A novel mechatronic system for evaluating elbow muscular spasticity relying on Tonic Stretch Reflex Threshold estimation

Muscular spasticity represents one of the most common motor disorder associated to lesions of the Central Nervous System, such as Stroke, and affects joint mobility up to the complete prevention of skeletal muscle voluntary control. Its clinical evaluation is hence of fundamental relevance for an effective rehabilitation of the affected subjects. Standard assessment protocols are usually manually performed by humans, and hence their reliability strongly depends on the capabilities of the clinical operator performing the procedures. To overcome this limitation, one solution is the usage of mechatronic devices based on the estimation of the Tonic Stretch Reflex Threshold, which allows for a quite reliable and operator-independent evaluation. In this work, we present the design and characterization of a novel mechatronic device that targets the estimation of the Tonic Stretch Reflex Threshold at the elbow level, and, at the same time, it can potentially act as a rehabilitative system. Our device can deliver controllable torque/velocity stimulation and record functional parameters of the musculo-skeletal system (joint position, torque, and multi-channel ElectroMyoGraphyc patterns), with the ultimate goals of: i) providing significant information for the diagnosis and the classification of muscular spasticity, ii) enhancing the recovery evaluation of patients undergoing through therapeutic rehabilitation procedures and iii) enabling a future active usage of this device also as therapeutic tool.Clinical relevance - The contribution presented in this work proposes a technological advancement for a device-based evaluation of motion impairment related to spasticity, with a major potential impact on both the clinical appraisal and the rehabilitation procedures

Dental Disorders and Salivary Changes in Patients with Laryngopharyngeal Reflux

Background: Laryngopharyngeal reflux (LPR) is a common inflammatory condition of the upper aerodigestive tract tissues related to the effects of gastroduodenal content reflux, characterized by a wide variety of clinical manifestations. The aim of our study was to evaluate the possible association between dental disorders and LRP, focusing on the role of salivary changes. Methods: Patient’s dental status was evaluated according to Schiff Index Sensitivity Scale (SISS), Basic Erosive Wear Examination (BEWE) and Decayed, Missing, and Filled Teeth (DMFT) scores. Reflux-associated symptoms were assessed according to Reflux symptom index (RSI). A qualitative and quantitative examination of saliva was performed. Results: Patients suffering from LPR had a higher incidence of dental disorders, regardless the presence of salivary pepsin, and thus, statistically significant higher scores of RSI (p = 0.0001), SISS (p = 0.001), BEWE (p < 0.001) and VAS (p < 0.001). Moreover, they had lower salivary flow compared with healthy patients. Conclusions: The finding of demineralization and dental caries on intraoral evaluation must raise the suspicion of LRP. Reflux treatments should also be aimed at correcting salivary alterations, in order to preserve the buffering capacity and salivary pH, thus preventing mucosal and dental damage

Search for the standard model Higgs boson in ℓν+jets final states in 9.7 fb(−1) of pp-bar collisions with the D0 detector

This is the publisher's version, also available electronically from http://journals.aps.org/prd/abstract/10.1103/PhysRevD.88.052008.We present, in detail, a search for the standard model Higgs boson, H, in final states with a charged lepton (electron or muon), missing energy, and two or more jets in data corresponding to 9.7  fb(−1) of integrated luminosity collected at a center-of-mass energy of s√=1.96  TeV with the D0 detector at the Fermilab Tevatron pp-bar Collider. The search uses b-jet identification to categorize events for improved signal versus background separation and is sensitive to associated production of the H with a W boson, WH→ℓνbb-bar; gluon fusion with the Higgs decaying to W-boson pairs, H→WW→ℓνjj; and associated production with a vector boson where the Higgs decays to W-boson pairs, VH→VWW→ℓνjjjj production (where V=W or Z). We observe good agreement between data and expected background. We test our method by measuring WZ and ZZ production with Z→bb-bar and find production rates consistent with the standard model prediction. For a Higgs boson mass of 125 GeV, we set a 95% C.L. upper limit on the production of a standard model Higgs boson of 5.8×σSM, where σSM is the standard model Higgs boson production cross section, while the expected limit is 4.7×σ(SM). We also interpret the data considering models with fourth generation fermions, or a fermiophobic Higgs boson

Moraxella catarrhalis acquisition, airway inflammation and protease-antiprotease balance in chronic obstructive pulmonary disease

<p>Abstract</p> <p>Background</p> <p><it>Moraxella catarrhalis </it>causes approximately 10% of exacerbations in chronic obstructive pulmonary disease (COPD) and also colonizes the lower airway in stable patients. Little is known about the effects of colonization by <it>M. catarrhalis </it>on airway inflammation and protease-antiprotease balance, and how these changes compare to those seen during exacerbations. Since COPD is a progressive inflammatory disease, elucidating the effects of bacterial colonization and exacerbation on airway inflammation is relevant to understanding disease progression in COPD. Our aims were (1) Analyze changes in airway inflammation in colonization and exacerbation of COPD due to <it>M. catarrhalis</it>; (2) Explore protease-antiprotease balance in colonization and exacerbation due to <it>M. catarrhalis</it>. Our hypothesis were (1) Acquisition of a new strain of M. catarrhalis in COPD increases airway inflammation from baseline and alters the protease-antiprotease balance towards a more proteolytic environment; (2) These changes are greater during exacerbations associated with <it>M. catarrhalis </it>as compared to colonization.</p> <p>Methods</p> <p>Thirty-nine consecutive COPD patients with 76 acquisitions of a new strain of <it>M. catarrhalis </it>over a 6-year period were identified in a prospective study. Seventy-six pre-acquisition sputum supernatant samples, obtained just before acquisition of <it>M catarrhalis</it>, and 76 acquisition samples (34 were associated with exacerbation, 42 with colonization) were analyzed for IL-8, TNF-α, Neutrophil Elastase (NE) and Secretory leukocyte protease inhibitor (SLPI). Changes were compared in paired samples from each patient.</p> <p>Results</p> <p>IL-8, TNF-α and NE were significantly elevated after acquisition of <it>M. catarrhalis</it>, compared to pre-acquisition samples (p =< 0.001 for all three). These changes were present in colonization (p = 0.015 for IL-8; p =< 0.001 for TNF-α and NE) as well as in exacerbation (p =< 0.001 for all three), compared to pre-acquisition levels. SLPI was significantly lower after acquisition (p =< 0.001), in colonization (p =< 0.001) as well as in exacerbation (p = 0.004), compared to pre-acquisition levels. SLPI levels correlated negatively with NE levels (R²= 0.07; p = 0.001).</p> <p>Conclusion</p> <p>Acquisition of <it>M. catarrhalis </it>in COPD causes increased airway inflammation and worsening protease-antiprotease imbalance during exacerbations and also in colonization, even in the absence of increased symptoms. These effects could contribute to progression of airway disease in COPD.</p

Neutrophil elastase reduces secretion of secretory leukoproteinase inhibitor (SLPI) by lung epithelial cells: role of charge of the proteinase-inhibitor complex

<p>Abstract</p> <p>Background</p> <p>Secretory leukoproteinase inhibitor (SLPI) is an important inhibitor of neutrophil elastase (NE), a proteinase implicated in the pathogenesis of lung diseases such as COPD. SLPI also has antimicrobial and anti-inflammatory properties, but the concentration of SLPI in lung secretions in COPD varies inversely with infection and the concentration of NE. A fall in SLPI concentration is also seen in culture supernatants of respiratory cells exposed to NE, for unknown reasons. We investigated the hypothesis that SLPI complexed with NE associates with cell membranes <it>in vitro</it>.</p> <p>Methods</p> <p>Respiratory epithelial cells were cultured in the presence of SLPI, varying doses of proteinases over time, and in different experimental conditions. The likely predicted charge of the complex between SLPI and proteinases was assessed by theoretical molecular modelling.</p> <p>Results</p> <p>We observed a rapid, linear decrease in SLPI concentration in culture supernatants with increasing concentration of NE and cathepsin G, but not with other serine proteinases. The effect of NE was inhibited fully by a synthetic NE inhibitor only when added at the same time as NE. Direct contact between NE and SLPI was required for a fall in SLPI concentration. Passive binding to cell culture plate materials was able to remove a substantial amount of SLPI both with and without NE. Theoretical molecular modelling of the structure of SLPI in complex with various proteinases showed a greater positive charge for the complex with NE and cathepsin G than for other proteinases, such as trypsin and mast cell tryptase, that also bind SLPI but without reducing its concentration.</p> <p>Conclusion</p> <p>These data suggest that NE-mediated decrease in SLPI is a passive, charge-dependent phenomenon <it>in vitro</it>, which may correlate with changes observed <it>in vivo</it>.</p