Localized Surface Plasmon Resonance-Based Colorimetric Assay Featuring Thiol-Capped Au Nanoparticles Combined with a Mobile Application for On-Site Parathion Organophosphate Pesticide Detection.

In this study, we employed a dual strategy for parathion organophosphate pesticide (parathion) detection; first, we used a localized surface plasmon resonance (LSPR)-based colorimetric sensor featuring thiol-capped Au NPs, namely cysteine (Cys)@Au NPs, 11-mercaptoundecanoic acid (11-MUA)@Au NPs, and glutathione (GSH)@Au NPs, via acetylcholinesterase (ACHE) and acetylthiocholine (ATCH) enzyme-mediated hydrolysis reactions; second, we developed a color analysis toxicity-sensing app (Toxin APP). Positively charged thiocholine (TCH) molecules, which were continuously generated via hydrolysis, subsequently conjugated with thiol-capped Au NPs, causing Au NP aggregation through electrostatic attractions. The degree of aggregation of the thiol-capped Au NPs was influenced by parathion concentrations in the range 0 to 108 ppt, because parathion acted as an ACHE inhibitor by controlling the amount of TCH generated. Based on the values of LSPR absorbance ratio, the limits of detection (LODs) of three types thiol-capped Au NPs were determined to be 100 ppt using ultraviolet-visible spectroscopy measurements. However, the aggregation efficiency of GSH@Au NPs was lower than that of the others regarding gradual changes in their color and LSPR absorbance band. Furthermore, we designed Toxin APP for color analysis which consists of three modules: processing, database collection, and communication. Toxin APP could on-site and precisely detect the color changes of GSH@Au NPs at parathion concentrations in the ranges of 100 ppt to 1, 10, and 100 ppm and could distinguish between OP and non-OP pesticides (e.g., fipronil) in tap water samples with high sensitivity and selectivity. Moreover, the concentration of residual parathion in real samples (tomato and strawberry) was quantified based on the color changes of GSH@Au NPs detected using Toxin APP. Therefore, the combination of an LSPR-based colorimetric assay and Toxin APP can be a reliable method for the facile and rapid detection of parathion in food and water samples.

[Relationship between hepatitis B virus X protein and hepatic cellular cancer].

Hepatic cellular cancer (HCC) is one of the most common cancers in the world, which is a serious threat to human health and life quality. More than 700,000 people die of HCC each year on average, and its incidence increases in many countries. Chronic hepatitis B virus (HBV) infection has been identified as a dominant risk factor for HCC. The pathogenesis of HBV-induced hepatocarcinogenesis is, however, incompletely understood. Evidence currently available supports a key role of the HBV X protein (HBx) in the cancer transformation and malignant tumor metastasis. HBx is a multifunctional regulator that may cooperate with the host factors to exert its effects on transcription, signal transduction, cell cycle progression, apoptosis, protein degradation, expression of oncogene and anti-oncogene. This review presents the current knowledge in the molecular pathogenesis of HBx in the induction of HCC.

[The etiological identification of an aseptic encephalitis outbreak (ten cases) in a hospital of Xiamen city, 2011].

OBJECTIVE: To identify the etiology of an aseptic encephalitis outbreak (ten cases) in a hospital of Xiamen city from 11 to 17 May, 2011. METHODS: A total of ten patients' throat swabs, anal swabs and cerebrospinal fluid were collected and detected by RT-PCR for pan-enterovirus. The samples containing detectable pan-enterovirus were tested by PCR with genotype-specific general primers located in VP1 region of enterovirus genotype A, B and C (HEV-A, B and C). The PCR products of VP1 segment were purified and sequenced, and phylogenetic analysis was performed. Meanwhile, the pathogens in those samples were isolated in Vero cell culture. Homologous analysis of VP1 sequences were carried out for the cultured virus samples and the original clinical samples to identify the outbreak etiology. RESULTS: Among the ten cases, seven cases were positive for pan-enterovirus nucleic acid. When tested by genotype-specific PCR, the throat and anal swab samples from those 7 patients were positive with HEV-B VP1 primers. Meanwhile, the HEV-B VP1 segments were sequenced and phylogenetic analyzed, which indicated the seven cases were all infected by enterovirus Echo 30. The sequences from those samples had homology of 95.3% - 97.1% with the epidemic strains in Zhejiang, 2004. Out of the seven cases, the sequences of XM2, XM3, XM4, XM8 throat swab samples and XM3, XM6 throat samples showed 99.4% - 100.0% homology which were different from the sequence of XM1, and the homology was 92.8% - 93.4%. Furthermore, the viruses were isolated using Vero cells from XM1, XM2, XM3, XM4 and XM8 throat swab samples, and the VP1 sequence showed more than 99.9% homology with the original specimens. CONCLUSION: The local outbreak of aseptic encephalitis was caused by Echo 30 of enterovirus genotype B, and the epidemic strains may have different genetic background.

A food-borne outbreak of gastroenteritis caused by different Salmonella serotypes in 2 universities in Xiamen, Fujian, China, in 2012.

We investigated a diarrhea outbreak in 2 universities to identify the etiological agent responsible, the source of infection, the mode of transmission, and the risk factors. A case-controlled study was conducted using case students and asymptomatic control students who were selected randomly and frequency-matched according to class and age, and the source of food or water intake was investigated. Of the total 22,404 students at the universities, 0.25% developed Salmonella Infections. A total of 96% (54/56) of the case students and 30% (35/117) of the control students consumed bread products provided by the same vendor (odds ratio [OR] = 63.3; 95% confidence interval [CI], 14.9-550.7). Among the students who consumed bread, 96% (52/54) of the case students and 9% (3/35) of the control students ate egg sandwiches (OR = 277.3; 95%CI, 43.9-1,750.8). Seven strains of Salmonella enteritidis and 6 strains of S. chester were isolated from the case students or food samples. Pulsed-field gel electrophoresis typing showed the same patterns. The outbreak of gastroenteritis was caused mainly by egg sandwiches contaminated with different serotypes of Salmonella.

A food-borne outbreak of gastroenteritis caused by norovirus GII in a university located in Xiamen City, China.

OBJECTIVES: We investigated a diarrhea outbreak that occurred at a university in China to identify the etiological agent of the outbreak, source of infection, mode of transmission, and risk factors. METHODS: In this case-control study, we compared the food sources and examined the food and water items consumed between the probable and confirmed cases and the asymptomatic control students, who were selected randomly and frequency-matched by class and age at a ratio of 1:2. RESULTS: Out of 7141 students (excluding teachers), 87 (1.2%) developed an illness. Thirty-three of 44 (75%) cases and 11 of 88 (13%) control students had consumed bread products supplied by an unlicensed small bakery (odds ratio 21, 95% confidence interval 8-60). Norovirus GII was detected in seven patients and in a food handler at the bread workshop and his 8-month-old son. CONCLUSIONS: The outbreak of gastroenteritis was caused mainly by bread products contaminated with norovirus GII. A food handler with an asymptomatic norovirus GII infection was the possible source of infection.

Genetic factors, viral infection, other factors and liver cancer: an update on current progress.

Primary liver cancer is one of the most common cancers at the global level, accounting for half of all cancers in some undeveloped countries. This disease tends to occur in livers damaged through alcohol abuse, or chronic infection with hepatitis B and C, on a background of cirrhosis. Various cancer-causing substances are associated with primary liver cancer, including certain pesticides and such chemicals as vinyl chloride and arsenic. The strong association between HBV infection and liver cancer is well documented in epidemiological studies. It is generally acknowledged that the virus is involved through long term chronic infection, frequently associated with cirrhosis, suggesting a nonspecific mechanism triggered by the immune response. Chronic inflammation of liver, continuous cell death, abnormal cell growth, would increase the occurrence rate of genetic alterations and risk of disease. However, the statistics indicated that only about one fifth of HBV carries would develop HCC in lifetime, suggesting that individual variation in genome would also influence the susceptibility of HCC. The goal of this review is to highlight present level of knowledge on the role of viral infection and genetic variation in the development of liver cancer.