Objective To discuss the clinical value of intravascular ultrasound (IVUS) in treatinginternal carotid arteries occlusion.Methods The patient was diagnosed with internal carotid artery occlusionthat was confirmed by CTA.Cerebral perfusion imaging showed that low perfusion area was consistent withischemic symptoms.Guided by IVUS,percutaneous transluminal angioplasty (PTA) was performed.By usingmicro-catheter coaxial technology,the micro guide wire was inserted in the carotid artery until it passedthrough the obstructed segment;After IVUS examination proved that the micro guide wire was in the truelumen of carotid artery,angiography through micro-catheter was carried out to confirm that the distal arterywas unobstructed;after adjusting the device position the embolism protector was placed.The plaque andlumen condition were assessed with IVUS,which was reevaluated after pre-expansion of balloon.After normaldirection blood flow was regained,the plaque stability was assessed with IVUS virtual organization sequence.Simple balloon dilatation therapy was adopted as the fibrous cap of plaque was in stable condition and thelumen stenosis rate was ＜40％.Results After balloon dilatation,the obstructed artery was reopened and theblood flow regained normal direction.IVUS examination showed that during the whole operation process thefibrous cap of plaque at the narrowed segment remained in stable condition,the lumen stenosis rate was ＜40％.Cerebral perfusion imaging revealed that after the treatment the low perfusion state was markedlyimproved.Conclusion IVUS plays an important guiding role in performing PTA for internal carotid arteryocclusion.This technique can increase the success rate of vascular recanalization and reduce the incidence ofcomplications.

Objective To observe the effect of electroacupuncture(EA) on the hippocampal expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in rats with vascular dementia(VD),so as to find out the underlying mo lecular mechanisms of EA in treating VD.Methods Thirty-two Wistar rats were randomly divided into a shamoperation group,a model group,a sham-acupuncture group,and an EA group (8 in each group).Permanent bilateral common carotid artery occlusion was performed to model vascular dementia in the model group,the shamacupuncture group and the EA group,while exposure but no occlusion of the bilateral common carotid were performed in the sham-operating group.Novel object recognition test was adopted to prove the establishment of VD rat model.All the rats were kept in an immobilization apparatus while receiving treatments.EA was applied ontoBaihui (GV20) and Zusanli (ST36) in EA group for 30 min,once daily for 7 days.Sham-acupuncture group were treated with needles inserted 0.5 mm superficially.And the sham-operation group and the model group were only immobilized.The protein expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in hippocampal tissue was detected by western blotting.Results The expression of GluA1 in the model group (1.216 ± 0.102) was significantly less than in the sham-operating group (1.918 ± 0.137) (P ＜ 0.05).The expression of GluA1 in the EA group (1.653 ± 0.169) was significantly higher than in the model group (1.216 ± 0.102) and in sham-acupuncture group (1.231 ±0.188) (P＜0.05).The expression of CaMKⅡ in the model group (1.516±0.392) was less than in the sham-operating group (2.187 ± 0.231) (P ＜ 0.05).The expression of CaMK Ⅱ in the EA group (2.733 ±0.387) was significantly higher than in the model group (1.516 ±0.392) and sham-acupuncture group (1.493 ±0.205) (P＜0.05).The expression ofpGluA1 in the model group (1.502 ±0.419) was less than in the sham-operating group (2.253 ± 0.244) (P ＜ 0.05).The expression of pGluA1 in the EA group (2.382 ± 0.308) was significantly higher than in the model group (1.502 ± 0.419) and the sham-acupuncture group (1.498 ± 0.223) (P ＜ 0.05).The expression of pCaMK Ⅱ in the model group (0.394 ± 0.227) was less than in the sham-operating group (0.667 ±0.175) (P＜0.05).The expression ofpCaMKⅡ in the EA group (1.189± 0.346) was significantly higher than in the model group (0.394 ± 0.227) and the sham-acupuncture group (0.408 ± 0.231) (P ＜ 0.05).Conclusion EA can enhance the protein expression and phosporylation of GluA1 and CaMK Ⅱ,causing silent synapses transforming into functional synapses,and consequently,long term potentiation was facilitated and cognitive impairment was improved by EA.

Objective To investigate whether functional electrical stimulation (FES) can improve the expression of proteins in the NMDAR1-pGLuR1 pathway so as to promote the recovery of motor function and sensation after stroke.Methods Eighty-one Wistar rats were used to make a photochemical brain model of local ischemia.Rats were randomly assigned into a sham, placebo stimulation or FES group.Rats in the placebo and FES groups had local ischemia induced in the M1 zone of the brain using the photosensitive dye Bengal rose.It was administered intravenously and a laser beam was then stereotactically positioned on the skull.The rats in the FES groups were stimulated for 30 minutes (10 minutes on, 10 minutes off, then 10 minutes on).The placebo group's treatment was similar, but without the electric current.The rats in the sham group received no intervention.The cylinder test and the adhesive-removal test were used to test the rats' motor function and sensation before the operation and before they were sacrificed.Cohorts were sacrificed after 3, 7 and 14 days of intervention.NMDA receptor and AMPA receptor were detected in the peri-ischemic cortex using western blotting.Results After 7 and 14 days the index of forelimb motor function in the cylinder test of the FES group was significantly better than that of the placebo group.The average adhesive-removal time of the FES group was also significantly faster compared with the placebo group.After 7 days the average expression of NMDAR1 in the FES group was significantly higher than in the placebo group.The average expression of GluR1 and pGluR1 in the FES group was significantly higher than in the placebo group after 14 days.Conclusion Functional electrical stimulation can improve motor function after ischemia through the NMDARAMPAR signal pathway, at least in rats.

Objective To investigate the effect of berberine on the polarization of mice RAW264.7 macrophages induced separately by lipopolysaccharide (LPS) and interleukin-4 (IL-4). Methods Mice RAW 264.7 macrophages cultured in vitro were divided into model group, medication group, and blank control group. Both model group and medication group were given either LPS (in final dose of 100 ng/mL) or IL-4 (in final dose of 10 ng/mL). Additionally, the medication group was treated with berberine in final dose of 20 μmol/L. The blank control group was given the same volume of phosphate buffered saline ( PBS). Real-time fluorescence quantitative polymerase chain reaction (PCR) was used to detect the mRNA expression of arginase-1 (Arg-1), inducible nitric oxide synthase ( iNOS) , suppressor of cytokine signaling2 ( SOCS2) and SOCS3. Enzyme-linked immunosorbent assay (ELISA) was used to determine the contents of tumor necrosis factor alpha (TNF-α) and IL-10. Results The content of TNF-αand the mRNA expression levels of iNOS and SOCS3 in macrophages induced by LPS were increased, and then were down-regulated by berberine (P<0.05 or P<0.01) . The content of IL-10 and the mRNA expression level of Arg-1 in macrophages induced by IL-4 were increased, and then were down-regulated by berberine ( P<0.05), but berberine had no effect on the mRNA expression level of SOCS2 ( P>0.05). Conclusion Berberine has an effect on inhibiting the M1 and M2 polarization of macrophages in vitro, suggesting that berberine may play a regulatory role in the dynamic balance of M1/M2.

Acute respiratory distress syndrome (ARDS) is a common complication of severe acute pancreatitis (SAP) and a leading cause of early death in SAP patients, but its pathogenesis is still unclear. In recent years, the role of gut microbiota and its metabolites in regulating SAP-related ARDS has attracted more and more attention, and in-depth studies on the pathogenesis of “intestine-lung axis” may provide new ideas for the research and development of drugs for SAP-related ARDS. This article summarizes the recent research advances in gut microbiota and its metabolites in SAP-related ARDS.

Objective To investigate the relationship between single nucleotide polymorphism (SNP) of BARD 1 gene and BRCA1 gene in epithelial ovarian cancer (EOC).Methods Nineteen EOC patients with BRCA1 gene mutation and 50 EOC cases without BRCA1 gene mutation between January 2016 and October 2016 were collected,and all EOC were diagnosed by pathological method.BARD1 gene variants were detected by next generation sequencing (NGS).The SNP of BARD1 gene was analyzed by Pearson linear correlation.Logistic regression analysis was used to research the clinicopathologic features and BRCA1 gene mutation associated with BARD1 gene SNP.Pearson's chi-square test was used to analyze the association between BARD1 gene Val507Met,Arg378Ser and Pro24Ser with different clinicopathologic features and BRCA1 gene mutation risk.Results (1) Eight BARD1 gene variants were found in 69 ovarian cancer patients,in which Val507Met,Arg378Ser and Pro24Ser were common variants,and the rate of mutation were all 54％ (37/69).(2) There was a significant linear correlation among Val507Met,Arg378Ser and Pro24Ser (all P＜0.01).(3) Obvious differences were found in Val507Met,Arg378Ser and Pro24Ser of BARD1 gene between BRCA1+ and BRCA1 (all P＜0.05).(4) No differences were found between BARD1 gene Val507Met,Arg378Ser and Pro24Ser and the clinicopathologic features (all P＞0.05),while obvious differences were found in BRCA1 gene mutation compared to the controls group.The risk of BRCA1 mutation in Val507Met and Arg378Ser were more evident in subjects with negative family history,positive menopause history,negative tubal ligation,onset age (≤60 years old) and sensitivity to platinum-based chemotherapy in EOC (all P＜0.05),while Pro24Ser was only more evident in positive menopause history of EOC (P＜0.05).Conclusions BARD1 Val507Met,Arg378Ser and Pro24Ser are the common genotypes,which are associated with BRCA1 mutation in EOC.The family history,menopause history,tubal ligation,onset age and sensitivity to platinum-based chemotherapy have effects on BARD1 SNP in the risk of BRCA1 gene mutation.

Objective To investigate the relationship between serum follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and clinicopathological features and prognosis of serous ovarian cancer retrospectively. Methods A total of 73 patients with serous ovarian cancer treated in the Department of Obstetrics and Gynecology of Tianjin Medical University General Hospital from January 2000 to December 2015 were included in this study. The relationship between serum FSH, LH, PRL and clinicopathological features was analyzed by Mann-Whitney U method. Kaplan-Meier (K-M) method was used to analyze survival rates of patients with different clinical features. Multivariate Cox proportional hazards regression analysis was used to analyze prognostic factors of serous ovarian cancer patients. Results The mean concentrations of serum FSH and LH were significantly higher in the>50 year-old group than those in the<50 year-old group (P<0.05). The mean concentrations of FSH and LH were significantly higher in menopause group than those in non-menopause group (P<0.05). There were no significant differences in serum levels of FSH and LH in patients with other different clinicopathological features (P>0.05). There was no significant correlation between serum PRL concentration and clinicopathological features (P>0.05). Analysis results showed that poor prognosis of patients was related with high serum levels of FSH (>40.13 IU/L), PRL (>14.96 μg/L) and FIGO stage (Ⅲ+Ⅳ) (P<0.05). There was no significant correlation between serum LH concentration and prognosis (P>0.05). COX regression analysis showed that the serum PRL>14.96 μg/L was risk factor for prognosis of serous ovarian cancer [HR(95%CI): 3.530(1.180-10.557),P=0.024]. Conclusion The serum levels of FSH and LH are significantly increased in postmenopausal women than those in menopause women. The serum level of PRL is correlated with the prognosis of serous ovarian cancer.

Objective To study the feasibility of using fractional flow reserve (FFR) to guide whether to perform coronary revascularization of non-culprit moderate stenosis in patients with unstable angina and estimate their clinical prognosis. Methods This study enrolled unstable angina patients with multivessel disease. First successful stenting of the culprit artery, then the other non-culprit moderate coronary stenosis were randomized into PCI guided by angiography or guided by FFR measurements. Death from any cause, nonfatal myocardial infarction, unplanned hospitalization leading to urgent revascularization and clinical manifestations with angina were followed during the first year. Results 71 patients were included, among them 35 patiens were randomly assigned to angiography-guided PCI and 36 patients to FFR-guided PCI. In FFR-guided PCI group, FFR was successfully measured in all of non-culprit moderate coronary stenosis. In 23 stenosis, the FFR was greater than 0.80, and stents were not placed in these stenosis. In 13 stenosis with FFR<0.8, stent were inplant and FFR was raised≥0.95 after stenting. The percentage of patients who had a primary end-point event was higher in the angiography-guided PCI group than the FFR-guided PCI group (P<0.05). Neither the rate of mortelity from any cause nor the rate of non-fatal myocardial infarction had significant difference between the 2 groups. Related to the target vessels rates of nonfatal myocardial infarction (5.6%vs. 28.6%) and target lesion revascularization (5.6%vs. 31.4%) were statistically different (P<0.01 and P<0.05, respectively). Conclusions In patients with unstable angina, it is safe to use FFR values to guide decisions on the revascularization of angiographically moderate non-culprit stenosis. Routine measurement of FFR in addition to angiographic guidance, as compared with PCI guided by angiography alone, results in a significant reduction in major adverse events at 1 year, particularly in urgent revascularization, and clinical manifestations with angina get better.

Objective To study the effects of different types of exercise training on learning and memory, as well as on the expression of synaptophysin (SYP) and on postsynaptic density protein 95 (PSD-95) in rats in which a model of vascular dementia had been created.Methods Forty male Wistar rats were divided randomly into a voluntary exercise group (V-EX) , a forced exercise group (F-EX) , an involuntary exercise group (I-EX) , a vascular dementia group (VD) and a sham-operation group (Sham) , with 8 rats in each group.Two-vessel occlusion (2-VO) of the arteria carotis communis was used to create a model of vascular dementia in all of the rats except those in the sham-operation group.Beginning one week after the surgery, the V-Ex rats were free to run in a running wheel.The F-EX rats were forced to run 270 m a day in an electric wheel.The I-EX rats were stimulated to imitate the gait pattern of their forelimbs running at 9 m/min three times a day for l0 minutes each time.No special training was given to the rats in the other 2 groups.Three weeks after the surgery, their learning and memory were tested using a novel object recognition test.Immediately after the test, their prefrontal cortex was sampled and the expression of SYP and PSD-95 was detected using western blotting.Results The average novel object recognition indices of the rats in the V-EX, F-EX and I-EX groups were all significantly higher than that of the VD group.Average PSD-95 expression was also significandy higher than in the VD group.Conclusion Exercise, whether voluntary, forced or induced by functional electrical stimulation can improve learning and memory in vascular dementia, at least in rats.The mechanism is possibly that the training can increase the expression of PSD-95 in the prefrontal cortex, though not SYP.

Objective To investigate the effect of sinomenine on the purinergic receptors A2A and P2X7 in endotoxemia mouse model and RAW264.7 macrophage model stimulated by lipopolysaccharide(LPS). Methods BALB/c mice were randomly divided into blank control group, model group and sinomenine group. Thirty minutes after the rats of sinomenine group were pretreated with intraperitoneal injection of sinomenine (40, 80, 160 mg/kg), the mice were given intraperitoneal injection of 15 mg/kg LPS to induce endotoxemia model. The serum levels of tumor necrosis factor-alpha(TNF-α) and interleukin-6(IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). The expression levels of purinergic receptor A2A and P2X7 in the liver and spleen were detected by reverse transcription-polymerase chain reaction(RT-PCR). RAW264.7 macrophages were divided into blank control group, LPS group and sinomenine group. Sinomenine group was firstly treated with sinomenine(300μmol/L) for 2 h, and then LPS group and sinomenine group were treated with LPS (100 ng/mL) for another 8 hours. TNF-α in the cell supernatant was measured by ELISA, and the expression levels of A2A and P2X7 in RAW264.7 cells were detected by RT-PCR. Results Stimulation with LPS could induce the increase of the mouse serum levels of TNF-α and IL-6 as well as the expression of A2A and P2X7 in mouse liver and spleen, and sinomenine had a counteraction on the above indexes(P<0.05) . In-vitro stimulation with LPS could induce the increase of the content of TNF-α and the expression of A2A and P2X7 in RAW264.7 cells , and sinomenine decreased TNF-α content and P2X7 expression (P<0.05) , but had an effect on enhancing A2A expression. Conclusion Sinomenine suppresses the expression of purinergic receptor P2X7 in mouse spleen and liver as well as in RAW264.7 macrophages, but its effect on the expression of A2A in various tissues and cells varies, whose related mechanism is needed further study.