Miracle-dz/UniFAR-FTUs huggingface dataset:
Incidence and mechanism of acute injuries in Iran Karate Championship 2010

There is a growing need for research in competitive activity of karateists. The aim of this study was to investigate the incidence, type and mechanism of injuries in Iranian professional men karate players. Seven hundred and sixty-seven men karate players (means ± SD; age, 21.7 ± 3.2 years, weight, 69.4 ± 8.9, height, 176.9 ± 6.4 cm) who participated in Iran men karate championships in 2010, took part in this study. An injury form was used to collect data. The form consisted of two sections: personal data (age, sex, height, weight, etc) and injury data. Variables such as incidence, location, causes and mechanisms of injury were considered and recorded after competitions. χ2 Test was used to analyse data. The results of this study showed that in the total of 739 matches (kata and kumite), 289 injuries occurred. Competitors have more injuries in the upper body than in the lower body (229 vs 60), (λ2 = 21.24, p<0.05). Incident rate of injuries was 15.4 injuries per 100 min of match (0.39 injuries per each match) and 376.7 injuries per 1000 athletes. Skeletal injury (44.2%) was the most common injury, face (32.6%) was the most common injured area, contusion (59.5%) was the main injury, opponent technical mistake (71 %) was the main cause of injuries and opponent's attack (54.6%) was the main mechanism of occurrence of injuries. So, decreased mistake kick, protective pads and the safe use of equipments and rules modification are the best ways of minimising the injuries in karate players.
The long-term outcomes of depression up to 10 years after stroke; the South London Stroke Register

Background Post-stroke depression is a frequent chronic and recurrent problem that starts shortly after stroke and affects patients in the long term. The health outcomes of depression after stroke are unclear. Aims (1) To investigate the associations between depression at 3 months and mortality, stroke recurrence, disability, cognitive impairment, anxiety and quality of life (QoL), up to 5 years post-stroke. (2) To investigate these associations in patients recovering from depression by year 1. (3) To investigate associations between depression at 5 years and these outcomes up to 10 years. Methods Data from the South London Stroke Register (1997–2010) were used. Patients (n at registration=3240) were assessed at stroke onset, 3 months after stroke and annually thereafter. Baseline data included sociodemographics and stroke severity measures. Follow-up assessments included anxiety and depression (Hospital Anxiety and Depression scale), disability, QoL and stroke recurrence. Multivariable regression models adjusted for age, gender, ethnicity, stroke severity and disability were used to investigate the association between depression and outcomes at follow-up. Results Depression at 3 months was associated with: increased mortality (HR: 1.27 (1.04 to 1.55)), disability (RRs up to 4.71 (2.96 to 7.48)), anxiety (ORs up to 3.49 (1.71 to 7.12)) and lower QoL (coefficients up to −8.16 (−10.23−6.15)) up to year 5. Recovery from depression by 1 year did not alter these risks to 5 years. Depression in year 5 was associated with anxiety (ORs up to 4.06 (1.92 to 8.58)) and QoL (coefficients up to −11.36 (−14.86 to −7.85)) up to year 10. Conclusions Depression is independently associated with poor health outcomes.
Remifentanil tolerance and hyperalgesia: short‐term gain, long‐term pain?

The unique pharmacology of remifentanil makes it a popular intra‐operative analgesic. Short‐acting opioids like remifentanil have been associated with acute opioid tolerance and/or opioid‐induced hyperalgesia, two phenomena which have different mechanisms and are pharmacologically distinct. Clinical studies show heterogeneity of remifentanil infusion regimens, durations of infusion, maintenance of anaesthesia, cumulative dose of remifentanil and pain measures, which makes it difficult to draw conclusions about the incidence of acute tolerance or hyperalgesia. However, it appears that intra‐operative remifentanil infusion rates of above 0.25 μg. kg−1.min−1 are associated with higher postoperative opioid consumption, suggesting tolerance. Infusion rates greater than 0.2 μg. kg−1.min−1 are characterised by lower mechanical/pressure/cold/pain thresholds, which suggests hyperalgesia. The use of concurrent multimodal analgesia, especially N‐methyl‐D‐aspartate receptor antagonists, may be an effective preventive strategy. The clinical significance and long‐term consequences of these entities is still uncertain.
Synthesis of nanosheet crystallites of ruthenate with an alpha-NaFeO2-related structure and its electrochemical supercapacitor property.

Unilamellar crystallites of conductive ruthenium oxide having a thickness of about 1 nm were obtained via elemental exfoliation of a protonic layered ruthenate, H(0.2)RuO(2). 0.5H(2)O, with an alpha-NaFeO(2)-related crystal structure. The obtained RuO(2) nanosheets possessed a well-defined crystalline structure with a hexagonal symmetry, reflecting the crystal structure of the parent material. The restacked RuO(2) nanosheets exhibited a high pseudocapacitance of approximately 700 F g(-1) in an acidic electrolyte, which is almost double the value of the nonexfoliated layered protonated ruthenate.
Effects of an alveolar recruitment manoeuvre guided by lung ultrasound on anaesthesia‐induced atelectasis in infants: a randomised, controlled trial

Atelectasis occurs in the majority of children undergoing general anaesthesia. Lung ultrasound has shown reliable sensitivity and specificity for diagnosing anaesthesia‐induced atelectasis. We assessed the effects of a recruitment manoeuvre on atelectasis using lung ultrasound in infants undergoing general anaesthesia. Forty infants, randomly allocated to either a recruitment manoeuvre group or a control group, received volume‐controlled ventilation with 5 cmH2O positive end‐expiratory pressure. Lung ultrasound examination was performed twice in each patient, the first a minute after starting mechanical ventilation of the lungs and the second at the end of surgery. Patients in the recruitment manoeuvre group received ultrasound‐guided recruitment manoeuvres after each lung ultrasound examination. The incidence of significant anaesthesia‐induced atelectasis at the second lung ultrasound examination was less in the recruitment manoeuvre group compared with the control group (25% vs. 80%; p = 0.001; odds ratio (OR) 0.083; 95% confidence interval (CI): 0.019–0.370). The median (IQR [range]) lung ultrasound scores for consolidation and B‐lines on the second examination were lower in the recruitment manoeuvre group compared with the control group; 6.0 (3.0–9.3 [0.0–14.0]) vs. 13.5 (11.0–16.5 [8.0–23.0]); p < 0.001 and 6.5 (3.0–12.0 [0.0–28.0]) vs. 15.0 (10.8–20.5 [7.0–28.0]); p < 0.001, respectively. The lung ultrasound scores for consolidation on the first and second examinations showed a negative correlation with age (r = −0.340, p = 0.008; r = −0.380, p = 0.003). We conclude that ultrasound‐guided recruitment manoeuvres with positive end‐expiratory pressure proved useful in reducing the incidence of anaesthesia‐induced atelectasis in infants, although 5 cmH2O positive end‐expiratory pressure alone was not sufficient to eliminate it. In addition, the younger the patient, the more susceptible they were to atelectasis.
Should blood glucose measurement be a standard of monitoring?

the same for the benefits as well, but by definition is only half of the story. However, as far as the current legal framework goes, it is clear that the approach that is to be adopted is what outcome is in the child’s best interests (see [1] for references), hence the use of this term in the guidelines. As for Russell’s comments regarding the time constraints of consent discussions, I would respectfully point out that the Working Party does not make the law; its remit was to offer guidance to anaesthetists on how to work within the law. If there is inadequate time to have the discussions required to satisfy the courts, then the Trust Board should be made aware that the conditions are such that it is not possible to act lawfully; it is for Trusts to address this problem, not anaesthetists to rush discussions or compromise standards [5]. It is also worth pointing out that the current Department of Health guidance [6] already states that the consent discussion should not take place just before surgery, hence the emphasis on consent as a process, and the establishment of pre-operative assessment clinics and provision of written information in advance of admission. Finally, there does not seem to be much difference between what the AAGBI guidance says and what Wellesley and Pownall are suggesting i.e. that referral to the courts may be appropriate in the case of 16 and 17-year-olds who refuse treatment. We are aware that the law in this area is likely to be reviewed by the Court of Appeal, and will take account of any changes in emphasis in future revisions. S. M. Yentis Chelsea and Westminster Hospital, London, UK Email: s.yentis@imperial.ac. uk
Thermodynamic and structural destabilization of apoE3 by hereditary mutations associated with the development of lipoprotein glomerulopathy[S]

Lipoprotein glomerulopathy (LPG) is a dominant inherited kidney disorder characterized by lipoprotein thrombi in glomerular capillaries. Single-amino-acid mutations in apoE have been associated with the development of the disease, although the mechanism is unknown. In an effort to gain mechanistic insight linking the presence of such mutations and the development of LPG, we evaluated the effects of three of the most common apoE3 variants associated with this disease, namely R145P(Sendai), R147P(Chicago), and R158P(Osaka or Kurashiki), on the structural and conformational integrity of the protein. All three variants were found to have significantly reduced helical content, to expose a larger portion of hydrophobic surface to the solvent, and to be significantly thermodynamically destabilized, often lacking functionally relevant unfolding intermediates. Furthermore, all variants were aggregation prone and had enhanced sensitivity to protease digestion. Finally, although the variants were able to form discoidal lipoprotein particles, discrete subpopulations of poorly formed or aberrant particles were evident. Furthermore, these lipoprotein particles were thermodynamically destabilized and aggregation prone. Overall, our data suggest that these mutations induce a generalized unfolding of the N-terminal domain of apoE3 toward a molten-globule-like structure. ApoE3 N-terminal domain unfolding due to mutation may constitute a common mechanism underlying the protein's association with the pathogenesis of LPG.
Presence of cerebral amyloid modulates phenotype and pattern of neurodegeneration in early Parkinson's disease

Objective To evaluate the frequency of cerebral amyloid in early Parkinson's disease (ePD) and provide a multimodal assessment of the influence of cerebral amyloid on disease phenotype. Methods We performed a multicentre cohort study of the Parkinson's Progression Markers Initiative (PPMI), including 369 drug-naïve patients with ePD and 174 healthy controls (HC). Cerebrospinal fluid (CSF) amyloid-β levels were transformed using the linear regression procedure. A cut-off of >198 pg/mL was used to define amyloid-negative (PD−) and amyloid-positive (PD+) subgroups. Grey matter (GM) density and hippocampal volume from the MRI was measured using Advanced Normalisation Tools (ANTs). We compared demographic, genetic, CSF, behavioural, functional and imaging modalities across ePD− and ePD+ groups. Results We observed that 16.5% of ePD have CSF evidence of amyloidosis. PD+ was significantly older than PD−, had a higher frequency of APOE e4 alleles and all CSF measures (total-tau, phosphorylated-tau and α-synuclein) were reduced. PD+ had reduced cognitive performance relative to PD− on Symbol–Digit Matching, Verbal Category Fluency and Delayed Recall tests. Imaging analysis in a subset of individuals (PD+ =43; PD− =241) revealed overlapping GM atrophy relative to HC in medial temporal, frontal and brainstem structures. Direct comparisons revealed PD+ GM reductions predominantly located in the frontal cortex while PD− had GM reductions in subcortical structures. These observations remain when controlling for age and APOE e4 allele status. Conclusions Cerebral amyloid in ePD yields a unique phenotype across all measured modalities that is consistent with a synergistic interaction between α-synuclein and amyloid pathology. Amyloid status should be considered when screening these individuals for trials involving disease-modifying agents.
Analysing case-control studies: adjusting for confounding

A case-control study examined the association between chronic Helicobacter pylori infection and coronary heart disease at young ages. In total, 1122 survivors of suspected acute myocardial infarction at age 30-49 years were recruited. For each case, a control matched for age and sex with no history of coronary heart disease was enrolled. Chronic infection with H pylori was confirmed serologically. Information on other risk factors for coronary heart disease was collected, including smoking behaviour, indicators of socioeconomic status, obesity, and blood lipid concentrations. Controls were asked about their current habits and history, whereas cases were asked about their habits and history just before their index myocardial infarction. Blood samples were obtained from cases within 24 hours of the onset of symptoms and from controls after collection of the information about risk factors.1 Early onset myocardial infarction was significantly associated with seropositive H pylori infection antibodies (odds ratio 2.28 (99% confidence interval 1.8 to 2.9)). The odds ratio was reduced to 1.87 (1.42 to 2.47) after adjustment for smoking and indicators of socioeconomic status and to 1.75 (1.29 to 2.36) after additional adjustment for blood lipid concentrations and obesity. Therefore, a moderate association existed between coronary heart disease and H pylori infection seropositivity that could not be fully explained by other risk factors. Which of the following statements, if any, are true? Statements a , c , and d are true, whereas b is false. The purpose of the case-control …
Perilipin-2-null mice are protected against diet-induced obesity, adipose inflammation, and fatty liver disease[S]

The cytoplasmic lipid droplet (CLD) protein perilipin-2 (Plin2) is expressed in multiple nonadipose tissues, where it is thought to play a role in regulating their lipid storage properties. However, the extent to which Plin2 functions in nutrient utilization and metabolism, or how it influences the consequences of over-feeding, remains unclear. In this study, we demonstrate that the absence of Plin2 prevents high-fat diet(HFD)-induced obesity in male and female mice. This response is associated with increased formation of subcutaneous beige adipocyte cells with uncoupling protein 1 expression, and amelioration of inflammatory foci formation in white adipose tissue and steatosis in the liver. Experiments demonstrate that Plin2 loss results in reduced energy intake and increased physical activity in response to HFD feeding. Our study provides the first evidence that Plin2 contributes to HFD-induced obesity by modulating food intake, and that its absence prevents obesity-associated adipose tissue inflammatory foci and liver steatosis.
Association between naturally occurring antiamyloid β autoantibodies and medial temporal lobe atrophy in Alzheimer's disease

The pathophysiology of Alzheimer's disease (AD) is thought to involve the accumulation and deposition of amyloid β (Aβ) peptide in the form of plaques. It is well known that decreased cerebrospinal fluid (CSF) Aβ42 concentrations occur early in AD. Besides this, τ protein becomes hyperphosphorylated (P-τ), getting unstable and unable to bind the microtubules and finally disintegrating into neurofibrillary tangles. The neuropathological process leads to a characteristic pattern of brain damage starting in the medial temporal lobe (MTL) that can be viewed and measured with structural MRI. Both CSF biomarkers (Aβ and P-τ) and MTL atrophy have been accepted as biomarkers of AD, supporting the diagnosis of AD even in preclinical stages.1 There is some correlation between MRI findings and CSF biomarkers. On one hand, atrophy of the MTL is a diagnostic marker for AD at the mild cognitive impairment stage, although this is not a such …
Impaired cerebral autoregulation: measurement and application to stroke

Cerebral autoregulation (CA) is a protective mechanism that maintains cerebral blood flow at a relatively constant level despite fluctuations of cerebral perfusion pressure or arterial blood pressure. It is a universal physiological mechanism that may involve myogenic, neural control as well as metabolic regulations of cerebral vasculature in response to changes in pressure or cerebral blood flow. Traditionally, CA has been represented by a sigmoid curve with a wide plateau between about 50 mm Hg and 170 mm Hg of steady-state changes in mean arterial pressure, defined as static CA. With the advent of transcranial Doppler, measurement of cerebral blood flow in response to transient changes in arterial pressure has been used to assess dynamic CA. However, a gold standard for measuring CA is not currently available. Stroke has been the leading cause of long-term adult disability throughout the world. A better understanding of CA and its response to pathological derangements can help assess the severity of stroke, guide management decisions, assess response to interventions and provide prognostic information. The objective of this review is to provide a comprehensive insight about physiology of autoregulation, measurement methodologies and clinical applications in stroke to help build a consensus for what should be included in an internationally agreed protocol for CA testing and monitoring, and to promote its translation into clinical bedside practice for stroke management.
Evidence for the presence of lipid-free monomolecular apolipoprotein A-1 in plasma[S]

The first step in reverse cholesterol transport is a process by which lipid-free or lipid-poor apoA-1 removes cholesterol from cells through the action of ATP binding cassette transporter A1 at the plasma membrane. However the structure and composition of lipid-free or -poor apoA-1 in plasma remains obscure. We previously obtained a monoclonal antibody (MAb) that specifically recognizes apoA-1 in preβ1-HDL, the smallest apoA-1-containing particle in plasma, which we used to establish a preβ1-HDL ELISA. Here, we purified preβ1-HDL from fresh normal plasma using said antibody, and analyzed the composition and structure. ApoA-1 was detected, but neither phospholipid nor cholesterol were detected in the purified preβ1-HDL. Only globular, not discoidal, particles were observed by electron microscopy. In nondenaturing PAGE, no difference in the mobility was observed between the purified preβ1-HDL and original plasma preβ1-HDL, or between the preβ1-HDL and lipid-free apoA-1 prepared by delipidating HDL. In sandwich ELISA using two anti-preβ1-HDL MAbs, reactivity with intact plasma preβ1-HDL was observed in ELISA using two MAbs with distinct epitopes but no reactivity was observed in ELISA using a single MAb, and the same phenomenon was observed with monomolecular lipid-free apoA-1. These results suggest that plasma preβ1-HDL is lipid-free monomolecular apoA-1.
Anti-inflammatory approaches to ischaemic stroke prevention

Stroke is a major cause of neurological morbidity and mortality. Atherosclerosis is a major contributor to first and recurrent stroke. A growing evidence base indicates that inflammation is a key process in the pathogenesis of atherosclerosis, leading to thromboembolic events. In this review, we summarise the evidence linking inflammation to stroke risk and discuss clinical trials addressing the ’inflammation hypothesis' in coronary disease and stroke. Trial registration number CONVINCE trial ClinicalTrials.gov number; NCT 02898610; Pre-results.
Parking monitor system based on magnetic field senso

To easily find an unoccupied parking space in a large car park is a problem for many drivers. Thus it is useful to have technical solutions which can provide information on parking space occupancy. A new monitor system is described in the following. It is based on passive magnetic field sensors. It provides occupancy information for car park users and helps them to place the car in a most efficient way
PPARγ ligand production is tightly linked to clonal expansion during initiation of adipocyte differentiation[S]

Adipocyte differentiation is orchestrated by the ligand-activated nuclear receptor PPARγ. Endogenous ligands comprise oxidized derivatives of arachidonic acid and structurally similar PUFAs. Although expression of PPARγ peaks in mature adipocytes, ligands are produced primarily at the onset of differentiation. Concomitant with agonist production, murine fibroblasts undergo two rounds of mitosis referred to as mitotic clonal expansion. Here we show that mouse embryonic fibroblasts deficient in either of two cell cycle inhibitors, the transcription factor p53 or its target gene encoding the cyclin-dependent kinase inhibitor p21, exhibit increased adipogenic potential. The antiadipogenic effect of p53 relied on its transcriptional activity and p21 expression but was circumvented by administration of an exogenous PPARγ agonist suggesting a linkage between cell cycling and PPARγ ligand production. Indeed, cell cycle inhibitory compounds decreased PPARγ ligand production in differentiating 3T3-L1 preadipocytes. Furthermore, these inhibitors abolished the release of arachidonic acid induced by the hormonal cocktail initiating adipogenesis. Collectively, our results suggest that murine fibroblasts require clonal expansion for PPARγ ligand production at the onset of adipocyte differentiation.
Mutations in BAG3 cause adult-onset Charcot-Marie-Tooth disease

Charcot-Marie-Tooth disease (CMT) is an umbrella term for more than 90 different genetic causes of inherited peripheral neuropathies (http://hihg.med.miami.edu/code/http/cmt/public_html/index.html#/) and has an estimated prevalence of 1 in 2500. Most cases present within the first two decades of life but increasing axonal genetic subtypes (CMT2) first present in adulthood. Identifying additional genes causing CMT2 is important because these can identify molecular pathways involved in axonal degeneration and enable development of rational therapies for these and related disorders. We have used whole exome sequencing (WES) to identify two families with CMT2 caused by mutations in the Bcl2-associated athanogene 3 (BAG3). Mutations in BAG3 have previously been shown to cause a myofibrillar myopathy1 2 often associated with cardiomyopathy that usually presents in childhood. Children have been reported with peripheral neuropathy in addition to myopathy3 and/or cardiomyopathy.4 ### Genetic testing Genomic analysis was focused on rare and conserved variants that followed an autosomal-dominant inheritance pattern in WES of both probands using the GEM.app/GENESIS software. We only considered variants that met the following criteria: (1) non-synonymous change; (2) minor allele frequency in Exome Aggregation Consortium (ExAC) database 3 or PhastCons >0.6; and (5) genotype quality >75. This analysis resulted in the identification of a variant in BAG3 (c.625C>T; p.Pro209Ser) that completely cosegregated with the presence of neuropathy in both large families (figure 1 …