Biomedical subjects

Jian Kang

Publications and source records attributed to Jian Kang.

58 records · Page 4Linked to original sources

PubMed2002

Targeted disruption of NBS1 reveals its roles in mouse development and DNA repair.

Nijmegen breakage syndrome (NBS) is an autosomal recessive hereditary disease that shares some common defects with ataxia-telangiectasia. The gene product mutated in NBS, named NBS1, is a component of the Mre11 complex that is involved in DNA strand-break repair. To elucidate the physiological roles of NBS1, we disrupted the N-terminal exons of the NBS1 gene in mice. NBS1(m/m) mice are viable, growth retarded and hypersensitive to ionizing radiation (IR). NBS1(m/m) mice exhibit multiple lymphoid developmental defects, and rapidly develop thymic lymphoma. In addition, female NBS1(m/m) mice are sterile due to oogenesis failure. NBS1(m/m) cells are impaired in cellular responses to IR and defective in cellular proliferation. Most systematic and cellular defects identified in NBS1(m/m) mice recapitulate those in NBS patients, and are essentially identical to those observed in Atm(-/-) mice. In contrast to Atm(-/-) mice, spermatogenesis is normal in NBS1(m/m) mice, indicating that distinct roles of ATM have differential requirement for NBS1 activity. Thus, NBS1 and ATM have overlapping and distinct functions in animal development and DNA repair.

Animals↗

PubMed2002

[The influence of nasal continual positive airway pressure on some vasoactive substances in patients with obstructive sleep apnea syndrome].

OBJECTIVE: To investigate the influence of nasal continual positive airway pressure (nCPAP) on the plasma levels of thromboxane B(2) (TXB(2)), renin, angiotensin II (AT-II), endothelin 1 (ET-1), cyclic AMP (cAMP) and cyclic GMP (cGMP) and evaluate their clinical significance. METHODS: 20 patients with OSAS without cardiovascular complications and 20 nromal controls were enrolled in the study, who were monitored with PSG, and then treated with nCPAP during the second night. All the plasma parameters were measured after PSG monitoring and nCPAP management with radio-immunoassay. RESULTS: Before nCPAP, plasma levels of TXB(2), renin, and AT-II were higher in patients with OSAS than those in control (P < 0.05); Meanwhile, the plasma levels of ET-1, cAMP, and cAMP/cGMP were significantly higher in patients group than those in control (P < 0.01). CONCLUSIONS: Patients with severe OSAS may have disturbances in neuro-regulation and changes in plasma level of TXB(2), renin, AT-II and ET-1, which indicates that the vasoactive substance might be related to the hypoxemia and disturbance in neuro-regulations, and might play an important role in the development of hypertension and other cardiovascular disorders. nCPAP therapy can correct the abnormalities of some vasoactive substances.

Angiotensin II↗

PubMed2002

[Study of serum leptin level in patients with obstructive sleep apnea].

OBJECTIVE: To explore the change of serum leptin in patients with obstructive sleep apnea syndrome (OSAS). METHODS: Polysomnography was performed in 58 patients with OSAS and in 21 simple obese controls without differences in age and body mass index (BMI). Serum leptin level was measured by radioimmunoassay. RESULTS: (1) The serum leptin level in patients with OSAS was higher, in both males (6.1 +/- 1.7) microg/L and females (19.5 +/- 9.9) microgram/L, than that in the simple obese controls [male (4.5 +/- 1.7) microgram/L, female (10.5 +/- 2.4) microgram/L] (P < 0.01, P < 0.05). (2) Serum leptin levels were significantly correlated with BMI in both OSAS patients (r = 0.64, P < 0.01) and simple obese controls (r = 0.59, P < 0.01), but only in OSAS patients was the leptin level significantly correlated with apnea and hypopnea index (AHI) (r = 0.47, P < 0.01) and with neck circumference (r = 0.64, P < 0.01). CONCLUSIONS: Serum leptin levels were higher in OSAS patients than in simple obese controls. Besides obesity and neck circumference, OSAS may also influence the leptin system, resulting in increased serum leptin level.

Body Mass Index↗

PubMed2002

[The effect of TNP-470 on the proliferation and apoptosis of lung adenocarcinoma cells].

OBJECTIVE: To investigate the effect of TNP-470 on the proliferation and apoptosis of lung adenocarcinoma cells and to explore the mechanism of the effect. METHODS: The TNP-470 with different concentrations was added to cultured lung adenocarcinoma cell strain AGZY-82A and the expressions of proliferating cell nuclear antigen (PCNA), p53, bcl-2, vascular endothelial growth factor (VEGF) and VEGF receptor Flk-1 of the tumor cells were assessed by immunohistochemical methods. RESULTS: The experimental data showed that TNP-470 inhibit the expressions of VEGF and Flk-1 by tumor cells with dose-dependence. In the group of cells without TNP-470 (control group) the expression could rates of VEGF and Flk-1 were 70.42% and 50%, respectively; while in the group of cells with 10(7) microgram/L TNP-470, the expression rates of VEGF and Flk-1 decreased to 13.2% and 7.2%, respectively. Under the lnfluence of 10(4) microgram/L TNP-470, the expression rates of VEGF, Flk-1 by the tumor cells decreased gradually with prolonging of the action time. After 6 hours of action, the expression rate of VEGF decreased to 14.4% and after 12 hours, the expression rate of Flk-1 decreased to 6.2%. In the control group the proliferation rate of PCNA-marked cells was (87.03 +/- 0.75)% and the positive expression rate of p53-marked cells was (3.67 +/- 0.39)%, while in the 10(7) microgram/L TNP-470 group the proliferation rate and positive rate of p53-marked cells were 0 and (63.28 +/- 0.84)%, respectively. No expression of bcl-2 in both control and low concentration TNP-470 group. Its expression increased gradually as the concentration induced. In the 10(4) microgram/L TNP-470 group the expression of PCNA by tumor cells decreased. But the expression of p53, bcl-2 increased gradually with prolonging of the action time. CONCLUSION: TNP-470 could inhibit the proliferation and promote the apoptosis of lung adenocarcinoma cells through reduction of the VEGF autocrine and down-regulation of the VEGF receptor.

Adenocarcinoma↗