Publications by authors named "Caterina Monaco"

Background: The effects of phosphodiesterase-type 5 (PDE5) inhibitors on the in vivo clitoral structure of women with diabetes have never been investigated.

Aim: To study the in vivo structural and hemodynamic changes of the clitoris in premenopausal women with type 1 diabetes on PDE5 inhibitors.

Methods: 38 premenopausal women with type 1 diabetes aged 36 -46 years.

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Polymorphonuclear neutrophil leucocytes (PMNs) are a critical part of innate immune defence against bacterial pathogens, and only a limited subset of microbes can escape killing by these phagocytic cells. Here we show that Neisseria meningitidis, a leading cause of septicaemia and meningitis, can avoid killing by PMNs and this is dependent on the ability of the bacterium to acquire L-glutamate through its GltT uptake system. We demonstrate that the uptake of available L-glutamate promotes N.

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recA1, recA13 and recA56 are considered null alleles of the Escherichia coli recA gene because they were shown to have essentially no activity in vivo. In this study, we used strains harboring the recA null alleles and their recA-proficient congenic counterpart to assess the lethal and the mutagenic effects elicited by near-UV(308 nm) coherent radiation generated by a XeCl excimer laser. We compared these effects with those produced by a conventional far-UV(254 nm) germicidal lamp.

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GdhR is a meningococcal transcriptional regulator that was previously shown to positively control the expression of gdhA, encoding the NADP-specific L-glutamate dehydrogenase (NADP-GDH), in response to the growth phase and/or to the carbon source. In this study we used reverse transcriptase-PCR-differential display (to identify additional GdhR-regulated genes. The results indicated that GdhR, in addition to NADP-GDH, controls the expression of a number of genes involved in glucose catabolism by the Entner-Doudoroff pathway and in l-glutamate import by an unknown ABC transport system.

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Meningococcal gdhA, encoding the NADP-specific l-glutamate dehydrogenase (NADP-GDH), is essential for systemic infection in an infant rat model. In this paper, a limited transcriptional analysis detected differences in gdhA expression among clinical isolates. In strains expressing high levels of gdhA mRNA, two promoters, gdhA P1 and gdhA P2, initiated transcription of gdhA.

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