Eignt compounds were isolated from the roots of Alinarubella Hance. They were identified as quinovic acid(Ⅰ), 3-oxo-urs-12-ene-27, 28-dioic acid (Ⅱ). quinovic acid-3? -O-?-D-glucopyranoside(Ⅲ ), quinovie acid-3?-O-?-L-rhamnopyranoside(Ⅳ). noreugenin (Ⅴ ), 7 -O-?-D-glucosyl- noreugenin(Ⅵ), scopo letin(Ⅶ), daucosterol(Ⅷ), by means of spectral analysis and reactions, Ⅱ, Ⅲ snd Ⅳ are isolated from the genus adina for the first time.

Object To carry out a systematic study on the chemical constituents of Carthamus tinctorius L. In order to reveal pharmacological active compounds for their further development. Methods Three constituents were separated by macroporous resin, silica gel, polyamide, Sephadex LH-20 and spectral analysis. Results The structures were elucidated by spectroscopic means including 1D, 2D NMR and ESI-MS; they are 1-ribityl-2, 3-diketo-1, 2, 3, 4-tetrahydro-6, 7-dimethyl-quinoxaline (Ⅰ), riboflavin (Ⅱ), and uracil-ribofuranose (Ⅲ). Conclusion Compounds Ⅰ-Ⅲ are isolated from C. tinctorius for the first time. Compound Ⅱ is a very important coenzyme for our bodies. It has been found that compound Ⅰ has the property of lowering the blood pressure of anesthetized dogs when administered in travenously.

Objective To discuss the effects of Liuwei Dihuang Decoction on expressions of TGF-β1 and complement regulatory protein CR1 of the renal on IgA nephropathy rats.Methods Forty SD rats were randomized into normal group, model group, tripterygium glycosides group and Liuwei Dihuang Decoction group after adaptive feeding for one week. Complex method was used to establish IgA nephropathy model. All administration groups were given relevant medicine for gavage for 4 weeks;urine routine, the number of urine erythrocyte and 24 h urine protein were detected;creatinine, urea nitrogen, total serum protein and serum alburin were detected from blood;the renal pathological changes were observed under light microscope by HE and Masson staining;the expressions of TGF-β1 and CR1 were detected by immunohistochemistry.Results Compared with model group,Liuwei Dihuang Decoction could significantly decrease the proteinuria and hematuria levels and renal fibrosis changes of IgA nephropathy model rats, reduce the expression of TGF-β1, and raise the expression of CR1 (P<0.05).Conclusion Liuwei Dihuang Decoction can delay the renal fibrosis in IgA nephropathy rats through reducing the degree of TGF-β1 and promoting the expression of CR1.

Objective To investigate the effect of progesterone on the expressions of inflammation-related factors of cortical cyclooxygenase-2 ( COX-2 ),prostaglandin E2 ( PGE2 ),inducible nitric oxide synthase (iNOS) and NF-κB in the cortex after traumatic brain injury (TBI) in rats so as to study the possible molecular mechanism of neuroprotective effect of progesterone on TBI.Methods Fortyfive male Spraque-Dawley rats were enrolled in the study and randomly divided into three groups,ie,sham operation group (n =15),TBI group (n =15) and progesterone treatment group (n =15).The rat model of TBI was duplicated with the improved Feeney' s method.The PROG treatment group was given i.p.injections of progesterone ( 16 mg/kg) at 1 and 6 hours after injury.The rats were sacrificed in three groups at 24 hours after injury and the specimens were removed.The changes of the positive cell numbers and protein level of COX-2,PGE2,iNOS and NF-κB in the cortex were examined by immunohistochemistry and Western blot.Results The positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the TBI group were distinctly higher than those of the sham operation group (P＜O.05).While the positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the progesterone treatment group were distinctly lower than those of the TBI group ( P ＜O.05).Conclusions Progesterone may exert protective effect on TBI through inhibiting NF-κB activity,blocking the inflammation response course of NF - κB and iNOS and decreasing the expressions of COX-2 and PGE2.

Objective To explore the neuroimmunomedulation mechanism of ICAM-1 and LFA-1 in children with febrile seizures (FS).Methods 40 children with FS were dividedinto simple FS(SFs)groupin20 cases and complex FS(CFS)groupin20 cases,and 30 health children matched with regard to age and sex were enrolled into control group.The real-time fluorescence quantitative PCR wag used to detect the expression of PBMC ICAM-1 mRNA.At the same time,the PBMC LFA-1 mRNA expression wfs studied with Send-QuantitativeRT-PCR analysis.Results The levels of PBMC ICAM-1 mRNA in SFS group were significantly higher than those in control group and CF$group(P<0.05).The levels ofPBMC ICAM-1 mRNA showed downtrend between CFS group and control group.but there was no statistical difference between the two groups(P>0.05).The levels of PBMC LFA-1 mRNA grey-scales in SFS group were significantly higher than those in control group and CFS group(P<0.05).In addition,the levels of PBMC LFA-1 mRNA in CFS group showed downtrend than those in control group,but there wti8 no statistical difference between the two groups(P>0.05).Conclusions The gene expression levels of PBMC ICAM-I/LFA-I in SFS group were different from those in CFS group.Inflammable immunopathology damage induced by ICAM-1/LFA-1 may play an important role in the pathogenesis of SFS.On the contrary,ICAM-1/LFA-1 may have seme neuroprotective effects on the pathogenesis of CFS.

Objective To compare the efficiency and safety between Aripiprazole and other traditional drugs for Tourette's syndrome treatment.Methods Databases such as China National Knowledge Infrastructure,Wanfang,VIP,China Biology Medicine Disc,PubMed and Web of Science were electronically searched for studies on Aripiprazole for Tourette's syndrome treatment.According to the inclusion and exclusion criteria,studies,extracted data,and assessed quality were screened.Meta-analysis was performed by using Stata 11.0 software.Results Four studies about Aripiprazole for Tourette's syndrome treatment with 396 patients (Aripiprazole group:201 cases;control group:195 cases) were synthetically and quantitatively analyzed.Meta-analysis results showed that Aripiprazole was better than other traditional agents (placebo,Tiapride,Haloperidol) [standardized mean difference (SMD) =0.21,95％ CI:0.10-0.32].The subgroup by time of treatment analysis results indicated that Aripiprazole was superior to other drugs in 2 weeks (SMD =0.28,95％ CI:0.06-0.50).There was no significant difference in the efficacy between Aripiprazole and other drugs for treatment of Tourette's syndrome in 4 weeks and 8 weeks after treatment (SMD =0.16,0.28;95％ CI:-0.05-0.38、-0.20-0.76).The subgroup by matched drugs results suggested that Aripiprazole was better than Tiapride (SMD =0.29,95 ％ CI:0.15-0.43),but was not significantly different from Haloperidol (SMD =-0.03,95％ CI:-0.28-0.22).There was no significant difference in side effects incidence between Aripiprazole and traditional drugs for treatment of Tourette's syndrome (RR =0.83,95 ％ CI:0.36-1.89).Conclusions Compared with the conventional drugs,Aripiprazole has better therapeutic efficacy in the treatment of Tourette's syndrome in children in 2 weeks.Aripiprazole is better than Tiapride,but equal to Haloperidol in the treatment of Tourette's syndrome.The safety of Aripiprazole needs to be further verified.

Objective To analyze the clinical features and gene mutation in mthylmalonic acidemia (MMA) accompanied by homocysteinemia (cblC), and review the relevant literatures. Methods The clinical features of 3 cases of MMA diagnosed by gene detection were retrospectively analyzed, and meanwhile the pertinent literatures of pathogenesis of MMA, especially combined with late-onset cblC and its gene detection, were reviewed. Results Patient 1 (26 days old) suffered from intermittent convulsions for 3 days, with isosuccinic acid 175.8 μmol/L, C3/C2 rate 1.363, homocysteine >?65 μmol/L and abnormal EEG. MMACHC gene detection found an exon deficiency (delEXON1), which has not been reported. Patient 2 ( 12 year old) was hospitalized for limb shaking, hyperspasmia and vomiting. His isosuccinic acid level was 334.3 μmol/L, C3/?C2 rate was 0.37, homocysteine >?65 μmol/L, and had abnormal EEG. MMACHC gene detection found the mutations of c.482G?>?A and c.609G?>?A. Patient 3 was hospitalized for intermittent convulsions for 20 days, whose isosuccinic acid, C3/?C2 rate, and homocysteine were increased. MMACHC gene detection found the mutations of c.394C?>?T and c.540del8 and c.540del8 had not been reported. Review of literatures discovered that MMA was combined with epileptic seizure in some patents, which further validate that the mutation in MMACHC gene c.482G?>?A may be related to the late-onset of cblC. Conclusions Gene detection contributes to the diagnosis of MMA; the mutation of MMACHC gene c.482G>A may be related to the late-onset of cblC; delEXON1 and c.540del8 are new mutations which have not been reported.

Objective To observe the effects of hedysari polysaccharide (HPS) on myocardial fibrosis and the expression of MMP-2/TIMP-2 in model mice of diabetic cardiomyopathy; To discuss the mechanism of action of prevention and treatment of myocardial fibrosis in diabetes.Methods Sixty mice were randomly divided into model group, rosiglitazone group and HPS high-, mediume- and low-dose groups. The normal group was 12 non-transgenic male BKS.Cg-Dock7m+/+Leprdb/JNjumice with the same age. Each group was given relevant medicine for gavage, for 8 weeks. Blood glucose of mice before and after medication 2, 4, 6, and 8 weeks was detected. The levels of MMP-2, MMP-2 and MMP-9 in myocardium were measured by Masson staining. The protein expressions of MMP-2 and TIMP-1 in myocardium were detected by Western blot.Results Compared with the model group, the blood glucose of HPS (high- and medium dose) groups and rosiglitazone group decreased significantly. Masson staining showed that the green fibers in the model group significantly increased and rosiglitazone group and HPS high-dose group decreased compared with the model group. Western blot showed that the expressions of MMP-2 in model group and MMP-2/TIMP-2 ratio were declined significantly, while the expression of MMP-2 was increased and TIMP-2 was decreased significantly, and the ratio of MMP-2/TIMP-2 increased in rosiglitazone group and HPS high- and medium-dose group.Conclusion HPS may reduce the degree of myocardial fibrosis in model mice with diabetic cardiomyopathy. The therapeutic effect of HPS may be to relieve myocardial fibrosis in model mice by increasing the ratio of MMP-2/TIMP-2.

BACKGROUND:Unicompartmental knee arthroplasty has become mainstream operation for treatment of unicompartmental osteoarthritis of the knee, but unicompartmental knee arthroplastystil has some problems, such as excessive bleeding-induced postoperative blood transfusion, increased blood transfusion rate, hospitalization expense and complication of blood transfusion. As tranexamic acid for total knee arthroplasty has achieved good effects. It is significant to investigate whether local application of tranexamic acid can effectively reduce blood loss in unicompartmental arthroplasty.
OBJECTIVE:To investigate the efficacy and safety of the intra-articular tranexamic acid injection in treating perioperative blood loss in patients undergoing unicompartmental knee arthroplasty.
METHODS:122 patients with knee osteoarthritis undergoing unicompartmental knee arthroplastyinthe Department of Orthopedics, the Second Affiliated Hospital ofDalian Medical University from January 2014 to August 2015wereenroled in this study. Al patients were randomly divided into two groups. Patients in the tranexamic acid group were injected with 10 mL of tranexamic acid (containing 1000 mg) + 10 mL of sodium chloride injection in the articular cavity before loosening the tourniquet. Patients in the control group received 20 mL of sodium chloride injection in the articular cavity. In both groups, the drainage tube was clipped for 3 hours after injection.At 48 hours after replacement, the drainage tube was puled out. We compared and analyzed hemoglobin levels and hematocrit at 2 days and 1 month postoperatively, total blood loss and drainage volume at 2 days postoperatively, the number of patients receiving blood transfusion, Hospital for Special Surgery scores of knee function at 1 week and 1 month postoperatively, and thrombosis at 1 week postoperatively, and evaluated effects of tranexamic acid on blood loss after unicompartmental knee arthroplasty.
RESULTS AND CONCLUSION:(1) Hemoglobin levels and hematocrit were significantly higher in the tranexamic acid group than in the control group at 2 days postoperatively (P< 0.05). No significant difference in hemoglobin levels and hematocrit was detected at 1 month postoperatively in both groups (P> 0.05). (2) Drainage volume and total blood loss were significantly less in the tranexamic acid group than in the control group at 2 days postoperatively (P< 0.05). (3) The number of patients receiving blood transfusion was significantly less in the tranexamic acid group (0 case) than in the control group (6 cases) (P< 0.05). (4) Scores of Hospital for Special Surgery were significantly higher in the tranexamic acid group than in the control group at 1 week postoperatively (P< 0.05). No significant difference in above socres was identified between the two groups at 1 month postoperatively. (5) No venous thrombosis was found at 1 week postoperatively in both groups. (6) These results confirm that during knee medial unicompartmental arthroplasty, intra-articular injection of tranexamic acid combined with 3 hours of blood occlusion can effectively reduce drainage volume, perioperative blood loss, blood transfusion, is beneficial to the early recovery of knee jointfunction after replacement, and does not increase the risk of lower extremity deep venous thrombosis.

Objective To investigate the clinical features of paroxysmal kinesigenic dyskinesia (PKD) and the mutation features of its pathogenic gene proline-rich transmenbrane protein 2 (PRRT2). Method The clinical manifestations and genetic tests of one case of PKD were retrospectively analyzed, and the related literatures were reviewed. Results A 10 year and 9 month male patient was recruited. The age of dyskinesias onset was 7 year and 6 month. The descriptions of the attacks were abnormal involuntary movements which were induced by sudden voluntary movements and presented with dystonia. The frequency of the attacks was three to ifve times per day with the duration lasting ten to twenty seconds, and there is no loss of consciousness. Treatment with oxcarbazepine is effective. A heterozygous mutation in PRRT2 gene, c.649_650insC (p. 217fs224X), was found by genetic testing, and the mutation was inherited from the patient’s mother who showed no symptom of PKD. Conclusion The onset age of PKD could be in the childhood and adolescence. The attack is provoked by sudden movements and the duration time is short. Treatment with antiepileptic drug is effective. The test of PRRT2 gene may help diagnosis. Mutation c.649_650insC is the hotspot mutation of the gene.