Radioactive 125I interstitial brachytherapy is easy to cause the intestinal tract tissue damage.Its mechanism possibly correlates to the quick renewal speed of the intestinal tract tissue and a majority of ceils in M, G2 and late S phases. The tolerant dose of intestinal tract tissue is approximately 160 Gy. If the absorbed dose is higher than the tolerant one, the intestinal tract tissue will be damaged. In the clinical practice of radio-active 125I interstitial brachytherapy, through the strict plan of the TPS system before the operation, by using ul-trasound, CT, MR/and other imaging technologies in the operating process and establishing the suitable barrier protection between the seeds and intestinal tract tissue, the radioactive damage of the intestinal tract tissue my be reduced.

Objective The relationship between XbaI polymorphism of ApoB gene and cerebral infarction(CI)among Chinese population was assessed by Meta-analysis.Methods All related case-control studies were collected from all publications,the relevant studies were identified after eliminating those poor-qualified studies.Meta-analysis was conducted for investigating heterogeneity among individual studies,and summarizing the effects across studies.Results The combined data statistics revealed the frequencies of the X-X+/X+X+ genotypes showed no statistically difference(Z=1.72,P=0.08).Through the subgroup analysis,it was obviously increase the risk of CI in Chinese northern population(OR=2.66,95%CI:1.67~4.24),but no statistically difference in Chinese southern population(OR=1.26,95%CI:0.90~1.77).Conclusions ApoB gene XbaI polymorphism may be significantly associated with susceptibility of CI in Chinese northern population,but not a definite risk for Chinese southern population.

Animals ; Aorta ; metabolism ; Hyperlipidemias ; metabolism ; Mice ; Mice, Inbred C57BL ; Nitric Oxide Synthase ; metabolism ; Physical Conditioning, Animal ; Physical Endurance

Adult ; Aortic Rupture ; pathology ; Death, Sudden, Cardiac ; etiology ; Heart Ventricles ; pathology ; Humans ; Male

This study aimed to investigate the immune adjuvant effect and mechanism induced by chitosan nanoparticles carrying pJME/GM-CSF. In this study, plasmid DNA (pJME/GM-CSF) was encapsulated in chitosan to prepare chitosan-pJME/GM-CSF nanoparticles using a complex coacervation process. Immunohistochemistry was used to detect the type of infiltrating cells at the site of intramuscular injection. The phenotype and functional changes of splenic DCs were measured by flow cytometry after different immunogens were injected intramuscularly. The killing activity of CTLs was assessed using the lactate dehydrogenase (LDH) release assay. The preparation of chitosan-pJME/GM-CSF nanoparticles matched the expected theoretical results. Our results also found that, after pJME/GM-CSF injection, the incoming cells were a mixture of macrophages, neutrophils, and immature DCs. Meanwhile, pJME/GM-CSF increased the expression of MHC class II molecules on splenic DCs, and enhanced their Ag capture and presentation functions. Cell-mediated immunity was induced by the vaccine. Furthermore, chitosan-pJME/GM-CSF nanoparticles outperformed the administration of standard pJME/GM-CSF in terms of DC recruitment, antigen processing and presentation, and vaccine enhancement. These findings reveal that chitosan could be used as delivery vector for DNA vaccine intramuscular immunizations, and enhance pJME/GM-CSF-induced cellular immune responses.
Adjuvants, Immunologic ; administration & dosage ; Animals ; Chitosan ; administration & dosage ; immunology ; Dendritic Cells ; immunology ; virology ; Encephalitis Virus, Japanese ; genetics ; immunology ; Encephalitis, Japanese ; immunology ; prevention & control ; virology ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor ; administration & dosage ; genetics ; immunology ; Humans ; Immunity, Cellular ; Japanese Encephalitis Vaccines ; administration & dosage ; genetics ; immunology ; Mice ; Mice, Inbred BALB C ; Nanoparticles ; administration & dosage ; Spleen ; immunology ; T-Lymphocytes, Cytotoxic ; immunology ; virology ; Vaccines, DNA ; administration & dosage ; genetics ; immunology

Adult ; Aged ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; pathology ; physiopathology ; Respiratory Function Tests

AimThe aim of this study was to establish a rodent model with similar characters of human metabolic syndrome(MS).Methods Three species mice and Wistar rats were fed with high energy chows(HEC)for 6 to 23 weeks.Animals were weighted every week.Fasting blood glucose(FBG)together with total cholesterol(TC)and low density lipoprotein-cholesterol(LDL-C)were investigated by oxidase test every two week.And fasting blood insulin(FINS)was determined by radioimmunoassay.Homeostasis model assessment of insulin resistance(HOMA-IR)was calculated as FBG×FINS/22.5.At the end of the experiment,oral glucose tolerance test(OGTT)was performed.Then animals were decapitated,and coel-fat and orchio-fat were collected and weighted to calculate the visceral fat coefficient(VFC).Results FBG,serum TC and LDL-C significantly increased(P<0.01)after 6 weeks feed of HEC in KM mice.The mice also formed abdominal obesity and insulin resistant together with impairment of glucose tolerance(P<0.05 or P<0.01).Though similar to the KM mice,C57BL/6 and BALB/c mice couldn't form abdominal obesity while the latter had increased body weight(P<0.05 or P<0.01).Wistar rats formed hyperlipidemia from 1 to 10 week and hyperglycemia from 10 to 23 week together with insulin resistance and impaired glucose tolerance(P<0.05 or P<0.01).Conclusion KM mice feed with HEC for 6 weeks could successfully establish metabolic syndrome mice model which might be suitable for drug-screening,the major characters includes the formation of abdominal obesity(increase of VFC),the increase of serum TC,LDL-C,FBG and HOMA-IR,and the decrease of OGTT.

60 Gy.The 5-year local control rates are 92%,71% and 87% respectively(P=0.9194),and 5-year overall survival rate are 68%,62% and 53% respectively(P=0.4194).There is no significant difference of overall survival and local control rate between these three dose groups.Five patients with dose of more than 50Gy died of late toxicities.Conclusions:Adjuvant radiotherapy for Stage Ⅱ and Ⅲ patients with rectal cancer dose not show dose response.There is no improvement of local control and survival due to the escalation of dose.The dose of conventional radiotherapy is better at less than 50Gy.Overdosage may lead to severe toxicities.

AIM To observe the protective effect of total flavone of Abelmoschl Manihot L medic(TFA) on myocardial ischemia reperfusion injury(IRI) in the rat heart in vitro. METHODS We adopted the method of in vivo perfusion set up by Langendorff to observe the changes of some markers, such as MDA,SOD,CPK,LDH,etc in the myocardial homogenate in the rat heart following ischemia and reperfusion. RESULTS TFA( 100,50,25 mg?L -1) can significantly reduce the lipid peroxidation product malondialdehyde(MDA), increase the activity of myocardium superoxide dismutase(SOD), decrease the transudation of creatine phosphokinase(CPK) and lactate dehydrogenase (LDH) from cardiomyocyte. And also, TFA caused an improvement of nitric oxide (NO) and its synthase, NOS. CONCLUSION TFA play a protective role on myocardial reperfusion injury in the rat in vitro via inhibition of lipid peroxidation, enhancement of anti-oxidation and relaxing of coronary artery.

Objective To observe the expression of cysteine rich-protein 61 (Cyr61) on renal tubular cells,to explore its effects against hypoxic induced kidney injury and the underlying mechanisms.Methods A stably Cyr61 expressed tubular cell line Cyr61-HK2 was established based on HK2 cells and recombinant Cyr61-lentivirus.BrdU incorporation assay was used for cell proliferation.The apoptosis of cells was analyzed by flow cytometry with Annexin V and propidiumiodide staining.Western bloting was used to detect the protein expression of BAD,Akt and ERK.Results (1) Cyr61-HK2 cells displayed more proliferation ability than HK2 cells.(2) Under hypoxia condition,the apoptosis of both HK2 and Cyr61-HK2 cells increased,but the apoptosis of Cyr61-HK2 cells was lesser than HK2 cells.(3) The expression of Cyr61 led to the phosphorylation of BAD,Akt and ERK on 0 h,0.5 h,1 h (all P ＜ 0.05).Conclusion The expression of Cyr61 can promote cell proliferation and dampen cell apoptosis induced by hypoxia,which may be involved in the Akt/ERK signal pathway.