Objective To investigate the CT features of ovarian cystadenofibroma(CFA)and to improve the diagnostic accuracy. Methods The clinical data and CT images of 7 patients with ovarian CFA were retrospectively analyzed.All cases underwent non-enhanced and contrast-enhanced CT scan.Results Ovarian lesions were unilateral in 5 cases,bilateral in 2 cases and totally 9 lesions were found.6 lesions were cystic,2 lesions were mainly solid and 1 lesion was mixed components.The maximum diameter of lesions ranged from 4.7-21.5 cm with an average of 8.2 cm.Lesions had smooth margins,and solid portions had different size vesicles. Cyst walls or septa showed various degree of thickening with calcification in 1 lesion and mural nodules in 5 lesions,and a small vesicle was visualized in only 1 of the mural nodules.Cystic portions appeared as fluid density without enhancement.Solid portions,thickened cyst walls and septa appeared as slight enhancement or no enhancement.No regional lymph node metastasis was found,no ascites or peritoneal implants as well.Conclusion Ovarian CFA has some characteristic of CT findings that may improve clinical diagnosis and differential diagnosis.

AIM: To apply the solid phase extraction (SPE) on salvianolic acids in Radix Salvia Miltiorrhizae by means of high performance liquid chromatography with mass spectroscopic detector (HPLC MSn). METHODS: A C 18 solid phase column and negative ion electrospray ionization (ESI) mode were used by orthogonal design to optimize four factors which might affect recoveries of samples, which included vacuum tightness, sample size, amount of eluting agent and eluting power. RESULTS: The optimized results were as follows: vacuum tightness was 0.002?106 Pa, sample size was 0.75 mL, amount of eluting agent was 15mL and eluting power was 1.0mL?s -1 . CONCLUSION: The established method is simple, reliable and suitable for the usual quality control method of salviamolic acids in Radix Salvia Miltiorrhizae.

Objective To evaluate the effects of isoflurane postconditioning on cerebral ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two male Sprague-Dawley rats,weighing 280-320 g,were randomly divided into 4 groups (n=8 each):group sham operation (group S),group I/R,group isoflurane preconditioning (group Ⅰ-pre),and group isoflurane postconditioning (group Ⅰ-post).Global cerebral I/R was induced by 4-vessel occlusion method described by Pulsinelli.1.5％ isoflurane was inhaled for 2h before ischemia in group Ⅰ-pre.1.5％ isoflurane was inhaled for 30 min immediately after onset of reperfusion in group Ⅰ-post.Neurological function was assessed and scored at 24h of reperfusion.The rats were sacrificed at 72h of reperfusion and hippocampi were isolated for determination of neuronal apoptosis (by TUNEL),caspase-3 expression (by immuno-histochemistry),and phosphorylated c-Jun N-terminal kinase (p-JNK) protein expression (by using Western blot) in hippocampal tissues.Apoptotic rate was calculated.Results Compared with S group,the number of grid cross was decreased,twist time was prolonged,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 and p-JNK protein was up-regulated in I/R,I-pre and Ⅰ-post groups (P ＜ 0.05).Compared in I/R group,the number of grid cross was increased,twist time was shortened,hanging time was prolonged,apoptotic rate was decreased,and the expression of caspase-3 and p-JNK protein was down-regulated in Ⅰ-pre and Ⅰ-post groups (P ＜ 0.05).Compared with I/R group,the number of grid cross was decreased,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 was up-regulated (P ＜ 0.05),and no significant changes in the expression of p-JNK protein were found in Ⅰ-post group (P ＞ 0.05).Conclusion Isoflurane postconditioning can reduce cerebral I/R injury,the efficacy is weaker than that of preconditioning and the mechanism is related to activation of JNK signal transduction pathway and inhibition of neuronal apoptosis in hippocampus of rats.

Objective:To investigate the hepatitis C virus (HCV) infection in hemodialysis patients.Methods:One hundred and fifty hemodialysis patients were tested for HCV-RNA using a reverse transcription-polymerase chain reaction (RT-PCR) assay and for anti-HCV IgG using an enzyme-linked mmunosorbent assay (ELISA).Result:The positive rate of anti-HCV IgG was 24%.The positive rate of HCV-RNA was 26.7%;the total positive rate of HCV markers was 35.3%.Conclusion:HCV infection rate in hemodialysis patients is higher than that of general population.The first-class risk factors for HCV infection is transfusion of blood,while the cross using of dialyzer and dialysis pipe-line is also one of the risk factors.

Objective To explore the common genetic abnormalities in childhood acute lymphoblastic leukemia(ALL) and their responses to early treatment response.Methods From December of 2010 to December of 2011,169 newly diagnosed ALL patients at the Department of Hematology,Beijing Children's Hospital Capital Medical University,were detected by karyotype analysis,reverse transcription polymerase chain reaction (RT-PCR) and fluorescent in situ hybridization (FISH),and the relationship between early treatment responses and genetic abnormalities was observed.Results Of the 169 cases,bone marrow cell specimens from 162 cases were successfully cultured,with the success rate reached to 95.9％,and 88 cases (52.1％) had chromosomal abnormalities.Fifty-five cases carried 8 types of fusion genes among the 153 patients who received RT-PCR examination,and the abnormal rate was 35.9％.Forty cases applied for the detection of mixed lineage leukemia (MLL) gene rearrangement by FISH,and 6 cases of them were positive.One hundred and five cases had genetic abnormalities and the detection rate reached to 62.1％ by using three combined methods.The genetic abnormalities were classified into 6 groups,they were t(12;21),t(1;19),t(9;22),MLL rearrangement,hyperdiploid and-6/6q-,-7/7q-respectively,and early therapy response in each group was compared,and statistically significant differences were found among 6 groups (x2 =22.954,19.432,14.045,P =0.001,0.001,0.016).Conclusions Conventional cytogenetics combined with RT-PCR and FISH can enhance the detection rate of genetic abnormalities in childhood ALL.Genetic abnormalities combined with early treatment response in ALL can better guide the clinical treatment and prognosis assessment.

Objective To screen the variation in NeuroD1 gene and to study its function in vitro and its clinical phenotypes and genetic characteristics in Chinese early-onset type 2 diabetic probands. Methods PCR-direct sequencing of NeuroD1 gene was performed in 85 early-onset type 2 diabetic probands, 95 late-onset type 2 diabetics with strong diabetic history and 87 non-diabetic control subjects. Distributions of the identified variation were calculated and compared among the three groups. Expression vectors with mouse NeuroD1 (mND1)cDNA wild type or mutant type and reporter vectors with human insulin promotor-linked luciferase were constructed. Then the above vectors were co-transfected into rat INS-1 cells. Relative luciferase activities were measured to compare transcriptional activities of insulin gene between WT and MT. Results S159P (T→C), a new mutation was identified in a proband, which was co-segregated with diabetes in 4 carriers from the paternal side. The functional study showed that the S159P mutant exhibited a 25% reduction in transcriptional activity of insulin gene as compared with the wild type. A45T (G→A), a common variation was identified. The AA + GA genotypic frequencies were markedly increased in early-onset type 2 diabetic probands as compared with late-onset type 2 diabetic probands and non-diabetic control subjects (P=0.006 and P=0.014, respectively). Conclusion The novel S159P mutation in the NeuroDl gene seems to contribute to the development of diabetes in the Chinese early-onset type 2 diabetic family. The A45T variation may increase susceptibility to or be in disequilibrium with early-onset type 2 diabetes mellitus in Chinese population. In addition, the A45T variation may affect the onset pattern of type 2 diabetes mellitns, such as early-onset but not late-onset type 2 diabetes mellitus.

Objective To evaluate the effect of isoflurane preconditioning on autophagy during focal cerebral ischemia-reperfusion (I/R) injury in rats.Methods Thirty-six healthy male Sprague-Dawley rats,weighing 250-280 g,aged 7-8 weeks,were divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),cerebral I/R group (group I/R) and isoflurane preconditioning group (group IP).Focal cerebral I/R was induced by 2 h middle cerebral artery occlusion followed by 24 reperfusion.Group IP inhaled 1.5％ isoflurane for 1 h per day for 5 consecutive days,the other two groups only inhaled 30％ oxygen,and focal cerebral I/R was induced at 24 h after the last inhalation.At 24 h of reperfusion,neurologic deficit was assessed and scored,the rats were then sacrificed,and brains were removed for determination of cerebral infarct size (using triphenyl tetrazolium chloride staining) and expression of microtubule-associated protein 1 light chain 3-Ⅱ (LC3-Ⅱ) and Beclin-1 (by Western blot).Results Compared with group S,the neurologic deficit scores and cerebral infarct size were significantly increased,and the expression of hippocampal LC3-Ⅱ and Beclin-1 was significantly up-regulated in I/R and IP groups (P＜0.05).Compared with group I/R,the neurologic deficit scores and cerebral infarct size were significantly decreased,and the expression of hippocampal LC3-Ⅱ and Beclin-1 was significantly upregulated in group IP (P ＜ 0.05).Conclusion The mechanism by which isoflurane preconditioning ameliorates focal cerebral I/R injury is related to enhancement of autophagy in the rats.

Objective To evaluate the effect of isoflurane preconditioning on the expression of hippocampal GluR1 subunits-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate(AMPA)receptors in a rat model of focal cerebral ischemia-reperfusion(I/R).Methods Forty-eight pathogen-free healthy male Sprague-Dawley rats,weighing 250-280 g,aged 7-8 weeks,were divided into 3 groups(n=16 each)using a random number table:sham operation group(group S),focal cerebral I/R group(group I/R)and isoflurane preconditioning group(group IPC).Focal cerebral I/R was induced by occlusion of the middle cerebral artery for 2 h followed by reperfusion to induce cognitive decline in I/R and IPC groups. Rats were exposed to 1.5% isoflurane for 1 h every day for 5 consecutive days,and the model was established at 24 h after the last exposure in group IPC. Eight rats in each group were selected to perform Morris water maze test for 6 consecutive days starting from 9 or 23 days after operation. The rats were sacrificed at 14 and 28 days after operation,and the hippocampal tissues were obtained for determination of the expression of GluR1 mRNA(by using real-time polymerase chain reaction)and GluR1 protein(by Western blot).Results Compared with group S,the escape latency was significantly prolonged at each time point after operation,the frequency of crossing the original platform quadrant and percentage of swimming distance at the original platform quadrant were decreased at 14 and 28 days after operation,and the expression of GluR1 protein and mRNA was down-regulated at 14 days after operation in I/R and IPC groups(P<0.05).Compared with group I/R,the escape latency was significantly shortened at 10-13 days after operation,the percentage of swimming distance at the original platform quadrant and frequency of crossing the original platform quadrant were increased at 14 days after the operation,and the expression of GluR1 protein and mRNA was up-regulated at 14 days after operation in group IPC(P<0.05).Conclusion The mechanism by which isoflurane preconditioninig improves the cognitive function is related to up-regulation of the expression of hippocampal GluR1 subunits-containing AMPA receptors in a rat model of focal cerebral I/R.

Objective To investigate the effect of isoflurane preconditioning on rat learning and memory in cerebral ischemia-reperfusion injury and its possible mechanism.Methods Thirty-six adult male Sprague-Daw ley rats w ere randomly divided into a sham operation group, a cerebral ischemia-reperfusion group, and an isoflurane preconditioning group (n=12 in each group). A model of middle cerebral artery occlusion and ischemic-reperfusion w as induced by a modified intraluminal suture method. The rats of the isoflurane preconditioning group inhaled 1.5%isoflurane for 1 hour per day for 5 d. At 24 h after the last preconditioning, a model of MCAO w as made. At 24 h after MCAO, the infarct volume w as detected by using 2,3,5 chlorinated diphenyl tetrazolium staining. At day 1, 3, 7, and 14 after MCAO, the modified Neurological Severity Score (mNSS) were performed. At day 9 after MCAO, the Morris w ater maze test w as used to evaluate the learning and memory of rats. At day 14, Western blotting w as used to detect the protein expression level of hippocampal tissue glutamate receptor 1 (GluR1) on the side of ischemia. Results No obvious infarcts w ere observed in the rats of the sham operation group. The infarct volume in the isoflurane preconditioning group w as significantly smal er than that of the cerebral ischemia-reperfusion group (26.383%±3.128%vs.19.107%±1.661%;P<0.05). No neurological deficit w as observed in the sham operation group (score 0). The mNSS scores at day 1, 3, 7, and 14 after MCAO in the isoflurane preconditioning group w ere decreased significantly (day 1:9.000 ±1.195 vs.11.500 ±1.414;day 3:6.6250 ±1.407 vs.6.625 ±1.407vs.6.625 ±1.407; day 7: 5.875 ±0.707 vs.7.375 ±1.407; and day 14:3.375 ±1.187 vs.5.125 ±1.246;al P<0.05). The Morris w ater maze show ed that the escape latencies at day 1-5 after MCAO in the isoflurane preconditioning group w ere al significantly shorter than those in the cerebral ischemia-reperfusion group (day 1: 95.992 ±15.734 s vs.103.008 ±11.654 s; day 2: 70.949 ±14.708 s vs. 94.705 ±14.709 s;day 3:39.660 ±7.413 s vs.65.716 ±10.155 s;day 4:22.692 ±5.778 s vs.35.240 ±8.553 s;day 5: 14.906 ±4.336 s vs.22.890 ±10.381 s; al P<0.05). The numbers of crossing platform (4.556 ± 1.333 vs.2.889 ±1.536 ) and the percentages of time spent in the target quadrant ( 33.014%±5.223%vs. 21.978%±6.697%) in the isoflurane preconditioning group w ere significantly increased than in the cerebral ischemia-reperfusion group (al P<0.01). The levels of hippocampal GluR1 protein on the ischemic sides in the sham operation group, ischemia-reperfusion group, and isoflurane preconditioning group w ere 0.871 ±0.153, 0.456 ±0.130, and 0.689 ±0.126, respectively. There w ere significant differences among the 3 groups ( F=18.329, P<0.001) and the isoflurane preconditioning group w as significantly higher than the ischemia-reperfusion group (P<0.05). Conclusions Isoflurane preconditioning can improve the learning and memory in cerebral ischemia-reperfusion in rats, its mechanism may be associated w ith the uprelagating GluR1 expression in the hippocampus.

Objective To evaluate the role of mitochondrial ATP-sensitive potassium (mitoKATP) channel in mitigation of cerebral ischemia-reperfusion (I/R) injury by isoflurane preconditioning in rats and the relationship with c-Jun N-terminal kinase (JNK) signaling pathway.Methods Thirty-two male Sprague-Dawley rats,weighing 280-320 g,were randomly divided into 4 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,isoflurane preconditioning group (group Ⅰ-pre),and 5-hydroxydecanoate (5-HD,a selective mitoKATP channel antagonist) group.Cerebral I/R was produced by modified 4-vessel technique described by Pulsinelli in anesthetized rats.In group Ⅰ-pre,the rats were exposed to 1.5％ isoflurane for 1 h everyday for 5 consecutive days before ischemia.In group 5-HD,5-HD 15 mg/kg was injected intraperitoneally at 30 min before ischemia and the other procedures were similar to those previously described in group Ⅰ-pre.Neurological behavior was evaluated at 24 h of reperfusion.The rats in each group were sacrificed at 72 h of reperfusion,and the brains were removed for determination of neuronal apoptosis (by TUNEL) and expression of caspase-3 and phosphor-JNK (p-JNK) protein (using Western blot) in hippocampal tissues.Apoptotic rate was calculated.Results Compared with group S,the number of grid cross was significantly decreased,hanging time was shortened,apoptotic rate was increased,and caspase-3 expression was up-regulated in I/R,Ⅰ-pre and 5-HD groups,the expression of p-JNK protein was up-regulated in IR and 5-HD groups,and no significant change was found in the expression of p-JNK protein in group Ⅰ-pre.Compare with group I/R,the number of grid cross was significantly increased,hanging time was prolonged,apoptotic rate was decreased,and the expression of caspase-3 and p-JNK protein was downregulated in group Ⅰ-pre,and no significant change was found in the parameters mentioned above in group 5-HD.Compared with group Ⅰ-pre,the number of grid cross was significantly decreased,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 and p-JNK protein was up-regulated in group 5-HD.Conclusion The mitoKATP channel is involved in mitigation of cerebral I/R injury by isoflurane preconditioning through blocking the JNK signaling pathway in rats.