Evaluation of a Hydrogel-Based Diagnostic Approach for the Point-of-Care Based Detection of .

Eleven primer pairs were developed for the identification of . The sensitivity and specificity of these primers were evaluated by Real Time (RT)-PCR melt curve analyses with DNA from 145 isolates and 40 other or non- species. Three primer pairs were further evaluated in a hydrogel-based RT-PCR detection platform, using DNA extracted from 50 cultures.

Multiplex Real-Time PCR Assay for Simultaneous Identification of Neisseria gonorrhoeae and Its Ciprofloxacin Susceptibility Status.

A real-time PCR (RT-PCR) assay was designed for the simultaneous identification of and its ciprofloxacin susceptibility status. A SYBR green-based multiplex RT-PCR format was used; it comprised two different forward primers and a common reverse primer to detect single nucleotide polymorphisms (SNPs) in of The primer pairs were evaluated for their sensitivity and specificity using genomic DNA from 254 isolates (82 were ciprofloxacin susceptible and 172 were ciprofloxacin resistant) and 23 non- species isolates. The performance of the primers was validated using genomic DNA from 100 different isolates (46 were ciprofloxacin susceptible and 54 were ciprofloxacin resistant) and 52 non- isolates.

Suppression of ERK activation in urethral epithelial cells infected with Neisseria gonorrhoeae and its isogenic minD mutant contributes to anti-apoptosis.

In gonococci-infected transduced human urethral epithelial cells (THUEC), the role of ERK, a mitogen-activated protein kinase (MAPK), in apoptosis is unknown. We observed lowering of ERK activation in THUEC following infection with anti-apoptosis-inducing Neisseria gonorrhoeae strain CH811. An isogenic cell division mutant of this strain, Ng CJSD1 (minD deficient), which is large and abnormally shaped, reduced ERK phosphorylation levels even more than its parental strain in THUEC.

Regulation of minD by oxyR in Neisseria gonorrhoeae.

In Neisseria gonorrhoeae, cytokinesis involves Escherichia coli homologues of minC, minD and minE which are encoded as part of a min operon. MinD, a 30 kD protein component of the MinC-MinD septum inhibitory complex, together with MinE, mediates cell division site selection. Gonococci mutated in minD display aberrant cytokinesis, abnormal morphology, defective microcolony formation and virulence.

A minD mutant of enterohemorrhagic E. coli O157:H7 has reduced adherence to human epithelial cells.

Adherence to epithelial cells is a prerequisite for intestinal colonization by the bacterial pathogen, enterohemorrhagic Escherichia coli (EHEC). The deletion of minD, a cell division gene, in EHEC caused reduced adherence to human epithelioid cervical carcinoma (HeLa) and human colonic adenocarcinoma (Caco-2) cells as compared to wild-type. The minD mutant formed minicells and filaments owing to aberrant cytokinesis.

Attenuated virulence of min operon mutants of Neisseria gonorrhoeae and their interactions with human urethral epithelial cells.

Neisseria gonorrhoeae, a sexually-transmitted gram-negative bacterium, causes gonorrhoea in humans. The min genes of N. gonorrhoeae are involved in cell division site selection with oxyR co-transcribed with these genes.

Cytosolic phospholipase a2 activation by Candida albicans in alveolar macrophages: role of dectin-1.

Candida albicans is an increasingly important pulmonary fungal pathogen. Resident alveolar macrophages are important in host defense against opportunistic fungal infections. Activation of Group IVA cytosolic phospholipase A(2)alpha (cPLA(2)alpha) in macrophages initiates arachidonic acid (AA) release for production of eicosanoids, which regulate inflammation and immune responses.

Murine infection model for Mycobacterium fortuitum.

Mycobacterium fortuitum is an atypical, non-tubercular, pathogenic, rapidly growing mycobacteria. As very little is known about its virulence determinants, the absence of an animal infection model was always sorely felt. A reliable and reproducible murine infection model has been developed in which non-replicating persistence of 10(5) CFU/g tissue in kidney was observed when a standardised dosage inoculum of 5x10(7) CFU was injected intravenously.