Abstract-Accumulating data indicate that metabolic syndrome is an inflammatory condition. Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with nephritis and cardiovascular disease. Evidence suggests that individuals with SLE are at risk for developing insulin resistance; however, this has not been directly examined. Using an established mouse strain with SLE (NZBWF1), we examined whether SLE is associated with increased body weight and fat deposition. Mean arterial pressure was significantly increased (140Ϯ4 versus 114Ϯ2 mm Hg; nՆ5) in SLE mice by 36 weeks of age compared with control mice (NZW/LacJ). Body weight in SLE mice was higher at each age compared with controls by 12%, 22%, and 34% (nϾ30). Visceral adipose tissue weight was increased in SLE by 44%, 74%, and 117% at 8, 20, and 36 weeks, respectively (nՆ12 etabolic syndrome can be characterized by a group of metabolic risk factors that includes central obesity, insulin resistance, dyslipidemia, increased blood pressure, and endothelial dysfunction. 1 Individuals with metabolic syndrome are at a markedly increased risk for developing hypertension and renal disease. Recent evidence indicates that inflammatory cytokines are elevated in patients with metabolic syndrome, 2-4 thus suggesting a role for chronic inflammation as an underlying mechanism for progression of this disease.Systemic lupus erythematosus (SLE) is a chronic inflammatory disorder that predominantly affects women during their reproductive years. The presence of autoantibodies (typically antinuclear antibodies) is used diagnostically, and although SLE can influence many organ systems, the skin, joints, and kidneys are typically affected. Like metabolic syndrome, a large percentage of individuals with SLE are hypertensive. Evidence suggests that individuals with SLE are also at increased risk for developing insulin resistance 5 and changes in body mass composition 6 ; however, this has not been adequately examined.The purpose of the present study was to test whether the progression of SLE is associated with changes in body composition, insulin sensitivity, and other characteristics of the metabolic syndrome. To examine this, we used a genetic mouse model of SLE (NZBWF1) that exhibits many features of human SLE, including a complex genetic origin, a bias for the female sex, immune complex glomerulonephritis, and the presence of antinuclear antibodies. We reported recently that these mice have hypertension and impaired endothelialdependent relaxation. 7 The results of the present study show that NZBWF1 mice also have several other characteristics of the metabolic syndrome that may contribute to the hypertension, including central obesity, insulin resistance, and hyperleptinemia. These data show that the NZBWF1 strain may be an important model to study the effects of obesity and insulin resistance on SLE-associated hypertension. Methods AnimalsFemale NZBWF1 (SLE) and NZW/LacJ (control) obtained from Jackson Laboratories (Bar Harbor, ME) were maintained on a 12-hour light/d...
The scapula has long been recognized as a key component in shoulder motion and a crucial part of the kinetic chain connecting the body's core and upper extremity. The pectoralis minor (PM) has garnered increasing attention as we better understand scapular kinematics and its role in shoulder pain and dysfunction. This is particularly important in patients with scapular dyskinesis and especially in overhead throwing athletes. The most of these patients achieve their recovery goals through nonoperative management, stretching, and strengthening protocols; however, some patients do not respond to nonoperative modalities. Several studies have recently shown improvement in shoulder motion and outcome scores after open surgical release of the PM from its scapular attachment. Arthroscopic release of the PM can be accomplished in the lateral decubitus position with standard shoulder arthroscopic portals.
Is there a correlation between increased posterior-inferior tibial slope angle and noncontact anterior cruciate ligament (ACL) injury? Does increasing the posterior-inferior tibial slope angle increase the risk of bilateral ACL injury? A computerized relational database (Access 2007; Microsoft Inc, Redmond, Washington) was used to conduct a retrospective review of patients undergoing bilateral or unilateral ACL reconstruction surgery or treatment by a single surgeon between 1995 and 2013. Included in the study were patients with bilateral and unilateral ACL injuries and patellofemoral pain syndrome with no associated ACL deficiency. Exclusion criteria included concomitant ligament injury, previous ACL reconstruction, and previous knee surgery. Also excluded were patients who did not have plain lateral radiographs. Fifty patients were randomly selected from each group. After controlling for age and Tegner activity level, the authors found that the posterior-inferior tibial slope angle was a significant predictor (P=.002) of noncontact ACL injury. Mean posterior-inferior tibial slope angle for the bilateral, unilateral, and control groups was 11.8°±2.3°, 9.3°±2.4°, and 7.5°±2.3°, respectively. In the group with unilateral ACL injury vs the group without ACL deficiency, a 1° increase in posterior-inferior tibial slope angle (P=.03) was associated with a 20% increase in unilateral ACL injury. In those with bilateral ACL injury vs those without ACL deficiency, a 1° increase in posterior-inferior tibial slope angle (P=.001) increased bilateral knee injury by 34%. The difference between the mean angles of the control group without ACL deficiency and both the bilateral injury and unilateral injury cohorts was statistically significant (P=.003). Increased posterior-inferior tibial slope angle is associated with an increased risk of noncontact bilateral and unilateral ACL injury. [Orthopedics. 2017; 40(1):e136-e140.].
Treatment of symptomatic meniscal tears continues to evolve as we improve our understanding of the biomechanical role of the meniscus and its long-term importance to the health of the knee joint. Suture repair of meniscal tears is challenging, yet the incidence of repairs among our colleagues continues to rise as we aim to preserve meniscal tissue. Many elements of performing a repair are tedious and difficult, including proper meniscal preparation, reduction, mattress suture placement, and fixation. The tear pattern and location present another layer of difficulty. The most widely used all-inside repair devices are harpoon-style devices and present their own challenges in using them without causing harm to the meniscus and surrounding cartilage. In this article, we describe a simple all-inside meniscal repair technique to improve the reproducibility and reliability of meniscal repairs using an accessory midbody meniscal portal and a surgical probe. This ensures proper placement of mattress sutures in a reduced meniscus, with a reduced risk of collateral injury to the meniscus and articular cartilage. Furthermore, this surgical technique is adaptable to any meniscal fixation method to the medial or lateral meniscus.
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