What Determines the Quality of Rehabilitation Clinical Practice Guidelines?: An Overview Study.

Objective: The aim of the study was to determine what factors determine the quality of rehabilitation clinical practice guidelines.

Design: Six databases were searched for articles that had applied the Appraisal of Guidelines for Research & Evaluation II quality assessment tool to rehabilitation clinical practice guidelines. The 573 deduplicated abstracts were independently screened by two authors, resulting in 81 articles, the full texts of which were independently screened by two authors for Appraisal of Guidelines for Research & Evaluation II application to rehabilitation clinical practice guidelines, resulting in a final selection of 40 reviews appraising 504 clinical practice guidelines.

Quality of Rehabilitation Clinical Practice Guidelines: An Overview Study of AGREE II Appraisals.

Objective: To evaluate the quality of rehabilitation Clinical Practice Guidelines (CPG), specifically with respect to their applicability.

Data Sources: The Medline, Embase, Web of Science, CINAHL, PsycINFO, and Cochrane Library databases were searched for papers published between 2017 and 2019 that applied the Appraisal of Guidelines for Research & Evaluation II (AGREE II) CPG quality assessment tool to rehabilitation CPGs.

Study Selection: Deduplicated abstracts (N=449) were independently screened by 2 authors, resulting in 47 articles.

Clinical Practice Guideline to Improve Locomotor Function Following Chronic Stroke, Incomplete Spinal Cord Injury, and Brain Injury.

Background: Individuals with acute-onset central nervous system (CNS) injury, including stroke, motor incomplete spinal cord injury, or traumatic brain injury, often experience lasting locomotor deficits, as quantified by decreases in gait speed and distance walked over a specific duration (timed distance). The goal of the present clinical practice guideline was to delineate the relative efficacy of various interventions to improve walking speed and timed distance in ambulatory individuals greater than 6 months following these specific diagnoses.

Methods: A systematic review of the literature published between 1995 and 2016 was performed in 4 databases for randomized controlled clinical trials focused on these specific patient populations, at least 6 months postinjury and with specific outcomes of walking speed and timed distance.

Impact of eliminating visual input on sitting posture and head position in a patient with spatial neglect following cerebral hemorrhage: a case report.

 Spatial neglect is a neurocognitive syndrome. Affected individuals pay little or insufficient attention to the space contralateral to the injured cerebral hemisphere, often resulting in or exacerbating disability following an acquired brain injury. Eliminating visual input may increase attention toward the contralesional side of space, and improve symptoms of spatial neglect; however this has never been examined in a clinical setting.

Understanding the Level of Concussion Knowledge in High School Sports in New Jersey.

Background: Coaches, athletic trainers (ATCs), and parents/guardians (parents) are important contributors to the proper identification and management of concussions in student-athletes. However, there are limited studies on the identification of concussion knowledge gaps that will help inform educational efforts and improve concussion outcomes in these groups.

Objective: To identify gaps and factors influencing concussion knowledge for high school athletics.

Feasibility and Preliminary Validation of an Online Version of the Ohio State University Traumatic Brain Injury Identification Method.

Objective: To test the feasibility and validity of an online version of an established interview designed to determine a lifetime history of traumatic brain injury (TBI).

Design: Cross-sectional.

Setting: General community.

The therapeutic value of cranioplasty in individuals with brain injury.

Primary Objective: To examine the effect of cranioplasty on recovery.

Research Design: Retrospective cohort study.

Method And Procedures: Retrospective chart review conducted in 2011 and 2012 on adult inpatients with craniectomy who completed a continuous episode of inpatient rehabilitation before and after receiving their cranioplasty.

Outcome Measures for Persons With Moderate to Severe Traumatic Brain Injury: Recommendations From the American Physical Therapy Association Academy of Neurologic Physical Therapy TBI EDGE Task Force.

Background And Purpose: The use of standardized outcome measures (OMs) is essential in assessing the effectiveness of physical therapy (PT) interventions. The purposes of this article are (1) to describe the process used by the TBI EDGE task force to assess the psychometrics and clinical utility of OMs used with individuals with moderate to severe traumatic brain injury (TBI); (2) to describe the consensus recommendations for OM use in clinical practice, research, and professional (entry-level) PT education; and (3) to make recommendations for future work.

Methods: An 8-member task force used a modified Delphi process to develop recommendations on the selection of OMs for individuals with TBI.

Presence of a dedicated trauma center physiatrist improves functional outcomes following traumatic brain injury.

Background: Maximizing long-term recovery following traumatic brain injury (TBI) is an important end point. We hypothesized that the addition of a dedicated physiatrist specializing in brain injury medicine to the trauma team would lead to improved functional outcomes.

Methods: Data from the Northern NJ TBI Model Systems were queried for all patients admitted to rehabilitation from four regional trauma centers, one with a full-time TBI physiatrist (PHYS) and three without (NO-PHYS).

Spatial Neglect Hinders Success of Inpatient Rehabilitation in Individuals With Traumatic Brain Injury: A Retrospective Study.

Background Current knowledge about spatial neglect and its impact on rehabilitation mostly originates from stroke studies. Objective To examine the impact of spatial neglect on rehabilitation outcome in individuals with traumatic brain injury (TBI). Methods The retrospective study included 156 consecutive patients with TBI (73 women; median age = 69.

Validity of the stroke rehabilitation assessment of movement scale in acute rehabilitation: a comparison with the functional independence measure and stroke impact scale-16.

Objective: To demonstrate sensitivity to change of the Stroke Rehabilitation Assessment of Movement (STREAM) as well as the concurrent and predictive validity of the STREAM in an acute rehabilitation setting.

Design: Prospective cohort study.

Setting: Acute, in-patient rehabilitation department within a tertiary-care teaching hospital in the United States.

Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis.

The importance of the DNA damage response (DDR) pathway in development, genomic stability, and tumor suppression is well recognized. Although 53BP1 and MDC1 have been recently identified as critical upstream mediators in the cellular response to DNA double-strand breaks, their relative hierarchy in the ataxia telangiectasia mutated (ATM) signaling cascade remains controversial. To investigate the divergent and potentially overlapping functions of MDC1 and 53BP1 in the ATM response pathway, we generated mice deficient for both genes.

Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair.

Histone lysine methylation has been linked to the recruitment of mammalian DNA repair factor 53BP1 and putative fission yeast homolog Crb2 to DNA double-strand breaks (DSBs), but how histone recognition is achieved has not been established. Here we demonstrate that this link occurs through direct binding of 53BP1 and Crb2 to histone H4. Using X-ray crystallography and nuclear magnetic resonance (NMR) spectroscopy, we show that, despite low amino acid sequence conservation, both 53BP1 and Crb2 contain tandem tudor domains that interact with histone H4 specifically dimethylated at Lys20 (H4-K20me2).

The tandem BRCT domain of 53BP1 is not required for its repair function.

53BP1 plays an important role in cellular response to DNA damage. It is thought to be the mammalian homologue of budding yeast Rad9 and/or fission yeast Crb2. Rad9/Crb2 are bona fide checkpoint proteins whose activation requires their corresponding C-terminal tandem BRCT (BRCA1 C-terminal) motifs, which mediate their oligomerization and phosphorylation at multiple sites following DNA damage.

53BP1 cooperates with p53 and functions as a haploinsufficient tumor suppressor in mice.

p53 binding protein 1 (53BP1) is a putative DNA damage sensor that accumulates at sites of double-strand breaks (DSBs) in a manner dependent on histone H2AX. Here we show that the loss of one or both copies of 53BP1 greatly accelerates lymphomagenesis in a p53-null background, suggesting that 53BP1 and p53 cooperate in tumor suppression. A subset of 53BP1-/- p53-/- lymphomas, like those in H2AX-/- p53-/- mice, were diploid and harbored clonal translocations involving antigen receptor loci, indicating misrepair of DSBs during V(D)J recombination as one cause of oncogenic transformation.

Chfr is required for tumor suppression and Aurora A regulation.

Tumorigenesis is a consequence of loss of tumor suppressors and activation of oncogenes. Expression of the mitotic checkpoint protein Chfr is lost in 20-50% of primary tumors and tumor cell lines. To explore whether downregulation of Chfr contributes directly to tumorigenesis, we generated Chfr knockout mice.

Early events in the DNA damage response.

The ability to sense DNA damage and activate response pathways that coordinate cell cycle progression and DNA repair is essential for the maintenance of genomic integrity and the viability of organisms. During the last couple of years, several proteins have been identified that participate very early in the DNA damage response. Here we review the current understanding of the mechanisms by which mammalian cells detect DNA lesions, especially double-strand breaks, and mediate the signal to downstream transducers.

Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrest.

Bloom's syndrome is a rare autosomal recessive genetic disorder characterized by chromosomal aberrations, genetic instability, and cancer predisposition, all of which may be the result of abnormal signal transduction during DNA damage recognition. Here, we show that BLM is an intermediate responder to stalled DNA replication forks. BLM colocalized and physically interacted with the DNA damage response proteins 53BP1 and H2AX.

53BP1 is required for class switch recombination.

53BP1 participates early in the DNA damage response and is involved in cell cycle checkpoint control. Moreover, the phenotype of mice and cells deficient in 53BP1 suggests a defect in DNA repair (Ward et al., 2003b).

UV-induced ataxia-telangiectasia-mutated and Rad3-related (ATR) activation requires replication stress.

Ataxia-telangiectasia-mutated and Rad3-related (ATR) plays an essential role in the maintenance of genome integrity and cell viability. The kinase is activated in response to DNA damage and initiates a checkpoint signaling cascade by phosphorylating a number of downstream substrates including Chk1. Unlike ataxia-telangiectasia-mutated (ATM), which appears to be mainly activated by DNA double-strand breaks, ATR can be activated by a variety of DNA damaging agents.

Accumulation of checkpoint protein 53BP1 at DNA breaks involves its binding to phosphorylated histone H2AX.

53BP1 participates in the cellular response to DNA damage. Like many proteins involved in the DNA damage response, 53BP1 becomes hyperphosphorylated after radiation and colocalizes with phosphorylated H2AX in megabase regions surrounding the sites of DNA strand breaks. However, it is not yet clear whether the phosphorylation status of 53BP1 determines its localization or vice versa.

p53 Binding protein 53BP1 is required for DNA damage responses and tumor suppression in mice.

53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53. It relocates to the sites of DNA strand breaks in response to DNA damage and is a putative substrate of the ataxia telangiectasia-mutated (ATM) kinase. To study the biological role of 53BP1, we disrupted the 53BP1 gene in the mouse.

DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1.

Activation of the ataxia telangiectasia mutated (ATM) kinase triggers diverse cellular responses to ionizing radiation (IR), including the initiation of cell cycle checkpoints. Histone H2AX, p53 binding-protein 1 (53BP1) and Chk2 are targets of ATM-mediated phosphorylation, but little is known about their roles in signalling the presence of DNA damage. Here, we show that mice lacking either H2AX or 53BP1, but not Chk2, manifest a G2-M checkpoint defect close to that observed in ATM(-/-) cells after exposure to low, but not high, doses of IR.