OBJECTIVETo explore the effect of Peitu Shengjin Recipe (PSR) on nutritional states and immune functions of stable phase chronic obstructive pulmonary disease (COPD) patients.

METHODSTotally 62 stable phase COPD patients were randomly assigned to the treatment group (30 cases) and the control group (32 cases). All patients inhaled Seretide (50/500 µg), twice per day. Besides, patients in the treatment group additionally received PSR, one dose per day. After three months of treatment, the COPD assessment test (CAT) score, the index of nutritional states [including body mass index (BMI) , thickness of skin fold (TSF), mid-arm muscle circumference (MAMC), serum albumin, serum prealbumin], and immune functions (including IgA, IgM, and IgG) were compared between the two groups.

RESULTSBy the end of the treatment, the CAT score decreased more obviously in the treatment group than in the control group (P < 0.05). The improvement of BMI, TSF, MAMC, serum albumin, and serum prealbumin was better in the treatment group than in the control group (P < 0.05). IgM and IgG also increased more in the treatment group (P < 0.05). There was no statistical difference in IgA between the two groups (P > 0.05).

CONCLUSIONSAdditionally use of PSR could improve nutritional states and immune functions of stable phase COPD patients to some extent. Meanwhile, it also could improve their health related quality of life.

Body Mass Index ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Nutritional Status ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; immunology ; Quality of Life ; Serum Albumin

Objective To investigate the release and intracellular localization of high mobility group box chromosomal protein 1(HMGBl)in the peripheral blood monocytes of rheumatoid arthritis(RA) patients and the inhibitive effect of thaiidomide.Methods 19 RA patients and 20 healthy controls were included in the study.Monocytes were separated from peripheral blood with Ficoll density gradient centrifugation.Monocytes were treated with 100 ng/ml tumor necrosis factor α(TNFa)or 100 ng/ml TNFα plus 40 μg/ml thalidomide and grown in an incubator at 37℃ with 5%CO,for 24 hours.The cuIture supernatants of the monocytes were collected.HMGB1 level in the culture medium was detected with Western blot.In addition,the intraceUular localization of HMGB1 in the fflonocytes was investigated with immunocytochemical analysis. Results Without stimulation. the release of HMGBl protein was significantly increased in the culture supernatants of peripheral blood monocytes from RA patients as compared with that from healthy controls(P<0.05).TNFα(100 ng/ml)did not further increase the release of HMGBl in the monocytes from the patients with RA.Thalidomide(40 μg/ml)could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFα(P<0.05).In the monocytes from RA patients,HMGBl was mainly localized in the nucleus.Treatment with TNFOL(100 ng/ml)for 24 hour resulted in a cytoplasmic translocation of HMGB1,which was inhibited significantly by thalidomide. Conclusion TNFα induces the release and cytoplasmic translocation of HMGBI in the peTipheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.

Abstract: With the development of molecular biology, non-coding sRNA has been found to play an important regulatory role in gene expression and protein activity, affecting various biological pathways including mosquito resistance against insecticides. Understanding the molecular regulatory mechanisms of drug resistance is essential for controlling mosquitoes, , of which metabolic resistance being the most critical mechanism, mainly referring to the high expression of metabolic detoxification enzyme-related genes (especially the cytochrome P450 enzyme system) in mosquitoes. On the basis of verification of insecticide resistance-related genes, further research on the correlation between sRNA and mosquito resistance-related genes provides new ideas and directions for further exploring the mechanism of mosquito resistance. The study of mosquito metabolic resistance mechanism is of great significance for the control of vector mosquitoes, drug resistance monitoring and novel insecticide development. This article reviews the progress of research on the resistance genes, sRNAs biosynthesis, genes involved in regulating mosquito metabolic detoxification enzymes and their applications.

Objective To demonstrate high mobility group box chromosomal protein 1(HMGBI) expression in synovium and joint,and to identify the role of HMGB1 in the pathogenesis of synovitis and joint destruction in adjuvant-induced arthritis(AA).Methods AA of 15 male rats were induced in SD rats by intradermal injection of 100?l Freud's complete adjuvant in the foot pad of the left hind paw.All rats were killed at the 18th day.Synovium and joints were collected for histopathology studies and determining the expression of HMGB1 by immunohistochemistry,and serum was collected for determining the expression of HMGB1 by western blotting analysis.Results Immunostaining of specimens from normal rats showed that HMGB1 was primarily confined to the nucleus of synoviocytes with occasional cytoplasmic staining.In contrast, inflammatory synovial tissues from AA rats showed a distinctly different HMGB1 staining pattern.Nuclear HMGBI expression was accompanied by a cytoplasmic staining in many mononuclear cells.The cytoplasmic HMGB1 expression in synovium of AA rats is significantly higher than that of normal rats.Additionally,HMGBI was highly expressed in the nuclei and cytoplasm of the subchondral chondrocytes and inflammatory cells in bone erosion in AA rats(P＜0.01),while fewer positive cytoplasmic staining of HMGB1 was found in chondrocytes and fewer positive nuclear staining was found in bone cells in normal rats.HMGB1 concentration was significantly higher in serum of AA rats than that in normal rats(P＜0.001).Conclusion The cytoplasmic HMGBI expression in synovium and joints is greatly upregulated;the level of HMGB1 in serum is increased in AA rats which suggests a patbogenetic role of HMGB1 in synovitis and bone destruction of adjuvant-induced arthritis.

Objective To study the effect of antiapoptosis factors PED/PEA-15 and XIAP on prostate cancer cells(PC-3)apoptosis.Methods The expressions of XIAP and PED/PEA-15 in prostate cancer cells(PC-3)were respectively assayed using the RT-PCR technique.XIAP and PED/ PEA-15 specific siRNA vectors were designed and constructed and then were transiently cotransfected into PC-3 cells under induction of liposome.The effects of siRNA vectors on PED/PEA-15 and XIAP transcription were assayed by RT-PCR technique,and the effect of XIAP and PED/PEA-15 on cancer cell apoptosis were determined by flow cytometry and microscope observation.Results PED/PEA- 15 and XIAP were both highly expressed in PC-3 cells.Enzyme digestion analysis and DNA sequencing confirmed that the PED/PEA-15 and XIAP-specific siRNA expression vectors were constructed successfully.The designed siRNA sequences of PED/PEA-15 and XIAP could specifically inhibit their transcription.The PC-3 cells which were cotransfected with PED/PEA-15 and XIAP- specific siRNA vectors were more sensitive to doxorubicin.The apoptosis rate of cotransfected cells was significantly increased.Conclusions PED/PEA-15 and XIAP might be involved in the development of prostate cancer.

Anthropometry ; Body Height ; Body Weight ; Breast Feeding ; Child ; Child Development ; China ; Female ; Growth Charts ; Humans ; Infant ; Infant, Newborn ; Male ; Public Health ; standards ; Reference Values ; Sex Factors ; World Health Organization

OBJECTIVEThe study aimed to test if Paridis Rhizoma total saponins (PRTS) could induce apoptosis of human gastric cancer cell MKN-45.

METHODBased on the previous researches, PRTS was set by different concentrations to treat human gastric cancer cell for 12 h (5, 10, 20 mg x L(-1)). Fluorescent staining methods were adopted to observe apoptotic morphological changes of MKN-45. The apoptosis rates were analyzed by flow cytometry with Annexin V-FITC/PI staining. The enzymatic activities of caspase-3 and caspase-8 were measured by ELISA. The protein levels of Fas and FasL were detected by Western blotting.

RESULTUnder a fluorescence microscope, MKN-45 treated by PRTS was seen typical apoptotic morphological features. PRTS significantly increased the rate of apoptosis. Compared with the control group, there exsited significant differences in apoptosis rate of PRTS concentration of 20 mg x L(-1) (P < 0.01); besides, the enzymatic activities of caspase-3 and caspase-8 were promoted obviously after the effect of PRTS on MKN-45 cells for 12 h (P < 0.01). The protein levels of Fas and FasL in the MKN-45 were upgraded significantly.

CONCLUSIONPRTS can induce apoptosis of human gastric cancer cell MKN-45 , which is concerned with caspase-3 and caspase-8 and upgraded Fas and FasL.

Apoptosis ; drug effects ; Caspase 3 ; genetics ; metabolism ; Caspase 8 ; genetics ; metabolism ; Cell Line, Tumor ; Drugs, Chinese Herbal ; pharmacology ; Fas Ligand Protein ; metabolism ; Humans ; Magnoliopsida ; chemistry ; Rhizome ; chemistry ; Saponins ; pharmacology ; Signal Transduction ; drug effects ; Stomach Neoplasms ; drug therapy ; genetics ; metabolism ; physiopathology ; fas Receptor ; metabolism

ObjectiveTo explore the role of BTBD10 overexpression in the proliferation of insulinoma cell line INS-1and its mechanism. MethodsThe recombined expression plasmid of pcDNA4.0-BTBD10 was constructed by gene cloning technique and was transfected into INS-1 cell by lipofectamine 2000. The stable overexpression BTBD10 of INS-1cell was selected at 48th hour after transfection.INS-1 cell proliferation activity was measured by MTT method.The expression of BTBD10,protein kinase B(Akt),phospho-Akt(p-Akt),mammal target of rapamycin (mTOR) and phospho-mTOR (p-mTOR) were determined by Western blot.ResultsThe stable overexpression BTBD10 of INS-1 cell wassuccessfullyconstructed.OverproductionofBTBD10promotedbetacellproliferation.The phosphorylation of Akt and mTOR was increased and the ratio of p-Akt/Akt and p-mTOR/mTOR was enhanced in the INS-1 overexpressed by BTBD10.But the expression of total Akt and mTOR presented no obvious changes. Conclusion The overexpression BTBD10 of INS-1 cell could activate of Akt/mTOR signalling pathway via stimulating phospho-mTOR and Akt,and enhance overall cell protein translation,so as to promote proliferation of INS-1 cell.

Objective To investigate the clinical characteristics and chronological change of ulcerative colitis(UC) in the Chinese PLA General Hospital in near 16 years. Methods Patients diagnosed with UC during the period from 1994 to 2009 in the Chinese PLA General Hospital were registered and their clinical profiles were analyzed. Results From 1994 to 2009, of 525 patients diagnosed with UC, with a median onset age of 42 years. The predominant form of UC was extensive colitis, which affected almost 33.3% (175/525), left-sided colitis was present in 21.3% (112/525) and rectum was present in 12.4%(65/525). The chronic relapsing type of UC was the most common (69.0%, 362/525 ), followed by the initial onset type (18. 1%, 95/525 ), chronic continuous type with intermittent exacerbations (9.7%,51/525), and acute fulminant type (3. 2%, 17/525 ). Two hundred and twenty-one patients (42. 1%,221/525) were graded as mild, 162 (30.9% , 162/525) as moderate, and 142(27.0%, 142/525) as severe UC. The proportion of mild colitis and rectum was significantly higher in patients with an onset age of over 60 years, compared with those with an onset age of less than 30 years( P ＜0. 05 ). The proportion of UC patients with old age onset ( P ＜ 0. 05 ), male sex ( P ＜ 0. 01 ), mild colitis ( P ＜ 0. 01 ), rectum ( P ＜0. 01 ) , relapse-free type ( P ＜ 0. 01 ) demonstrated a chronological increase from 1994 to 2009.Conclusions The distinctive clinical features and chronological change were seen in UC patients in recent years. Compare to those with an onset at less than 30 years, the proportion of mild colitis and rectum was significantly larger in patients with an onset at over 60 years of age, and the proportion of UC patients with old age onset, male sex, mild colitis, rectum, relapse type were less.

AIM: In order to explore the pathogenesis of ulcerative colitis (UC), an experimental colitis in mouse was induced by the hapten dinitrochlorobenzene (DNCB), and the activity of leukocyte migration inhibitory factor (LMIF) was measured at the same time. METHODS: 67 BALB/c mice were randomly divided into control (60% ethanol) and DNCB groups. After they were sensitized by smearing 3.3% DNCB on the abdominal skin, they were challenged with DNCB at concentration of 0.1%, 0.2% and 0.4% respectively by instillation once a day. The weight, stool viscosity and hematochezia were observed and accumulated as disease active index (DAI) score. The pathological changes in colon tissue were judged macropathologically and by means of microscope. LMIF activity was determined by the absorbance (A) of migrated leukocytes. RESULTS: Compared to control group, the increases in DAI accumulate score, pathologic score, and LMIF activity in DNCB groups were observed. CONCLUSION: Mouse colitis was induced by DNCB, which was accompanied by an increase in LMIF activity. [