Objective To summarize the clinical features,neuroimaging findings and pathological characteristics of demyelinating pseudotumors(DPT)of the brain,and to differentiate it from glioma. Methods The clinical features,neuroimaging findings and pathological characteristics of 35 patients with demyelinating pseudotumors of the brain were summarized,and the diagnosis for 18 of them was confirmed by bioscopy.Results Demyelinating pseudotumors affected adults of both sexes.The onset age of patients ranged from 9 to 69 years old.There was no definite antecedent,and the clinical syndromes were atypical. Neuroimaging scans showed multiple lesions in cerebral hemisphere,while the lesion in brain stem and spinal cord was single.The symptom and neuroimaging were not parallel.While with many or large lesions, the symptoms and signs were less.The lesions were not enhanced on CT scan,but appeared round or patch enhancement on MRI scan.Nine patients with DWI all appeared high density.The myelin basic protein was useful for diagnosis.The typical pathological changes were demyelination,perivascular inflammatory infiltration and reactive gliosis.The Creutzfeuldt cells were also found in these patients.The lesions might become small or disappear after treatment,but could not serve as the criterion to exclude brain neoplasm. Conclusions DPT is a distinct demyelination disease entity,which is confusable with brain neoplasm.It is difficult to distinguish DPT from brain neoplasm with the clinical features and conventional neuroimaging scan.But DWI scan is useful.The pathological changes accord with demyelination,and Creutzfeuldt cells are also found.It is important to apply corticosteroid treatment or biopsy rather than being anxious to excise the lesions.

Objective To analyze the clinical,imaging and pathological features of cortical vein thrombosis (CoVT).Methods Three cases of cortical vein thrombosis were diagnosed in our hospital from February 2010 to October 2012.We reviewed and summarized their clinical manifestation,radiological feature and pathological characteristics.Results All patients were young with acute onset.The main clinical manifestations included headache,epilepsy or limbs weakness.Two cases had intracranial hypertension.One case had decreased activity of protein S.One had increased plasma homocysteine.Brain computed tomography scan showed hypodensity lesion with some hyperdensity inside.Cranial routine magnetic resonance imaging showed long signal in T1-weighed image and T2-weighed image,with occasional short T1 signal inside.Contrast-enhanced magnetic resonance imaging revealed heterogeneous enhancement.All of 3 cases underwent brain biopsy because of the suspected diagnosis of brain tumor.Brain pathology showed the local necrosis and hemorrhage,dilated small vein with congestion or thrombosis.Neuronal degeneration,hyperplasia of gliocyte,hyperplasia of endotheliocyte in small blood vessels with reaction of histiocytes was also displayed.Duration from initial visit to final diagnosis was from 14 days to 2 months.Conclusions CoVT has various clinical and radiological manifestations and it is easy to misdiagnose as brain tumor.Careful analysis of clinical and imaging data could improve its diagnostic accuracy.Brain biopsy would also be helpful for diagnosis.

Objective To investigate the correlation between the expression of adhesion molecule CD146 and the vulnerability of carotid atherosclerotic plaque.Methods The plaque samples were collected from 40 patients who underwent the carotid endarterectomy and were divided into the stable plaque group and the instable plaque group by ultrasound imaging.Five carotid artery samples were taken from the healthy donors as the control.Immunohistochemistry was applied to test the CD146 expression in all samples.Results Higher expression of CD146 was observed in the atherosclerotic plaques than in the healthy control.Moreover,statistical difference was found in the expression of CD146 in the plaques between the instable plaque group and the stable plaque group (0.31 ± 0.19 vs 0.17 ± 0.07,P ＜ 0.05).The expression of CD146 was positively correlated with the necrotic area (r =0.471 8,P =0.019 9) and the matrix metalloproteinase (MMP)-9 expression in the plaques (r =0.535 6,P =0.000 9).Conclusion The CD146 expression is correlated with the vulnerability of carotid atherosclerotic plaque.

Objective To observe the effects of Dengzhanhua Capsule on kidney tissue inflammatory cytokines in chronic renal failure rats;To explore its possible mechanism for the efficacy in chronic renal failure. Methods Sixty SD rats were randomly divided into normal control group, model group, benazepril group and Dengzhanhua group, 15 rats in each group. Chronic renal failure rat model was established by Platt 5/6 nephrectomized. Benazepril (0.29 mg/100 g) was given to rats in the benazepril group by gastrogavage. Dengzhanhua Capsule (0.3 g/100 g) was given to rats in the Dengzhanhua group by gastrogavage. Normal saline was given to rats in the normal group and the model group by gastrogavage. The whole treatment period was twelve weeks. Expressions of TGF-β1 and PAI-1 were determined by semi-quantitative RT-PCR after treatment. Concentrations of kidney tissue inflammatory cytokines IL-6 and TNF-α were determined by ELISA. Results Expressions of TGF-β, PAI-1 and IL-6, TNF-αin benazepril group and Dengzhanhua group were significantly lower than those in model group (P<0.05). Compared with benazepril group, it was significantly lower in Dengzhanhua group (P<0.05). Conclusion Dengzhanhua Capsule can reduce kidney tissue inflammatory in chronic renal failure rats, and inhibit renal fibrosis.

Objective To observe the effect of exposure of emphysema with intermittent hypoxia on oxidative stress injury of myocardial cells in rats. Methods Sixty male Wistar rats were divided randomly into four experimental groups(each n=15). The normal control group was bred normally. The emphysema group was exposed to cigarette smoke twice a day(once 30 minutes). The intermittent hypoxia(IH)group was exposed to intermittent hypoxia circumstance 8 hours/day,and the emphysema with IH group was exposed to cigarette smoke twice a day (once 30 minutes)and intermittent hypoxia circumstance 8 hours/day. Each group was exposed for 8 weeks. At the beginning of 9 weeks,the blood gas analysis was performed in 5 rats selected randomly from each group,and the rest rats were sacrificed and their hearts and lungs were taken. Under light microscope,the lung tissues stained with hematoxylin-eosin(HE)were examined. The lung pathology and the results of blood gas analysis showed that the emphysema with IH rat model was established successfully. The levels of malonaldehyde(MDA)and superoxide dismutase(SOD)in rat myocardium were measured by enzyme-linked immunosorbent assay(ELISA),and the subunit p22phox mRNA expressions of nicotinamide adenine dinucleotide phosphate(NADPH)-oxidase were detected by real-time reverse transcription-polymerase chain reaction(RT-PCR). Results Compared with the normal group, the MDA levels and p22phox mRNA expressions were increased obviously in emphysema group, IH group and emphysema with IH group〔MDA(μmol/g):2.93±0.54, 3.58±0.63, 4.51±0.72 vs. 1.75±0.56, p22phox mRNA:0.043±0.004,0.067±0.015,0.123±0.016 vs. 0.018±0.002,all P<0.05〕,but the activities of SOD were decreased significantly(U/mg:36.07±4.79,33.51±7.12,24.29±5.36 vs. 46.08±5.12,all P<0.05). In emphysema with IH group,the increase of MDA levels and p22phox mRNA expressions and decrease of SOD levels were more remarkable compared with those in emphysema group and IH group(all P<0.05). The expression of p22phox mRNA was positively correlated with MDA level(r=0.734,P<0.001). Conclusion The myocardial tissue oxidative stress injury in rats induced by emphysema with intermittent hypoxia exposure is more serious than that induced by exposure of either emphysema or intermittent hypoxia alone,NADPH oxidase possibly being the important medium of myocardial cell response to oxidative stress.

Objective To analyze the role of cysteinyl aspartate specific proteinase-1 (caspase-1) in a mouse model of D-galactosamine (D-GalN) and lipopolysaccharide (LPS) induced acute liver failure (ALF) and to study the possible mechanism. Methods C57BL/ 6 mice were randomly divided into four groups including control group, Z-WEHD-FMK (caspase-1 inhibitor) treatment group, ALF model group and Z-WEHD-FMK-treated ALF group. The mouse model of ALF was established by intraperitoneally injec-ting the mice with D-GalN (450 mg/ kg) and LPS (10 μg/ kg). The damages in liver tissues were evaluated based on the histopathological examination and the levels of alanine transaminase (ALT) and aspartate trans-aminase (AST) in serum samples. Western blot assay was performed to analyze the expression of caspase-1 and the phosphorylation of glycogen synthase kinase 3β (GSK-3β). The qRT-PCR was used to measure the expression of inflammatory cytokines at transcriptional level. Results The expression of caspase-1 at both mRNA and protein levels were gradually increased during the development of ALF. Compared with the mice with ALF, those in the Z-WEHD-FMK-treated ALF group showed less severe liver damages on histopatholog-ical examination and decreased levels of ALT and AST in serum samples [ALT: (479. 2±39. 5) U/ L vs (998. 5±60. 4 ) U/ L, P<0. 05; AST: ( 478. 5±28. 6) U/ L vs ( 1 180. 7±91. 4) U/ L, P<0. 05]. The expression of TNF-α, IL-1β, IL-18 and IL-33 at transcriptional level were significantly suppressed in mice with ALF upon the Z-WEHD-FMK intervention. Results of the Western blot assay indicated that Z-WEHD-FMK suppressed the activities of GSK-3β by enhancing its phosphorylation. Conclusion This study demon-strated that caspase-1 could promote the activation of GSK-3β resulting in the development of inflammation responses and liver damages during the development of ALF in mice.

Objective To investigate the effects of peroxisome proliferator-activated receptor α( PPARα) on macrophage-mediated inflammatory responses with the interference of lipopolysaccharide and the possible mechanism.Methods The bone marrow stem cells were isolated from the femora of mice.The granulocyte-macrophage colony stimulating factor ( GM-CSF) was used to stimulate the in vitro differentiation from bone marrow stem cells into primary macrophages.An in vitro model with cultured cells expressing in-flammatory cytokines was established by treating the primary macrophages with lipopolysaccharide ( LPS) .A specific chemical agonist, Wy-14643, was used to activate PPARα. Autophagy inhibitors including 3-methyladenine (3-MA) and small interfering RNA against Atg7 ( Atg7 siRNA) were used to inhibit the autophagy.Western blot assay was performed to detect the expression of autophagy-related proteins ( Atg5, Atg7, Beclin-1 and LC3).The transcriptional levels of TNF-α, IL-1β, IL-6, Atg5, Atg7 and Beclin-1 were analyzed by qRT-PCR.Results Compared with the macrophages treated with LPS alone, those pretreated with various concentrations of Wy-14643 (10 μmol/L, 25 μmol/L and 50 μmol/L) showed inhibited ex-pression of proinflammatory cytokines ( TNF-α,IL-1βand IL-6) and enhanced expression of autophagy-relat-ed proteins (Atg5, Atg7 and Beclin-1) at mRNA level in a dose-dependent manner.The expression of auto-phagy-related proteins (Atg5, Atg7, Beclin-1 and LC3) by macrophages was promoted with the pretreatment of Wy-14643 as indicated by Western blot assay.The transcriptional levels of TNF-α, IL-1βand IL-6 were increased in Wy-14643 pretreated-macrophages after stimulation with 3-MA or Atg7 siRNA .Conclusion PPARαsuppressed the macrophage-mediated inflammatory responses by promoting autophagy, suggesting that the PPARα-autophagy pathway might be one of the signaling pathways regulating LPS induced-inflamma-tory responses.

Objective To analyze the clinical,imaging and pathological features of cortical vein thrombosis (CoVT). Methods Ten patients with CoVT (4 patients with CoVT alone and 6 patients with CoVT and venous sinus thrombosis)treated at Navy General Hospital from January 2006 to Jun 2013 were collected retrospectively.Its etiology,imaging,and pathological features of brain tissue in 3 patients were analyzed. Results Of the 10 patients with CoVT,3 were female and 7 were male.Their mean age was 31 ± 15 years old.(1)Brain CT scan and MRI showed hemorrhagic cerebral infarction,and contrast-enhanced MRI showed scattered heterogeneous enhancement within lesions. DSA could find CoVT at different parts.(2)3 patients underwent brain biopsy because they were initially diagnosed as brain tumor. Pathological examination showed glial cell,endothelial proliferation and phagocytic reaction.Scattered spotty bleeding was observed,and significant expansion of small veins,A few of them had blood stasis and thrombosis. Conclusion CoVT is one kind of intracranial venous thrombosis. It is more common occurred in young and middle aged adults,and most of them were venous sinus thrombosis.It is caused by retrograde thrombosis and spread to cortical veins.CoVT is easily to be misdiagnosed as brain tumor.Combination of clinical and imaging findings is needed for accurate diagnosis.

Objective To evaluate the efficacy of itraconazole oral solution for prevention of invasive fungal infection ( IFI ) in neutropenic patients with acute leukemia after chemotherapy.Methods Clinical data of 136 neutropenic patients with acute leukemia after chemotherapy at the Department of Hematology,Nanfang Hospital from January 2008 to December 2010 were retrospectively analyzed.Patients were divided into itraconazole group ( n =67 ) and control group ( n =69).There were 36 patients with acute nonlymphocytic leukemia ( ANLL),31 with acute lymphoblastic leukemia (ALL) in itraconazole group;while in control group,there were 30 patients with ANLL,38 with ALL and 1 with biphenotypic acute leukaemia (BAL).Patients in itraconazole group received intraconazole after chemotherapy until the neutrophil count was increased to 0.5 × 109/L or the body temperature returned to normal and without any imaging evidence of IFI.The incidence of IFI and clinical features were compared between the groups using SPSS 13.0 software.Pearson x2 test was used for nominal variables,for measurement data,t (normal distribution) or Mann-Whitney U (skewed distribution) test were used.Results There were 12 cases ( 17.9％ ) suffering from IFI in itraconazole group and 32 cases (46.4％) in the control group (x2 =12.59,P ＜ 0.01 ).For ANLL patients,the incidence of IFI in itraconazole group was significantly lower than that in control group ( 16.7％ vs.56.7％,x2 =11.53,P ＜0.01 ).In itraconazole group,the incidence of IFI in female patients was significantly lower than that in male patients ( 8.6％ vs.28.1％,x2 =4.35,P ＜0.05 ).And for the female patients,the incidence of IFI in itraconazole group was significantly lower than thatin the control group (8.6％ vs.44.7％,x2 =11.98,P＜0.01).Conclusion Itranconzole oral solution can effectively prevent IFI in neutropenic patients with acute leukemia after chemotherapy,especially for the female patients with ANLL.

AIM:To explore the regulatory effect of chemokine CCL 3 on exosome secretion from human bone marrow mesenchymal stem cells(hBMSCs).METHODS: hBMSCs were stimulated with chemokine CCL 3 at different concentrations in vitro.The proliferation of hBMSCs was measured by CCK-8 assay and viable cell counting.Exosome se-cretion from hBMSCs was qualitatively analyzed by transmission electron microscope(TEM)and flow cytometry, and the quantitative analysis was carried out by flow cytometry and nanoparticle tracking analysis(NTA).RESULTS:Compared with control group,the viability of the hBMSCs detected by CCK-8 assay was increased when hBMSCs were treated with CCL3(P<0.05).The results of viable cell counting demonstrated that the number of hBMSCs was raised in CCL 3 group in a dose-dependent manner(P<0.05).The results of flow cytometry showed that hBMSCs expressed 3 CCL3-related spe-cific receptors,CCR1,CCR5 and CCR9.Compared with control group,the fluorescence intensity of CCR9 in CCL3 group was obviously enhanced.However,no significant difference of fluorescence intensity for CCR 5 and CCR1 was observed be-tween the 2 groups.The results of NTA demonstrated that the secretion capacity of CCL 3-induced hBMSCs was far less than that in control group(P<0.05).However, the microvesicles larger than 100 nm in CCL3 groups were increased(P<0.05).The above results indicated that the higher concentration of CCL 3 induced the lower secretion of exosomes.In addi-tion,the results of flow cytometry demonstrated that CCL 3-induced hBMSCs showed lower quantity of CD 9 +exosomes than those in control group(P<0.01).CONCLUSION:CCL3 promotes the proliferation of hBMSCs but depresses the secre-tion of exosomes in a dose-dependent manner.CCL3 affects the size distribution of exosomes and increases the number of nonfunctional microvesicles of larger than 100 nm in size.CCL3 induces the expression of CCR9 in hBMSCs.