is an important zoonotic pathogen in swine and humans that causes sepsis and meningitis. Our previous study in Thailand showed that the prevalence of infection in humans, especially in northern areas of Thailand, and the transmission of the pathogen occurred mainly through the consumption of traditional raw pork products. Considering the high incidence proportion and mortality rate of the disease as an important public health problem, we implemented a food safety campaign in the Phayao Province in northern Thailand in 2011. We evaluated the effects of a food safety campaign by comparing the sociodemographic, clinical, and bacteriological characteristics of cases before and after the campaign. The follow-up study showed a marked decrease of the incidence proportion in the first 2 years, indicating the effectiveness of the campaign. In the third year, however, the incidence proportion slightly increased again, indicating the existence of deep-rooted cultural behaviors and the necessity of continuous public health intervention. Furthermore, epidemiological analysis of the cases made it possible to estimate the infectivity of the pathogen via the oral route of infection. In the present study, we showed the effectiveness of the food safety campaign for controlling the infection, and we present a role model public health intervention for prevalent areas affected by infection in humans.
Overlapping subclones from the Rhizobium trifolii symbiosis plasmid pRt843a were generated by using in vivo and in vitro methods. Subclones were assayed for symbiotic phenotype by introducing them into a derivative of R. trifolii ANU843 cured of its symbiosis plasmid and testing the transconjugant strains for the ability to induce nitrogen-fixing nodules on clover. One subclone spanning 32 kilobase pairs (kb) of DNA from pRt843a was found to restore nitrogen fixation ability. This subclone included all known nodulation genes of R. trifolii ANU843 and the nitrogenase structural genes nifHDK. In addition, regions homologous tofixABC, nifA, nifB, nifE, and nipN genes of other nitrogen-fixing bacteria were identified in this 32-kb subclone by DNA-DNA hybridization. Transposon mutagenesis of this subclone confirmed that regions containing these nif andflx genes were required for induction of nitrogen-fixing nodules on clover. In addition, a region located 5 kb downstream of the niJK gene was found to be required for induction of nitrogen-fixing nodules. No homology to known nif and fix genes could be detected in this latter region.Bacteria of the genus Rhizobium are able to fix atmospheric nitrogen in symbiotic association with leguminous plants. Development of this symbiosis is a complex multistep process requiring induction of many Rhizobium genes (see references 31, 32, and 47 for recent reviews).. Most of these genes have been located on single large plasmids termed symbiosis plasmids (pSym), which range in size from 180 kilobase pairs (kb) in R. trifolii to 1,600 kb in R. meliloti (10,20). The number of pSym-encoded genes that are actually required for successful development of a nitrogenfixing symbiosis, by any Rhizobium strain, is still unknown. New genes and even new regions of Sym plasmids that are essential for symbiotic nitrogen fixation continue to be identified (1, 46). We are endeavoring to systematically identify all pSym-encoded genes that are needed for a functional symbiosis between R. trifolii ANU843 and clover plants.In R. trifolii ANU843, it has been established that less than 14 kb of the 180-kb symbiosis plasmid (pRt843a) are required for nodule formation on clover roots (53). R. trif6lii containing this 14-kb nodulation (Nod) region but lacking the rest of pSym reach a stage in the symbiosis at which bacteria are released from infection threads into the plant cell cytoplasm. However, the released bacteria fail to differentiate into an endosymbiotic bacteroid form. These bacterial cells often lack an intact peribacteroid membrane and do not develop the large pleomorphic shape typical of wild-type Rhizobium (53). Rhizobium strains containing only the 14-kb fragment also do not fix nitrogen, since the structural genes for the nitrogenase enzyme (nifHDK), as well as several other genes shown to be required for nitrogen fixation, are not included on this fragment.Identification of nitrogen fixation genes in Rhizobium spp. has generally been accomplished by heterologous DNA * Corresponding author. h...
Methylenetetrahydrofolate reductase is a key enzyme in folate metabolism, which affects DNA synthesis and methylation and is possibly linked to colorectal carcinogenesis. Alcohol and acetaldehyde have an adverse effect on folate metabolism. This study investigated the relationship of functional MTHFR C677T and ALDH2 polymorphisms to colorectal adenomas with reference to alcohol consumption in a case-control study of male officials in the Self-Defense Forces (SDF) who received a preretirement health examination at two SDF hospitals. The study subjects were 452 cases of colorectal adenoma and 1050 controls with no polyp who underwent total colonoscopy. Genotypes were determined by the PCR-RFLP method using genomic DNA extracted from the buffy coat. Statistical adjustment was made for age, hospital, rank in the SDF, body mass index, cigarette-years and alcohol intake. Neither MTHFR C677T nor ALDH2 showed a measurable association with colorectal adenoma. While high alcohol consumption was associated with a moderately increased risk of colorectal adenoma, neither of the two polymorphisms showed a significant effect on the association between alcohol and colorectal adenoma. F olate metabolism has drawn much attention in relation to colorectal carcinogenesis.(1,2) Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme regulating folate metabolism. MTHFR irreversibly converts 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate.(2) The substrate of MTHFR, 5,10-methylenetetrahydrofolate, is required for conversion of deoxyuridylate to thymidylate. Insufficient thymidylate results in uracil misincorporation into DNA, leading to single-strand and double-strand breaks and increasing the incidence of DNA misrepair.(3,4) On the other hand, 5-methyltetrahydrofolate is a methyl donor in the remethylation of homocystein to methionine, which is required for DNA methylation. Imbalanced DNA methylation has been implicated in colorectal carcinogenesis. (5,6) The MTHFR C677T polymorphism is a common functional polymorphism in exon 4, resulting in an alanine-tovaline substitution at codon 222.(7) The homozygous variant (677TT) has no more than 30% of normal enzyme activity, and heterozygotes (677CT) also seem to have lower activity of the enzyme.(7) Several, (8)(9)(10)(11)(12) but not all, (13)(14)(15) epidemiological studies have shown a decreased risk of colorectal cancer associated with the MTHFR 677TT genotype, especially in individuals with high folate intake and /or low alcohol intake. On the other hand, a limited number of studies addressed the relationship between the MTHFR C677T polymorphism and colorectal adenoma, a well-established precursor lesion of colorectal cancer. (16)(17)(18)(19)(20) These studies generally showed no association between the MTHFR C677T polymorphism and the risk of colorectal adenoma, but reported variable associations between alcohol intake and colorectal adenoma, dependent on the MTHFR C677T polymorphism. (16 -20) Alcohol has fairly consistently been shown to be associated with increas...
JapicCTI-121902 for Phase II study, JapicCTI-101075 for Phase III study (http://www.clinicaltrials.jp/user/cte_main.jsp).
The immunogenicity and safety of an inactivated cell culture Japanese encephalitis vaccine (CC-JEV) were compared with those of an inactivated mouse brain-derived Japanese encephalitis vaccine (MB-JEV) in phase III clinical multicenter trials conducted in children. The vaccines contain the same Japanese encephalitis virus strain, the Beijing-1 strain. Two independent clinical trials (trials 1 and 2) were conducted. Trial 1 was conducted in 468 healthy children. Each subject was injected with 17 g per dose of either CC-JEV or MB-JEV, and the immunogenicity and safety of the vaccines were investigated. Trial 1 showed that CC-JEV was more immunogenic and reactive than MB-JEV at the same dose. Therefore, to adjust the immunogenicity of CC-JEV to that of MB-JEV, a vaccine that has had a good track record regarding its efficacy for a long time, trial 2 was conducted in 484 healthy children. To improve the stability, CC-JEV was converted from a liquid type to a freeze-dried type of vaccine. Each subject was injected subcutaneously with either 4 g per dose of CC-JEV, 8 g per dose of CC-JEV, or 17 g per dose of MB-JEV twice, at an interval of 2 to 4 weeks, followed by an additional booster immunization 1 to 15 months after the primary immunization. Based on the results of trial 2, 4 g per dose of the freeze-dried CC-JEV (under the label Encevac) was selected as a substitute for the MB-JEV. Encevac was approved and launched in 2011 and has since been in use as a 2nd-generation Japanese encephalitis vaccine in Japan. (These studies have been registered at the JapicCTI under registration no. JapicCTI-132063 and JapicCTI-080586 for trials 1 and 2, respectively.) J apanese encephalitis (JE) is an infectious disease caused by the JE virus (JEV), which is mediated by mosquitoes, such as Culex tritaeniorhynchus (1, 2). JE occurs not only in Japan but also in many other Asian countries, including Korea, Taiwan, China, Vietnam, Thailand, Malaysia, Myanmar, and India (3). The number of cases and fatalities due to JE are reported to be about 20,000 and 600 per year, respectively (1). To prevent this infectious disease, a JE vaccine derived from infected mouse brain tissue has been in use for a long time in Japan and other countries. Concurrently, a live-attenuated vaccine developed from a passaged culture of the JEV SA14 strain in primary hamster kidney cells and animals (mice and hamsters) with successive plaque purifications in primary chicken embryo cells, SA14-14-2, has been in use since 1989 in China and other countries (4). Moreover, an inactivated vaccine produced using the SA14-14-2 vaccine strain has been licensed in the United States, Europe, Canada, and Australia (5).In Japan, mouse brain-derived JE vaccine (MB-JEV) was initially produced using mouse brains inoculated with JEV Nakayama-NIH as a vaccine virus strain. At that time, MB-JEV was produced by adding formalin to the centrifugal supernatant of a 5% emulsion of mouse brain to inactivate the JE virus (6). Later, the quality of MB-JEV was improved through purificatio...
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