Objective To observe the effects of different hypothermia on cerebral oxygen metabolism during cardiopulmonary bypass(CPB).Methods 20 patients undergoing valvular replacements were randomly divided in two groups:shallow hypothermia group(30℃) and middle hypothermia group(26℃).Blood gas analysis and lactate concentration in arterial and internal jugular vein blood were monitored at 3 time points during operation,from which the arterial-internal jugular venous oxygen content difference(Ca-jvO 2),cerebral oxygen extraction ratio(ERO 2),cerebral lactate production(ADVL) were calculated.Results CaO 2,Ca-jvO 2 and ERO 2 of the two groups were significantly reduced(P0 05) at the same time points.Ca-jvO 2 at the T 3 time point was both lower(P

Objective:To investigate the protective effect of N-acetylcysteine(NAC)on right ventricular remodeling in a rat model of monocrotaline-induced pulmonary arterial hypertension ( PAH ) .Methods: PAH rats were induced by a single injection of monocrotaline(60 mg/kg,sc)and were ad ministered with NAC[500 mg/(kg? d)]for 6 weeks.At the end of 4 weeks,the right ventricular systolic pressure ( RVSP ) and mean pulmonary artery pressure ( mPAP ) were monitored via the right jugular vein catheterization into the right ventricle .Right ventricle ( RV ) to left ventricle ( LV )+septum ( S ) were calculated.Right ventricular morphological change was observed by HE staining .Sirius red was used to demonstrate collagen deposition .The expressions of collagenⅠ,collagen Ⅲ, NADPH oxidase 4 ( NOX4 ) and nuclear factor-kappa B ( NF-κB ) were analyzed by RT-PCR and ( or ) Western blot.Results:NAC attenuated RVSP ,mPAP and right ventricular remodeling index ( RV/LV+S) of PAH rats induced by monocrotaline after treatment for 4 weeks.Furthermore ,monocrotaline-induced right ventricular collagen accumulation and collagen Ⅰand collagenⅢexpression were both significantly suppressed by NAC .The expressions of NOX 4 and NF-κB were obviously decreased in right ventricule from PAH rats with NAC treatment.Conclusion:NAC ameliorates right ventricular remodeling of PAH induced by monocrotaline in rats through down regulating the expression of NOX 4 and antioxidant activity ,and inhibiting activation of NF-κB and collagen accumulation .

BACKGROUND: Type Ⅰ and type Ⅲ collagen, the main components of cardiac stroma,have supporting,protective and restrictive effects on myocardial cells. They are essential for the heart to maintain its normal shape and function. OBJECTIVE:To explore the effects of types Ⅰ and Ⅲ collagen on cardiac function by observing their changes in atrium myocardium of children with ventricular septal defect (VSD). DESIGN: A case analysis. SETTTING: Department of Cytobiology, Xinxiang Medical College. PARTICIPANTS: Six children who had died from accidents were selected from the Pediatric Department of the First Affiliated Hospital,Xinxiang Medical College, between January and August 2003. Informed consent was obtained form their relatives. They were 4 males and 2 females,ranging from 1 to 15 years in age. Congenital heart diseases were excluded by naked-eye anatomical examination,and right atrium tissues were collected for the study. Meanwhile, 21 children with VSD, 12 males and 9 females aged 1-17 years,were recruited from the Department of Cardiac-thoracic Surgery of the same hospital. METHODS:A small amount of fresh myocardium was cut from the right atrium at the edge of incision. Peroxidase-labeled strepto-avidin immunohistochemical method was adopted to detect the expression of types Ⅰ and Ⅲ collagen protein in atrium myocardium, which was analyzed using image analysis to calculate the area composition ratio of type Ⅰ and type Ⅲ collagen in atrium myocardium(representing the relative area percentage of collagen protein) and area percentage (representingthe expression percentage of collagen protein). MAIN OUTCOME MEASURES:Expression of typeⅠand type Ⅲ collagen protein in atrium myocardium. RESULTS: Six normal controls and 21 patients with VSD entered the final statistical analysis. ① Type Ⅰcollagen of normal atrium was strip-like fibers with different diameters connected with each other,whereas type Ⅲ collagen was scattered in spots and pieces. ② The distribution of type Ⅰ and Ⅲ collagen of atrium in VSD patients was mostly similar to that of the normal controls; only part of them displayed extreme rearrangement, that is,type Ⅰcollagen presenting large-speckle increment,breakage or disappearance, while type Ⅲ collagen increased in stripes and bundles. ③ The area percentage and area composition ratio of type Ⅰ and type Ⅲ collagen:type Ⅰ collagen expressed more than type Ⅲ collagen in normal myocardium [area percentage: (48.82±12.35)％ vs (40.02±13.53)％, t=2.173, P ＜ 0.05;area composition: (15.87±6.03) μm2 vs (13.62 6.94) μm2, t=2.221, P ＜ 0.05].Likewise, type Ⅰ collagen expressed more highly than type Ⅲ collagen in VSD myocardium [area percentage: (55.37±10.42)％ vs (50.27±14.36) ％,t=2.173, P ＜ 0.05; area composition: (24.93±9.62) μm2 vs (19.22 12.03) μm2,t=2.221, P＜ 0.05]. The content of both type Ⅰ and type Ⅲ collagen in VSD children was obviously higher than that in normal children(t=2.153-2.234,P ＜ 0.05). CONCLUSION: In children with VSD, part of type Ⅰ and type Ⅲ collagen is found rearranged and increased in atrium, which may result from the interstitial compensation due to cardiac dysfunction.

Objective To study the expression of PTEN and Caspase-3 proteins in esophageal squamous cell carcinoma(ESCC) and to analyze the relationships between the expressions of the proteins and clinicopathologic factors as well as prognosis.Methods 64 cases of ESCCs,16 cases of pericarcinoma tissues and 16 cases of dysplasia epithelium were immunohistochemically stained.All 64 patients who underwent surgical treatment up to January 2005 were regularly followed up through letters and check-ups.Results The positive expression rate in pericarcinoma tissues,dysplasia and ESCC were significantly down-regulated((P

Objective To investigate expressional pattern of the Connexin 43 in atrial myocytes of ventricular septal defect children. Methods The expressional role of the Connexin 43 in atrial myocytes of ventricular septal defect children were observed and determinated by immunohistochemistry and digital image analysis technology. Results 1.The Connexin 43 granules of 1-3 year-old-group normal children were mainly distributed on cell side surface,which took on beening spot-,belt-or chain-shaped,but seldom at intercalated disks. The Connexin 43 of 7-16 year-old-group normal children were abundantly distributed on cell side surface and intercalated disks. 2.The Connexin 43 of 1-3 year-old-group ventricular septal defect children were not noly distributed on cell side surface but could be detected at intercalated disks and cytoplasm,a few granules were irregular in arrangement.The Connexin 43 of 7-16 year-old-group ventricular septal defect children were distributed on cell side surface and in cytoplasm but seldom existed at intercalated disks,and arranged in irregular order. 3.The experimental results showed insignificant difference in the expressional amount of the Connexin 43 in atrial myocytes between the ventricular septal defect children and normal children. Conclusion The Cx 43 distributional pattern in atrial myocytes of ventricular septal defect children was changed,but its expressional amount was indistinct,which suggested that ventricular septal defect affected only the Cx43 expressional pattern.

Objective:To explore the mechanism of zoledronic acid (ZOL) affects osteogenic differentiation and bone formation through the regulation of sirtuin 3 (SIRT3) / P53 expression.Methods:Bone marrow mesenchymal stem cells (BMSCs) were induced to differentiate into osteogenic cells, the expression of SIRT3 in the cells was detected, and the targeting regulation relationship between SIRT3 and P53 was analyzed. The intracellular expressions of SIRT3 and P53 were intervened and ZOL was used to treat the cells. MTT method, Western blot method and kit were used to detect cell viability, osteogenesis-related genes Osteoprotegerin (OPG), runt-related transcription factor 2 (Runx2) expression, alkaline phosphatase (ALP) activity and alizarin red S (ARS) staining, respectively. Ovariectomy (OVX) was used to construct a rat model and explore the effect of ZOL on the progression of osteoporosis (OP) in vivo.Results:ZOL promoted osteogenic differentiation of BMSCs. The expression of SIRT3 was down-regulated in the serum of OP patients (0.78±0.23) compared with that of healthy subjects (1.00±0.26 vs. 0.78±0.23. t=3.85, P<0.001). During the osteogenic differentiation of BMSCs, the expression level of SIRT3 gradually increased with the prolonged induction of osteogenesis. Compared with the p53 protein expression and BMSCs activity in the control group, SIRT3 knockout could increase the expression level of p53 protein (0.59±0.05 vs. 1.01±0.11. t=6.02, P=0.004) but inhibited the activity of BMSCs (100.00±8.41 vs. 51.26±5.59. t=8.36, P=0.001). After ZOL treatment, the inhibitory effect of SIRT3 on cell viability (49.61±5.11 vs. 87.61±7.31. t=7.38, P=0.002) and osteogenesis was relieved, and the level of P53 was inhibited (1.10±0.10 vs. 0.69±0.04. t=6.59, P=0.003). P53 overexpression partially offseted the effects of ZOL on cell viability (84.61±6.52 vs. 66.54±5.47. t=3.68, P=0.021) and osteogenesis. Compared with the sham surgery group, the OVX group showed inhibition of osteogenesis in rats, and ZOL treatment significantly improved osteogenic inhibition. ZOL treatment increased the expression level of SIRT3 protein in bone tissue of OVX rats, but inhibited the expression level of P53. Conclusion:ZOL promoted osteogenic differentiation and bone formation of BMSCs by promoting the ubiquitination and degradation of P53 by SIRT3.

Objective To investigate the imaging features of dysplastic nodules with a focus of hepatocellular carcinoma ( DN-HCC ) on contrast-enhanced ultrasound ( CEUS ) and to improve the diagnostic accuracy . Methods The clinical data of 60 patients and CEUS imaging of 62 hepatic nodules [DN-HCCs , n =54 ;dysplastic nodules (DN) , n =8] pathologically proved were reviewed retrospectively . According to Contrast Enhanced Ultrasound Liver Imaging Reporting and Data System (CEUS LI-RADS) , the lesions were categorized . Results Significantly different CEUS patterns between DN-HCCs and DNs were observed ( P < 0 .05) . During the arterial phase ,54 DN-HCC lesions showed various enhancement patterns [ hypervascular ,59 .3％ ( 32/54 ) ;nodule-in-nodule ,9 .3％ ( 5/54 ) ;isovascular ,13 .0％ ( 7/54 ) and hypovascular ,18 .5％ (10/54)] . Of the 54 DN-HCC lesions ,44 .4％ (24/54) showed washout during the late phase .Of the 8 DN lesions ,62 .5％ (5/8) showed iso-enhancement during the arterial phase ,25％ (2/8) showed hypo-enhancement ,and 12 .5％ (1/8) showed hyper-enhancement . No DN lesion showed washout during the late phase .According to CEUS LI-RADS (LR) algorithm ,27 .8％ (15/54) DN-HCCs were LR-5 ,46 .3％ (25/54) DN-HCCs were LR-4 ,25 .9％ (14/54) DN-HCCs and 100％ (8/8) DNs were LR-3 . Regarding hyper-enhancement ( including local hyper-enhancement ) during the arterial phase or hypo-enhancement (including local hypo-enhancement) during the late phase as the diagnostic standard of DN-HCC , the diagnostic sensitivity , specificity and accuracy value were 83 .3％ , 87 .5％ and 83 .9％ , respectively . Conclusions The imaging features of hyper-enhancement during the arterial phase or hypo-enhancement during the late phase on CEUS are useful to diagnose DN-HCCs .

Anoctamin 1 (ANO1) is a kind of calcium-activated chloride channel involved in nerve depolarization. ANO1 inhibitors display significant analgesic activity by the local peripheral and intrathecal administration. In this study, several thiophenecarboxylic acid and benzoic acid derivatives were identified as novel ANO1 inhibitors through the shape-based virtual screening, among which the 4-arylthiophene-3-carboxylic acid analogues with the best ANO1 inhibitory activity were designed, synthesized and compound