Background:\r\n', u'There are two virus known as Nam Dinh Virus, and Colti group B be found in Viet Nam. These viruses have appeared in the South, the Middle and the Highland. They haven\u2019t been reported in the Southern provinces and Can Thoas well. \r\n', u'Objectives: \r\n', u'To identify the circulation of Nam Dinh virus strain, and coltivirus group B strain in Can Tho, Southern Viet Nam, and their existence in nature.\r\n', u'Subjects and method: \r\n', u'Thirty-four mosquito samples (7, 453 individual mosquitoes) from Culex quinque faciatus and Culex pseudovishnui were collected in Can Tho provice, southern Vietnam 2005.\r\n', u'Isolatingviruses on Aedes albopictuc clone C6/36, Vero cells, and using PT- PCR and ELISA Sandwich for identification. \r\n', u'Results:\r\n', u'2 Nam Dinh virus strains, 2 coltivirus group B strains and 1 flavivirus strain (insect flavivirus) were isolated from Culex quinque faciatus, and no virus was isolated from Culex pseudovishnui.\r\n', u'Conclusion: \r\n', u'The identification of the transmission of Nam dinh Virus, and coltivirus group B in Can Tho province by isolating virus from Culex quinque faciatus has shown the evidence for natural vertical transmission of these viruses.\r\n', u'
Viruses ; Coltivirus ; Flavivirus ; Arboviruses ; Culex ;

Corticotropin releasing factor (CRF) is known to be involved in the stress response and in some degenerative brain disorders. In addition, CRF has a role as a neuromodulator in adult cerebellar circuits. Data from developmental studies suggest a putative role for CRF as a trophic factor during cerebellar development. In this study, we investigated the trophic role for CRF family of peptides by culturing cerebellar neurons in the presence of CRF, urocortin or urocortin II. Primary cell cultures of cerebella from embryonic day 18 mice were established, and cells were treated for either 1, 5 or 9 days with Basal Medium Eagles complete medium alone or complete medium with 1 micrometer CRF, urocortin, or urocortin II. The number of GABA-positive neurons in each treatment condition was counted at each culture age for monitoring the changes in neuronal survival. Treatment with 1 micrometer CRF or 1 micrometer urocortin increased the survival of GABAergic neurons at 6 days in vitro and 10 days in vitro, and this survival promoting effect was abolished by treatment with astressin in the presence of those peptides. Based on these data, we suggest that CRF or urocortin has a trophic role promoting the survival of cerebellar GABAergic neurons in cultures.
gamma-Aminobutyric Acid/*metabolism ; Time Factors ; Receptors, Corticotropin-Releasing Hormone/*metabolism ; Peptides/chemistry ; Neurons/*metabolism ; Mice, Inbred C57BL ; Mice ; Immunohistochemistry ; Image Processing, Computer-Assisted ; Corticotropin-Releasing Hormone/biosynthesis/*physiology ; Cerebellum/*embryology/*metabolism ; Cells, Cultured ; Cell Survival ; Animals

Objective: To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia. Methods: The in vitro antiinflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The level of NO produced in the culture media was determined by Griess method. The iNOS and COX-2 protein expressions were analyzed by Western blot. The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. Mice mortality was monitored for 5 days after injection of LPS. The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques. Results: The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vivo models. The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions. In the septic shock model, ELA dose-dependently protected mice from LPS-induced mortality. Further study on the isolated components of ELA indicated that 9,10-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract. Conclusions: These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS, and COX-2 and protects mice from LPS-induced mortality in septic shock model.