Objective To study butylphthalide on acute cerebral infarction with leukoaraiosis patients cognitive function. Methods 80 patients with acute cerebral infarction combined with leukoaraiosis in Yuncheng Central Hospital from June 2014 to June 2015 were selected, all patients had cognitive dysfunction, and randomly divided into study group and control group with 40 cases in each group. The two groups were given conventional treatment of cerebral infarction, the study group was given the butylphthalide soft capsules two tablets, three times once day orally for three months, we used MMSE and MoCA scale to assess the cognitive status of the patients in the two groups at four, eight, and 12 weeks after treatment. The changes of liver function during treatment were analyzed. Results In the treatment, the two groups of patients with MMSE were improved, in four weeks of treatment, the MMSE scores of the study group was higher than the control group, but there was no significant difference between the two groups, eight weeks and 12 weeks, the MMSE scores of the study group was significantly higher than the control group, and the difference between the two groups was statistically significant (P<0.05), the MOCA score of patients in the study group gradually become normal, and significantly higher than the control group, after treatment for four weeks, eight weeks and 12 weeks the difference was statistically significant (P<0.05), the study group patients first had abnormal liver function in the treatment, recovered after stopping the medication. Conclusion Butylphthalide can improve the cognitive function of patients with acute cerebral infarction combined with leukoaraiosis, the increase of transaminase caused by treatment has no significant effect on clinical medication, which is worthy of further popularization and application.

Objective To construct a shRNA lentiviral vector targeting the gene encoding tumor necrosis factor alpha-induced protein 8 (TNFAIP8) in RAW264. 7 cells, a mouse macrophage cell line, and to investigate the effects of TNFAIP8 gene silencing on the functions of mouse macrophages. Methods The shRNA sequence targeting TNFAIP8 gene was designed and DNA oligos containing small hairpin frame was synthesized. The double-stranded DNA was cloned into pLKO. 1-TRC vector after annealing. The recombi-nant vector was verified by using double enzyme digestion and gene sequencing. Lentiviruses were prepared by transfecting the constructed vector into 293T cells. Fluorescent quantitative RT-PCR and Western blot as-say were performed to detect the expression of TNFAIP8 at mRNA and protein levels after infecting the RAW264. 7 cells with lentiviruses. Flat dish adhesion experiment and wound-healing assay were used to evaluate the effects of TNFAIP8 gene silencing on the adhesion and migration of RAW264. 7 cells. Results The recombinant lentiviral vector was successfully constructed as indicated by double enzyme di-gestion and gene sequencing analysis. The expression of TNFAIP8 in RAW264. 7 cells at both mRNA and protein levels were significantly down-regulated after lentivirus infection (P<0. 05). Moreover, TNFAIP8 gene silencing significantly impaired the cell adhesion ability of RAW264. 7 cells after 15 min, 30 min or 2 hours of culture. Compared with the cells in control group, the RAW264. 7 cells harboring silenced TN-FAIP8 gene looked round with a smaller number of cellular extensions. The wound-healing assay showed that less TNFAIP8 gene-silenced RAW264. 7 cells migrated into the wounded area as compared with the cells in control group after 24 hours of culture (P<0. 05). The wound-healing rates of the experimental and control groups were 25% and 50%, respectively. Conclusion The recombinant lentiviral vector containing shRNA targeting the TNFAIP8 gene was successfully constructed. Transfecting the RAW264. 7 cells with the con-structed vector significantly silenced the expression of TNFAIP8 gene and inhibited the adhesion and migra-tion of these cells.

Objective To study clinicopathologic features of ALK-positive large B-cell lymphoma.Methods The clinical data,histopathological characteristics,immunophenotype and fluorescence in situ hybridization (FISH) result of a patient with ALK-positive large B-cell lymphoma were analyzed and discussed combined with related literatures.Results A 30-years-old male patients with the left neck lymphadenectasis was studied.Histological evaluation revealed the tumor grew in sheets in the nodal,with round nuclei,dispersed chromatin,a single prominent central nucleolus and moderate amounts of eosinophilic to amphophilic cytoplasm.The neoplastic cells exhibited immunoblastic/plasmablastic morphology.Immunohistochemistry measurement showed that the tumor cells were marked positively by CD138,ALK-1,CD45RO,CD4,Perforin,CD117 and Kappa proteins,while negatively by CD3,CD8,CD20,CD30,CD38,CD57,CD79a,Pax-5,EMA and AE1/AE3 proteins.FISH test demonstrated the presence of ALK gene translocation.The patient was given 4 cycles of CHOP chemotherapy after surgery.However,the conditions deteriorated after 4 months.Now the patient continued to receive treatment.Conclusion ALK-positive large B-cell lymphoma represents a distinct variant of diffuse large B-cell lymphoma,and the tumor has special histological features along with a distinct immunophenotype and ALK gene rearrangement.

Aim To study the in virto interaction o f Cefathiamidine in combination with Ciprofloxacin against clinical isolates of Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis. Methods The activity of each drug alone was determined against all the isolates. Chequerborad synergy testing was then performed against all the isolat es. Results The percentage of the FIC index less than 0.5, from 0.5 t o 1,from 1 to 2,more than 2 was 53.3%～93.3%,6.7%～46.7%,0%,0% respectiv ely. Conclusion Synergism and additivity of cefathiamidine comb ined with ciprofloxacin respectively against 90 strains of Gram positive cocci w ere the main inter actions, there were little autonomy and no antagonism.

Exfoliative cytology is a required course for medical diploma students majoring in pathological diagnosis and technology. However there exist no ready-made teaching materials to use or teaching models to follow.This paper discusses the attempts made to achieve preferable teaching result by formulating syllabus based on training scheme by carefully picking teaching content,combining case analysis with multimedia instruction and making new method of assessment.

Objective To investigate the expression and clinical significance of p63, CD_(44v6) and human papilloma virus (HPV) 16/18 in carcinoma of cervix and precancerous lesion and to study their role in the pathogenesis of the infiltrative carcinoma of the cervix(ICC). Methods 145 patients were selected, among whom were 60 cases of ICC, 55 cases of cervical intraepithelial neoplasia (CIN) and 30 cases of normal cervical epidermis (NCE). Immunohistochemistry streptavidin peroxidase (SP) was used to detect the expressions of p63 and CD_(44v6) protein and hybridization in situ was used to measure HPV 16/18 gene on tissue microarray. Results HPV 16/18, p63 and CD_(44v6) in ICC were significantly higher than those in CIN and NCE groups (P < 0.05). The expressions of HPV 16/18 gene in CIN I 、CIN II and CIN III were 27.3 % , 43.8 %, 70.6 % respectively. p63 protein was mainly expressed in squamous cell carcinoma, but not in adenocarcinoma. p63-positive rate was related to the grade of squamous cell carcinoma and clinical stage. CD_(44v6) positive rate was related to the pathological grade and clinical stage. Moreover, the positive rate of lymph node metastasis was significantly higher than the cases without metastasis (P <0.05). The expression of HPV16/18 was positively correlated with that of p63 in ISCC (P <0.05, Cp =0.49). Conclusion HPV16/18 possibly participate in the pathogenesis and progress of cervical squamous carcinoma. p63, as the cancer gene, may participate in the occurrence and development of cervical cancer caused by HPV 16/18. p63 could be a differentiation indicator of cervical squamous carcinoma, and it could be one of the markers which would be differentiated into squamous cell in malignant tumour. CD_(44v6) could be used as one of the indicators of distant metastasis of cervical cancer.

Objective To investigate the dysregulation of HER-2 protein and gene in non-small cell lung cancer (NSCLC), and to identify the association between clinicopathological features,prognosis and HER-2 aberrations amongst protein and gene. Methods 140 NSCLC tissues (89 squamous cell carcinoma, 51 adenocarcinoma) with operative section and detailed case were taken from pathology department of Shanxi Cancer Hospital from Jan 2006 to Feb 2007, while 70 normal tissues were set as control group. Immunohistochemistry was applied to detect the state of HER-2 protein expression,and fluorescence in situ hybridization (FISH) was applied to test the status of gene amplification. Results In normal and NSCLC tissues, over-expression of HER-2 was detected in 0 case and 17 (12.14 %) cases (P < 0.05), respectively. The over-expression of HER-2 was associated with the pathological type of NSCLC, which was detected more frequently in adenocarcinoma (χ2 = 4.19, P = 0.04), rather than the gender, age, smoke history, clinical stages, and lymphatic metastasis of patients. 40 (28.57 %) cases presented HER-2 gene copy number ≥3, including 6 (4.29 %) patients with HER-2 gene amplification, 34 (24.29 %) patients with HER-2 gene multicopy. HER-2 gene amplification was associated with the pathological type (P = 0.024), smoke history (P = 0.048) and age (P = 0.015), rather than lymphatic, gender, clinical stages. None clinicopathological features were presented correlation with HER-2 gene multicopy (P > 0.05). There was no significantly difference in survival between patients with and without HER-2 protein over-expression and HER-2 gene dysregulation (P > 0.05). HER-2 protein over-expression was associated with HER-2 gene amplification (P > 0.05), while no relationship between HER-2 protein overexpression and HER-2 gene multicopy (P < 0.01). Conclusions The over-expression of HER-2 is related to pathological type of NSCLC with more frequent expression in adenocarcinoma. The incidence rate of HER-2 gene amplification in patients with adenocarcinoma histology, never-smokers, and young age is high. The HER-2 protein over-expression and gene dysregulation show no relation with the prognosis of NSCLC.

Objective To investigate the protein expression and genetic alterations of c-myc in primary systemic anaplastic large cell lymphoma (ALCL) and discuss its relationship with clinicopathologic features and immunophenotypes.Methods 87 cases of ALCL were selected.Immunohistochemical method was used to detect the protein expression of c-myc,ALK,CD3,CD10,CD20,CD30 and EMA.c-myc and ALK genetic alterations were detected by using fluorescence in situ hybridization (FlSH).The interrelationships between protein expression,genetic alterations and clinicopathological parameters were analysed statistically.Results Immunohistochemical results:of 87 cases,ALK protein was expressed in 54 cases (62.1％).c-myc protein was expressed in 27 cases (31.0 ％).ALK and c-myc were co-expressed in 20 cases (23.0 ％).c-myc protein expression,ALK and c-myc co-expression increased with the upgrade of ALCL clinical stages,and the expression was higher in International Prognostic Index (IPI) high-risk groups than in low-risk groups (P ＜ 0.05).FISH test results:of 87 ALCL cases,there were 50 cases (57.5 ％) of ALK rearrangements and 19 cases (21.8 ％) of ALK aneuploidy.c-myc rearrangement was detected in none of 87 ALCL cases,but there was aneuploidy in 19 cases (21.8 ％).The differences of c-myc aneuploidy in ALK positive and negative groups were statistically insignificant (P ＞ 0.05),while they were statistically significant in c-myc groups (P ＜ 0.05) and in different IPI groups (P ＜ 0.05).Conclusion c-myc protein expression and aneuploidy were related with ALCL clinical stages and IPI,which could be used as an indicator of estimating ALCL malignant degree and predicting prognosis.

Objecitv e To investigate the effects of a recombinant protein osteoclast inhibitory lectin related protein 2( OCILRP2)-Fc on LPS-induced endotoxemia by blocking OCILRP 2 signaling pathway and to in-vestigate the roles of OCILRP2 during inflammation.Methods Real-time PCR was used to detect OCILRP2 ex-pression at mRNA level in RAW264.7cells before and after in vitro stimulation with LPS.A mouse model of en-dotoxemia was established by intraperitoneal injection of BALB /c mice with a median lethal dose of LPS .Two hours prior to LPS treatment, mice were intraperitoneally injected with OCILRP2-Fc, human IgG or PBS, re-spectively .Several parameters including the survival rate of BALB/c mice with and without LPS treatment , spleen weight for arterial hyperemia analyzing , histopathological changes of lung and liver by HE staining , serum levels of inflammatory cytokines (IL-6, IL-12, TNF-αand IFN-γ)by ELISA , NF-κB activity by Western blot, were analyzed .Results Real-time PCR showed that LPS elevated in vitro OCILRP2 expression at mRNA level in macrophages (P<0.05).Upon the treatment of OCILRP2-Fc, BALB/c mice suffered from endotoxemia showed obviously increased survival rate , decreased spleen hyperemia , attenuated pathological injury of lung and liver, reduced levels of IL-6, IL-12, TNF-αand IFN-γin serum samples (P <0.05) as compared with mice treated with human IgG and PBS .LPS induced NF-κB p65 phosphorylation and IκB degradation were inhibited by OCILRP2-Fc treatment.Conclusion OCILRP2-Fc protects mice from endotoxemia by blocking OCILRP 2 signaling, which suggests that OCILRP2 plays an important role in LPS induced inflammation.

Objective To assess the value of computed tomography (CT) and magnetic resonance imaging (MRI) in the diagnosis of pancreatic neuroendocrine neoplasms (PNEN) and to analyze the factors influencing thepreoperative imaging diagnosis of PNEN.Methods From January 2016 to November 2016, patients with PNEN diagnosed by surgery and biopsy were collected. CT and MRI data of them were analyzed. The CT values or signal intensity of the lesions and the pancreatic parenchyma were measured and the contrast-to-noise ratio (CNR) of the lesion was calculated. Detecting sensitivity and diagnosis accuracy of CT and MRI were compared. Detecting sensitivity of different MRI sequences was also analyzed. Diagnosis accuracy of non-functional PNEN and functional PNEN was compared and analyzed. Lesion CNR was compared between arterial phase and portal venous phase of the contrast enhanced CT. The sensitivity, accuracy and constituent ratio were compared by nonparametric analysis. Independent sample t test and one-way analysis of variancewere performed for the quantitative parameters comparison. Results A total of 54 patients with 56 lesions of PNEN were included for two of whom had two lesions each. CT and MRI were both performed in 44 patients (46 lesions).Detecting sensitivity and diagnosis accuracy of CT were 97.8% (45/46) and87.0% (40/46), respectively. Detecting sensitivity of MRI were 97.8% (45/46) and89.1% (41/46), respectively. There was no significant difference in detecting sensitivity and diagnosis accuracy between CT and MRI (both P>0.05). The CNR of lesion in arterial phase was higher than that of portal venous phase(4.7±3.8 vs 3.4±2.5), and the difference was statistically significant (t=2.949, P<0.05). Detecting rates of T1 weighted imaging with fat suppression (T1WI-FS) image, T2 weighted imaging with fat suppression (T2WI-FS) image, diffusion weighted imagingand dynamic contrast enhanced T1WI-FS image were 90.0% (45/50), 88.0%(44/50), 86.0%(43/50), and 91.7% (44/48), respectively. There was no significant difference in detecting rate among these images sequences (Q=2.526, P=0.510). Tumor diameter in non-functional PNEN was significantly larger than that in functional PNEN ((2.9±1.6) cm vs (1.7±0.7) cm)(t=3.479,P<0.05). The overall diagnosis rate of non-functional PNEN with CT and MRI before operation was 70.8% (17/24), which was significantly lower than that of functional PNEN (100.0%, 31/31) (χ2=10.360，P=0.002).Conclusions CT and MRI are both sensitive in detectingPNEN, and they were two complementary modalities. CT image in arterial phase delineated the lesion better than that in portal venous phase. MRI images with different sequences can becomplementary and there is no significant difference in detecting sensitivity for PNEN among different sequences. CT and MRI play an equal rolein the diagnosis of PNEN before operation. Because of atypical CT and MRI findings, the diagnosis of non-functional PNEN is more difficult thanfunctional PNEN.