Objective To study the effect of pioglitazone(PIO) on AdipoR1 and cholesterol ester(CE) in foam cells derived from THP-1-derived macrophages.Methods THP-1-derived macrophages were incubated with increasing concentrations of PIO for 24 hours.After co-cultured with low density lipoprotein(LDL),the accumulation of cholesterol in macrophages was measured by fluorescence spectrophotometric method.The lipid peroxide within cells was detected by TBARS method,the foam cells were observed by oil red staining.AdipoR1 levels were determined by Western blot.Results Compared with the ox-LDL group (0 μmol/L),oil red O-positive cells of the PIO protective groups were greatly reduced.TC,CE,MDA of the PIO protective groups were also obviously decreased.TC (53.6 ± 1.2) μg/mg,CE (30.2 ± 3.6) μg/mg,MDA (3.42 ± 0.06) μg/mg of 5 μμ mol/L PIO group were lower than those of 0μmol/L PIO group[(98.2 ± 3.5),(65.5 ± 6.5),(8.50 ± 1.21)] μg/mg (P ＜ 0.05).TC (25.6 ± 1.8) μg/mg,CE (22.5 ± 4.5) μg/mg,MDA (1.90 ± 0.42) μg/mg of 50 μmol/L PIO group.TC (16.8 ± 2.2) μg/mg,CE(5.9 ± 1.4) μg/mg,MDA (0.65 ± 0.05) μg/mg of 100μmol/L PIO group.Concomitantly,PIO significantly increased AdipoR1 protein expresion,AdipoR1 of 5μmol/L PIO group(0.06±0.05) was higher than that of 0μmol/L PIO group(0.03 ±0.07).AdipoR1 of 50μmol/L PIO group(0.11 ±0.07) was higher than that of 5μmol/L PIO group (0.06 ± 0.05).AdipoR1 of 100 μmol/L PIO group (0.40 ± 0.05) was obviously higher than that of 50 μ mol/L PIO group (0.11 ± 0.07).Conclusion PIO inhibited THP-1-derived formation by up-regulation the expression of AdipoR1,which may play an important role in the development and progression of atherosclerosis.

Objective To investigate the molecular mechanism of epithelial-mesenchymal transition (EMT) induced by activated vascular endothelial growth factor receptor-1 ( VEGFR-I ) in cell line MHCC97-H.Methods MHCC97-H cells were cultured in DMEM with 1％ fetal bovine serum (control group),10 μmol/L PP2 (PP2 group),10 μmol/L PBS (PBS group),50 μmol/L VEGF-B (VEGF-B group),l0μmol/L PP2 and 50 μmol/L VEGF-B (PP2 +VEGF group),10 μmol/L PBS and 50 μmol/L VEGF-B (PBS + VEGF-B group),respectively.Protein expressions of epithelial marker E-cadherin,α-catenin and mesenchymal marker vimentin and N-cadherin were detected by Western blot.The expression sites of E-cadherin,α-catenin and mesenchymal marker vimentin and N-cadherin were detected by cell immunofluorescence.The ability of invasion and migration of cell line MHCC97-H were assessed by cell invasion and migration test.All data were analyzed by the t test.Results The expressions of E-cadherin,α-catenin,vimentin and N-cadherin were 3.23 +0.76,3.01 ±0.25,3.01 +0.22 and 2.63 +0.40 in the control group,4.18 +0.32,3.29 +0.11,4.85 +0.36 and 3.02 +0.52 in the PP2 group,2.83 +0.65,3.03 +0.27,1.37 ±0.24 and 2.98 ±0.36 in the PBS group,2.06 ±0.15,2.84 ±0.76,5.79 ± 0.38 and 5.54 ± 0.28 in the VEGF-B group,6.12 ± 0.08,5.45 ± 0.37,3.36 ± 0.42 and 3.26 ±0.13 in the PP2 + VEGF-B group and 1.36 ±0.54,1.26 ±0.45,4.05 ±0.17 and 1.05 ±0.33 in the PBS +VEGF-B group.There was a significant difference in the expressions of E-cadherin and α-catenin between the PP2 +VEGF-B group and the VEGF-B group (t =7.625,9.931,P ＜ 0.05 ).The expressions of vimentin and N-cadherin in the PP2 + VEGF-B group were significantly lower than those in the VEGF-B group (t =12.001,11.910,P ＜ 0.05).Six hours after the treatment with VEGF-B,the numbers of MHCC97-H migrated were 19 ± 1,5 ± 2and 16 ± 1 in the VEGF-B group,PP2 + VEGF-B group and PBS + VEGF-B group,respectively.The number of MHCC97-H cells migrated in the VEGF-B group was greater than that in the PP2 ± VEGF-B group ( t =13.566,P ＜ 0.05 ).The number of MHCC97-H cells passed through the Boyden chamber was 4 + 2,which was significantly less than 16 ± 1 of the VEGF-B group (t =12.350,P ＜0.05).Conclusion EMT induced by activated VEGFR-1 was mediated via c-Src kinase signal transduction in MHCC91-H cell line,and c-Src may be a potential target to interfere the invasion and migration of hepatic cancer cells.

A 54 years old male patient with chronic leg ulcers was admitted in our hospital in November 2017. He was diagnosed as pyoderma gangrenosum by the pathological examination. Then the wound was treated with simple vacuum sealing drainage combined with irrigation of oxygen loaded fluid. This therapy overcame the shortage of hypoxia in the Tibetan Plateau on wound healing, resulting in a better wound healing. The patient was eventually cured and discharged from hospital.

The biological samples of oral genetic diseases and rare diseases are extremely precious. Collecting and preserving these biological samples are helpful to elucidate the mechanisms and improve the level of diagnose and treatment of oral genetic diseases and rare diseases. The standardized construction of biobanks for oral genetic diseases and rare diseases is important for achieving these goals. At present, there is very little information on the construction of these biobanks, and the standards or suggestions for the classification and coding of biological samples from oral and maxillofacial sources, and this is not conducive to the standardization and information construction of biobanks for special oral diseases. This consensus summarizes the background, necessity, principles, and key points of constructing the biobank for oral genetic diseases and rare diseases. On the base of the group standard "Classification and Coding for Human Biomaterial" (GB/T 39768-2021) issued by the National Technical Committee for Standardization of Biological Samples, we suggest 76 new coding numbers for different of biological samples from oral and maxillofacial sources. We hope the consensus may promote the standardization, and smartization on the biobank construction as well as the overall research level of oral genetic diseases and rare diseases in China.