Effect of Bisphosphonates on Anodized and Heatâ Treated Titanium Surfaces: An Animal Experimental Study

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141247/1/jper1035.pd

Mechanical Properties of Coal Ash Particle-Reinforced Recycled Plastic-Based Composites for Sustainable Railway Sleepers

This experimental research investigates the mechanical properties of municipal plastic waste-based particulate composites reinforced with coal ash (CA), the by-product of thermal power plants, for sustainable railway sleepers. Six series of sustainable composites filled with inorganic mineral fillers, including CA, were prepared by a twin-screw extruder and a compression molding machine. The effect of mix design variables-such as filler type, contents and the particle size of the filler-on mechanical properties-including tensile, compression and flexural properties-and morphology were characterized. The scanning electron microscopy (SEM) was employed to examine the morphology of the composites, which revealed the uniform dispersion of fillers in the polymer matrix. The study results conclude that the recycled plastic-based composite with the addition of CA up to 60% is suitable for railway sleeper applications. This experimental study may provide new insight into the railway applications of the developed composites under service loading conditions including traffic loading and earthquake

Homeobox gene Dlx-2 is implicated in metabolic stress-induced necrosis

<p>Abstract</p> <p>Background</p> <p>In contrast to tumor-suppressive apoptosis and autophagic cell death, necrosis promotes tumor progression by releasing the pro-inflammatory and tumor-promoting cytokine high mobility group box 1 (HMGB1), and its presence in tumor patients is associated with poor prognosis. Thus, necrosis has important clinical implications in tumor development; however, its molecular mechanism remains poorly understood.</p> <p>Results</p> <p>In the present study, we show that Distal-less 2 (Dlx-2), a homeobox gene of the Dlx family that is involved in embryonic development, is induced in cancer cell lines dependently of reactive oxygen species (ROS) in response to glucose deprivation (GD), one of the metabolic stresses occurring in solid tumors. Increased Dlx-2 expression was also detected in the inner regions, which experience metabolic stress, of human tumors and of a multicellular tumor spheroid, an <it>in vitro </it>model of solid tumors. Dlx-2 short hairpin RNA (shRNA) inhibited metabolic stress-induced increase in propidium iodide-positive cell population and HMGB1 and lactate dehydrogenase (LDH) release, indicating the important role(s) of Dlx-2 in metabolic stress-induced necrosis. Dlx-2 shRNA appeared to exert its anti-necrotic effects by preventing metabolic stress-induced increases in mitochondrial ROS, which are responsible for triggering necrosis.</p> <p>Conclusions</p> <p>These results suggest that Dlx-2 may be involved in tumor progression via the regulation of metabolic stress-induced necrosis.</p

Clinical and Radiological Outcomes of Modified Phemister Operation with Coracoclavicular Ligament Augmentation Using Suture Anchor for Acute Acromioclavicular Joint Dislocation

Background Modified Phemister operation has been widely used for the treatment of acute acromioclavicular (AC) joint dislocation. Additionally, the use of suture anchor for coracoclavicular (CC) fixation has been reported to provide CC stability. This study was conducted to evaluate the clinical and radiological results of a modified Phemister operation with CC ligament augmentation using suture anchor for acute AC joint dislocation. Methods Seventy-four patients underwent the modified Phemister operation with CC ligament augmentation using suture anchor for acute AC joint dislocation and were followed-up for an average of 12.3 months. The visual analogue scale (VAS), range of motion, Constant score, and Korean shoulder scoring system (KSS) were used for clinical assessment. Acromioclavicular interval (ACI), coracoclavicular distance (CCD), and acromioclavicular distance (ACD) were obtained to evaluate the radiological assessments. Results At the last follow-up, the mean VAS Score was 1.7 points, the mean joint range of the forward flexion was 164.6°, external rotation at the side was 61.2°, and internal rotation to the posterior was a level of T12. The mean Constant score and the mean KSS was 82.7 points and 84.2 points, respectively. At the mean ACI, CCD, and ACD, significant differences were found preoperatively and at the last follow-up. When the ACI, CCD, and ACD were compared with the contralateral unaffected shoulder at the last follow-up, the affected shoulders had significantly higher values. Conclusions The modified Phemister operation with CC ligament augmentation using suture anchor is clinically and radiologically effective at acute AC joint dislocation

Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration

Background: Perturbation in cell adhesion and growth factor signalling in satellite cells results in decreased muscle regenerative capacity. Cdon (also called Cdo) is a component of cell adhesion complexes implicated in myogenic differentiation, but its role in muscle regeneration remains to be determined. Methods: We generated inducible satellite cell-specific Cdon ablation in mice by utilizing a conditional Cdon allele and Pax7 CreERT2. To induce Cdon ablation, mice were intraperitoneally injected with tamoxifen (tmx). Using cardiotoxin-induced muscle injury, the effect of Cdon depletion on satellite cell function was examined by histochemistry, immunostaining, and 5-ethynyl-2&apos;-deoxyuridine (EdU) incorporation assay. Isolated myofibers or myoblasts were utilized to determine stem cell function and senescence. To determine pathways related to Cdon deletion, injured muscles were subjected to RNA sequencing analysis. Results: Satellite cell-specific Cdon ablation causes impaired muscle regeneration with fibrosis, likely attributable to decreased proliferation, and senescence, of satellite cells. Cultured Cdon-depleted myofibers exhibited 32 ± 9.6% of EdU-positive satellite cells compared with 58 ± 4.4% satellite cells in control myofibers (P &lt; 0.05). About 32.5 ± 3.7% Cdon-ablated myoblasts were positive for senescence-associated β-galactosidase (SA-β-gal) while only 3.6 ± 0.5% of control satellite cells were positive (P &lt; 0.001). Transcriptome analysis of muscles at post-injury Day 4 revealed alterations in genes related to mitogen-activated protein kinase signalling (P &lt; 8.29 e−5) and extracellular matrix (P &lt; 2.65 e−24). Consistent with this, Cdon-depleted tibialis anterior muscles had reduced phosphorylated extracellular signal-regulated kinase (p-ERK) protein levels and expression of ERK targets, such as Fos (0.23-fold) and Egr1 (0.31-fold), relative to mock-treated control muscles (P &lt; 0.001). Cdon-depleted myoblasts exhibited impaired ERK activation in response to basic fibroblast growth factor. Cdon ablation resulted in decreased and/or mislocalized integrin β1 activation in satellite cells (weak or mislocalized integrin1 in tmx = 38.7 ± 1.9%, mock = 21.5 ± 6%, P &lt; 0.05), previously linked with reduced fibroblast growth factor (FGF) responsiveness in aged satellite cells. In mechanistic studies, Cdon interacted with and regulated cell surface localization of FGFR1 and FGFR4, likely contributing to FGF responsiveness of satellite cells. Satellite cells from a progeria model, Zmpste24−/− myofibers, showed decreased Cdon levels (Cdon-positive cells in Zmpste24−/− = 63.3 ± 11%, wild type = 90 ± 7.7%, P &lt; 0.05) and integrin β1 activation (weak or mislocalized integrin β1 in Zmpste24−/− = 64 ± 6.9%, wild type = 17.4 ± 5.9%, P &lt; 0.01). Conclusions: Cdon deficiency in satellite cells causes impaired proliferation of satellite cells and muscle regeneration via aberrant integrin and FGFR signalling. © 2020 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley &amp; Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders1

Successful Hemostasis with Recombinant Activated Factor VII in a Patient with Massive Hepatic Subcapsular Hematoma

Recombinant activated coagulation factor VII (rFVIIa) is known to be effective in the management of acquired deficiencies of factor VII and platelet function defects. But recently, rFVIIa has been successfully used to treat ongoing bleeding in disseminated intravascular coagulopathy (DIC) condition. The patient reported here was suspected to be suffering from toxic hepatitis on admission. After percutaneous liver biopsy, bleeding occurred and did not stop even after right hepatic artery embolization. The patient developed a severe hemorrhage that resulted in hypovolemic shock, hemoperitoneum, and a massive subcapsular hematoma. The patient then developed DIC due to massive transfusion, as well as acute liver necrosis. The patient was given 400 μg/kg of rFVIIa. Recombinant factor VIIa was administered in an attempt to control the bleeding. This stabilized the hemoglobin levels of the patient. The patient gradually recovered in 4 months. In conclusion, this case suggests that rFVIIa can be successfully used for the hemostasis of uncontrolled bleeding in DIC

ZNF746/PARIS overexpression induces cellular senescence through FoxO1/p21 axis activation in myoblasts

Various stresses, including oxidative stress, impair the proliferative capacity of muscle stem cells leading to declined muscle regeneration related to aging or muscle diseases. ZNF746 (PARIS) is originally identified as a substrate of E3 ligase Parkin and its accumulation is associated with Parkinson’s disease. In this study, we investigated the role of PARIS in myoblast function. PARIS is expressed in myoblasts and decreased during differentiation. PARIS overexpression decreased both proliferation and differentiation of myoblasts without inducing cell death, whereas PARIS depletion enhanced myoblast differentiation. Interestingly, high levels of PARIS in myoblasts or fibroblasts induced cellular senescence with alterations in gene expression associated with p53 signaling, inflammation, and response to oxidative stress. PARIS overexpression in myoblasts starkly enhanced oxidative stress and the treatment of an antioxidant Trolox attenuated the impaired proliferation caused by PARIS overexpression. FoxO1 and p53 proteins are elevated in PARIS-overexpressing cells leading to p21 induction and the depletion of FoxO1 or p53 reduced p21 levels induced by PARIS overexpression. Furthermore, both PARIS and FoxO1 were recruited to p21 promoter region and Trolox treatment attenuated FoxO1 recruitment. Taken together, PARIS upregulation causes oxidative stress-related FoxO1 and p53 activation leading to p21 induction and cellular senescence of myoblasts. © 2020, The Author(s).1