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Related Lesions (relate + lesion)
Selected AbstractsSuperficial digital flexor tendon lesions in racehorses as a sequela to muscle fatigue: A preliminary studyEQUINE VETERINARY JOURNAL, Issue 6 2007M. T. Butcher Summary Reasons for performing study: Racing and training related lesions of the forelimb superficial digital flexor tendon are a common career ending injury to racehorses but aetiology and/or predisposing causes of the injury are not completely understood. Objectives: Although the injury takes place within the tendon, the lesion must be considered within the context of the function of the complete suspensory system of the distal limb, including the associated muscles. Methods: Both muscle and tendon function were investigated in vivo using implanted strain gauges in 3 Thoroughbred horses walking, trotting and cantering on a motorised treadmill. These data were combined with assessments of muscle architecture and fibre composition to arrive at an overview of the contribution of each muscle-tendon unit during locomotion. Results: The superficial digital flexor muscle has fatigue-resistant and high force production properties that allow its tendon to store and return elastic energy, predominantly at the trot. As running speed increases, deep digital flexor tendon force increases and it stabilises hyperextension of the fetlock, thus reinforcing the superficial digital flexor in limb load support. The deep digital flexor muscle has fast contracting properties that render it susceptible to fatigue. Conclusion: Based on these measurements and supporting evidence from the literature, it is proposed that overloading of the superficial digital flexor tendon results from fatigue of the synergistic, faster contracting deep digital flexor muscle. Potential relevance: Future research investigating distal limb system function as a whole should help refine clinical diagnostic procedures and exercise training approaches that will lead to more effective prevention and treatment of digital flexor tendon injuries in equine athletes. [source] Neuropathology of Alzheimer's DiseaseMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 1 2010Daniel P. Perl MD Abstract Alois Alzheimer first pointed out that the disease which would later bear his name has a distinct and recognizable neuropathological substrate. Since then, much has been added to our understanding of the pathological lesions associated with the condition. The 2 primary cardinal lesions associated with Alzheimer's disease are the neurofibrillary tangle and the senile plaque. The neurofibrillary tangle consists of abnormal accumulations of abnormally phosphorylated tau within the perikaryal cytoplasm of certain neurons. The senile plaque consists of a central core of beta-amyloid, a 4-kD peptide, surrounded by abnormally configured neuronal processes or neurites. Other neuropathological lesions are encountered in cases of Alzheimer's disease, but the disease is defined and recognized by these 2 cardinal lesions. Other lesions include poorly understood changes such as granulovacuolar degeneration and eosinophilic rodlike bodies (Hirano bodies). The loss of synaptic components is a change that clearly has a significant impact on cognitive function and represents another important morphological alteration. It is important to recognize that distinguishing between Alzheimer's disease, especially in its early stages, and normal aging may be very difficult, particularly if one is examining the brains of patients who died at an advanced old age. It is also noted that instances of pure forms of Alzheimer's disease, in the absence of other coexistent brain disease processes, such as infarctions or Parkinson's disease,related lesions, are relatively uncommon, and this must be taken into account by researchers who employ postmortem brain tissues for research. Mt Sinai J Med 77:32&–42, 2010. © 2010 Mount Sinai School of Medicine [source] Defining the Canonical Form of T-Cell-Mediated Rejection in Human Kidney TransplantsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2010K. S. Famulski Banff defines T-cell-mediated rejection (TCMR) using nonspecific lesions and arbitrary cutoffs, with no external gold standard. We reexamined features of TCMR using exclusively molecular definition independent of histopathology. The definition was derived from mouse kidney transplants with fully developed TCMR, and is based on high expression of transcripts reflecting IFNG effects and alternative macrophage activation. In 234 human kidney transplant biopsies for cause phenotyped by microarrays, we identified 26 biopsies meeting these criteria. After excluding three biopsies with unrelated diseases, all 23 biopsies had typical Banff lesions of TCMR (inflammation, tubulitis), with v lesions in 10/23. Banff histopathology diagnosed 18 as TCMR, 1 as mixed and 4 as borderline. Despite marked changes in transcriptome indicating tissue injury and dedifferentiation, all kidneys with molecularly defined TCMR, even with v lesions or late rejection, demonstrated excellent recovery of function at 6 months with no graft loss (mean follow-up 2.5 years). Thus TCMR defined exclusively by molecules manifests TCMR,related lesions and function impairment, but good recovery and survival, even with late rejection or arteritis. This combination of pathologic, clinical and molecular features constitutes the typical or canonical T-cell-mediated rejection. [source] Apolipoprotein E,dependent accumulation of Alzheimer disease,related lesions begins in middle age,ANNALS OF NEUROLOGY, Issue 6 2009Eloise Kok BScHons Objective To study the prevalence and age dependency of senile plaques (SP) and neurofibrillary tangles (NFT), the brain changes characteristic of Alzheimer disease (AD), and their association with apolipoprotein E (APOE) genotypes in a community-dwelling normal population. Methods This neuropathological study used both silver staining and A, immunohistochemistry in brain tissue microarrays, including SP coverage and NFT counts from frontal cortex and hippocampus, and APOE genotyping, and was performed on a consecutive prospective series of 603 subjects (aged between 0 and 97 years) of an unselected population living outside of institutions. Cases were subjected to autopsy following sudden or unexpected out-of-hospital death, covering 22.1% of the mortality of Tampere, Finland and its surroundings. None died of AD, although 22 (3.7%) were demented and 10 (1.7%) had memory problems. Results Of the series, 30.8% had SP, and 42.1% had NFT; these occurred more commonly among females and showed a strong relationship with age. Both changes had already appeared at around 30 years of age, reaching an occurrence of almost 100% in the oldest. SP were more frequent in APOE ,4-carriers compared with noncarriers in every age group except the oldest (>90 years). The difference was most evident during the ages 50 to 59 years, where 40.7% of ,4-carriers had SP, compared with 8.2% in noncarriers (odds ratio, 8.39; 95% confidence interval, 2.55,27.62). The difference in NFT prevalence between APOE genotypes was not statistically significant in any age group. Interpretation The brain changes associated with AD may already begin developing early in middle age, especially among APOE ,4 carriers. Ann Neurol 2009;65:650,657 [source] | ||||||||||