Data Fusion of Electronic Nose and Electronic Tongue for Detection of Mixed Edible-Oil

For the problem of the waste of the edible-oil in the food processing, on the premise of food security, they often need to add new edible-oil to the old frying oil which had been used in food processing to control the cost of the production. Due to the fact that the different additive proportion of the oil has different material and different volatile gases, we use fusion technology based on the electronic nose and electronic tongue to detect the blending ratio of the old frying oil and the new edible-oil in this paper. Principal component analysis (PCA) is used to distinguish the different proportion of the old frying oil and new edible-oil; on the other hand we use partial least squares (PLS) to predict the blending ratio of the old frying oil and new edible-oil. Two conclusions were proposed: data fusion of electronic nose and electronic tongue can be used to detect the blending ratio of the old frying oil and new edible-oil; in contrast to single used electronic nose or single used electronic tongue, the detection effect has increased by using data fusion of electronic nose and electronic tongue

Data Fusion of Electronic Nose and Electronic Tongue for Discrimination of Chinese Liquors

The aim of this work is to improve the performance of electronic nose system and electronic tongue system by fusing the data of different sensor types, and a data fusion technique is presented in this paper. Eight different commercial brands of liquor were discriminated by using electronic nose and electronic tongue. Principle Component Analysis (PCA) was applied on the data of electronic nose and electronic tongue respectively, the classification result was not good enough. However, the result was improved by using the data fusion technique. Therefore, this technique can enhance the ability of PCA. Bayesian classifier and Bayesian classifier based on PCA were used to further classify the samples, two conclusions were proposed: compared with the single application of electronic tongue or electronic nose, the fusion technique has improved the classification accuracy; in contrast with the Bayesian classification, Bayesian classification based on PCA method has increased the classification speed trebly

Gene therapy for C-26 colon cancer using heparin-polyethyleneimine nanoparticle-mediated survivin T34A

Ling Zhang1,*, Xiang Gao1,2,*, Ke Men1, BiLan Wang1, Shuang Zhang1, Jinfeng Qiu1, Meijuan Huang1, MaLing Gou1, Ning Huang2, ZhiYong Qian1, Xia Zhao1, YuQuan Wei11State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, 2Department of Pathophysiology, College of Preclinical and Forensic Medical Sciences, Sichuan University, Chengdu, People’s Republic of China*These authors contributed equally to this workBackground: Gene therapy provides a novel method for the prevention and treatment of cancer, but the clinical application of gene therapy is restricted, mainly because of the absence of an efficient and safe gene delivery system. Recently, we developed a novel nonviral gene carrier, ie, heparin-polyethyleneimine (HPEI) nanoparticles for this purpose.Methods and results: HPEI nanoparticles were used to deliver plasmid-expressing mouse survivin-T34A (ms-T34A) to treat C-26 carcinoma in vitro and in vivo. According to the in vitro studies, HPEI nanoparticles could efficiently transfect the pGFP report gene into C-26 cells, with a transfection efficiency of 30.5% ± 2%. Moreover, HPEI nanoparticle-mediated ms-T34A could efficiently inhibit the proliferation of C-26 cells by induction of apoptosis in vitro. Based on the in vivo studies, HPEI nanoparticles could transfect the Lac-Z report gene into C-26 cells in vivo. Intratumoral injection of HPEI nanoparticle-mediated ms-T34A significantly inhibited growth of subcutaneous C-26 carcinoma in vivo by induction of apoptosis and inhibition of angiogenesis.Conclusion: This research suggests that HPEI nanoparticle-mediated ms-T34A may have a promising role in C-26 colon carcinoma therapy.Keywords: gene therapy, mouse survivin-T34A, colon cancer, polyethyleneimine, nanoparticles, cancer therap

Identification of the genetic determinants of Salmonella enterica serotype Typhimurium that may regulate the expression of the type 1 fimbriae in response to solid agar and static broth culture conditions

<p>Abstract</p> <p>Background</p> <p>Type 1 fimbriae are the most commonly found fimbrial appendages on the outer membrane of <it>Salmonella enterica </it>serotype Typhimurium. Previous investigations indicate that static broth culture favours <it>S</it>. Typhimurium to produce type 1 fimbriae, while non-fimbriate bacteria are obtained by growth on solid agar media. The phenotypic expression of type 1 fimbriae in <it>S</it>. Typhimurium is the result of the interaction and cooperation of several genes in the <it>fim </it>gene cluster. Other gene products that may also participate in the regulation of type 1 fimbrial expression remain uncharacterized.</p> <p>Results</p> <p>In the present study, transposon insertion mutagenesis was performed on <it>S</it>. Typhimurium to generate a library to screen for those mutants that would exhibit different type 1 fimbrial phenotypes than the parental strain. Eight-two mutants were obtained from 7,239 clones screened using the yeast agglutination test. Forty-four mutants produced type 1 fimbriae on both solid agar and static broth media, while none of the other 38 mutants formed type 1 fimbriae in either culture condition. The flanking sequences of the transposons from 54 mutants were cloned and sequenced. These mutants can be classified according to the functions or putative functions of the open reading frames disrupted by the transposon. Our current results indicate that the genetic determinants such as those involved in the fimbrial biogenesis and regulation, global regulators, transporter proteins, prophage-derived proteins, and enzymes of different functions, to name a few, may play a role in the regulation of type 1 fimbrial expression in response to solid agar and static broth culture conditions. A complementation test revealed that transforming a recombinant plasmid possessing the coding sequence of a NAD(P)H-flavin reductase gene <it>ubiB </it>restored an <it>ubiB </it>mutant to exhibit the type 1 fimbrial phenotype as its parental strain.</p> <p>Conclusion</p> <p>Genetic determinants other than the <it>fim </it>genes may involve in the regulation of type 1 fimbrial expression in <it>S</it>. Typhimurium. How each gene product may influence type 1 fimbrial expression is an interesting research topic which warrants further investigation.</p

Astragaloside IV alleviates 1-deoxysphinganine-induced mitochondrial dysfunction during the progression of chronic kidney disease through p62-Nrf2 antioxidant pathway

Introduction: Chronic kidney disease (CKD) can lead to significant elevation of 1-deoxysphingolipids (1-deoxySL). The increase of 1-deoxySL in turn can result in mitochondrial damage and oxidative stress, which can cause further progression of CKD.Methods: This study assessed the therapeutic effect of Astragaloside IV (AST) against 1-deoxySL-induced cytotoxicity in vitro and in rats with CKD. HK-2 cells were exposed to 1-deoxysphinganine (doxSA) or doxSA + AST. doxSA-induced mitochondrial dysfunction and oxidative stress were evaluated by immunostaining, real-time PCR, oxidative stress sensor, and transmission electron microscopy. The potential effects of AST on kidney damage were evaluated in a rat 5/6 nephrectomy (5/6 Nx) model of CKD.Results: The findings of in vitro experiments showed that doxSA induced mitochondrial damage, oxidative stress, and apoptosis. AST markedly reduced the level of mitochondrial reactive oxygen species, lowered apoptosis, and improved mitochondrial function. In addition, exposure to AST significantly induced the phosphorylation of p62 and the nuclear translocation of Nrf2 as well as its downstream anti-oxidant genes. p62 knock-down fully abolished Nrf2 nuclear translocation in cells after AST treatment. However, p62 knock-down did not affect TBHQ-induced Nrf2 nuclear translocation, indicating that AST can ameliorate doxSA-induced oxidative stress through modulation of p62 phosphorylation and Nrf2 nuclear translocation.Conclusion: The findings indicate that AST can activate Nrf2 antioxidant pathway in a p62 dependent manner. The anti-oxidative stress effect and the further mitochondrial protective effect of AST represent a promising therapeutic strategy for the progression of CKD

Factors associated with low cure rate of tuberculosis in remote poor areas of Shaanxi Province, China: a case control study

<p>Abstract</p> <p>Background</p> <p>The directly observed therapy-short course (DOTS) strategy was introduced in Shaanxi province, China to improve tuberculosis (TB) control by means of improved case detection (target: > = 70%) and treatment success rates (target: > = 85%) in new smear positive (SS+) TB patients. At a provincial level the targets were both reached in 2005. However in 30 (28%) out of 107 counties of Shaanxi province the cure rate was below 85%. This study aimed to investigate patient and treatment characteristics associated with non-cure after tuberculosis (TB) treatment in these counties.</p> <p>Methods</p> <p>In this case-control study, new smear positive TB cases in 30 counties with a cure rate <85% were included. Cured patients were compared to non-cured patients using logistic regression analysis to assess determinants for non-cure.</p> <p>Results</p> <p>Of the 659 patients included, 153 (23.2%) did not have cure as treatment outcome. Interruption of treatment was most strongly associated with non-cure (OR = 8.7, 95% CI 3.9-18.4). Other independent risk factors were co-morbidity, low education level, lack of appetite as an initial symptom of TB disease, diagnosis of TB outside of the government TB control institutes, missing sputum re-examinations during treatment, and not having a treatment observer. Twenty-six percent of patients did not have a treatment observer. The non-cure rate was better for those with a doctor (odds ratio (OR) 0.38, 95% confidence interval (CI) 0.17-0.88) as treatment observer than for those with a family member (OR 0.62, 95%CI 0.37-1.03). The main reason for interrupted treatment mentioned by patients was presence of adverse effects during treatment (46.5%).</p> <p>Conclusions</p> <p>Interruption of treatment was most strongly associated with non-cure. Although treatment observation by medical staff is preferred, in order to diminish the proportion of patients who do not have a treatment observer and thereby reduce the proportion of patients who interrupt treatment, we suggest making it possible for family members, after sufficient training, to be treatment observers in remote areas where it is logistically difficult to have village doctors observe treatment for all patients.</p

All-cause mortality and risk factors in a cohort of retired military male veterans, Xi'an, China: an 18-year follow up study

<p>Abstract</p> <p>Background</p> <p>Risk factors of all-cause mortality have not been reported in Chinese retired military veterans. The objective of the study was to examine the risk factors and proportional mortality in a Chinese retired military male cohort.</p> <p>Methods</p> <p>A total of 1268 retired military men aged 55 or older were examined physically and interviewed using a standard questionnaire in 1987. The cohort was followed up every two years and the study censored date was June30, 2005 with a follow-up of up to 18 years. Death certificates were obtained from hospitals and verified by two senior doctors. Data were entered (double entry) by Foxbase, and analysis was carried out by SAS for Windows 8.2. Multivariate Cox proportional hazard regression model was used to compute hazard ratio (HR) and 95% confidence interval (CI).</p> <p>Results</p> <p>The total person-years of follow-up was 18766.28. Of the initial cohort of 1268 men, 491 had died, 748 were alive and 29 were lost to follow up. Adjusted mortality (adjusted for age, blood pressure, body mass index, cholesterol, triglycerides, alcohol, exercise, and existing disease) was 2,616 per 100,000 person years. The proportional mortality of cancer, vascular disease and Chronic Obstructive Pulmonary Disease (COPD) were 39.71%, 28.10% and 16.90% respectively. Multivariate analysis showed that age, cigarettes per day, systolic blood pressure, triglyceride, family history of diseases (hypertension, stroke and cancer), existing diseases (stroke, diabetes and cancer), body mass index, and age of starting smoking were associated with all-cause mortality, HR (95%CI) was1.083(1.062–1.104), 1.026(1.013–1.039), 1.009(1.003–1.015), 1.002(1.001–1.003), 1.330(1.005–1.759), 1.330(1.005–1.759), 1.444(1.103–1.890), 2.237(1.244–4.022), 1.462(1.042–2.051), 2.079(1.051–4.115), 0.963(0.931–0.996)and 0.988(0.978–0.999)respectively. Compared with never-smokers, current smokers had increased risks of total mortality [HR 1.369(1.083–1.731)], CHD [HR 1.805 (1.022–3.188)], and lung cancer [HR 2.939 (1.311–6.585)].</p> <p>Conclusion</p> <p>The three leading causes of diseases were cancer, CHD and stroke, and COPD. Aging, cigarette smoking, high systolic blood pressure, high triglyceride, family history of cancer, hypertension and stroke, existing cases recovering from stroke, diabetes and cancer, underweight, younger age of smoking were risk factors for all-cause mortality. Quitting cigarette smoking, maintaining normal blood pressure, triglyceride and weight are effect control strategies to prevent premature mortality in this military cohort.</p

Impact of Darker, Intermediate and Lighter Phenotypes of Body Melanization on Desiccation Resistance in Drosophila melanogaster

A possible link between melanization and desiccation resistance can be inferred if within population differences in melanization find significant correlations with desiccation resistance and its mechanistic basis i.e. rate of water loss/hr. Accordingly, darker, intermediate and lighter phenotypes of body melanization were analyzed in wild and laboratory reared Drosophila melanogaster L. (Diptera: Clyclorrapha) populations from highland and lowland sites located in close proximity at five different latitudinal locations (11.15 °N to 31.06°N) within the Indian subcontinent. In large population samples, occurrence of significant within population variability made it possible to assort non-overlapping phenotypes of body coloration (i.e. lighter (< 25%), intermediate (30 to 40%) and darker (> 45%)) for all the populations which were further investigated for desiccation resistance and rate of water loss/hr. Significantly, higher desiccation resistance but much reduced rate of water loss/hr were observed in darker and intermediate phenotypes in all the populations. By contrast, lighter phenotypes exhibited lower desiccation tolerance but higher rate of water loss/hr. A regression analysis between traits provided similar slope values for wild and laboratory populations. For all three physiological traits, predicted trait values from multiple regression analysis as a simultaneous function of annual average temperature and relative humidity, matched the observed values. We infer that parallel changes in melanization and desiccation resistance may result from decreasing annual average temperature and relative humidity along increasing latitude as well as altitude on the Indian subcontinent

TNF-α and TGF-β Counter-Regulate PD-L1 Expression on Monocytes in Systemic Lupus Erythematosus

Monocytes in patients with systemic lupus erythematosus (SLE) are hyperstimulatory for T lymphocytes. We previously found that the normal program for expression of a negative costimulatory molecule programmed death ligand-1 (PD-L1) is defective in SLE patients with active disease. Here, we investigated the mechanism for PD-L1 dysregulation on lupus monocytes. We found that PD-L1 expression on cultured SLE monocytes correlated with TNF-α expression. Exogenous TNF-α restored PD-L1 expression on lupus monocytes. Conversely, TGF-β inversely correlated with PD-L1 in SLE and suppressed expression of PD-L1 on healthy monocytes. Therefore, PD-L1 expression in monocytes is regulated by opposing actions of TNF-α and TGF-β. As PD-L1 functions to fine tune lymphocyte activation, dysregulation of cytokines resulting in reduced expression could lead to loss of peripheral T cell tolerance