The obstructive sleep apnea-hypopnea syndrome(OSAHS)is considered as a complex genetic disorder with high mor- bidity and mortality.More and more evidence indicate that it has familial aggregation and genetic predisposition.Some gene phenotypes related to upper airway anomalies,abnormal breathing control,obesity,hypertension and insulin resistance might act to increase suscepti- bility to OSAHS.This article reviews current knowledge about a genetic approach to the causes and risk factors for sleep apnea.

AIM To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of suramin. METHODS Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group(F), hypoxia hypercapnia +suramin group (S). The levels of VEGF in serum and in lung tissue were measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, the expression of VEGF was observed by immunohistochemistry, the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS ①Mean pulmonary arterial pressure(mPAP), weight ratio of RV to LV+S, the leves of VEGF in serum and in lung tissue of group F were significantly higher than that of group N and group S (P

AIM: To study the effect of chronic hypoxic hypercapnia on gene expression of thromboxane synthase and prostacyclin synthase in pulmonary arterioles. METHODS: Sprague-Dawley rats were randomly divided into two groups: control group and hypoxic hypercapnic group. TXS mRNA and PGI 2-S mRNA were observed in pulmonary arterioles by in situ hybridization. RESULTS:mPAP, weight ratio of right ventricle (RV) to left ventricle plus septum(LV+S), contents of TXB 2 and 6-keto-PGF1 ? in plasma and lung and TXS mRNA in pulmonary arterioles were much higher in rats of hypoxic hypercapnic group than those of control group. Differences of PGI 2-S mRNA in pulmonary arterioles were not significant in two groups. Light microscopy showed hypertrophy of vessel smooth muscle cells and vessel cavity straitness were found in hypoxic hypercapnic group. CONCLUSION: Changes of gene expressions of thromboxane synthase and prostacyclin synthase and imbalance of TXA 2/PGI 2 may play an important role in hypoxic hypercapnic pulmonary hypertension.

AIM: To clarify the role of nitric oxide (NO) system in development of chronic hypoxic hypercapnic pulmonary hepertension. METHODS: Male Sprague-Dawley rats were randomly divided into control group and hypoxic hypercapnic group. NO content of plasma was determined, constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) were examined using the technique of immunohistochemistry, expression of cNOS mRNA and iNOS mRNA of arteriole were detected by in situ hybridization. RESULTS: Plasma NO concentration, cNOS activity and cNOS mRNA expression in arteriole of chronic hypoxic hypecapnic group were significantly lower than that of control group ( P

OBJECTIVE To study the therapeutic effect and the underlying mechanism of asiatico?side on bleomycin-induced rat interstitial pulmonary fibrosis(IPF). METHODS Male Sprague-Dawley (SD)rats were divided into normal control group,bleomycin 5 mg·kg-1 model group and asiaticoside 50 mg · kg-1 group. The model and asiaticoside group were administrated with bleomycin 5 mg · kg-1 to induce IPF,while the asiaticoside group was administrated with asiaticoside 50 mg·kg-1 by gastric perfusion. Hematein eosin(HE)and Masson staining were carried out to analyze the histopathological changes in the lung. Lung homogenates were used to examine hydroxyproline(HYP) content,and serum samples were used to measure the concentration of interferon-γ(IFN-γ),interleukin-4(IL-4) and tumor necrosis factor-α(TNF-α). In addition,immunohistochemical methods were used to locate lung transforming growth factor-β1(TGF-β1)and adenosine 2A receptor(A2AR)expression,and Western blotting was used to examine the expression levels of TGF-β1 and A2AR. RESULTS On the 7th,14th and 28th days,the scores of pulmonary inflammation were higher in model group than in control group (P<0.01),and the asiaticoside group showed mitigated alveolitis(P<0.01,P<0.05) compared with model group. Compared with control group,the scores of pulmonary fibrosis in model group were elevated(P<0.01),and the asiaticoside group showed reduced pulmonary fibrosis(P<0.05). On the 14th and 28th days,HYP content in the model group〔1.85±0.10,(2.48±0.18)mg·g-1〕was higher than in the control group〔0.79 ± 0.07,(0.84 ± 0.08)mg · g-1〕(P<0.01),but HYP content in the asiaticoside group〔1.32±0.131,(1.71±0.13)mg·g-1〕was lower than in the model group(P<0.05). IL-4 and TNF-αin the asiaticoside group were lower than in model group(P<0.05),but were higher in the model group than in the control group(P<0.01,P<0.05). The expression level of TGF-β1 protein in the asiaticoside group was lower than in the model group(P<0.05),but was higher in the model group than in the control group(P<0.05). The expression level of A2AR protein in the asiaticoside group was higher than in the model group(P<0.05),but was lower in the model group than in the control group(P<0.05). CONCLUSION Asiaticoside can mitigate bleomycin-induced IPF by inhibiting the expression of IL-4, TNF-αand TGF-β1,and raising the level of A2AR.

AIM: To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of SHENYI Capsule. METHODS: Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group (F), and hypoxia hypercapnia+SHENYI Capsule group (S). The levels of VEGF in serum and lung tissue are measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, and the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum, and lung tissue of group F were significantly higher than those of group N and group S (P

Objective To investigate the correlation between expression of Panton-Valentine leukocidin gene and accessory gene regulator among different clinical isolates of Staphylococcus aureus.Methods All non-duplicate Staphylococcus aureus clinical isolates were isolated from various clinical specimens of the patients at 4 hospitals from January 2003 to December 2010.Panton-Valentine leukocidin genes among Staphylococcus aureus clinical isolates were detected by PCR and DNA sequencing.The expressions of lukS-PV and agrA were determined by real-time PCR.Results Ninty-six S.aureus isolates including 58 hospital-acquired and 28 community-acquired isolates were positive for PVL genes,among which 54 from blood,33 from pus and 9 from sputum.Ten isolates cannot be classified due to lack of information.Sixty-seven and 29 PVL-positive isolates were isolated from the specimens of adults and children.The median relative quantities of lukSmRNA of the isolates from pus and blood were 1.500 and 0.818.The quantity of lukSmRNA among the isolates from pus was significantly higher than that from blood (U =634,P =0.025).The median relative quantities of lukSmRNA of the isolates from children and adults were 1.292 and 0.540,respectively.The quantity of lukSmRNA among the isolates from children was significantly higher than that from adults (U =660,P =0.013).The median relative quantities of lukSmRNA among community-acquired and hospital-acquired isolates were 1.034 and 0.536,respectively.The quantity of lukSmRNA among community-acquired isolates was significantly higher than that from hospital-acquired isolates (U =338,P =0.012).The correlation coefficients between lukSmRNA and agrAmRNA of total isolates,pus isolates and blood isolates were 0.592 (P ＜ 0.01),0.810 (P ＜ 0.0l) and 0.543 (P ＜0.01),respectively.While the correlation coefficients of those among the isolates from children and adults were 0.804 (P ＜ 0.01) and 0.476 (P ＜ 0.01).The correlation coefficients of those among the isolates from community-acquired and hospital-acquired isolates were 0.767 (P ＜ 0.01) and 0.556 (P＜0.01).Conclusions The quantity of lukSmRNA of Staphylococcus aureus isolates from pus was significantly higher than that from blood.The agr may have positive regulation effect on the expression of lukS/F-PV,especially among the isolates from pus and children.(Chin J Lab Med,2013,36:313-317)

AIM: To study the effect of safflower injection on expression of COX-2 mRNA in chronic hypoxic hypercapnic rat pulmonary arterioles.METHODS: Sprague-Dawley rats were randomly divided into normal control group,hypoxic hypercapnic group(B),hypoxic hypercapnia+ safflower injection group(C).The concentration of TXB2 and 6-Keto-PGF1? in plasma and in lung were detected by the technique of radioimmunoassay.COX-2 mRNA was observed in arterioles from rats by the technique of in situ hybridization.RESULTS: ① Mean pulmonary arterial pressure(mPAP),weight ratio of right ventricle(RV) to left ventricle plus septum(LV+S) were much higher in B group than those in control group.No significant difference of mean carotid arterial pressure(mCAP) was observed in three groups.② The concentration of TXB2 and the ratio of TXB2/6-keto-PGF1? were significantly higher in B group than those in control group.③ Light microscopy showed that vessel wall area/total area,the density of medial smooth muscle cells and the thickness of medial smooth cell layer were significantly higher in B group than those in control group.Electron microscopy showed proliferation of medial smooth muscle cells and collagenous fibers in pulmonary arterioles in B group.Safflower injection reversed the changes mentioned above.④ Expression of COX-2 mRNA in pulmonary arterioles was much higher in C group than those in B group.Differences of COX-1 mRNA in pulmonary arterioles were not significant between these two groups.CONCLUSION: Safflower injection increases the expression of COX-2 mRNA in chronic hypoxic hypercapnic rat pulmonary arterioles,indicating an important mechanism that safflower injection inhibits the formation of hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling.

AIM: To study the role and the mechani sm of heme oxygenas/endogenous carbon monoxide on nitric oxide synthase/nitric oxide system in rats with pulmo nary hypertension induced by hypoxic hypercapnia. METHODS: Spr ague-Dawley rats w ere randomly divided into three groups: control group (A group),hypoxic hypercap n ic group (B group), hypoxic hypercapnia+hemin group (C group). Blood CO concentr at ion (COHb%),NO concentration,HO-1 activity, iNOS, cNOS in blood serum and lung h omogenate were measured, respectively. RESULTS: ① mPAP and RV /(LV+S) of B g roup were significantly higher than those of A and C group( P

AIM:To establish a fast , accurate and economical technique for culturing mouse pulmonary arte-riolar smooth muscle cells ( PASMCs ) , and to explore the effects of hypoxia on the proliferation and apoptosis of the PASMCs.METHODS:In sterile condition, the pulmonary artery was isolated from the male BALB/c mice by digesting with collagenase I, and the cells were cultured in fetal bovine serum-coated flask.Centrifugal procedure was not used dur-ing the cell passage .The cell morphology was observed under an inverted phase-contrast microscope .α-Smooth muscle ac-tin was identified by immunocytochemistry and immunofluorescence .The effects of hypoxia on the proliferation and apopto-sis of the PASMCs were detected by CCK-8 assay and TUNEL assay .RESULTS:PASMCs were identified by the methods of immunocytochemistry , immunofluorescence staining and observation of morphology .Unlike the rat PASMCs with typical subcultured peak-vally pattern, the mouse PASMCs showed a lot different without a peak-vally pattern.The cells could be subcultured after 5 d to 7 d and there was 3 to 5 generations depending on the activity of the cells .CCK-8 assay demonstra-ted that the A values of PASMCs exposed to hypoxia increased after 24 h ( P<0.05) as compared with normoxia .TUNEL result showed that the apoptotic index of the PASMCs in hypoxia decreased after 24 h (P<0.05).CONCLUSION:This technique for obtaining cultured mouse PASMCs is simple , fast, accurate and economical .The digestion time is easy to control.Hypoxia promotes the proliferation and inhibits the apoptosis of PASMCs .