Health-Related Quality of Life and Injuries in Physical Education Students: A Multi-Group Model According to the Degree of Adherence to the Mediterranean Diet.

The Mediterranean diet is considered a healthy eating pattern. It has been shown to improve people's quality of life. When a person suffers injuries, their quality of life suffers. This research aims to accomplish the following: (a) to study the differences in the effect of the health-related quality of life on injuries according to the degree of adherence to the Mediterranean diet, (b) to analyse the existing differences in the variables that make up the health-related quality of life according to the degree of adherence to the Mediterranean diet, and (c) to analyse the degree of adherence to the Mediterranean diet according to whether the participants have suffered any injury. The study was descriptive, cross-sectional, and exploratory in a sample of 556 physical education students. The PREDIMED questionnaire, the SF-36 questionnaire, and a self-administered questionnaire were used. The results showed that high adherence to the Mediterranean diet was associated with higher quality of life and lower injury rates. It was also observed that high adherence to the Mediterranean diet improved the effect of the quality of life on injuries. In conclusion, the Mediterranean diet is beneficial for the quality of life of young university students.

Mediterranean diet adherence on self-concept and anxiety as a function of weekly physical activity: an explanatory model in higher education.

Introduction: Scientific literature has now demonstrated the benefits of an active lifestyle for people's psychological health. Based on the above statement, the aim was to (a) evaluate and adjust a structural equation model containing the variables anxiety, self-concept, and Mediterranean diet adherence and (b) contrast the proposed theoretical model by studying the differences between the variables according to the level of weekly physical activity in a sample of 558 university students. Methods: A non-experimental, exploratory, cross-sectional investigation has been proposed. Instruments such as the PREDIMED Questionnaire, the Beck Anxiety Inventory, the International Physical Activity Questionnaire, and the Form 5 Self-Concept Questionnaire were used to collect data. Results and discussion: The results illustrate that students showing low adherence to the Mediterranean diet had higher levels of anxiety (M = 0.95) than those showing a high degree of adherence (M = 0.75). It is also observed that young people with a high degree of adherence to the Mediterranean diet report higher scores in the different dimensions of self-concept compared to young people with a low degree of adherence. In conclusion, it is affirmed that young people who show a high degree of adherence to this dietary pattern show lower levels of anxiety and greater recognition of the different areas of their self-concept.

Preferred surgical techniques for secondary intraocular lens implantation in adults with aphakia.

AIM: To identify the current surgical management of aphakia and the outcomes and complications of each technique. METHODS: This cross-sectional study included ophthalmic surgeons with at least one-year experience in surgery for aphakia. A study questionnaire was formulated to collect data in Saudi Arabia and other regional countries. The questionnaire included 22 questions on demographics, preferred surgical techniques, complications and the factors related to surgeon decision and the choice for managing aphakia. RESULTS: The study included 145 participants (111; 76.6% were males) with mean age of 46.7 ± 11.5 years. The mean duration of cataract surgery experience was 17.6 ± 11.1 years. Most participants (86.2%) were trained in cataract surgery. Scleral fixation of intraocular lens (SFIOL) was the most commonly preferred technique, followed by iris fixation IOL, and anterior chamber IOL (75.2%, 9%, and 15.9%, respectively). The main determinants for selection of a surgical technique were simplicity (56.6%), surgical instrument availability (48.3%), and training on the technique (47.6%). The most frequent postoperative complications were pupil distortion, high intraocular pressure (IOP), pupillary capture of the IOL, and IOL decentration. CONCLUSIONS: SFIOL is the preferred surgical technique for managing aphakia. The decision to choose one technique over another is complex and is based on several factors, including technical difficulty, previous training, anatomical variations, ocular comorbidities, and the potential complications. The most frequent complications after surgical correction of aphakia are pupil distortion, high IOP, pupillary capture of the IOL, and decentered IOLs.

Glioblastoma Cells Counteract PARP Inhibition through Pro-Survival Induction of Lipid Droplets Synthesis and Utilization.

Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor in adults. Poly (ADP-ribose) polymerase inhibitors (PARPi) represent a new class of anti-neoplastic drugs. In the current study, we have characterized the mechanism by which glioblastoma cells evade the effect of PARPi as anti-tumor agents. We have found that suppression of PARP activity exerts an anti-stemness effect and has a dual impact on autophagy, inducing its activation in the first 24 h (together with down-regulation of the pro-survival mTOR pathway) and preventing autophagosomes fusion to lysosomes at later time-points, in primary glioma cells. In parallel, PARPi triggered the synthesis of lipid droplets (LDs) through ACC-dependent activation of de novo fatty acids (FA) synthesis. Notably, inhibiting ß-oxidation and blocking FA utilization, increased PARPi-induced glioma cell death while treatment with oleic acid (OA) prevented the anti-glioma effect of PARPi. Moreover, LDs fuel glioma cells by inducing pro-survival lipid consumption as confirmed by quantitation of oxygen consumption rates using Seahorse respirometry in presence or absence of OA. In summary, we uncover a novel mechanism by which glioblastoma escapes to anti-tumor agents through metabolic reprogramming, inducing the synthesis and utilization of LDs as a pro-survival strategy in response to PARP inhibition.

Tankyrases as modulators of pro-tumoral functions: molecular insights and therapeutic opportunities.

Tankyrase 1 (TNKS1) and tankyrase 2 (TNKS2) are two homologous proteins that are gaining increasing importance due to their implication in multiple pathways and diseases such as cancer. TNKS1/2 interact with a large variety of substrates through the ankyrin (ANK) domain, which recognizes a sequence present in all the substrates of tankyrase, called Tankyrase Binding Motif (TBM). One of the main functions of tankyrases is the regulation of protein stability through the process of PARylation-dependent ubiquitination (PARdU). Nonetheless, there are other functions less studied that are also essential in order to understand the role of tankyrases in many pathways. In this review, we concentrate in different tankyrase substrates and we analyze in depth the biological consequences derived of their interaction with TNKS1/2. We also examine the concept of both canonical and non-canonical TBMs and finally, we focus on the information about the role of TNKS1/2 in different tumor context, along with the benefits and limitations of the current TNKS inhibitors targeting the catalytic PARP domain and the novel strategies to develop inhibitors against the ankyrin domain. Available data indicates the need for further deepening in the knowledge of tankyrases to elucidate and improve the current view of the role of these PARP family members and get inhibitors with a better therapeutic and safety profile.

Selective modulation by PARP-1 of HIF-1α-recruitment to chromatin during hypoxia is required for tumor adaptation to hypoxic conditions.

BACKGROUND: The adaptation to hypoxia is mainly controlled by the HIF transcription factors. Increased expression/activity of HIF-1α correlates with poor prognosis in cancer patients. PARP-1 inhibitors are used in the clinic to treat BRCAness breast/ovarian cancer and have been shown to regulate the hypoxic response; therefore, their use could be expanded. METHODS: In this work by integrating molecular/cell biology approaches, genome-wide ChIP-seq, and patient samples, we elucidate the extent to which PARP-1 exerts control over HIF-1-regulated genes. RESULTS: In human melanoma, PARP-1 and HIF-1α expression are strongly associated. In response to a hypoxic challenge poly(ADP-ribose) (PAR) is synthesized, HIF-1α is post-transcriptionally modified (PTM) and stabilized by PARylation at specific K/R residues located at its C-terminus. Using an unbiased ChIP-seq approach we demonstrate that PARP-1 dictates hypoxia-dependent HIF-recruitment to chromatin in a range of HIF-regulated genes while analysis of HIF-binding motifs (RCGTG) reveals a restriction on the recognition of hypoxia responsive elements in the absence of PARP-1. Consequently, the cells are poorly adapted to hypoxia, showing a reduced fitness during hypoxic induction. CONCLUSIONS: These data characterize the fine-tuning regulation by PARP-1/PARylation of HIF activation and suggest that PARP inhibitors might have therapeutic potential against cancer types displaying HIF-1α over-activation.

Parp3 promotes astrocytic differentiation through a tight regulation of Nox4-induced ROS and mTorc2 activation.

Parp3 is a member of the Poly(ADP-ribose) polymerase (Parp) family that has been characterized for its functions in strand break repair, chromosomal rearrangements, mitotic segregation and tumor aggressiveness. Yet its physiological implications remain unknown. Here we report a central function of Parp3 in the regulation of redox homeostasis in continuous neurogenesis in mice. We show that the absence of Parp3 provokes Nox4-induced oxidative stress and defective mTorc2 activation leading to inefficient differentiation of post-natal neural stem/progenitor cells to astrocytes. The accumulation of ROS contributes to the decreased activity of mTorc2 as a result of an oxidation-induced and Fbxw7-mediated ubiquitination and degradation of Rictor. In vivo, mTorc2 signaling is compromised in the striatum of naïve post-natal Parp3-deficient mice and 6 h after acute hypoxia-ischemia. These findings reveal a physiological function of Parp3 in the tight regulation of striatal oxidative stress and mTorc2 during astrocytic differentiation and in the acute phase of hypoxia-ischemia.

Successful surgical management of post-penetrating or deep lamellar keratoplasty Acquired Corneal Sub-Epithelial Hypertrophy (ACSH): A case series.

INTRODUCTION: Acquired Corneal Sub-Epithelial Hypertrophy (ACSH) has been described in patients with peripheral superficial corneal opacities following penetrating keratoplasty and might present similar to Salzmann's nodular degeneration (SND) or peripheral hypertrophic sub-epithelial corneal degeneration (PHSCD). We describe the clinical presentation, topographic findings and the surgical outcome of three cases, which fit the appearance and characteristics of ACSH. PRESENTATION OF CASES: Three patients (3 eyes) with paracentral or peripheral corneal opacification were reviewed to describe their clinical examination (SL), morphology of the opacity (depth, diameter and density) and document their topographic changes before and after surgical intervention by peeling of the epithelium with or without superficial keratectomy under the microscope in addition to brief description of their histopathological examination. DISCUSSION: All 3 cases were secondary to corneal procedures [Penetrating keratoplasty (PKP) in 1 for pseudophakic bullous keratopathy and deep anterior lamellar keratoplasty (DLK) in 2 for advanced keratoconus]. All cases presented with reduced vision, astigmatic changes in topography or manifest refraction. The visual acuity, symptoms, and topographical findings all improved after treatment. Histopathologically, all cases fit the newly described entity of ACSH. CONCLUSION: Careful clinical judgement guided by corneal topography are needed for proper the diagnosis of acquired corneal opacification that results in reduction of vision to identify ACSH from other similar conditions (PHSCD and SND). Peeling of the thickened epithelial and sub-epithelial tissue is curative avoiding the need for corneal re-grafting.

PARP1 and Poly(ADP-ribosyl)ation Signaling during Autophagy in Response to Nutrient Deprivation.

Autophagy is considered to be the primary degradative pathway that takes place in all eukaryotic cells. Morphologically, the autophagy pathway refers to a process by which cytoplasmic portions are delivered to double-membrane organelles, called autophagosomes, to fuse with lysosomes for bulk degradation. Autophagy, as a prosurvival mechanism, can be stimulated by different types of cellular stress such as nutrient deprivation, hypoxia, ROS, pH, DNA damage, or ER stress, promoting adaptation of the cell to the changing and hostile environment. The functional relevance of autophagy in many diseases such as cancer or neurodegenerative diseases remains controversial, preserving organelle function and detoxification and promoting cell growth, although in other contexts, autophagy could suppress cell expansion. Poly(ADP-ribosyl)ation (PARylation) is a covalent and reversible posttranslational modification (PTM) of proteins mediated by Poly(ADP-ribose) polymerases (PARPs) with well-described functions in DNA repair, replication, genome integrity, cell cycle, and metabolism. Herein, we review the current state of PARP1 activation and PARylation in starvation-induced autophagy.

PARP3 comes to light as a prime target in cancer therapy.

Poly(ADP-ribose) polymerase 3 (PARP3) is the third member of the PARP family that catalyze a post-translational modification of proteins to promote, control or adjust numerous cellular events including genome integrity, transcription, differentiation, cell metabolism or cell death. In the late years, PARP3 has been specified for its primary functions in programmed and stress-induced double-strand break repair, chromosomal rearrangements, transcriptional regulation in the zebrafish and mitotic segregation. Still, deciphering the therapeutic value of its inhibition awaits additional investigations. In this review, we discuss the newest advancements on the specific functions of PARP3 in cancer aggressiveness exemplifying the relevance of its selective inhibition for cancer therapy.

PARP3, a new therapeutic target to alter Rictor/mTORC2 signaling and tumor progression in BRCA1-associated cancers.

PARP3 has been shown to be a key driver of TGFß-induced epithelial-to-mesenchymal transition (EMT) and stemness in breast cancer cells, emerging as an attractive therapeutic target. Nevertheless, the therapeutic value of PARP3 inhibition has not yet been assessed. Here we investigated the impact of the absence of PARP3 or its inhibition on the tumorigenicity of BRCA1-proficient versus BRCA1-deficient breast cancer cell lines, focusing on the triple-negative breast cancer subtype (TNBC). We show that PARP3 knockdown exacerbates centrosome amplification and genome instability and reduces survival of BRCA1-deficient TNBC cells. Furthermore, we engineered PARP3-/- BRCA1-deficient or BRCA1-proficient TNBC cell lines using the CRISPR/nCas9D10A gene editing technology and demonstrate that the absence of PARP3 selectively suppresses the growth, survival and in vivo tumorigenicity of BRCA1-deficient TNBC cells, mechanistically via effects associated with an altered Rictor/mTORC2 signaling complex resulting from enhanced ubiquitination of Rictor. Accordingly, PARP3 interacts with and ADP-ribosylates GSK3ß, a positive regulator of Rictor ubiquitination and degradation. Importantly, these phenotypes were rescued by re-expression of a wild-type PARP3 but not by a catalytic mutant, demonstrating the importance of PARP3's catalytic activity. Accordingly, reduced survival and compromised Rictor/mTORC2 signaling were also observed using a cell-permeable PARP3-specific inhibitor. We conclude that PARP3 and BRCA1 are synthetic lethal and that targeting PARP3's catalytic activity is a promising therapeutic strategy for BRCA1-associated cancers via the Rictor/mTORC2 signaling pathway.

PARP3 controls TGFß and ROS driven epithelial-to-mesenchymal transition and stemness by stimulating a TG2-Snail-E-cadherin axis.

Several members of the Poly(ADP-ribose) polymerase (PARP) family are essential regulators of genome integrity, actively prospected as drug targets for cancer therapy. Among them, PARP3 is well characterized for its functions in double-strand break repair and mitotis. Here we report that PARP3 also plays an integral role in TGFß and reactive oxygen species (ROS) dependent epithelial-to-mesenchymal transition (EMT) and stem-like cell properties in human mammary epithelial and breast cancer cells. PARP3 expression is higher in breast cancer cells of the mesenchymal phenotype and correlates with the expression of the mesenchymal marker Vimentin while being in inverse correlation with the epithelial marker E-cadherin. Furthermore, PARP3 expression is significantly upregulated during TGFß-induced EMT in various human epithelial cells. In line with this observation, PARP3 depletion alters TGFß-dependent EMT of mammary epithelial cells by preventing the induction of the Snail-E-cadherin axis, the dissolution of cell junctions, the acquisition of cell motility and chemoresistance. PARP3 responds to TGFß-induced ROS to promote a TG2-Snail-E-cadherin axis during EMT. Considering the link between EMT and cancer stem cells, we show that PARP3 promotes stem-like cell properties in mammary epithelial and breast cancer cells by inducing the expression of the stem cell markers SOX2 and OCT4, by increasing the proportion of tumor initiating CD44high/CD24low population and the formation of tumor spheroid bodies, and by promoting stem cell self-renewal. These findings point to a novel role of PARP3 in the control of TGFß-induced EMT and acquisition of stem-like cell features and further motivate efforts to identify PARP3 specific inhibitors.

PARP-1 regulates metastatic melanoma through modulation of vimentin-induced malignant transformation.

PARP inhibition can induce anti-neoplastic effects when used as monotherapy or in combination with chemo- or radiotherapy in various tumor settings; however, the basis for the anti-metastasic activities resulting from PARP inhibition remains unknown. PARP inhibitors may also act as modulators of tumor angiogenesis. Proteomic analysis of endothelial cells revealed that vimentin, an intermediary filament involved in angiogenesis and a specific hallmark of EndoMT (endothelial to mesenchymal transition) transformation, was down-regulated following loss of PARP-1 function in endothelial cells. VE-cadherin, an endothelial marker of vascular normalization, was up-regulated in HUVEC treated with PARP inhibitors or following PARP-1 silencing; vimentin over-expression was sufficient to drive to an EndoMT phenotype. In melanoma cells, PARP inhibition reduced pro-metastatic markers, including vasculogenic mimicry. We also demonstrated that vimentin expression was sufficient to induce increased mesenchymal/pro-metastasic phenotypic changes in melanoma cells, including ILK/GSK3-ß-dependent E-cadherin down-regulation, Snail1 activation and increased cell motility and migration. In a murine model of metastatic melanoma, PARP inhibition counteracted the ability of melanoma cells to metastasize to the lung. These results suggest that inhibition of PARP interferes with key metastasis-promoting processes, leading to suppression of invasion and colonization of distal organs by aggressive metastatic cells.

Poly(ADP-ribose) signaling in cell death.

Poly(ADP-ribosyl)ation (PARylation) is a reversible protein modification carried out by the concerted actions of poly(ADP-ribose) polymerase (PARP) enzymes and poly(ADP-ribose) (PAR) decomposing enzymes such as PAR glycohydrolase (PARG) and ADP-ribosyl hydrolase 3 (ARH3). Reversible PARylation is a pleiotropic regulator of various cellular functions but uncontrolled PARP activation may also lead to cell death. The cellular demise pathway mediated by PARylation in oxidatively stressed cells has been described almost thirty years ago. However, the underlying molecular mechanisms have only begun to emerge relatively recently. PARylation has been implicated in necroptosis, autophagic cell death but its role in extrinsic and intrinsic apoptosis appears to be less predominant and depends largely on the cellular model used. Currently, three major pathways have been made responsible for PARP-mediated necroptotic cell death: (1) compromised cellular energetics mainly due to depletion of NAD, the substrate of PARPs; (2) PAR mediated translocation of apoptosis inducing factor (AIF) from mitochondria to nucleus (parthanatos) and (3) a mostly elusive crosstalk between PARylation and cell death/survival kinases and phosphatases. Here we review how these PARP-mediated necroptotic pathways are intertwined, how PARylation may contribute to extrinsic and intrinsic apoptosis and discuss recent developments on the role of PARylation in autophagy and autophagic cell death.

Mejoría en el score de riesgo cardiovascular por la cirugía bariátrica / Improvement in the cardiovascular risk score due to bariatric surgery

Introducción: La obesidad se ha considerado como un factor de riesgo para desarrollar eventos coronarios agudos. Los principales factores para desarrollar este tipo de enfermedades están presentes en la mayoría de los pacientes sometidos a cirugía bariátrica. Objetivo: Evaluar el riesgo cardiovascular de los pacientes sometidos a cirugía bariátrica en forma preoperatoria y postoperatoria tras un seguimiento a dos años. Sede: Hospital General ''Dr. Manuel Gea González''. Diseño: Estudio retrospectivo, longitudinal, observacional y comparativo. Material y métodos: Pacientes de la clínica de cirugía bariátrica, operados con la técnica de bypass gástrico, calculando el riesgo cardiovascular de forma preoperatoria y posteriormente a dos años de seguimiento. Resultados: Se incluyeron 64 pacientes (13 hombres y 51 mujeres). La edad promedio de los hombres fue 42 años su índice de masa corporal promedio fue 49.44 kg/m², la puntuación del riesgo cardiovascular preoperatoria fue: 5.15 (2-9). Al seguimiento a dos años su índice de masa corporal promedio disminuyó a 36.23 kg/m², la puntuación del riesgo cardiovascular fue: 2.38 (0-5). En las mujeres la edad promedio fue de 36 años, su índice de masa corporal promedio previo a la cirugía fue 45.32 kg/m², la puntuación del riesgo cardiovascular fue: 4.3 (-10 a 13). A un seguimiento de dos años su índice de masa corporal promedio fue 28.64 kg/m² (20.1-42.1), la puntuación del riesgo cardiovascular fue -4.1 (-11 a 8). Conclusión: La cirugía bariátrica no sólo ha demostrado ser un método eficaz y seguro para la disminución del peso corporal en pacientes con obesidad mórbida, también aquí se demuestra que disminuye el riesgo cardiovascular que poseen estos pacientes.

Introduction: Obesity has been considered a risk factor for acute coronary events. The main factors to develop this type of diseases are present in most of the patients subjected to bariatric surgery. Objective: To assess the cardiovascular risk of patients subjected to bariatric surgery preoperatively and at 2-years follow-up. Setting: General Hospital ''Dr. Manuel Gea González''. Design: Retrospective, longitudinal, observational, and comparative study. Patients and methods: Patients from the bariatric surgery clinic, operated with the gastric bypass technique, calculating the cardiovascular risk preoperatively and at 2-year follow-up. Results: The study included 64 patients (13 men and 51 women). Average age of men was 42 years, their average body mass index was 49.44 kg/m², preoperative cardiovascular risk score was 5.15 (2-9). At 2-year follow-up, their BMI diminished to 36.23 kg/m², the cardiovascular risk score was 2.38 (0-5). In women, average age was of 36 years, their body mass index before surgery was of 45.32 kg/m², the cardiovascular risk score was 4.3 (-10 a 13). At 2-year follow-up, their average body mass index reduced to 28.64 kg/m² (20.1-42.1), and the cardiovascular risk score was -4.1 (-11 to 8). Conclusion: Bariatric surgery has not only been demonstrated as an efficacious and safe method to reduce body weight in patients with morbid obesity but also to diminish the cardiovascular risk depicted by these patients.

PARP inhibitors: new partners in the therapy of cancer and inflammatory diseases.

Poly(ADP-ribose) polymerases (PARPs) are defined as cell signaling enzymes that catalyze the transfer of ADP-ribose units from NAD(+) to a number of acceptor proteins. PARP-1, the best characterized member of the PARP family, which currently comprises 18 members, is an abundant nuclear enzyme implicated in cellular responses to DNA injury provoked by genotoxic stress. PARP is involved in DNA repair and transcriptional regulation and is now recognized as a key regulator of cell survival and cell death as well as a master component of a number of transcription factors involved in tumor development and inflammation. PARP-1 is essential to the repair of DNA single-strand breaks via the base excision repair pathway. Inhibitors of PARP-1 have been shown to enhance the cytotoxic effects of ionizing radiation and DNA-damaging chemotherapy agents, such as the methylating agents and topoisomerase I inhibitors. There are currently at least five PARP inhibitors in clinical trial development. Recent in vitro and in vivo evidence suggests that PARP inhibitors could be used not only as chemo/radiotherapy sensitizers, but also as single agents to selectively kill cancers defective in DNA repair, specifically cancers with mutations in the breast cancer-associated genes (BRCA1 and BRCA2). PARP becomes activated in response to oxidative DNA damage and depletes cellular energy pools, thus leading to cellular dysfunction in various tissues. The activation of PARP may also induce various cell death processes and promotes an inflammatory response associated with multiple organ failure. Inhibition of PARP activity is protective in a wide range of inflammatory and ischemia-reperfusion-associated diseases, including cardiovascular diseases, diabetes, rheumatoid arthritis, endotoxic shock, and stroke. The aim of this review is to overview the emerging data in the literature showing the role of PARP in the pathogenesis of cancer and inflammatory diseases and unravel the solid body of literature that supports the view that PARP is an important target for therapeutic intervention in critical illness.

PARP-1 is involved in autophagy induced by DNA damage.

Autophagy is a lysosome-dependent degradative pathway frequently activated in tumor cells treated with chemotherapy or radiation. PARP-1 has been implicated in different pathways leading to cell death and its inhibition potentiates chemotherapy-induced cell death. Whether PARP-1 participates in the cell's decision to commit to autophagy following DNA damage is still not known. To address this issue PARP-1 wild-type and deficient cells have been treated with a dose of doxorubicin that induces autophagy. Electron microscopy examination and GFP-LC3 transfection revealed autophagic vesicles and increased expression of genes involved in autophagy (bnip-3, cathepsin b and l and beclin-1) in wild-type cells treated with doxo but not in parp-1(-/-) cells or cells treated with a PARP inhibitor. Mechanistically the lack of autophagic features in PARP-1 deficient/PARP inhibited cells is attributed to prevention of ATP and NAD(+) depletion and to the activation of the key autophagy regulator mTOR. Pharmacological or genetical inhibition of autophagy results in increased cell death, suggesting a protective role of autophagy induced by doxorubicin. These results suggest that autophagy might be cytoprotective during the response to DNA damage and suggest that PARP-1 activation is involved in the cell's decision to undergo autophagy.

The Kelman Duet phakic intraocular lens: 1-year results.

PURPOSE: To evaluate the efficacy and safety of the Kelman Duet phakic intraocular lens (PIOL) for correction of moderate and high myopia. METHODS: Kelman Duet PIOLs were implanted in 169 eyes of 110 patients with moderate or high myopia. In all cases, implantation of the lens was feasible through an incision of less than 2.5 mm without complications. Uncorrected visual acuity (UCVA), manifest refraction, best spectacle-corrected visual acuity (BSCVA), intraocular pressure, central corneal endothelial change, and complications were recorded preoperatively and during 12 months of follow-up. RESULTS: Following PIOL implantation, 23 (13.61%) eyes required LASIK retreatment for the correction of residual astigmatic refractive error and were excluded from the refractive analysis. Best spectacle-corrected visual acuity remained the same or improved in 95.04% of eyes, 81.30% of eyes (100) were within +/-1.00 diopter (D) of emmetropia, and 57.72% (71) were within +/-0.50 D. Intraocular pressure increased slightly in the first 4 weeks postoperatively but stabilized to the preoperative level by 3 months. Mean endothelial cell loss at 12 months was 5.43%. Oval pupils developed in 10.1% of eyes. Haptic exchange or reposition was performed in 7.76% of cases. CONCLUSIONS: The Kelman Duet PIOL was safe and effective for the correction of moderate to high myopia in this study with 1-year follow-up and offered the advantage of using a 2.5-mm or less incision width. Accurate haptic sizing remains a challenge and haptic exchange to correct haptic size mismatching is possible.

Lucha contra la ceguera por cataratas en zona rural del estado Aragua: programa Sight-first / Struggle against the blindness by cataracts in the rural zone of the Aragua state: Sight-first program

Este estudio analiza un programa realizado en el Estado Aragua, Venezuela, en la lucha contra la ceguera por cataratas. Se realizó en cuatro municipios del citado estado, donde la población se caracteriza por ser de bajos recursos y baja posibilidad de atención oftalmológica. El criterio diagnóstico y terapéutico se basó en la ceguera por cataratas sin enfermedades subyacentes, en mayores de 50 años de edad. El programa consta de tres etapas: la primera incluye tamizaje y diagnóstico. Luego en la segunda, se procede a la cirugía y por último el seguimiento de los pacientes intervenidos. Tuvo una cobertura de 13,48 por ciento (989 de 7.333 habitantes). De los 989 pacientes, 80 fueron diagnosticados y operados. Estos pacientes, que eran un peso familiar y por ende condenados a una vida intradomiciliaria por no contar con los recursos para asistir al centro oftalmológico más cercano, fueron restituídos a su vida cotidiana