0.05),but significantly lower than control group when run-out L-CN(P

BACKGROUND: The conventional X-ray imaging has low absorption contrast for lymphoedema, and the resolution is about mm level, which is not conducive to early diagnosis. Micro-imaging of biological soft tissues can be achieved by phase-contras imaging technique. OBJECTIVE: Using synchrotron radiation in-line phase contrast imaging technique to achieve the lymphoedema model imaging and observe the lesions characteristic of lymphatic vessels. DESIGN, TIME AND SETTING: Observational experiment. The lymphoedema model was prepared at the Capital Medical University from May to June in 2009. And the experiment was completed in Shanghai Synchrotron Radiation Facility (SSRF) BL13W1 in June 2009. MATERIALS: Five New Zealand rabbits were prepared for lower extremity lymphoedema models. METHODS: The lower extremity lymph node eradicates operation was performed on rabbits to result in lower extremity lymphoedema. And the synchrotron radiation in-line phase contrast imaging technology was used to collect the projected image of specimens within the 180°, and to reconstruct three-dimensional image. MAIN OUTCOME MEASURES: Severity of lymphatic vessels and the wall thickness. RESULTS: The lymphatic vessel was swollen, bent and distorted. And the lymphatic vessel generates lateral branches in order to promote lymphatic drainage, which was clearly observed from the image obtained by phase contrast imaging technology.CONCLUSION: The use of synchrotron radiation type coaxial imaging technology can be achieved for lymphedema model for micro-imaging, which has certain significance to the early diagnosis of lymphedema.

Objective To evaluate the relationship between intestinal metaplasia (IM) and helicobacter pylori infection in elderly patients with chronic gastritis. Methods The patients over 60 years old and diagnosed as chronic gastritis by endoscopy from January 2008 to December 2009 were divided into two groups by pathological appearance. One group was chronic gastritis with IM (IM group), the other was chronic gastritis without IM (NIM group). The infection of helicobacter pylori, activity of inflammation, atrophy of gland, and folliculus lymphaticus in gastric mucosa were observed. Results The infection of helicobacter pylori, infiltration of neutrophil and atrophy ratio of gland were significantly higher in IM group than in NIM group (52.7% vs. 37.3%, 35.5% vs.24.0 %, 36.6 % vs. 3.5%, x2 = 10. 677, 7.641, 95. 606; P = 0. 001, 0. 006, 0. 000, respectively).There was no statistical difference in presentation of folliculus lymphaticus between IM group and NIM group (x2 = 0.003, P=0. 957). The infiltration of neutrophil and presentation of folliculus lymphaticus were significantly higher in helicobacter pylori positive patients than in helicobacter pylori negative patients (45.8% vs. 14.8%, 42.6% vs. 4.2%, both P=0.000). Conclusions The appearance of IM seems to be related with helicobacter pylori infection, activity inflammation and atrophy of gland. The presentation of folliculus lymphaticus seems to be closely related with helicobacter pylori infection. The eradication treatment of helicobacter pylori infection in the elderly chronic gastritis patients should be strengthened.

Objective: The present study investigates the effects of Tanreqing injection, a compound Chinese herbal medicine, on the proliferation of leukemia cells in vitro and discusses the potential mechanisms. Methods: Tanreqing injection was diluted to a series of concentrations (1:2, 1:4, 1:8, 1:16, 1:32, 1:64, 1:128, 1:256 and 1:512) by volume and then independently applied to treat chronic myeloid leukemia K562 cells and T cell acute lymphocytic leukemia Molt4 cells at the proliferative stage. Cell growth was observed at different time intervals under a microscope. Cell proliferation was determined by cell counting kit-8 assay and the survival curve was delineated. The inhibitory rate and the half inhibitory concentration (IC50) were calculated. Molt4 cells were stained with propidium iodide (PI) and PI/Annexin V and then the cell cycle and apoptosis were analyzed by using flow cytometry. In addition, a real-time quantitative polymerase chain reaction was subjected to detect the expressions of apoptosis-related genes (bcl-2 and caspase-3) after Tanreqing treatment. Results: Tanreqing injection had inhibitory effects on the proliferation of K562 cells and Molt4 cells. The most toxic concentrations were observed between 1:2 and 1:16 where cells were almost necrotic. The inhibitory effect manifested in a concentration- and time-dependent manner. The IC50 of K562 and Molt4 was 1:333 and 1:142, respectively. After 1:32 Tanreqing injection treatment for 72 h, the number of Molt4 cells in the S phase significantly decreased (P<0.05), and the apoptosis rate markedly increased (P<0.05). In addition, increased caspase-3 expression and decreased bcl-2 expression were also observed (P<0.05). Conclusion: Tanreqing injection can both inhibit the proliferation and promote the apoptosis of leukemia cells in vitro, whereby the potential mechanism seems to be mediated in part by decreasing S phase ratio, down-regulating bcl-2 expression and up-regulating caspase-3 expression.

Objective To examine whether tissue inhibitor of metalloproteinases-1 (TIMP-1) is involved in arterial calcification of chronic renal failure (CRF) rats. Methods CRF model was induced in male Wistar rats by garage daily with 2% adenine 250 mg/kg. The calcification of aorta, femoral artery, renal artery and coronary artery was evaluated histomorphometrically by van Kossa-stained sections at 2-, 4-, 6- and 8-week respectively. RT-PCR and Western blot were used to observe the expressive levels of TIMP-1 mRNA and protein. Expressions of TIMP-1, osteopentin (OPN) and core binding factor α1 (Cbfα-1) protein were analyzed by immunhistochemistry. Results Serum urea nitrogen, creatinine, inorganic phosphate, calcium-phosphorus product and intact parathyroid hormone (iPTH) increased significantly in the model animals compared with control group after 2 weeks (P<0.01). Medial calcification was found in above four arteries of model groups after 6 weeks. RT-PCR and Western blot showed that TIMP-1 expression of model group was significantly higher than that of control group (P< 0.05), and obviously elevated in a time-dependent manner. The expression of TIMP-1 and OPN in calcified aortic smooth muscle cells increased obviously (P<0.05), and positive immunostaining of Cbfα-1 was found. The expression of TIMP-1 was positively correlated with OPN and Cbfα-1 (r=0.317, P=0.000; r=0.485, P=0.000). Conclusions The pathology of arterial calcification in CRF rats induced by adenine is similar to CRF patients, which may serve as a useful model of CRF with arterial calcification. The up-regulation of TIMP-1 seems to participate in the formation and development of vascular calcification in CRF.

The effect of diet with various fatty acid composition on insulin resistance in male OLETF ratswas observed. The results showed that it was beneficial to insulin sensitivity in rats fed with ? 3 polyunsaturated fatty acid rich food.

Objective To make a systematic review of pressure ulcers risk factors in critically ill patients. Methods We systematically reviewed all articles related to the pressure ulcers risk factors in critically ill patients. The Cochrane Library, PubMed, EMBASE, Web of Science Core Collection, CNKI, WANFANG and SinoMed were searched to August 2016. Results In total, 13 eligible articles were included. These studies included 18, 184 critically ill patients, six studies were classified as high quality, and seven were classified as moderate quality. Risk factors for the development of pressure ulcers include age, ICU stay, diabetes, mean arterial pressure<60-70 mmHg (1 mmHg=0.133 kPa), mechanical ventilation and mechanical ventilation, drugs, sedation and postural changes. Conclusions There is no single factor that can explain the occurrence of pressure ulcers. So it is in a variety of factors interaction, the occurrence of a significant increase in risk.

Bromodomain and extra-terminal domain(BET)Bromodomain has become a new target for the treatment of cancers and other human disorders. Nowadays,several classes of its potent and selective small-molecule inhibitors have been identified,many of which are in clinical trials. Preclinical and clinical data have shown that BET Bromodomain inhibitors have good prospects. Howev-er,there are potential therapeutic deficiencies,such as drug resistance. At present,attempts are being made to develop BET Bromodo-main inhibitors and degraders based on polypharmacology,combining BET Bromodomain with other targets of different mechanisms. In this paper,small-molecule kinase/BET inhibitors,small-molecule histone deacetylases(HDAC)/BET inhibitors and BET protein degraders are reviewed,which may provide guidance for further research on BET protein.

Objective To investigate the accumulation and maturation status of pulmonary conventional dendritic cells (cDCs) in the early phase of acute lung injury (ALI),and to explore the way of the inflammatory responses and lung injury modulated by cDCs in vivo.MethodsMale C57BL/6 mice were randomly ( random number) divided into the normal control group,6 h-ALI group and 24 h-ALI group.Murine model of ALI was made by intra-tracheal administration of lipopolysaccharide (LPS) and lung specimens were taken 6 h or 24 h later.The accumulation and maturation status of pulmonary cDCs were assessed by flow cytometry.IL-6 and TNF-α were quantified to evaluate the lung inflammation.Transcription factors T-bet/GATA-3 mRNA ratio was determined to estimate the balance between Th1/Th2 responses.IFN-γand IL-4 were quantified to evaluate Thl-specific and Th2-specific cytokine production respectively.Lung injury was estimated by lung wet weight/body weight ratio (LWW/BW) and histopathological assessment.Comparison between groups was performed using one -way ANOVA.ResultsCompared with normal control group,LPS challenge resulted in higher level of IL-6 and TNF-α,increased LWW/BW ratio and significant histopathological changes (P ＜0.01 ).The accumulation and maturation of pulmonary cDCs in 6 h-ALI group were significantly increased after LPS challenge (P ＜0.01 ),while the accumulation and maturation of pulmonary cDCs in 24 h-ALI group were significantly lower than that in 6 h-ALI group ( P ＜0.01 ).Compared with normal control group,the expression of T-bet mRNA in 24 h-ALI group was markedly enhanced ( P ＜ 0.01 ) and the production of IFN-γ was increased as well ( P ＜ 0.01 ).ConclusionsThe accumulation and maturation of pulmonary cDCs peaked within 24 h after LPS challenge,pulmonary cDCs may initiate and amplify acute lung inflammation of ALI by enhancing the Th1 immune response and ensuing cytokine production.

Objective To investigate function of Arg327Ile (R327I) and Arg327Ala(R327A) FⅨ mutants and to study the molecular pathogenesis of haemophilia B(HB) caused by R3271 mutation.Methods Hygromycin-resistant cell line was screened and the secretion of FⅨ antigen into the medium was measured by ELISA.The cell line with appropriate expression levels of F Ⅸ antigen was selected for culture.Recombinant F Ⅸ (rF Ⅸ ) was purified from concentrated medium by two step methods of Q-Sepharose Fast Flow and anion exchange chromatography.The concentration and purity of rF Ⅸ were determined by ELISA and SDS-PAGE,respectively.The activation of wild-type ( WT),R327I and R327A of rFⅨ by FⅦa/TF/Ca2+ or FⅪa/Ca2+ was identified by Western blot in different time periods.The FⅨa and FⅧa complex formed by interaction with different concentrations of FⅧa was used to activate F X,the apparent dissociation constant (Kd) for FⅧa binding was calculated by the kinetic results.The kinetic data of the activation of FX by WT,R327I and R327A FⅨa with or without FⅧa were calculated.Results The amount of WT,R327I and R327A rFⅨ were 450,210,64 μg,and the purity of rFⅨ was confirmed by SDSPAGE.Both R3271 and R327A could be normally activated by FⅧa/TF/Ca2+ or FⅪa/Ca2+.Kd for FⅧa binding showed that the binding capacities of R327I and R327A were 4 and 5 times lower than WT,respectively.The catalytic efficiencies of R327I and R327A F Ⅸ a for F X were 6 and 8 times lower with FⅧa,and 3 and 7.4 times lower without F Ⅷ a,respectively.Conclusions R327I and R327A rF Ⅸ mutants impair their binding to the FⅧa.The site on R327 contributes to FⅧa binding.It is partly related to the activation of FX.The low FⅧa binding to R327I FⅨa may cause HB.