Missed games, financial losses, and characteristics of eye injuries in the National Basketball Association during the 2010-2011 to 2017-2018 seasons.

PURPOSE: The purpose is to report financial loss, demographic metrics, and mechanisms of injury associated with eye injuries in the National Basketball Association (NBA) from the 2010-2011 to 2017-2018 seasons. METHODS: We performed a retrospective review of eye injuries in the NBA from the 2010-2011 to 2017-2018 seasons using publicly available information from Basketball Reference and the Pro Sports Transactions websites. Only injuries of the eye and adnexa that caused players to miss games in the regular season and playoffs were included in the study. Financial loss was calculated based on the regular season salary of the players and normalized for inflation with 2018 as the base year. RESULTS: There were 30 eye injuries causing a total of 106 missed games and $7,486,770 in financial losses across eight seasons. Linear regressions showed a moderately positive increase in eye injuries (Pearson's r = 0.68, P = 0.07, and 0.79 injuries per year/1000 game-days increase) and financial losses (Pearson's r = 0.67, P = 0.07, and $185.75 increase per year/1000 game-days) over time. There were significantly more games missed due to orbital fractures than games missed due to contusions/lacerations (11.5 vs. 2.8 missed games, P = 0.01). CONCLUSION: We demonstrate an increasing trend of eye injuries in the NBA, resulting in increased financial loss. Injuries may be varied in type and affect the number of games missed.

Adequacy of samples obtained via percutaneous core-needle rebiopsy for EGFR T790M molecular analysis in patients with non-small cell lung cancer following acquired resistance to first-line therapy: A systematic review and meta-analysis.

MICRO ABSTRACT: Rebiopsies characterizing resistance mutations in patients with non-small cell lung cancer (NSCLC) can guide personalized medicine and improve overall survival rates. In this systematic review, we examine the suitability of percutaneous core-needle biopsy (PT-CNB) to obtain adequate samples for molecular characterization of the acquired resistance mutation T790M. This review provides evidence that PT-CNB can obtain samples with high adequacy, with a mutation detection rate that is in accordance with prior literature. BACKGROUND: Non-small cell lung cancer (NSCLC) comprises 85% of all lung cancers and has seen improved survival rates with the rise of personalized medicine. Resistance mutations to first-line therapies, such as T790M, however, render first-line therapies ineffective. Rebiopsies characterizing resistance mutations inform therapeutic decisions, which result in prolonged survival. Given the high efficacy of percutaneous core-needle biopsy (PT-CNB), we conducted the first systematic review to analyze the ability of PT-CNB to obtain samples of high adequacy in order to characterize the acquired resistance mutation T790M in patients with NSCLC. METHODS: We performed a comprehensive literature search across PubMed, Embase, and CENTRAL. Search terms related to "NSCLC," "rebiopsy," and "PT-CNB" were used to obtain results. We included all prospective and retrospective studies that satisfied our inclusion and exclusion criteria. A random effects model was utilized to pool adequacy and detection rates of the chosen articles. We performed a systematic review, meta-analysis, and meta-regression to investigate the adequacy and T790M detection rates of samples obtained via PT-CNB. RESULTS: Out of the 173 studies initially identified, 5 studies met the inclusion and exclusion criteria and were chosen for our final cohort of 436 patients for meta-analysis. The pooled adequacy rate of samples obtained via PT-CNB was 86.92% (95% CI: [79.31%, 92.0%]) and the pooled T790M detection rate was 46.0% (95% CI: [26.6%, 66.7%]). There was considerable heterogeneity among studies (I2 > 50%) in both adequacy and T790M detection rates. CONCLUSION: PT-CNB can obtain adequate samples for T790M molecular characterization in NSCLC lung cancer patients. Additional prospective studies are needed to corroborate the results in this review.

Trends in Anti-VEGF Injection Medicare Part B Claims among Male and Female Ophthalmologists from 2012-2016.

Background: Compared to male ophthalmologists, female ophthalmologists have significantly reduced salaries, fewer faculty roles and authored publications, garnered less federal research funding, and achieved less editorial advancement. We aimed to use the most recently available Centers for Medicare and Medicaid Services data to characterize trends and differences in anti-VEGF reimbursements coded for by male and female ophthalmologists.Methods: We used Medicare Fee-For Service Provider Utilization and Payment Data: Part B Provider public use files for 2012-2016 to quantify service and reimbursement patterns for anti-VEGF injections between male and female ophthalmologists. Five outcome variables were studied: number of providers, average Medicare payment amount, total payment, number of services, and number of Medicare beneficiaries.Results: Number of services performed per female provider was 71.2% that of a male ophthalmologist in 2012, and this percentage did not change from 2012 to 2016 (95%CI [0.63, 0.804], [0.984, 1.04], respectively). Female providers had 76.1% of beneficiaries as males in 2012, and this percentage stayed constant throughout the years (95%CI [0.69, 0.84] and [0.99, 1.03], respectively). The total payment difference between female and males was $102,175 per provider in 2012, and this gap widened by $18,292 yearly (95% CI [-162599.17, -41760.47], [-33060.35, -3524.38], respectively).Conclusion: While male and female providers saw considerable increases in aflibercept services and payments in the 5-year period, the gap between male and female reimbursements widened significantly. Moving forward, analysis of large-scale Medicare datasets provides a tangible report card on how effective our attitudes and policies are in cultivating equal opportunity.

Eye injuries in the National Hockey League from 2010 to 2018: an analysis of injury rates, mechanisms, and the National Hockey League visor policy.

OBJECTIVE: We aim to assess the efficacy of widespread visor adoption by assessing eye injury rates during the 2010-2018 seasons. We also compare injury rates, missed games, and financial losses to previously reported data in order to track progress over time. Lastly, we characterize the mechanism and type of eye injuries sustained by National Hockey League (NHL) players to examine risk areas within NHL games. DESIGN: We performed a retrospective review of NHL player injuries using official NHL team reports, ProSportsTransactions, and TSN Sports. PARTICIPANTS: All NHL players who suffered an eye injury from 2010 to 2018 were included; 31 injuries matched this criterion. METHODS: Trends in injuries, missed games, and financial losses over time were analyzed using Pearson's correlation coefficients. Wilcoxon-Mann-Whitney tests were performed to compare our data with eye injury data. Fisher's exact test was performed to assess significance between mechanism and type of eye injury and outcome. RESULTS: There were 31 total eye injuries causing 233 missed games and a total of US$8 951 000 in financial losses across the 2010-2018 seasons. There was a strong decrease in the number of eye injuries (r = -0.83, p = 0.01) and a moderate decrease in number of missed games (r = -0.62, p = 0.09). Injuries due to direct puck strikes contributed to over US$6.5 million in financial losses and led to significantly more missed games compared with stick injuries (14.6 vs 4.3). CONCLUSION: We tangibly demonstrate the financial and physical effects of recent safety interventions and indicate areas for improved safety in the NHL.

History of traumatic brain injury interferes with accurate diagnosis of Alzheimer's dementia: a nation-wide case-control study.

Traumatic brain injury (TBI) and Alzheimer's disease (AD) bear a complex relationship, potentially increasing risk of one another reciprocally. However, recent evidence suggests post-TBI dementia exists as a distinct neurodegenerative syndrome, confounding AD diagnostic accuracy in clinical settings. This investigation sought to evaluate TBI's impact on the accuracy of clinician-diagnosed AD using gold standard neuropathological criteria. In this preliminary analysis, data were acquired from the National Alzheimer's Coordinating Centre (NACC), which aggregates clinical and neuropathologic information from Alzheimer's disease centres across the United States. Modified National Institute on Aging-Reagan criteria were applied to confirm AD by neuropathology. Among participants with clinician-diagnosed AD, TBI history was associated with misdiagnosis (false positives) (OR = 1.351 [95% CI: 1.091-1.674], p = 0.006). Among participants without clinician-diagnosed AD, TBI history was not associated with false negatives. TBI moderates AD diagnostic accuracy. Possible AD misdiagnosis can mislead patients, influence treatment decisions, and confound research study designs. Further work examining the influence of TBI on dementia diagnosis is warranted.

Mitochondrial Biology and Neurological Diseases.

Mitochondria are extremely active organelles that perform a variety of roles in the cell including energy production, regulation of calcium homeostasis, apoptosis, and population maintenance through fission and fusion. Mitochondrial dysfunction in the form of oxidative stress and mutations can contribute to the pathogenesis of various neurodegenerative diseases such as Parkinson's (PD), Alzheimer's (AD), and Huntington's diseases (HD). Abnormalities of Complex I function in the electron transport chain have been implicated in some neurodegenerative diseases, inhibiting ATP production and generating reactive oxygen species that can cause major damage to mitochondria. Mutations in both nuclear and mitochondrial DNA can contribute to neurodegenerative disease, although the pathogenesis of these conditions tends to focus on nuclear mutations. In PD, nuclear genome mutations in the PINK1 and parkin genes have been implicated in neurodegeneration [1], while mutations in APP, PSEN1 and PSEN2 have been implicated in a variety of clinical symptoms of AD [5]. Mutant htt protein is known to cause HD [2]. Much progress has been made to determine some causes of these neurodegenerative diseases, though permanent treatments have yet to be developed. In this review, we discuss the roles of mitochondrial dysfunction in the pathogenesis of these diseases.

Protective role of SIRT5 against motor deficit and dopaminergic degeneration in MPTP-induced mice model of Parkinson's disease.

Parkinson's disease (PD) is characterized by progressive loss of nigrostriatal dopaminergic neurons that results in motor deficits including resting tremor, rigidity, bradykinesia, and postural instability. Despite decades of intensive study, the underlying molecular mechanisms are not fully understood. Multiple lines of evidence indicate that mitochondrial dysfunction and oxidative stress contribute to neuronal death, which is the key feature of neurodegeneration. Mitochondria are pivotal organelles that host essential functions in neuronal viability including energy production, oxidative phosphorylation, calcium buffering, redox homeostasis and apoptosis. SIRT5, which localizes in the mitochondrial matrix, is nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase. The physiological and pathophysiological functions of SIRT5 in vivo remain elusive although it is known to be an important energy sensor. Here, we investigated the role of SIRT5 in the pathogenesis of PD mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We present evidence that SIRT5 deficiency, by itself, does not affect motor and non-motor functions; however, lack of SIRT5 exacerbates MPTP-induced motor deficits. Consistently, MPTP-exposed SIRT5 knockout mice exhibited more severe nigrostriatal dopaminergic degeneration than that observed in wild-type controls. Furthermore, deletion of SIRT5 leads to a larger decrease, relative to control, in the expression level of manganese superoxide dismutase (SOD2), a mitochondria-specific antioxidant enzyme, after MPTP induction. These findings indicate that SIRT5 ameliorates MPTP-induced nigrostriatal dopaminergic degeneration via preserving mitochondrial antioxidant capacity.

Progressive multiple alignment using sequence triplet optimizations and three-residue exchange costs.

In this paper we demonstrate a practical approach to construct progressive multiple alignments using sequence triplet optimizations rather than a conventional pairwise approach. Using the sequence triplet alignments progressively provides a scope for the synthesis of a three-residue exchange amino acid substitution matrix. We develop such a 20 x 20 x 20 matrix for the first time and demonstrate how its use in optimal sequence triplet alignments increases the sensitivity of building multiple alignments. Various comparisons were made between alignments generated using the progressive triplet methods and the conventional progressive pairwise procedure. The assessment of these data reveal that, in general, the triplet based approaches generate more accurate sequence alignments than the traditional pairwise based procedures, especially between more divergent sets of sequences.