Granulocyte macrophage-colony stimulating factor (GM-CSF) is a muhifunctional growth factor. It stimulates the proliferation, differemiation and maturity of hematopoietic progenitor cell (HPC), and transfers from bone marrow to periphery, inducing multiple cell proliferation or differentiation. In recent years, some studies have indicated that GM-CSF plays an important role in anti-apoptosis, inducing neuronal differentiation and angiogenesis, which will he a new supplement to the treatment of ischemic cerebrovascular disease. This article reviews the effects of GM-CSF in the treatment of ischemic cerebrovascular disease.

After the merozoite entered the erythrocyte,the membrane debris in the parasitophorous vacuoles of early ring form was passed out through a narrow external aperture in erythro-cyte to the exterior.The trophozoite was oval or irregular in shape.Ingestion of host cell cytoplasm occurred cystostomally.The asexual parasite possessed acristate mitochondria and was surrounded by a single-membraned pellicle.The gametocyte possessed cristate mitochondria and was surrounded by two unit membranes.The cytoplasm of mature macrogametocytes contained many ribosomes,mitochondria and osmiophilic bodies and a small nucleus while microgametocytes contained fewer ribosomes,osmiophilic bodies and mitochondria and a large nucleus.Three characteristic morphological alterations were observed within the host cells,that is,small vesicles,cytoplasmic cleft and caveola-vesicle complex.The clefts within the cytoplasm of the host erythrocytes were present in all human malarial parasites.The small vesicles distributed all over the cytoplasm were surrounded by a unit membrane.The caveola-vesicle complex consisted of caveolae was surrounded by small vesicles and probably corresponds to a Schuffner's dot.(Figs.1-13)

Objective To study the mithridatism of VMAT 2 in transgeneic CHO cell.Methods Using technology of transgene from PC 12 to CHO, MTT reduction assay was used to detect the toxic effect on MPP + to wtCHO and cDNACHO,meanwhile the role of reserpine was observed,including the toxic effect to MPP + on specific blocking agent of VMAT 2.Results cDNACHO to the sensitivity of MPP + was much less than that of wtCHO over concentration of 0.5 mmol/L MPP +; cDNACHO had the same sensitive as wtCHO to rotenon;after the reserpine was added,the above role disappeared,but wtCHO reserpine was given alone,it couldn't change its sensitivity to MPP +.Conclusion VMAT 2 has protective effect on cDNACHO by transporting MPP + to vesicles; PC 12 possesses the antitoxic components.

Objective To investigate the relationship between tumor necrosis factor-α (TNF-α) in ischemic brain tissue and bran edema after cerebral ischemia-reperfusion in rats.Methods Eighty four male SD rats were randomly assigned to either a cerebral ischemia reperfusion group (n =44) or a sham-operation group (n =40). A model of middle cerebral artery occlusion for 120 minutes followed by reperfusion was induced in rats using the suture method. The infarct size was determined by 2, 3, 5-triphenyi terazoloride (TTC) staining at 6 h,24 h, 3 d, and 7 d respectively after the reperfusion. Dry-wet weight method was used to measure brain water content and evaluate the extent of brain edema. The enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of TNF-α in ischemic brain tissue. Results TNF-α level in ischemic brain tissue was increased at 6 h (445.8 ±91.7 pg/ml) after the reperfusion, and reached the peak at day 3 (715.5 ±121.3 pg/ml). There were significant differences compared to the sham-operation group and other time points (all P＜0.001). After that, it was decreased gradually, but it was still higher than that in the shamoperation group at day 7 (478.1 ± 145.5 pg/ml vs. 148.5 ± 101.7 pg/ml, P＜0.005). The initial change of the water content in brain tissue lagged behind the increased TNF-α. It did not increase significantly until 24 h after cerebral ischemia-reperfusion (P ＜0.001). It reached the peak at day 3 (P ＜0.001), and it was still higher than that in the control group at day 7 (P ＜0.05). The evolution of cerebral infarct volume was in accordance with the changes of TNF-α level. Conclusions TNF-α is associated with the changes of brain edema and infarct volume,and it is harmful to brain tissue.

Objective To investigate the effect of songling xuemaikang(SL-xmk)pretreatment on the expression of matrix metalloproteinase-9(MMP-9)after focal cerebral ischemia-reperfusion in rats.Methods A total of 45 male Sprague-Dawley rats were randomly allocated into SL-xmk pretreatment,sham operation,and normal saline control group.Preventive gavage was per-formed for 8 weeks in rats using SL-xmk(937.50 mg/kg)suspension in the SLxmk pretreatment group(n = 15);the preventive gavage was performed in rats using the equal volume of normal saline in the sham operation(n = 15)and normal saline control(n = 15)groups.At the end of the pretreatment process,a model of middle cerebral artery occlusion(MCAO)in rats was induced by suture method for 2 hours and reperfusion for 24 hours.The effects of SL-xmk pretreatment on the neurologic deficit scores after transient MCAO,brain water content,and infarct volume in rats were observed.Immunohistochemical staining was used to detect the MMP-9 immunoreactive positive cells in ischemic brain tissue.Results The neurologjc deficit scores(1.21 ± 0.25 vs.2.37 ± 0.35,P = 0.000),the brain water content (76.24% ± 7.09% vs.88.78% ± 6.57%,P = 0.000),the percentage of infarct volume (22.62% ±2.17% vs.27.84% ±3.43%,P =0.000),and the numbers of MMP-9 positive cells(16.20 ± 2.17/mm vs.20.60 ± 2.71/mm,P = 0.000)were all significantly lower than those in the control group.Conclusions SL-xmk pretreatment may significantly inhibit the expression of MMP-9 in the brain tissue of focal cerebral ischemia-reperfusion rats and reduce brain water content and infarct volume.

Objective To determine the frequency of depression in patients with Parkinson' s disease(PD) and healthy controls over 50 years of age and to analyze the characteristics and influencing factors of PD with depression(PDD) in Nanjing.Methods One hundred and twenty-six PD patients were diagnosed and assessed using Self-rating Depression Scale (SDS) and Hamilton Depression Scale (HAMD).The frequency,characteristics and influencing factors of depression were statistically analyzed,and the factor analysis of HAMD was carried out.Also,one hundred and twenty-four healthy subjects over the age of 50 were selected as the control group.Ressults The incidence of depression in PD group was 48.4％ ( 61/126):15.1％ (19/126) for mild depression,27.8％ (35/126) for moderate depression,5.6％ (7/126) for severe depression.The incidence of depression in the control group was 9.7％ (12/124):5.7％ (7/124) for mild depression,2.4％ (3/124) for moderate depression,1.6％ (2/124) for severe depression.There was a significant difference between these two groups( x2 =45.36,P ＜ 0.01 ).Univariate and Logistic regression analysis revealed that a high frequency of depression occurred in patients with long PD duration,high H-Y stage and UPDRS Ⅲ.According to each factor analysis of HAMD,the scores of cognitive impairment,tardiness,anxiety and sleep disturbances of the PD patients with depressive syndromes were higher than that of the control group.Conclusion Depression is a relatively common complication of PD in Nanjing which is associated with long PD duration,severity of motor disturbances and increasing H-Y stage.

Background::Thoracic aortic aneurysm (TAA) is a fatal cardiovascular disease, the pathogenesis of which has not yet been clarified. This study aimed to identify and validate the diagnostic markers of TAA to provide a strong theoretical basis for developing new methods to prevent and treat this disease.Methods::Gene expression profiles of the GSE9106, GSE26155, and GSE155468 datasets were acquired from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using the "limma" package in R. Least absolute shrinkage and selection operator (LASSO), support vector machine-recursive feature elimination (SVM-RFE), random forest, and binary logistic regression analyses were used to screen the diagnostic marker genes. Single-sample gene set enrichment analysis (ssGSEA) was used to estimate immune cell infiltration in TAA.Results::A total of 16 DEGs were identified. The enrichment and functional correlation analyses showed that DEGs were mainly associated with inflammatory response pathways and collagen-related diseases. Collagen type I alpha 1 chain ( COL1A1) and synaptotagmin like 2 ( SYTL2) were identified as diagnostic marker genes with a high diagnostic value for TAA. The expression of COL1A1 and SYTL2 was considerably higher in TAA vascular wall tissues than in the corresponding normal tissues, and there were significant differences in the infiltration of immune cells between TAA and normal vascular wall tissues. Additionally, COL1A1 and SYTL2 expression were associated with the infiltration of immune cells in the vascular wall tissue. Single-cell analysis showed that COL1A1 in TAA was mainly derived from fibroblasts and SYTL2 mainly from cluster of differentiation (CD)8 + T cells. In addition, single-cell analysis indicated that fibroblasts and CD8 + T cells in TAA were significantly higher than those in normal arterial wall tissue. Conclusions::COL1A1 and SYTL2 may serve as diagnostic marker genes for TAA. The upregulation of SYTL2 and COL1A1 may be involved in the inflammatory infiltration of the vessel wall and poor extracellular matrix remodeling, promoting the progression of TAA.