Background: The purpose of this study was to assess postsurgical outcomes in active patients after primary repair of acute and chronic proximal hamstring tears. Hypothesis: Surgical treatment of both acute and chronic proximal hamstring avulsion injuries would result in improved patient outcomes using validated outcome scores and a hamstring-specific questionnaire, and operative repair of these injuries results in excellent outcomes with a high level of patient satisfaction, pain relief, and return to function. Study Design: Case series; Level of evidence, 4. Methods: Fifty-two patients who underwent proximal hamstring repair (26 male and 26 female; average age, 47.7 years) completed the Lower Extremity Functional Scale (LEFS), a custom LEFS, the Marx Activity Scale, a custom Marx scale, a proximal hamstring score (which combines the sum of the custom LEFS and Marx), and a proximal hamstring questionnaire with subjective questions. Forty patients were characterized as having acute repairs, and 12 patients had chronic repairs. All patients underwent surgical repair with 5 suture anchors on the ischial tuberosity through a transverse incision. The rehabilitation protocol was also similar with the use of a hip orthosis for 6 to 8 weeks, allowing progressive weightbearing and range of motion. Results: The mean follow-up in our study was 33 months (range, 12-76 months). The mechanism of injury in 28 patients was eccentric hip flexion and knee extension in the ipsilateral knee typically caused by a slip and fall accident. One patient’s injury was caused by trauma to the proximal hamstring. In 23 patients, hamstring injuries were sports related. Overall, 51 (98%) were satisfied with their outcome after surgery. The LEFS, Marx, custom LEFS, custom Marx, and proximal hamstring scores for patients with acute injuries were 76.2, 10.0, 71.4, 20, and 91.7, respectively. For those with chronic injury, the scores were 71.5, 10.4, 70.8, 18.7, and 89.8, respectively. The scores were not statistically different for LEFS, Marx, custom LEFS, and proximal hamstring scores ( P = .22, P = .6, P = .72, and P = .6, respectively). Patients with acute injury did have a greater custom Marx score ( P = .001). Postoperatively, 5 patients (9.6%) had burning pain or numbness in the posterior thigh or foot, and 25 (48%) had at least some discomfort sitting. Thirty-five patients (67%) reported they could participate in strenuous activities at their latest follow-up. All patients estimated their strength recovery at ≥75%. Conclusion: Results of this study indicate successful outcomes for both acute and chronic repairs, although patients with the acute repairs had higher functional and hamstring scores, and estimated hamstring strength.

To determine whether changes in glycogen synthase kinase-3beta (GSK-3beta) phosphorylation contribute to muscle hypertrophy, we delineated the effects of GSK-3beta activity on C(2)C(12) myotube size. We also examined possible insulin-like growth factor I (IGF-I) signaling of NFAT (nuclear factors of activated T cells)-inducible gene activity and possible modulation of NFAT activation by GSK-3beta. Application of IGF-I (250 ng/ml) or LiCl (10 mM) alone (i.e., both inhibit GSK-3beta activity) increased the area of C(2)C(12) myotubes by 80 and 85%, respectively. The application of IGF-I (250 ng/ml) elevated GSK-3beta phosphorylation and reduced GSK-3beta kinase activity by approximately 800% and approximately 25%, respectively. LY-294002 (100 microM) and wortmannin (150 microM), specific inhibitors of phosphatidylinositol 3'-kinase, attenuated IGF-I-induced GSK-3beta phosphorylation by 67 and 92%, respectively. IGF-I suppressed the kinase activity of GSK-3beta. IGF-I (250 ng/ml), but not LiCl (10 mM), induced an increase in NFAT-activated luciferase reporter activity. Cotransfection of a constitutively active GSK-3beta (cGSK-3beta) inhibited the induction by IGF-I of NFAT-inducible reporter activity. LiCl, which inhibits GSK-3beta, removed the block by cGSK-3beta on IGF-I-inducible NFAT-responsive reporter gene activity. These data suggest that the IGF-I-induced increase in skeletal myotube size is signaled, in part, through the inhibition of GSK-3beta.

IV.

Currently, the repertoire of cellular and molecular pathways that control skeletal muscle atrophy and hypertrophy are not well defined. It is possible that intracellular regulatory signaling pathways are active at different times during the muscle hypertrophy process. The hypothesis of the given experiments was that cellular signals related to protein translation would be active at early time points of skeletal muscle regrowth, whereas transcriptional signals would be active at later time points of skeletal muscle regrowth. The phosphorylation status of p38 MAPK and JNK increased at the end of limb immobilization but returned to control values at recovery day 3. Transient increases in phosphorylation and in protein concentration occurred during recovery of soleus muscle mass. Phosphorylation of Akt, p70S6k, and signal transducer and activator of transcription 3 (STAT3) peaked on recovery day 3 compared with day 0. Glycogen synthase kinase (GSK)-3beta phosphorylation was increased on the sixth and fifteenth recovery day. In addition, transient peaks in seven protein concentrations occurred at different times of recovery: STAT3, calcineurin A (CaNA), CaNB, and beta4E-BP1 protein concentrations peaked on the third recovery day; p70S6k, STAT3, Akt, and GSK3-beta peaked on the sixth recovery day; and GSK3-beta peaked on the fifteenth recovery day. The apexes of STAT3 and GSK3-beta protein concentrations remained elevated for two recovery time points. Thus the time course of increase in molecules of signaling pathways differed as the young rat soleus muscle regrew from an atrophied state.

Root tears are a subset of meniscal injuries that result in significant knee joint pathology. Occurring on either the medial or lateral side, root tears are defined as radial tears or avulsions of the posterior horn attachment to bone. After a root tear, there is a significant increase in tibio-femoral contact pressure concomitant with altered knee joint kinematics. Previous cadaver studies from our institution have shown that root repair of the medial meniscus is successful in restoring joint biomechanics to within normal limits. Indications for operative management of meniscal root tears include (1) a symptomatic medial meniscus root tear with minimal arthritis and having failed non-operative treatment, and (2) a lateral root tear in associated with an ACL tear. In this review, we describe diagnosis, imaging, patient selection, and arthroscopic surgical technique of medial and lateral meniscus root injuries. In addition we highlight the pearls of repair technique, associated complications, post-operative rehabilitation regimen, and expected outcomes.

Our previous transgenic analyses revealed that a 600-base pair ␤-myosin heavy chain (␤MyHC) promoter conferred mechanical overload (MOV) and non-weightbearing (NWB) responsiveness to a chloramphenicol acetyltransferase reporter gene. Whether the same DNA regulatory element(s) direct ␤MyHC expression following MOV or NWB activity in vivo remains unknown. We now show that a 293-base pair ␤MyHC promoter fused to chloramphenicol acetyltransferase (␤293) responds to MOV, but not NWB activity, indicating a segregation of these two diverse elements. Inclusion of the ␤MyHC negative regulatory element (؊332 to ؊300; ␤NRE) within transgene ␤350 repressed expression in all transgenic lines. Electrophoretic mobility shift assays showed highly enriched binding activity only in NWB soleus nuclear extracts that was specific to the distal region of the ␤NRE sense strand (d␤NRE-S; ؊332 to ؊311). Supershift electrophoretic mobility shift assay revealed that the binding at the distal region of the ␤NRE sense strand was antigenically distinct from cellular nucleic acidbinding protein and Y-box-binding factor 1, two proteins shown to bind this element. Two-dimensional UV crosslinking and shift Southwestern blotting analyses detected two proteins (50 and 52 kDa) that bind to this element. These in vivo results demonstrate that segregated ␤MyHC promoter elements transcriptionally regulate ␤MyHC transgene expression in response to two diverse modes of neuromuscular activity.The sarcomeric myosin heavy chain (MyHC) 1 is a major contractile protein that is encoded by a multigene family constituted by eight members (1). Each member has been shown to be responsive to a complex set of intrinsic and extrinsic signals that collectively regulate their expression in a defined developmental stage-and muscle fiber type-specific pattern. Within the MyHC gene family, the ␤MyHC is the one member whose regulated expression in both cardiac and skeletal muscle has been most extensively studied. Expression of the ␤MyHC gene has been detected in the ventricular myocardium and skeletal muscles comprising the hind limb of fetal mice, whereas in the adult, its expression is primarily restricted to skeletal muscles or muscle regions composed predominately of slow twitch type I fibers (2, 3). In vitro investigations of the control of ␤MyHC gene transcription have led to the identification of a control region located within the proximal promoter (nucleotides Ϫ300 to Ϫ188 of the human ␤MyHC gene) region (4 -7). This control region was found to be composed of three discrete DNA regulatory elements termed MCAT-like, C-rich and ␤e3, which are highly conserved in location and sequence across species (4 -7). The absolute requirement for these elements to obtain high levels of gene expression was demonstrated in transient transfection studies where the independent disruption of any of these conserved elements decreased and/or abolished musclespecific expression of ␤MyHC reporter genes (4 -7).Located just upstream from the ␤MyHC control region is a highly conserved ne...

Athletes underwent revision arthroscopic posterior capsulolabral repair at an incidence of 6.4%. Revision patients had significantly poorer outcome scores and return to play when compared with those who did not undergo revision surgery with risk factors being dominant shoulder surgery, female sex, concomitant rotator cuff injury, the use of 3 or fewer anchors, and smaller glenoid bone width. These data are essential for patient selection, optimal treatment techniques, and patient education as posterior shoulder instability failure requiring revision has not previously been evaluated.

Perioperative nerve blocks provide effective pain management after hip arthroscopy but must be used with caution to decrease risk of falls. Intra-articular and portal site injections with local anesthetics and preoperative celecoxib can decrease opioid consumption. There is a lack of high-quality evidence on this topic, and further research is needed to determine the best approach to manage postoperative pain and optimize patient satisfaction.