A study published in BMCMedicine finds that retinal nerve fiber layer (RNFL) thinning is independently associated with increased incident cardiovascular (CVD) risk, making RNFL thickness as a potential retinal fingerprint for CVD events screening.
]. However, we should point out that the additive NRI of 21.8% was mainly based on the small sample with incident cardiovascular events. Twenty-one out of 29 patients with cardiovascular events could not be reclassified with the novel prediction model yet and the absolute NRI was 2.0%. Despite the improved prediction by the addition of pRNFL thickness, the small sample size may limit the power effect and more evidence from large-scale longitudinal studies is of necessity.
To the best of our knowledge, this is the first prospective study to investigate the association between RNFL thickness and incident CVD events. The major strengths of this study were its large sample size, the relatively long follow-up period of nearly 8 years, the prospective design of two cohorts for comprehensive analysis of RNFL thickness within the macula and peripapillary regions and the rigorous findings after adjustments for numerous covariates.
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Optimisation of AAV-NDI1 Significantly Enhances Its Therapeutic Value for Correcting Retinal Mitochondrial DysfunctionAAV gene therapy for ocular disease has become a reality with the market authorisation of LuxturnaTM for RPE65-linked inherited retinal degenerations and many AAV gene therapies currently undergoing phase III clinical trials. Many ocular disorders have a mitochondrial involvement from primary mitochondrial disorders such as Leber hereditary optic neuropathy (LHON), predominantly due to mutations in genes encoding subunits of complex I, to Mendelian and multifactorial ocular conditions such as dominant optic atrophy, glaucoma and age-related macular degeneration. In this study, we have optimised the nuclear yeast gene, NADH-quinone oxidoreductase (NDI1), which encodes a single subunit complex I equivalent, creating a candidate gene therapy to improve mitochondrial function, independent of the genetic mutation driving disease. Optimisation of NDI1 (ophNdi1) substantially increased expression in vivo, protected RGCs and increased visual function, as assessed by optokinetic and photonegative response, in a rotenone-induced murine model. In addition, ophNdi1 increased cellular oxidative phosphorylation and ATP production and protected cells from rotenone insult to a significantly greater extent than wild type NDI1. Significantly, ophNdi1 treatment of complex I deficient patient-derived fibroblasts increased oxygen consumption and ATP production rates, demonstrating the potential of ophNdi1 as a candidate therapy for ocular disorders where mitochondrial deficits comprise an important feature.
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‘Cultural Betrayal Trauma Theory’ Adds Another Devastating Layer to Recent ShootingsThe alleged shooters in Monterey Park and Half Moon Bay being of Asian descent adds a new layer of hurt, writes Jennifer M. Gómez
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Migraine attacks are of peripheral origin: the debate goes on - The Journal of Headache and PainBackground Despite the pervasiveness of migraine, the underlying pathophysiological mechanisms initiating migraine attacks are far from well understood and are matter of scientific debate. Objective In this narrative review, we discuss key evidence for that suggest a peripheral origin or central origin and provide directions for future studies that may provide further clarification. Discussion Migraine pathogenesis is considered to involve the trigeminovascular system, a term that encompasses the trigeminal nerve and its axonal projections to the intracranial blood vessels. Beyond any doubt both peripheral and central mechanisms are involved in migraine pathogenesis, but an unresolved question is the how the initial activation occurs in a migraine attack. Evidence favoring a peripheral origin of migraine attacks, i.e., initial events occur outside of the blood–brain barrier, include the importance of sensitization of perivascular sensory afferents early on in a migraine attack. Evidence favoring a central origin include the occurrence of prodromal symptoms, migraine aura, and activation of structures within the central nervous system early in and during a migraine attack. Conclusions Both peripheral and central mechanisms are likely involved in a migraine attack, e.g., peripheral nociceptive input is necessary for pain transmission and cortical activity is necessary for pain perception. Yet, the debate of whether migraine attacks are initiated a peripheral or central site remains unresolved. The increased focus on prodromal symptoms and on the development of a human model of migraine aura will possibly provide key arguments needed to answer this question in the near future. Until then, we cannot draw firm conclusions and the debate goes on. Video link Video recording of the debate held at the 1st International Conference on Advances in Migraine Sciences (ICAMS 2022, Copenhagen, Denmark) is available at: https://www.youtube.com/watch?v=NC0nlcKohz0 . Graphical Abstrac
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Exploring the relationship between breastfeeding and the incidence of infant illnesses in Ireland: evidence from a nationally representative prospective cohort study - BMC Public HealthBackground Ireland has one of the lowest BF rates in the world. This study investigates the association between breastfeeding and infant health in Ireland. Methods A cross-sectional, secondary analysis of data collected from Growing Up in Ireland (GUI): the National Longitudinal Study of Children was conducted. The average morbidity for 2212. infants exclusively breastfed for at least 90 days (EBF90days) was compared to data for 3987 infants in the non-breastfed (Non-BF) group. Data were weighted using entropy balancing to ensure the comparability of groups. Sensitivity analyses considered alternative definitions of the breastfeeding group. Results Infants who were EBF90days were significantly less likely to be admitted to hospital (CI: − 0.06 to − 0.03), spent less nights in hospital (CI: − 0.37 to − 0.11), and were less likely to develop respiratory diseases including asthma (CI: − 0.03 to − 0.01), chest infections (CI: − 0.12 to − 0.08), snuffles/common colds (CI: − 0.07 to − 0.02), ear infections (CI: − 0.08 to − 0.04), eczema (CI: − 0.08 to − 0.04), skin problems (CI: − 0.04 to − 0.00), wheezing or asthma (CI: − 0.06 to − 0.03), vomiting (CI: − 0.03 to − 0.00), and colic (CI: − 0.04 to − 0.01). Further outcomes such as current health of the infant at time of interview (CI: − 0.04 to − 0.00), feeding problems (CI: − 0.04 to − 0.02) and sleeping problems (CI: − 0.02 to − 0.00) indicated a protective effect of EBF90days versus Non-BF. However, these infants were also more likely to fail to gain weight (CI: 0.01 to 0.02) and were at a slightly higher risk of developing nappy rash (CI: 0.00 to 0.02). Conclusion Exclusive breastfeeding for 90+ days is associated with protection against childhood morbidity. Given the protective effect of breastfeeding on adverse health effects in infants, policy makers should prioritise policies that support, promote and protect exclusive breastfeeding.
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Optimisation of AAV-NDI1 Significantly Enhances Its Therapeutic Value for Correcting Retinal Mitochondrial DysfunctionAAV gene therapy for ocular disease has become a reality with the market authorisation of LuxturnaTM for RPE65-linked inherited retinal degenerations and many AAV gene therapies currently undergoing phase III clinical trials. Many ocular disorders have a mitochondrial involvement from primary mitochondrial disorders such as Leber hereditary optic neuropathy (LHON), predominantly due to mutations in genes encoding subunits of complex I, to Mendelian and multifactorial ocular conditions such as dominant optic atrophy, glaucoma and age-related macular degeneration. In this study, we have optimised the nuclear yeast gene, NADH-quinone oxidoreductase (NDI1), which encodes a single subunit complex I equivalent, creating a candidate gene therapy to improve mitochondrial function, independent of the genetic mutation driving disease. Optimisation of NDI1 (ophNdi1) substantially increased expression in vivo, protected RGCs and increased visual function, as assessed by optokinetic and photonegative response, in a rotenone-induced murine model. In addition, ophNdi1 increased cellular oxidative phosphorylation and ATP production and protected cells from rotenone insult to a significantly greater extent than wild type NDI1. Significantly, ophNdi1 treatment of complex I deficient patient-derived fibroblasts increased oxygen consumption and ATP production rates, demonstrating the potential of ophNdi1 as a candidate therapy for ocular disorders where mitochondrial deficits comprise an important feature.
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