Comitant strabismus etiology: extraocular muscle integrity and central nervous system involvement—a narrative review

Strabismus is not a condition in itself but the consequence of an underlying problem. Eye misalignment can be caused by disease, injury, and/or abnormalities in any of the structures and processes involved in visual perception and oculomotor control, from the extraocular muscles and their innervations to the oculomotor and visual processing areas in the brain. A small percentage of all strabismus cases are the consequence of well-described genetic syndromes, acquired insult, or disease affecting the extraocular muscles (EOMs) or their innervations. We will refer to them as strabismus of peripheral origin since their etiology lies in the peripheral nervous system. However, in most strabismus cases, that is comitant, non-restrictive, non-paralytic strabismus, the EOMs and their innervations function properly. These cases are not related to specific syndromes and their precise causes remain poorly understood. They are generally believed to be caused by deficits in the central neural pathways involved in visual perception and oculomotor control. Therefore, we will refer to them as central strabismus. The goal of this narrative review is to discuss the possible causes behind this particular type of eye misalignment and to raise awareness among eyecare professionals about the important role the central nervous system plays in strabismus etiology, and the subsequent implications regarding its treatment. A non-systematic search was conducted using PubMed, Medline, Cochrane, and Google Scholar databases with the keywords “origins,” “causes,” and “etiology” combined with “strabismus.” A snowball approach was also used to find relevant references. In the following article, we will first describe EOM integrity in central strabismus; next, we will address numerous reasons that support the idea of central nervous system (CNS) involvement in the origin of the deviation, followed by listing several possible central causes of the ocular misalignment. Finally, we will discuss the implications CNS etiology has on strabismus treatment.Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature.Peer ReviewedPostprint (published version

Initial clinical and treatment patterns of advanced differentiated thyroid cancer: ERUDIT study

Advanced differentiated thyroid cancer; Epidemiological study; Survival prognostic factorsCáncer de tiroides diferenciado avanzado; Estudio epidemiológico; Factores pronósticos de supervivenciaCàncer de tiroide diferenciat avançat; Estudi epidemiològic; Factors pronòstics de supervivènciaBackground Up to 30% of differentiated thyroid cancer (DTC) will develop advanced-stage disease (aDTC) with reduced overall survival (OS). Objective The aim of this study is to characterize initial diagnosis of aDTC, its therapeutic management, and prognosis in Spain and Portugal. Methods A multicentre, longitudinal, retrospective study of adult patients diagnosed with aDTC in the Iberian Peninsula was conducted between January 2007 and December 2012. Analyses of baseline characteristics and results of initial treatments, relapse- or progression-free survival ((RP)FS) from first DTC diagnosis, OS, and prognostic factors impacting the evolution of advanced disease were evaluated. Results Two hundred and thirteen patients (median age: 63 years; 57% female) were eligible from 23 hospitals. Advanced disease presented at first diagnosis (de novo aDTC) included 54% of patients, while 46% had relapsed from early disease (recurrent/progressive eDTC). At initial stage, most patients received surgery (98%) and/or radioiodine (RAI) (89%), with no differences seen between median OS (95% CI) (10.4 (7.3–15.3) years) and median disease-specific-survival (95% CI) (11.1 (8.7–16.2) years; log-rank test P = 0.4737). Age at diagnosis being <55 years was associated with a lower risk of death (Wald chi-square (Wc-s) P < 0.0001), while a poor response to RAI to a higher risk of death ((Wc-s) P < 0.05). In the eDTC cohort, median (RP)FS (95% CI) was of 1.7 (1.0–2.0) years after RAI, with R0/R1 surgeries being the only common significant favourable factor for longer (RP)FS and time to aDTC ((Wc-s) P < 0.05). Conclusion Identification of early treatment-dependent prognostic factors for an unfavourable course of advanced disease is possible. An intensified therapeutic attitude may reverse this trend and should be considered in poor-performing patients. Prospective studies are required to confirm these findings.ERUDIT study was sponsored and funded by Eisai Farmacéutica S.A. (Madrid, Spain)

Mecanismo de fuerza constante

Número de publicación: ES2683962 A1 (28.09.2018) También publicado como: ES2683962 B2 (21.02.2019) Número de Solicitud: Consulta de Expedientes OEPM (C.E.O.) P201700551 (28.03.2017)Mecanismo de fuerza constante del tipo de los utilizados para mantener un nivel de fuerza constante sobre el eslabón de entrada. El mecanismo incorpora una guía curva (1), cuya cara exterior define dos pistas de rodadura laterales (3a, 3b) sobre las que ruedan sendas ruedas (5a, 5b). Ambas ruedas (5a, 5b) están montadas sobre un mismo eje (6), sobre el que actúa un resorte de extensión (8). El otro extremo de este resorte se articula a un eje fijo (7). Por acción de una cadena de rodillos (10) las ruedas (5a, 5b) se desplazan sobre sendas pistas de rodadura laterales (3a, 3b) mientras que el resorte de extensión (8) se opone al movimiento. La geometría de la curva definida por las pistas de rodadura laterales (3a, 3b) es tal que la fuerza aplicada sobre la cadena de rodillos (10) se mantiene constante para cualquier posición de las ruedas (5a, 5b).Universidad de Almería y Universidad de Sevill

Mecanismo da síncope em nadadoras de elite

Os atletas podem ter baixa tolerância ao ortostatismo. O mecanismo envolvido ainda nao é bem conhecido. Nossa hipótese se baseia em que as mulheres nadadoras de alta performance desmaiam facilmente durante o teste de inclinaçao, tilt test (TT), provavelmente devido a um pobre controle barorreflexo. A frequência cardíaca e as variabilidades da pressao arterial diastólica, a sensibilidade barorreflexa, a hemodinâmica cardíaca e a velocidade do fluxo cerebral foram analisadas durante o TT em um grupo de 8 mulheres recorde mundial de longa distância em águas abertas (travessia do Canal da Mancha). Cinco indivíduos (63%) tinham uma resposta positiva ao TT e três, negativa. A prova demonstrou ao início uma frequência cardíaca mais alta, componentes de baixa frequência na análise da variabilidade, uma relaçao baixa frequência/alta frequência (

Mecanismo da síncope em nadadoras de elite

Os atletas podem ter baixa tolerância ao ortostatismo. O mecanismo envolvido ainda nao é bem conhecido. Nossa hipótese se baseia em que as mulheres nadadoras de alta performance desmaiam facilmente durante o teste de inclinaçao, tilt test (TT), provavelmente devido a um pobre controle barorreflexo. A frequência cardíaca e as variabilidades da pressao arterial diastólica, a sensibilidade barorreflexa, a hemodinâmica cardíaca e a velocidade do fluxo cerebral foram analisadas durante o TT em um grupo de 8 mulheres recorde mundial de longa distância em águas abertas (travessia do Canal da Mancha). Cinco indivíduos (63%) tinham uma resposta positiva ao TT e três, negativa. A prova demonstrou ao início uma frequência cardíaca mais alta, componentes de baixa frequência na análise da variabilidade, uma relaçao baixa frequência/alta frequência (

Kinetic Modelling of ELM-induced Fast-ion Transport and Acceleration in the ASDEX Upgrade Tokamak

Universidad de Sevilla PP2016-7145EUROfusion Consortium 63305

Plasma β-III tubulin, neurofilament light chain and glial fibrillary acidic protein are associated with neurodegeneration and progression in schizophrenia

Schizophrenia is a progressive disorder characterized by multiple psychotic relapses. After every relapse, patients may not fully recover, and this may lead to a progressive loss of functionality. Pharmacological treatment represents a key factor to minimize the biological, psychological and psychosocial impact of the disorder. The number of relapses and the duration of psychotic episodes induce a potential neuronal damage and subsequently, neurodegenerative processes. Thus, a comparative study was performed, including forty healthy controls and forty-two SZ patients divided into first-episode psychosis (FEP) and chronic SZ (CSZ) subgroups, where the CSZ sub group was subdivided by antipsychotic treatment. In order to measure the potential neuronal damage, plasma levels of β-III tubulin, neurofilament light chain (Nf-L), and glial fibrillary acidic protein (GFAP) were performed. The results revealed that the levels of these proteins were increased in the SZ group compared to the control group (P < 0.05). Moreover, multiple comparison analysis showed highly significant levels of β-III tubulin (P = 0.0002), Nf-L (P = 0.0403) and GFAP (P < 0.015) in the subgroup of CSZ clozapine-treated. In conclusion, β-III tubulin, Nf-L and GFAP proteins may be potential biomarkers of neurodegeneration and progression in SZFundação para a Ciência e a Tecnologia | Ref. SFRH/BD/135623/20Instituto de Salud Carlos III | Ref. P16/00405Ministerio de Sanidad, Igualdad y Política Social | Ref. 2017I054Agencia del Conocimiento en Salud | Ref. PRIS2-17Xunta de Galicia | Ref. IN607C-2017/02Xunta de Galicia | Ref. IN607B 2018/1

Plasma?-III tubulin, neurofilament light chain and glial fibrillary acidic protein are associated with neurodegeneration and progression in schizophrenia

Schizophrenia is a progressive disorder characterized by multiple psychotic relapses. After every relapse, patients may not fully recover, and this may lead to a progressive loss of functionality. Pharmacological treatment represents a key factor to minimize the biological, psychological and psychosocial impact of the disorder. The number of relapses and the duration of psychotic episodes induce a potential neuronal damage and subsequently, neurodegenerative processes. Thus, a comparative study was performed, including forty healthy controls and forty-two SZ patients divided into first-episode psychosis (FEP) and chronic SZ (CSZ) subgroups, where the CSZ sub group was subdivided by antipsychotic treatment. In order to measure the potential neuronal damage, plasma levels of beta-III tubulin, neurofilament light chain (Nf-L), and glial fibrillary acidic protein (GFAP) were performed. The results revealed that the levels of these proteins were increased in the SZ group compared to the control group (P < 0.05). Moreover, multiple comparison analysis showed highly significant levels of beta-III tubulin (P = 0.0002), Nf-L (P = 0.0403) and GFAP (P < 0.015) in the subgroup of CSZ clozapine-treated. In conclusion, beta-III tubulin, Nf-L and GFAP proteins may be potential biomarkers of neurodegeneration and progression in SZ

Orange juice–derived flavanone and phenolic metabolites do not acutely affect cardiovascular risk biomarkers: a randomized, placebo-controlled, crossover trial in men at moderate risk of cardiovascular disease

Background: Epidemiological data suggest inverse associations between citrus flavanone intake and cardiovascular disease (CVD) risk. However, insufficient randomized controlled trial (RCT) data limit our understanding of mechanisms by which flavanones and their metabolites potentially reduce cardiovascular (CV) risk factors. Objective: We examined the effects of orange juice or a dose-matched hesperidin supplement on plasma concentrations of established and novel flavanone metabolites and their effects on CV risk biomarkers in men at moderate CVD risk. Methods: In an acute, randomized, placebo-controlled crossover trial, 16 fasted participants (aged 51-69 y) received orange juice or a hesperidin supplement (both providing 320 mg hesperidin) or control (all matched for sugar and vitamin C content). At baseline and 5 h post-intake, endothelial function (primary outcome), further CV risk biomarkers (i.e. blood pressure, arterial stiffness, cardiac autonomic function, platelet activation and NADPH oxidase gene expression) and plasma flavanone metabolites were assessed. Prior to each intervention, a diet low in flavonoids, nitrate/nitrite, alcohol and caffeine was followed and a standardized low-flavonoid evening meal was consumed. Results: Orange juice intake significantly elevated mean (± SEM) plasma concentrations of 8 flavanone (1.75 ± 0.35 µmol/L, P < 0.0001) and 15 phenolic metabolites (13.27 ± 2.22 µmol/L, P < 0.0001) compared with control at 5 h post-consumption. Despite increased plasma flavanone and phenolic metabolite concentrations, CV risk biomarkers were unaltered. Following hesperidin supplement intake, flavanone metabolites were not different to control, suggesting altered absorption/metabolism compared with the orange juice matrix. Conclusions: Following single-dose flavanone intake within orange juice, we detected circulating flavanone and phenolic metabolites collectively reaching a concentration of 15.20 ± 2.15 µmol/L but observed no effect on CV risk biomarkers. Longer-duration RCTs are required to further examine the previous associations between higher flavanone intakes and improved cardiovascular health and to ascertain the relative importance of food matrix and flavanone-derived phenolic metabolites