The Continual Forming and Contribution of Infective Juveniles Produced Via Endotokia Matricida of Entomopathogenic Nematodes in the Family of Steinernematidae and Heterorhabditidae

The non-feeding developmentally arrested infective juveniles (IJs) of entomopathogenic nematodes in the family of Steinernematidae and Heterorhabditidae seek out a susceptible insect host and initiate infections. The aim of the research was to examine the continualforming and contribution of IJs produced via endotokia matricida (IJs-EM) of Heterorhabditis bacteriophora, Steinernema glaseri, and S. carpocapsae. The research was conducted at the Laboratory of Nematology of the Saga University, Japan (April 2001-April2002) and the Laboratory of Nematology of the Indonesian Legume and Tuber Crops Research Institute (June 2003-October 2004). The nematode progenies were investigated using the greater wax moth, Galleria mellonella, pre-inoculated with 50 IJs at 25°C.Results showed that three reproductive adult generations were observed at day 18th. There were 135,000, 128,000 and 133,000 IJs per insect cadaver produced in H. bacteriophora, S. glaseri and S. carpocapsae, respectively. Endotokia matricida contributed a higher number of IJs than that of a normal mode of IJs production. The ratios are 81%, 28% and 64% for H. bacteriophora, S. glaseri, and S. carpocapsae of the IJs total production, respectively. Among the generations, the highest contribution of IJs was come from thethird adult generation bearing endotokia matricida, i.e., 63%, 24% and 51% for the three nematode species. Although the IJs-EM were more transparent compared to the normal IJs, they were morphologically similar. The results show that endotokia matricida has a pivotal role in a species maintenance and survival strategy of entomopathogenic nematodes in extreme environmental conditions

Abnormalities of the FHIT gene in human oral carcinogenesis

The abnormalities of the fragile histidine triad (FHIT) gene in tissue samples of oral squamous cell carcinomas (SCCs) along with several leukoplakias and an erythroplakia were examined to determine whether the FHIT gene is actually a frequent target in vivo for alteration during oral carcinogenesis. Abnormal transcripts of the FHIT gene were found in eight of 15 oral SCCs. Although these abnormal transcripts varied widely, deletion patterns incorporating a deletion of exon 5 were the most common. Loss of heterozygosity (LOH) analysis demonstrated that the abnormal FHIT transcripts found in cancer cells were attributable to abnormalities of the FHIT gene. Abnormal FHIT transcripts were also observed in two of seven premalignant lesions. Interestingly, in the case of one patient with a premalignant lesion showing an abnormal FHIT transcript, subsequent oral SCC developed during a 3-year follow-up period. On the other hand, in the two patients from whom both leukoplakia and SCC samples were taken simultaneously, abnormal FHIT transcripts were found only in the SCCs. Although the functional role of FHIT remains to be clarified, these results suggest that the FHIT alteration is actually involved in carcinogenesis of the oral epithelium. © 2000 Cancer Research Campaig

Mice deficient in CD38 develop an attenuated form of collagen type II-induced arthritis

CD38, a type II transmembrane glycoprotein expressed in many cells of the immune system, is involved in cell signaling, migration and differentiation. Studies in CD38 deficient mice (CD38 KO mice) indicate that this molecule controls inflammatory immune responses, although its involvement in these responses depends on the disease model analyzed. Here, we explored the role of CD38 in the control of autoimmune responses using chicken collagen type II (col II) immunized C57BL/6-CD38 KO mice as a model of collagen-induced arthritis (CIA). We demonstrate that CD38 KO mice develop an attenuated CIA that is accompanied by a limited joint induction of IL-1β and IL-6 expression, by the lack of induction of IFNγ expression in the joints and by a reduction in the percentages of invariant NKT (iNKT) cells in the spleen. Immunized CD38 KO mice produce high levels of circulating IgG1 and low of IgG2a anti-col II antibodies in association with reduced percentages of Th1 cells in the draining lymph nodes. Altogether, our results show that CD38 participates in the pathogenesis of CIA controlling the number of iNKT cells and promoting Th1 inflammatory responses

Drosophila Eggshell Production: Identification of New Genes and Coordination by Pxt

Drosophila ovarian follicles complete development using a spatially and temporally controlled maturation process in which they resume meiosis and secrete a multi-layered, protective eggshell before undergoing arrest and/or ovulation. Microarray analysis revealed more than 150 genes that are expressed in a stage-specific manner during the last 24 hours of follicle development. These include all 30 previously known eggshell genes, as well as 19 new candidate chorion genes and 100 other genes likely to participate in maturation. Mutations in pxt, encoding a putative Drosophila cyclooxygenase, cause many transcripts to begin expression prematurely, and are associated with eggshell defects. Somatic activity of Pxt is required, as RNAi knockdown of pxt in the follicle cells recapitulates both the temporal expression and eggshell defects. One of the temporally regulated genes, cyp18a1, which encodes a cytochromome P450 protein mediating ecdysone turnover, is downregulated in pxt mutant follicles, and cyp18a1 mutation itself alters eggshell gene expression. These studies further define the molecular program of Drosophila follicle maturation and support the idea that it is coordinated by lipid and steroid hormonal signals

The Drosophila melanogaster host model

The deleterious and sometimes fatal outcomes of bacterial infectious diseases are the net result of the interactions between the pathogen and the host, and the genetically tractable fruit fly, Drosophila melanogaster, has emerged as a valuable tool for modeling the pathogen–host interactions of a wide variety of bacteria. These studies have revealed that there is a remarkable conservation of bacterial pathogenesis and host defence mechanisms between higher host organisms and Drosophila. This review presents an in-depth discussion of the Drosophila immune response, the Drosophila killing model, and the use of the model to examine bacterial–host interactions. The recent introduction of the Drosophila model into the oral microbiology field is discussed, specifically the use of the model to examine Porphyromonas gingivalis–host interactions, and finally the potential uses of this powerful model system to further elucidate oral bacterial-host interactions are addressed

Data for: Correlation between asymptomatic excessive transmural injury after pulmonary vein isolation and a bonus freeze protocol using the second-generation 28 mm cryoballoon for paroxysmal atrial fibrillation

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