AIM: To investigate the effects of pioglitazone , a peroxisome proliferator-activated receptor γ( PPARγ) agonist, on the cognitive impairments and inflammatory cytokine production induced by isoflurane in aged mice . METHODS:Male C57BL/6J mice ( 11-month-old, n =136 ) were assigned randomly into 5 groups: control group ( Con) , isoflurane group ( Iso) , 10 mg/kg pioglitazone +isoflurane group ( Pi10+Iso) , 20 mg/kg pioglitazone +isoflu-rane group (Pi20+Iso) and 20 mg/kg pioglitazone alone group (Pi20).The mice in all isoflurane-treated groups were ex-posed to oxygen mixed with 1.4%isoflurane for 2 h.The mice in Con group and in Pi20 group were exposed to oxygen only for 2 h.Pioglitazone was suspended in 1% carboxymethyl cellulose (CMC).Pioglitazone (10 mg/kg or 20 mg/kg) was gavaged 2 h prior to the exposure of isoflurane or oxygen alone .The same volume of 1% CMC was gavaged in Con group and in Iso group.Fear conditioning tests were performed to determine the learning and memory abilities 48 h after isoflurane exposure.Fresh cerebral cortice and hippocampi were dissected to measure the protein expression of PPAR γby Western blotting, and the contents of IL-1βand TNF-αwere analyzed by ELISA 6 h after isoflurane exposure .RESULTS: Com-pared with Con group, the response of freezing behavior decreased (P<0.05) and IL-1βcontent in the hippocampus in-creased ( P<0.05) in Iso group.Compared with Iso group , the response of freezing behavior and PPARγprotein expres-sion level had no significant change ( P>0.05) in Pi10+Iso group, but the response of freezing behavior and PPARγpro-tein expression level increased significantly (P<0.05) and IL-1βcontent in the hippocampus decreased (P<0.05) in Pi20+Iso group.IL-1βcontent in the cerebral cortex and TNF-αlevels both in the cerebral cortex and the hippocampus showed no significant difference among all groups (P>0.05).CONCLUSION:Pioglitazone attenuates cognitive impair-ments and the elevates the level of IL-1βin the hippocampus induced by isoflurane in aged mice .

Dendritic cells act as the major antigen presenting cells in the body and play a central role in intri-guing the adaptive immune response. Protective immunity against schistosome and immuno-pathological response in host caused by eggs are both closely associated with Th2 response. Further understanding on immune mechanism will contribute to the development of vaccines against schistosome infection, as well as the relief of the pathological lesion in schistosomiasis. This article discusses the central role of dendritic cells in the mechanism of Th2 response induced by schistosome (including eggs).

ObjectiveTo observe the efficacy of maintenance hormonal treatment after response to chemotherapy in advanced breast cancer. Methods8 patients with advanced breast cancer were treated with chemotherapy,maintenance hormonal therapy were given after response to chemotherapy.The efficacy was evaluated every 2 cycles of chemotherapy and 2 months of endocrine therapy according to RECIST standard.Results8 patients received chemotherapy for 2-8 cycles (median 4 cycles). All patients got PR, the duration of chemotherapy was 1-6 months (median 2 months), the time to failure of chemotherapy was 4 months. Until the last follow-up day (31th December 2010), the time to progression was 6-86 months (median 13.5 months).Survival was 6-86 months(median 21.5 months).Seven patients quit the chemotherapy due to severe side effects of hematologic toxicity,fatigue or nausea vomiting.One patient died because of allergy to paclitaxol.Conclusion Maintenance hormonal treatment after patients with metastatic breast cancer response to chemotherapy may prolong the duration of effective therapy and improve the QOL.

Objectives To study the effect of VIM in Enterovirus 71 (EV71) infection of (human brain microvascular endothelial cells (HBMEC) and elaborating the mechanism of EV71 infection in the nervous system. Methods Knocked out the VIM by CRISPR technology , the differences in EV71 absorption , replication , release between wild VIM and VIM knocked-out (VIM-KO) HBMEC were detected by fluorescence quantitative PCR. Results 4 ℃ absorption experiment conformed that EV71 adsorption in VIM- KO is 40% less than in the normal HBMEC. After EV71 infect HBMEC for 48 h (48 h p. i.), the quantitative PCR result showed intracellular viral RNA in VIM-KO was only 1/12 of that in the normal HBMEC. Also the extracellular viral RNA was quantified, and the number of cells in VIM-KO had been reduced 1.4 times compared with the normal HBMEC. Conclusions Once VIM knocking out, EV71 attachment has been obviously reduced. Meanwhile, the level of viral RNA replication and release are decreased compared with the normal HBMEC. VIM may be an attachment receptor of EV71 in HBMEC , when the virus invades HBMEC with the binding of VIM. Moreover , VIM plays an important role in the replication and release of EV71.

Cryptosporidium spp.are protozoan parasites that infect the epithelial cells of the gstrointestinal tract of hosts.In humans,cryptosporidiosis is usually a self-limiting infection in immunocompetent individuals,but severe diarrhea and dissemination to extra-intestinal sites can occur in high-risk individuals,such as the very young,the elderly,immunedeficiency individuals,particularly in HIV-positive patients.So far,molecular epidemiological data have confirmed the presence of 30 species and over 40 genotypes with genus Cryptosporidium,with 21 species and genotypes being found in humans.The majority of human cryptosporidiosis cases are responsible for C.hominis and C.parvum.Human cases caused by C.meleagridis,C.ubiquitum,C.felis and C.canis have been increasing.Besides that,with data accumulation of molecular epidemiology of human cryptosporidiosis,some more Cryptosporidium species and genotypes were newly identified in humans.This paper mainly reviews epidemiology status of these new emerging Cryptosporidium species and genotypes in humans.

Objective To observe the effects of Hedan tablet on cytokines and oxidation factors in APOE-/-mouse, and to explore its effect on atherosclerosis and to explore its behind mechanism. Methods APOE-/-mice (n=50) were randomly divided into control group, model group, low dose Hedan tablet treatment group, high dose Hedan tablet treatment group and simvastatin treatment group. Mice in control group were given normal feed while mice in other groups were fed with high cho?lesterol diet. Hedan or Simvastatin was administrated intra-gastrically while normal saline was given to model group in the same route. After 12 weeks, mice were sacrificed to observe the mRNA level of tumor necrosis factor-α(TNF-αmRNA) in aorta by RT-PCR. Mean while, serum levels of interleukin-1 (IL-1), interleukin-10 (IL-10), malonaldehyde (MDA) and su?peroxide dismutase (SOD) were determined in different groups. Results Compared with control group, TNF-αmRNA tran?scription level as well as serum levels of IL-1 and MDA significantly increase while serum levels of IL-10 and SOD de?creased remarkably in model group, (P<0.01). Compared with model group, mRNA levels of TNF-αas well as serum levels of IL-1 and MDA were significantly decreased while serum levels of IL-10, SOD were greatly increased in low dose and high dose Hedan tablet treatment groups as well as in simvastatin treatment group (P<0.01). Conclusion Hedan tablet inhibit the formation of atherosclerosis through its anti-oxidation role and anti-inflammation role.

Aim To investigate the effect of isoflurane on the phosphorylation of p38 mitogen-activated protein kinase (MAPK)in the hippocampus of neonatal rats, and the effect of p38 MAPK pathway on isoflurane-in-duced neuronal apoptosis.Methods Forty-eight neo-natal rats on postnatal day 7 were assigned randomly into four groups:DMSO group (group Air +DMSO), p38 MAPK inhibitor SB203580 group (group Air +SB20 ),isoflurane +DMSO group (group Iso +DM-SO),and isoflurane +SB203580 group (group Iso +SB20 ).Rats were exposed to air or isoflurane (volume fraction of 0.01 1 )for 4h.The p38 inhibitor SB203580 (20 nmol)or DMSO (volume fraction of 0.1 )5μl was intraventricularly administered 30 min before the expo-sure.The brains of some rats in each group were per-fused and embedded by paraffin 6h after the exposure. Neuronal apoptosis in the hippocampal CA1 area was detected by terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL)(n =6). The hippocampal tissues of the other rats in each group were dissected 6h after the exposure,and the protein expressions of phospho-p38 (p-p38 ),p38,cleaved caspase-3,phospho-NF-κB (p-NF-κB ),Bcl-2 and Bax were detected by Westem blot (n =6).Results The number of TUNEL positive cells in the hippocam-pal CA1 region in group Iso +DMSO increased by 4.8 fold compared with that in group Air +DMSO (P <0.01 ),while the number of TUNEL positive cells in group Iso +SB20 decreased by 3 /5 compared with that in group Iso +DMSO (P <0.01 ).The protein expres-sion of cleaved caspase-3 in group Iso +DMSO signifi-cantly increasd (P =0.003)compared to that in group Air +DMSO,which was significantly decreasd in group Iso +SB20 (P =0.007 ).In addition,isoflurane also increased the protein expression of p-p38,p-NF-κB and Bax,decreased the level of Bcl-2,and reduced the ratio of Bcl-2 /Bax compared with control animals (P <0.01 ,P =0.004,P <0.01 ,P <0.01 ,P <0.01 ,respectively).Howerver,SB203580 partly at-tenuated the isoflurane-induced protein change above. Conclusion Isoflurane induces neuroapoptosis in neo-natal rat hippocampus by the activation of p38 MAPK pathway.

Objective To observe the destroyed architecture of splenic lymphoid follicles in mice infected with Schistosoma japonicum by immunohistochemistry. Methods The mice infected with S. japonicum(20 cercariae/mouse)for 8 weeks were sacrificed,and the splenic samples were paraffin embedded and sliced. The sections were first stained by hematoxylin and eosin to observe the massive structure of splenic lymphoid follicles,and then B cells,follicular dendritic cells(FDC)and germinal center cells were labeled with anti-B220,anti-CD21 or anti-Ki67 antibodies respectively by immunohistochemistry to observe the distribution of the specific cells of lymphoid follicles. Results The results of HE staining showed that the structure of lym-phoid follicles in spleens of infected mice was blurred,the number and area of follicles were significantly reduced compared to those of the normal mice. The immunohistochemical staining showed that the splenic T/B lymphocyte segregation ,FDC network and germinal centers of the infected mice all disappeared. Conclusion The structure of splenic lymphoid follicles in the mice infected with S. japonicum is obviously damaged.

To preliminarily study the pro⁃angiogenic activity of Echinococcus granulosus hydatid cysts against hu⁃ man umbilical vein endothelial cells in vitro and the transcriptional level of potential pro⁃angiogenic factors. Methods The hydatid cysts and protoscolex derived from experimentally infected mice were collected and cultured in vitro，then the human umbilical vein endothelial cells were stimulated by the supernatant and cyst fluid respectively，and the angiogenesis was observed and analyzed through a microscope and the angiogenesis mode of the software NIH Image J. Meanwhile，the mouse homologous proteins of matrix metalloproteinase⁃9（MMP⁃9）and high mobility group box B1（HMGB1）were identified in E. granulosus genome through sequence alignment，and their transcriptional levels in the cyst wall and protoscolex were analyzed. Results The culture supernatant of hydatid cysts significantly promoted human umbilical vein endothelial cells into tubes（F = 73.03，P < 0.001），the transcriptions of MMP⁃9 and HMGB1 were detected in the cyst wall and protoscolex，and the transcriptional level of MMP⁃9 was higher in protoscolex（t = -11.65，P < 0.001），while the level of HMGB1 was higher in hydatid cysts（t = 6.43，P = 0.003）. Conclusion Some parasite⁃derived pro⁃angiogenic molecules may exist in the supernatant of E. granulosus hydatid cysts，while further researches are required into their exact mechanisms.

Objective:This study aims to evaluate the clinical effect and adverse reactions of oxaliplatin or irinotecan plus capecitabine treatment for colorectal liver metastases. Methods:Data from 125 cases of colorectal liver metastasis patients were continuously enrolled and randomized into two groups, i.e., 63 in group one (treatment group) and the other 62 in group two (the control group). Capecitabine was administered at 1 000 mg/m2 doses, twice a day from d1 to d14, to all patients. Irinotecan was administered at 150 mg/m2 in d1 to group one, and oxaliplatin was administered at 130 mg/m2 in d1 to group two. The drug administration cycle lasted for 21 days in both regimens, with at least 6 administration cycles. The total course was for 6 months at most. The therapeutic efficacy, median progression-free survival time, median survival time, short-term clinical effect, and adverse drug reaction were monthly determined. Results:The overall response rates and disease control rates were 33.3%and 66.7%in group one, respectively, and 35.5%and 70.9%in group two, respectively, with no significant differences between the groups (P>0.05). The median survival time and median progression-free survival time were 14 months and 5 months in group one, respectively, and 12 months and 5 months in group two, with no significant differences between the two groups (P>0.05). The level-Ⅲand-Ⅳadverse drug reactions mainly include hematological toxicity, gastrointestinal reactions, and hand-foot syndrome. The diarrhea frequency is obviously higher in group one than in group two, and the difference between the two groups is sta-tistically significant (P<0.05). No significant differences were observed in the other adverse reactions between the groups (P>0.05). Conclusion:The Oxaliplatin or Irinotecan plus Capecitabine treatment is effective for colorectal liver metastases, which enhances survival rate and reduces patient suffering because of it has less side effects and good tolerance. The treatment must be further generalized and clinically applied.