Delayed Transfer of the Extensor Carpi Radialis Brevis Branch of the Radial Nerve to the Anterior Interosseous Nerve for Restoration of Thumb and Index Finger Flexion: Case Report.

High median nerve injuries (HMNIs) are rare lesions involving the upper extremities and affect the median nerve from its origin to the emergence of the anterior interosseous nerve (AIN). Proximal reconstruction has long been considered the gold standard in treating HMNI, but thumb and index flexion and pinch and grip weakness are consistently not recovered. We report the surgical results of a patient affected by an HMNI with partial spontaneous recovery after a gunshot wound. AIN function was successfully restored in a delayed fashion by transferring the radial nerve branch to the extensor carpi radialis brevis to the AIN.

DNA damage in BALB/c mice infected with Lacazia loboi and its relation to nutritional status.

BACKGROUND: Jorge Lobo's disease, also known as lacaziosis, is a cutaneous-subcutaneous mycosis with chronic evolution. It is caused by the fungus Lacazia loboi. Herein we report a study that relates the genotoxicity caused by L. loboi in isogenic mice with nutritional status, through a normal or restricted diet. METHODS: DNA damage was assessed in the peripheral blood by the comet assay (tail intensity). RESULTS: The results for leukocytes showed increases in the mean tail intensity in mice under dietary restriction, in infected mice under dietary restriction and in infected mice ingesting a normal diet. CONCLUSION: These results indicate that dietary restriction and L. loboi infection may increase DNA damage levels in mice, as detected by the comet assay.

Analysis of the expression of toll-like receptors 2 and 4 and cytokine production during experimental Leishmania chagasi infection.

Toll-like receptors (TLRs) recognise pathogen-derived molecules and influence immunity to control parasite infections. This study aimed to evaluate the mRNA expression of TLRs 2 and 4, the expression and production of the cytokines interleukin (IL)-12, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL-17, IL-10 and transforming growth factor (TGF)-ß and the production of nitric oxide (NO) in the spleen of mice infected with Leishmania chagasi. It also aimed to evaluate any correlations between mRNA expression TLR2 and 4 and cytokines and NO production. Infection resulted in increased TLR2-4, IL-17, TNF-α and TGF-ß mRNA expression during early infection, with decreased expression during late infection correlating with parasite load. IFN-γ and IL-12 mRNA expression decreased at the peak of parasitism. IL-10 mRNA expression increased throughout the entire time period analysed. Although TGF-ß, TNF-α and IL-17 were highly produced during the initial phase of infection, IFN-γ and IL-12 exhibited high production during the final phase of infection. IL-10 and NO showed increased production throughout the evaluated time period. In the acute phase of infection, there was a positive correlation between TLR2-4, TNF-α, IL-17, NO, IL-10 and TGF-ß expression and parasite load. During the chronic phase of infection, there was a positive correlation between TLR2-4, TNF-α, IL-17 and TGF-ß expression and parasite load. Our data suggest that infection by L. chagasi resulted in modulation of TLRs 2 and 4 and cytokines.

DNA damage and nitric oxide production in mice following infection with L. chagasi.

Leishmania chagasi, which causes visceral leishmaniasis in South America, is an obligate intracellular protozoan. Production of nitric oxide by macrophages during the inflammatory response is one of the main microbicidal mechanisms against this parasite. The goal of this study was to evaluate whether L. chagasi infection causes DNA damage in peripheral blood and spleen cells of Balb/c mice and whether such damage may be related to NO production. Balb/c mice were either infected with L. chagasi or maintained as controls. The single-cell gel electrophoresis (comet) assay was used to measure DNA damage in peripheral blood and spleen cells, and the Griess reaction was used to measure NO production in the spleen. L. chagasi infection induced DNA damage in peripheral blood and spleen cells of infected mice. Macrophages from the control group, challenged with L. chagasi, showed significantly (p<0.05) greater NO production, compared to non-challenged cells. Treatment of spleen cells with N(G)-monomethyl-l-arginine (LNMMA) caused a significant reduction of NO production and DNA damage (p<0.05). Our results indicate that L. chagasi induces DNA damage in the peripheral blood and spleen cells and that NO not only causes killing of the parasite but also induces DNA damage in adjacent cells.