Venous thromboembolism ( VTE ) is a common vascular disease.It has become an important public health problem because of its high incidence, recurrence and mortality rate.Because the clinical symptom of VTE is relatively hidden, it is difficult to diagnose and treat it.This article focuses on the clinical diagnosis,treatment and laboratory examination of VTE.

Objective To study the relationship between the abnormality of mitochondrinl DNA (mtDNA) copy number and the clinical parameters and microsatellite instability (MSI) in colorectal cancer. Methods Total DNA was extracted from cancer and pericancer tissue from 50 colorectal cancer (CRC) biopsy samples. Non-ceding region sequencing was done and the copy number of mtDNA was quantitated with real-time PCR in mitochondrial NDI gene. The relationship between clinical indicators, mtMSI and mitochondrial copy number was detected. Results The mean copy number of mtDNA 312±185 in the tumor tissue was significantly lower than that 525±125 of the corresponding non-tumor tissue of these patients (P<0.001). No significant correlation was found between mtDNA copy number and other variables including age, gender, pathological type and clinical stage (P > 0. 05). However, there was a significant correlation between copy number and mtMSI (P<0.001). Conclusion There is a significant reduction of mtDNA in CRC patients, which may be caused by mtMSL

Objective To summarize the experience and efficiency of coils in endovascular aortic repair.Methods From September 2008 to December 2013,48 patients received endovascular aortic repair in combination of coil embolization including abdominal aortic aneurysm in 32 patients, and aortic dissection in 16.Results Coils were successfully implanted in all cases.One patient with ruptured abdominal aortic aneurism (AAA) underwent emergency endovascular aortic repair and died of multiple organ failure the day after surgery.One patient died of pulmonary artery embolization 3 hours after TEVAR.44 patients were followed up ranging from 7 to 60 months.In AAA group, 25 patients received endovascular exclusion in combination with internal iliac artery embolization, four of them had claudication due to gluteal ischemia but without other severe complications.Post-operative CTA found endovascular thrombosis in aneurysm.In the aortic dissection group, one patient died of pulmonary infection.During the follow up, there was no AAA dissection, and AAA rupture.Post-operative CT confirmed thrombus in cavity.There were no scaffold and coil translocation and surrounding tissue injury.Conclusions Endovascular aortic repair in combination with coil embolization is a complementary treatment to aortic diseases.

Objective To investigate the pathological characteristics of lymph nodes,liver and bone morrow in adult-onset still' s disease (AOSD).Methods The clinical data of three AOSD patients were collected and their biopsy of enlarged lymph nodes,liver and bone marrow were analyzed by histology and immunohistochemistry.Results In AOSD lymphadenopathy,there were high lymph node hyperplasia,partial architecture damage and an intense paracortical hyperplasia along with diffused infiltration of large immunoblasts,activated lymphocytes,Langerhans cells,histocytes,neutrophils and chronic inflammatory cells.Bone marrow biopsy showed a significant increase in the proportion of granulocytes and erythrocytes,with apparently increased segmented neutrophils.Hepatic biopsy showed hepatocellular spotty necrosis.Meanwhile,there was some infiltration of lymphocytes and neutrophils in the periportal fibrosis area.Immunohistochemical staining showed CD21 expression in lymphoid follicle remnants and B cell markers with few T markers in most of immunoblasts.Conclusion The pathological characterizations of lymph nodes,liver and bone marrow provide important clues to the diagnosis of AOSD as well as its differential diagnosis.

AIM To study if the activated T lymphocytes induced by hepatocellular carcinoma (HCC) rejection antigenic peptide SLIVHLNEV (mutant peptide of C met) pulsed dendritic cells (DCs) can provide protection against tumor challenge in nude mice HCC model and in vitro . METHODS SLIVHLNEV was eluted from HCC cell line HHCC by mild acid buffer and was identified by the mass spectrometry technique. SLIVHLNEV pulsed DCs isolated from HLA A2+ ruptured spleen were co cutured with isogeneic T lymphocytes. Cytotoxicity was tested using lactate dehydrogenase (LDH) release assay. The induced cytotoxic T lymphocytes (CTLs) were implanted into nude mice in order to protect them against transplanted HHCC tumor cells. The inhibition effect of CTLs on the growth of implanted tumor in nude mice was also observed. RESULTS The CTLs induced by SLIVHLNEV pulsed DCs had unique ability to kill HHCC tumor cells in vitro. They also protected the nude mice against the further challenge of HHCC tumor cells and inhibited the growth of implanted tumor. CONCLUSION DC based HCC rejection antigenic peptide SLIVHLNEV vaccine can induce powerful immune reaction both in nude mice HCC model and in vitro.

Aim To investigate radioprotective effects of platelet factor 4 (PF4) on hemopoiesis of mice after γ -ray irradiation and their mechanisms. Methods The mice were injected with PF4 twice at 6h intervals; and 20 h after the second injection they were given one irradiation of 7.5Gy 60Co γ -ray. 8d later the colony forming unit of granulocyte-macrophage (CFU-GM), colony forming of unit spleen (FU-S), number and DNA contents in bone marrow cells (BMCs) were examined by flow cytometry. Results 8d after irradiation, a significant difference was shown between DNA contents in BMCs and cell cycles of the PF4-injected mice and those of the irradiated mice (P∨ 0.01), whereas little difference was found between those of the irradiated mice and the controls (P∧ 0.05). Conclusion PF4 can obviously protect hemopoietic stem cells (HSCs) of mice from radiation injury and promote proliferation of HSCs after radiation.

Objective To evaluate the role of P2X3 receptors in dorsal root ganglion in development of incisional pain in rats.Methods Twenty-four healthy male SD rats weighing 200-220 g were randomly divided into 3 groups(n = 8 each): control group(group C),incisional pain(group IP)and P2X3 receptor antagonist + IP group(group A).In group IP and A,a 1 cm longitudinal incision was made in the plantar surface of left hindpaw according to the method described by Brennan et al.in isoflurane-anesthetized rats.P2X3 receptor antagonist TNP-ATP 200 nmol was injected into the plantar surface of left hindpaw 30 min after plantar incision was made in group A,while equal volume of normal saline was given instead of TNP-ATP in group C and IP.The behavior of the hindpaw of the rats were assessed using cumulative pain score within 1 h after injection.The animals were sacri ficed 2 h after injection and the dorsal root ganglion was removed for determination of P2X3 receptor expression and intracellular Ca2+ concentrations.ResultsThe cumulative pain scores,P2X3 receptor expression and Ca2 + concentrations were significantly higher in group IP and A than in group C(P ＜ 0.05).The cumulative pain scores,P2X3 receptor expression and Ca2+ concentrations were significantly lower in group A than in group IP(P ＜0.05).Conclusion P2X3 receptors in dorsal root ganglion is involved in the development of incisional pain through increasing intracellular Ca2+ concentrations in rats.

Objective:To investigate the expression and function of CD226 on NK s ubsets and its coexpression with other activation receptor and inhibition recept or on NK cells. Methods:The expression of CD226 on CD56 bright and CD56 dim NK subsets and coe xpress ion with CD16 and NKG2A in PBMC and MLC in the presence or absence of IL-2 or IL-15 were detected by double fluorescent staining and flow cytometry analysis. The level of IFN-? in the supernatants of PBMC culture and MLC treated with o r without IL-2 or IL-15 were evaluated by ELISA. 51Cr release assay w as employed to measure the specific lysis of NK cells killing target K562 cells. Results:CD226 was mainly expressed on CD56 dim NK subsets in PBMC. When s imulated by IL-2, CD226 expression was shifted to CD56 bright NK subsets, while IL-15 increased the subpopulation of NKG2A+CD226+double positive cell s. In MLC-generated NK cells, CD226 was mainly expressed on CD56 dim NK su bsets, and also shifted to CD56 bright NK subsets in the addition of IL-15 . Furt hermore, the percentage of CD16+CD226+和NKG2A+CD226+ subsets were increa sed when stimulated by IL-2 or IL-15. There was great increase in IFN-? lev el in the supernatants of PBMC culture in the presence of IL-2 or IL-15, but no difference in the supernatants of MLC treated with or without two cytokine s. Moreover, the cytotoxicity of NK cells in PBMC and MLC were greatly enhanced by IL-2 or IL-15. Conclusion:CD226 is mainly expressed on CD56 bright NK subsets in IL-2 or IL-1 5 activated NK cells, and is coexpressed with CD16 and NKG2A preferentiatly, whi ch maybe involve in the modulation of cytotoxicity of NK cells based on the balance of coexpressed activation and inhibition receptors. [

Objective:To study the effects of rat interleukin-10 (rIL-10) gene treatment on the expression of collagen , matrix metalloproteinase 13(MMP13) and their specific inhibitors the tissue inhibitor of metalloproteinase 1(TIMP1) in porcine serum in-duced liver fibrosis rats then to explore the anti-fibrotic effect of rL-10.Methods:Thirty SD rats were divided into normal control and fibrosis model group.Normal control group (group C) was intraperitoneally injected with 0.5 ml normal sodium twice a week for 8 week, while the fibrosis model group was injected with equal volume of pig serum for 8 week.At the beginning of the 5th week, fibrosis model group was further randomly divided into a fibrosis model subgroup ( group M ) , rIL-10 gene treatment subgroup ( group I ) and empty vector control subgroup(group P).Rats in group C and M were injected with Ringer’s solution as a reagent control via the tail vein weekly, rats in group I were injected with the rIL-10 plasmid pcDNA3-rIL-10, and rats in group P were injected with empty vector pcDNA3.All rats were sacrificed at the end of 8th week, and the liver tissue samples were collected to observe deposition of collegan in liver tissue by sirius red staining and detected the expression of MMP 13 and TIMP1 in the liver tissue by SP immunohistochemistry .Re-sults:Sirius red staining showed that the area of the collegan deposition was dramatically increased in fibrosis model subgroup and emp -ty vector control subgroup compared with the normal control group , and the area of the collagen deposition was dramatically decreased in rIL-10 gene treatment subgroup compared with the fibrosis model and empty vector control subgroup .Immunohistochemistry analysis showed that the expression of MMP 13 and TIMP1 in fibrosis model subgroup and empty vector control subgroup was significantly higher than the normal control group , but compared with normal control group , expression of MMP13 was significantly increased and expres-sion of TIMP1 was significantly decreased in rIL-10 gene treatment subgroup .Compared with fibrosis model subgroup and empty vector control subgroup, the expression of MMP13 and TIMP1 was dramatically decreased in rIL-10 gene treatment subgroup.Conclusion:rIL-10 gene treatment attenuates the area of collagen deposition in liver fibrosis rats associated with downregulation of TIMP 1.

AIM: To study the role of hypoxia precondit io ning (HP) in hypoxia-reoxygenation (HR)-induced apoptosis in neonatal rat cardio myocytes and the possible mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were divided into three groups: normal group, HP+H/R group and H/R group. Acridine orange (AO) sta ining was performed to detect morphological changes of apoptotic cells. Apoptosi s rates of cardiomyocytes were detected by flow cytometry. Colorimetric assay wa s used to detect caspase-3 activity. Expression of Bcl-2 protein was detected by immunohistochemistry combined with computer image analysis. RESULTS: Apoptotic cells were detected by AO staining after hypo xia of 6 h followed by 3 h-reoxygenation. The hypodiploid apoptotic peak was det ected by flow cytometry with the apoptotic rates of (29.7?5.4)%. A significan tly reduced apoptotic rates of (7.8?1.3)% was detected in HP group(P