OBJECTIVETo observe the effects of qingchang huashi recipe (QHR) on the dendritic cells (DCs) of experimental colitis rats, thus exploring its possible mechanisms for treating ulcerative colitis (UC).

METHODSThe UC rat model was induced by TNBS/anhydrous alcohol. Forty male Wistar rats were randomly divided into 4 groups, i.e., the normal group, the model group, the QHR group, and the Mesalazine group, 10 in each group. Since the 2nd day of modeling, corresponding medication was respectively administered to each treatment group by gastrogavage for 10 successive days. The number of DCs in the colonic mucosa was observed using iMmunohistochemical assay. The DCs ratio in the mesenteric lymph nodes, and the expressions of surface molecules MHC-II and CD86 were detected using flow cytometry.

RESULTSCompared with the model group, the number of DCs in the colonic mucosa significantly decreased, the expression of MHC-II in the mesenteric lymph nodes significantly decreased in the QHR group and the Mesalazine group, showing statistical difference (P < 0.01). There was no statistical difference between the two groups (P > 0.05). There was no statistical difference in the DCs ratios and the CD86 expression among the 4 groups (P > 0.05).

CONCLUSIONQHR could decrease the infiltration of DCs in the colonic mucosa, and suppress the activation of DCs in the mesenteric lymph nodes, which might be one of its mechanisms for treating UC.

Animals ; Colitis, Ulcerative ; drug therapy ; physiopathology ; Dendritic Cells ; cytology ; drug effects ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Intestinal Mucosa ; cytology ; Lymph Nodes ; cytology ; Lymphocyte Count ; Male ; Mesentery ; cytology ; Phytotherapy ; Rats ; Rats, Wistar

Fifty-six patients with Graves' ophthalmopathy(GO)were treated with antithyroid drug and oral prednisone for three months,TSH receptor antibody(TRAb)level was reduced,GO activity and severity of some patients were ameliorated but still positively associated with TRAb.It suggests that TRAb not only triggers off GO but also plays a possible role in the maintenance of the autoimmune process in GO.

Objective To estalish an accurate method for determining the content of astragaloside Ⅳ in Shouqing Granula. Method TLC scanner was selected to detect astragaloside Ⅳ with silica gela thin layer. The sample was separated by using chloroform-methanol-water (13 : 6 : 2) below 10 ℃ overnight with the under layer solution, ?_s=530 nm, ?_R=700 nm. Results The linear ranges of astragaloside Ⅳ was 0.22～ 0.73 ?g, the average recovery was 97.72%, RSD=0.69%. Conclusion The method was simple and accurate, and can be used for the quality control of Shouqing Granula.

Establishment of quality management system (QMS) plays a critical role in the clinical data management (CDM). The objectives of CDM are to ensure the quality and integrity of the trial data. Thus, every stage or element that may impact the quality outcomes of clinical studies should be in the controlled manner, which is referred to the full life cycle of CDM associated with the data collection, handling and statistical analysis of trial data. Based on the QMS, this paper provides consensus on how to develop a compliant clinical data management plan (CDMP). According to the essential requirements of the CDM, the CDMP should encompass each process of data collection, data capture and cleaning, medical coding, data verification and reconciliation, database monitoring and management, external data transmission and integration, data documentation and data quality assurance and so on. Creating and following up data management plan in each designed data management steps, dynamically record systems used, actions taken, parties involved will build and confirm regulated data management processes, standard operational procedures and effective quality metrics in all data management activities. CDMP is one of most important data management documents that is the solid foundation for clinical data quality.
Clinical Trials as Topic ; Data Collection ; standards ; Database Management Systems ; standards ; Information Storage and Retrieval ; standards

BACKGROUNDDiabetic macrovascular complications are important causes of cardiovascular and cerebrovascular diseases and also one of the major causes of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Phlorizin has been reported to be effective in reducing the blood glucose level in diabetic mellitus, while little is known about its effects on vascular complications. This study aimed to observe the effects of phlorizin on the aorta of diabetes db/db mice and explore its mechanism.

METHODSDiabetic db/db mice (n = 16) and age-matched db/m mice (n = 8) were divided into three groups: normal control group (CC group, db/m mice, n = 8), untreated diabetic group (DM group, db/db mice, n = 8) and diabetic group treated by phlorizin (DMT group, db/db mice, n = 8). Phlorizin (20 mg/kg body weight) was given in normal saline solution intragastrically for 10 weeks. Animals were weighed weekly. At the 10th weekend, all mice were fasted overnight and then sacrificed. Fasting blood was collected, and the aortas were dissected. The blood samples were analyzed for fasting blood glucose (FBG), serum advanced glycation end products (AGEs), malondialdehyde (MDA) and superoxide dismutase (SOD) activity, the aortic ultrastructure was studied.

RESULTSThe weight and serum concentration of FBG, AGEs, and MDA in the DM group were higher than that in the CC group (P < 0.01), and they were significantly lower in the DMT group (P < 0.05). Serum SOD activity was lower than that in the CC group (P < 0.01), and it is significantly higher in the DMT group (P < 0.05). The severity of aorta damage in the DMT group was less than that in the DM group.

CONCLUSIONSPhlorizin protected the db/db mice from diabetic macrovascular complications, attributed to the decreasing of blood glucose and AGEs level, and its antioxidant potential. This study may provide a new natural medicine for treating diabetic macrovascular complications.

Animals ; Aorta, Thoracic ; pathology ; Blood Glucose ; analysis ; Diabetic Angiopathies ; drug therapy ; pathology ; Glycation End Products, Advanced ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phlorhizin ; therapeutic use ; Superoxide Dismutase ; metabolism

OBJECTIVETo observe the improvement effects of puerarin on glycated brain damages in rat model induced by D-galactose.

METHODThe model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks, and all rats were treated with puerarin (high dose 300 mg x kg(-1), middle dose 150 mg x kg(-1), low dose 75 mg x kg(-1)) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products (fructosamine in serum, glycohaemoglobin, advanced glycation end-products) and AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope.

RESULTHigh dose and middle dose of puerarin can decrease the activity of aldose reductase in red blood cells (P < 0.01), and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P < 0.01). Also, puerarin can decrease the content of AGEs in brain and the level of calcium ions in brain cells (P < 0.05, P < 0.01), and decrease lesions degree in mitochondria in brain hippocampus cells.

CONCLUSIONPuerarin can produce the protective effects on glycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.

Aldehyde Reductase ; metabolism ; Animals ; Brain ; metabolism ; pathology ; Calcium ; metabolism ; Erythrocytes ; enzymology ; Female ; Fructosamine ; blood ; Galactose ; antagonists & inhibitors ; Glycated Hemoglobin A ; metabolism ; Glycation End Products, Advanced ; metabolism ; Hippocampus ; ultrastructure ; Isoflavones ; isolation & purification ; pharmacology ; Male ; Mitochondria ; ultrastructure ; Neuroprotective Agents ; pharmacology ; Plants, Medicinal ; chemistry ; Pueraria ; chemistry ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the safety and effectiveness of endoscopic mucosal resection (EMR) in the treatment of colorectal polyps.

METHODEMR was applied in the treatment of colorectal polyps.

RESULTSA total of 3578 polyps in 2609 patients were all completely resected except 2 cases and the integrated rate of samples was 99.6%. Intra- and post-operation complications occurred in 22 cases(0.8%), including 7 intraoperative bleeding, 5 postoperative bleeding, and 10 thermal burn, which were cured by symptomatic treatment. A total of 1530 (58.6%) cases were followed-up with 3-12 months and no relapse was found in former place of excision.

CONCLUSIONEMR can be applied in resection of colorectal polyps effectively and safely.

Aged ; Endoscopy, Gastrointestinal ; Humans ; Intestinal Mucosa ; surgery ; Intestinal Polyps ; surgery ; Postoperative Hemorrhage ; Recurrence

This study was aimed to investigate the reversing effect of arsenic trioxide (As2O3) on methylation status and the regulatory effect on transcription of malignant lymphoma cell line CA46 p16 gene as well as their possibe mechanisms. The hypermethylated malignant lymphoma cell line CA46 was used as a subject of experiment for studying relation of gene methylation with expression. The effect of As2O3 on the proliferation and viability of CA46 was detected by SRB method, the change of p16 methylation status after exposure to As2O3 was determined by nMSP, the expressions of p16, DNMT1, DNMT3A, DNMT3B mRNA were assayed by RT-PCR, the influence of As2O3 on CA46 cell cycle was analyzed by flow cytometry using analytical method for DNA ploidy. The results showed that the methylation level of p16 gene was obviously reduced after treatment with As2O3 for 72 hours and the hypermethylation of p16 gene was successfully reversed; the expression of p16 gene in untreated (control) group was low while it was enhanced in treated groups; the gray scale ratios of p16 gene to beta-actin in groups treated with As2O3 of concentration 0.5, 1.0 and 2.0 micromol/L were 0.33+/-0.10, 0.57+/-0.11 and 0.67+/-0.09 respectively, exhibiting a significant difference in comparison with 0.73+/-0.13 of positive control (p<0.01); as compared with the untreated group, the expression of DNMT3A and DNMT3B in treated groups was obviously down-regulated in a concentration-dependent manner, while expression of DNMT1 was nearly unchanged; as compared with control, all the 3 different concentrations of As2O3 could inhibit the proliferation of CA46 cells and increase the cell number in G0/G1 phase. It is concluded that the As2O3 may up-regulate the expression of p16 gene, recover the activity of p16 gene, thereby promote the regulatory function on cell cycle resul-ting in arrest of cells in G0/G1 phase and inhibit growth of tumor cells through depressing the expression of DNMT3A and DNMT3B and/or directly reversing the methylation status of p16 gene.
Arsenicals ; pharmacology ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p16 ; genetics ; metabolism ; DNA Methylation ; drug effects ; Genes, p16 ; Humans ; Lymphoma ; genetics ; Oxides ; pharmacology ; Transcriptional Activation

OBJECTIVETo evaluate the efficacy and safety of alendronate for the treatment of osteoporosis/osteopenia secondary to hyperthyroidism.

METHODSFrom April 2008 to November 2009, 27 patients with hyperthyroidism with osteoporosis/ osteopenia measured by dual energy X-ray absorptiometry (DXA) were included in this study, and then they were randomly divided into two groups (group A and group B) by simple random sampling. Group A consisted of 14 patients treated with antithyroid drug and caltrate D, the antithyroid drug change with thyroid function, and caltrate D 600 mg per day. Group B consisted of 13 patients treated with antithyroid drug, caltrate D and alendronate, antithyroid drug and caltrate D the same as group A, and alendronate 70 mg weekly. Meanwhile, 21 healthy voluntary adults were chosen as control group. And compared with the control group which was treated with nothing. Followed-up for one year, the bone mineral density (including T-score, Z-score, BMD) in lumbar spine (LS), femoral neck (FN) and distal radius (DR) and general information, were compared before and after treatment.

RESULTSBMD at FN and DR were significantly higher at 12 months after treatment than at the baseline in group A (P = 0.000); T-score, Z-score, and BMD at the LS, FN and DR were all significantly higher at 12 months after treatment than at the baseline in group B (P < 0.05), but these data could not arrive to normal level. In group A, the percentage increased in BMD at the LS, FN, and DR were (4.34 +/- 10.5)%, (3.21 +/- 1.38)%, (1.95 +/- 0.44)%, respectively, at 12 months after treatment. In group B, the percentage increased in BMD at the LS, FN, and DR were (6.10 +/- 8.12)%, (4.10 +/- 5.64)%, (3.10 +/- 3.23)%, respectively, at 12 months after treatment. There was significant difference in the rate of increase between two groups (P < 0.05). AKP decreased, weight, BMI increased, and thyroid function decreased, after treatment than those before in both of the two groups. (P < 0.05).

CONCLUSIONAlendronate can significantly increase BMD in treating patients with hyperthyroidism and osteoporosis/osteopenia. Compared with anti-thyroid drugs alone, treatment with alendronate can obtain more clinical effect and also very safety.

Adult ; Alendronate ; therapeutic use ; Bone Density ; Bone Density Conservation Agents ; therapeutic use ; Bone Diseases, Metabolic ; drug therapy ; etiology ; Female ; Humans ; Hyperthyroidism ; complications ; drug therapy ; Male ; Middle Aged ; Osteoporosis ; drug therapy ; etiology

OBJECTIVETo investigate the prevalence of JAK2V617F and MPLW515L/K mutation in patients with slightly elevated platelets (BPC) or hemoglobin (Hb) not meeting the criteria of polycythemia vera (PV) or essential thrombocythemia (ET).

METHODSGenomic DNA from bone marrow or blood mononuclear cells was screened with allele specific polymerase chain reaction (AS-PCR) for JAK2V617F and MPLW515L/K mutation. The history of thrombosis was assessed retrospectively by patients files.

RESULTSOf 30 patients, 14 (46.7%) were positive for the JAK2V617F mutation, none of them had the MPLW515L/ K. Five of these 14 patients had a history of thrombosis. Follow-up results were available in 22 patients. Among them, 12 patients with JAK2V617F mutation turned out to be MPD in 6-24 months; only 2 out of 10 patients without this mutation evolved to MPD.

CONCLUSIONJAK2V617F mutation could be one of the diagnosis criteria of early MPD. No MPLW515L/K expression was found in early MPD.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Early Diagnosis ; Female ; Follow-Up Studies ; Humans ; Janus Kinase 2 ; genetics ; metabolism ; Male ; Middle Aged ; Mutation ; Myeloproliferative Disorders ; diagnosis ; genetics ; metabolism ; Receptors, Thrombopoietin ; genetics ; metabolism ; Young Adult