Objective To describe the pathogenic and serological test results of the plague in China from 2001 to 2009, and human and animal plague distribution. Methods Through access to information of the plague surveillance report in China from 2002 to 2010, national plague pathogenic and serological test results and the epidemic situation were analyzed from 2001 to 2009. Results From 2001 to 2009, 2966 strains of Yersinia pestis were isolated in the seven provinces which were Guizhou, Guangxi, Yunnan, Qinghai, Tibet, Gansu and Inner Mongolia. Of these, 1 138 000 animals were detected by bacteriological method, 1998 strains of Yersinia pestis were isolated;379 227 groups of intermediary animals were detected, 927 strains of Yersinia pestis were isolated;41 strains of Yersinia pestis were isolated from human body. Animal serums of 1 169 702 were detected by indirect hemagglutination assay(IHA), of these 3177 animal serums were positive, 168 human serums were positive;53 323 animal samples were detected by reverse indirect hemagglutination assay(RIHA), of these 500 were positive. There were outbreak or epidemic of plague in 9 types of plague foci, 2925 strains of Yersinia pestis were isolated. Two animals and 6 fleas were judged as new reservoir and new vector. There were 23 counties of 6 provinces were judged as plague new natural foci counties. Conclusions The plague epidemic in China is still serious between 2001 and 2009. There are nine types of foci in the active state.

Objective To summarize the imaging characteristics of the hepatic epithelioid hemangioendothelioma (EHE).Methods The clinical data of 6 patients with hepatic EHE who were admitted to the Yantaishan Hospital (3 patients), Zhangzhou Hospital of Traditional Chinese Medicine (2 patients) and Zhangqiu Hospital of Traditional Chinese Medicine (1 patient) between March 2007 and June 2014 were retrospectively analyzed.All the patients underwent plain scan and dynamic enhanced scan of computed tomography (CT), and the number,shape, size, location, density or signal, level and method of enhancement of the lesions were observed and analyzed.Six patients were followed up by outpatient imaging examination up to June 2014, and the changes of lesions were observed.Results Among the 6 patients, 1 solitary lesion and 5 multiple lesions were detected, and the total lesions were 125 including 1 patient with 75 lesions.The lesions were round or round-like and originated commonly from the right lobe of liver and hepatic subcapsular with a maximum diameter of 0.5-3.5 cm.Plain scan of CT showed that the lesions in 6 patients had low density with the clear boundary.MRI showed that low T1 WI signal and high or slightly high T2WI signal of the lesions were detected in 4 patients.Two patients had liver capsular retraction sign.The ring-like enhancement of 1 lesion and homogeneous enhancement of 5 lesions were found by dynamic enhanced scan of CT in 6 patients and enhanced scan of MRI in 4 patients.Enhanced signal in all the lesions was detected in the delayed phase.Veins into or through lesions were found in 3 lesions, with normal or narrowing vascular cavity.One patient had visible lollipop sign.Of the 6 patients, 5 were confirmed as with metastatic carcinoma of liver, and 1 was suggested as with cholangiocarcinoma.Six patients were diagnosed with hepatic EHE by pathological examination using hepatic biopsy technique.Among the 2 patients with hepatic EHE who didn't receive antineoplastic treatment after the diagnosis, 1 patient received CT examination at year 2 after first visit, which showed capsular retraction sign, and then was diagnosed as with secondary hepatic cirrhosis by MRI at 4 years after first visit.Another patient was diagnosed as with hepatic cirrhosis by CT examination at year 6.5 after first visit.One patient was diagnosed with tumor recurrence of hepatic left lobe by CT reexamination at postoperative year 4, and underwent ultrasound-guided radio frequency ablation (RFA) treatment based on no enlargement of tumor during 1-year follow-up, and then returned a normal condition after half year follow-up.Other 3 patients undergoing operation were followed up at postoperative year 1 , 4, 5 with no recurrence and metastasis.Conclusions Intrahepatic single or multiple nodules and delayed reinforcement by dynamic enhanced scan of CT and MRI are the typical imaging performances of hepatic EHE.There are certain characteristics in the liver the lollipop sign, capsular retraction sign and veins into or through the lesions.Mutual fusion and fibrosis of lesions leading ultimately to secondary liver cirrhosis may be characteristics of EHE growth.

AIM: To investigate in vitro effects of cholecystokinin octapeptide(CCK-8) on the expressions of B7.1 and B7.2 and the costimulatory activity of T lymphocytes in unstimulated macrophages.METHODS: Mouse peritoneal macrophages were isolated and incubated with CCK-8(10-12-10-6 mol/L) for indicated time.The B7.1 and B7.2 expressions of murine peritoneal macrophages were analyzed by flow cytometry.CD4+T cells were isolated from mouse spleen using immunomagnetic beads,and cultured with 1/4 numbers of macrophages which were pretreated with CCK-8 and/or anti-B7.1 antibody,anti-B7.2 antibody,CCK1R antagonist CR1409,CCK2R antagonist CR2945 for 24 h.ConA was added into the culture medium to stimulate CD4+T cell proliferation.The proliferation was determined by measuring -TdR incorporation in a ?-scintillation counter.RESULTS: B7.1 and B7.2 expressions and costimulatory activity of peritoneal macrophages were enhanced by CCK-8 in a dose-dependent manner,and the maximal effects occurred at the concentrations of 10-9 mol/L to 10-7 mol/L.Anti-B7.2 antibody,but not anti-B7.1 antibody,reduced the modulatory role of CCK-8 on costimulatory activity.Both CR1409 and CR2945 reversed the effect of CCK-8 on costimulation,and the role of CR1409 was more significant.CONCLUSION: CCK-8 enhances macrophage costimulatory activity by upregulating B7.2 expression,which is mediated by CCK1R and CCK2R.CCK1R might be the major receptor responsible for the modulation of CCK-8 on costimulation.

AIM: To study the effects of cholecystokinin octapeptide (CCK-8) on T-lymphocyte subsets in keyhole limpet haemocyanin (KLH)-immunized mice.METHODS: Female BALB/c mice were immunized with KLH and injected with different dosages of CCK-8 or saline simultaneously. Positive CD4+and CD8+ T cells in peripheral blood or splenocytes were measured by flow cytometry. The production and mRNA level of Th1 cytokine, IFN-? and Th2 cytokine, IL-4 in the splenocytes were evaluated by ELISA and RT-PCR, respectively. In addition, lung tissue sections were made with HE staining.RESULTS: CCK-8 downregulated the positive CD4+and CD8+ T lymphocytes both in peripheral blood and in splenocytes in KLH-immunized mice, resulting in the reduction of CD4+/CD8+ ratio.CCK-8 improved the production of IFN-?, elevated IFN-? gene transcription, whereas cut down the production of IL-4, decreased IL-4 gene transcription. CCK-8 lightened the pulmonary inflammation induced by KLH.CONCLUSION: CCK-8 inhibits CD4+T lymphocytes activation, Th2 cytokine mRNA expression and protein production in KLH-immunized mice, indicating that CCK-8 modulates adaptive immune response.

Aim To investigate the role of GC in indu-cing apoptosis of amygdaloid neurons.Methods Cul-turing primary neurons of amygdala,the neurons were identified by immunefluorescence techniques with anti-body against microtubule associated protein-2 (MAP2 ) and antibody against GC receptor.Using flow cytome-try to detect the effects of different concentrations of dexamethasone on the amygdala neuron apoptosis. Then the experiment was divided into four groups:CON ,DEX ,DEX +MIF and MIF .The rate of apopto-sis of the four groups was detected by TUNEL tech-nique and the expressions of BAX mRNA of four groups by Real-time PCR technique.Results (1 )Compared with the control group, the percentage of apoptotic cells increased significantly with DEX(10 -8 mol·L-1~10 -6 mol · L-1 )treatment in a concentration-de-pendent manner.(2)the TUNEL test showed that the percentage of apoptotic cells of DEX group increased significantly,compared with control group.While it decreased significantly in DEX+MIF group,compared with DEX group.There was no difference between MIF group and control group.(3 )Compared with control group,the expressions of BAX mRNA of DEX group increased significantly.While the expressions of BAX mRNA of DEX +MIF group decreased significantly, compared with the DEX group.There was no difference between MIF group and control group.Conclusion GC can independently induce the apoptosis of primary cultured neurons in the amygdala by combining with GC receptor.

AIM: To investigate the inhibitory effect s of a synthetic CRE-transcription factor decoy oligodeoxynucleotide (CRE-decoy ODN) on the upregulation of the expression of cholecystokinin (CCK) and fosB mRN A induced by chronic morphine administration in SK-N-SH cells. METHODS: The CRE cis-element, TGACGTCA, was palindromic, a sy nthetic single-stranded phosphorothioate oligodeoxynucleotide composed of the CR E sequence self-hybridizes to form a duplex/hairpin. The CRE-palindromic decoy a nd control oligodeoxynucleotides were added to the medium (1 h before exposure t o morphine) at 150 nmol/L in the presence of cationic lipid DOTAP. After the cel ls were treated with 100 ?mol/L morphine for 48 h, 10 ?mol/L naloxone was use d for 15 min. The effects of CRE-decoy ODN on the DNA-binding activity of CREB, the expression of CCK and fosB mRNA were detected by electrophoresis mobi lity shift assay (EMSA) and RT-PCR, respectively. The stability of cell-incorpo rated [ 32P]-labeled CRE-decoy ODN was extracted with phenol:chloroform a nd then subjected to 20% nondenaturing polyacrylamide gel electrophoresis and au toradiography. RESULTS: Chronic morphine administration and acute naloxone-prec ipitated withdrawal significantly activated the DNA-binding activity of CREB and the expression of CCK and fosB mRNA in SK-N-SH cells. The CRE-decoy ODN pen etrated into the cells, specifically downregulated these indexes. CONCLUSIONS: CRE-decoy ODN can significantly downregulates the e xpre ssion of CCK and fosB mRNA through specifically suppressing the DNA-binding activity of CREB activated by chronic morphine administration in SK-N-SH cells.

Objective To detect the Yersinia pestis plasmid and molecular weight along the Qinghai-Tibet Railway.Methods Yersinia pestis plasmids molecular weight detected and analyzed using alkaline lysis,phenol-chloroform extraction of Yersinia pestis plasmid by agarose gel electrophoresis.Results The 18 Yersinia pestis strains of Qinghai-Tibet Railway contained 6×106,45×106,52×106,65×106,92×106plasmid,varing in the range of the 52×106-92×106.Conclusions The Yersinia pestis of Qinghai-Tibet Railway has a standardplasmid graphics,with the biggest Yersinia pestis plasmid changing in a certain regular degree,which providessignificance in the study of plague natural foci of the spatial structure and the genetic.characteristics of Yersiniapestis.

Objective T o observe cardiac ultrastructure and the expression of heat shock protein 70 (H SP70) and hypoxia inducible factor-1α (H IF-1α) in electric shock death rats and to explore the application of these indexes as the basis of m edical identification in electric shock death. Methods Seventy-tw o SD rats w ere random ly divided into electric shock death group, postm ortem electric shock group and the control group. T he changes of m yocardial ultrastructure w ere observed by transm ission electron m icro-scope, and the expressions of m yocardial H SP70 and H IF-1α w ere observed by im m unohistochem ical technology. Results M yocardial m yofibril fracture, m itochondrial cristae and m em brane dissolution, and disordered arrangem ent of Z lines and M lines w ere observed in electric shock rats. H SP70 and H IF-1αw ere strong positive expressions in the electric shock death group, significantly com pared w ith the con-trol and postm ortem electric shock groups (P<0.05). Conclusion T he expressions of H SP70 and H IF-1αw ere obviously increased in electric shock death group, w hich m ay be used as the diagnostic indicator of electric shock death.

The T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) is an inhibitory receptor mainly expressed on active T-cells, or natural killer cells (NK cells) that activate negative stimulus signals in immune cells by combining with multiple ligands on the surface of target cells including tumor cells and infected cells. TIGIT plays an important regulatory role in the immune pathogenesis of tumors, viral infections and various autoimmune diseases by inhibiting the over activation of cells and the over secretion of proinflammatory cytokines. Recent researches show that TIGIT is highly expressed in T cells and NK cells of cancer patients, and is related to disease progression and poor clinical prognosis. Researchers try to enhance the activity of T cells or NK cells by blocking the binding of TIGIT and its ligand for therapeutic intervention. At present, there have been many reports about the use of anti-TIGIT monoclonal antibody treatment in different mouse tumor models leading to tumor regression, TIGIT has received extensive attention in cancer immunotherapy as a promising target for next generation cancer immunotherapy. Several clinical trials are currently evaluating the efficacy of anti-TIGIT monoclonal antibodies (mAbs) in patients with several cancers. The most advanced candidate, tiragolumab, has exhibited remarkable efficacy in programmed cell death ligand 1 (PD-L1)-positive non-small cell lung carcinoma (NSCLC) patients in phase Ⅱ clinical trials, in combination with PD-L1 blockade. However, the specific mechanism of TIGIT blockade remains to be fully elucidated.

AIM:To observe the changes in heme oxygenase-1(HO-1) expression in the lung after ischmia-reperfusion of hind limbs in rats.METHODS:Hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury was made by following reperfusion. Lung tissue was obtained from the animals subjected to sham operation, 4 h ischemia without reperfusion and 4 h, 8 h, 16 h, 24 h, 48 h reperfusion following 4 h ischemia. The levels of HO-1 mRNA and protein were measured at different times by Northern blot and Western blot. Immunohistochemistry technique was used to determine the cell types responsible for limb ischemic reperfusion induced HO-1 expression. RESULTS:After ischemia-reperfusion of limbs, HO-1 mRNA increased by 4 h, reached a peak at 16 h, and returned toward baseline at 24-48 h. This time course correlated with increased HO-1 protein. Immunohistochemical studies showed HO-1expressed in a variety of cell types, including the airway epithelium, alveolar macrophages and vascular smooth muscular cells. There were no positive signals in sham group and ischemia group both in mRNA levels and protein levels. CONCLUSION:The expression of HO-1 in the lung is not induced by limb ischemia or sham operation, but induced by limb reperfusion after ischemia in rats.