Objective To evaluate the value of transvaginal ultrasound in the diagnosis of tubal pregnancy.Methods The retrospective analysis was made according to transvaginal ultrasound inspection on 77 patients and their sonographic appearance and ultrasonic diagnosis of tubal pregnancy proved by surgery and pathology.Results The two-dimensional sonogram mainly showed the adnexal masses and the liquid area opaca in the pelvic cavity.The masses were divided into three types:germ heart-beat type,gestational sac type,and uneven mixed mass type.According to distinctive two-dimensional sonographic appearance,the accuracy rates of transvaginal ultrasound in the diagnosis of rupture,nonrupture,and abortion tubal pregnancy were 87.23%,100%,and 34.62%,respectively.In combination with pelvic mass,indirect sign of effusion,and patient history,the accuracy rates of ultrasonic diagnosis in the above clinical classifications were 95.74%,100%,and 84.61%,respectively.The accuracy rate of the total ultrasonic diagnosis was 92.21%.Conclusions Transvaginal ultrasound has higher accuracy in the diagnosis of rupture and nonrupture tubal pregnancy,but it lacks distinctive sonographic appearance in the diagnosis of the majority of abortion tubal pregnancy,which is the main reason for affecting the accuracy of ultrasonic diagnosis of tubal pregnancy.

Objective To evaluate the characteristics of the haemodynamics of the hysteromyoma and its diagnosis value. Methods To apply the transvaginal color doppler ultrasound to detect the blood flow parameters of the uterine artery and the muscular tumor’s peripheral and inner area from 68 patients with hysteromyoma, compared with the blood flow parameters of the uterine artery from 50 normal women so as to analyze their difference. Results (1) In the hysteromyoma group, the maximum blood flow velocity during the systolic phase (SP) and the minimum blood flow velocity during the end-diastolic phase (ED) of uterine artery are significantly higher than those in the normal group(P

ObjectiveTo evaluate the cytogenetic characteristics of the patients with acute myelomonocytic leukemia (AML-M4), acute monocytic leukemia (AML-M5)and myelodysplastic syndrome (MDS).MethodsChromosomes of bone marrow cells were prepared by short-term culture.Karyotype analysis was performed in 100 AML-M4,46 AML-M5 and 115 MDS by R-banding technique.Results26 ％ (26/100) AML-M4 had clonal cytogenetic abnormalities which mainly include +8,t(8;21) and -7.26 ％ (12/46) AML-M5 had clonal cytogenetic abnormalities which mainly include +11. 39 ％(45/115)had clonal cytogenetic abnormalities which mainly include +8, Hypodiploid and -7. ConclusionCytogenetic detection is very important for the diagnosis of myelodysplastic syndrome and acute myelocytic leukemia.

Objective:To explore the e ect of QingreJiedu herbs in combination with Jiegeng decoction on expression of NF-?B p65 in ALI induced by LPS.Methods:Male Sprague-Dawley rats were randomly divided into normal group,model control group,QingreJiedu group,and the group of QingreJiedu herbs in combination with Jiegeng decoction.The model of ALI was made by injected with a single dose of LPS through vena femorali,the pathologic morphology,MPO activity and the expression of NF-?B p65 was observed.Result:Compared with normal group,infiltration.of PMNs,capillary congestion and swelling were found in model control group,and the content of MPO and expression of NF-?B p65 in the nuclear were significantly increased(P

A method was developed for the determination of sodium caprylate in human serum albumin by reversed phase high performance liquid chromatography(RP-HPLC) after pre-column derivatization. The caprylic acid, extracted from human serum albumin by hexane, was treated with ω-bromoacetophenone and 18-crown-6 for 30 min at 50 ℃, and analyzed on a Nova-Park C_(18)(150 mm×3.9 mm, 4 μm) column with methanol-water(75∶ 25, V/V) as the mobile phase. The internal standard was enanthic acid, the flow rate was 1.0 mL/min and the detection wavelength was 262 nm. The extraction yield of caprylic acid was 97.9% and that of enanthic acid was 98.2%. The linear range of sodium caprylate was 9.00×10~(-4)-1.44×10~(-2) mol/L(r=0.9995). The average recovery of caprylic acid was 99.7%, RSD was less than 0.9%. The present method is reliable and relatively simple and can be used for the determination of sodium caprylate in human serum albumin.

Objective To investigate the effect of recombinant intestinal trefoil factor(rITF)on the intestinal mucosa of acute necrotizing pancreatitis(ANP)rats and explore the mechanism.Methods 60 male SD rats were randomly divided into control group(n=20),ANP group(n=20),rITF group(n=20).ANP was induced by retrograde injection of 5%sodium taurocholate(100μl/100 g)into biliopancreatic duct.Rats in rITF group were injected with rITF(0.5 mg/100 g)before and after ANP induction.The rats in ANP group and control group received same amount of normal sailne.Each group were sacrificed 12 h or 24 h later.respectively.Blood sample was taken to determine the serum level of amylase.Terminal ileum was resected to observe the pathologic changes;immunohistochemistry method was applied to detect the activity of NF-κB;the expression of TNF-α mRNA,ICAM-1 mRNA in intestinal mucosa was measured by RT-PCR.Results Intestinal injury score of ANP group was higher than that ofcontrol group(P＜0.05),intestinal injury score of ANP 12 h group was higher than that of rITF 12 h group(P＜0.05),but there was no significant difference between ANP 24 h group and rITF 24 h group.The number of positive NF-κB cells was 26±4,55±8,49±4,respectively;the relatively expression of TNF-α mRNA in terminal ileum was 0.050±0.005,1.040±0.031 and 0.792±0.0256,respectively;the relatively expression of ICAM-1 mBNA was 0.045±0.010,0.795±0.037 and 0.400±0.031,respectively,in control group,ANP group and rITF 12 h group.The corresponding values in the ANP group were significantly increased compared with those values in the control group (P＜0.05 or P＜0.01).Conclusions rITF may protect the intestinal mucosa.the mechanism may include inhibit NF-κB activation,down-regulate TiNF-α mBNA,ICAM-1 mRNA expression.

Objective To determine the expressions of miR-200a, miR-141, miR-205 and miR-34a in epithelial ovarian cancer (EOC) samples and to explore their clinical significance. Methods According to FIGO staging, 44 EOC pa?tients were divided into two groups:early FIGO stage (stageⅠ-Ⅱ, n=15) and late FIGO stage (stageⅢ-Ⅳ, n=29). Expres?sions of 4 miRNAs were detected by real time quantitative PCR, and were compared between two groups. The correlation of 4 miRNAs was calculated. EOC patients were divided into high miRNA expression group and low expression group according to the median value of miRNAs expression. Kaplan-Meier survival analysis and Cox multivariate analysis were used to com?pare the age, FIGO state, tumor residual after operation and post-operative chemotherapy of ovarian cancer between two groups. Results The expression of miR-141 was elevated in stagesⅢandⅣcompared with that of stagesⅠand Ⅱ(P=0.036). There was a positive correlation between expression of miR-141, miR-200a and miR-205, but a negative correlation with miR-34a (P<0.05). There was a positive correlation between miR-200a and miR-205 (P<0.05). Lower miR-200a ex?pression was associated with shorter progress free survival in ovarian cancer analyzed by log-rank test ( P=0.035). The sur?vival rate was significantly higher in FIGO stages ⅠandⅡthan that of FIGO stagesⅢandⅣ(P<0.05). Cox regression analysis revealed that miR-200a, FIGO stage and age were influential factors of overall survival time and progress-free sur?vival time of ovarian cancer, while miR-141, miR-205, miR-34a and tumor residual after operation and post-operative che?motherapy were not influential factors. Conclusion The expression of miR-200a is closely correlated with the progress and prognosis of ovarian cancer and may be used as an independent indicator for ovarian cancer prognosis.

AIM: To investigate the effects of auricularia auricular polysaccharide (AAP) on chronic cerebral ischemia injury in rats. METHODS: The chronic cerebral ischemia mode1 was made by permanent middle cerebral artery occlusion (MCAO) on the right side. AAP at different doses (50 mg/kg and 100 mg/kg) was intragastrically administered at the onset of ischemia and in the following days after operation, once a day for 4 weeks. After 4 weeks of MCAO, Morris water maze test was introduced to examine the learning and memory functions. Nissl staining was performed to detect the survival neurons in hippocampal slices. Level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissue were measured. RESULTS: Rats treated with AAP showed a shorter escaping latency in spacial navigation test because the AAP treated rats spent less time to find the platform in spatial probe test. More survival neurons in hippocampal slices were observed from AAP treated rats. Also, the MDA level in brain tissue was reduced and SOD activity in brain tissue was increased in the AAP treated rats with MCAO. CONCLUSION: AAP protects rats from chronic brain ischemic injury, in which its anti-oxidative effect might be involved.

Objective To explore the effects and possible mechanism of calcium-sensing receptor(CaSR) in rat myocardial H9c2 cells hypertrophy model using angiotensin Ⅱ (Ang Ⅱ).Methods Cardiac hypertrophy model was established by treating cultured H9c2 cells with Ang Ⅱ in vitro.Hypertrophic H9c2 cells were treated with gadolinium chloride (GdCl3,a specific agonist of CaSR) and/or with Calhex231 (a specific inhibitor of CaSR) and 3-methyladenine (3-MA,a specific inhibitor of autophagy) to divided into 5 groups (six in each group):control,Ang Ⅱ,GdCl3 + Ang lⅡ,GdCl3 + Calhex231 + Ang Ⅱ,GdCl3 + 3-MA + Ang Ⅱ groups.To evaluate the status of H9c2 cells hypertrophy,protein content was determined through a coomassie brilliant blue protein kit and the expression of Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) and the phosphorylation form (pCaMK Ⅱ/CaMK Ⅱ) was analyzed by Western blotting.The protein expression of CaSR,autophagy maker [Beclin-1,micmtubule-associated protein 1 light chain 3(LC3)Ⅱ/LC3 Ⅰ,P62] and Ca2+/calmodulin-dependent-protein kinase-kinase-β (CaMKKβ)-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway was analyzed by Western blotting.Results ①GdCl3 further increased H9c2 cells protein content [control group:(2.52 ± 0.84) g/L,Ang Ⅱ group:(8.72 ± 3.60) g/L GdCl3 + Ang Ⅱ group:(14.17 ± 4.49) g/L,all P ＜ 0.05] and the expression of CaSR (control group:0.22 ± 0.04,Ang Ⅱ group:0.43 ± 0.02,GdCl3 + Ang Ⅱ group:0.63 ± 0.08,all P ＜ 0.05) and pCaMK Ⅱ/CaMKⅡ (control group:0.25 ± 0.05,AngⅡ group:0.51 ± 0.03,GdCl3 + AngⅡ group:0.77 ± 0.06,all P＜ 0.05) induced by Ang Ⅱ.Calhex231 suppressed the increasing of hypertrophy indicators induced by GdCl3 [GdCl3 + Calhex231 + AngⅡ group,CaSR:0.41 ± 0.16,protein content:(9.92 ± 2.54) g/L,pCaMK Ⅱ/CaMKⅡ:0.58 ± 0.08,all P ＜ 0.05].②GdCl3 promoted the effect of Ang Ⅱ in regulation of autophagy such as Beclin-1 protein increased (control group:0.31 ± 0.06,AngⅡ group:0.55 ± 0.09,GdCl3 + AngⅡ group:0.74 ± 0.08,all P ＜ 0.05),LC3 Ⅱ/LC3 Ⅰ increased (control group:0.28 ± 0.06,Ang Ⅱ group:0.56 ± 0.10,GdCl3 + Ang Ⅱ group:1.00 ± 0.15,all P ＜ 0.05) and P62 protein decreased (control group:0.54 ± 0.03,AngⅡ group:0.34 ± 0.02,GdCl3 + AngⅡ group:0.15 ± 0.03,all P ＜ 0.05).Moreover,Calhex231 suppressed autophagy induced by GdCl3 (GdCl3 + Calhex231 + Ang Ⅱ group,Beclin-1:0.53 ± 0.14,LC3 Ⅱ/LC3 Ⅰ:0.57 ± 0.12,P62:0.28 ± 0.05,all P ＜ 0.05).③GdCl3 increased pCaMKKβ/CaMKKβ (control group:0.43 ± 0.09,AngⅡ group:0.76 ± 0.12,GdCl3 + AngⅡ group:1.19 ± 0.21,all P ＜ 0.05),pAMPK/AMPK (control group:0.38 ± 0.11,AngⅡ group:0.68 ± 0.08,GdCl3 + AngⅡ group:1.18 ± 0.08,all P ＜ 0.05) and decreased pmTOR/mTOR (control group:0.90 ± 0.10,Ang Ⅱ group:0.54 ± 0.04,GdCl3 + AngⅡ group:0.29 ± 0.09,all P ＜ 0.05).Furthermore,Calhex231 blocked the effect of GdCl3 on the above-mentioned proteins changes (GdCl3 + Calhex231 + Ang Ⅱ group,pCaMKKβ/CaMKKβ:0.75 ± 0.06,pAMPK/AMPK:0.57 ± 0.05,pmTOR/mTOR:0.51 ± 0.08,all P ＜ 0.05).Conclusion Inhibiting calcium-sensing receptor expression has reversed H9c2 cell hypertrophy induced by Ang Ⅱ,which may be related to suppressing autophagy and suppressing CaMKKβ-AMPK-mTOR pathway.

Objective To evaluate the effects of butorphanol pretreatment on myocardial damage induced by limb ischemia/reperfusion (I/R) in rats.Methods One hundred and eight male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =36 each) using a random number table:sham operation group (group S),I/R group and butorphanol pretreatment group (group B).Limb ischemia was induced by occlusion of bilateral hind limbs for 2 h followed by reperfusion in I/R and B groups.At 10 min before ischemia,butorphanol 0.2 mg/kg was injected via the right jugular vein in group B,while the equal volume of normal saline was injected in group I/R.Six rats were chosen randomly before ischemia (baseline,T0) and at 2,6,12,24 and 48 h after reperfusion (T1-5) and blood samples were taken from the abdominal aorta for determination of the serum creatine kinase isoenzyme-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration.The animals were then sacrificed and myocardial specimens were obtained for determination of myocardial apoptosis (using TUNEL) and the expression of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated protein kinase (ERK) (using Western blot analysis).Apoptosis index was calculated.Results Compared with group S,the serum CK-MB and cTnI levels were significantly increased at T1-5,and the apoptosis index and expression of JNK and ERK were increased at T2-5 in group I/R (P ＜ 0.05).Compared with group I/R,the pathological changes of myocardium were significantly reduced at T4,the serum CK-MB and cTnI levels were decreased at T2-5,the apoptosis index was decreased at T4,5,the expression of ERK was up-regulated at T2-5,and the expression of JNK was down-regulated at T2-4 (P ＜ 0.05).Conclusion Butorphanol pretreatment can reduce apoptosis in myocardial cells through activating MAPK signal transduction pathway,up-regulating ERK expression and down-regulating JNK expression,thus attenuating myocardial damage induced by limb I/R in rats.