Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated patellofemoral osteoarthritis can be a disabling disease. When conservative treatment fails, surgical options can be unpredictable and may be considered too aggressive for middle-aged and active people. We analysed the clinical and radiological results of a new coronal osteotomy involving thinning of the patella in a selected group of patients with isolated patellofemoral osteoarthritis. Since 1991, 31 patients (35 knees) have been treated, of whom 34 were available for follow-up at a mean of 9.1 years. The Knee Society Score, the Patellar score and the Short-form-36 questionnaire were used for clinical evaluation. We also examined the radiological features to confirm bone consolidation and assess the progression of osteoarthritis. A significant improvement in the functional scores and radiological parameters was noted. All patients except one were satisfied with the operation. Radiological progression of the patellofemoral osteoarthritis was slowed but radiological femorotibial osteoarthritis progressed in 23 (65%) cases, with a total knee replacement becoming necessary in four cases without technical problems in resurfacing the patella. We compared the results with other forms of surgical treatment reported in the literature. This treatment offers good clinical and radiological results, presenting an alternative method of managing patellofemoral osteoarthritis.
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PMID:The patellar thinning osteotomy in patellofemoral arthritis: four to 18 years' follow-up. 2088 76

Heart failure is a progressive and disabling disease. The incidence of heart failure is also on the rise, particularly in the elderly of industrialized societies. This is in part due to an increased ageing population, whom initially benefits from improved, and life-extending cardiovascular therapy, yet ultimately succumb to myocardial failure. A major cause of heart failure is ischemia secondary to the sequence of events that is dyslipidemia, atherosclerosis, and myocardial infarction. In the case of heart failure postmyocardial infarction, ischemia can lead to myocardial cell death by both necrosis and apoptosis. The extent of myocyte death postinfarction is associated with adverse cardiac remodeling that can contribute to progressive heart chamber dilation, ventricular wall thinning, and the onset of loss of cardiac function. In cardiomyocytes, recent studies indicate that myocardial ischemic injury activates the unfolded protein stress response (UPR) and this is associated with increased apoptosis. This paper focuses on the intersection of ischemia, the UPR, and cell death in cardiomyocytes. Targeting of the myocardial UPR may prove to be a viable target for the prevention of myocyte cell loss and the progression of heart failure due to ischemic injury.
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PMID:The Myocardial Unfolded Protein Response during Ischemic Cardiovascular Disease. 2253 6