New pinhole sulcus implant for the correction of irregular corneal astigmatism.

PURPOSE: To evaluate the effect on visual acuity of the implantation of a new intraocular pinhole device (Xtrafocus) in cases of irregular corneal astigmatism with significant visual impairment. SETTING: University of São Paulo, São Paulo, Brazil. DESIGN: Prospective case series. METHODS: Pseudophakic eyes of patients with irregular corneal astigmatism were treated with the pinhole device. The causes of irregular corneal astigmatism were keratoconus, post radial keratotomy (RK), post-penetrating keratoplasty (PKP), and traumatic corneal laceration. The device was implanted in the ciliary sulcus in a piggyback configuration to minimize the effect of corneal aberrations. Preoperative and postoperative visual parameters were compared. The main outcome variables were manifest refraction, uncorrected and corrected distance and near visual acuities, subjective patient satisfaction, and intraoperative and postoperative adverse events and complications. RESULTS: Twenty-one patients (ages 35 to 85 years) were included. There was statistically significant improvement in uncorrected and corrected (CDVA) distance visual acuities. The median CDVA improved from 20/200 (range 20/800 to 20/60) preoperatively to 20/50 (range 20/200 to 20/20) in the first month postoperatively and remained stable over the following months. Manifest refraction remained unchanged, while a subjective visual performance questionnaire revealed perception of improvement in all the tested working distances. No major complication was observed. One case presented with decentration of the device, which required an additional surgical intervention. CONCLUSIONS: The intraocular pinhole device performed well in patients with irregular astigmatism caused by keratoconus, RK, PKP, and traumatic corneal laceration. There was marked improvement in visual function, with high patient satisfaction.

Clostridium difficile-induced colitis in mice is independent of leukotrienes.

Clostridium difficile is the major cause of antibiotic-associated diarrhea and pseudomembranous colitis in healthcare settings. However, the host factors involved in the intestinal inflammatory response and pathogenesis of C. difficile infection (CDI) are largely unknown. Here we investigated the role of leukotrienes (LTs), a group of pro-inflammatory lipid mediators, in CDI. Notably, the neutrophil chemoattractant LTB4, but not cysteinyl (cys) LTs, was induced in the intestine of C57BL/6 mice infected with either C. difficile strain VPI 10463 or strain 630. Genetic or pharmacological ablation of LT production did not ameliorate C. difficile colitis or clinical signs of disease in infected mice. Histological analysis demonstrated that intestinal neutrophilic inflammation, edema and tissue damage in mice during acute and severe CDI were not modulated in the absence of LTs. In addition, CDI induced a burst of cytokines in the intestine of infected mice in a LT-independent manner. Serum levels of anti-toxin A immunoglobulin (Ig) G levels were also not modulated by endogenous LTs. Collectively, our results do not support a role for LTs in modulating host susceptibility to CDI in mice.

The acute phase of Trypanosoma cruzi infection is attenuated in 5-lipoxygenase-deficient mice.

In the present work we examine the contribution of 5-lipoxygenase- (5-LO-) derived lipid mediators to immune responses during the acute phase of Trypanosoma cruzi infection in 5-LO gene knockout (5-LO(-/-)) mice and wild-type (WT) mice. Compared with WT mice, the 5-LO(-/-) mice developed less parasitemia/tissue parasitism, less inflammatory cell infiltrates, and a lower mortality. This resistance of 5-LO(-/-) mice correlated with several differences in the immune response to infection, including reduced PGE2 synthesis; sustained capacity of splenocytes to produce high levels of interleukin (IL)-12 early in the infection; enhanced splenocyte production of IL-1ß, IL-6, and IFN-γ; rapid T-cell polarization to secrete high quantities of IFN-γ and low quantities of IL-10; and greater numbers of CD8(+)CD44(high)CD62L(low) memory effector T cells at the end of the acute phase of infection. The high mortality in WT mice was associated with increased production of LTB4/LTC4, T cell bias to produce IFN-γ, high levels of serum nitrite, and marked protein extravasation into the peritoneal cavity, although survival was improved by treatment with a cys-LT receptor 1 antagonist. These data also provide evidence that 5-LO-derived mediators negatively affect host survival during the acute phase of T. cruzi infection.