A study of the viscoelastic effect in a bone remodeling model

The present paper addresses the following question can a simple regulatory bone remodeling model predict effects of viscosity on the trabecular morphology? For that, we propose an extension of a previous bone remodeling model by taking into account the viscosity properties of the tissue. Zener’s law is used to describe the mechanical behavior of the bone and a specific law of the apparent bone density rate is proposed. Based on stability analysis, numerical simulations are then performed to investigate the viscosity role on simulations of the bone remodeling process. We show that the viscous contribution affects the evolution of the apparent bone density, by slowing down the adaptation process, which seems to be confirmed by simulations with real data obtained from rat tibia.     

Damaged-bone adaptation under steady homogeneous stress

In this work an extension of the adaptive-elasticity theory is proposed in order to include the contribution of bone microdamage as a stimulus. Some aspects of damaged-bone tissue adaptation, brought about by a change of the daily loading history, are investigated. In particular, under the assumption of a small strain approximation and isothermal conditions, the solution of the remodeling rate equation for steady homogeneous stress is discussed and the damage effect upon the remodeling time constant is shown. The result is both theoretical and numerical, based on a recent theory of internal damaged-bone remodeling (Ramtani, S., and Zidi, M., 1999, "Damaged-Bone Remodeling Theory: Thermodynamical Approach, " Mechanics Research Communications, Vol. 26, pp. 701-708. Ramtani, S., and Zidi, M., 2001, "A Theoretical Model of the Effect of Continum Damage on a Bone Adaption Model," Journal of Biomechanics, Vol. 34, pp. 471-479) and motivated by the works of Cowin, S. C., and Hegedus, D. M., 1976, "Bone Remodeling I: Theory and Adaptive Elasticity," Journal of Elasticity, Vol. 6, pp. 471-479 and Hegedus, D. H., and Cowin, S. C., 1976, "Bone Remodeling II: Small Strain Adaptive Elasticity," Journal of Elasticity, Vol. 6, pp. 337-352.     

Stability analysis and finite element simulation of bone remodeling model

Bone remodeling is widely viewed as a dynamic process--maintaining bone structure through a balance between the opposed activities of osteoblast and osteoclast cells--in which the stability problem is often pointed out. By an analytical approach, we present a bone remodeling model applied to n unit-elements in order to analyze the stationary states and the condition of their stability. In addition, this theory has been simulated in a computer model using the Finite Element Method (FEM) to show a relationship between the bone remodeling process and the stability analysis.     

A theoretical model of the effect of continuum damage on a bone adaptation model

Throughout life, bone is continuously turning over by the well-regulated processes of bone formation and resorption. Everyday activities damage bone, and this damage is normally repaired in a continuous remodelling process. When an imbalance in this remodelling process occurs, bones may become more susceptible to fracture. This paper is devoted to a theoretical modelling of the competition between damage and internal remodelling in bones. The general theory of adaptive damaged-elastic materials proposed here as a model for the physiological process of damaged-bone remodelling follows the general framework of continuum thermodynamics where new damaged-bone remodelling law and associated thermodynamical restrictions are stated, and specialized to the case of small strain in isothermal processes. An attempt is also made to derive: (a) the damage force (adaptive damage energy release rate ) which controls the microcracks propagation and arrest, and (b) the damage rule by introducing damage thresholds and loading/unloading conditions.     

Association of Lymphotoxin Alpha Polymorphism with Type 1 Diabetes in a Tunisian Population

We investigated the association of the lymphotoxin (LT)-α gene polymorphism +249A/G with type 1 diabetes. The distribution of genotypes of the LT-α +249A/G single nucleotide polymorphism (SNP) was assessed in 115 diabetic patients and 123 normoglycemic control subjects, using PCR-restriction fragment length polymorphism analysis. Among unselected patients, the SNP was significantly associated with increased risk of diabetes (χ² = 8.44, p = 0.014) and was found to be more pronounced among female (χ² = 8.37, p = 0.02) than male (χ² = 6.11, p = 0.047) patients. A significant association was detected between LT-α +249A/G and increased risk of diabetes, in particular for young-onset patients (χ² = 6.92, p = 0.031). Moreover, we reported significant differences in levels of HbA1c, triglycerides, alanine transaminase, and anti-glutamic acid decarboxylase-65 among alleles. Additional studies with extended patient age groups and different ethnicities are needed to confirm our findings.     

Soluble HLA-G induces NF–кB activation in natural killer cells

Human leukocyte antigen (HLA)-G is an immunomodulatory molecule discovered for the first time in the maternal–fetal interface. In cancer context, where high number of natural killer (NK) cells is described, the presence of HLA-G in its soluble form is thought to be essential for NK cells signaling. To evaluate intracellular signaling in NK cells upon HLA-G soluble forms stimulation, we investigate the role of soluble HLA-G (HLA-G5- and HLA-G1 shedding form) stimulation on classical nuclear factor (NF)–κB pathway activation. We reported that these two forms of soluble HLA-G could activate NF–κB in NK cells. NF–κB activation in NK cells does implicate neither phosphatidylinositol 3-kinase (PI3K) nor MEK (MAP kinase kinase) as demonstrated after specific inhibition experiments. We demonstrated elsewhere that NF–κB activation in NK cells is not implicated in cytotoxicity inhibition by HLA-G. Our findings may suggest the important role played by NF–κB activation after soluble HLA-G stimulation in other NK cells function.     

Pro-inflammatory cytokines and microRNAs in male infertility

Molecular Biology Reports - Male infertility is a problem that affects 10–15% of men of reproductive age. In particular, gametogenesis is a complex process in which inflammation may play a...     

A High Throughput Genotyping Approach Reveals Distinctive Autosomal Genetic Signatures for European and Near Eastern Wild Boar

The lack of a Near Eastern genetic signature in modern European porcine breeds indicates that, although domestic pigs from the Fertile Crescent entered Europe during the Neolithic, they were completely replaced by their European counterparts in a short window of time. Whilst the absence of such genetic signature has been convincingly demonstrated at the mitochondrial level, variation at the autosomal genomes of European and Near Eastern Sus scrofa has not been compared yet. Herewith, we have explored the genetic relationships among 43 wild boar from Europe (N = 21), Near East (N = 19) and Korea (N = 3), and 40 Iberian (N = 16), Canarian (N = 4) and Mangalitza (N = 20) pigs by using a high throughput SNP genotyping platform. After data filtering, 37,167 autosomal SNPs were used to perform population genetics analyses. A multidimensional scaling plot based on genome-wide identity-by-state pairwise distances inferred with PLINK showed that Near Eastern and European wild boar populations are genetically differentiated. Maximum likelihood trees built with TreeMix supported this conclusion i.e. an early population split between Near Eastern and European Sus scrofa was observed. Moreover, analysis of the data with Structure evidenced that the sampled Iberian, Canarian and Mangalitza pigs did not carry any autosomal signature compatible with a Near Eastern ancestry, a finding that agrees well with previous mitochondrial studies.     

Carotid artery mechanical properties and stresses quantified using in vivo data from normotensive and hypertensive humans

The goal of this study was to model the in vivo non-linear mechanical behavior of human common carotid arteries (CCAs) and then to compare wall stresses and associated contributions of micro-constituents in normotensive (NT) and treated hypertensive (HT) subjects. We used an established theoretical model of 3D arterial mechanics that assumes a hyperelastic, anisotropic, active–passive, and residually stressed wall. In vivo data were obtained non-invasively from CCAs in 16 NT (21–64 years old) and 25 treated HT (44–69 years old) subjects. The associated quasi-static boundary value problem was solved semi-analytically over a cardiac cycle while accounting for surrounding perivascular tissue. Best-fit values of model parameters, including those describing contributions by intramural elastin, fibrillar collagen, and vascular smooth muscle, were estimated by a non-linear least-squares method. The model (1) captured temporal changes in intraluminal pressure, (2) estimated wall stress fields that appeared to reflect the presence or absence of age and disease, and (3) suggested changes in mechanical characteristics of wall micro-constituents despite medical treatment of hypertension. For example, age was positively correlated with residual stresses and altered fibrillar collagen in NT subjects, which indirectly validated the modeling, and HT subjects had higher levels of stresses, increased smooth muscle tone, and a stiffer elastin-dominated matrix despite treatment. These results are consistent with prior reports on effects of age and hypertension, but provide increased insight into evolving contributions of cell and matrix mechanics to arterial behavior in vivo.