RESUMO
We report an outbreak of dengue in Darfur, western Sudan, during September 2014-April 2015. Dengue virus-specific PCR testing of 50 samples from nonmalaria febrile illness case-patients confirmed 35 dengue cases. We detected 7 cases of dengue shock syndrome and 24 cases of dengue hemorrhagic fever.
Assuntos
Vírus da Dengue , Dengue/epidemiologia , Dengue/virologia , Surtos de Doenças , Vírus da Dengue/classificação , Vírus da Dengue/genética , Feminino , Humanos , Masculino , Estações do Ano , Dengue Grave/epidemiologia , Sudão/epidemiologiaRESUMO
Periodontitis is one of the severe complications in diabetic patients and gingival epithelium plays an initial role on the onset and progression of this disease. However the potential mechanism is yet sufficiently understood. Meanwhile, the research on the correlational experimental animal models was also insufficient. Here, we established periodontitis with type 2 diabetes in db/db and Tallyho/JngJ (TH) mice and periodontitis with type 1 diabetes in streptozotocin induced diabetes C57BL/6J (STZ-C57) mice by oral infection of periodontal pathogen Porphyromonas gingivalis W50. We demonstrated that periodontal infected mice with high blood glucose levels showed dramatically more alveolar bone loss than their counterparts, in which infected db/db mice exhibited the most bone defects. No contrary impact could be observed between this periodontal infection and onset and severity of diabetes. The expressions of PTPN2 were inhibited whereas the expression of JAK1, STAT1, and STAT3 increased dramatically in gingival epithelia and the serum TNF-α also significantly increased in the mice with diabetic periodontitis. Our results indicated that the variations of inflammation-related protein expressions in gingival epithelia might lead to the phenotype differences in the mice with diabetic periodontitis.
