Objective To investigate the prognostic factors of young stroke patients with conventional treatment,and provide the basis for clinical diagnosis and treatment of stroke.Methods The clinical data of 72 cases of young stroke patients with conventional treatment were analyzed retrospectively.The prognostic factors were analyzed.Results In seventy-two cases of young stroke patients,18 cases of conventional treatment failed (25.00％,18/72).Univariate analysis showed that smoking,alcohol,underlying disease,dysphagia,barthel index (BI) score,U.S.national institutes of health stroke scale (NIHSS) score and Oxford handicap scale (OHS) score was closely related with the prognosis (P ＜ 0.05 or ＜ 0.01).Logistic analysis showed that the age,BI score,NIHSS score,OHS score and underlying diseases was the independent prognostic factor for young stroke patients.Eighteen cases who failed in conventional treatment fails accepted comprehensive rehabilitation treatment.Compared with that before treatment,1,3,6 months after treatment BI,NIHSS and OHS scores were significantly decreased (P ＜ 0.05).Conclusions BI,NIHSS,OHS score and underlying diseases are the independent prognostic factor for young stroke patients.Surgery and postoperative comprehensive rehabilitation in young stroke patients who failed in conventional treatment can improve patient's outcomes and prognosis.

Dexamethasone ; therapeutic use ; Glucocorticoids ; pharmacology ; therapeutic use ; Humans ; Infant, Newborn ; Meconium Aspiration Syndrome ; drug therapy ; physiopathology ; Methylprednisolone ; therapeutic use ; Prednisolone ; therapeutic use

OBJECTIVETo research the mechanism of dopamine (DA) controlled memory in mice.

METHODSMice received i.p. injection of scopolamine (0.3 mg/kg, SCOP 0.3, and 3.0mg/kg, SCOP 3.0, respectively, n = 10) and saline (NS, n = 10) for 60 days in experiment 1. Memory of mice was detected by dark avoidance behavior in the 53" d and the 60"' d. Animals were sacrificed after the memory test; brain tissues were processed for Fos-ir and TH-ir by immunohistochemistry. Mice were divided into four groups according results of expri-ment 1, they received i.p. injection of apomorphine (0.1 mg/kg, APO 0.1, 0.5 mg/kg, APO 0.5, and 2.0 mg/kg, APO2.0 respectively, n = 10).

RESULTSMemory was inhibited in mice injected scopolamine 3.0 mg/kg. Latency was significantly less than in NS group, only 1/ 4 that of NS group (P > 0.05). The number of mistake of SCOP 3.0 group increased about four times than that of NS group (P > 0.05). But there was no difference of latency and number of mistake between SCOP 0.3 and NS group in expriment 1. Scopolamine-induced memory deficit was associated with decreased cellular activation, indicated by Fos immunoreactive (ir) staining, in NAcc CA1 and CA3 (P < 0.05), and also associated with decreases in the number of cells labeled for tyrosine hydroxylase (TH-ir), the rate limiting enzyme for dopamine conversion (P < 0.01) and the number of cells co-labeled for TH-ir/Fos-ir (P <0.01) in the ventral tegmental area(VTA), apomorphine lessened scopolamine-induced memory deficit in experiment 2. The number of cells co-labeled for TH-ir/Fos-ir (P <, 0.05) was increased in VTA after apomorphine treatment.

CONCLUSIONApomorphine lessened scopolamine-induced memory deficit in mice by increasing DA activities in VTA.

Animals ; Apomorphine ; pharmacology ; Disease Models, Animal ; Dopamine Agonists ; pharmacology ; Male ; Memory Disorders ; chemically induced ; drug therapy ; Mice ; Scopolamine Hydrobromide ; toxicity

Objective To explore the efficacy of GM6001,tissue inhibitor expression and significance of matrix metalloproteinase?9(MMP?9)in mice model of oxygen?induced retinal neovascularization(RNV)and evaluate the inhibition effect of MMP?9 inhibitor(GM6001)on RNV. Meth?ods Mice were placed in oxygen boxes to establish oxygen?induced RNV animal models. The GM6001 treated or hyperxia control groups received an intravitreal injection of 1μL GM6001(100μmol/L)or PBS at day 11 after birth. The normal control and hyperxia group were not treated. HE staining was used to detect RNV in retinal whole mounts,the mRNA level and protein expression of MMP?9 were measured by RT?PCR,Western blot and immunohistochemistry,respectively. Results RNV in the GM6001 treated group was decreased significantly compared with the hyperxia group and hyperxia control group. Compared with the normal control group,higher protein and mRNA expression of MMP?9 were observed in the hy?perxia group and hyperxia control group. The expression of MMP?9 protein and mRNA were decreased in the GM6001 treated group compared with the hyperxia control group(P<0.05). Conclusion The abnormal expression of MMP?9 was closely correlated with RNV. The development of RNV can be markedly inhibited by MMP?9 inhibitor(GM6001),which,we believe,will provide new molecular targets and therapeutic strategy for retinopathy of prematurity treatment.

Animals ; Blood Cell Count ; Blood Cells ; Decompression Sickness ; blood ; Male ; Rabbits

Adenocarcinoma, Follicular ; epidemiology ; genetics ; metabolism ; pathology ; Carcinoma, Papillary ; pathology ; DNA-Binding Proteins ; metabolism ; Diagnosis, Differential ; Genes, ras ; genetics ; Humans ; Point Mutation ; Prognosis ; Thyroglobulin ; metabolism ; Thyroid Neoplasms ; epidemiology ; genetics ; metabolism ; pathology ; Transcription Factors

Cell Line, Tumor ; Genetic Vectors ; Humans ; Male ; Neuraminidase ; genetics ; metabolism ; Prostate ; metabolism ; Prostatic Neoplasms ; metabolism ; pathology

Aged ; Bone and Bones ; pathology ; Carcinoma, Small Cell ; complications ; pathology ; Female ; Humans ; Hyoid Bone ; pathology ; Plasmacytoma ; complications ; Small Cell Lung Carcinoma ; Thyroid Gland ; pathology ; Thyroid Neoplasms ; pathology

OBJECTIVE:To reduce the types of drugs which was not consistent with the accounts in monthly checking of out-patient department,reduce the wastage of dismounted drugs and improve dismounted drug management. METHODS:Through qual-ity control circle(QCC),analyzing the reasons for inconformity of accounts and drugs,adopting relevant countermeasures of staff training,cipher prescription,counter storage,managed by designated person,expiry data management and so on,the process of dismounted drug management was formulated and implemented. The types of drugs which was not consistent with the accounts and activity growth value of circle members were analyzed statistically before,during and after QCC. RESULTS:The types of drugs which was not consistent with the accounts were 33.6,21.2 and 13.6 before,during and after QCC,decreasing by 59.5%. The ac-tivity growth value of circle members were all positive value. CONCLUSIONS:QCC of outpatient pharmacy can effectively reduce the types of drugs which is not consistent with the accounts in monthly checking,standardize dismounted drug management and im-prove pharmaceutical care quality.

Objective: This work aimed to construct stable MCF-7 cell sublines from which staphylococcal nuclease domain con-taining 1 (SND1) expression was interfered to analyze the effect of SND1 silencing on the proliferation and metastasis of MCF-7 cells. Methods: The lentivirus that could mediate SND1 silencing was prepared. MCF-7 cells were infected with the lentiviruses to construct stable sub-cell lines. Quantitative real-time polymerase chain reaction and Western blot analysis were employed to determine SND1 ex-pression level. MTS, wound healing, and transwell assays were applied to analyze the effect of SND1 silencing on the proliferation, mi-gration, and invasion of MCF-7 cells. Results: A lentivirus expression vector that contains sequences encoding shRNAs targeting SND1 and an shRNA negative control were successfully established. The lentiviruses (LV-SH1, LV-SH2, LV-SH3, and 和 LV-NC) were then collected and packaged. Stabilized MCF-7 sublines were prepared through infection with lentiviruses. The most efficient MCF-7 stable cell subline, MCF-SH3, was selected for SND1 silencing. Compared with the control cell, the proliferation, migration, and inva-sion potential of MCF-SH3 were significantly decreased. Conclusion: SND1 could promote the proliferation, migration, and invasion of breast cancer cells. Thus, silencing SND1 expression will inhibit such proliferation, migration, and invasion. These results indicated that the unusual expression of SND1 is associated with breast cancer and may participate in cancer progression by affecting prolifera-tion, migration, and invasion.