Study on the effect and mechanism of the dysfunction of CD4(+) T cells in the disease process of chronic cardiac failure.

Objective: To study the effect and mechanism of the dysfunction of CD4(+) T cells in the disease process of chronic cardiac failure (CHF).

Methods: According to different group technologies, 100 CHF patients were divided into the following groups: ischemia group and non-ischemia group, heart function Ⅲ-Ⅳ group and heart function Ⅰ-Ⅱ group, event group and non-event group, and 50 healthy volunteers were included in the control group. Real-time PCR was used to detect transcription factors T-bet and GATA-3 of Th1 and Th2; flow cytometry was applied to determine the ratio of Th17 and Treg cells; ELISA was employed to test cytokines IFN-γ, IL-4, IL-17 and IL-10 of peripheral blood Th1, Th2, Th17 and Treg cells, respectively; ultrasonic cardiogram was used to exploit to LVEF and LVEDd; and electrochemilu minescene immunoassay was used to examine plasma BNP.

[Impacts of hypoxia on the features and chemoresistance of cancer stem cells in Hep-2 cells and underlying mechanism].

Objective: To investigate the effects of hypoxia on the features and chemoresistance of cancer stem cells in Hep-2 cells and underlying mechanism.

Methods: The shRNA interference recombinant plasmid targeting HIF-1α was synthesized and transfected into Hep-2 cells. The HIF-1α knockdown Hep-2 cells were established after clonal selection and the expression of HIF-1α was measured.

[Expression of hypoxia inducible factor-1α and correlated target genes in human laryngeal carcinoma].

Objective: To detect the expression of hypoxia inducible factor 1 alpha (HIF-1α), glucose transporter protein-1 (GLUT-1) and vascular endothelial growth factor (VEGF) in human laryngeal carcinoma tissue, and to study the relationship between hypoxia and HIF-1α, GLUT-1, VEGF in human laryngeal carcinoma Hep-2 cells and to explore the effect of HIF-1α, GLUT-1 and VEGF as endogenous hypoxic markers on laryngeal carcinoma.

Methods: The expression levels of HIF-1α, GLUT-1 and VEGF were detected in 35 cases of laryngeal carcinoma by SP immunohistochemical methods and in Hep-2 cells by SP immunocytochemical methods. The relationship between HIF-1α and GLUT-1, VEGF protein expression was analyzed.

[Expression of S-phase kinase associated protein 2 in laryngeal carcinoma and its molecular mechanisms involved in regulation of proliferation and apoptosis of Hep-2 cells].

Objective: To investigate the expression of S-phase kinase associated protein 2 (Skp2) in human laryngeal squamous cell carcinomas and to explore the effect of silencing of Skp2 by RNAi on the proliferation and apoptosis and the expressing of p27 protein as well as change of cell cycle in laryngeal carcinoma cell line Hep-2 cell.

Methods: The expression of Skp2 in laryngeal carcinoma tissues of different differentiation grade was detected by immunohistochemistry. According to the encoding sequence of mRNA of Skp2, two pieces of oligonucleotide sequences were designed and synthesized.

[Silencing of signal transducer and activator of transcription 3 gene expression using RNAi enhances the efficacy of radiotherapy for laryngeal carcinoma in vivo].

Objective: To study the inhibitory effect of signal transducer and activator of transcription 3 (STAT3) shRNA generated by vector pSilence in conjunction with radiotherapy on laryngeal squamous cell carcinoma of nude mice xenograft tumor.

Methods: The animal models of xenotransplanted human laryngeal carcinoma cell line Hep-2 were set up in 28 nude mice which were divided into 4 groups at random: the negative plasmid control group, the group that received pshSTAT3 (pGPU6/GFP/NeoshSTAT3) transfection, the radiation group, and the group of pshSTAT3 transfection combined with irradiation. Tumor volume was determined regularly.

[Molecular mechanisms involved in regulation of proliferation and apoptosis by STAT3 antisense oligonucleotide and chemotherapy in laryngeal cancer cells].

Objective: To study the mechanism of STAT3 antisense oligonucleotide (STAT3 AS-ON) in combination with DDP in the treatment of laryngeal cancer.

Methods: STAT3 AS-ON, DDP, or STAT3 AS-ON + DDP was added into culture media. The expression and phosphorylation levels of STAT3 protein in Hep-2 cells were measured by Western Blot.

[Role of clonality analysis by X-chromosome inactivation in the diagnosis of cervical lymph node occult micrometastasis from squamous carcinoma of the head and neck].

Objective: To investigate the role of clonality analysis by X-chromosome inactivation in the diagnosis of cervical lymph node metastasis from squamous carcinoma of the head and neck.

Methods: Twenty cases of clinical NOM0 squamous carcinoma of the head and neck with either pathologically confirmed or suspected occult micrometastasis in the cervical lymph node were recruited. Interested DNA samples were procured through tissue microdissection and one-step proteinase K digestion, and the clonality analysis was carried out by means of restriction enzyme digestion and amplification of human androgen receptor markers (HUMURA) to check out the status of X-chromosome inactivation.

[Subdiaphragmatic vagotomy reduces the responses of fever and discharge of neurons in PVN to LPS].

Aim: To study the possibility that responses of fever and discharge of neurons in PVN to intraperitoneal administration of LPS are mediated by vagal afferents.

Methods: Rectal temperature of rat was detected by digital temperature detecting instrument. Glass micropipette placed in PVN was used to record unit discharges of neurons in it, before and after LPS was injected into PVN in normal rats and vagotomy rats.

[The activation of vagus afferent in response to lipopolysaccharide the role of interleukin-1].

To study the possibility of activation of vagus afferent in response to lipopolysaccharide (LPS) through interleukin-1 (IL-1), Wistar rats were randomly divided into LPS group and saline (NS) group. The expression of c-Fos, CD14 and Mac-1 were detected by immunohistochemistry staining. IL-1 bioactivity was determined by L929 cell proliferation.