Positional accommodative intraocular lens power error induced by the estimation of the corneal power and the effective lens position

Purpose:

To evaluate the predictability of the refractive correction achieved with a positional accommodating intraocular lenses (IOL) and to develop a potential optimization of it by minimizing the error associated with the keratometric estimation of the corneal power and by developing a predictive formula for the effective lens position (ELP).

Materials and Methods:

Clinical data from 25 eyes of 14 patients (age range, 52–77 years) and undergoing cataract surgery with implantation of the accommodating IOL Crystalens HD (Bausch and Lomb) were retrospectively reviewed. In all cases, the calculation of an adjusted IOL power (P_IOLadj) based on Gaussian optics considering the residual refractive error was done using a variable keratometric index value (n_kadj) for corneal power estimation with and without using an estimation algorithm for ELP obtained by multiple regression analysis (ELP_adj). P_IOLadj was compared to the real IOL power implanted (P_IOLReal, calculated with the SRK-T formula) and also to the values estimated by the Haigis, HofferQ, and Holladay I formulas.

Results:

No statistically significant differences were found between P_IOLReal and P_IOLadj when ELP_adj was used (P = 0.10), with a range of agreement between calculations of 1.23 D. In contrast, P_IOLReal was significantly higher when compared to P_IOLadj without using ELP_adj and also compared to the values estimated by the other formulas.

Conclusions:

Predictable refractive outcomes can be obtained with the accommodating IOL Crystalens HD using a variable keratometric index for corneal power estimation and by estimating ELP with an algorithm dependent on anatomical factors and age.     

Chromatic-achromatic perimetry in four clinic cases: Glaucoma and diabetes

Background:Some diseases that affect the visual system may show loss of chromatic-achromatic sensitivity before obvious physical signs appear in the usual examination of the eye''s posterior segment. A perimetric study has been conducted with four typical patients with glaucoma and diabetes, at different stages of the disease.Results:The results seem to indicate losses in the achromatic-parvocellular perimetry and both chromatic perimetry tests, undetected by conventional SAP.Conclusions:Our results illustrate that our patients without visible retinal alterations show signs of suspicion in multichannel perimetry.     

miR-146a is a pivotal regulator of neutrophil extracellular trap formation promoting thrombosis

Neutrophil extracellular traps (NET) induce a procoagulant response linking inflammation and thrombosis. Low levels of miR-146a, a brake of inflammatory response, are involved in higher risk of cardiovascular events, but the mechanisms explaining how miR-146a exerts its function remain largely undefined. The aim of this study was to explore the impact of miR-146a deficiency in NETosis both in sterile and non-sterile models in vivo, and to investigate the underlying mechanism. Two models of inflammation were used: (i) Ldlr^-/- mice transplanted with bone marrow from miR-146a^-/- or wild-type mice were fed a high-fat diet, generating an atherosclerosis model; and (ii) an acute inflammation model was generated by injecting lipopolysaccharide (1 mg/kg) into miR-146a^-/- and wildtype mice. miR-146a deficiency increased NETosis in both models. Accordingly, miR-146a^-/- mice showed significantly reduced carotid occlusion time and elevated levels of NET in thrombi following FeCl3-induced thrombosis. Infusion of DNAse I abolished arterial thrombosis in both WT and miR-146a^-/- mice. Interestingly, miR-146a-deficient mice have aged, hyperreactive and pro-inflammatory neutrophils in their circulation which are more prone to form NET independently of the stimulus. Furthermore, we demonstrated that patients with community-acquired pneumonia with reduced miR-146a levels associated with the T variant of the functional rs2431697 had an increased risk of cardiovascular events due, in part, to an increased generation of NET.     

Protective role of melatonin and retinol palmitate in oxidative stress and hyperlipidemic nephropathy induced by adriamycin in rats

Abstract: We have studied the effects of melatonin and retinol palmitate (RP) on the nephropathy and oxidative stress induced by a single and high dose of adriamycin (AD) in Wistar male rats. A dose of melatonin (75 μg/ kg/day) and a dose of RP (0.25 g oily solution/kg/day, sc) were injected 3 and 9 days before and after the administration of AD (25 mg/kg, i.p.), respectively. After the decapitation, samples were taken from the neck vascular trunk in order to determine the triglycerides, total cholesterol, phospholipids, HDL-cholesterol, total proteins, urea, lipoperoxides, and reduced glutathione (GSH). We estimated the lipoperoxide and glutathione (GSH) contents in renal homogenates, and the excretion of proteins in urine over a 24 hr period. The administration of AD caused significant increases in proteinuria and in the other parameters studied [lipids (triglycerides, total cholesterol, phospholipids, and HDL-cholesterol), nonprotein nitrogen compounds, and lipoperoxides]. AD increased the lipoperoxide content, but it decreased the GSH content in the kidney. Both melatonin and RP, although melatonin more significantly, decreased the intensity of the changes produced by the administration of AD alone. In fact, melatonin was quite efficient in reducing the formation of lipoperoxides, restoring renal GSH content and decreasing remarkably the severity of proteinuria. These results support the powerful antioxidant action of melatonin at renal level and a lower antioxidant action of retinol. Likewise, these data reinforce the hypothesis which supports the pathogenetic role and the close relation between the oxidative stress and the expression of the nephropathy induced by AD. However, in spite of this obvious antioxidant effect of melatonin in the kidney, additional studies are required to establish accurately the role of this pineal indole in the regulation and dynamics of the antioxidative defense enzyme system, which neutralizes the damaging effect of free radicals, both endogenous and exogenous, in this organ.     

Quadruple-2 protease inhibitors (PI)-therapy does not accelerate viral decay and suppression in PI-naive HIV-1 infected patients with severe immunosuppression and high viral load as compared with standard triple therapy

To analyse if a four-drug combination including two protease inhibitors (PIs) accelerates viral decay and suppression as compared with standard triple therapy in heavily immunosuppressed HIV-1 infected patients, an open label clinical trial was designed. PIs naive patients receiving their first highly active antiretroviral therapy were included if their CD4 cell count was lower than 200/mm3 and their HIV viral load (VL) >100,000 RNA copies/mL. Every patient received two analogues and was randomized in two groups receiving either one PI (saquinavir soft gel capsule) or two PIs (saquinavir + nelfinavir). Viral efficacy (VL <50), time to reach VL <50, viral clearance rate constant and plasmatic elimination half-life were determined. In all, 30 patients were enrolled. No viral variable was significatively improved by the four-drug combination in the short term. No clinical benefit should be expected with a four-drug (two PIs) regimen in patients with low CD4+ cell count and high VL.