Objective To investigate the effects of vitamin D deficiency on pregnancy and fetal development in mice. Methods All female ICR mice were randomly divided into two groups. In control group, mice were fed with standard feeds (vitamin D3 >800 IU/kg). In vitamin D deficiency group (VDD), female mice were fed with feeds with vitamin D depletion (vitamin D3 <25 IU/kg). For mating purposes, four females were housed overnight with two males starting at 9 : 00 PM. Females were checked 7 : 00 AM the next morning, and the presence of a vaginal plug was designated as gestational day (GD) 0. All pregnancy mice were sacrificed on GD18. For each litter, the number of live fetuses, dead fetuses and resorption sites were counted. Live fetuses in each litter were weighed. Crown-rump lengths were examined. And skeletal development of all live fetuses in each litter was evaluated. Re-sults The pregnancy rate was lower in VDD group than that in control group(P<0.05). The number of live fetu-ses was significantly decreased(P<0.05). By contrast, the numbers of dead fetuses and resorption sites were sig-nificantly increased(P<0.05). In addition, the average weights of fetuses and placenta were reduced in vitamin D deficiency group. Moreover, vitamin D deficiency resulted in skeletal development retardation in fetuses. Conclu-sion Vitamin D deficiency impairs pregnancy and developmental outcomes in mice.

With the development and the expansion of higher medical education,lack of course resource became a “bottleneck” which restricted the development of medical schools.Teaching hospitals played some roles in medical education,but there was a huge gap in teaching ability between these hospitals and the hospitals affiliated with universities.The Clinical College analyzed the current situation of teaching ability in teaching hospitals and did the preliminary research for the solutions of this situation.

From the current state of the medical environment and health issues,we dis-cuss the necessity of physician-patient communication skills and find the way to enhance the skills of interns.

Nitric oxide (NO) plays an important pathophysiological role in osteoarthritis and cartilage metabolism. To determine the relationship between NO and the synthesis of type II collagen in cartilage, we measured levels of type II collagen by ELISA and procollagen (II) mRNA by RT-PCR in cultured lapine chondrocytes that were incubated with some kinds of reagents. 0.2mM sodium nitroprusside (SNP, a NO donor) can release high levels of NO, decreasing type II collagen, suppressing the expression of procollagen (II) mRNA (COL2A1).At the same time, chondrocytes showed a large increase in NO synthesis, a decrease in type II collagen and COL2A1 mRNA in response to 100u/ml IL-1. When 1mg/ml N-nitro-L-arginine methyl easter (NAME, an inhibitor of NO synthase) was mixed with IL-1, NO production was inhibited, the amounts of type II collagen recovered partially and COL2A1 mRNA recovered completely.These data indicate NO can inhibit type II collagen synthesis as IL-1 downstream molecule by suppressing procollagen (II) mRNA.

AIM: To study the chloride channel activity [ICl_(Ca)] in vascular smooth cells of the spontaneously hypertensive rats (SHR). METHODS: The vascular beds of mesenteric arteries were isolated from the pentobarbital anesthetized rats and perfused with 37 ℃ PSS at a constant flow rate. The vasoconstriction response to norepinphrine (NE) was determined by changes in perfused pressure. The strips of the rat arteries were mounted in an organ chamber filled with 37 ℃ PSS and the vascular tension was measured. RESULTS: (1) The contractile responses of mesenteric arteries to NE in SHR were greater than that in Wistar rats. (2) The inhibitory magnitude of the contractile response by niflumic acid in SHR was significantly less than that in Wistar rats and showed dose-dependent manner. (3) Decreasing the extracellular Cl~- concentration increased the contractile response to NE significantly and the amplitude of enhanced contractile response in SHR was greater than that in Wistar rats. CONCLUSION: It can be concluded that NE-induced contraction is enhanced in SHR, which is partly due to an increase in Cl~- efflux through the Ca~(2+)-activated Cl~- channels. The chloride channel activity may increase in association with the elevation of vascular tone and blood pressure.

Objective To explore the association between vitamin D deficiency and nonalcoholic fatty liver disease (NAFLD).Methods From April to June 2013,104 outpatients met NAFLD diagnostic criteria were enrolled.At the same period,98 age and gender matched healthy individuals were enrolled as control.The clinical data were collected through questionnaire,physical examination and lab tests.The severity of hepatic steatosis was dertermined with upper abdominal ultrasound examination.The serum concentration of 25 (OH )D was detected by radio-immunology.The association between vitamin D deficiency and NAFLD was analyzed with two independent sampling t analysis,chi-square test,analysis of variance (ANOVA)and Logistic regression analysis.Results The clinical indexes including body mass index (BMI ), abdominal circumference, blood pressure, aspartate aminotransferase, alanine aminotransferase,glutamyl ranspeptidase,lactate dehydrogenase,uric acid,triglyceride,overall cholesterol, lower density lipoprotein cholesterol and fasting blood glucose of NAFLD group were higher than those of the healthy control group,and the differences were statistically significant (all P < 0.05).But the level of higher density lipoprotein cholesterol of NAFLD group was lower than that of the healthy control group, and the difference was statistically significant (t=-2.941 ,P =0.004).However there was no significant difference in serum 25 (OH)D concentration,the level of calcium and phosphorus (all P >0.05).The results of stratification analysis in age and BMI indicated that the rate of 25 (OH )D deficiency (<37.5 nmol/L)in NAFLD patients aged less than 30 was higher than that of healthy control group (χ2 =6.679, OR = 13.71,P = 0.025 );the rate of 25 (OH)D deficiency in NAFLD patients with BMI≤25 kg/m2 was higher than that of healthy control group (χ2 = 3.734,OR = 4.97,P < 0.01).Among BMI≤25 kg/m2 group,after the adjustment of age,gender and metabolic syndrome,the results of multiple group Logistic regression analysis indicated that serum 25(OH)D concentration was negatively correlated to NAFLD (OR= 1 .16,95 % CI :1 .03 to 1 .30,P = 0.032).Conclusion Vitamin D deficiency might be a risk factor in pathogenesis of NAFLD patients with age less than 30 year old and BMI ≤25 kg/m2 .

Aim To investigate the effect of N-acetylcysteine (NAC) pretreatment/posttreatment on lipopolysaccharide (LPS)-induced intra-uterine fetal death (IUFD) and intra-uterine growth retardation (IUGR) in mice.Methods In the first experiment,all pregnant mice except controls received an intraperitoneal (75 ?g?kg-1) injection of LPS on gd 15~17.In LPS+NAC groups,the pregnant mice were treated with NAC before and/or after LPS. The saline-and NAC-treated pregnant mice served as controls. The dams were sacrificed on gd 18. In the second experiment,all pregnant mice except controls received an intraperitoneal (75 ?g?kg-1) injection of LPS on gd 15. In LPS+NAC groups,the pregnant mice were treated with NAC before and/or after LPS. The saline-and NAC-treated pregnant mice served as controls. The dams were sacrificed at 1.5 h or 6 h after LPS.Results pretreatment with NAC significantly alleviated LPS-induced fetal mortality and reversed LPS-induced growth development retardation.Correspondingly,pretreatment with NAC significantly attenuated LPS-induced elevation in TNF-? concentration in maternal serum and amniotic fluid and lipid peroxidation in maternal and fetal livers. By contrast to pretreatment,posttreatment with NAC had no effect on LPS-induced TNF-? production and lipid peroxidation,and did not protect against LPS-induced IUFD and IUGR and in fact aggravated LPS-induced preterm labor.Conclusion Pretreatment with NAC attenuates LPS-induced IUFD and IUGR,whereas posttreatment with NAC aggravates LPS-induced preterm labor.

Objective To explore the protective effect of folic acid supplementation in different ways on lipopolysaccharide-induced external malformations and skeletal malformations in mice.Methods The pregnant mice were divided into six groups randomly,including saline control group,FA control group,LPS group,LPS+FAig group,LPS+FAip group,and LPS+FAdw group.All dams were medicated on gestational day 8～12,and then sacrificed on gestational day 18,for each litter,the number of live fetuses,dead fetuses,resorption fetuses and external malformations of live fetuses were all counted.All fetuses were subsequently evaluated the skeletal malformations.Results A low dose of LPS injection during the second trimester resulted in external and skeletal malformations.Exencephaly and encephalomeningocele were two of the most common external malformations,skeletal malformations consisted mainly of the incompletion of supraoccipital ossification,sternal malformation and rib malformation.FA supplementation by three ways all attenuated the external and skeletal malformations.And the best protective effect was by oral administration.The incidence of external,sternal and rib malformation was all decreased.Conclusions Three ways can prevent the mice during the second trimester from the external and skeletal malformations caused by LPS injection,and the best protective effect was by intragastric administration.

Objective To analyze the clinical significance of modified thyroidectomy by trans-isthmus approach.Methods The clinical data of 5 751 patients who underwent thyroidectomy from Jan.1996 to Jan.2006 were retrospectively analyzed.All cases were divided into two groups.The modified operation group(n=3288) was treated by trans-isthmus thyroidectomy.Another group(n=2463) was treated by routine approach.The operation time,bleeding volume,and complications were observed and compared.Results In modified operation group,the mean operation time,bleeding volume,temporary injury of recurrent laryngeal nerve,tracheal discomfort,and hypocalcemia were significantly decreased than those in routine approach group(P

Purpose To assess the clinical application of non-contrast-enhanced MR angiography (NCE-MRA) using flow sensitive dephasing (FSD) prepared steady-state free precession (SSFP) for displaying hand arteries of patients with rheumatoid arthritis. Materials and Methods Twenty-two patients with rheumatoid arthritis were recruited in this study. All the patients undertook hand NCE-MRA and three-dimensional dynamic CE-MRA on a 1.5T MR scanner. The informed consent was obtained from each subject. Image quality was assessed independently by two experienced radiologists at three arterial segments (wrist arteries, palm arteries, andfinger arteries) with a four-point scale. Signal to noise ratio (SNR), contrast to noise ratio (CNR), and vessel sharpness were evaluated by a magnetic resonance physicist. The results and image quality were statistically compared between the two MRA techniques.Results Twenty-two patients of 24 hands successfully underwent NCE-MRA and CE-MRA scan. Among 72 vascular segments, 69 segments of NCE-MRA were diagnostic, which was higher than that of CE-MRA (96% vs 83%,P<0.05). Otherwise, the image quality, SNR, CNR and vessel sharpness of NCE-MRA were all superior to those of CE-MRA (P<0.05).Conclusion NCE-MRA using FSD-prepared SSFP allows clear depiction of the hand arterial tree, and the image quality is superior to that of dynamic CE-MRA. It is a potential tool for evaluating the disease of hand arteries.