A porous fibrous hyperelastic damage model for human periodontal ligament: Application of a microcomputerized tomography finite element model

The periodontal ligament (PDL) is a soft biological tissue that connects the tooth with the trabecular bone of the mandible. It plays a key role in load transmission and is primarily responsible for bone resorption and most common periodontal diseases. Although several numerical studies have analysed the biomechanical response of the PDL, most did not consider its porous fibrous structure, and only a few analysed damage to the PDL. This study presents an innovative numerical formulation of a porous fibrous hyperelastic damage material model for the PDL. The model considers two separate softening phenomena: fibre alignment during loading and fibre rupture. The parameters for the material model characterization were fitted using experimental data from the literature. Furthermore, the experimental tests used for characterization were computationally modelled to verify the material parameters. A finite element model of a portion of a human mandible, obtained by microcomputerized tomography, was developed, and the proposed constitutive model was implemented for the PDL. Our results confirm that damage to the PDL may occur mainly because of overpressure of the interstitial fluid, while large forces must be applied to damage the PDL fibrous network. Moreover, this study clarifies some aspects of the relationship between PDL damage and the bone remodelling process

Serum macrophage migration inhibitory factor (MIF) levels after allogeneic hematopoietic stem cell transplantation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72178/1/j.1751-553X.2007.01016.x.pd

Severe brain atrophy after long-term survival seen in siblings with familial amyotrophic lateral sclerosis and a mutation in the optineurin gene: a case series

<p>Abstract</p> <p>Introduction</p> <p>Previous studies have shown widespread multisystem degeneration in patients with sporadic amyotrophic lateral sclerosis who develop a total locked-in state and survive under mechanical ventilation for a prolonged period of time. However, the disease progressions reported in these studies were several years after disease onset. There have been no reports of long-term follow-up with brain imaging of patients with familial amyotrophic lateral sclerosis at an advanced stage of the disease. We report the cases of siblings with amyotrophic lateral sclerosis with homozygous deletions of the exon 5 mutation of the gene encoding optineurin, in whom brain computed tomography scans were followed up for more than 20 years.</p> <p>Case presentation</p> <p>The patients were a Japanese brother and sister. The elder sister was 33 years of age at the onset of disease, which began with muscle weakness of her left lower limb. Two years later she required mechanical ventilation. She became bedridden at the age of 34, and died at the age of 57. A computed tomography scan of her brain at the age of 36 revealed no abnormality. Atrophy of her brain gradually progressed. Ten years after the onset of mechanical ventilation, atrophy of her whole brain, including the cerebral cortex, brain stem and cerebellum, markedly progressed. Her younger brother was 36 years of age at the onset of disease, which presented as muscle weakness of his left upper limb. One year later, he showed dysphagia and dysarthria, and tracheostomy ventilation was performed. He became bedridden at the age of 37 and died at the age of 55. There were no abnormal intracranial findings on brain computed tomography scans obtained at the age of 37 years. At the age of 48 years, computed tomography scans showed marked brain atrophy with ventricular dilatation. Subsequently, atrophy of the whole brain rapidly progressed as in his elder sister.</p> <p>Conclusion</p> <p>We conclude that a homozygous deletion-type mutation in the optineurin gene may be associated with widespread multisystem degeneration in amyotrophic lateral sclerosis.</p

RESVERATROL INCLUSION COMPLEX WITH β-CYCLODEXTRIN (RCD): CHARACTERIZATION AND EVALUATION OF TOXICITY IN WISTAR RATS

Objective: The aim of this study was to characterise the resveratrol inclusion complex with β-cyclodextrin (RCD) and evaluate their toxicity in wistar rats.Methods: The RCD were prepared in ultra-turrax. For characterization of the RCD were used: Fourier transform infra-red Spectroscopy, Nuclear Magnetic Resonance (NMR), Differential Scanning Calorimetry (DSC) and X-ray powder diffraction. The RCD and others 4 treatments were performed by the chronic oral administration in 35 rats during 60 ds. After the treatments they were euthanized and the serum blood were collected to analyzed some hemogram and biochemical parameters including aspartyl aminotransferase (AST); alanine aminotransferase (AST); phosphatase alkaline (ALP); total bilirubin (TB); direct bilirubin (DB); total protein (TP); total cholesterol (TC), triacylglycerol (TAG), very low-density lipoprotein (VLDL), high-density lipoprotein (HDL), calcium, iron and phosphate using fully automated biochemistry analyzer.Results: The characterization results indicated a successful formation of the RCD. All hematological parameters analysed were within the normal values in all the groups. Furthermore, the hemogram and biochemical parameters were significantly (P&gt;0.05) similar to the control group.Conclusion: The daily oral administration during 60 d of RCD are not harmful on blood parameters of Wistar rats. Thus, RCD can be used safely for treatment of some metabolic diseases

Serum macrophage migration inhibitory factor reflects adrenal function in the hypothalamo-pituitary-adrenal axis of septic patients: an observational study

<p>Abstract</p> <p>Background</p> <p>The hypothalamo-pituitary-adrenal (HPA) axis modulates the inflammatory response during sepsis. Macrophage migration inhibitory factor (MIF), which counteracts the anti-inflammatory activity of glucocorticoid (GC), is one of the mediators of the development of inflammation. An inflammatory imbalance involving GC and MIF might be the cause or result of adrenal insufficiency. Our objective was to clarify the relationship between serum MIF and adrenal function in the HPA axis of sepsis patients using the adrenocorticotropic hormone (ACTH) stimulation test.</p> <p>Methods</p> <p>An observational study was performed in a university intensive care unit over a two-year period. Of 64 consecutive sepsis patients, 41 were enrolled. The enrolled patients underwent an ACTH stimulation test within 24 h of the diagnosis of severe sepsis or septic shock. Clinical and laboratory parameters, including serum MIF and cortisol, were measured.</p> <p>Results</p> <p>Based on their responses to the ACTH stimulation test, the patients were divided into a normal adrenal response (NAR) group (n = 22) and an adrenal insufficiency (AI) group (n = 19). The AI group had significantly more septic shock patients and higher prothrombin time ratios, serum MIF, and baseline cortisol than did the NAR group (<it>P </it>< 0.05). Serum MIF correlated significantly with the SOFA (Sequential Organ Failure Assessment) score, prothrombin time ratio, and delta max cortisol, which is maximum increment of serum cortisol concentration after ACTH stimulation test (rs = 0.414, 0.355, and -0.49, respectively, <it>P </it>< 0.05). Serum MIF also correlated significantly with the delta max cortisol/albumin ratio (rs = -0.501, <it>P </it>= 0.001). Receiver operating characteristic curve analysis identified the threshold serum MIF concentration (19.5 ng/mL, <it>P </it>= 0.01) that segregated patients into the NAR and AI groups.</p> <p>Conclusions</p> <p>The inverse correlation between serum MIF and delta max cortisol or the delta max cortisol/albumin ratio suggests that high serum MIF reflects an insufficient adrenal response in the HPA axis. Serum MIF could be a valuable clinical marker of adrenal insufficiency in sepsis patients.</p

Protection from Intracellular Oxidative Stress by Cytoglobin in Normal and Cancerous Oesophageal Cells

Cytoglobin is an intracellular globin of unknown function that is expressed mostly in cells of a myofibroblast lineage. Possible functions of cytoglobin include buffering of intracellular oxygen and detoxification of reactive oxygen species. Previous work in our laboratory has demonstrated that cytoglobin affords protection from oxidant-induced DNA damage when over expressed in vitro, but the importance of this in more physiologically relevant models of disease is unknown. Cytoglobin is a candidate for the tylosis with oesophageal cancer gene, and its expression is strongly down-regulated in non-cancerous oesophageal biopsies from patients with TOC compared with normal biopsies. Therefore, oesophageal cells provide an ideal experimental model to test our hypothesis that downregulation of cytoglobin expression sensitises cells to the damaging effects of reactive oxygen species, particularly oxidative DNA damage, and that this could potentially contribute to the TOC phenotype. In the current study, we tested this hypothesis by manipulating cytoglobin expression in both normal and oesophageal cancer cell lines, which have normal physiological and no expression of cytoglobin respectively. Our results show that, in agreement with previous findings, over expression of cytoglobin in cancer cell lines afforded protection from chemically-induced oxidative stress but this was only observed at non-physiological concentrations of cytoglobin. In addition, down regulation of cytoglobin in normal oesophageal cells had no effect on their sensitivity to oxidative stress as assessed by a number of end points. We therefore conclude that normal physiological concentrations of cytoglobin do not offer cytoprotection from reactive oxygen species, at least in the current experimental model

Macrophage Migration Inhibitory Factor Activates Hypoxia-Inducible Factor in a p53-Dependent Manner

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