Validity and reliability of an iPhone App to assess time, velocity and leg power during a sit-to-stand functional performance test.

No procede.The purposes of this study were: (i) Analyze the concurrent validity and reliability of an iPhone App for measuring time, velocity and power during a single sit-to-stand (STS) test compared with measurements recorded from a force plate; and (ii) Evaluate the relationship between the iPhone App measures with age and functional performance. Forty-eight healthy individuals (age range: 26-81 years) were recruited. All participants completed a STS test on a force plate with the movement recorded on an iPhone 6 at 240 frames-per-second. Functional ability was also measured using isometric handgrip strength and self-paced walking time tests. Intraclass correlation coefficients (ICC), Pearson's correlation coefficient, Cronbach's alpha (α) and Bland-Altman plots with 95% confidence intervals (CI) were used to test validity and reliability between instruments. The results showed a good agreement between all STS measurement variables; time (ICC=0.864, 95%CI=0.77-0.92; α=0.926), velocity (ICC=0.912, 95%CI=0.85-0.95; α=0.953) and power (ICC=0.846, 95%CI=0.74-0.91; α=0.917) with no systematic bias between instruments for any variable analyzed. STS time, velocity and power derived from the iPhone App show moderate to strong associations with age (|r|=0.63-0.83) and handgrip strength (|r|=0.4-0.64) but not the walking test. The results of this study identify that this iPhone App is reliable for measuring STS and the derived values of time, velocity and power shows strong associations with age and handgrip strength.No.Actividad Física y DeporteTerapia y Rehabilitació

Interpreting systematic reviews: are we ready to make our own conclusions? A cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Independent evaluation of clinical evidence is advocated in evidence-based medicine (EBM). However, authors' conclusions are often appealing for readers who look for quick messages. We assessed how well a group of Malaysian hospital practitioners and medical students derived their own conclusions from systematic reviews (SRs) and to what extent these were influenced by their prior beliefs and the direction of the study results.</p> <p>Methods</p> <p>We conducted two cross-sectional studies: one with hospital practitioners (<it>n </it>= 150) attending an EBM course in June 2008 in a tertiary hospital and one with final-year medical students (<it>n </it>= 35) in November 2008. We showed our participants four Cochrane SR abstracts without the authors' conclusions. For each article, the participants chose a conclusion from among six options comprising different combinations of the direction of effect and the strength of the evidence. We predetermined the single option that best reflected the actual authors' conclusions and labelled this as our best conclusion. We compared the participants' choices with our predetermined best conclusions. Two chosen reviews demonstrated that the intervention was beneficial ("positive"), and two others did not ("negative"). We also asked the participants their prior beliefs about the intervention.</p> <p>Results</p> <p>Overall, 60.3% correctly identified the direction of effect, and 30.1% chose the best conclusions, having identified both the direction of effect and the strength of evidence. More students (48.2%) than practitioners (22.2%) chose the best conclusions (<it>P </it>< 0.001). Fewer than one-half (47%) correctly identified the direction of effect against their prior beliefs. "Positive" SRs were more likely than "negative" SRs to change the participants' beliefs about the effect of the intervention (relative risk (RR) 1.8, 95% confidence interval 1.3 to 2.6) and "convert" those who were previously unsure by making them choose the appropriate direction of effect (RR 1.9, 95% confidence interval 1.3 to 2.8).</p> <p>Conclusions</p> <p>The majority of our participants could not generate appropriate conclusions from SRs independently. Judicious direction from the authors' conclusions still appears crucial to guiding our health care practitioners in identifying appropriate messages from research. Authors, editors and reviewers should ensure that the conclusions of a paper accurately reflect the results. Similar studies should be conducted in other settings where awareness and application of EBM are different.</p> <p>Please see Commentary: <url>http://www.biomedcentral.com/1741-7015/9/31/</url>.</p

RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration.

In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity. Reduction in synapse number is a consistent early feature of neurodegenerative diseases, suggesting deficient compensatory mechanisms. Although much is known about toxic processes leading to synaptic dysfunction and loss in these disorders, how synaptic regeneration is affected is unknown. In hibernating mammals, cooling induces loss of synaptic contacts, which are reformed on rewarming, a form of structural plasticity. We have found that similar changes occur in artificially cooled laboratory rodents. Cooling and hibernation also induce a number of cold-shock proteins in the brain, including the RNA binding protein, RBM3 (ref. 6). The relationship of such proteins to structural plasticity is unknown. Here we show that synapse regeneration is impaired in mouse models of neurodegenerative disease, in association with the failure to induce RBM3. In both prion-infected and 5XFAD (Alzheimer-type) mice, the capacity to regenerate synapses after cooling declined in parallel with the loss of induction of RBM3. Enhanced expression of RBM3 in the hippocampus prevented this deficit and restored the capacity for synapse reassembly after cooling. RBM3 overexpression, achieved either by boosting endogenous levels through hypothermia before the loss of the RBM3 response or by lentiviral delivery, resulted in sustained synaptic protection in 5XFAD mice and throughout the course of prion disease, preventing behavioural deficits and neuronal loss and significantly prolonging survival. In contrast, knockdown of RBM3 exacerbated synapse loss in both models and accelerated disease and prevented the neuroprotective effects of cooling. Thus, deficient synapse regeneration, mediated at least in part by failure of the RBM3 stress response, contributes to synapse loss throughout the course of neurodegenerative disease. The data support enhancing cold-shock pathways as potential protective therapies in neurodegenerative disorders

Assessment of splenic function

Hyposplenic patients are at risk of overwhelming post-splenectomy infection (OPSI), which carries mortality of up to 70%. Therefore, preventive measures are warranted. However, patients with diminished splenic function are difficult to identify. In this review we discuss immunological, haematological and scintigraphic parameters that can be used to measure splenic function. IgM memory B cells are a potential parameter for assessing splenic function; however, more studies are necessary for its validation. Detection of Howell–Jolly bodies does not reflect splenic function accurately, whereas determining the percentage of pitted erythrocytes is a well-evaluated method and seems a good first-line investigation for assessing splenic function. When assessing spleen function, 99mTc-labelled, heat-altered, autologous erythrocyte scintigraphy with multimodality single photon emission computed tomography (SPECT)-CT technology is the best approach, as all facets of splenic function are evaluated. In conclusion, although scintigraphic methods are most reliable, they are not suitable for screening large populations. We therefore recommend using the percentage of pitted erythrocytes, albeit suboptimal, as a first-line investigation and subsequently confirming abnormal readings by means of scintigraphy. More studies evaluating the value of potentially new markers are needed

Limits on WWZ and WW\gamma couplings from p\bar{p}\to e\nu jj X events at \sqrt{s} = 1.8 TeV

We present limits on anomalous WWZ and WW-gamma couplings from a search for WW and WZ production in p-bar p collisions at sqrt(s)=1.8 TeV. We use p-bar p -> e-nu jjX events recorded with the D0 detector at the Fermilab Tevatron Collider during the 1992-1995 run. The data sample corresponds to an integrated luminosity of 96.0+-5.1 pb^(-1). Assuming identical WWZ and WW-gamma coupling parameters, the 95% CL limits on the CP-conserving couplings are -0.33<lambda<0.36 (Delta-kappa=0) and -0.43<Delta-kappa<0.59 (lambda=0), for a form factor scale Lambda = 2.0 TeV. Limits based on other assumptions are also presented.Comment: 11 pages, 2 figures, 2 table

Search For Heavy Pointlike Dirac Monopoles

We have searched for central production of a pair of photons with high transverse energies in $p\bar p$ collisions at $\sqrt{s} = 1.8$ TeV using $70 pb^{-1}$ of data collected with the D\O detector at the Fermilab Tevatron in 1994--1996. If they exist, virtual heavy pointlike Dirac monopoles could rescatter pairs of nearly real photons into this final state via a box diagram. We observe no excess of events above background, and set lower 95% C.L. limits of $610, 870, or 1580 GeV/c^2$ on the mass of a spin 0, 1/2, or 1 Dirac monopole.Comment: 12 pages, 4 figure

Zgamma Production in pbarp Collisions at sqrt(s)=1.8 TeV and Limits on Anomalous ZZgamma and Zgammagamma Couplings

We present a study of Z +gamma + X production in p-bar p collisions at sqrt{S}=1.8 TeV from 97 (87) pb^{-1} of data collected in the eegamma (mumugamma) decay channel with the D0 detector at Fermilab. The event yield and kinematic characteristics are consistent with the Standard Model predictions. We obtain limits on anomalous ZZgamma and Zgammagamma couplings for form factor scales Lambda = 500 GeV and Lambda = 750 GeV. Combining this analysis with our previous results yields 95% CL limits |h{Z}_{30}| < 0.36, |h{Z}_{40}| < 0.05, |h{gamma}_{30}| < 0.37, and |h{gamma}_{40}| < 0.05 for a form factor scale Lambda=750 GeV.Comment: 17 Pages including 2 Figures. Submitted to PR

A Measurement of the W Boson Mass

We report a measurement of the W boson mass based on an integrated luminosity of 82 pb$^{-1}$ from \ppbar collisions at $\sqrt{s}=1.8$ TeV recorded in 1994--1995 by the \Dzero detector at the Fermilab Tevatron. We identify W bosons by their decays to $e\nu$ and extract the mass by fitting the transverse mass spectrum from 28,323 W boson candidates. A sample of 3,563 dielectron events, mostly due to Z to ee decays, constrains models of W boson production and the detector. We measure \mw=80.44\pm0.10(stat)\pm0.07(syst)~GeV. By combining this measurement with our result from the 1992--1993 data set, we obtain \mw=80.43\pm0.11 GeV.Comment: 11 pages, 5 figure

Acute Cellular Alterations in the Hippocampus After Status Epilepticus

The critical, fundamental mechanisms that determine the emergence of status epilepticus from a single seizure and the prolonged duration of status epilepticus are uncertain. However, several general concepts of the pathophysiology of status epilepticus have emerged: (a) the hippocampus is consistently activated during status epilepticus; (b) loss of GABA-mediated inhibitory synaptic transmission in the hippocampus is critical for emergence of status epilepticus; and, finally (c) glutamatergic excitatory synaptic transmission is important in sustaining status epilepticus. This review focuses on the alteration of GABAergic inhibition in the hippocampus that occurs during the prolonged seizures of status epilepticus. If reduction in GABAergic inhibition leads to development of status epilepticus, enhancement of GABAergic inhibition would be expected to interrupt status epilepticus. Benzodiazepines and barbiturates are both used in the treatment of status epilepticus and both drugs enhance GABA A receptor-mediated inhibition. However, patients often become refractory to benzodiazepines when seizures are prolonged, and barbiturates are often then used for these refractory cases of status epilepticus. Recent evidence suggests the presence of multiple GABA A receptor isoforms in the hippocampus with different sensitivity to benzodiazepines but similar sensitivity to barbiturates, thus explaining why the two drug classes might have different clinical effects. In addition, rapid functional plasticity of GABA A receptors has been demonstrated to occur during status epilepticus in rats. During status epilepticus, there was a substantial reduction of diazepam potency for termination of the seizures. The loss of sensitivity of the animals to diazepam during status epilepticus was accompanied by an alteration in the functional properties of hippocampal dentate granule cell GABA A receptors. Dentate granule cell GABA A receptor currents from rats undergoing status epilepticus had reduced sensitivity to diazepam and zinc but normal sensitivity to GABA and pentobarbital. Therefore, the prolonged seizures of status epilepticus rapidly altered the functional properties of hippocampal dentate granule cell GABA A receptors, possibly explaining why benzodiazepines and barbiturates may not be equally effective during treatment of the prolonged seizures of status epilepticus. A comprehensive understanding of the cellular and molecular events leading to the development, maintenance, and cytotoxicity of status epilepticus should permit development of more effective treatment strategies and reduction in the mortality and morbidity of status epilepticus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65664/1/j.1528-1157.1999.tb00873.x.pd