Use of a factor analysis to assess biomechanical factors of American Sign Language in native and non-native signers.

Prior studies suggest that native (born to at least one deaf or signing parent) and non-native signers have different musculoskeletal health outcomes from signing, but the individual and combined biomechanical factors driving these differences are not fully understood. Such group differences in signing may be explained by the five biomechanical factors of American Sign Language that have been previously identified: ballistic signing, hand and wrist deviations, work envelope, muscle tension, and "micro" rests. Prior work used motion capture and surface electromyography to collect joint kinematics and muscle activations, respectively, from ten native and thirteen non-native signers as they signed for 7.5 min. Each factor was individually compared between groups. A factor analysis was used to determine the relative contributions of each biomechanical factor between signing groups. No significant differences were found between groups for ballistic signing, hand and wrist deviations, work envelope volume, excursions from recommended work envelope, muscle tension, or "micro" rests. Factor analysis revealed that "micro" rests had the strongest contribution for both groups, while hand and wrist deviations had the weakest contribution. Muscle tension and work envelope had stronger contributions for native compared to non-native signers, while ballistic signing had a stronger contribution for non-native compared to native signers. Using a factor analysis enabled discernment of relative contributions of biomechanical variables across native and non-native signers that could not be detected through isolated analysis of individual measures. Differences in the contributions of these factors may help explain the differences in signing across native and non-native signers.

Relationships of brain cholesterol and cholesterol biosynthetic enzymes to Alzheimer's pathology and dementia in the CFAS population-derived neuropathology cohort.

Altered cholesterol metabolism is implicated in brain ageing and Alzheimer's disease. We examined whether key genes regulating cholesterol metabolism and levels of brain cholesterol are altered in dementia and Alzheimer's disease neuropathological change (ADNC). Temporal cortex (n = 99) was obtained from the Cognitive Function and Ageing Study. Expression of the cholesterol biosynthesis rate-limiting enzyme HMG-CoA reductase (HMGCR) and its regulator, SREBP2, were detected using immunohistochemistry. Expression of HMGCR, SREBP2, CYP46A1 and ABCA1 were quantified by qPCR in samples enriched for astrocyte and neuronal RNA following laser-capture microdissection. Total cortical cholesterol was measured using the Amplex Red assay. HMGCR and SREBP2 proteins were predominantly expressed in pyramidal neurones, and in glia. Neuronal HMGCR did not vary with ADNC, oxidative stress, neuroinflammation or dementia status. Expression of HMGCR neuronal mRNA decreased with ADNC (p = 0.022) and increased with neuronal DNA damage (p = 0.049), whilst SREBP2 increased with ADNC (p = 0.005). High or moderate tertiles for cholesterol levels were associated with increased dementia risk (OR 1.44, 1.58). APOE ε4 allele was not associated with cortical cholesterol levels. ADNC is associated with gene expression changes that may impair cholesterol biosynthesis in neurones but not astrocytes, whilst levels of cortical cholesterol show a weak relationship to dementia status.

Movement compensation is driven by the deltoid and teres minor muscles following severe rotator cuff tear.

BACKGROUND: Rotator cuff tears are common in older adults, negatively affecting function. Previous simulation-based studies reported more posterior and superior oriented glenohumeral loading with increased cuff tear severity and task performance, although corresponding muscle compensation strategies are unclear. Our objective is to determine how shoulder muscle forces change with increased rotator cuff tear severity during functional task performance. METHODS: Eight musculoskeletal models of increasing tear severity were developed to represent no rotator cuff tear to massive three-tendon tears. Simulations were performed using each combination of model and kinematics for five functional tasks. Individual muscle forces were averaged for each task and tear severity, then normalized by the sum of the muscle forces across the shoulder. Forces were compared across tear severity and muscle. FINDINGS: For muscle force contribution, interactions between tear severity and muscle and a main effect of muscle were seen for all tasks (P < 0.0001). Middle deltoid increased force contribution by >10% in the greatest tear severity model compared to no cuff tear model for all tasks (all P < 0.0001). Teres minor contribution increased by 7.7%, 5.6%, and 11% in the greatest tear severity model compared to the no cuff tear model for forward reach, axilla wash, and upward reach 105° tasks, respectively (all P < 0.0001). INTERPRETATION: Functional tasks elicit compensatory responses from uninjured muscles following severe cuff tears, notably in middle deltoid and teres minor, leading to posterior-superior glenohumeral loading. The muscles are potential targets for strengthening to avoid injury from sustained increased muscle force.

Nitric oxide-mediated dispersal in single- and multi-species biofilms of clinically and industrially relevant microorganisms.

Strategies to induce biofilm dispersal are of interest due to their potential to prevent biofilm formation and biofilm-related infections. Nitric oxide (NO), an important messenger molecule in biological systems, was previously identified as a signal for dispersal in biofilms of the model organism Pseudomonas aeruginosa. In the present study, the use of NO as an anti-biofilm agent more broadly was assessed. Various NO donors, at concentrations estimated to generate NO levels in the picomolar and low nanomolar range, were tested on single-species biofilms of relevant microorganisms and on multi-species biofilms from water distribution and treatment systems. Nitric oxide-induced dispersal was observed in all biofilms assessed, and the average reduction of total biofilm surface was 63%. Moreover, biofilms exposed to low doses of NO were more susceptible to antimicrobial treatments than untreated biofilms. For example, the efficacy of conventional chlorine treatments at removing multi-species biofilms from water systems was increased by 20-fold in biofilms treated with NO compared with untreated biofilms. These data suggest that combined treatments with NO may allow for novel and improved strategies to control biofilms and have widespread applications in many environmental, industrial and clinical settings.