84 research outputs found

    Uniqueness in the determination of loads in multi-span beams and plates

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    Most of the results available on the inverse problem of determining loads acting on elastic beams or plates under transverse vibration refer to single beam or single plate. In this paper, we consider the determination of sources in multi-span systems obtained by connecting either two Euler-Bernoulli elastic beams or two rectangular Kirchhoff-Love elastic plates. The material of the structure is assumed to be homogeneous and isotropic. The transverse load is of the form g(t)f(x), where g(t) is a known function of time and f(x) is the unknown term depending on the position variable x. Under slight a priori assumptions, we prove a uniqueness result for f(x) in terms of observations of the dynamic response taken at interior points of the structure in an arbitrary small interval of time. A numerical implementation of the method is included to show the possible application of the results in the practical identification of the source term

    Chronic Multiple Knee Ligament Injuries: Epidemiological Analysis of More Than One Hundred Cases

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    INTRODUCTION: Diagnosis and treatment of multiple ligament injuries of the knee remain a real challenge for most surgeons. OBJECTIVE: To find out the epidemiological profile of patients surgically treated at a Reference Service with more than one chronic ligament injury in the knee joint. MATERIALS AND METHODS: Of a total of 978 operated patients, 109 presented at least two associated ligament injuries in the same knee. Demographic and clinical variables were evaluated. RESULTS: The anterior cruciate ligament group presented a larger number of cases of ligament injuries related with sports practice and falls, while the posterior cruciate ligament and anterior cruciate ligament + posterior cruciate ligament groups presented more cases related to traffic accidents and trauma with object (weight on the knee) (p<0.001). The varus group presented significantly higher values of time since injury (p<0.01). In the group with new anterior cruciate ligament injury (neoligament) associated with other ligament injuries the disruption times were higher, showing statistical significance (p<0.001). CONCLUSIONS: Anterior cruciate ligament injury associated with other ligament injuries other than posterior cruciate ligament injury are related to sports practice and falls. Posterior cruciate ligament injury associated to other ligament injuries, including or not anterior cruciate ligament injury, are related to traffic accidents and direct trauma caused by an object on the knee. Significant delay between primary ligament injuries and their reconstructions generates varus deformity of the affected knee. In spite of the large delay in seeking medical treatment, few patients with neoligament anterior cruciate ligament injury and other combined disruptions will develop varus deformity

    Nuclear Factor (NF) κB polymorphism is associated with heart function in patients with heart failure

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    <p>Abstract</p> <p>Background</p> <p>Cardiac remodeling is generally an adverse sign and is associated with heart failure (HF) progression. NFkB, an important transcription factor involved in many cell survival pathways, has been implicated in the remodeling process, but its role in the heart is still controversial. Recently, a promoter polymorphism associated with a lesser activation of the <it>NFKB1 </it>gene was also associated with Dilated Cardiomyopathy. The purpose of this study was to evaluate the association of this polymorphism with clinical and functional characteristics of heart failure patients of different etiologies.</p> <p>Methods</p> <p>A total of 493 patients with HF and 916 individuals from a cohort of individuals from the general population were investigated. The <it>NFKB1 </it>-94 insertion/deletion ATTG polymorphism was genotyped by High Resolution Melt discrimination. Allele and genotype frequencies were compared between groups. In addition, frequencies or mean values of different phenotypes associated with cardiovascular disease were compared between genotype groups. Finally, patients were prospectively followed-up for death incidence and genotypes for the polymorphism were compared regarding disease onset and mortality incidence in HF patients.</p> <p>Results</p> <p>We did not find differences in genotype and allelic frequencies between cases and controls. Interestingly, we found an association between the ATTG<sub>1</sub>/ATTG<sub>1 </sub>genotype with right ventricle diameter (<it>P </it>= 0.001), left ventricle diastolic diameter (P = 0.04), and ejection fraction (EF) (P = 0.016), being the genotype ATTG<sub>1</sub>/ATTG<sub>1 </sub>more frequent in patients with EF lower than 50% (<it>P </it>= 0.01). Finally, we observed a significantly earlier disease onset in ATTG1/ATTG<sub>1 </sub>carriers.</p> <p>Conclusion</p> <p>There is no genotype or allelic association between the studied polymorphism and the occurrence of HF in the tested population. However, our data suggest that a diminished activation of <it>NFKB1</it>, previously associated with the ATTG<sub>1</sub>/ATTG<sub>1 </sub>genotype, may act modulating on the onset of disease and, once the individual has HF, the genotype may modulate disease severity by increasing cardiac remodeling and function deterioration.</p

    FAM5C Contributes to Aggressive Periodontitis

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    Aggressive periodontitis is characterized by a rapid and severe periodontal destruction in young systemically healthy subjects. A greater prevalence is reported in Africans and African descendent groups than in Caucasians and Hispanics. We first fine mapped the interval 1q24.2 to 1q31.3 suggested as containing an aggressive periodontitis locus. Three hundred and eighty-nine subjects from 55 pedigrees were studied. Saliva samples were collected from all subjects, and DNA was extracted. Twenty-one single nucleotide polymorphisms were selected and analyzed by standard polymerase chain reaction using TaqMan chemistry. Non-parametric linkage and transmission distortion analyses were performed. Although linkage results were negative, statistically significant association between two markers, rs1935881 and rs1342913, in the FAM5C gene and aggressive periodontitis (p = 0.03) was found. Haplotype analysis showed an association between aggressive periodontitis and the haplotype A-G (rs1935881-rs1342913; p = 0.009). Sequence analysis of FAM5C coding regions did not disclose any mutations, but two variants in conserved intronic regions of FAM5C, rs57694932 and rs10494634, were found. However, these two variants are not associated with aggressive periodontitis. Secondly, we investigated the pattern of FAM5C expression in aggressive periodontitis lesions and its possible correlations with inflammatory/immunological factors and pathogens commonly associated with periodontal diseases. FAM5C mRNA expression was significantly higher in diseased versus healthy sites, and was found to be correlated to the IL-1β, IL-17A, IL-4 and RANKL mRNA levels. No correlations were found between FAM5C levels and the presence and load of red complex periodontopathogens or Aggregatibacter actinomycetemcomitans. This study provides evidence that FAM5C contributes to aggressive periodontitis

    Invariant Natural Killer T Cell Agonist Modulates Experimental Focal and Segmental Glomerulosclerosis

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    A growing body of evidence demonstrates a correlation between Th2 cytokines and the development of focal and segmental glomerulosclerosis (FSGS). Therefore, we hypothesized that GSL-1, a monoglycosylceramide from Sphingomonas ssp. with pro-Th1 activity on invariant Natural Killer T (iNKT) lymphocytes, could counterbalance the Th2 profile and modulate glomerulosclerosis. Using an adriamycin(ADM)-based model of FSGS, we found that BALB/c mice presented albuminuria and glomerular degeneration in association with a Th2-like pro-fibrogenic profile; these mice also expressed a combination of inflammatory cytokines, such as IL-4, IL-1α, IL-1β, IL-17, TNF-α, and chemokines, such as RANTES and eotaxin. In addition, we observed a decrease in the mRNA levels of GD3 synthase, the enzyme responsible for GD3 metabolism, a glycolipid associated with podocyte physiology. GSL-1 treatment inhibited ADM-induced renal dysfunction and preserved kidney architecture, a phenomenon associated with the induction of a Th1-like response, increased levels of GD3 synthase transcripts and inhibition of pro-fibrotic transcripts and inflammatory cytokines. TGF-β analysis revealed increased levels of circulating protein and tissue transcripts in both ADM- and GSL-1-treated mice, suggesting that TGF-β could be associated with both FSGS pathology and iNKT-mediated immunosuppression; therefore, we analyzed the kidney expression of phosphorylated SMAD2/3 and SMAD7 proteins, molecules associated with the deleterious and protective effects of TGF-β, respectively. We found high levels of phosphoSMAD2/3 in ADM mice in contrast to the GSL-1 treated group in which SMAD7 expression increased. These data suggest that GSL-1 treatment modulates the downstream signaling of TGF-β through a renoprotective pathway. Finally, GSL-1 treatment at day 4, a period when proteinuria was already established, was still able to improve renal function, preserve renal structure and inhibit fibrogenic transcripts. In conclusion, our work demonstrates that the iNKT agonist GSL-1 modulates the pathogenesis of ADM-induced glomerulosclerosis and may provide an alternative approach to disease management
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