Correlation between kinetic and kinematic measures, clinical tests and subjective self-evaluation questionnaires of the affected upper limb in people after stroke

IntroductionAssessment of stroke recovery should include multiple sources of information in order to obtain a complete understanding of the individual’s rehabilitation progress. Self-evaluation questionnaires’ scores do not always correspond to the scores of commonly used clinical evaluation tools. The purpose of this study was to assess the relationship between self-evaluation questionnaires, clinical tests, and kinematic and kinetic analyses of the affected upper limb after stroke, and to determine the correlation between these measures and self-reported general function 2–4 years after the stroke.MethodsTwenty-six subjects recovering from stroke were included in the study. Spearman’s correlation coefficient was used to measure the correlation between Stroke Impact Scale (SIS), Motor activity Log (MAL), Fugl-Meyer Assessment (FMA) and Action Reach Arm Test (ARAT) scores, and kinematic and kinetic analyses. A logistic regression was used to assess the extent to which these measures may predict the participants’ functional self-reported status 2–4 years post stroke.ResultsSections regarding hand function, hand force and general ADL of the self-evaluation questionnaires correlated with kinematic variables. However, only questionnaires that focus on hand function correlated with clinical tests. Mean and maximal hand velocity had the strongest correlations with self-evaluation questionnaires and with the clinical tests, more than other kinematic variables. Self-evaluation questionnaires and clinical tests were found to be correlated with hand kinetic metrics force-to-time ratio and number of force peaks. SIS hand force domain, mean velocity and maximal velocity predicted self-reported general function 2–4 years after the stroke.ConclusionSelf-evaluation questionnaires should be considered for wider use in the clinical evaluation of a patient’s stroke recovery, since they add important information on the individual’s functional status, which is not reflected in the clinical tests

Toward an Equity-Driven Conceptual Model of COVID-19 Vaccine Decision-Making for People with IDD

COVID-19 presented a public health emergency in the U.S., resulting in severe illness, hospitalizations, high mortality rates, and long-term adverse health care conditions. Several studies examined the disparities in transmission rates, barriers to care, and negative health outcomes for persons with disabilities, particularly people with intellectual and developmental disabilities (I/DD). While data revealed similar trends among Black, Hispanic or Latino/a/x/e, Native, Indigenous, and Asian people, outcomes are compounded for people of color with I/DD. Several historical, pervasive, systemic, structural, and attitudinal barriers have constrained healthcare access and adequate treatment, instigating feelings of distrust among those in systems of care. Although vaccination is effective in minimizing adverse outcomes, COVID-19 vaccine policies and rollouts have also followed inequitable patterns in distribution and accessibility. To better address the concerns and needs of communities, a multidisciplinary team at a University Center of Excellence in Developmental Disabilities (UCEDD) engaged in a generative, multistep, systematic process to explore factors that influence vaccine confidence among people with I/DD, their families, and support circles, particularly people of color with IDD. Garnering data and input from multiple sources, we uncovered several complexities around vaccination, which include (a) accessibility; (b) context, history, and sociocultural concerns; (c) policies; (d) communication and media; and (e) a continuum of vaccine confidence and supported decision-making. Findings from these efforts underscore the centrality of equity and trust, with implications for practitioners, institutions, policymakers, and public health strategists. Furthermore, our model can serve as a useful framework for people invested in promoting healthcare equity in vaccination for people with I/DD and with multiple marginalized identities

A nonplanar slow rupture episode during the 2000 Miyakejima dike intrusion

Magmatic intrusions release extensional strain in the Earth's crust upon availability of magma. Intrusions are typically accompanied by earthquake swarms and by surface faulting that is often larger than what is expected from the magnitude of the induced earthquakes. The 2000 Miyakejima dike intrusion triggered the largest volcanic earthquake swarm monitored so far, with five Ml>6 earthquakes. We analyze the seismicity and deformation induced by the Miyakejima dike with the aim of constraining the timescale and mechanisms of slow strain release during the episode. In six earthquake bursts lasting few hours and migrating at 3c1 km h 121 we find candidates for slow earthquakes. Each burst nucleated at the tips of previous bursts, suggesting stress interaction. The variability of fault plane solutions indicates that the bursts occurred on a complex system of fractures, consistent with weakly consolidated surface layers strained by spatially inhomogneous stresses that change in time, such as those induced by a dike. Based on dislocation models, we find that deformation is best explained by aseismic slip (in addition to the seismic burst), with a moment 1.3 to 2.3 times larger than the earthquakes' seismic moment, and opening of 0.20 \ub1 0.07 m on the dike. The aseismic slip occurred over a few hours, with moment, duration, and migration velocity consistent with that of previously observed slow slip events. We argue that the seismic bursts are likely driven by slow slip, sharing most properties with tectonic slow slip events and swarms, but occurring on a set of nonaligned faults

MiR-27a Functions as a Tumor Suppressor in Acute Leukemia by Regulating 14-3-3θ

<div><p>MicroRNAs (miRs) play major roles in normal hematopoietic differentiation and hematopoietic malignancies. In this work, we report that miR-27a, and its coordinately expressed cluster (miR-23a∼miR-27a∼miR-24-2), was down-regulated in acute leukemia cell lines and primary samples compared to hematopoietic stem-progenitor cells (HSPCs). Decreased miR-23a cluster expression in some acute leukemia cell lines was mediated by c-MYC. Replacement of miR-27a in acute leukemia cell lines inhibited cell growth due, at least in part, to increased cellular apoptosis. We identified a member of the anti-apoptotic 14-3-3 family of proteins, which support cell survival by interacting with and negatively regulating pro-apoptotic proteins such as Bax and Bad, as a target of miR-27a. Specifically, miR-27a regulated 14-3-3θ at both the mRNA and protein levels. These data indicate that miR-27a contributes a tumor suppressor-like activity in acute leukemia cells via regulation of apoptosis, and that miR-27a and 14-3-3θ may be potential therapeutic targets.</p> </div

Effects of c-MYC on expression of the miR-23a cluster.

<p>(A) Knock down of c-MYC expression in P493B cells by doxycycline-treatment. Cells were treated with 0 µg/ml (white bar), 0.1 µg/ml (grey bar) or 0.3 µg/ml (black bar) doxycycline for 48 hr, harvested, and total RNA isolated. Levels of miR-23a cluster member expression were measured via qRT-PCR, using U18 as an endogenous control, and normalized to untreated (0 µg/ml Dox) cells (2^−ΔΔCt = 1). (B) and (C) The effects of pharmacologic inhibition of c-MYC on miR-23a (B) and miR-27a (C) in REH, KOPN8, SUPB15, and K562 cell lines were determined by treatment with 2 doses of 10058-F4 (25 µM [grey bar] and 50 µM [black bar]) or vehicle (white bar) for 48 hr. Fold-expression of mature miR-23a and miR-27a were assessed by qRT-PCR and analyzed as above. Effect of the c-MYC inhibitor on miR-23a and miR-27a expression was determined by comparison of treated cells to the mean expression (±SEM) of vehicle-treated cells Significance was determined by a Student's t-test where p<0.05 (*) indicated significance (n = 2–6 independent experiments). (D) and (E) The effect of siRNA knock-down of endogenous c-MYC on expression of miR-23a (D) and miR-27a (E) in K562, Karpas45, and Molt16 cells were assessed by transfection with 50 nM (grey bar) or 100 nM (black bar) of an siRNA-c-MYC pool or 100 nM of control siRNA (white bar). Expression levels of miR-23a and miR-27a and significance of results were assessed as in (B) and (C). n≥3 independent experiments for all samples.</p