No abstract available.
Malaria*

Deep infection of Achilles tendon is one of the serious complications that occur after open repair of the tendon. It sometimes leads to a very large tendon defect during the course of treatment. We report on a case of massive defect in Achilles tendon, which was successfully treated with Achilles tendon allograft and flexor hallucis longus tendon transfer.
Achilles Tendon* ; Allografts* ; Tendon Transfer ; Tendons*

Acute sprain of the ankle requires comprehensive history taking and physical examination in diagnosing the type of severity and deciding on the plan of treatment. Literature supports functional treatment as the treatment of choice for grade I and II injuries. During the acute phase, the goal of treatment focuses on controlling pain and swelling. PRICE (protection, rest, ice, compression, and elevation) is a well-established protocol at this phase. There is some evidence that application of ice and use of nonsteroidal anti-inflammatory drugs improves healing and speeds recovery. Then the functional treatment (motion restoration and strengthening exercises) is administered to progress the rehabilitation appropriately in order to facilitate healing and restore the mechanical strength and proprioception. Early mobilization has been shown to result in more rapid return to work and daily activities than immobilization. Grade III injuries still generate controversy in terms of the best management available, and more studies on early mobilization, cast immobilization, or surgery are needed. Even the Cochrane reviews published to date are not conclusive.
Ankle Injuries* ; Ankle* ; Diagnosis* ; Early Ambulation ; Ice ; Immobilization ; Physical Examination ; Proprioception ; Rehabilitation ; Return to Work ; Sprains and Strains

STUDY DESIGN: In vitro cell culture. PURPOSE: The purpose of the study was to investigate the effect of high glucose on premature stress-induced senescence of rat notochordal cells. OVERVIEW OF LITERATURE: Glucose-mediated increase of oxidative stress is a major causative factor for the development of diseases associated with diabetes mellitus such as senescence. However, no information is available for the effect of high glucose on premature stress-induced senescence of rat notochordal cells. METHODS: Notochordal cells were isolated from 4-week-old rats, cultured and placed in either 10% fetal bovine serum (FBS, normal control) or 10% FBS plus two high glucose concentrations (0.1 M and 0.2 M, experimental conditions) for 1 and 3 days. We identified and quantified the mitochondrial damage (mitochondrial transmembrane potential), reactive oxygen species (ROS) and antioxidants, such as manganese superoxide dismutase (MnSOD) and catalase, for each condition. We also identified and quantified senescence and telomerase activity. Finally, we determined the expression of proteins related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB) pathways. RESULTS: Two high glucose concentrations enhanced the disruption of mitochondrial transmembrane potential and excessive generation of ROS in notochordal cells for 1 and 3 days, respectively. The expressions of MnSOD and catalase were increased in notochordal cells treated with both high glucose concentrations at 1 and 3 days. The telomerase activity declined at 1 and 3 days. Two high glucose concentrations increased the occurrence of stress-induced senescence of notochordal cells by p16-pRB pathways at 1 and 3 days. CONCLUSIONS: Despite compensatory expression of antioxidants, high glucose-induced oxidative stress accelerates stress-induced senescence in rat notochordal cells. This may result in dysfunction of notochordal cells, leading to accelerated premature disc degeneration. The prevention of excessive generation of oxidative stress by strict blood glucose control is important to prevent or to delay premature disc degeneration in young patients with diabetes mellitus.
Aging* ; Animals ; Antioxidants ; Blood Glucose ; Catalase ; Cell Aging ; Cell Culture Techniques ; Diabetes Mellitus ; Glucose* ; Humans ; Intervertebral Disc Degeneration ; Membrane Potentials ; Notochord* ; Oxidative Stress ; Rats* ; Reactive Oxygen Species ; Superoxide Dismutase ; Telomerase