Topic modeling applied to business research: A latent dirichlet allocation (LDA)-based classification for organization studies

More than 1.5 million academic documents are published each year, and this trend shows an incremental tendency for the following years. One of the main challenges for the academic community is how to organize this huge volume of documentation to have a sense of the knowledge frontier. In this study we applied Latent Dirichlet Allocation (LDA) techniques to identify primary topics in organization studies, and analyzed the relationships between academic impact and belonging to the topics detected by LDA

Undiagnosed osteoid osteoma of the spine presenting as painful scoliosis from adolescence to adulthood: a case report

Presented here is a case of a young woman, with an undiagnosed osteoid osteoma of the spine, which presented with painful scoliosis in adolescence and was treated by bracing until her accession to adulthood. A more thorough investigation, years after the initial one, revealed the tumor. Surgical excision and stabilization offered the long-awaited cure. Misdiagnosis resulted in intractable pain for years, deformity, the discomfort of brace therapy, and the frustration of a prolonged yet ineffective treatment

Abnormal ECG Findings in Athletes: Clinical Evaluation and Considerations.

PURPOSE OF REVIEW: Pre-participation cardiovascular evaluation with electrocardiography is normal practice for most sporting bodies. Awareness about sudden cardiac death in athletes and recognizing how screening can help identify vulnerable athletes have empowered different sporting disciplines to invest in the wellbeing of their athletes. RECENT FINDINGS: Discerning physiological electrical alterations due to athletic training from those representing cardiac pathology may be challenging. The mode of investigation of affected athletes is dependent on the electrical anomaly and the disease(s) in question. This review will highlight specific pathological ECG patterns that warrant assessment and surveillance, together with an in-depth review of the recommended algorithm for evaluation

The Hellenic type of nondeletional hereditary persistence of fetal hemoglobin results from a novel mutation (g.-109G>T) in the HBG2 gene promoter

Nondeletional hereditary persistence of fetal hemoglobin (nd-HPFH), a rare hereditary condition resulting in elevated levels of fetal hemoglobin (Hb F) in adults, is associated with promoter mutations in the human fetal globin (HBG1 and HBG2) genes. In this paper, we report a novel type of nd-HPFH due to a HBG2 gene promoter mutation (HBG2:g.-109G>T). This mutation, located at the 3′ end of the HBG2 distal CCAAT box, was initially identified in an adult female subject of Central Greek origin and results in elevated Hb F levels (4.1%) and significantly increased Gγ-globin chain production (79.2%). Family studies and DNA analysis revealed that the HBG2:g.-109G>T mutation is also found in the family members in compound heterozygosity with the HBG2:g.-158C>T single nucleotide polymorphism or the silent HBB:g.-101C>T β-thalassemia mutation, resulting in the latter case in significantly elevated Hb F levels (14.3%). Electrophoretic mobility shift analysis revealed that the HBG2:g.-109G>T mutation abolishes a transcription factor binding site, consistent with previous observations using DNA footprinting analysis, suggesting that guanine at position HBG2/1:g.-109 is critical for NF-E3 binding. These data suggest that the HBG2:g-109G>T mutation has a functional role in increasing HBG2 transcription and is responsible for the HPFH phenotype observed in our index cases

Return to play with hypertrophic cardiomyopathy: are we moving too fast? A critical review.

The diagnosis of a potentially lethal cardiovascular disease in a young athlete presents a complex dilemma regarding athlete safety, patient autonomy, team or institutional risk tolerance and medical decision-making. Consensus cardiology recommendations previously supported the 'blanket' disqualification of athletes with hypertrophic cardiomyopathy (HCM) from competitive sport. More recently, epidemiological studies examining the relative contribution of HCM as a cause of sudden cardiac death (SCD) in young athletes and reports from small cohorts of older athletes with HCM that continue to exercise have fueled debate whether it is safe to play with HCM. Shared decision-making is endorsed within the sports cardiology community in which athletes can make an informed decision about treatment options and potentially elect to continue competitive sports participation. This review critically examines the available evidence relevant to sports eligibility decisions in young athletes diagnosed with HCM. Histopathologically, HCM presents an unstable myocardial substrate that is vulnerable to ventricular tachyarrhythmias during exercise. Studies support that young age and intense competitive sports are risk factors for SCD in patients with HCM. We provide an estimate of annual mortality based on our understanding of disease prevalence and the incidence of HCM-related SCD in different athlete populations. Adolescent and young adult male athletes and athletes participating in a higher risk sport such as basketball, soccer and American football exhibit a greater risk. This review explores the potential harms and benefits of sports disqualification in athletes with HCM and details the challenges and limitations of shared decision-making when all parties may not agree

SMARCB1 loss induces druggable cyclin D1 deficiency via upregulation of MIR17HG in atypical teratoid rhabdoid tumors

Atypical teratoid rhabdoid tumor (ATRT) is a fatal pediatric malignancy of the central neural system lacking effective treatment options. It belongs to the rhabdoid tumor family and is usually caused by biallelic inactivation of SMARCB1, encoding a key subunit of SWI/SNF chromatin remodeling complexes. Previous studies proposed that SMARCB1 loss drives rhabdoid tumor by promoting cell cycle through activating transcription of cyclin D1 while suppressing p16. However, low cyclin D1 protein expression is observed in most ATRT patient tumors. The underlying mechanism and therapeutic implication of this molecular trait remain unknown. Here, we show that SMARCB1 loss in ATRT leads to the reduction of cyclin D1 expression by upregulating MIR17HG, a microRNA (miRNA) cluster known to generate multiple miRNAs targeting CCND1. Furthermore, we find that this cyclin D1 deficiency in ATRT results in marked in vitro and in vivo sensitivity to the CDK4/6 inhibitor palbociclib as a single agent. Our study identifies a novel genetic interaction between SMARCB1 and MIR17HG in regulating cyclin D1 in ATRT and suggests a rationale to treat ATRT patients with FDA- approved CDK4/6 inhibitors. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156416/2/path5493.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156416/1/path5493_am.pd

The effect of different skin-ankle brace application pressures on quiet single-limb balance and electromyographic activation onset of lower limb muscles

<p>Abstract</p> <p>Background</p> <p>Several studies have been carried out in order to investigate the effect of ankle bracing on ankle joint function and performance. However, no study so far has examined the role of skin-brace interface pressure in neuromuscular control. The aim of this study was to investigate the effect of different skin-ankle brace interface pressures on quiet single limb balance and the electromyographic (EMG) activation sequence of four lower limb muscles.</p> <p>Methods</p> <p>Thirty three male physical education students who volunteered to take part in the study were measured under three ankle brace conditions: i) without brace, ii) with brace and 30 kPa application pressure and iii) with brace and 60 kPa application pressure. Single limb balance (anteroposterior and mediolateral parameter) was assessed on the dominant lower limb, with open and closed eyes, on a force platform, simultaneously with the EMG recording of four lower lower limb muscles' (gastrocnemius, peroneus longus, rectus femoris and biceps femoris) activation onset.</p> <p>Results</p> <p>The results showed that overall balance (total stability parameter) was not significantly affected in any of the three ankle brace conditions. However, the anteroposterior centre of pressure excursion and centre of pressure excursion velocity were significantly increased with the application of ankle brace, both with 30 and 60 kPa application pressures. Furthermore, it was found that single limb balance was significantly worse with closed eyes compared to open eyes. EMG measurements showed that the sequence of lower limb activation onset was not affected in any of the three ankle brace application conditions. The results of this study showed that the application of an ankle brace with two different skin-brace interface pressures had no effect on overall single limb balance and the sequence of lower limb muscle activation.</p> <p>Conclusion</p> <p>These findings suggest that peripheral joint receptors are either not adequately stimulated by the brace application and therefore are not able to alter the balance control strategy of the CNS, or that they play a less important role in the control of single limb balance. Further research is needed in this area with more dynamic and functional measurements, before the safe use of ankle bracing can be widely recommended.</p

Cyp26b1 Regulates Retinoic Acid-Dependent Signals in T Cells and Its Expression Is Inhibited by Transforming Growth Factor-β

The vitamin A metabolite, retinoic acid (RA), plays important roles in the regulation of lymphocyte properties. Dendritic cells in gut-related lymphoid organs can produce RA, thereby imprinting gut-homing specificity on T cells and enhancing transforming growth factor (TGF)-β-dependent induction of Foxp3+ regulatory T cells upon antigen presentation. In general, RA concentrations in cells and tissues are regulated by its degradation as well. However, it remained unclear if T cells could actively catabolize RA.We assessed the expression of known RA-catabolizing enzymes in T cells from mouse lymphoid tissues. Antigen-experienced CD44+ T cells in gut-related lymphoid organs selectively expressed Cyp26b1, a member of the cytochrome P450 family 26. However, T cells in the spleen or skin-draining lymph nodes did not significantly express Cyp26b1. Accordingly, physiological levels of RA (1-10 nM) could induce Cyp26b1 expression in naïve T cells upon activation in vitro, but could not do so in the presence of TGF-β. Overexpression of Cyp26b1 significantly suppressed the RA effect to induce expression of the gut-homing receptor CCR9 on T cells. On the other hand, knocking down Cyp26b1 gene expression with small interfering RNA or inhibiting CYP26 enzymatic activity led to enhancement of the RA-induced CCR9 expression.Our data demonstrate a role for CYP26B1 in regulating RA-dependent signals in activated T cells but not during TGF-β-dependent differentiation to Foxp3+ regulatory T cells. Aberrant expression of CYP26B1 may disturb T cell trafficking and differentiation in the gut and its related lymphoid organs

Implementation of Guidelines for the Management of Arterial Hypertension. The Impulsion Study

This study assessed the effects of a pilot best practice implementation enhancement program on the control of hypertension. We enrolled 697 consecutive known hypertensive patients with other vascular risk factors but free from overt vascular disease. There was no “control” group because it was considered unethical to deprive high-risk patients from “best medical treatment”. Following a baseline visit, previously trained physicians aimed to improve adherence to lifestyle measures and drug treatment for hypertension and other vascular risk factors. Both at baseline and at study completion (after 6 months), a 1-page form was completed showing if patients achieved treatment targets. If not, the reasons why were recorded. This program enhanced compliance with lifestyle measures and increased the use of evidence-based medication. There was a substantial increase in the number of patients who achieved treatment targets for blood pressure (p<0.0001) and other vascular risk factors. In non-diabetic patients (n=585), estimated vascular risk (PROCAM risk engine) was significantly reduced by 41% (p<0.0001). There was also a 12% reduction in vascular risk according to the Framingham risk engine but this did not achieve significance (p=0.07). In conclusion, this is the first study to increase adherence to multiple interventions in hypertensive patients on an outpatient basis, both in primary care and teaching hospitals. Simple, relatively low cost measures (e.g. educating physicians and patients, distributing printed guidelines/brochures and completing a 1-page form) motivated both physicians and patients to achieve multiple treatment goals. Further work is needed to establish if the improvement observed is sustained. [ClinicalTrials.gov NCT00416611]