Objective: To prepare the calcitonin oral microparticle. Methods: The oral delivery system of salmon calcitonin was made using diketopiperazine microparticles as carrier by the method of sole solifification. The parameters including the shape of microparticle,dissolving in vitro , the effect of reducing bleed calcium and bioavailability etc . were observed. Results: The diameter of the microparticles was 1 3 ?m, and the drug concentration was 0.42%. The rate of encapsulating was 91.1%. The drug did not release within 2 h in artificial gastric fluid and completely released in artificial intestinal fluid within 6 h. The microparticles had obvious effect of reducing bleed calcium 3 h after it was taken, the effect lasted for 12 h. Conclusion: The microparticles of salmon calcitonin release slowly and have better effects of reducing bleed calcium by oral delivery system.

Nowadays,the incidence of intellectual disabilities(ID) increased in the elder,and they would meet the following problems:life transitions,future life planning and understanding emotions,etc.This paper discusses the measures to be made for ageing person with ID from three aspects:assessing and managing illness,caregiving stress and the role of psychologists.

Objective:To evaluate the efficacy of computed tomography (CT)-guided implantation of radioactive ~(125)I seeds in the treatment of residual foci of nasopharyngeal carcinoma after radiotherapy.Methods:Twenty-five nasopharyngeal carcinoma patients who had residual foci after radiotherapy were implanted radioactive ~(125)I seeds from January 2007 to January 2008 in our hospital. Three-dimensional treatment planning system (TPS) was used to calculate the quantity and total dosage of ~(125)I seeds. The radioactive ~(125)I seeds were implanted into residual foci under CT guidance. The dosage distribution of radioactive ~(125)I seeds were verified after surgery. The nasopharyngeal endoscopy CT scans were performed at 3, 6, and 12 months after surgery and the short-term efficacy and adverse reaction were evaluated. Results:Out of the 25 patients, 20 patients had complete response (CR), 2 patients had partial response (PR), 2 patients had no change (NC), and 1 patient had progressive diseases (PD). The overall effective rate (CR+PR) was 88.0%. All patients had no serious postoperative complications. Conclusion:CT-guided implantation of radioactive ~(125)I seed was an effective and safe method in the treatment of the residual foci of nasopharyngeal carcinoma after radiotherapy.

Adult ; Femur Head Necrosis ; chemically induced ; drug therapy ; Glucocorticoids ; therapeutic use ; Humans ; Male ; Paraquat ; poisoning

Human leukemias are considered as clonal malignancies initiated at stage as early as hematopoietic stem/progenitor cells. The drug resistance and relapse are two major causes for treatment failure of leukemia. Recently, the discovery of leukemia stem/progenitor cells (LSPC) and subsequent research have provided a cue to elucidate the pathogenesis of leukemia and to explore the strategies of targeted therapy against LSPC. This review summarizes the molecular characteristics of LSPC and some research advances of therapy targeting LSPC including therapy targeting to surface molecules of LSPC, interference of interaction between LSPC and bone marrow microenvironment, regulation mechanisms of some specific molecular and so on.
Humans ; Leukemia ; therapy ; Neoplastic Stem Cells ; Stem Cell Transplantation

Objective To explore the relationship between DNA repair gene XRCC1 and XPD polymorphisms and individual susceptibility to prostate cancer. Methods PCR-restriction fragment length polymorphism assay was used to analyze the XRCC1 (C26304T and G28152A) and XPD A35931C polymorphisms in 358 prostate cancer patients and 312 healthy controls. Unconditional logistic regression analysis was performed to calculate odd ratio (OR) and 95% confidence interval (CD for estimating the correlation between different genotypes and prostate cancer risks. Results Forty-seven(13.1%) cases present XRCC1 28152AA genotype in prostate cancer group, while 24 cases in the control group (7. 1%), individuals with this genotype had a significantly increased risk for prostate cancer (OR 1. 924, 95%CI=1.126 - 3. 288, P=0. 017). There was no significant difference between two groups at XRCC1 C26304T and XPD A35931C sites. Combined analysis of the three sites polymorphisms showed that individuals with XRCC1 28152 AA and XPD 35931AC+CC genotype had a higher risk of prostate cancer than those with three wild genotypes (OR = 3. 087,95%CI 1. 081 - 8.813;OR = 3. 376,95%CI 1.067-10.683;OR 3. 216,95%CI=1. 439-7.188,P = 0. 004). Analysis stratified by age of onset, PSA, Gleason score and T stage revealed that XRCC1 28152AA and XPD 35931 AC+CC high-risk genotype was especially associated with early age at onset of prostate cancer (P<0. 05). Conclusions The XRCC1 and XPD genotypes may be contributed to the risk of developing prostate cancer, particularly for younger patients.

Objective To explore the expression feature of long non-coding RNA (lncRNA) 1010001N08Rik in hyperoxia-induced bronchopulmonary dysplasia (BPD) and predict the mechanism that 1010001N08Rik might be involved in the occurrence and development of BPD by a series of bioinformatics analysis.Method The sequence,genomic position and structure characteristics of 1010001N08Rik were acquired from UCSC genome browser,and its target gene was predicted by Ensemble database.We successfully established the animal model of BPD by making newborn C57BL/6J mice exposed to 95％ concentrations of ambient oxygen for seven days.The expression of 1010001N08Rik and Gata 6 were detected using real-time quantitative polymerase chain reaction (PCR).Student's t test was used to compare their expression levels during the BPD process.Result The relative expression of 1010001N08Rik in BPD process at d1,d3,d5,d7 was 1.21 ± 0.33,2.02 ± 0.41,2.95 ± 0.45,4.20-± 0.48 respectively,and there were significant difference between adjacent time points (P ＜ 0.05).The relative expression of Gata 6 mRNA was 0.92 ±0.30,1.10 ± 0.31,0.86 ± 0.24,0.45-± 0.08 respectively,and there was significant difference between d5 and d7 (P ＜0.05).1010001N08Rik had highly conserved property among different species.The chromosomal regions of 1010001N08Rik existed transcriptional factors binding locations and epigenetic regulation clues,and its possible candidate target gene was Gata 6.Conclusion The expression of 1010001N08Rik increased during the formation process of BPD.Bioinformatics analysis and preliminary experiment results suggested that 1010001N08Rik might participate in the process of BPD by down-regulating Gata 6 expression.

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) onpromotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to induce the liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells.qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1. Liquid chromatography-mass spectrometry (LC-MS) and co-immunoprecipitation (Co-IP) were conducted to identify proteins interacting with PID1.Chromatin immunoprecipitation(ChIP)was operated to measure the modification of H3K4me3 of PID1 promoter.RESULTS PID1 restriction improved insulin resistance,hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover,PID1 liver-specific protooncogenes via hydrodynamics-based transfection established a primary hepatocellular carcinoma mouse model,induced an immunosuppressive environment,with the reduction of CD3+,CD4+,CD8+T cells,retarded maturation of dendritic cells(DCs),pronounced differentiation of regulatory T cells(Tregs),and recruitment of MDSC.In addition,PID1 overexpression activated prolifer-ation related genes, promoted anti-inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor(EGFR)and activation of downstream KRAS/ERK pathway.As such,PID1 exist trimethylation of histone H3 at lysine 4(H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function.IR accelerates liver cancer development and progression partially dependent on the activation of PID1.

Objective To investigate the role of expression of tall-like receptor 4 (TLR4) on medullary system cell (neutrophii, platelet) and endothelial cell surface in polymorphonuclear neutrophils (PMN) recruitment in rata with acute necrotizing pancreatitis. Methods C3H/He-J mice and C3H/He-N mice were divided into 4 groups by bone marrow transplantation: mosaic of medullary system cell TLR4-/- and endothelial cell TLR4 +/+ ; mosaic of medullary system cell TLR4 +/+ and endothelial cell TLR4-/-; mosaic of medullary system cell TLR4 +/+ and endothelial cell TLR4 -/-; mosaic of medullary system cell TLR4-/- and endothelial cell TLR4-/-, another control group was also established. ANP was induced in all these groups by intraperitoneal injection of cerulein and caudal vein injection of lipopolysaccharide. Serum amylase, pancreatic tissue naphthol AS-D chloroacetate esterase, MPO activity, TRL4 mRNA expression in peripheral blood granuloeyte was determined by RT-PCR, TRL4 protein expression in pancreatic tissue was measured by immunohistochemisty. Results Compared with that of control group, the levels of serum amylase in the 4 groups all significantly elevated and there was no difference among these 4 groups. Pathological scores of pancreas in the 4 groups were 5.52 ± 1.21, 5.18 ± 1.02, 2.03 ± 0. 82, 1.92 ± 0. 78, respectively; MPO activities were (1.834 ± 0. 170) U/g, (2. 596 ±0. 138) U/g, (0. 367 ±0. 018) U/g, (0. 202 ±0. 018) U/G, respectively; AS-D counts were 66.88 ± 2.17, 75.00 ± 2.43, 21.50 ± 2.38, 20.00 ± 2.19, respectively ; the expressions of TLR4mRNA of granular cell in peripheral blood were 0. 037 ± 1. 047 E-2, 1. 489 ± 8. 084 E-2, 1.470 ± 5. 210E-2, 0. 017 ± 6. 668 E-3, respectively; the 2 groups with endothelial eel1 TLR4 +/+ had strongly positive expression of TLR4 protein in vascular endothelial cell ; while the 2 groups with endothelial cell TLR4-/- had no expression; the pancreatic injuries, MPO activities, AS-D counts and TLR4 protein in the 2 groups with endothelial cell TLR4 +/+ were significantly higher than those in the 2 groups with endothelial cell TLR4-/-. Conclusions It was endothelial cell, not peripheral blood granulocyte, which played a key role in the process of neutrophil recruitment and pathological injure of ANP.

Objective To investigate the significance of expression of toll-like receptor on medullary system cell and endothelial cell surface in PMN recruiting in severe acute pancreatitis.Method In this study,26 C3H/He-J mice and 26 C3H/He-N mice were derided into 4 groups by bone marrow transplantation:group A, mosaic of medullary system cell TLR4-/- and endothelial cell TLR4+/+,group B, mosaic of medullary system cell TLR4+/+ and endothelial cell TLR4-/- ;group C, homozygote ofTLR4+/+ ;group D, homozygote of TLR4-/-. SAP was induced to all these mice. Amylase, TRIA of granular cell in peripheral blood,TRL4 expression in pancreas, Naphthol AS-D chloroacetate esterase, MPO activity were tested. Results Amylase level increased in all mice, there was no differences of the amylase level among groups, TRIA of granular cell in peripheral blood in group B and C was significant higher than A and D(P<0.05), TLR4 in pancreas were positive in group A and C, negative in group B and D, AS-D count and M PO activity in group A and C were higher than that in group B and D (P < 0. 05 ). Conclusions It was endothelial cell, not peripheral blood granulocyte, that plays a key role in recuiting neutrophils that triggers severe acute pancreatitis.