Cross-cultural adaptation and validation of the Greek Version of the SARC-F for evaluating sarcopenia in Greek older adults

Objective:To translate and validate into Greek, the SARC-F questionnaire, a screening tool for sarcopenia.Methods:Questionnaire was back-translated and culturally adapted into Greek according to guidelines proposed by the World Health Organization. A convenience sample of 197 Greek elderly people (71.6±7.8 years, 68.5% women) was recruited, 64 of which were classified as persons at risk of sarcopenia according to the SARC-F. Internal consistency, test-retest and inter-rater reliability were evaluated. Validity (sensitivity, specificity, predictive positive value and predictive negative value) was assessed against the definition from the European Working Group of Sarcopenia in Older People (EWGSOP2), which is considered gold standard. Receiver-operating characteristic analysis was also performed to calculate the area under the curve.Results:SARC-F demonstrated high internal consistency (Cronbach’s alpha of 0.93) and excellent inter-rater and test-retest reliability, with intraclass correlation coefficient (ICC) of 0.91 (95% CI 0.79-0.96), and 0.93 (95% CI 0.91-0.95), respectively. According to the definition of sarcopenia from the EWGSOP2, 53 (26.85) participants were identified as probable sarcopenic and 23 (11.6%) as sarcopenic. Sensitivity of the tool for sarcopenia was 34.4 and specificity was 93.2. Positive predictive values were 26.4 and negative predictive values were 66.6%.Conclusion:Τhe SARC-F was successfully adapted into Greek language. The Greek SARC-F revealed low sensitivity but high specificity with EWGSOP2 sarcopenia definitions, indicating that it can detect with precision the absence of sarcopenia.     

Melatonin ameliorates cardiac remodelling in fructose-induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channels

Molecular Biology Reports - Metabolic syndrome comprises a group of disorders, including cardiac abnormalities. Ventricular arrhythmias observed in metabolic syndrome are due to the impaired...     

Protective role of zinc in liver damage in experimental diabetes demonstrated via different biochemical parameters

Diabetes mellitus is a serious worldwide metabolic disease, which is accompanied by hyperglycaemia and affects all organs and body system. Zinc (Zn) is a basic cofactor for many enzymes, which also plays an important role in stabilising the structure of insulin. Liver is the most important target organ after pancreas in diabetic complications. In this study, we aimed to investigate the protective role of Zn in liver damage in streptozotocin (STZ)‐induced diabetes mellitus. There are four experimental groups of female Swiss albino rats: group I: control; group II: control + ZnSO₄; group III: STZ‐induced diabetic animals and group IV: STZ‐diabetic + ZnSO₄. To induce diabetes, STZ was injected intraperitoneally (65 mg/kg). ZnSO₄ (100 mg/kg) was given daily to groups II and IV by gavage for 60 days. At the end of the experiment, rats were killed under anaesthesia and liver tissues were collected. In the diabetic group, hexose, hexosamine, fucose, sialic acid levels, arginase, adenosine deaminase, tissue factor activities and protein carbonyl levels increased, whereas catalase, superoxide dismutase, glutathione‐S‐transferase, glutathione peroxidase, glutathione reductase and Na⁺/K⁺‐ATPase activities decreased. The administration of Zn to the diabetic group reversed all the negative effects/activities. According to these results, we can suggest that Zn has a protective role against STZ‐induced diabetic liver damage.     

The effect of ellagic acid on caspase-3/bcl-2/Nrf-2/NF-kB/TNF-α /COX-2 gene expression product apoptosis pathway: a new approach for muscle damage therapy

Molecular Biology Reports - The goal of this study was to determine the protective role of ellagic acid (EA) against CCl4-induced muscle injury in rats. In this study, 36 Wistar albino rats...     

Protein Interactions and Fluctuations in a Proteomic Network using an Elastic Network Model

Abstract

A set of protein conformations are analyzed by normal mode analysis. An elastic network model is used to obtain fluctuation and cooperativity of residues with low amplitude fluctuations across different species. Slow modes that are associated with the function of proteins have common features among different protein structures. We show that the degree of flexibility of the protein is important for proteins to interact with other proteins and as the species gets more complex its proteins become more flexible. In the complex organism, higher cooperativity arises due to protein structure and connectivity.     

Altered -3 substrate specificity of Escherichia coli signal peptidase 1 mutants as revealed by screening a combinatorial peptide library

Signal peptidase functions to cleave signal peptides from preproteins at the cell membrane. It has a substrate specificity for small uncharged residues at -1 (P1) and aliphatic residues at the -3 (P3) position. Previously, we have reported that certain alterations of the Ile-144 and Ile-86 residues in Escherichia coli signal peptidase I (SPase) can change the specificity such that signal peptidase is able to cleave pro-OmpA nuclease A in vitro after phenylalanine or asparagine residues at the -1 position (Karla, A., Lively, M. O., Paetzel, M. and Dalbey, R. (2005) J. Biol. Chem. 280, 6731-6741). In this study, screening of a fluorescence resonance energy transfer-based peptide library revealed that the I144A, I144C, and I144C/I86T SPase mutants have a more relaxed substrate specificity at the -3 position, in comparison to the wild-type SPase. The double mutant tolerated arginine, glutamine, and tyrosine residues at the -3 position of the substrate. The altered specificity of the I144C/I86T mutant was confirmed by in vivo processing of pre-beta-lactamase containing non-canonical arginine and glutamine residues at the -3 position. This work establishes Ile-144 and Ile-86 as key P3 substrate specificity determinants for signal peptidase I and demonstrates the power of the fluorescence resonance energy transfer-based peptide library approach in defining the substrate specificity of proteases.     

Graded alterations of RBC aggregation influence in vivo blood flow resistance

Although the effects of red blood cell (RBC) aggregation on low-shear rate blood viscosity are well known, the effects on in vivo flow resistance are still not fully resolved. The present study was designed to explore the in vivo effects of RBC aggregation on flow resistance using a novel technique to enhance aggregation: cells are covalently coated with a block copolymer (Pluronic F-98) and then suspended in unaltered plasma. RBC aggregation was increased in graded steps by varying the Pluronic concentration during cell coating and was verified by microscopy and erythrocyte sedimentation rate (ESR), which increased by 200% at the highest Pluronic level. RBC suspensions were perfused through an isolated in situ guinea pig hindlimb preparation while the arterial perfusion pressure was held constant at 100 mmHg via a pressure servo-controlled pump. No significant effects of enhanced RBC aggregation were observed when studies were conducted in preparations with intact vascular control mechanisms. However, after inhibition of smooth muscle tone (using 10(-4) M papaverin), a significant change in flow resistance was observed in a RBC suspension with a 97% increase of ESR. Additional enhancements of RBC aggregation (i.e., 136 and 162% increases of ESR) decreased flow resistance almost to control values. This was followed by another significant increase in flow resistance during perfusion with RBC suspensions with a 200% increase of ESR. This triphasic effect of graded increases of RBC aggregation is most likely explained by an interplay of several hemodynamic mechanisms that are triggered by enhanced RBC aggregation.     

Fungal growth inside saline-filled implants and the role of injection ports in fungal translocation: in vitro study

Infection is a serious complication of breast augmentation and tissue expansion with inflatable devices. Several reports have shown that fungi may be able to survive, colonize, and even cause infection in saline-filled devices. The mechanism of how they penetrate, spread, and colonize inside the inflatable implants is not exactly understood. The authors assessed both the expander membrane and the port in terms of leakage and penetration of Candida albicans and Aspergillus niger in an in vitro model. Thirty saline-filled expanders connected to the injection port were placed in sterile containers filled with tryptic soy broth culture medium to simulate the clinical situation in phases I and II. Intact and multipunctured ports were used in the first and second phases of the study, respectively. Either the container or the implant was inoculated with one of these fungi, and six implants in containers without fungal inoculation served as controls. As a third phase, intraluminal survival of fungi was investigated in saline-filled containers (n = 12) in 21 days. The silicone membrane, with its intact connecting tube and port, was impermeable to these fungi, whereas both fungi were able to diffuse inside-out or outside-in through the punctured ports. C. albicans did not survive beyond 18 days in saline, whereas A. niger continued to multiply at day 21. Chemical analyses of the implant fluids revealed that the contents of the culture medium diffused into the implants in phases I and II. The data show that an intact silicone membrane is impermeable to fungi, and punctured ports allow translocation of fungi into the implants. Fungi can grow and reproduce in a saline-only environment, and their survival periods differ among the species. Furthermore, their survival may be enhanced by the influx of substances through the implant shell.     

Differential effects of mechanical ventilatory strategy on lung injury and systemic organ inflammation in mice

Patients with acute respiratory distress syndrome are at increased risk for developing multiorgan system dysfunction. The goal of this study was to establish an in vivo murine model to assess the differential effects of ventilation-protective strategies on the development of acute lung injury and systemic organ inflammation. C57B/6 mice were randomized to mechanical ventilation (MV) with conventional, high (17 ml/kg) or protective, low (6 ml/kg) tidal volume (VT) after intratracheal hydrochloric acid or no intervention. Mean arterial pressure was continuously monitored during MV and did not differ between groups. After 4 h, lung injury was assessed by measurement of wet/dry lung weight, lung lavage protein concentration and cell count, and histology. Concentration of IL-6, TNF-alpha, VEGF, and VEGF receptor-2 (VEGFR2) was measured in lung, liver, kidney, and heart. Results were compared with control, spontaneously breathing mice. Lung injury and altered pulmonary cytokine expression were not detected after MV of healthy mice with low or high VT. Although MV did not significantly alter IL-6 or TNF-alpha in systemic organs, VEGF concentration significantly increased in liver and kidney. After acid aspiration, mice ventilated with high VT manifested lung injury and increased IL-6 and VEGFR2 in lung, liver, and kidney, whereas VEGF increased only in liver and kidney. MV with low VT after acid aspiration attenuated lung injury, both IL-6 and VEGFR2 expression in lung and systemic organs, and hepatic, but not renal, increased VEGF. Our data suggest that MV strategy has differential effects on systemic inflammatory changes and thus may selectively predispose to systemic organ dysfunction.     

Partial rescue of functional interactions of a nonpalmitoylated mutant of the G-protein G alpha s by fusion to the beta-adrenergic receptor

Most heterotrimeric G-protein alpha subunits are posttranslationally modified by palmitoylation, a reversible process that is dynamically regulated. We analyzed the effects of Galpha(s) palmitoylation for its intracellular distribution and ability to couple to the beta-adrenergic receptor (betaAR) and stimulate adenylyl cyclase. Subcellular fractionation and immunofluorescence microscopy of stably transfected cyc(-) cells, which lack endogenous Galpha(s), showed that wild-type Galpha(s) was predominantly localized at the plasma membrane, but the mutant C3A-Galpha(s), which does not incorporate [(3)H]palmitate, was mostly associated with intracellular membranes. In agreement with this mislocalization, C3A-Galpha(s) showed neither isoproterenol- or GTPgammaS-stimulated adenylyl cyclase activation nor GTPgammaS-sensitive high-affinity agonist binding, all of which were present in the wild-type Galpha(s) expressing cells. Fusion of C3A-Galpha(s) with the betaAR [betaAR-(C3A)Galpha(s)] partially rescued its ability to induce high-affinity agonist binding and to stimulate adenylyl cyclase activity after isoproterenol or GTPgammaS treatment. In comparison to results with the WT-Galpha(s) and betaAR (betaAR-Galpha(s)) fusion protein, the betaAR-(C3A)Galpha(s) fusion protein was about half as efficient at coupling to the receptor and effector. Chemical depalmitoylation by hydroxylamine of membranes expressing betaAR-Galpha(s) reduced the high-affinity agonist binding and adenylyl cyclase activation to a similar degree as that observed in betaAR-(C3A)Galpha(s) expressing membranes. Altogether, these findings indicate that palmitoylation ensured proper localization of Galpha(s) and facilitated bimolecular interactions of Galpha(s) with the betaAR and adenylyl cyclase.