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Abstract. Sporadic cases of melioidosis have been reported in Hainan, China for decades; however, to the best of our knowledge, there are no accurate source-identification investigations confirming that melioidosis is endemic. Four indigenous melioidosis cases were identified, which prompted the performance of contact microbiologic and molecular techniques to evaluate endemicity. Environmental samples were collected from various locations surrounding each patient's residence. The samples were screened for Burkholderia pseudomallei (B. pseudomallei) using Ashdown culture medium, and confirmed by polymerase chain reaction and 16S ribosomal DNA sequencing. Clinical and environmental isolates of B. pseudomallei were evaluated by multilocus sequence typing (MLST) and 4-locus multilocus variable number tandem repeat analysis (MLVA-4) for evidence of homology between them. Analysis by MLST indicated that one environmental sample and one clinical colony were sequence type-46, as well as type (8,3,11,9) by MLVA-4. The evidence indicates a likely geographical and epidemiological association. Taken together, B. pseudomallei from the environmental samples in addition to the high molecular homology between the clinical and environmental isolates indicates, at least, regional endemicity of melioidosis in Hainan, China.

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Connexin43 (Cx43)-mediated gap junctions are vital in maintaining corneal endothelium homeostasis. Tumor necrosis factor-alpha (TNF-α) is among the most important inflammatory factors which cause corneal endothelial dysfunction in various eye diseases. However, the effect of TNF-α on Cx43-mediated gap junctions of the corneal endothelium remains undefined. In the current research, we determined the effect of TNF-α on gap junction intercellular communication (GJIC) in rabbit corneal endothelium. To evaluate alterations of GJIC, if any, we treated ex vivo cultured rabbit corneal endothelium with different concentrations of TNF-α (2-20 ng/ml). The localization of Cx43 was analyzed by immunostaining, while RT-qPCR and western blot were used to profile the expression of Cx43 and zonula occludens-1 (ZO-1). The association between ZO-1 and Cx43 was evaluated using immunoprecipitation and double staining. GJIC activity was determined by the scrap loading and dye transfer assay (SLDT). Our data demonstrated that a high concentration of TNF-α (10 ng/ml and 20 ng/ml) disrupts the Cx43 mediated gap junction distribution in rabbit corneal endothelium and suppresses the expression of Cx43 protein. Furthermore, rabbit corneal endothelial GJIC was inhibited due to the decreased association between the ZO-1 and Cx43 proteins. Current results demonstrate that TNF-α inhibits corneal endothelial GJIC via decreasing the association between ZO-1 and Cx43, disrupting the distribution of Cx43, and downregulating the expression of Cx43 protein. This study offers a new theoretical foundation for diagnosing and treating corneal endothelial cell decompensation induced by elevated TNF-α in various eye diseases.