastatic lymph node ratio [MLR < 0.04 (1/25), n = 180; 0.04-0.06 (1/25-1/15), n = 687; ≥ 0.06 (1/15), n = 98] for 5-year survival analysis. The significance of intergroup differences between the survival curves was assessed by a log-rank test., Results: The 5-year survival rate of the entire GC + SLNM patient population was 49.9%. Stratification analysis showed significant differences in survival time (post-operative days) according to age: ≤ 50 years-old: 950.7 ± 79.0 vs 50-64 years-old: 1697.8 ± 65.9 vs ≥ 65 years-old: 1996.2 ± 57.6, all P < 0.05. In addition, younger age (≤ 50 years-old) correlated significantly with mean survival time (r = 0.367, P < 0.001). Stratification analysis also indicated an inverse relationship between increasing MLR and shorter survival time: < 0.04: 52.8% and 0.04-0.06: 51.1% vs ≥ 0.06: 40.5%, P < 0.05. The patients with the shortest survival times and rates were younger and had a high MLR (≥ 0.06): ≤ 50 years-old: 496.4 ± 133.0 and 0.0% vs 50-65 years-old: 1180.9 ± 201.8 and 21.4% vs ≥ 65 years-old: 1538.4 ± 72.4 and 37.3%, all P < 0.05. The same significant trend in shorter survival times and rates for younger patients was seen with the mid-range MLR group (0.04-0.06), but the difference between the two older groups was not significant. No significant differences were found between the age groups of patients with MLR < 0.04. Assessment of clinicopathological parameters identified age group, Borrmann type, histological type and tumor depth as the most important predictors of the survival rates and times observed for this study population., Conclusion: GC patients below 51 years of age with MLR of SLNM above 0.06 have shorter life expectancy than their older counterparts.
- Published
- 2013
- Full Text
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