Simulations suggest walking with reduced propulsive force would not mitigate the energetic consequences of lower tendon stiffness.

Aging elicits numerous effects that impact both musculoskeletal structure and walking function. Tendon stiffness (kT) and push-off propulsive force (FP) both impact the metabolic cost of walking and are diminished by age, yet their interaction has not been studied. We combined experimental and computational approaches to investigate whether age-related changes in function (adopting smaller FP) may be adopted to mitigate the metabolic consequences arising from changes in structure (reduced kT).

Quantifying mechanical and metabolic interdependence between speed and propulsive force during walking.

Walking speed is a useful surrogate for health status across the population. Walking speed appears to be governed in part by interlimb coordination between propulsive (F) and braking (F) forces generated during step-to-step transitions and is simultaneously optimized to minimize metabolic cost. Of those forces, F generated during push-off has received significantly more attention as a contributor to walking performance.

Muscle metabolic energy costs while modifying propulsive force generation during walking.

We pose that an age-related increase in the metabolic cost of walking arises in part from a redistribution of joint power where muscles spanning the hip compensate for insufficient ankle push-off and smaller peak propulsive forces (F). Young adults elicit a similar redistribution when walking with smaller F via biofeedback. We used targeted F biofeedback and musculoskeletal models to estimate the metabolic costs of operating lower limb muscles in young adults walking across a range of F.

Imaging and Simulation of Inter-muscular Differences in Triceps Surae Contributions to Forward Propulsion During Walking.

Forward propulsion during the push-off phase of walking is largely governed at the ankle by differential neuromechanical contributions from the biarticular medial (MG) and lateral gastrocnemii (LG) and the uniarticular soleus (SOL). However, the relative contribution of these individual muscles to forward propulsion is equivocal, with important implications for the design and control of wearable assistive devices and for targeted therapeutics. The aim of this study was to evaluate the agreement between empirical and model-predicted triceps surae (i.

Heart rate measures from the Apple Watch, Fitbit Charge HR 2, and electrocardiogram across different exercise intensities.

This study compared heart rate (HR) measurements for the Fitbit Charge HR 2 (Fitbit) and the Apple Watch devices with HR measurements for electrocardiogram (ECG). Thirty young adults (15/15 females/males, age 23.5 ± 3.

Familial Risk in Patients With Carcinoma of Unknown Primary.

Importance: Carcinoma of unknown primary (CUP) accounts for 3% to 5% of all cancers and is associated with poor prognosis. Familial clustering of different cancer sites with CUP is unknown and may provide information regarding etiology, as well as elevated cancer risks in relatives.

Objective: To quantify the risk of cancer by site in first- and second-degree relatives and first cousins of individuals with CUP.

Increased Risk of Colorectal Cancer Among Family Members of All Ages, Regardless of Age of Index Case at Diagnosis.

Background & Aims: It is not clear whether familial risk of colorectal cancer (CRC) varies with age of index CRC patients or their relatives. We quantified the risk of CRC in first-degree relatives (FDRs), second-degree relatives, and first-cousin relatives of individuals with CRC, stratified by ages and sexes of index patients and ages of relatives.

Methods: CRCs diagnosed between 1980 and 2010 were identified from the Utah Cancer Registry and linked to pedigrees from the Utah Population Database.

Increased risk of colorectal neoplasia among family members of patients with colorectal cancer: a population-based study in Utah.

Background & Aims: Colorectal cancer (CRC) frequently develops in multiple members of the same families, but more data are needed to prepare effective screening guidelines. We quantified the risk of CRC and adenomas in first-degree relatives (FDRs) and second-degree relatives and first cousins of individuals with CRC, and stratified risk based on age at cancer diagnosis.

Methods: We performed a case-control study of Utah residents, 50-80 years old, who underwent colonoscopy from 1995 through 2009.

Epidemiology and familial risk of synchronous and metachronous colorectal cancer: a population-based study in Utah.

Background & Aims: Patients diagnosed with colorectal cancer (CRC) are at risk for synchronous and metachronous lesions at the time of diagnosis or during follow-up evaluation. We performed a population-based study to evaluate the rate, predictors, and familial risk for synchronous and metachronous CRC in Utah.

Methods: All newly diagnosed cases of CRC between 1980 and 2010 were obtained from the Utah Cancer Registry and linked to pedigrees from the Utah Population Database.

Parental influence on systemic sclerosis.

Objective: To examine parental influence on the development of systemic sclerosis (SSc; scleroderma). We designed 3 studies: mitochondrial inheritance, birth order (a possible surrogate marker for microchimerism), and paternal age at conception (a possible surrogate for telomere erosion) to examine their association with development of SSc.

Methods: SSc was defined by International Classification of Diseases, Ninth and Tenth Revision codes (ICD-9 710.

Characteristics of missed or interval colorectal cancer and patient survival: a population-based study.

Background & Aims: Colorectal cancers (CRCs) diagnosed within a few years after an index colonoscopy can arise from missed lesions or the development of a new tumor. We investigated the proportion, characteristics, and factors that predict interval CRCs that develop within 6-60 months of colonoscopy.

Methods: We performed a population-based cohort study of Utah residents who underwent colonoscopy examinations from 1995 through 2009 at Intermountain Healthcare or the University of Utah Health System, which provide care to more than 85% of state residents.

Maternal prenatal weight gain and autism spectrum disorders.

Background: The rising population of individuals identified with an autism spectrum disorder (ASD) calls for further investigation of its underlying etiology. A disturbance in the fetal steroid hormone environment may be a mechanism in which environmental and genetic risk factors interact. The mother, fetus, and placenta collectively create the fetal steroid environment.

Risk of colorectal cancer and adenomas in the families of patients with adenomas: a population-based study in Utah.

Background: Guidelines recommend that individuals with a first-degree relative (FDR) diagnosed with colorectal cancer (CRC) or advanced adenoma before age 60 years should undergo colonoscopy starting at age 40 years. The authors quantified the risk of adenomas and CRC in FDRs, second-degree relatives (SDRs), and third-degree relatives (TDRs) of patients diagnosed with adenomas and advanced adenomas.

Methods: A population-based, retrospective, case-control study was performed of residents of the state of Utah aged 50 years to 80 years who underwent colonoscopy between 1995 and 2009 at Intermountain Healthcare or the University of Utah.

Establishing a familial basis for papillary thyroid carcinoma using the Utah Population Database.

Importance: Determining if relatives of patients diagnosed as having papillary thyroid carcinoma (PTC) are at increased risk of developing the same cancer--and if so, which relatives and to what degree--would help identify those who require closer clinical attention. This could lead to earlier cancer detection and improved prognoses.

Objective: To define the familial risk of PTC using a unique population research database.

Familial risk of childhood cancer and tumors in the Li-Fraumeni spectrum in the Utah Population Database: implications for genetic evaluation in pediatric practice.

We used the Utah Population Database to examine risk of cancer in relatives of 4,482 pediatric cancer cases (≤18 years old) diagnosed from 1966 to 2009 compared to matched population controls. We quantified cancer risk in relatives of children with cancer to determine evidence of familial aggregation and to inform risk assessment and counseling for families. Odds ratios that reflect risk were obtained using conditional logistic regression models adjusting for number of biological relatives, their degree of genetic relatedness and their person-years at risk.

Excess mortality and causes of death in autism spectrum disorders: a follow up of the 1980s Utah/UCLA autism epidemiologic study.

This study's purpose was to investigate mortality among individuals with autism spectrum disorders (ASD) ascertained during a 1980s statewide autism prevalence study (n = 305) in relation to controls. Twenty-nine of these individuals (9.5 %) died by the time of follow up, representing a hazard rate ratio of 9.

Total hip arthroplasty, hip osteoarthritis, total knee arthroplasty, and knee osteoarthritis in patients with developmental dysplasia of the hip and their family members: a kinship analysis report.

Background: Developmental dysplasia of the hip (DDH) is a familial condition with a wide phenotypic expression. Families with high rates of DDH may have individuals with subtle phenotypic expression that can progress to osteoarthritis and require total hip arthroplasty (THA). This study compares the rates of THA in relatives of individuals with DDH with individuals in control families.

Hemangioma is associated with atopic disease.

Objective: To determine if atopic disease is associated with infantile hemangioma.

Study Design: Case control study.

Setting: State of Utah inpatient and outpatient records obtained from the Department of Health, Intermountain Healthcare medical records, and the University of Utah Health Care medical records using the Utah Population Database.

Is gastroschisis truly a sporadic defect?: familial cases of gastroschisis in Utah, 1997 to 2008.

Background: Gastroschisis remains an epidemiologic and pathogenetic dilemma, with genetics not thought to play a significant role in its etiology. The purpose of this study was to determine which gastroschisis cases in the Utah Birth Defect Network (UBDN) were related and the excess familial risk among multigenerational families.

Methods: Gastroschisis cases born from 1997 through 2008 were identified from the statewide population-based UBDN and linked with the Utah Population Database (UPDB) to access multigenerational pedigrees.

Familial clustering of hemangiomas.

Objectives: To assess the degree of relationship among individuals with hemangiomas and to evaluate the relative risk (RR) for family members of individuals with hemangiomas.

Design: Retrospective case-control study.

Setting: Utah Population Database.

Inflammatory bowel disease aggregation in Utah kindreds.

Background: The observed heritability of inflammatory bowel disease (IBD) is incompletely explained by known genetic risk factors. Kindred-specific genetic variants that cause IBD may be a source of "missing heritability." Given that they have been previously difficult to identify, we sought to identify high-risk IBD kindreds.

Heritability of vasculopathy, autoimmune disease, and fibrosis in systemic sclerosis: a population-based study.

Objective: To investigate the familiality of systemic sclerosis (SSc) in relation to Raynaud's phenomenon (RP) (a marker of vasculopathy), other autoimmune inflammatory disease, and fibrotic interstitial lung disease (ILD).

Methods: A genealogic resource, the Utah Population Database (UPDB), was used to test heritability of RP, other autoimmune disease, and ILD. Diseases were defined by International Classification of Diseases, Ninth Revision codes and identified from statewide discharge data, the University of Utah Health Science Center Enterprise Data Warehouse, and death certificates and were linked to the UPDB for analysis.

Quantification of the familial contribution to juvenile idiopathic arthritis.

Objective: We previously demonstrated that there is familial aggregation of juvenile idiopathic arthritis (JIA). Using a large JIA cohort, we sought to identify additional clusters of JIA cases and to calculate robust estimates of the relative risk (RR) of JIA in the siblings and cousins of JIA probands. We also estimated the population attributable risk (PAR) of familial factors in JIA.