Objective To clarify the association of onset and maintenance of metabolic syndrome (MS) with energy metabolism imbalance,especially with dialysate glucose load in peritoneal dialysis (PD) patients.Methods Using retrospective self-controlled study,the changes of MS,dialysate glucose load and dietary energy intake (DEI) in 126 PD patients in about 1 year were collected and analyzed to define the effect of energy intake on MS.Resting energy expenditure (REE) was measured and physical activity level (PAL) was evaluated based on the activity records in PD patients with unchanged MS state and their impacts on MS were analyzed.Results The incidence of changing from non-MS to MS was higher in glucose load increasing group than that of glucose load unchanged or decreasing group.When glucose load increased,patients developing MS had significantly increased serum triglyceride (TG) level (P＜0.01) and significantly decreased serum high density lipoprotein cholesterol (HDL-C) level (P＜0.05),while the waist circumference and blood glucose level did not alter significantly.In patients changing from MS to non-MS,their serum C reactive protein (CRP) levels significantly decreased during the follow-up (P＜0.05).No significant difference was found in DEI in patients changing from MS to non-MS.However,in patients changing from non-MS to MS,their DEI decreased during the follow up (P＜0.05).In a subgroup analysis in 36 PD patients who maintained their metabolic status and did not change their glucose load,there was no difference in REE per body surface per day between the MS group and the nonMS group (t=0.840,P＞0.05).However,the PAL was lower in the MS group than that of the nonMS group (t=2.358,P＜0.05).Conclusions The increase of dialysate glucose load may be an important factor leading to the onset of MS,by altering serum TG and HDL-C level.Inflammation and the sedentary life also contribute to the MS state.

Humans ; Hyoid Bone ; pathology ; Male ; Middle Aged ; Syndrome

To obtain high-yield avilamycin-producing strains,low energy N~+ ion implantation technology and screening of streptomycin-re- sistant mutants are used in the study on breeding mutation.The results show that,“saddle”region,which range is from 3?10~(15) to 5?10~(15) ions/cm~2,has got better induced mutation action.It also means that the strain's resistant mutation and yield mutation closely correlate to each other,and the method of streptomycin resistant screening is feasible.We have isolated a high-yield strain SVT-45 which the productivi- ty is 195% higher than the original strain's in the rotation-flask experiments.These results showed that the ion implantation was an effective method for microbe mutagensis.

Objective To investigate the effect of chymase on the proliferation of rat cardiac fibroblasts (CFs) and the role of transforming growth factor-?1 (TGF-?_1).Methods Cultured CFs of neonatal SD rats were isolated by trypsinization.Cell number and DNA synthesis were evaluated by MTT assay (A_(490) value) and [~3H]-deoxythy- midine [~3H]-TdR incorporation.The mRNA expression of TGF-?_1 in CFs was determined by RT-PCR.Results Chymase increased CFs numbers and [~3H]-TdR incorporation in a dose-dependent manner.The A_(490) value of CFs stimulated by 15,30 and 60 ng/mL chymase was 0.263?0.033,0.348?0.031 and 0.387?0.026,respectively, which were all significantly higher than that of control (0.201?0.019,P

Cholesterol ester transfer protein (CETP) is a key regulator of high density lipoprotein (HDL). Owing to its important role in the reverse of cholesterol transport, CETP has become a hotspot target in modulating lipid drug design. In this paper, structure based pharmacophore (SBP) models for CETP inhibitors were built based on the protein structure 4F2A from Protein Database (PDB). The best pharmacophore contained six hydrophobic features, one hydrogen bond acceptor feature and nine excluded volume features, with the N and CAI value was 3.33 and 2.31 respectively. Then the model was used to search the traditional Chinese medicine database (TCMD) and 629 compounds originated from 315 TCM herbs were obtained. Molecular docking was also used to validate SBP by analyzing the critical amino acid residue and the interaction between potential active compounds and receptor. In this study, several TCM herbs, like Lycii Frutus and Schisandrae chinensis fructus, which contained more optimal SBP based screening results, have been reported hypolipidemic effect, and need to be studied deeply in a more focused research on herbal active constituents. Therefore, this study could provide reliable fundamental data for exploring the action mechanisms of TCM, and be applicable to identify lead candidates, which can be utilized as starting scaffolds for natural CETP inhibitors.
Cholesterol Ester Transfer Proteins ; antagonists & inhibitors ; Drug Evaluation, Preclinical ; methods ; Medicine, Chinese Traditional ; Molecular Docking Simulation

Objective To observe the effect of hypoxia reoxygenation on activity of superoxide dismutase(SOD)and MDA content as well as[Ca~(2+)],concentration and mitochondria membrane poten- tial of intestinal epithelial cell-6(IEC-6)in IEC culture medium and explore the protective effect and mechanism of serum containing Ziqi-liquid(a preparation of Chinese herbal medicine)on hypoxia reoxy- genation damaged IEC-6.Methods Hypoxia reoxygenation damage model of IEC-6 was made.SOD activity and MPA content in IEC-6 culture medium were determined by ultraviolet spectrometry after hy- poxia reoxygenation and treatment with Ziqi-liquid.Meanwhile,MMP changes and[Ca~(2+)]concentration were detected by laser scanning confocal microscopy.Results After hypoxia reoxygenation,SOD and MMP were significantly decreased,but MDA content and[ Ca~(2+)] concentration significantly increased (P＜0.01),and significantly facilitated by serum containing Ziqi-liquid.Conclusion Hypoxia reoxy- genation can damage IEC-6,but the serum containing Ziqi-liquid has significant protective effect on it.

This study was aimed to investigate the cytogenetic characteristics of hematopoietic cells (HC) and bone marrow mesenchymal stoma cells (BMMSC) isolated from patients with myelodysplastic syndrome (MDS) and healthy individuals as normal controls, and to clarify whether HC and BMMSC are simultaneously involved and participate in pathogenesis and development of MDS. Both marrows of 22 newly diagnosed patients with MDS and 7 healthy individuals were collected; BMMSC were isolated and amplified by using established culture system, as well as were identified according to morphologic features and surface antigens detected by flow cytometry; the characteristics of BMMSC from MDS patients were analyzed; the BMMSC karyotyping analysis of MDS patients was performed by banding of HC and BMMSC with pancreatin-Giemsa technique (GTG) and in accordance with ISCN (2005) requirements; the cytogenetic characteristics of HC and BMMSC were compared. The results showed that in vitro culture system for isolation and amplification was successfully established. The light microscopy and flow cytometry confirmed that BMMSC possessed characteristics showing long and thin spindle form and expressing CD29, CD73, CD90 antigens, and unexpressing CD34, CD45 antigens. In BMMSC of 14 MDS patients (64%), the cytogenetic abnormalities were found usually involving the loss of chromosomal material (92%), among which clonal loss was observed in 7 cases (50%). The detection indicated a random loss of chromosomal material in significant proportion of BMMSC. A high proportion of chromosomal material random loss may be a marker of chromosomal instability in BMMSC of MDS patients, the detection also showed that completely consistent aberration types did not exist between HC and BMMSC. The aberrations were observed in 3 cases of MDS with normal karyotype of HC, its aberration rate (33%) was obviously lower than that in MDS patients with abnormal karyotypes (92%). It is concluded that the cytogenetic abnormalities exist in BMMSC of MDS patients, the unbalanced aberration of chromosomal materials may be a genetic instability marker of BMMSC. The difference of aberration types in BMMSC from HC suggests that genetic susceptibility of BMMSC and HC is similar, but no completely identical, which indicates the potential involvement of BMMSC in pathogenesis of MDS. Studying this potential role of BMMSC can be helpful to further understanding of MDS biological characteristics and provide the new approaches for diagnosis and therapy of MDS.
Adult ; Aged ; Aged, 80 and over ; Bone Marrow Cells ; pathology ; Case-Control Studies ; Chromosome Aberrations ; Female ; Humans ; Male ; Mesenchymal Stromal Cells ; pathology ; Middle Aged ; Myelodysplastic Syndromes ; genetics ; pathology ; Young Adult

AIMTo determine the effects of azide methyl anthraquinone derivative (AMAD) on growth inhibition and inducing apoptosis of multidrug resistant (MDR) KBv200 cells and parental drug-sensitive KB cells.

METHODSCytotoxicity was determined by tetrazolium (MTF) assay. Reactive oxygen species (ROS) levels and mitochondrial membrane potential (deltapsi(m)) in cells were labeled with DCFH-DA and DiOC6 and tested by flow cytometry. Annexin V stain and DNA ladder were used to examine the apoptosis of KB and KBv200 cells induced by AMAD.

RESULTSAMAD was shown to inhibit the growth of KB and KBv200 cells significantly in a concentration-dependent manner, with mean IC50 of 0.36 and 0.45 micromol x L(-1), respectively. The generation of ROS increased obviously after the cells were treated with AMAD for 12 h, up to the peak in 24 h, meanwhile the levels of deltapsi(m) were time-dependently decreased. DNA fragmentation appeared on the agarose gel. Annexin V stain showed AMAD induced apoptosis of KB and KBv200 cells also in a concentration-dependent manner.

CONCLUSIONAMAD showed inhibitory effect on both MDR KBv200 cells and parental drug-sensitive KB cells. The mechanism of action was associated with the increase of the cellular ROS level and the decrease of the mitochondrial membrane potential induced by AMAD, which result in cell apoptosis.

Anthraquinones ; administration & dosage ; chemistry ; pharmacology ; Antineoplastic Agents ; administration & dosage ; chemistry ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Humans ; KB Cells ; Mitochondria ; physiology ; Molecular Structure ; Mouth Floor ; Mouth Neoplasms ; pathology ; Reactive Oxygen Species ; metabolism ; Vincristine ; pharmacology

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

BACKGROUNDIn addition to the well-known antibodies against human leukocyte antigens (HLA)-induced kidney-graft rejection, polymorphic major-histocompatibility-complex (MHC) class I-related chain A (MICA) antigens can elicit antibodies and have been suggested to play a role in the antibody-mediated allograft rejection (AMR). We carried out a prospective study of MICA antibodies in post-renal transplant patients to determine the association between MICA antibodies, C4d staining, histological features, and graft outcome.

METHODSWe tested 52 patients who had biopsy results due to graft dysfunction. The MICA antibodies in concurrent sera were determined by Luminex. All patients were followed up for one year after renal biopsy. The influence of antibody production on the function of graft was analyzed.

RESULTSAntibodies against MICA were positive in 15 out of the 52 patients (28.9%). The presence of MICA antibodies was associated with renal-allograft deterioration. During one-year follow-up, the estimated glomerular filtration rate (eGFR) decreased (24.0 ± 3.4)% among recipients with anti-MICA antibodies. However, among recipients without anti-MICA antibodies, the eGFR has declined only (8.4 ± 3.0)% (P = 0.017). The association between C4d staining, histological features and MICA antibody production was found no significant difference.

CONCLUSIONBesides anti-HLA antibodies, the presence of post-transplant MICA antibody is associated with poor graft outcome and increases the risk of graft failure.

Adult ; Antibodies ; blood ; immunology ; Female ; Histocompatibility Antigens Class I ; immunology ; Humans ; Kidney Transplantation ; immunology ; Male ; Middle Aged ; Prospective Studies ; Transplantation, Homologous ; immunology