The levels of serum lipids, lipoproteins and apoproteins were determined in 36 age over 90 year long-living people, 43 patients with old myocardial infarction (OMI) and 56 normal subjects of the age 40 to 64 years old. The resutts showed that: the ratioes of HDL-c/TC, HDL-c/LDL-c and ApoA_1/ApoB_(100) of the long-living people were higher than that of the patients with OMI; the levels of TC, TG, LDL-c, VLDL-c, ApoB_(100) and ApoA_1 in longevity group were lower than that of OMI group; no significant difference of HDL-c level was found between longevity and OMI group. Compared with normal group, the serum concentration of ApoA_1/ApoB_(100) ratio, TG and VLDL-c in the long-living group were obviously higher, and the serum concentration of ApoB_(100), ApoA_1 and HDL-c significantly lower. No significant differences were found in the levels of TC, LDL-c, and in the ratioes of HDL-c/TC and HDL-c/LDL-c between longevity and normal group. Stepwise regression analysis showed that the serum ApoB_(100) concentration and ApoA_1/ApoB_(100) ratio was the most important factor of longevity. It was suggested that the internal balance of serum lipids and lipoprotein metabolism in long-living people was good co-ordination, and the lower ApoB_(100) level and higher ApoA_1/ApoB_(100) ratio were probably parameters of longevity.

Objective To explore the possible immunological mechanism of laminarin sulfate in the prevention of experimental atherosclerosis. Methods Serum soluble interleukin 2 receptor (sIL-2R) , circulating immuno-complex, sub units of T lymphocyte, inter leukin-6(IL-6) , in-terleukin-8(IL-8), tumor necrosis factor-a (TNF-a) and lipid metabolism were determined by ELISA, RIA in rats and quails. Results The lipid metabolism and immunologic function were prominent disturbance in animals after feeding with high-lipid food. However, Laminarin sulfate has obvious regulating effects on above-mentioned index. Conclusions The mechanism of laminarin sulfate in the prevention of atherosclerosis might be closely related to the regulation of the disturbance of lipid metabolism and to the regulation of the immunologic function of the body.

Objective: To study the attenuating effect of angiotensin I type 1 receptor antagonist losartan and an-giotensin converting enzyme inhibitor captopril on aortic atherosclerosis in rabbits. Methods: Thirty-one male New Zealand rabbits were randomly divided into 5 groups:control group,high cholesterol diet group,losartan group, captopril group and combined drug administration groupdosartan+captopril). The animals were killed after 16 weeks and the serum total cholesterol ,triglyceride, high and low density cholesterol .atherosclertic ratio,endothelin,NO,plaque area percentage,aortic cholesterol content and vascular smooth muscle cell (VSMC) apoptosis were determined. Results:The plaque area percentage,aortic cholesterol contents and endothelin levels of 3 drug treatment groups were significantly lower than that of high cholesterol group,NO contents and VSMC apoptosis were significantly higher. Conclusion:Losartan and captopril can attenuate aortic atherosclerosis induced by high cholesterol diet .combined administration of the 2 drugs at low doses are more effective. The mechanism may be related to the protection of endothelial function and the effect on apoptosis of VSMC.

Animals ; Helminthiasis ; pathology ; Humans ; Moniliformis ; pathogenicity

AIM: To investigate the relationships between antiproliferative mechanisms of probucol and protein expressions of signaling molecules ERK1/2, MKP-1, HO-1 and Trx-1 in rat aortic smooth muscle cells (RASMCs) stimulated with ox-LDL. METHODS: The effects of probucol on cell cycle, cell proliferation and the expressions of ERK1/2, MKP-1, HO-1 and Trx-1 in the presence of ox-LDL were observed by means of MTT test, FCM and Western blotting. RESULTS: (1) Probucol significantly inhibited the proliferation of RASMCs stimulated with ox-LDL. A value in 100 μmol/L probucol+35 mg/L ox-LDL group was reduced by 34.9% as compared to ox-LDL group (P<0.01). (2) Probucol protected against ox-LDL-induced RASMCs proliferation through inducing cell growth arrest at G_0/G_1 phase and cell apoptosis. (3) ox-LDL increased the expression of p-ERK1/2 by 34.7% (P<0.01) and decreased MKP-1 by 60.0% (P<0.01), respectively, as compared to control. Probucol attenuated the increase in ox-LDL-stimulated p-ERK1/2 level by 15.7%, but increased MKP-1 expression by 2 times (P<0.01). (4)ox-LDL at concentration of 35 mg/L decreased the intracellular Trx-1 expression by 28.9% (P<0.05), and slightly increased the level of HO-1 expression as compared to control (P<0.05). Probucol enhanced the expression of Trx-1 by 91.6% (P<0.01) and HO-1 by 31.9% (P<0.01), respectively as compared to ox-LDL group. CONCLUSION: Probucol inhibits ox-LDL-stimulated the proliferation of RASMCs through increases in MKP-1/HO-1 expression, suppression of cell cycle progression and induction of cell apoptosis.

AIM: To investigate the effect of probucol on proliferation of rat vascular smooth muscle cells(VSMC) stimulated by basic fibroblast growth factor (bFGF) and/or hydrogen peroxide(H 2O 2). METHODS: Effects of probucol on VSMC proliferation and DNA synthesis stimulated by bFGF and/or H 2O 2 were observed by means of MTT test, cell number count and [ 3H]-TdR incorporation. RESULTS: ①Probucol significantly inhibited proliferation and DNA synthesis in VSMC stimulated by bFGF and/or H 2O 2, with dosage-dependent manner. Cell number, A value and [ 3H]-TdR incorporation in group probucol+bFGF and group probucol+H 2O 2 were reduced by 40.0%, 39.1%, 45 5% and 46 9%, 45 0%, 39 5%, respectively, compared with group bFGF and group H 2O 2 ( P 0.05). CONCLUSION: Probucol dramatically inhibited proliferation and DNA synthesis in VSMC stimulated by bFGF and/or H 2O 2, but had no inhibitory effect on the cell proliferation prestimulated by bFGF and /or H 2O 2. [

Objective To study the changes of trans-diaphragmatic pressure (Ptra) and its correlation with esophageal pressure (Peso) through ARDS piglet model.Methods Five piglets were enrolled in the study.Peso,gastric pressure (Pgas) and intra-thoracic pressure (Pint) was monitored through balloon inserted.The data before ARDS serve as control.ARDS was produced in the piglets through saline lavage.The pressure were observed and the Ptra were calculated.The pressure changes and correlation between Ptra and Peso were analyzed as well.Linear regression with the coefficient of determination and t-test were used as appropriate.Significance was assumed for P ＜ 0.05.Results Peso,Pgas and Pint before ARDS were 7.3 ± 1.9,25.5 ± 2.4,- 1.23 ± 0.21 cmH2O,Ptra was 18.2 ± 1.6 cmH2O.While after ARDS,the data were 4.7 ± 1.4,31.1 ± 3.1 and - 1.79 ± 0.28 cmH2O,and Ptra was 26.4 ± 2.1 cmH2 O,and all these changes were obviously ( P ＜ 0.05 ).The correlation between Pint and Peso,Pint and Ptra (A) and Ptra ( B ) were 0.93 ± 0.025,0.88 ± 0.023 and 0.87 ± 0.37 before ARDS.After ARDS,the correlation changed to be 0.82 ±0.21,0.81 ±0.20 and 0.78 ±0.31.Although a bit decreased,the correlation was still positive (P ＜ 0.01 ).Conclusions There existed good correlations between Peso and Ptra as well as between Pint and Peso before or after ARDS.Ptra was increased obviously after ARDS,which could lead to respiratory muscle fatigue.

Objective To evaluate the clinical characteristics and pathological features of Meckel's diverticulum(MD) in children.Methods 244 MD cases admitted between January 2010 and December 2014 were retropectively analyzed.Results In fifty patients,MD was an incidental finding at laparotomy or laparoscopy for unrelated entities.Among the remaining 194 symptomatic patients,there were 76 patients presenting GI bleeding,forty eight patients were identified with perforated Meckel's diverticulum,thirty six patients suffered from intestinal obstruction.34 patients had MD caused severe complications such as volvulus and intestinal necrosis,diverticular perforation and peritonitis.61 out of 76 GI bleeding patients underwent a 99mTc scan,and positive tracer was found in 42 patients.Among the 19 negative 99mTc scan patients,8 received capsule endoscopy and only 3 patients were suspected of diverticulum.242 patients underwent one stage resection of the diverticulum.Histology revealed ectopic gastric mucosa or ectopic pancreatic tissue in 128 patients.One patient died of volvulus and intestinal necrosis postoperatively,and two suffered from adhesive intestinal obstruction during one to five year's follow up.Conclusions It is necessary to maintain a high suspicion of MD in the pediatric age group with symptoms of abdominal pain,gastrointestinal hemorrhage or intestinal obstruction.Ectopic mucosa assumes the ultimate responsibility for major complications of MD.

To construct and validate a deep learning-based bone age prediction model for children living in both plain and highland regions.

Objective To study the clinicopathologic features , diagnosis and differential diagnosis of succinate dehydrogenase ( SDH ) deficient gastrointestinal stromal tumors ( GISTs ) as a unique tumor subtype.Methods SDHB and SDHA immunohistochemistry was performed in 120 gastric GISTs, in addition to CD117, DOG-1, CD34, smooth muscle actin (SMA), desmin,S-100 protein, cytokeratin (CK) and Ki-67.Subset of the cases was further evaluated for the presence of mutations in CKIT exons 9, 11, 13 and 17 mutations and platelet derived growth factor receptor alpha ( PDGFRA) exons 12 and 18.Results Eight of 120 (6.6%) GIST cases were found SDH-deficient including 3 male and 5 female patients (median age of 36.2 years;ranging 16 to 65 years of age).The tumors involved antrum (6 cases), lesser curvature (1 case) and fundus (1 case).Macroscopically, the dominant tumor masses varied from 3 to 10 cm in diameter with a multinodular or plexiform pattern involving the gastric wall .Microscopically ,tumor cells had predominantly epithelioid morphology , with occasional mixed spindle cell nodules .Lymphovascular invasion was identified in 5 cases.Immunohistochemistry for SDHB was negative in all 8 cases, and SDHA was negative in 5 cases.All 8 SDHB negative cases also expressed CD 117, DOG-1 and CD34, but were negative for SMA, desmin, S-100 and CK.All 8 cases were found to have wild-type CKIT and PDGFRA genes. Available clinical follow-up were obtained in 7 cases, ranging from 2 to 60 months ( median follow-up 23.3 months) , and all patient were alive .Three cases were found to have liver metastases at their first diagnosis , and one developed omental and mesenteric metastases in 17 months.Conclusions SDH-deficient GIST is a distinct subtype of GIST , with a predilection to occur in young and female patients .Characteristic pathological findings include multinodular gastric wall involvement , epithelioid cell morphology , frequently lymphovascular invasion with occasional lymph node and liver metastases , but an overall indolent clinical behavior.Immunohistochemistry for SDHB is required for the diagnosis .