Acostalohmann4909

PURPOSE The purpose of this study is to develop and assess the accuracy of a new intraocular lens (IOL) power calculation method based on machine learning techniques. METHODS The following data were retrieved for 260 eyes of 260 patients undergoing cataract surgery preoperative simulated keratometry, mean keratometry of posterior surface, axial length, anterior chamber depth, lens thickness, and white-to-white diameter; model and power of implanted IOL; and subjective refraction at 3 months post surgery. These data were used to train different machine learning models (k-Nearest Neighbor, Artificial Neural Networks, Support Vector Machine, Random Forest, etc). Implanted lens characteristics and biometric data were used as input to predict IOL power and refractive outcomes. For external validation, a dataset of 52 eyes was used. The accuracy of the trained models was compared with that of the power formulas Holladay 2, Haigis, Barrett Universal II, and Hill-RBF v2.0. RESULTS The SD of the prediction error in order of lowest to highest was the new method (designated Karmona) (0.30), Haigis (0.36), Holladay 2 (0.38), Barrett Universal II (0.38), and Hill-RBF v2.0 (0.40). Using the Karmona method, 90.38% and 100% of eyes were within ±0.50 and ±1.00 D respectively. CONCLUSIONS The method proposed emerged as the most accurate to predict IOL power.PURPOSE Peripapillary hyperreflective ovoid mass-like structures (PHOMS) are novel and not well characterized findings occurring in several disorders of the optic nerve. The aim of this study is to present two cases of tilted disc syndrome (TDS) and one case with optic disc drusen undergoing a multimodal imaging approach. METHODS In this case series, a qualitative evaluation of the OCTA findings in regions with PHOMS was performed. RESULTS Structural OCT revealed the presence of PHOMS. OCTA identified the presence of a vascular complex within this hyperreflective structure. CONCLUSIONS Assuming that PHOMS are thought to correspond to herniating nerve fibers or be secondary to axoplasmic stasis, this vascular complex may represent a displacement of the deeper vessels deputed at the irroration of the optic nerve into the retina or, alternatively, might be secondary to an increase in vascular endothelial growth factor (VEGF) levels and a subsequent development of neovessels.Small synthetic molecules mimicking the three-dimensional structure of α-helices may find applications as inhibitors of therapeutically relevant protein-protein and protein-nucleic acid interactions. However, the design and use of multi-facial helix mimetics remains in its infancy. Here we describe the synthesis and application of novel bilaterally substituted p-terphenyl compounds containing positively-charged aminoalkyl groups in relative 1,4 positions across the aromatic scaffold. These compounds were specifically designed to mimic all faces of the arginine-rich α-helix of the HIV-1 protein Rev, which forms deeply embedded RNA complexes and plays key roles in the virus replication cycle. Two of these molecules recognized the Rev site in the viral RNA and inhibited the formation of the RRE-Rev ribonucleoprotein complex, a currently unexploited target in HIV chemotherapy. Cellular assays revealed that the most active compounds blocked HIV-1 replication with little toxicity, and likely exerted this effect through a multi-target mechanism involving inhibition of viral LTR promoter-dependent transcription and Rev function. Further development of this scaffold may open new avenues for targeting nucleic acids and may complement current HIV therapies, none of which involve inhibitors interfering with the gene regulation processes of the virus.The development of therapeutic approaches based on direct cardiac reprogramming of fibroblasts into induced-cardiomyocytes (iCM) has emerged as an attractive strategy to repair the injured myocardium. The identification of the mechanisms driving lineage conversion represents a crucial step toward the development of new and more efficient regenerative strategies. To this aim, here we show that pre-treatment with the Bmi1 inhibitor PTC-209 is sufficient to increase the efficiency of Chemical-induced Direct Cardiac Reprogramming both in mouse embryonic fibroblasts and adult cardiac fibroblasts. see more PTC-209 induces an overall increase of spontaneously beating iCM at end-stage of reprogramming, expressing high levels of late cardiac markers Troponin T and myosin muscle light chain-2v. The inhibition of Bmi1 expression occurring upon PTC-209 pre-treatment was maintained throughout the reprogramming protocol, contributing to a significant gene expression de-regulation. RNA profiling revealed that, upon Bmi1 inhibition a significant down-regulation of genes associated with immune and inflammatory signalling pathways occurred, with repression of different genes involved in interleukin, cytokine and chemokine pathways. Accordingly, we observed the down-regulation of both JAK/STAT3 and MAPK/ERK1-2 pathway activation, highlighting the crucial role of these pathways as a barrier for cardiac reprogramming. These findings have significant implications for the development of new cardiac regenerative therapies.Cell cycle proteins that are often dysregulated in malignant cells, such as cyclin-dependent kinase 4 (CDK4) and CDK6, have attracted considerable interest as potential targets for cancer therapy. In this context, multiple inhibitors of CDK4 and CDK6 have been developed, including three small molecules (palbociclib, abemaciclib and ribociclib) that are currently approved for the treatment of patients with breast cancer and are being extensively tested in individuals with other solid and haematological malignancies. Accumulating preclinical and clinical evidence indicates that the anticancer activity of CDK4/CDK6 inhibitors results not only from their ability to block the cell cycle in malignant cells but also from a range of immunostimulatory effects. In this Review, we discuss the ability of anticancer cell cycle inhibitors to modulate various immune functions in support of effective antitumour immunity.