Glenohumeral contact forces in reversed anatomy shoulder replacement

A major requirement to design an implant is to develop our understanding of the applied internal forces during everyday activities. In the absence of any basic apparatus for measuring forces directly, it is essential to rely on modelling. The major aim of this study was therefore to understand the biomechanical function of subjects with the reversed anatomy Bayley?Walker prosthesis, using an inverse dynamic shoulder model. In this context, the muscle and joint forces of 12 Bayley–Walker subjects were compared to those of 12 normal subjects during 12 activities of daily living.Maximum glenohumeral contact forces for normal and Bayley–Walker subjects were found to be 77% (±15) and 137% (±21) body weight for lifting a 2 kg shopping bag, and the least forces 29% (±4) and 67% (±8) body weight for reaching to opposite axilla, respectively. For normal subjects, middle deltoid, supraspinatus and infraspinatus were found to be the most active muscles across the subjects and tasks. On the other hand, for implanted subjects with a lack of rotator cuff muscles, the middle deltoid and coracobrachialis muscles were found to be the most active. The biomechanical model can therefore be used in order to gain knowledge about the pathology as well as possible post surgical rehab for subjects with reversed shoulder replacement.     

Oxidative stress--mediated alterations in glucose dynamics in a genetic animal model of type II diabetes

Insulin resistance, characterized by an inexorable decline in skeletal muscle glucose utilization and/or an excessive hepatic glucose production, constitutes a major pathogenic importance in a cluster of clinical disorders including diabetes mellitus, hypertension, dyslipidemia, central obesity and coronary artery disease. A novel concept suggests that heightened state of oxidative stress during diabetes contributes, at least in part, to the development of insulin resistance. Several key predictions of this premise were subjected to experimental testing using Goto-Kakizaki (GK) rats as a genetic animal model for non-obese type II diabetes. Euglycemic-hyperinsulinemic clamp studies with an insulin infusion index of 5 mU/kg bw/min were used to measure endogenous glucose production (EGP), glucose infusion rate (GIR), glucose disposal rate (GDR) and skeletal muscle glucose utilization index (GUI). Moreover, the status of oxidative stress as reflected by the urinary levels of isoprostane and protein carbonyl formation were also assessed as a function of diabetes. Post-absorptive basal EGP and circulating levels of insulin, glucose and free fatty acid (FFA) were elevated in GK rats, compared to their corresponding control values. In contrast, steady state GIR and GDR of the hyperglycemic/hyperinsulinemic animals were reduced, concomitantly with impaired insulin's ability to suppress EGP. Insulin stimulated [3H]-2-deoxyglucose (2-DG) uptake (a measure of glucose transport activity) by various types of skeletal muscle fibers both in vivo and in vitro (isolated muscle, cultured myoblasts) was diminished in diabetic GK rats. This diabetes-related suppression of skeletal muscle glucose utilization was associated with a decrease in insulin's ability to promote the phosphorylation of tyrosine residues of insulin receptor substrate-1 (IRS-1). Similarly, the translocation of GLUT-4 from intracellular compartment to plasma membrane in response to insulin was also reduced in these animals. Oxidative stress-based markers (e.g. urinary isoprostane, carbonyl-bound proteins) were elevated as a function of diabetes. Nullification of the heightened state of oxidative stress in the GK rats with alpha-lipoic acid resulted in a partial amelioration of the diabetes-related impairment of the in vivo and in vitro insulin actions. Collectively, the above data suggest that 1) insulin resistance in GK rats occurs at the hepatic and skeletal muscle levels, 2) muscle cell glucose transport exhibited a blunted response to insulin and it is associated with a major defect in key molecules of both GLUT-4 trafficking and insulin signaling pathways, 3) skeletal muscle insulin resistance in GK rats appears to be of genetic origin and not merely related to a paracrine or autocrine effect, since this phenomenon is also observed in cultured myoblasts over several passages and finally heightened state of oxidative stress may mediate the development of insulin resistance during diabetes.     

Constitutive modeling of menisci tissue: a critical review of analytical and numerical approaches

Biomechanics and Modeling in Mechanobiology - Menisci are fibrocartilaginous disks consisting of soft tissue with a complex biomechanical structure. They are critical determinants of the kinematics...     

Nonlinear Mechanical Properties of Prestressed Branched Fibrous Networks

Random fiber networks constitute the solid skeleton of many biological materials such as the cytoskeleton of cells and extracellular matrix of soft tissues. These random networks show unique mechanical properties such as nonlinear shear strain-stiffening and strain softening when subjected to preextension and precompression, respectively. In this study, we perform numerical simulations to characterize the influence of axial prestress on the nonlinear mechanical response of random network structures as a function of their micromechanical and geometrical properties. We build our numerical network models using the microstructure of disordered hexagonal lattices and quantify their nonlinear shear response as a function of uniaxial prestress strain. We consider three different material models for individual fibers and fully characterize their influence on the mechanical response of prestressed networks. Moreover, we investigate both the influence of geometric disorder keeping the network connectivity constant and the influence of the randomness in the stiffness of individual fibers keeping their mean stiffness constant. The effects of network connectivity and bending rigidity of fibers are also determined. Several important conclusions are made, including that the tensile and compressive prestress strains, respectively, increase and decrease the initial network shear stiffness but have no effect on the maximal shear modulus. We discuss the findings in terms of microstructural properties such as the local strain energy distribution.     

Lacticaseibacillus casei in Diet of Juvenile Convict Cichlid Fish (Amatitlania nigrofasciata): Evaluating Growth Performance,Digestive Enzyme Activities,Immune Responses,and Stress Resistance

Probiotics and Antimicrobial Proteins - In this study, growth performance, body composition, digestive enzymes activity, mucosal and immunological parameters, cultivable bacterial populations, and...     

Centering the Organizing Center in the Arabidopsis thaliana Shoot Apical Meristem by a Combination of Cytokinin Signaling and Self-Organization

Plants have the ability to continously generate new organs by maintaining populations of stem cells throught their lives. The shoot apical meristem (SAM) provides a stable environment for the maintenance of stem cells. All cells inside the SAM divide, yet boundaries and patterns are maintained. Experimental evidence indicates that patterning is independent of cell lineage, thus a dynamic self-regulatory mechanism is required. A pivotal role in the organization of the SAM is played by the WUSCHEL gene (WUS). An important question in this regard is that how WUS expression is positioned in the SAM via a cell-lineage independent signaling mechanism. In this study we demonstrate via mathematical modeling that a combination of an inhibitor of the Cytokinin (CK) receptor, Arabidopsis histidine kinase 4 (AHK4) and two morphogens originating from the top cell layer, can plausibly account for the cell lineage-independent centering of WUS expression within SAM. Furthermore, our laser ablation and microsurgical experiments support the hypothesis that patterning in SAM occurs at the level of CK reception and signaling. The model suggests that the interplay between CK signaling, WUS/CLV feedback loop and boundary signals can account for positioning of the WUS expression, and provides directions for further experimental investigation.     

Modelling the effects of hydrogen passivation and strain on the field emission from armchair-graphene nanoribbon using a modified non-equilibrium Green’s function method

In this report, we introduced a modified non-equilibrium Green’s function method to investigate the structural effects on the field emission current from an armchair graphene nanoribbon. We introduce a modified self-energy which is useful to study the effects of potential barrier in the field emission devices. Investigation into the effects of hydrogen passivation and applied strain can be realised using our modified formalism. Also a practical method to consider the effect of device parameters, such as channel length, anode–cathode separation and gate potential can be provided by the proposed formalism. The quantum effects of the emitter’s structure on the field emission are achievable by our introduced method.     

Impaired TGF-β signaling and a defect in resolution of inflammation contribute to delayed wound healing in a female rat model of type 2 diabetes

Wound healing (WH) impairment is a well-documented phenomenon in clinical and experimental diabetes. Sex hormones, in addition to a number of signaling pathways including transforming growth factor-β1 (TGF-β1)/Smads and TNF-α/NF-κB in macrophages and fibroblasts, appear to play a cardinal role in determining the rate and nature of WH. We hypothesized that a defect in resolution of inflammation and an enhancement in TNF-α/NF-κB activity induced by estrogen deficiency contribute to the impairment of TGF-β signaling and delayed WH in diabetes models. Goto-Kakizaki (GK) rats and full thickness excisional wounds were used as models for type 2 diabetes (T2D) and WH, respectively. Parameters related to the various stages of WH were assessed using histomorphometry, western blotting, real-time PCR, immunofluorescence microscopy and ELISA-based assays. Retarded re-epithelialization, suppressed angiogenesis, delayed wound closure, reduced estrogen level and heightened states of oxidative stress were characteristic features of T2D wounds. These abnormalities were associated with a defect in resolution of inflammation, shifts in macrophage phenotypes, increased β3-integrin expression, impaired wound TGF-β1 signaling (↓p-Smad2/↑Smad7) and enhanced TNF-α/NFκB activity. Human/rat dermal fibroblasts of T2D, compared to corresponding control values, displayed resistance to TGF-β-mediated responses including cell migration, myofibroblast formation and p-Smad2 generation. A pegylated form of soluble TNF receptor-1 (PEG-sTNF-RI) or estrogen replacement therapy significantly improved re-epithelialization and wound contraction, enhanced TGFβ/Smad signaling, and polarized the differentiation of macrophages toward an M2 or "alternatively" activated phenotype, while limiting secondary inflammatory-mediated injury. Our data suggest that reduced estrogen levels and enhanced TNF-α/NF-κB activity delayed WH in T2D by attenuating TGFβ/Smad signaling and impairing the resolution of inflammation; most of these defects were ameliorated with estrogen and/or PEG-sTNF-RI therapy.