Job Accommodation of American is effective to ensure the equal employment of domestic disabilities. This paper introduced its legal basis, contents and procedures.

Aim To investigate the effect of pioglitazone on the AdipoR1 and AdipoR2 expression of HU-VECs induced by intermittent high glucose.Methods After exposed to intermittent high glucose for 5 d,HUVECs were incubated with pioglitazone(10,1 or 0.1 ?mol?L-1) for 24 hours.The AdipoR1 and AdipoR2 mRNA expression levels in HUVECs were also determined by real-time PCR.Results After exposed to intermittent high glucose for 5 days,HUVECs were treated with pioglitazone(10,1 or 0.1 ?mol?L-1) for 24 h.10,1?mol?L-1 of pioglitazone treatment enhanced AdipoR1 mRNA level(both P

ERP system is introduced. Combined with the deficiencies of management of medical consumable materials in supply chain and high-value materials, the application of ERP to workflow, fundamental material, operation and high-value material management are explored. It indicates that although with some deficiencies, this ERP system optimizes business process and then improves work efficiency of management of medical consumable materials greatly.

AIM:To investigate molecular regulatory mechanism of K-ras to girdin protein in COS7 cells and expression of K-ras and girdin in colorectal carcinoma tissues .METHODS:The lentiviral vector carrying K-ras gene was constructed and transfected in the COS 7 cells.The expression of K-ras, girdin proteins and other related proteins in COS 7 cells and colorectal carcinoma tissues was observed by Western blot .RESULTS:The COS7 cells with K-ras over-expres-sion showed an irregular cell morphology .The results of Western blot indicated that the downstream signal protein levels of p-ERK1/2, p-Stat3 and girdin were significantly increased in the COS 7 cells with K-ras over-expression.Transfection with the K-ras siRNA into the COS7 cells significantly reduced the protein levels of p-ERK1/2, p-Stat3 and girdin.In the color-ectal carcinoma tissues (7 cases), 5 cases had higher expression of K-ras and girdin compared with pericarcinous tissues . CONCLUSION:K-ras regulates girdin expression through the signal pathway of K-ras-ERK1/2-Stat3-girdin.

Objective To detect the fetal external ear observation on standard sections and the best time with ultrasonography. Methods Total 2212 normal fetuses 17-40 weeks of gestation were divided into six groups. Fetal ears were obtained on transverse-incline view at cervical vertebra level (section A) and mandible level (section B), on parasagittal view (section C) and coronal view (section D) at external ear level. Fetal ears were evaluated and analyzed statistically. Results Among 2212 normal fetuses, 3454 ears (78.07%), 1694 ears (38.29%), 3454 ears (78.07%) and 2304 ears (52.08%) were obtained on section A, B, C and D, respectively. The obtained-rate of fetal ears on section A was the same as section C at the same week of gestation, but was significant higher than that of section B and section D (P<0.05). The obtained-rate of fetal ears was statistical different between section B and section D at the groups of 25-40 weeks (P<0.01). The obtained-rate of fetal ears was negatively correlated with gestational age (P<0.01). Conclusion It is useful and easy to observe the fetal external ear with ultrasonography to detect fetal ear abnormalities. Section A and section C are recommended to be standard observation sections for fetal external ear. Section B and section D can be used as supplementary for section A and section C. The best time for fetal external ear observation with ultrasonography is 17-24+6 weeks gestation.

Objective To investigate the dynamic level changes and significance of triggering receptor expressed on myeloid cells-1 (TREM-1) in the injury brain tissues of rats caused by pneumolysin (PLY).Methods Sixty-four SD rats were randomly and equally divided into PLY group and control group,0.1 mL PLY and isopyknic normal saline was given through left internal carotid artery respectively.Brain tissue gross and histological changes were observed at different time(4 h,6 h,12 h,24 h),meanwhile the expression levels of neurocyte damage marker glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) protein were detected by immunohistochemistry;and the expression levels of TREM-1,tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected respectively by enzyme-linked immunosorbent assay.Results The observation of brain tissue gross and histological changes indicated the existence of brain injury,and the expression levels of GFAP,NSE,TNF-α and IL-6 protein increased from 4 h after PLY were injected and augmented dynamically as time went on,compared with the control group at corresponding time points,the differences were statistically significant (all P ＜ 0.05).The level of TREM-1 in the PLY group reached a peak at the 4 h time point,but decreased somewhat at the 6 h time point,the level of TREM-1 was still higher than that in control group,the differences were statistically significant(all P ＜ 0.05).However,the level of TREM-1 in the PLY group declined obviously at 12 h and 24 h time points,compared with that in control group,there were no significant differences (all P ＞ 0.05).Conclusions The expression levels of TREM-1 up-regulated obviously in the early stage of brain damage induced by PLY,which might be involved in the pathological process of brain damage by promoting the expression of TNF-α and IL-6.

AIM:There is little evidence proving the molecular mechanism of WenxinKeli ( WXKL) .This study tried to explore the gene ex-pression profile and pathology alteration of WXKL-treated rabbits with myocardial infarction .METHOD: Twenty male adult rabbits were randomly divided into 4 groups:sham, model, WXKL and captopril groups .Model, WXKL and captopril groups underwent the ligation of the left anterior descending coronary artery , while sham group went through an identical procedure without ligation .WXKL (817 mg? kg-1? d-1), captopril (8 mg? kg -1? d-1) and distilled water (model and sham) were administered orally to the rabbits. 4 weeks later, hearts were taken out for expression chip and pathological staining (HE, Masson and TUNEL) after echocardiography. RESULT:WXKL could down-regulate genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (cathepsin C and TTC5) and neuro-hormonal system (ACE and EDN1), and up-regulate angiogenesis promoting gene like RSPO 3, which explained why WXKL group represented with better cardiac function , less histopathological injury and slighter apoptosis .CONCLUSION:WXKL plays an important role in suppressing inflammation , inhibiting renin-angiotensin system and alleviating apoptosis , and might be a promising Chinese medicine in treating patients with myocardial infarction .

Animals ; Drugs, Chinese Herbal ; therapeutic use ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; drug therapy ; etiology ; prevention & control ; Phytotherapy

bnormality in these parameters was improved.

[ ABSTRACT] AIM: To study the protective effects of cannabinoid CB2 receptor agonist JWH133 on rat acute lung injury induced by paraquat (PQ).METHODS: Male Sprague-Dawley rats (n=72) were randomly divided into 4 groups.PQ group:PQ was administered intraperitoneally at the dose of 20 mg/kg;Low-dose JWH133 pretreatment group ( L-JWH133 group):JWH133 (5 mg/kg, ip) was administered 1 h before PQ exposure;high-dose JWH133 pretreatment group ( H-JWH133 group):JWH133 (20 mg/kg, ip) was administered 1 h before PQ exposure;control group:1 mL sa-line was administered intraperitoneally.Arterial blood, bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 8 h, 1 d and 3 d after PQ exposure.PaO2 and the levels of TNF-αand IL-1βin BALF were measured via blood gas analyzer and ELISA, respectively.The pathological changes and lung injury scores were assessed at 3 d after PQ expo-sure.NF-κB and AP-1 protein levels were also determined by Western blotting.RESULTS:The decrease in PaO2 , struc-tural injury of the lung tissues, interstitial pulmonary edema, and the increase in IL-1βand TNF-αin BALF were observed in PQ-treated rats compared with control group.JWH133 pretreatment reduced the degree of lung tissue injury, decreased the levels of IL-1βand TNF-αin BALF and the NF-κB and AP-1 protein expression in the lung tissue compared with PQ group, especially in H-JWH133 group.CONCLUSION:CB2 receptor agonist JWH133 inhibits NF-κB and AP-1 protein expression in the lung tissues, and reduces the secretion of IL-1βand TNF-αin BALF after paraquat exposure, thus atten-uating paraquat-induced acute lung injury.