Column-editor : Susan M. Kleiner
Jeffrey B. Driban, Easwaran Balasubramanian, Mamta Amin, Michael R. Sitler, Marvin C. Ziskin and Mary F. Barbe
Joint trauma is a risk factor for osteoarthritis (OA), which is becoming an increasingly important orthopedic concern for athletes and nonathletes alike. For advances in OA prevention, diagnosis, and treatment to occur, a greater understanding of the biochemical environment of the affected joint is needed.
To demonstrate the potential of a biochemical technique to enhance our understanding of and diagnostic capabilities for osteoarthritis.
Outpatient orthopedic practice.
8 subjects: 4 OA-knee participants (65 ± 6 y of age) and 4 normal-knee participants (54 ± 10 y) with no history of knee OA based on bilateral standing radiographs.
The independent variable was group (OA knee, normal knee).
Main Outcome Measures:
16 knee synovial-protein concentrations categorized as follows: 4 as pro-inflammatory, or catabolic, cytokines; 5 as anti-inflammatory, or protective, cytokines; 3 as catabolic enzymes; 2 as tissue inhibitors of metalloproteinases [TIMPs]; and 2 as adipokines.
Two anti-inflammatory cytokines (interleukin [IL]-13 and osteoprotegerin) and a pro-inflammatory cytokine (IL-1β) were significantly lower in the OA knees. Two catabolic enzymes (matrix metalloproteinase [MMP]-2 and MMP-3) were significantly elevated in OA knees. TIMP-2, an inhibitor of MMPs, was significantly elevated in OA knees.
Six of the 16 synovial-fluid proteins were significantly different between OA knees and normal knees in this study. Future research using a similar multiplex ELISA approach or other proteomic techniques may enable researchers and clinicians to develop more accurate biochemical profiles of synovial fluid to help diagnose OA, identify subsets of OA or individual characteristics, guide clinical decisions, and identify patients at risk for OA after knee injury.
Column-editor : Susan Kleiner
Zeynep Hazar Kanik, Seyit Citaker, Canan Yilmaz Demirtas, Neslihan Celik Bukan, Bulent Celik and Gurkan Gunaydin
, maximal isometric quadriceps strength, vertical jump height, and blood analyses (creatine kinase [CK], lactate dehydrogenase [LDH], myoglobin, and C-reactive protein). Power analysis indicated that the required sample size to evaluate a time × group interaction (with 80% of statistical power and P < .05
Lijing Wang, Ligong Duan, Xukun Li and Guoping Li
Calpains and calpastatin can degrade muscle proteins, but no research has investigated the expression pattern of calpains and calpastatin after exhaustive exercise.
To investigate the alterations in expression of μ-, m-, and n-calpain and calpastatin after exhaustive exercise and its association with muscle injury.
64 rats divided into 2 groups, a nonexercise control group and an acute-exhaustive-exercise (AEE) group. Biopsies in the AEE group were taken at different times after exercise.
Calpastatin protein expression and m-calpain activity increased early after exercise, but both n-calpain protein expression and μ-calpain activity generally decreased with time. n-Calpain mRNA expression was down- regulated from late after exercise.
The increased m-calpain activity might promote muscle-protein degradation and muscle injury. On the contrary, calpastatin might execute a protective function against muscle injury. The change in p-calpain activity was found earlier than muscle injury and therefore might serve as a useful predictor of muscle injury.
Emily R. Hunt, Shelby E. Baez, Anne D. Olson, Timothy A. Butterfield and Esther Dupont-Versteegden
immediately after the insult modulates the potentially damaging inflammatory processes. 30 , 31 Increases in peak torque seen after massage suggest that it also can accelerate muscle recovery and hasten the return of normal function. 23 Moreover, massage also induces an upregulation of protein synthesis and
Walter Herzog, Timothy R. Leonard, Venus Joumaa and Ashi Mehta
According to the cross-bridge theory, the steady-state isometric force of a muscle is given by the amount of actin–myosin filament overlap. However, it has been known for more than half a century that steady-state forces depend crucially on contractile history. Here, we examine history-dependent steady-state force production in view of the cross-bridge theory, available experimental evidence, and existing explanations for this phenomenon. This is done on various structural levels, ranging from the intact muscle to the myofibrillar and isolated contractile protein level, so that advantages and limitations of the various preparations can be fully exploited and overcome. Based on experimental evidence, we conclude that steady-state force following active muscle stretching is enhanced, and this enhancement has a passive and an active component. The active component is associated with the cross-bridge kinetics, and the passive component is associated with a calcium-dependent increase in titin stiffness.
João C. Dias, Melissa W. Roti, Amy C. Pumerantz, Greig Watson, Daniel A. Judelson, Douglas J. Casa and Lawrence E. Armstrong
Dieticians, physiologists, athletic trainers, and physicians have recommended refraining from caffeine intake when exercising because of possible fluid-electrolyte imbalances and dehydration.
To assess how 16-hour rehydration is affected by caffeine ingestion.
59 college-age men.
Subjects consumed a chronic caffeine dose of 0 (placebo), 3, or 6 mg · kg−1 · day−1 and performed an exercise heat-tolerance test (EHT) consisting of 90 minutes of walking on a treadmill (5.6 km/h) in the heat (37.7 °C).
There were no between-group differences immediately after and 16 hours after EHT in total plasma protein, hematocrit, urine osmolality, specific gravity, color, and volume. Body weights after EHT and the following day (16 hours) were not different between groups (P > .05).
Hydration status 16 hours after EHT did not change with chronic caffeine ingestion.
Zhongren Sun, Xiaoning Li, Zhiqiang Su, Ying Zhao, Li Zhang and Mingyuan Wu
Bone marrow stromal cells (BMSCs) can be differentiated into neuronal cells and are used to treat spinal cord injury (SCI).
This study investigated whether electroacupuncture enhances BMSC’s effects on SCI in rats.
The effects of transplantation of phosphate-buffered saline or BMSC, electroacupuncture, and a combination of BMSC transplantation and electroacupuncture on SCI were evaluated using a combined behavioral score (CBS). Expressions of neuronal marker neuron-specific enolase (NSE) and gliocyte-specific marker glial fibrillary acidic protein (GFAP) of transplanted BMSC were detected using immunohistochemistry to assess the effect of electroacupuncture on differentiation of BMSC into neuronal cells.
The combination of BMSC transplantation and electroacupuncture significantly alleviated CBS in rats with SCI compared with the separate treatment of BMSC or electroacupuncture. In addition, electroacupuncture increased the NSE- and GFAP-positive transplanted BMSCs in spinal cord.
Combined treatment showed a better effect, and the mechanisms may be partially caused by enhanced differentiation of BMSC into neuronal cells. Future studies are needed to confirm this.
Tessa Gordon, Esther Udina, Valerie M.K. Verge and Elena I. Posse de Chaves
Injured peripheral but not central nerves regenerate their axons but functional recovery is often poor. We demonstrate that prolonged periods of axon separation from targets and Schwann cell denervation eliminate regenerative capacity in the peripheral nervous system (PNS). A substantial delay of 4 weeks for all regenerating axons to cross a site of repair of sectioned nerve contributes to the long period of separation. Findings that 1h 20Hz bipolar electrical stimulation accelerates axon outgrowth across the repair site and the downstream reinnervation of denervated muscles in rats and human patients, provides a new and exciting method to improve functional recovery after nerve injuries. Drugs that elevate neuronal cAMP and activate PKA promote axon outgrowth in vivo and in vitro, mimicking the electrical stimulation effect. Rapid expression of neurotrophic factors and their receptors and then of growth associated proteins thereafter via cAMP, is the likely mechanism by which electrical stimulation accelerates axon outgrowth from the site of injury in both peripheral and central nervous systems.