Core Strength Testing: Developing Normative Data for Three Clinical Tests

Background/Purpose: Research suggests that core endurance is related to function and injury. Core endurance tests are commonly used in the clinic and yet limited data about normative values exist. This study aims to establish normative values and assess the effect of specific variables on these values in adults 18-55 years old for three clinical core endurance tests. Subjects/Methods: Fifty-five subjects, 20 male and 35 female with a mean age of 29 participated in this study. Subjects were required to complete a general health and exercise history questionnaire. Each subject was then randomly assigned a test order and tested by one of four student researchers. The core endurance tests performed were right side plank (RSP), left side plank (LSP), 60 degree flexion test (Fl) and trunk extensor (Ext) endurance test. Analyses/Results: Analyses included one-way ANOVA and multiple regression to determine where differences existed between groups and to understand what variables influenced test outcomes. Significant results existed for the following variables: gender M/F (RSP p=.002, LSP p=.003), exercise Y/N (Ext p=.02, Fl p=.003), active runners Y/N (RSP p=.03 Fl p=.0002), strength training Y/N (RSP p=.03, LSP p=.02), core exercise Y/N (LSP p=.02), previous and/or current competitive athletes Y/N (Ext p=.045, RSP p=.01, Fl p=.01) and lower extremity injury Y/N (Ext p=.03). Multiple regression revealed exercise time was the most significant predictor of RSP (p=.01) and core exercise time and overall exercise time were highest predictors of LSP (p=.001). Conclusion: Our results suggest that gender and exercise play a significant role in core endurance. Data suggests regular general exercise and strength training may have a stronger correlation with increased overall core endurance than participating in exercises specific to the core musculature. Implications: Normative values about these core endurance tests can be used in clinical practice to assess core endurance in the general population

Sex-related differences in endothelial function and blood viscosity in the elderly population

Elderly represents a growing population and cardiovascular diseases (CVD) is one of the leading causes of mortality in this population. Sex differences are involved in CVD with middle-aged males being at higher risk than females. After menopause, females are no longer protected by hormones and the role of sex on cardiovascular parameters involved in CVD, such as endothelial function and blood viscosity, is still unclear. The purpose of this study was to investigate the effect of sex on endothelial function, blood viscosity and CVD in elderly. Clinical investigation and blood analyses were performed on 182 (93 females and 89 males) elderly participants (mean age: 75.83 ± 1.22). Health status of participants were classified. Sex differences in endothelial function, blood viscosity, high density lipoprotein (HDL), hematocrit, and red blood cell (RBC) aggregation were assessed. CVD prevalence was higher in males (27.0%) than in females (5.4%) (p < 0.001). Females had higher vasoreactivity (p = 0.014) and HDL (p < 0.001) level than males. Blood viscosity was higher in males than in females at any shear rate (p < 0.001). Hematocrit was greater in males than in females (p < 0.001) while RBC aggregation did not differ between the two populations. To conclude, females have less CVD than age-matched males that might be due to their greater vascular function and lower blood viscosity

Clinical outcomes of 130 patients with primary and secondary lung tumors treated with Cyberknife robotic stereotactic body radiotherapy

Background: Authors report clinical outcomes of patients treated with robotic stereotactic body radiotherapy (SBRT) for primary, recurrent and metastatic lung lesions. Patients and methods: 130 patients with 160 lesions were treated with Cyberknife SBRT, including T1-3 primary lung cancers (54%), recurrent tumors (22%) and pulmonary metastases (24%). The mean biologically equivalent dose (BED10Gy) was 151 Gy (72–180 Gy). Median prescribed dose for peripheral and central lesions was 3x20 Gy and 3x15 Gy, respectively. Local control (LC), overall survival (OS), and cause-specific survival (CSS) rates, early and late toxicities are reported. Statistical analysis was performed to identify factors influencing local tumor control. Results: Median follow-up time was 21 months. In univariate analysis, higher dose was associated with better LC and a cut-off value was detected at BED10Gy ≤ 112.5 Gy, resulting in 1-, 2-, and 3-year actuarial LC rates of 93%, vs 73%, 80% vs 61%, and 63% vs 54%, for the high and low dose groups, respectively (p = 0.0061, HR = 0.384). In multivariate analysis, metastatic origin, histological confirmation and larger Planning Target Volume (PTV) were associated with higher risk of local failure. Actuarial OS and CSS rates at 1, 2, and 3 years were 85%, 74% and 62%, and 93%, 89% and 80%, respectively. Acute and late toxicities ≥ Gr 3 were observed in 3 (2%) and 6 patients (5%), respectively. Conclusions: Our favorable LC and survival rates after robotic SBRT, with low rates of severe toxicities, are coherent with the literature data in this mixed, non-selected study population

A map of neurofilament light chain species in brain and cerebrospinal fluid and alterations in Alzheimer\u27s disease

Neurofilament light is a well-established marker of both acute and chronic neuronal damage and is increased in multiple neurodegenerative diseases. However, the protein is not well characterized in brain tissue or body fluids, and it is unknown what neurofilament light species are detected by commercial assays and whether additional species exist. We developed an immunoprecipitation-mass spectrometry assay using custom antibodies targeting various neurofilament light domains, including antibodies targeting Coil 1A/1B of the rod domain (HJ30.13), Coil 2B of the rod domain (HJ30.4) and the tail region (HJ30.11). We utilized our assay to characterize neurofilament light in brain tissue and CSF of individuals with Alzheimer\u27s disease dementia and healthy controls. We then validated a quantitative version of our assay and measured neurofilament light concentrations using both our quantitative immunoprecipitation-mass spectrometry assay and the commercially available immunoassay from Uman diagnostics in individuals with and without Alzheimer\u27s disease dementia. Our validation cohort included CSF samples from 30 symptomatic amyloid-positive participants, 16 asymptomatic amyloid-positive participants, 10 symptomatic amyloid-negative participants and 25 amyloid-negative controls. We identified at least three major neurofilament light species in CSF, including N-terminal and C-terminal truncations, and a C-terminal fragment containing the tail domain. No full-length neurofilament light was identified in CSF. This contrasts with brain tissue, which contained mostly full-length neurofilament and a C-terminal tail domain fragment. We observed an increase in neurofilament light concentrations in individuals with Alzheimer\u27s disease compared with healthy controls, with larger differences for some neurofilament light species than for others. The largest differences were observed for neurofilament light fragments including NfL165 (in Coil 1B), NfL324 (in Coil 2B) and NfL530 (in the C-terminal tail domain). The Uman immunoassay correlated most with NfL324. This study provides a comprehensive evaluation of neurofilament light in brain and CSF and enables future investigations of neurofilament light biology and utility as a biomarker

Clinical outcomes of 130 patients with primary and secondary lung tumors treated with Cyberknife robotic stereotactic body radiotherapy

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Even a Previous Light-Active Physical Activity at Work Still Reduces Late Myocardial Infarction and Stroke in Retired Adults Aged>65 Years by 32%: The PROOF Cohort Study

Background: Work may contribute significantly to daily physical activity (PA) and sedentary behavior (SB). Physical inactivity and SB at work might be two major risk factors for premature morbidity. Therefore, the aim of this research was to describe self-reported past PA and SB at work and during leisure time within the PROOF cohort subjects, and to determine consequences of PA and SB on late health of these now retired workers.Material and Methods: The PROOF cohort study was used to prospectively allow assessment of the predictive value of PA and SB at work and during leisure time among a healthy retired French population, with regard to cardiovascular and cerebrovascular events. PA (MET-h/week) and SB (h/d) were assessed using the Population Physical Activity Questionnaire (POPAQ) and the modified Global Physical Activity Questionnaire (GPAQ). Odds ratios (ORs with 95% CIs) for cardiovascular and cerebrovascular events were associated with each level of PA at work: light (<3 METs), moderate (3–5.9 METs), vigorous (≥6 METs) and were compared to SB at work.Results: Out of the 1011 65-year-old subjects initially included, the 15-year follow-up has been currently completed for 688 (68%) subjects; 89 deaths (all-cause mortality, 9%) and 91 fatal and non-fatal cardiovascular and cerebrovascular events (9%), were reported. An active work (light, moderate, or vigorous intensity) was associated with a 21% reduced risk of cardiovascular (myocardial infarction) and cerebrovascular events (stroke) (OR = 0.79, 95% CI: 0.32–0.91, p < 0.02) compared to sedentary work. This relationship was already significant for light intensity work (32%; i.e., OR = 0.68, 95% CI: 0.31–0.87, p < 0.02).Conclusion: There is strong causal evidence linking PA and SB at work with late cardiovascular and cerebrovascular disease. All in all, the risk for onset of myocardial infarction and stroke was lower among those who had a previous active work compared to those with previous sedentary work. Even previous light active work produced substantial health benefits.Clinical Trial Registration:www.ClinicalTrials.gov, identifier: NCT00759304

Mechanisms that Govern how the Price of Anarchy varies with Travel Demand

Selfish routing, represented by the User-Equilibrium (UE) model, is known to be inefficient when compared to the System Optimum (SO) model. However, there is currently little understanding of how the magnitude of this inefficiency, which can be measured by the Price of Anarchy (PoA), varies across different structures of demand and supply. Such understanding would be useful for both transport policy and network design, as it could help to identify circumstances in which policy interventions that are designed to induce more efficient use of a traffic network, are worth their costs of implementation. This paper identifies four mechanisms that govern how the PoA varies with travel demand in traffic networks with separable and strictly increasing cost functions. For each OD movement, these are expansions and contractions in the sets of routes that are of minimum cost under UE and minimum marginal total cost under SO. The effects of these mechanisms on the PoA are established via a combination of theoretical proofs and conjectures supported by numerical evidence. In addition, for the special case of traffic networks with BPR-like cost functions having common power, it is proven that there is a systematic relationship between link flows under UE and SO, and hence between the levels of demand at which expansions and contractions occur. For this case, numerical evidence also suggests that the PoA has power law decay for large demand

Global, regional, and national burden of chronic kidney disease, 1990–2017 : a systematic analysis for the Global Burden of Disease Study 2017

Background Health system planning requires careful assessment of chronic kidney disease (CKD) epidemiology, but data for morbidity and mortality of this disease are scarce or non-existent in many countries. We estimated the global, regional, and national burden of CKD, as well as the burden of cardiovascular disease and gout attributable to impaired kidney function, for the Global Burden of Diseases, Injuries, and Risk Factors Study 2017. We use the term CKD to refer to the morbidity and mortality that can be directly attributed to all stages of CKD, and we use the term impaired kidney function to refer to the additional risk of CKD from cardiovascular disease and gout. Methods The main data sources we used were published literature, vital registration systems, end-stage kidney disease registries, and household surveys. Estimates of CKD burden were produced using a Cause of Death Ensemble model and a Bayesian meta-regression analytical tool, and included incidence, prevalence, years lived with disability, mortality, years of life lost, and disability-adjusted life-years (DALYs). A comparative risk assessment approach was used to estimate the proportion of cardiovascular diseases and gout burden attributable to impaired kidney function. Findings Globally, in 2017, 1·2 million (95% uncertainty interval [UI] 1·2 to 1·3) people died from CKD. The global all-age mortality rate from CKD increased 41·5% (95% UI 35·2 to 46·5) between 1990 and 2017, although there was no significant change in the age-standardised mortality rate (2·8%, −1·5 to 6·3). In 2017, 697·5 million (95% UI 649·2 to 752·0) cases of all-stage CKD were recorded, for a global prevalence of 9·1% (8·5 to 9·8). The global all-age prevalence of CKD increased 29·3% (95% UI 26·4 to 32·6) since 1990, whereas the age-standardised prevalence remained stable (1·2%, −1·1 to 3·5). CKD resulted in 35·8 million (95% UI 33·7 to 38·0) DALYs in 2017, with diabetic nephropathy accounting for almost a third of DALYs. Most of the burden of CKD was concentrated in the three lowest quintiles of Socio-demographic Index (SDI). In several regions, particularly Oceania, sub-Saharan Africa, and Latin America, the burden of CKD was much higher than expected for the level of development, whereas the disease burden in western, eastern, and central sub-Saharan Africa, east Asia, south Asia, central and eastern Europe, Australasia, and western Europe was lower than expected. 1·4 million (95% UI 1·2 to 1·6) cardiovascular disease-related deaths and 25·3 million (22·2 to 28·9) cardiovascular disease DALYs were attributable to impaired kidney function. Interpretation Kidney disease has a major effect on global health, both as a direct cause of global morbidity and mortality and as an important risk factor for cardiovascular disease. CKD is largely preventable and treatable and deserves greater attention in global health policy decision making, particularly in locations with low and middle SDI

CSF Tau phosphorylation at Thr205 is associated with loss of white matter integrity in autosomal dominant Alzheimer disease

BACKGROUND: Hyperphosphorylation of tau leads to conformational changes that destabilize microtubules and hinder axonal transport in Alzheimer\u27s disease (AD). However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s). METHODS: In autosomal dominant AD (ADAD) mutation carriers (MC) and non-carriers (NC) we compared cerebrospinal fluid (CSF) phosphorylation at tau sites (pT217, pT181, pS202, and pT205) and total tau with WM measures, as derived from diffusion tensor imaging (DTI), and cognition. A WM composite metric, derived from a principal component analysis, was used to identify spatial decline seen in ADAD. RESULTS: The WM composite explained over 70% of the variance in MC. WM regions that strongly contributed to the spatial topography were located in callosal and cingulate regions. Loss of integrity within the WM composite was strongly associated with AD progression in MC as defined by the estimated years to onset (EYO) and cognitive decline. A linear regression demonstrated that amyloid, gray matter atrophy and phosphorylation at CSF tau site pT205 each uniquely explained a reduction in the WM composite within MC that was independent of vascular changes (white matter hyperintensities), and age. Hyperphosphorylation of CSF tau at other sites and total tau did not significantly predict WM composite loss. CONCLUSIONS: We identified a site-specific relationship between CSF phosphorylated tau and WM decline within MC. The presence of both amyloid deposition and Tau phosphorylation at pT205 were associated with WM composite loss. These findings highlight a primary AD-specific mechanism for WM dysfunction that is tightly coupled to symptom manifestation and cognitive decline