Comparison of three newer generation freely available intraocular lens power calculation formulae across all axial lengths

Purpose:The aim of this study is to evaluate the accuracy of three newer generation formulae (Barrett Universal II, EVO, Hill-RBF 2.0) for calculation of power of two standard IOLs—the Acrysof IQ and Tecnis ZCB00 across all axial lengths.Methods:In this retrospective series, 206 eyes of 206 patients, operated for cataract surgery with above two IOLs over the last 6 months, were included in the study. Preoperative biometry measurements were obtained from LenstarLS900. By using recommended lens constants, the mean error for each formula was calculated and compared. Then, the optimized IOL constants were calculated to reduce the mean error to zero. Mean and median absolute errors were calculated for all eyes and separately for short (AL<22.5 mm), medium (22.5–24.5 mm), and long eyes (>24.5 mm). Absolute errors and percentages of eyes within prediction errors of ±0.25 D, ±0.50 D, ±0.75 D, and ±1.00 D were compared.Results:Prediction error with using recommended lens constants was significantly lower in the Barrett Universal II formula as compared to the other two formulae. However, after optimizing lens constants, there were no significant differences in the absolute errors between the three formulae. The formulae ranked by mean absolute error were as follows: Barrett Universal II (0.304 D), EVO (0.317 D), and Hill-RBF (0.322) D. There were no significant differences between absolute errors in the three formulae in each of the short-, medium-, and long-eye subgroups.Conclusion:With proper lens constant optimization, the Barrett Universal II, EVO, and Hill-RBF 2.0 formulae were equally accurate in predicting IOL power across the entire range of axial lengths.     

Effect of cigarette smoking and 3.2% ethanol alone or together on RBC and platelet counts in rats

The present study was conducted on 32 rats divided into four groups. Group C served as control, Group S rats were exposed to cigarette smoke alone, Group SE to cigarette smoke and ethanol (3.2%) and Group E to ethanol alone for twelve weeks. The basal RBC and platelet count were determined and compared with the values obtained at the end of 12 weeks. A significant increase in RBC and platelet counts was seen in Groups S (P < 0.001 and P < 0.01 respectively) and SE (P < 0.01 for both counts). The increase in group SE is less than that seen in Group S. Ethanol consumption alone has shown a significant decrease (P < 0.01) in RBC count and apparent decrease in platelet count as compared to control. This study indicates that cigarette smoke is damaging to health alone or when combined with ethanol.     

Inhibition of calpain prevents NMDA-induced cell death and β-amyloid-induced synaptic dysfunction in hippocampal slice cultures

Background and purpose:

Alzheimer''s disease (AD) is a multifactorial, neurodegenerative disease, which is in part caused by an impairment of synaptic function, probably mediated by oligomeric forms of amyloid-β (Aβ). While the Aβ pathology mainly affects the physiology of neurotransmission, neuronal decline is caused by excitotoxic cell death, which is mediated by the NMDA receptor. A comprehensive therapeutic approach should address both Aβ-induced synaptic deficits, as well as NMDA receptor-mediated neurodegeneration, via one molecular target. This study was designed to test whether calpain could be involved in both pathological pathways, which would offer a promising avenue for new treatments.

Experimental approach:

Application of the specific, water-soluble calpain inhibitor A-705253 was used to inhibit calpain in hippocampal slice cultures. We examined whether inhibition of calpain would prevent Aβ-induced deficits in neurotransmission in CA1, as well as NMDA-induced neuronal cell death.

Key results:

A-705253 dose-dependently prevented excitotoxicity-induced neurodegeneration at low nanomolar concentrations, determined by propidium iodide histochemistry. Inhibition of the NMDA receptor similarly protected from neuronal damage. Caspase staining indicated that calpain inhibition was protective by reducing apoptosis. Electrophysiological analysis revealed that inhibition of calpain by A-705253 also fully prevented Aβ oligomer-induced deficits in neurotransmission. The protective effect of calpain was compared to the clinically available NMDA receptor antagonist memantine, which was also effective in this model.

Conclusions and implications:

We suggest that inhibition of calpain exhibits a promising strategy to address several aspects of the pathology of AD that may go beyond the available therapeutic intervention by memantine.     

Oncogene proteins and proliferation antigens in thymomas: increased expression of epidermal growth factor receptor and Ki67 antigen.

AIMS--To examine thymomas for proteins encoded by oncogenes and to determine whether their presence correlates with tumour growth and associated myasthenia gravis. METHODS--Sections of 24 thymomas were incubated with anti-EGF receptor (EGF-R), anti-Ki67 antigen, anti-p53, and anti-bcl-2 antibodies, and then stained using the alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique. Cell suspensions and epithelial cell cultures from some of the tumours were also studied. RESULTS--Whereas EGF-R expression was not detected in any of the controls (but only in a 20 week old fetus), it was detected in neoplastic epithelial cells of all thymomas, and was most strongly expressed in metastases and in samples from donors with severe myasthenia gravis. Ki67 labelling was also increased, especially in the larger thymomas. Epithelial expression of both of these markers was confirmed in fresh cell suspensions and monolayer cultures from the five available cases. In contrast, p53 and bcl-2 were not detected in the neoplastic cells, but bcl-2 was present in the intermingling thymocytes. CONCLUSIONS--Neoplastic thymoma cells express EGF-R and Ki67, but there is no concomitant increase in the expression of p53 and bcl-2 proteins. Increased EGF-R expression may result in increased proliferation of neoplastic cells and also in myasthenia gravis. Measurement of EGF-R concentrations may be of prognostic value. The bcl-2 staining pattern in T lymphocytes illustrates the broad spectrum of maturational stages in thymoma lymphocytes.     

L-selectin mediates neutrophil rolling in inflamed venules through sialyl LewisX-dependent and -independent recognition pathways

The glycoprotein (GP) L-selectin initiates adhesive interactions between leukocytes and endothelial cells (EC). It functions as a lymphocyte-lectin homing receptor recognizing carbohydrate determinants of the peripheral lymph node addressing on high endothelial venules. It also mediates neutrophil rolling, the earliest interaction of neutrophils with acutely inflamed venules. Neutrophil L-selectin presents sialyl-LewisX (sLe(X)) as a ligand to P- and E-selectin in vitro, and we have proposed that this is a major mechanism of L- selectin-mediated rolling in vivo. In contrast, the contribution of neutrophil L-selectin as a receptor protein recognizing one (or more) ligand(s) on inflamed EC is unclear. To address this question, an sLe(X)-negative murine pre-B cell line, L1-2, that can neither bind vascular selectins nor roll in inflamed rabbit venules, was transfected with human L-selectin cDNA. L-selectin expression in stable transfectants was sufficient to confer significant rolling in vivo. Rolling was unaffected by neuraminidase treatment but completely blocked by anti-L-selectin monoclonal antibody (MoAb) DREG-56. Thus, L- selectin can initiate leukocyte interactions with EC determinants potentially through recognition of endothelial carbohydrates. In contrast, when human neutrophils were tested, rolling was reduced, but not abolished, by MoAb DREG-56. Likewise, treatment with neuraminidase or anti-sLe(X) MoAbs decreased, but did not abrogate, neutrophil rolling, consistent with residual EC recognition via L-selectin. Combination of MoAb DREG-56 and neuraminidase resulted in almost complete loss of rolling, as did removal of glycosylated L-selectin by chymotrypsin. Together with the demonstrable rolling of L-selectin transfectants, our results support the concept of a bidirectional interaction between L-selectin bearing sLe(X) on neutrophils and activated EC in vivo. These findings also suggest that L-selectin may mediate rolling of lymphocytes that lack carbohydrate ligands for E- or P-selectin, although probably less efficiently than through bidirectional recognition.