Adenoviridae ; genetics ; Genes, p53 ; Genetic Therapy ; methods ; Genetic Vectors ; Humans ; Neoplasms ; therapy ; RNA Interference ; Tumor Suppressor Protein p53 ; genetics

Psoriasis is a recrudescent chronic inflammatory dermatosis which is called“tinea”in ancient times. Its pathogenesis is not only associated with changes in the blood and body fluids, but also has close connection with external infection of six evil factors. This article sorted data of pathogenesis and treatment from the perspective of external infection of six evil factors, and discovered that pathogenesis of psoriasis includes external factors of four evils of wind, cold, damp and heat and internal factors of blood deficiency and blood dryness. Ancient treatment was based on dispelling wind, clearing away heat and moistening dryness. The pathogenesis can be summarized as follows:wind and poison attack skin and hinder blood production. The treatment can be “let in air for detoxification, enrich blood and moister dryness, cooling and activating blood”, blood and functional status of organs of patients should be observed, with a purpose to provide references and basis for modern clinical prevention and treatment of psoriasis.

OBJECTIVE:To evaluate the effects of compound amino acids capsul es on hypoalbuminemia in patients with chronic renal failure undergoing hemodialysis.METHODS:30hemodialysis patients were selected to orally take2compound amino acids capsules(0.35g per capsule)twice daily for12weeks,renal and liver function and levels of serum albumin and pre-albumin were measured before and after the experiment.RESULTS:The levels of serum albumin and pre-albumin were increased significantly after the treatment,it were(30.5?4.6)g/L vs(35.9?7.1)g/L,and(213.0?46.9)mg/L vs(275.8?52.3)mg/L respectively(P

Objective To investigate the effect of interferon alfα-2b on the ultrastructure and Caspase-3 levels in villus in early pregnancy with bacterial vaginal disease (BV). Method Early pregnant women were divided into two groups. The treated group included 25 early pregnant women with BV who chose to have an early termination and were treated with rhINFα-2b. The controling group included 30 early pregnant women without any genital tract infectious diseases. The caspase-3 levels in trophocytes were detected by immunochemistry and the ultrastructural changes were observed in villus by transmission electron microscopy. Result (1)There was no apparent difference of ultrastructural changes between the two groups. (2)There was no statistical significance of the levels of caspase-3 between the two groups (P>0.05). Conclusion The excessive apoptosis do not occur in the trophocytes when treated with INFα-2b.

Animals ; Botulinum Toxins ; adverse effects ; therapeutic use ; Bruxism ; drug therapy ; Dystonia ; drug therapy ; Humans ; Joint Dislocations ; drug therapy ; Sialorrhea ; drug therapy ; Temporomandibular Joint Disorders ; drug therapy

AIM To determine the relationship between the elevation of endogenous inhibitor of nitric oxide synthase (NOS)N G,N G-asymmetric dimethylarginine (ADMA) and metabolic control in diabetic rats. METHODS Diabetes was induced in Sprague-Dawley rats by a single intraperitoneal injection of streptozotocin. At 72 h after injection, half of diabetic rats received insulin treatment for 8 weeks (20 U?kg -1?d -1,ih, bid). Serum levels of ADMA were measured by high-performance liquid chromatography. Thoracic aortic rings from non-diabetic age-matched control, untreated diabetic, and insulin-treated diabetic rats were tethered in isolated organ baths,contracted with 1 ?mol?L -1 phenylephrine, and challenged with either the endothelium-dependent vasodilator acetylcholine or the endothelium-independent vasodilator sodium nitroprusside. Serum concentrations of glucose, glycosylated serum protein, and malondialdehyde, derived from lipid peroxidation were also examined to estimate metabolic control.RESULTS Serum levels of ADMA significantly elevated in untreated diabetic rats compared with control rats. This elevation of ADMA was accompanied by impairment of relaxation response to acetylcholine but not sodium nitroprusside in aortic rings. Chronic insulin treatment not only prevented the elevation of serum ADMA, but also improved the impaired endothelium-dependent relaxation in diabetic rats. Serum levels of glucose, glycosylated serum protein, and malondialdehyde were significantly increased in parallel with the elevation of ADMA in untreated diabetic rats compared with control rats. These parameters were normalized after diabetic rats received insulin treatment. CONCLUSION These results provide the first evidence that the elevation of endogenous inhibitor of NOS in streptozotocin-induced diabetic rats is close related to metabolic control of the disease.

Objective To evaluate the effects of penehyclidine hydrochloride (PHC) on the expression of Toll like receptor-4 (TLR4) and nuclear factor kappa B (NF-κcB) in a rat model of sepsis-induced acute lung injury (ALI).Methods Seventy-two adult male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =24 each) using a random number table:shame operation group (group S),ALI group and PHC group.Sepsis-induced ALl was induced by cecal ligation and puncture in anesthetized rats.In group PHC,PHC 0.45 mg/kg was intramuscularly injected immediately after cecal ligation and puncture.At 6,12,24 and 36 h after ligation,the broncho-alveolar lavage fluid (BALF) was collected for detection of TNF-α and IL-6 concentrations and the lungs were removed for determination of the expression of TLR4 (using RT-PCR and Western blot) and NF-κBp65 (using Western blot) in lung tissues and for microscopic examination.The pathological changes of lungs were scored.The wet to dry lung weight (W/D) ratio was calculated and the activity of myeloperoxidase (MPO) in lung tissues was measured.Results As compared with S group,the IL-6 concentrations in BALF at 6,12 and 24 h after ligation,TNF-α concentration in BALF at 6 and 12 h after ligation,and the expression of TLR4 and NF-κBp65,pathological scores,W/D ratio and MPO activity at each time point were significantly increased in ALI group (P ＜ 0.05).Compared with ALI group,the TNF-α concentration in BALF at 6 and 12 h after ligation,and IL-6 concentrations in BALF,the expression of TLR4 and NF-κBp65,pathological scores,W/D ratio and MPO activity at each time point were significantly decreased in group PHC (P ＜ 0.05).Conclusion PHC inhibits NF-κB activation and decreases inflammatory responses through blocking TLR4 expression in lung tissues,thus attenuating sepsis-induced ALI in rats.

Modern medicine makes it possible to turn those former impossible ideas into reality.Meanwhile,more and more social and ethical issues are also drawing public attention arising from the development of modern medicine.This paper explores reasonable and feasible countermeasures to cope with the ethical issues brought by modern medical development from a cultural perspective.

Background Studies confirmed that hydroxycamptothecin cause the apoptosis of human Tenon capsule fibroblasts (HTFs) by protein kinase R-like endoplasmic reticulum stress kinase (PERK) single pathway.Autophagy and apoptosis are programmed cell death following stress reaction,so they remain a close association.However,the effect of hydroxycamptothecin on the autophagy of HTFs and its mechanism are still unclear.Objective This study was to explore the promoting effect of PERK signal pathway on hydroxycamptothecin inducing the autophagy of HTFs.Methods This study procedure was approval by Ethic Committee of Nanjing Medical University.Human Tenon capsule tissue was obtained from fresh adult donors.HTFs were cultured and passaged by explant-culture method and identified by immunofluorescence for vimentin and keratin.pLVX-PERK lentiviral packed by 293T cells was transfected into HTFs to obtain stable PERK-knockout cell line by puromycin selection.Then the HTFs were treated with 0.10 g/L of hydroxycamptothecin for 5 minutes and consecutively cultivated for 24 hours,and the untreated cells were used as the control group.Western blot assay was used to detect the expressions of autophagy specific proteins in the cells,including autophagy related gene 5 (ATG-5),Beclin-1,light chain 3 (LC-3).Cyto-ID staining was used to identify the autophagosome in the cells.The experimental results were analyzed and compared between different treating groups.Results The gray scales for the expressions of Beclin 1,ATG-5,LC-3-Ⅰ and LC-3-Ⅱ proteins in HTFs were 0.365:±0.045,0.765 ±0.055,0.120±0.030 and 0.215 ±0.035 in the control group,and those in the hydroxycamptothecin treated group were 0.980±0.070,1.495±0.095,0.585±0.025 and 0.785±0.055,showing a significant decline in the hydroxycamptothecin treated group(P=0.018,0.022,0.007,0.013).The green fluorescence of the autophagosome was stronger in the hydroxycamptothecin treated group compared with the control group.Western blot revealed that the gray scale of PERK expression in the cells was 0.130±0.030 in the PERK-knockout group,with a significant reduce in comparison with 0.765 ±0.055 of the control group (P =0.010).However,no obvious distinctions were seen in the band intensities of the expressions of Beclin-1,ATG-5 and LC-3 proteins between the two groups.Western blot indicated that the grey scale of the PERK expression in the cells was 1.790± 0.060 in the 0.10 g/L hydroxycamptothecin group,which was significantly higher than 0.880 ± 0.070 of the control group (P =0.010).Expression levels (gray scales) of Beclin-1,ATG-5,LC-3-Ⅰand LC-3-Ⅱ in the PERK-knockout+ 0.10 g/L hydroxycamptothecin group were 0.475 ± 0.045,0.390 ± 0.040,0.055 ± 0.015 and 0.075 ± 0.025,which were significantly lowed in comparison with 0.955 ± 0.065,0.765 ± 0.055,0.155 ± 0.015 and 0.280 ± 0.030 of the control+ 0.10 g/L hydroxycamptothecin group (P =0.026,0.031,0.042,0.034).In addition,the fluorescence intensity of autophagosomes was weaker in the PERK-knockout+0.10 g/L hydroxycamptothecin group compared with the control+0.10 g/L hydroxycamptothecin group.Conclusions Hydroxycamptothecin induces the autophagy of HTFs by PERK signal pathway.

Objective To construct mouse granulocyte-macrophage colony stimulating factor (mGM-CSF) gene eukaryotic expressing plasmid pcDNA3-GM-CSF, to transfect the recombinant into erythroleukemia cell line FBL-3, and identify their biological activity.Methods GM-CSF gene eukaryotic expressing plasmid was constructed by subclone and recombinant was transfected into FBL-3 cells by electroporation. After screening by G418 and cloning by limiting dilution,we obtained positive cell clones(FBL-3-GM-CSF). PCR and RT-PCR were used to identify the integration and stable expression of GM-SF gene in FBL-3-GM-CSF cells. The biological activity was confirmed by the hematopoietic progenitor cell proliferative assay and hematopoietic progenitor cell colony formation assay. Results Mouse GM-CSF cDNA was amplified from the prokaryotic expressing plasmid PET-30a(+)-GM-CSF by PCR firstly and BamH Ⅰ and EcoRⅠrestriction sites were introduced. The inserted fragment was cut by BamH Ⅰ and EcoR Ⅰ digestion and ligated into pcDNA3 vector. The pcDNA3-GM-CSF eukaryotic expressing plasmid was constructed. The recombinant was cleared with appropriate endoneucleases and sequenced. The findings showed that the orientation of the insert was correct, while no rearrangement or mutation was found. PCR and RT-PCR assay showed that GM-CSF gene had integrated into FBL-3-GM-CSF cells and stably expressed. The hematopoietic progenitor cell proliferative assay and hematopoietic progenitor cell colony formation assay demonstrated that the cultured supernatant of FBL-3-GM-CSF cells of expressing GM-CSF should obviously stimulate proliferation of murine marrow mononuclear cells, and could stimulate hematopoietic progenitor cell colony formation. The number of colony formation was 54.67?4.83. The rate of colony formation was 0.547 %.Conclusions GM-CSF gene eukaryotic expressing plasmid is constructed successfully. A cell clone, which can express stably GM-CSF gene and possess biological activity,is obtained. Our studies have founded the base for the preparation of GM-CSF gene-modified vaccine of tumor cell and the study of feasibility of immune therapy of leukemia.