OBJECTIVETo compare the angiogenesis in unstable and stable plaques and to investigate the potential role of neovessels in creating vulnerable sites for atherosclerotic plaques.

METHODSSpecimens of coronary arteries were obtained from 52 autopsy cases with acute coronary syndromes. Plaque morphology was studied by use of stained slides. 922 tissue blocks of late-stage lesions were classified into two groups: (1) unstable plaque (n = 153), the plaque was characterized by a large extracellular lipid core (more than 40% of the plaque area); (2) stable plaque (n = 769), lipid core less than 40% of the plaque area. Forty blocks were selected randomly from each group and serial sections were stained immunohistochemically with a polyclonal antibody against F VIII RAg. Computer-aided planimeter was used for quantitative analysis.

RESULTSIn unstable plaques, the occurrence of neovessels was more frequent and the neovessel density (number/mm(2)) was significantly increased as compared to that of stable plaques (frequency: 80.4% vs 66.6%, P < 0.01; shoulder: 22.16 +/- 19.96 vs 10.04 +/- 11.52, base: 21.68 +/- 20.44 vs 9.68 +/- 11.52, fibrous cap: 3.80 +/- 5.32 vs 1.48 +/- 2.28, P < 0.05). Most neovessels were located in the shoulder region and at the base of plaques.

CONCLUSIONSThese findings suggest that neovessels in coronary atherosclerotic plaques are closely associated with the decreased stabilization of the plaques.

Aged ; Aged, 80 and over ; Coronary Artery Disease ; pathology ; Coronary Vessels ; pathology ; Female ; Humans ; Male ; Neovascularization, Pathologic ; pathology

OBJECTIVESTo analyze the relationship between oxidized low density lipoprotein (oxLDL), angiogenesis and stabilization of atherosclerotic plaques in human coronary arteries; and to investigate the role of oxLDL in creating vulnerable sites in atherosclerotic plaques.

METHODSSamples of coronary arteries were obtained at autopsies of 42 patients with acute coronary syndrome. Eighty randomly selected blocks were studied by immunohistochemistry using antibodies against oxLDL and endothelial cells (factor VIII). Computer-aided planimeter was used for quantitative analysis.

RESULTSIn unstable plaques, percentage of immunoreactive areas for oxLDL was significantly higher than that in stable plaques. Most of the oxLDL were located in shoulder region of these plaques, as compared to the fibrous cap and basal regions. The details of distribution of oxLDL were as follows: shoulder region (20.43 +/- 3.12 for unstable plaques and 17.65 +/- 4.22 for stable plaques), fibrous cap (4.77 +/- 2.03 for unstable plaque and 2.80 +/- 0.22 for stable plaques) and basal region (5.65 +/- 1.65 for unstable plaques and 3.22 +/- 1.02 for unstable plaques). OxLDL was also a main component in the lipid core. In the shoulder region, there was a significant positive correlation between neovascularization and oxLDL (r = 0.8247, P = 0.000).

CONCLUSIONSThe amount of oxLDL is significantly higher in unstable atherosclerotic plaques, especially over the shoulder region. OxLDL in coronary atherosclerotic plaques is thus an important factor in determining stabilization of the plaques. OxLDL may induce influx of inflammatory cells which subsequently leads to decreased plaque stabilization.

Angina, Unstable ; metabolism ; pathology ; Coronary Artery Disease ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Lipoproteins, LDL ; metabolism ; Myocardial Infarction ; metabolism ; pathology ; Neovascularization, Pathologic ; metabolism ; pathology

Objective To study the influence on the metabolism of Pu-erarin on the pharmacokinetics of glipizide capsule in healthy and diabetic rabbits.Methods Healthy New Zealand rabbits randomly assigned , one group was modeled , each group had 5 rabbits.Glipizide (5 mg) was taken orally once to every rabbit.After 2 weeks of clearing stage, Puerarin (18 mg· kg -1) was administered daily by auricular vein injection qd for 3 d, then glipizide was taken orally at the same dosage on the 4 d.The blood was drawn from ear vein before and after administe-ring glipizide in every rabbit.Then the blood concentration of glipizide was measured by HPLC.The pharmacokinetic parameter was calculated with pharmacokinetic software DAS 2.0.The pharmacokinetics of glipiz-ide in rabbits administered with or without Puerarin were analyzed by auto-control.Results The concentration time -curves were fit to the one-compartment model.In healthy group , administered with Puerarin , the t1/2 were (4.2 ±0.5),(3.58 ±0.7) h,ρmax were (15.5 ±0.8), (8.4 ±0.6 ) mg· L-1 , AUC0-35 were ( 134.8 ±0.7 ) , ( 77.2 ±1.4 ) mg· h· L -1; respectively before and after.In diabetic group , t1/2 were (7.6 ±0.9),(5.6 ±0.9) h,ρmax were (13.4 ±0.8),(10.6 ±0.9) mg· L-1,AUC0-35 were (10.5 ±0.8),(7.7 ±1.6) mg· h· L-1 respectively before and after.There were notable differences on t1/2 ,ρmax , AUC values of glipizide in rabbits administered with or without Puerarin ( P <0.05 ).Conclusion Puerarin shows significant impact on the pharmacokinetics of glipizide.

OBJECTIVETo investigate the influence of ICAM-1 469K/E gene polymorphisms on the risk of atrophic gastritis and dysplasia.

METHODSThe ICAM-1 469K/E gene polymorphisms in a total of 372 subjects were detected by polymerase chain reaction-direct sequencing. All of the subjects were from Linqu County, a high risk area of gastric cancer in Shandong Province of northern China. All cases were initially diagnosed as normal or superficial gastritis at the beginning of this study. After a 5-year follow-up, the cases were subdivided into no progression group (no histological progression, n=137), progression group I (progressed to severe chronic atrophic gastritis, n=194) and progression group II (progressed to low-grade dysplasia, n=41).

RESULTSIn all 372 subjects, the frequencies of KK, KE or EE genotype of ICAM-1 K469E were 50.5%, 39.2% and 10.2%, respectively. No significant differences were observed in the ICAM-1 469K/E genotype frequencies between the progression group I and no progression group (P>0.05). The frequencies of KK genotype (68.3%) were significantly higher in the progression group II than in the no progression group (49.6%, P=0.035), and also than in the progression group I (47.4%, P=0.015). An increased risk of the progressing to dysplasia from normal or superficial gastritis was found in the individuals with ICAM-1 469KK genotype [odds ratio (OR)=2.21, 95%CI, 1.10-4.42].

CONCLUSIONICAM-1 469K/E gene polymorphisms are significantly associated with the risk of gastric low-grade dysplasia, but not related with severe chronic atrophic gastritis in a population with high risk of gastric cancer in Linqu County, Shandong Province, China.

Adult ; Female ; Follow-Up Studies ; Gastritis ; genetics ; pathology ; Gastritis, Atrophic ; genetics ; pathology ; Genotype ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; Male ; Middle Aged ; Odds Ratio ; Polymorphism, Genetic ; Precancerous Conditions ; genetics ; pathology ; Risk ; Stomach Neoplasms ; genetics ; pathology

A randomized crossover study was performed to compare the effects of low glycemic index diets (LGI)and high glycemic index diets(HGI)on blood glucose,lipid profile and control of body weight in patients with type 2 diabetes.Compared with HGI group,the fasting serum insulin,Homa-IR,LDL-C and body weight significantly decreased in LGI group(P

OBJECTIVETo explore roles of mRNA and protein expressions of organic anion transporting polypeptide (oatp2b1) of rats with high fat diet and overstrain induced Pi deficiency syndrome in the transporting of damp turbidity.

METHODSTotally 24 SD rats were randomly divided into three groups, i.e., the normal group, the overstrain group, and the high fat diet group, 8 in each group. After successful modeling, one piece of tissues such as spleen, kidney, liver, lung, stomach, small intestine, and large intestine was taken from each rat. Rats of the overstrain group were bonded by specially made bondage cylinder, 3 h each time on odd days, and forced to swim in cold water (10 +/- 1) degrees C for 7 min on even days alternatively for twelve weeks. Rats in the model group and the normal group were fed with standard routine granular forage for 12 weeks. Rats in the high fat diet group were fed with high fat forage for twelve weeks. All rats drank and ate freely. The mRNA and protein expressions of oatp2b1 were detected in the seven tissues using RT-PCR and Western blot.

RESULTSThe mRNA expression of oatp2b1 in liver and kidney tissues of rats in the high fat diet group was higher when compared with that of the normal group and the overstrain group (P < 0.01, P < 0.05). The oatp2b1 mRNA expression in the normal group was sequenced from high to low as liver > lung > spleen > larger intestine > small intestine > kidney > stomach. The oatp2b1 mRNA expression in the overstrain group was sequenced from high to low as liver > lung > larger intestine > spleen > kidney > stomach > small intestine. The oatp2b1 mRNA expression in the high fat diet group was sequenced from high to low as liver > lung > spleen > small intestine > kidney > larger intestine > stomach. The oatp2b1 protein expression in the lung tissue was sequenced from high to low as the overstrain group > the normal group > the high fat diet group (P > 0.05). The oatp2b1 protein expression in the spleen tissue was sequenced from high to low as the high fat diet group > the normal group > the overstrain group (P > 0.05). The oatp2b1 protein expression in the kidney tissue was sequenced from high to low as the normal group > the overstrain group > the high fat diet group (P > 0.05). The oatp2b1 protein expression in the liver tissue was sequenced from high to low as the normal group > the high fat diet group > the overstrain group (P > 0.05). Of them, the oatp2b1 protein expressed extremely less in the stomach, large intestine, and small intestine. The oatp2b1 protein expression in the normal group was sequenced from high to low as lung >spleen > liver, kidney > stomach, larger intestine, and small intestine. The oatp2b1 protein expression in the overstrain group was sequenced from high to low as lung > spleen > kidney > liver > stomach, larger intestine, and small intestine. The oatp2b1 protein expression in the high fat diet group was sequenced from high to low as spleen > lung > kidney > liver > stomach, larger intestine, and small intestine. However, there was no statistical significance among the three groups by pair-wise comparison (P > 0.05).

CONCLUSIONSKidney and liver might play important roles in the transportation and transformation of damp under the state of Pi deficiency syndrome. Oatp2b1 may be one of the material bases involved in the transportation and transformation of damp turbidity. Pi's function of governing transportation and transformation of damp might not only include the functions of the gastrointestinal tract, but also include partial liver and kidney functions.

Animals ; Diet, High-Fat ; Disease Models, Animal ; Fatigue ; diagnosis ; metabolism ; Kidney ; metabolism ; Liver ; metabolism ; Male ; Medicine, Chinese Traditional ; Organic Anion Transporters ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the effectiveness and safety of sirolimus-eluting stents (SESs) for treatment of in-stent restenosis (ISR).

METHODSAll 27 patients with ISR and clinical evidence of ischemia had been treated with SESs. Among them, 23 patients had diffuse and complex lesions, and 5 of them received 2 SESs. Clinical and angiographic follow-up were performed for all patients and the results were analyzed.

RESULTSAll stents were implanted successfully. There were no remained stenosis and major in-hospital complications. Average follow-up time was 8.9 +/- 2.1 (5-14) months, with a clinical follow-up rate of 96.3% and angiographic follow-up rate of 92.6%. During the follow-up, there was none of death. One patient had recurrent angina with an angiographic evidence of the proximal edge restenosis of the stent. Mild neointimal hyperplasia in the proximal edge was found in 2 patients, but the stenosis was less than 25%. No late lumen loss was found in other 24 patients. The late lumen loss of the in-stent averaged 0.09 +/- 0.02 mm, and of the distal edge vessel averaged 0.10 +/- 0.03 mm, and of the proximal edge vessel averaged 0.20 +/- 0.06 mm. The rate of target vessel revascularization was 3.8%.

CONCLUSIONThe SES implantation is safe and feasible for the treatment of in-stent restenosis, which could effectively prevent neointimal hyperplasia and recurrent restenosis of the lesion.

Adult ; Aged ; Coronary Angiography ; Coronary Restenosis ; diagnostic imaging ; therapy ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Sirolimus ; administration & dosage ; Stents

OBJECTIVETo investigate the biological characteristics of childhood T-lineage acute lymphoblastic leukemia (T-ALL) and their clinical significance.

METHODSImmunophenotyping was performed by three-color flow cytometry analysis using CD45 /SSC gating in 23 children with newly diagnosed T-ALL. Meanwhile cytogenetic analysis was performed.

RESULTSCD3(+) expression of T-lineage antigens was apparently higher than CD7(+) and CD5(+) expression. CD19(+) expression of B-lineage antigens was apparently higher than CD22(+), CD10(+) and CD20(+) expression. Myeloid antigen was expressed in 4 cases (17%). CD34(+) and HLA-DR(+) were observed in 4 cases (17%) and 5 cases (22%), respectively. cCD3(+) and cCD79(+) were expressed in 23 cases (100%) and 22 cases (96%), respectively. The chromosome detection in 8 cases with T-ALL showed hyperdiploid or Ph(+) chromosome (one case each). The fusion gene detection in 5 cases showed MLL rearrangements in two cases and positive SIL/TAL1 fusion gene in one case. CD3 expression was related with the complete remission rate.

CONCLUSIONSImmunophenotyping is an important tool for diagnosis of T-ALL. However, the immunophenotype of T-ALL is heterogeneous. So, immunophenotyping along with cytogenetic and molecular genetic analysis is needed in the treatment and prognosis evaluation of T-ALL.

Child ; Child, Preschool ; Chromosome Aberrations ; Female ; Humans ; Immunophenotyping ; Male ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; genetics ; immunology

BACKGROUNDMechanical stress plays an important role in the maintenance of bone homeostasis. Current hypotheses suggest that interstitial fluid flow is an important component of the system by which tissue level strains are amplified in bone. This study aimed to test the hypothesis that the short-term and appropriate fluid shear stress (FSS) is expected to promote the terminal differentiation of pre-osteoblasts and detect the expression profile of microRNAs in the FSS-induced osteogenic differentiation in MC3T3-E1 cells.

METHODSMC3T3-E1 cells were subjected to 1 hour of FSS at 12 dyn/cm(2) using a parallel plate flow system. After FSS treatment, cytoskeleton immunohistochemical staining and microRNAs (miRNAs) were detected immediately. Osteogenic gene expression and immunohistochemical staining for collagen type I were tested at the 24th hour after treatment, alkaline phosphatase (ALP) activity assay was performed at 24th, 48th, and 72 th hours after FSS treatment, and Alizarin Red Staining was checked at day 12.

RESULTSOne hour of FSS at 12 dyn/cm(2) induced actin stress fiber formation and rearrangement, up-regulated osteogenic gene expression, increased ALP activity, promoted synthesis and secretion of type I collagen, enhanced nodule formation, and promoted terminal differentiation in MC3T3-E1 cells. During osteogenic differentiation, expression levels of miR-20a, -21, -19b, -34a, -34c, -140, and -200b in FSS-induced cells were significantly down-regulated.

CONCLUSIONThe short-term and appropriate FSS is sufficient to promote terminal differentiation of pre-osteoblasts and a group of miRNAs may be involved in FSS-induced pre-osteoblast differentiation.

Actins ; chemistry ; Alkaline Phosphatase ; metabolism ; Animals ; Cell Differentiation ; Cells, Cultured ; Collagen Type I ; biosynthesis ; Core Binding Factor Alpha 1 Subunit ; genetics ; Cyclooxygenase 2 ; genetics ; Gene Expression Profiling ; Mice ; MicroRNAs ; physiology ; Osteoblasts ; cytology ; Osteogenesis ; Stress, Mechanical ; Stress, Physiological

BACKGROUNDEnamel demineralization occurs frequently during orthodontic treatment. In this study, we evaluated the changes of the density of mutans streptococcus (MS) in plaque after bracket bonding and using fluoride adhesive on maxillary incisors by real time fluorescence-quantitative polymerase chain reaction (RT-FQ PCR).

METHODSThe study was designed as a self-paired test. Brackets were bonded with fluoride adhesive on the left side, while non-fluoride adhesive on the right side for each patient. Plaque samples were taken from the surfaces around the brackets of four maxillary incisors before brackets bonding and after the bonding 4 weeks later. The amount of MS was measured by RT-FQ PCR. The data obtained were analyzed statistically using the SPSS 11.5 version and the alpha level was set at 0.05 (2-tailed).

RESULTSThe amount of MS in plaque increased significantly after bracket bonding (P < 0.01), whereas no significant differences were observed among four maxillary incisors both before and after brackets bonding (P > 0.05), and among the incisors using and not using fluoride adhesive (P > 0.05).

CONCLUSIONSThe increase of the density of MS in plaque after bracket bonding is one of the etiological factors for enamel demineralization in orthodontic patients. The result of this study did not support what we observed clinically that the incidence of enamel demineralization for lateral incisors was higher than that for central incisors. Using fluoride adhesive for bonding did not affect the amount of MS in plaque in our study. Further study is needed.

Adhesives ; Adolescent ; Dental Bonding ; Dental Plaque ; microbiology ; Female ; Fluorescence ; Fluorides ; administration & dosage ; Humans ; Male ; Orthodontic Brackets ; Polymerase Chain Reaction ; methods ; Streptococcus mutans ; genetics ; isolation & purification ; Tooth Demineralization