Implantação de controle de versão de software no subprojeto informatização do Siger.

Gerência de configuração de software. Gerência de configuração de software no subprojeto informatização do Siger. implantação de controle de versão no subprojeto informatização do Siger. Conclusões.bitstream/item/76661/1/CNPTIA-COM.TEC.-8-98.pd

Plantar Pressure Distribution Patterns During Gait in Diabetic Neuropathy Patients with a History of Foot Ulcers

OBJECTIVE: To investigate and compare the influence of a previous history of foot ulcers on plantar pressure variables during gait of patients with diabetic neuropathy. INTRODUCTION: Foot ulcers may be an indicator of worsening diabetic neuropathy. However, the behavior of plantar pressure patterns over time and during the progression of neuropathy, especially in patients who have a clinical history of foot ulcers, is still unclear. METHODS: Subjects were divided into the following groups: control group, 20 subjects; diabetic neuropathy patients without foot ulcers, 17 subjects; and diabetic neuropathy patients with at least one healed foot ulcer within the last year, 10 subjects. Plantar pressure distribution was recorded during barefoot gait using the Pedar-X system. RESULTS: Neuropathic subjects from both the diabetic neuropathy and DNU groups showed higher plantar pressure than control subjects. At midfoot, the peak pressure was significantly different among all groups: control group (139.4±76.4 kPa), diabetic neuropathy (205.3±118.6 kPa) and DNU (290.7±151.5 kPa) (p=0.008). The pressure-time integral was significantly higher in the ulcerated neuropathic groups at midfoot (CG: 37.3±11.4 kPa.s; DN: 43.3±9.1 kPa.s; DNU: 68.7±36.5 kPa.s; p=0.002) and rearfoot (CG: 83.3±21.2 kPa.s; DN: 94.9±29.4 kPa.s; DNU: 102.5±37.9 kPa.s; p=0.048). CONCLUSION: A history of foot ulcers in the clinical history of diabetic neuropathy subjects influenced plantar pressure distribution, resulting in an increased load under the midfoot and rearfoot and an increase in the variability of plantar pressure during barefoot gait. The progression of diabetic neuropathy was not found to influence plantar pressure distribution

Propriocepção na artroplastia total de joelho em idosos: uma revisão da literatura

Proprioception is the conscious or unconscious ability to perceive the motion and joint position through the articular mechanoreceptors. Proprioception is extremely important in geriatric patients, because such deficits may increase the risk of falls. Patients with total knee arthroplasty usually lose some proprioceptives afferents, and the consequences of this impairment are still contradictory among researchers. The posterior cruciate ligament is one of the primary stabilizers of the knee joint, andit may or may not be removed in total knee arthroplasty. The present paper reviewed the literature in order to discuss proprioception in patients with replaced knees. We also highlighted the importance of keeping the posterior cruciate ligament after surgery. Our conclusion raised controversial issues. However, most of the past studies agree that jointproprioception decreases after total knee arthroplasty and also agree on the importance to preserve posterior cruciate ligament.Propriocepção é a capacidade de perceber, de modo consciente ou inconsciente, o movimento e o posicionamento articular através dosmecanorreceptores articulares. Na população geriátrica, a propriocepção é extremamente importante, pois deficits aumentam os riscos para a queda. Em pacientes com artroplastia total de joelho, algumas aferênciasproprioceptivas são perdidas na cirurgia e suas conseqüências ainda geram controvérsias entre pesquisadores. O ligamento cruzado posterior é um elemento estabilizador primário do joelho que pode ser ou não preservado nas artroplastias totais. O presente trabalho buscou realizar uma revisão da literatura com o objetivo de rever a propriocepção em pacientes com artroplastia total de joelho, a partir do levantamento atual da literatura, e especificamente a importância da preservação do ligamento cruzado posterior nas próteses. A conclusão traz controvérsias, no entanto, a maioria dos autores defendem a idéia de que a artroplastia total de joelho diminui a propriocepção da articulação e que o ligamento cruzado posterior deve ser preservado sempre que possível

A novel role for the extracellular matrix glycoprotein-Tenascin-X in gastric function.

KEY POINTS: Tenascin X (TNX) functions in the extracellular matrix of skin and joints where it maintains correct intercellular connections and tissue architecture TNX is associated exclusively with vagal-afferent endings and some myenteric neurones in mouse and human stomach, respectively. TNX-deficient mice have accelerated gastric emptying and hypersensitivity of gastric vagal mechanoreceptors that can be normalized by an inhibitor of vagal-afferent sensitivity. Cultured nodose ganglion neurones showed no changes in response to capsaicin, cholecystokinin and potassium chloride in TNX-deficient mice. TNX-deficient patients have upper gastric dysfunction consistent with those in a mouse model. Our translational studies suggest that abnormal gastric sensory function may explain the upper gut symptoms present in TNX deficient patients, thus making it important to study gastric physiology. TNX deficiency should be evaluated routinely in patients with connective tissue abnormalities, which will enable a better understanding of its role and allow targeted treatment. For example, inhibitors of vagal afferents-baclofen could be beneficial in patients. These hypotheses need confirmation via targeted clinical trials. ABSTRACT: Tenascin-X (TNX) is a glycoprotein that regulates tissue structure via anti-adhesive interactions with collagen in the extracellular matrix. TNX deficiency causes a phenotype similar to hypermobility Ehlers-Danlos syndrome involving joint hypermobility, skin hyperelasticity, pain and gastrointestinal dysfunction. Previously, we have shown that TNX is required for neural control of the bowel by a specific subtype of mainly cholinergic enteric neurones and regulates sprouting and sensitivity of nociceptive sensory endings in mouse colon. These findings correlate with symptoms shown by TNX-deficient patients and mice. We aimed to identify whether TNX is similarly present in neural structures found in mouse and human gastric tissue. We then determined whether TNX has a functional role, specifically in gastric motor and sensory function and nodose ganglia neurones. We report that TNX was present in calretinin-immunoreactive extrinsic nerve endings in mouse and human stomach. TNX deficient mice had accelerated gastric emptying and markedly increased vagal afferent responses to gastric distension that could be rescued with GABAB receptor agonist. There were no changes in nodose ganglia excitability in TNX deficient mice, suggesting that vagal afferent responses are probably the result of altered peripheral mechanosensitivity. In TNXB-deficient patients, significantly greater symptoms of reflux, indigestion and abdominal pain were reported. In the present study, we report the first role for TNX in gastric function. Further studies are required in TNX deficient patients to determine whether symptoms can be relieved using GABAB agonists