Kinetic Monte Carlo theory of sliding friction

The sliding friction as a function of scanning velocity at the nanometer scale was simulated based on a modified one-dimensional Tomlinson model. Monte Carlo theory was exploited to describe the thermally activated hopping of the contact atoms, where both backward and forward jumps were allowed to occur. By comparing with the Monte Carlo results, improvements to current semiempirical solutions were made. Finally, experimental results of sliding friction on a NaCl(100) as a function of normal load and scanning velocity where successfully simulated. © 2009 The American Physical Society.Fil: Furlong, Octavio Javier. University of Wisconsin Milwaukee; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; ArgentinaFil: Manzi, Sergio Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; ArgentinaFil: Pereyra, Victor Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Matemática Aplicada de San Luis "Prof. Ezio Marchi". Universidad Nacional de San Luis. Facultad de Ciencias Físico, Matemáticas y Naturales. Instituto de Matemática Aplicada de San Luis "Prof. Ezio Marchi"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; ArgentinaFil: Bustos Giunta, Victor Angel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Luis. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich". Universidad Nacional de San Luis. Facultad de Ciencias Físico Matemáticas y Naturales. Instituto de Física Aplicada "Dr. Jorge Andrés Zgrablich"; ArgentinaFil: Tysoe, Wilfred T.. University of Wisconsin Milwaukee; Estados Unido

A role for apoptosis in temporomandibular joint disc degeneration. A contemporary review

The temporomandibular joint (TMJ) connects the mandible to the skull. TMJ disorders induce degenerative tissue changes in TMJ disc that are largely the result of maladaption to abnormal joint loading. Histopathological studies have documented an association between TMJ arthropathy and loss of tissue cellularity, via apoptosis-related processes, that result in diminished extracellular matrix generation, organization, and repair. However, the exact molecular mechanisms underpinning the development and progression of such degenerative changes are still unclear. We review the most recent findings regarding the involvement of apoptotic mechanisms in TMJ disc degeneration. Although a number of aspects of TMJ disc degeneration have been thoroughly investigated, data on the involvement of apoptotic mechanisms and their mediators are few and quite recent; indeed most of the research conducted on fibrous cartilage apoptosis has focused on the intervertebral disc

How to determine in a transparent and fair way the authors of a research paper

Para que una persona sea merecedora de la autoría de una investigación debe haber realizado alguna contribución académica sustancial para que esta pudiera llevarse a cabo y, además, ser capaz de dar cuenta públicamente de la integridad de sus procesos y sus resultados. Este artículo resume: 1) la matriz propuesta por L. W. Roberts para contribuir a definir las autorías durante las etapas iniciales de la investigación, 2) los criterios de autoría del Comité Internacional de Editores de Revistas Médicas para definir quiénes merecen dichos créditos y quiénes no, 3) la taxonomía de 14 roles propuesta por la Declaración CRediT para transparentar las tareas realizadas por cada una de las personas proclamadas autoras de una investigación biomédica y 4) las principales conductas que degradan la transparencia de las autorías.For a person to deserve an investigation authorship he/she must have made some substantial academic contribution so that that research could be carried out and, in addition, must be able to publicly account for the integrity of their processes and their results. This article summarizes: 1) the matrix proposed by Roberts to help defining authorship during the initial stages of the investigation; 2) authorship criteria of the International Committee of Medical Journal Editors to define who deserves such credits and who does not; 3) the 14-role taxonomy proposed by the CRediT Declaration to transparent the tasks performed by each of the proclaimed authors of a biomedical research; 4) the main behaviors that degrade the transparency of authorships.Fil: Terrasa, Sergio Adrian. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Italiano; ArgentinaFil: Posadas Martinez, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Italiano; ArgentinaFil: Giunta, Diego Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Italiano; Argentin

The Effects of Exercise and Kinesio Tape on Physical Limitations in Patients with Knee Osteoarthritis

(2) exercise KT with tension application (stabilizing effect) grou

Differential course of HIV-1 infection and apolipoprotein E polymorphism

Abstract We studied the course of infection with human immunodeficiency virus type 1 (HIV-1) in relation to apolipoprotein E (APOE) polymorphism found for 209 Italians treated at Infectious Disease Clinics in Rome and Modena. Clinically, patients were classified into four groups according to the yearly rate of decline in CD4+ cell count (LTNP: long-term non-progression; SLOW, 'NORMAL' or RAPID). Patients at both extremes of the clinical spectrum, i.e. those who rapidly progressed to AIDS and those with stable high CD4 cell counts, had few APOE ɛ4 and ɛ2 alleles (P = 0.04). Detailed clinical information was then used to construct four model-based clinical profiles using grade-of-membership analysis (GoM), predictive of APOE genotypic frequencies: 1. The clinical profile associated with good long-term prognosis lacked ɛ2 (P=0.01); 2. Disease progression to AIDS was associated with ɛ4 and ɛ2, most evident for zidovudine-lamivudine regimens without a protease inhibitor (P = 0.03); and, 3. AIDS patients had low ɛ4 and ɛ2 frequencies, consistent with a high mortality rate among ɛ4+ and ɛ2+ AIDS patients. These findings suggest allele-specific immunomodulatory effects involving inherited APOE isoform important enough to alter the clinical course of HIV infection and, possibly, drug efficacy. They imply a connection between lipid metabolism and immunity potentially relevant to common disorders

Is inflammaging an auto[innate]immunity subclinical syndrome?

The low-grade, chronic, systemic inflammatory state that characterizes the aging process (inflammaging) results from late evolutive-based expression of the innate immune system. Inflammaging is characterized by the complex set of five conditions which can be described as 1. low-grade, 2. controlled, 3. asymptomatic, 4. chronic, 5. systemic, inflammatory state, and fits with the antagonistic pleiotropy theory on the evolution of aging postulating that senescence is the late deleterious effect of genes (pro-inflammatory versus anti-inflammatory)that are beneficial in early life. Evolutionary programming of the innate immune system may act via selection on these genetic traits. Here I propose that the already acquired knowledge in this field may pave the way to a new chapter in the pathophysiology of autoimmunity: the auto-innate-immunity syndromes. Indeed, differently from the well known chapter of conventional autoimmune diseases and syndromes where the main actor is the adaptive immunity, inflammaging may constitute the subclinical paradigm of a new chapter of autoimmunity, namely that arising from an autoimmune inflammatory response of the innate-immune-system, an old actor of immunity and yet a new actor of autoimmunity, also acting as a major determinant of elderly frailty and age-associated diseases

Beneficial effects of PACAP in osteoarthritis cartilage. An “in vivo” and an “in vitro” morphological and biochemical study

Osteoarthritis (OA); the most common form of degenerative joint disease; is associated with variations in pro-inflammatory growth factor levels; inflammation and hypocellularity resulting from chondrocyte apoptosis (1). Pituitary adenylate cyclaseactivating polypeptide (PACAP) is a neuropeptide endowed with a range of trophic effects in several cell types; including chondrocytes (2). However; its role in OA has not been studied. To address this issue; we investigated whether PACAP expression is affected in OA cartilage obtained from experimentally-induced OA rat models; and then studied the effects of PACAP in isolated chondrocytes exposed to IL-1β in vitro to mimic the inflammatory milieu of OA cartilage. OA induction was established by histomorphometric and histochemical analyses. Changes in PACAP distribution in cartilage or its concentration in synovial fluid (SF) were assessed by immunohistochemistry and ELISA. Results showed that PACAP abundance in cartilage tissue and SF was high in healthy controls. OA induction decreased PACAP levels both in affected cartilage and SF. In vitro; PACAP prevented IL-1β-induced chondrocyte apoptosis; as determined by MTT assay; Hoechst staining and western blots of apoptotic-related proteins. These changes were also accompanied by decreased i-NOS and COX-2 levels; suggesting an anti-inflammatory effect. Altogether, these findings support a potential role for PACAP as a chondroprotective agent for the treatment of OA

Mesenchymal stem cell-based tissue engineering strategy for cartilage regeneration: A morphomolecular study

Articular cartilage is an avascular and aneural tissue with poor self-repair capacity. Pathological conditions leading to the cartilage degeneration, such as osteoarthritis (OA), have prompted the development of strategies aimed to its regeneration, such as mesenchymal stem cells (MSCs)-based tissue engineering approach. The aim of this study was to investigate if chondrocytes, differentiated from rat adipose tissue derived-MSCs (AMSCs) and seeded on Collagen Cell Carrier (CCC) scaffolds, are able to constitute a morphologically and biochemically healthy hyaline cartilage. To this purpose the AMSCs were primarily differentiated in chondrocytes through chondrogenic medium and subsequently cultured for 6 weeks on CCC scaffolds. The expression of osteoblast (Runt-related transcription factor 2 (RUNX2) and osteocalcin), chondrocyte (collagen I, II and lubricin) and apoptosis (caspase-3) biomarkers were evaluated in undifferentiated AMSCs, AMSCs-derived chondrocytes cultured in monolayer and AMSCs-derived chondrocytes seeded on CCC scaffolds, by different techniques such as immunohistochemistry, ELISA, Western blot and gene expression analyses. AMSCs-derived chondrocytes cultured on CCC scaffolds showed the increased expression of collagen II and lubricin, whereas the expression of collagen I, RUNX2, osteocalcin and caspase-3 resulted decreased when compared to the other groups. In conclusion, the results of this study suggest a possible role of AMSCs and the use of CCC scaffolds for therapeutic strategies aimed to the articular cartilage regeneration

The effects of physical activity (treadmill and vibration stimulation training) on Caspase-3 and Lubricin expression in articular cartilage in rats with glucorticoid-induced osteoarthritis

Glucocorticoids are considered the most powerful anti-inflammatory and immunomodulating drugs. However a number of side effects is well documented in different diseases, also in the articular cartilage where increase or decrease the synthesis of extracellular matrix components hormone dependent. The objective of this study has been to test the effects of procedures or drugs affecting bone metabolism on articular cartilage in rats with prednisolone-induced osteoarthritis and to evaluate the outcomes of physical activity on the articular cartilage by treadmill and vibration platform training. The animals were divided into 5 groups, bone and cartilage evaluations used whole-body scans, and histomorphometric analysis. Lubricin and caspase-3 expression were evaluated by immunohistochemistry, western blot analysis and biochemical analysis. These results confirm the beneficial effect of physical activity on the articular cartilage. The effects of drug therapy with glucocorticoids decrease the expression of lubricin and increase the expression of caspase-3 in the rats, while after physical activity the values return normal equipared to control group. Our findings suggest that it might be possible that the mechanical stimulation in the articular cartilage could release lubricin antibody that are capable of inhibiting caspase-3 activity preventing chondrocytes death. We can assume that the physiological balance between lubricin and caspase-3 could mantein the integrity of cartilage. So in certain diseases such as osteoporosis, mechanical stimulation could be a possible therapeutic treatment. With our results we can venture the hypothesis that a mild physical activity could also be used as a therapeutic treatment for cartilage disease such as osteoarthritis

EARLINET instrument intercomparison campaigns: Overview on strategy and results

This paper introduces the recent European Aerosol Research Lidar Network (EARLINET) quality-assurance efforts at instrument level. Within two dedicated campaigns and five single-site intercomparison activities, 21 EARLINET systems from 18 EARLINET stations were intercompared between 2009 and 2013. A comprehensive strategy for campaign setup and data evaluation has been established. Eleven systems from nine EARLINET stations participated in the EARLINET Lidar Intercomparison 2009 (EARLI09). In this campaign, three reference systems were qualified which served as traveling standards thereafter. EARLINET systems from nine other stations have been compared against these reference systems since 2009. We present and discuss comparisons at signal and at product level from all campaigns for more than 100 individual measurement channels at the wavelengths of 355, 387, 532, and 607 nm. It is shown that in most cases, a very good agreement of the compared systems with the respective reference is obtained. Mean signal deviations in predefined height ranges are typically below ±2 %. Particle backscatter and extinction coefficients agree within ±2  ×  10−4 km−1 sr−1 and ± 0.01 km−1, respectively, in most cases. For systems or channels that showed larger discrepancies, an in-depth analysis of deficiencies was performed and technical solutions and upgrades were proposed and realized. The intercomparisons have reinforced confidence in the EARLINET data quality and allowed us to draw conclusions on necessary system improvements for some instruments and to identify major challenges that need to be tackled in the future