Learning from Mistakes – a Case of Pediatric Patient with Recurrent Whitlow.

Background: Herpetic whitlow is a herpes simplex virus infection of the fingers or thumb characterized by erythema accompanied by painful non-purulent vesicles.

Aim: To draw attention to the typical appearance of herpetic whitlow and to distinguish it from bacterial infections and other skin diseases because of their different management.

Materials And Methods: The patient’s history, dermatological status, and scrapings from the vesicles were taken.

Nitric oxide and prostaglandin response to group B streptococcal infection in the lung.

Group B streptococcus (GBS) causes a complex inflammatory process that involves prostaglandins (PG) and nitric oxide (NO). The goal of this study was to examine the inflammatory response to GBS in the lung and the co-regulation of the PG and NO pathways, if any, both in vitro and in vivo. Sprague Dawley rats were treated with various combinations of GBS, aminoguanidine (AG), a selective inducible nitric oxide synthase (iNOS) inhibitor, and L-arginine (LA), a NO donor.

Dynamics of cellular entry and drug delivery by dendritic polymers into human lung epithelial carcinoma cells.

Dendrimers and hyperbranched polymers are emerging as potentially ideal drug delivery vehicles because they provide a significant amount of tailorability and a large density of functional groups. This study explores the dynamics of cellular entry of dendrimers and hyperbranched polymers alone, and in the complexed form with ibuprofen, into A549 human lung epithelial carcinoma cells using UV/Vis spectroscopy, flow cytometry and fluorescence microscopy. Both dendrimers and hyperbranched polymers appear to enter these cells rapidly.

Nitric oxide-dependent regulation of pro-inflammatory cytokines in group B streptococcal inflammation of rat lung.

Group B Streptococcus (GBS) infection leading to sepsis and lung injury is a major cause of neonatal morbidity and mortality. Lung injury may result from overproduction of pro-inflammatory mediators (cytokines), caused by nitric oxide (NO). Our objective was to characterize the molecular signaling events involving the pro-inflammatory mediators interleukin-6 (IL-6) and macrophage inflammatory protein (MIP-2) in the presence of aminoguanidine (AG), an inducible nitric oxide synthase (iNOS) specific inhibitor, in lung tissue from GBS-treated young rats.

Group B Streptococci and inducible nitric oxide synthase: modulation by nuclear factor kappa B and ibuprofen.

Group B Streptococci (GBS) neonatal infections cause a complex inflammatory process involving numerous biochemical mediators. Nitric Oxide (NO) is generated by many cell types in response to different inflammatory signals. Nuclear factor kappa B (NFkappaB) plays an important role in the inflammatory process and may induce a number of biochemical mediator genes, including the inducible nitric oxide synthase (iNOS).