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The occurrence and the consistency of the popliteomeniscal fascicle between the popliteus tendon and the lateral meniscus have been the subject of debate. It is difficult to diagnose and treat popliteomeniscal fascicle tears. Furthermore, popliteomeniscal fascicle tears are difficult to identify with arthroscopy. This article describes the diagnostic factors for popliteomeniscal fascicle tears and the safe, effective operative techniques that can be used for their treatment. We suggest that popliteomeniscal fascicle tears are diagnosed when the following 3 conditions are confirmed: (1) existence of mechanical symptoms such as pain, locking, and giving way in the lateral compartment of the knee; (2) identification of hypermobility of the lateral meniscus through arthroscopic probing; and (3) occurrence of an osteochondral lesion in the posterior area of the lateral femoral condyle. In the case of popliteomeniscal fascicle tears, the tear area can be repaired with a suture hook and polydioxanone with an all-inside technique. If the joint space is narrowing because of soft-tissue tightness, it can be repaired with a zone-specific cannula through an inside-out technique.

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BackgroundThe purpose of this study was to investigate the incidence of acromial fracture after reverse total shoulder arthroplasty (RTSA) and clinical and radiological outcomes of treatment of the fracture.MethodsA systematic review was performed to identify studies that reported the results of treatment of acromial fractures after RTSA. A literature search was conducted by two investigators using four databases (PubMed, Embase, Cochrane, and Ovid Medline).ResultsFifteen studies (2,857 shoulders) satisfied our inclusion criteria. The incidence of acromial fracture after RTSA was 4.0% (114 / 2,857). The mean age of the patients at the time of fracture was 72.9 years (range, 51 to 91 years). The mean time from RTSA to diagnosis of acromial fracture was 9.4 months (range, 1 to 94 months). One hundred shoulders (87.7%) were treated conservatively and 14 shoulders (12.3%) were treated surgically. The mean follow-up period after acromial fracture was 33.8 months. The overall union rate was 50.0% (43.8% for conservative treatment and 87.5% for operative treatment). The fracture incidence was significantly different among the medial glenoid and medial humerus prosthesis design (8.4%), the lateral glenoid and medial humerus design (4.0%), and the medial glenoid and lateral humerus design (2.8%). The mean values at final follow-up were as follows: visual analog scale score, 2.2; American Shoulder and Elbow Surgeons score, 59.1; Constant score, 59.7; and Simple Shoulder Test, 5.8. The mean forward flexion, abduction, and external rotation were 102.3°, 92.3°, and 25.8°, respectively.ConclusionsAcromial fractures after RTSA are a complication neither uncommon nor negligible. In the absence of studies with high-level evidence, there is a controversy on the outcomes after treatment. Further well-designed prospective randomized controlled studies with a long-term follow-up should be performed to ascertain the diagnosis, treatment, and prognosis of acromial fractures after RTSA.

Prolonged hyperglycemia results in pancreatic β-cell dysfunction and apoptosis, referred to as glucotoxicity. Although both oxidative and endoplasmic reticulum (ER) stresses have been implicated as major causative mechanisms of β-cell glucotoxicity, the reciprocal importance between the two remains to be elucidated. The aim of this study was to evaluate the differential effect of oxidative stress and ER stress on β-cell glucotoxicity, by employing melatonin which has free radical-scavenging and antioxidant properties. As expected, in β-cells exposed to prolonged high glucose levels, cell viability and glucose-stimulated insulin secretion (GSIS) were significantly impaired. Melatonin treatment markedly attenuated cellular apoptosis by scavenging reactive oxygen species via its plasmalemmal receptor-independent increase in antioxidant enzyme activity. However, treatments with antioxidants alone were insufficient to recover the impaired GSIS. Interestingly, 4-phenylbutyric acid (4-PBA), a chemical chaperone that attenuate ER stress by stabilizing protein structure, alleviated the impaired GSIS, but not apoptosis, suggesting that glucotoxicity induces oxidative and ER stress independently. We found that cotreatment of glucotoxic β-cells with melatonin and 4-PBA dramatically improved both their survival and insulin secretion. Taken together, these results suggest that ER stress may be the more critical mechanism for prolonged high-glucose-induced GSIS impairment, whereas oxidative stress appears to be more critical for the impaired β-cell viability. Therefore, combinatorial therapy of melatonin with an ER stress modifier may help recover pancreatic β-cells under glucotoxic conditions in type 2 diabetes.

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