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These altered joint coordination and stiffness could be considered as a protective strategy utilized to effectively absorb energy, stabilize the body and ankle, and prevent excessive ankle inversion. However, this strategy could result in greater mechanical demands on the knee joint.Total knee arthroplasty (TKA) surgery improves knee joint kinematics and kinetics during gait for most patients, but a lack of evidence exists for the level and incidence of improvement that is achieved. The objective of this study was to quantify patient-specific improvements in knee biomechanics relative to osteoarthritis (OA) severity levels. Seventy-two patients underwent 3-dimensional (3D) gait analysis before and 1 year after TKA surgery, as well as 72 asymptomatic adults and 72 with moderate knee OA. A combination of principal component analysis and discriminant analyses were used to categorize knee joint biomechanics for patients before and after surgery relative to asymptomatic, moderate, and severe OA. Post-TKA, 63% were categorized with knee biomechanics consistent with moderate OA, 29% with severe OA, and 8% asymptomatic. The magnitude and pattern of the knee adduction moment and angle (frontal plane features) were the most significant contributors in discriminating between pre-TKA and post-TKA knee biomechanics. Standard of care TKA improves knee biomechanics during gait to levels most consistent with moderate knee OA and predominately targets frontal plane features. These results provide evidence for the level of improvement in knee biomechanics that can be expected following surgery and highlight the biomechanics most targeted by surgery.Obese (OB) youth demonstrate altered knee mechanics and worse lower-extremity performance compared with healthy weight (HW) youth. Our objectives were to compare sagittal plane knee landing mechanics between OB and HW youth and to examine the associations of knee and hip extension peak torque with landing mechanics in OB youth. Twenty-four OB and 24 age- and sex-matched HW youth participated. Peak torque was measured and normalized to leg lean mass. Peak knee flexion angle and peak internal knee extension moment were measured during a single-leg hop landing. Paired t tests, Pearson correlation coefficients, and Bonferroni corrections were used. OB youth demonstrated worse performance and lower knee extension (OB 12.76 [1.38], HW 14.03 [2.08], P = .03) and hip extension (OB 8.59 [3.13], HW 11.10 [2.89], P = .005) peak torque. Furthermore, OB youth demonstrated lower peak knee flexion angles (OB 48.89 [45.41 to 52.37], HW 56.07 [52.59 to 59.55], P = .02) and knee extension moments (OB -1.73 [-1.89 to -1.57], HW -2.21 [-2.37 to -2.05], P = .0001) during landing compared with HW youth. Peak torque measures were not correlated with peak knee flexion angle nor internal knee extension moment during landing in either group (P > .01). OB youth demonstrated altered landing mechanics compared with HW youth. However, no associations among peak torque measurements and knee landing mechanics were present.This study investigated (a) site- and direction-dependent variations of passive triceps surae aponeurosis stiffness and (b) the relationships between aponeurosis stiffness and muscle strength and walking performance in older individuals. Seventy-nine healthy older adults participated in this study. Shear wave velocities of the triceps surae aponeuroses at different sites and in two orthogonal directions were obtained in a prone position at rest using supersonic shear imaging. The maximal voluntary isometric contraction torque of the plantar flexors and normal (preferred) and fast (fastest possible) walking speeds (5-m distance) were also measured. The shear wave velocities of the adjoining aponeuroses were weakly associated with plantar flexion torque (r = .23-.34), normal (r = .26), and fast walking speed (r = .25). this website The results show clear spatial variations and anisotropy of the triceps surae aponeuroses stiffness in vivo, and the aponeurosis stiffness was associated with physical ability in older adults.Glucokinase-maturity onset diabetes of the young (GCK-MODY) represents a rare genetic disorder due to mutation in the glucokinase (GCK) gene. The low incidence of vascular complications in GCK-MODY makes it a natural paradigm for interrogating molecular mechanisms promoting vascular health under prolonged hyperglycemia. Clinical rate of misdiagnosis has remained high, and a reliable serum lipid biomarker that precedes genetic screening can facilitate correct diagnosis and treatment. Herein, we comprehensively quantitated 565 serum lipids from 25 classes in 105 subjects (42 nondiabetic controls, 30 GC K-MODY patients, 33 drug-naïve, and newly-onset T2D patients). At false-discovery rate (FDR) less then 0.05, several phosphatidylcholines (PCs) and plasmalogen PCs were specifically increased in GCK-MODY, while triacylglycerols (TAGs) and diacylglycerols (DAGs) were reduced. Correlation matrices between lipids uncovered coregulation between plasmalogen PCs (PCps) and glycerolipid precursors was distinctly enhanesultant increases in the production of HDL-PCps and PUFA-PCs provides an active, circulating form of protection towards the vasculature of GCK-MODY, thereby lowering the incidence of vascular complications despite chronic exposure to hyperglycemia since birth.Cancer cells develop protective adaptations against oxidative DNA damage, providing a strong rationale for targeting DNA repair proteins. There has been a high degree of recent interest in inhibiting the mammalian Nudix pyrophosphatase MutT Homolog 1 (MTH1). MTH1 degrades 8-oxo-dGTP, thus limiting its incorporation into genomic DNA. MTH1 inhibition has variously been shown to induce genomic 8-oxo-dG elevation, genotoxic strand breaks in p53-functional cells, and tumor-inhibitory outcomes. Genomically incorporated 8-oxo-dG is excised by the base excision repair enzyme, 8-oxo-dG glycosylase 1 (OGG1). Thus, OGG1 inhibitors have been developed with the idea that their combination with MTH1 inhibitors will have anti-tumor effects by increasing genomic oxidative DNA damage. However, contradictory to this idea, we found that human lung adenocarcinoma with low OGG1 and MTH1 were robustly represented in patient datasets. Furthermore, OGG1 co-depletion mitigated the extent of DNA strand breaks and cellular senescence in MTH1-depleted p53-wildtype lung adenocarcinoma cells.
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