9 results match your criteria: "University of Huazhong Science and Technology[Affiliation]"

Cytokine storm syndrome in coronavirus disease 2019: A narrative review.

J Intern Med

February 2021

From the, Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, China.

Cytokine storm syndrome (CSS) is a critical clinical condition induced by a cascade of cytokine activation, characterized by overwhelming systemic inflammation, hyperferritinaemia, haemodynamic instability and multiple organ failure (MOF). At the end of 2019, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, China, and rapidly developed into a global pandemic. More and more evidence shows that there is a dramatic increase of inflammatory cytokines in patients with COVID-19, suggesting the existence of cytokine storm in some critical illness patients.

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The ataxia telangiectasia-mutated and Rad3-related (ATR) kinase functions as a central node in the DNA damage response signaling network. The mechanisms by which ATR activity is amplified and/or maintained are not understood. Here we demonstrate that BRIT1/microcephalin (MCPH1), a human disease-related protein, is dispensable for the initiation but essential for the amplification of ATR signaling.

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[Promotive effect of decreased cyclin E threshold on cell proliferation].

Ai Zheng

November 2004

Center of Gastroenterological Surgery/Cancer Research Institute, Tongji Hospital, Tongji Medical College, University of Huazhong Science and Technology, Wuhan, Hubei 430 030, P.R. China.

Background & Objective: Many studies showed that high expression of Cyclin E promotes cell proliferation, but contrary data was also reported that cell proliferation didn't decrease with low expression of Cyclin E. In addition, we observed that many tumor cells have strong capability of proliferation with low expression of Cyclins, including Cyclin E. This study was to analyze effect of reduced Cyclin E threshold on proliferation of acute lymphocyte leukemia cell line MOLT-4 to explain the above phenomena.

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[Mdr-1 ribozyme in the reversal of multidrug resistance in human ovarian cancer].

Zhonghua Zhong Liu Za Zhi

September 2003

Department of Obstetrics & Gynecology, Tongji Hospital, Tongji Medical College, University of Huazhong Science and Technology. Wuhan 430030, China.

Objective: To study the mechanism of multidrug resistance and its reversal by mdr-1 ribozyme in human ovarian cancer.

Methods: The expression of mdr-1 and p-glycoprotein (p-gp) was studied by confocal laser microscope (Confocal), RT-PCR and Western blot analysis in adriamycin-resistant human ovarian cancer cell line (A2780/ADM) and adriamycin-sensitive one (A2780). The mdr-1 ribozyme was transfected into the A2780/ADM by Lipofectamine 2000 to overcome the multidrug resistance in ovarian cancer.

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Objective: To study whether the liver cirrhosis and portal hypertension are associated with a -786T-->C mutation at promoter and VNTR polymorphism in intron 4 and a 894 G-->T mutation at exon 7 of the eNOS.

Methods: A case control study of 106 patients with liver cirrhosis due to HBV was performed in comparison with 108 controls with the help of PCR-SSCP or RFLP.

Results: There was no difference in the gene frequency of allele G of promoter between LC(+) group and other groups.

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[Role of apoptosis-associated genes and caspase-3 in cisplatin-resistant human ovarian cancer cell lines].

Zhonghua Fu Chan Ke Za Zhi

March 2003

Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, University of Huazhong Science and Technology, Wuhan 430030, China.

Objective: To explore the role of apoptosis-associated genes and caspase-3 activity in cisplatin (DDP)-resistant human ovarian cancer cell lines.

Methods: The expressions of apoptosis-associated genes (bcl-2, bax, bcl-X(L) and bcl-X(S)) and the activity of caspase-3 were studied by reverse transcription-polymerase chain reaction (RT-PCR) and western blot in the cisplatin-resistant (A2780/DDP, COC1/DDP) and sensitive human ovarian cancer cells (A2780 and COC1). The apoptotic rates of A2780, COC1, A2780/DDP and COC1/DDP were measured with flow cytometry when treated with cisplatin.

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Objective: To assess the association of human leucocyte antigen (HLA)-DRB1 allele with the genetic susceptibility to cirrhosis due to hepatitis B virus(HBV).

Methods: One hundred and six patients with cirrhosis due to HBV in Hubei area were investigated for HLA-DRB1 gene by polymerase chain reaction-sequence specific primers technique. The results were compared with those from 108 normal healthy people.

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[Tumor necrosis factor alpha HLA-DRB(1) gene polymorphism and genetic susceptibility to cirrhosis].

Zhonghua Nei Ke Za Zhi

December 2002

The Institute of Liver Disease, Tongji Hospital, Tongji Medical College, University of Huazhong Science and Technology, Wuhan 430030, China.

Objective: To study the relationship between the gene polymorphism of HLA-DRB(1) and tumor necrosis factor (TNF)alpha with the genetic susceptibility to cirrhosis.

Methods: The gene polymorphism of DRB(1) and TNF alpha of 106 cases of cirrhosis due to HBV and 108 controls were detected by means of polymerase chain reaction-sequence specific primer and RFLP techniques.

Results: The frequency of DRB(1) * 120X and TNF2/1 was increased in the patients as compared with the controls (35.

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Background & Objective: Cisplatin-based chemotherapy is an important way for treatment of ovarian cancer, but resistance to cisplatin is one of the reasons of treatment failure of ovarian cancer. This study was designed to investigate the relationship between apoptosis-associated proteins and caspase-3 activity as well as their effects on chemoresistance in human ovarian cancer cell lines.

Methods: The expression of apoptosis-associated proteins (bcl-2, bcl-xL, bax, bcl-xs), the activity of caspase-3 and cleavage of poly ADP-ribose polymerase (PARP) were determined with Western blot analysis in the cisplatin-resistant cell (COC1/DDP) and cisplatin-sensitive human ovarian cancer cell (COC1).

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