PubMed · 10088430
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T Harada. 1999. [Acute tonsillitis].. https://pubmed.ncbi.nlm.nih.gov/10088430/
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Previous studies have shown that proinflammatory cytokines, such as tumor necrosis factor (TNF), are expressed after acute hemodynamic overloading and myocardial ischemia/infarction. To define the role of TNF in the setting of ischemia/infarction, we performed a series of acute coronary artery occlusions in mice lacking one or both TNF receptors. Left ventricular infarct size was assessed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-type (both TNF receptors present) and mice lacking either the type 1 (TNFR1), type 2 (TNFR2), or both TNF receptors (TNFR1/TNFR2). Left ventricular infarct size as assessed by TTC staining was significantly greater (P < 0.005) in the TNFR1/TNFR2-deficient mice (77.2% +/- 15.3%) when compared with either wild-type mice (46.8% +/- 19.4%) or TNFR1-deficient (47.9% +/- 10.6%) or TNFR2-deficient (41.6% +/- 16.5%) mice. Examination of the extent of necrosis in wild-type and TNFR1/TNFR2-deficient mice by anti-myosin Ab staining demonstrated no significant difference between groups; however, the peak frequency and extent of apoptosis were accelerated in the TNFR1/TNFR2-deficient mice when compared with the wild-type mice. The increase in apoptosis in the TNFR1/TNFR2-deficient mice did not appear to be secondary to a selective up-regulation of the Fas ligand/receptor system in these mice. These data suggest that TNF signaling gives rise to one or more cytoprotective signals that prevent and/or delay the development of cardiac myocyte apoptosis after acute ischemic injury.
In this study, experimental allergic encephalomyelitis (EAE) rats and rats exhibiting EAE expressing high circulating anti-nerve growth factor antibody were daily monitored for clinical signs and chronic relapses. Eighty-five days after EAE induction, blood, spinal cord and brain stem were used for histological examination, nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) evaluation. The results showed that NGF-deprived rats display more severe clinical signs of disease. These effects were associated with a significant reduction of NGF in the brain stem and spinal cord but not of BDNF, which decreased only in spinal cord. These observations provide additional support to the hypothesis of a protective NGF role in rats exhibiting EAE.
STUDY DESIGN: A correlative design using stepwise regression analysis. OBJECTIVE: To explore the variation in spinal isometric strength that can be accounted for by anticipation of pain, sensory perception of pain, functional disability belief, and the fear-avoidance belief in chronic low back pain patients. SUMMARY OF THE BACKGROUND DATA: Several biobehavioral factors contribute to the persistence of pain behavior in chronic patients. Recent studies suggest a need to explore the relation between reduced physical performance and the sensory and cognitive perception of pain. METHODS: Sixty-three patients with chronic low back pain 20 to 56 years of age participated in this study. Visual Analogs Scales, the Fear-Avoidance Belief questionnaire, and the Disability Belief questionnaire were used to measure the sensory and cognitive dimensions of pain. Spinal isometric strength was measured by the Medx lumbar extension machine. RESULTS: Analysis of variance and the stepwise regression analysis demonstrated that anticipation of pain and the fear-avoidance belief about physical activity significantly predicted variation in the spinal isometric strength deficit P < 0. 001. True pain experienced during the testing and answers to the Disability Belief questionnaire were not related. CONCLUSION: The results of this study strongly support the hypothesis that spinal physical capacity in chronicity is not explained solely by the sensory perception of pain. The anticipation of pain and the fear-avoidance belief about physical activities were the strongest predictors of the variation in physical performance.