Exercise hormone irisin prevents physical inactivity-induced cognitive decline in mice.

We previously reported that physical inactivity (PI) induces cognitive decline and depressive states, which were ameliorated by regular exercise. However, the mechanism underlying the preventive effect of exercise remains unelucidated. Irisin has recently been identified as an exercise-inducible myokine that improves cognitive impairment. Plasma irisin levels increase during physical exercise; therefore, PI could lead to a decline in cognitive function by reducing plasma irisin. Therefore, this study aimed to examine whether irisin is associated with cognitive decline and mental deterioration altered by PI and exercise. The mice were housed for eight weeks in the PI cage, whose living space was one-sixth that of a standard cage. Simultaneously, the mice were subjected to regular exercise in the presence or absence of an irisin-neutralizing antibody. PI increased the epididymal fat mass without increasing body weight, muscle mass, or plasma corticosterone levels. Additionally, PI induced anxiety, depressive states, and a decline in working memory. In contrast, regular exercise after PI elevated irisin levels in plasma and increased fibronectin type III domain-containing 5 (FNDC5) and peroxisome proliferator-activated receptor gammacoactivator 1α expression in skeletal muscle. Regular exercise also increased hippocampal brain-derived neurotrophic factor (BDNF) expression and BrdU-positive cells, alleviating cognitive decline and mental deterioration induced by PI. The beneficial effects of exercise were compromised by the administration of an irisin-neutralizing antibody. Moreover, plasma irisin level was positively correlated with working memory, hippocampal BDNF levels, and hippocampal cell proliferation. These findings suggest that exercise-inducible irisin is critical for maintaining cognitive function in the PI state.

Regular Low-Intensity Exercise Prevents Cognitive Decline and a Depressive-Like State Induced by Physical Inactivity in Mice: A New Physical Inactivity Experiment Model.

Regular exercise has already been established as a vital strategy for maintaining physical health via experimental results in humans and animals. In addition, numerous human studies have reported that physical inactivity is a primary factor that causes obesity, muscle atrophy, metabolic diseases, and deterioration in cognitive function and mental health. Regardless, an established animal experimental method to examine the effect of physical inactivity on physiological, biochemical, and neuroscientific parameters is yet to be reported. In this study, we made a new housing cage, named as the physical inactivity (PI) cage, to investigate the effect of physical inactivity on cognitive function and depressive-like states in mice and obtained the following experimental results by its use. We first compared the daily physical activity of mice housed in the PI and standard cages using the nano-tag method. The mice's physical activity levels in the PI cage decreased to approximately half of that in the mice housed in the standard cage. Second, we examined whether housing in the PI cage affected plasma corticosterone concentration. The plasma corticosterone concentration did not alter before, 1 week, or 10 weeks after housing. Third, we investigated whether housing in the PI cage for 10 weeks affected cognitive function and depressive behavior. Housing in an inactive state caused a cognitive decline and depressive state in the mice without increasing body weight and plasma corticosterone. Finally, we examined the effect of regular low-intensity exercise on cognitive function and depressive state in the mice housed in the PI cage. Physical inactivity decreased neuronal cell proliferation, blood vessel density, and gene expressions of vascular endothelial growth factors and brain-derived neurotrophic factors in the hippocampus. In addition, regular low-intensity exercise, 30 min of treadmill running at a 5-15 m/min treadmill speed 3 days per week, prevented cognitive decline and the onset of a depressive-like state caused by physical inactivity. These results showed that our novel physical inactivity model, housing the mice in the PI cage, would be an adequate and valuable experimental method for examining the effect of physical inactivity on cognitive function and a depressive-like state.

Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters.

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

Olive leaf extract prevents obesity, cognitive decline, and depression and improves exercise capacity in mice.

Obesity is a risk factor for development of metabolic diseases and cognitive decline; therefore, obesity prevention is of paramount importance. Neuronal mitochondrial dysfunction induced by oxidative stress is an important mechanism underlying cognitive decline. Olive leaf extract contains large amounts of oleanolic acid, a transmembrane G protein-coupled receptor 5 (TGR5) agonist, and oleuropein, an antioxidant. Activation of TGR5 results in enhanced mitochondrial biogenesis, which suggests that olive leaf extract may help prevent cognitive decline through its mitochondrial and antioxidant effects. Therefore, we investigated olive leaf extract's effects on obesity, cognitive decline, depression, and endurance exercise capacity in a mouse model. In physically inactive mice fed a high-fat diet, olive leaf extract administration suppressed increases in fat mass and body weight and prevented cognitive declines, specifically decreased working memory and depressive behaviors. Additionally, olive leaf extract increased endurance exercise capacity under atmospheric and hypoxic conditions. Our study suggests that these promising effects may be related to oleanolic acid's improvement of mitochondrial function and oleuropein's increase of antioxidant capacity.

A BCI Based Alerting System for Attention Recovery of UAV Operators.

As unmanned aerial vehicles have become popular, the number of accidents caused by an operator's inattention have increased. To prevent such accidents, the operator should maintain an attention status. However, limited research has been conducted on the brain-computer interface (BCI)-based system with an alerting module for the operator's attention recovery of unmanned aerial vehicles. Therefore, we introduce a detection and alerting system that prevents an unmanned aerial vehicle operator from falling into inattention status by using the operator's electroencephalogram signal. The proposed system consists of the following three components: a signal processing module, which collects and preprocesses an electroencephalogram signal of an operator, an inattention detection module, which determines whether an inattention status occurred based on the preprocessed signal, and, lastly, an alert providing module that presents stimulus to an operator when inattention is detected. As a result of evaluating the performance with a real-world dataset, it was shown that the proposed system successfully contributed to the recovery of operator attention in the evaluating dataset, although statistical significance could not be established due to the small number of subjects.

Comprehensive gene expression profiling of human astrocytes treated with a hepatic encephalopathy-inducible factor, alpha 1-antichymotripsin.

Astrocytes are major glial cells that play a critical role in brain homeostasis. Abnormalities in astrocytic function, such as hepatic encephalopathy (HE) during acute liver failure, can result in brain death following brain edema and the associated astrocyte swelling. Recently, we have identified alpha 1-antichymotripsin (ACT) to be a biomarker candidate for HE. ACT induces astrocyte swelling by upregulating aquaporin 4 (AQP4); however, the causal connection between these proteins is not clear yet. In this study, we utilized a microarray profile to screen the differentially expressed genes (DEGs) in astrocytes treated with ACT. We then performed Gene Ontology, REACTOME, and the comprehensive resource of mammalian protein complexes (CORUM) enrichment analyses of the identified DEGs. The results of these analyses indicated that the DEGs were enriched in pathways activating adenylate cyclase (AC)-coupled G protein-coupled receptors (GPCRs) and therefore were involved in the cyclic adenosine monophosphate (cAMP) signaling. These results indicate that ACT may act as a ligand of Gs-GPCRs and subsequently upregulate cAMP. As cAMP is known to upregulate AQP4 in astrocytes, these results suggest that ACT may upregulate AQP4 by activating AC GPCRs and therefore serve as a therapeutic target for acute HE.

Drinking hydrogen water enhances endurance and relieves psychometric fatigue: a randomized, double-blind, placebo-controlled study 1.

Acute physical exercise increases reactive oxygen species in skeletal muscle, leading to tissue damage and fatigue. Molecular hydrogen (H2) acts as a therapeutic antioxidant directly or indirectly by inducing antioxidative enzymes. Here, we examined the effects of drinking H2 water (H2-infused water) on psychometric fatigue and endurance capacity in a randomized, double-blind, placebo-controlled fashion. In Experiment 1, all participants drank only placebo water in the first cycle ergometer exercise session, and for comparison they drank either H2 water or placebo water 30 min before exercise in the second examination. In these healthy non-trained participants (n = 99), psychometric fatigue judged by visual analogue scales was significantly decreased in the H2 group after mild exercise. When each group was divided into 2 subgroups, the subgroup with higher visual analogue scale values was more sensitive to the effect of H2. In Experiment 2, trained participants (n = 60) were subjected to moderate exercise by cycle ergometer in a similar way as in Experiment 1, but exercise was performed 10 min after drinking H2 water. Endurance and fatigue were significantly improved in the H2 group as judged by maximal oxygen consumption and Borg's scale, respectively. Taken together, drinking H2 water just before exercise exhibited anti-fatigue and endurance effects.

Structure determination and quantification of a new flavone glycoside with anti-acetylcholinesterase activity from the herbs of Elsholtzia ciliata.

Three acacetin triglycosides (compounds 1, 2 and 3) were isolated from the herbs of Elsholtzia ciliata (Labiatae). The structure were identified as 7-O-ß-D-glucopyranosyl-(1 â†’ 2)[α-L-rhamnopyranosyl-(1 â†’ 6)]-ß-D-glucopyranoside (compound 1), 7-O-(6-O-acetyl)-ß-D-glucopyranosyl-(1 â†’ 2)[α-L-rhamnopyranosyl-(1 â†’ 6)]-ß-D-glucopyranoside (compound 2) and 7-O-(6-O-acetyl)-ß-D-glucopyranosyl-(1 â†’ 2)[(4-O-acetyl)-α-L-rhamnopyranosyl-(1 â†’ 6)]-ß-D-glucopyranoside (compound 3) of acacetin. The structures of these compounds were determined on the basis of 2D-NMR spectroscopic data. Compound 3 has not been isolated from a natural source. In addition, the three compounds were quantitatively analysed by HPLC. Acetylcholinesterase (AChE) inhibition activity was assayed to find anti-Alzheimer's activity, since this enzyme increases the concentration of acetylcholine (ACh), a neurotransmitter, responsible for brain's memory. Acacetin, the aglycone of the three compounds, exhibited a potent anti-cholinesterase activity (IC50, 50.33 ± 0.87), though its glycosides (1, 2 and 3) were less active. HPLC analysis demonstrated that the three compounds were contained in the MeOH extract in the order of compounds 2 (12.63 mg/g extract) > 3 (3.10 mg/g) > 1 (2.92 mg/g).

Bio-artificial bone formation model with a radial-flow bioreactor for implant therapy-comparison between two cell culture carriers: porous hydroxyapatite and ß-tricalcium phosphate beads.

Bone grafting is necessary before dental implant treatment in patients with jaw bone defects. Currently, autologous bone grafting is a major burden on the patient. However, it is impossible to form a sufficient foundation for the implant with a bone-filling agent alone. It is, therefore, necessary to prepare hybrid artificial bone tissue containing osteoblasts and osteoclasts. In this study, mouse MC3T3-E1 pre-osteoblast cells and human embryonic-derived osteoblastic cell line hFOB1.19 were cultured in radial-flow bioreactors (RFB) to form three-dimensional artificial bone filled with porous beads of ß-tricalcium phosphate (ß-TCP) or hydroxyapatite (HA)-which are clinically used as bone-filling agents-as cell culture carriers. When circulation culturing was performed in the growth medium for the first 10-12 days, glucose consumption was increased in the cultures with HA beads in comparison to the cultures with ß-TCP beads. When cultured in the differentiation culture medium during the second half of the culture period, the glucose consumption decreased in the culture with HA beads. A DNA microarray analysis suggested that osteogenesis progressed fast in three-dimensional culture filled with HA beads and that partly differentiation into osteoblasts was prominent in cultures with ß-TCP beads. In the growth process of MC3T3-E1 cells, the vitamin A metabolism was also activated, the synthesis and degradation of retinoic acid was enhanced, and the metabolism of the same process decreased at the end of differentiation in three-dimensional cultures. Three-dimensional circulation culture in RFB is considered to be useful for the formation of hybrid bio-artificial bone tissue.

Alpha-1 antichymotrypsin is involved in astrocyte injury in concert with arginine-vasopressin during the development of acute hepatic encephalopathy.

BACKGROUND AND AIMS: We developed a bio-artificial liver (BAL) using a radial-flow bioreactor and rescued mini-pig models with lethal acute liver failure (ALF). The point of the rescue is the recovery from hepatic encephalopathy (HE). HE on ALF has sometimes resulted in brain death following brain edema with astrocyte swelling. Several factors, including ammonia and glutamine, have been reported to induce astrocyte swelling and injury. However, many clinicians believe that there are any other factors involved in the development of HE. Therefore, the aim of this study was to identify novel HE-inducible factors, particularly those inducing astrocyte dysfunction. METHODS: Mini-pig plasma samples were collected at three time points: before the administration of toxins (α-amanitin and LPS), when HE occurred after the administration of toxins, and after treatment with extracorporeal circulation (EC) by the BAL. To identify the causative factors of HE, each plasma sample was subjected to a comparative proteome analysis with two-dimensional gel electrophoresis and mass spectrometry. To assess the direct effects of candidate factors on the astrocyte function and injury, in vitro experiments with human astrocytes were performed. RESULTS: Using a proteome analysis, we identified alpha-1 antichymotrypsin (ACT), which was increased in plasma samples from mini-pigs with HE and decreased in those after treatment with EC by BAL. In in vitro experiments with human astrocytes, ACT showed growth-inhibitory and cytotoxic effects on astrocytes. In addition, the expression of water channel protein aquaporin-4, which is induced in injured astrocytes, was increased following ACT treatment. Interestingly, these effects of ACT were additively enhanced by adding arginine-vasopressin (AVP) and were canceled by adding an AVP receptor antagonist. CONCLUSIONS: These results suggest that ACT is involved in astrocyte injury and dysfunction in concert with AVP during the development of acute HE.

Acute immobilization stress following contextual fear conditioning reduces fear memory: timing is essential.

BACKGROUND: Histone acetylation is regulated in response to stress and plays an important role in learning and memory. Chronic stress is known to deteriorate cognition, whereas acute stress facilitates memory formation. However, whether acute stress facilitates memory formation when it is applied after fear stimulation is not yet known. Therefore, this study aimed to investigate the effect of acute stress applied after fear training on memory formation, mRNA expression of brain-derived neurotrophic factor (BDNF), epigenetic regulation of BDNF expression, and corticosterone level in mice in vivo. METHODS: Mice were subjected to acute immobilization stress for 30 min at 60 or 90 min after contextual fear conditioning training, and acetylation of histone 3 at lysine 14 (H3K14) and level of corticosterone were measured using western blot analysis and enzyme-linked immunosorbent assay (ELISA), respectively. A freezing behavior test was performed 24 h after training, and mRNA expression of BDNF was measured using real-time polymerase chain reactions. Different groups of mice were used for each test. RESULTS: Freezing behavior significantly decreased with the down-regulation of BDNF mRNA expression caused by acute immobilization stress at 60 min after fear conditioning training owing to the reduction of H3K14 acetylation. However, BDNF mRNA expression and H3K14 acetylation were not reduced in animals subjected to immobilization stress at 90 min after the training. Further, the corticosterone level was significantly high in mice subjected to immobilization stress at 60 min after the training. CONCLUSION: Acute immobilization stress for 30 min at 60 min after fear conditioning training impaired memory formation and reduced BDNF mRNA expression and H3K14 acetylation in the hippocampus of mice owing to the high level of corticosterone.

Oral administration of inosine produces antidepressant-like effects in mice.

Inosine, a breakdown product of adenosine, has recently been shown to exert immunomodulatory and neuroprotective effects. We show here that the oral administration of inosine has antidepressant-like effects in two animal models. Inosine significantly enhanced neurite outgrowth and viability of primary cultured neocortical neurons, which was suppressed by adenosine A1 and A2A receptor agonists. Oral administration of inosine to mice transiently increased its concentration in the brain and enhanced neuronal proliferation in the dentate gyrus, accompanied by phosphorylation of mitogen-activated protein kinase and increase in transcript level of brain-derived neurotrophic factor. In stress models, oral inosine prevented an increase in immobility time in forced swim test after chronically unexpected stress and mitigated a reduction in sucrose preference after chronic social defeat stress. These results indicate that oral administration of inosine has the potential to prevent depressive disorder via adenosine receptors.

The management of the displaced medial wall in complex acetabular fractures using plates and additional cerclage.

Reduction for displaced quadrilateral plates in complicated acetabular fractures is difficult and requires wide exposure. The purpose of this study is to assess the usefulness of the additional cable in this complicated fracture and to evaluate the potential danger of compressing the superior gluteal artery and nerve with cable application. We evaluated 31 hips (these included 25 hips with fractures of both columns, two posterior wall and column fractures, three anterior column and posterior hemitransverse fractures, and one high T-shaped fracture) with an average six-year follow-up. Clinical outcomes were evaluated using a modification of the Matta grading system and radiographic arthritic grades. We assessed the postoperative clinical outcomes in relation with other variables such as anatomical reduction, delayed operation, seagull sign, and femoral head injuries. We determined whether the superior gluteal artery and nerve were compressed by cerclage with the help of femoral angiography and EMG. Clinical outcomes were graded as very good to excellent for 18 patients, good for five, fair for three and poor for five. Preoperative femoral head injury (P = 0.011), a seagull sign (P = 0.001), poor reduction (P = 0.015), and delayed reduction (P = 0.05) were found to statistically influence clinical results. We found that there were no injuries to the superior gluteal artery and nerve in spite of using a cable. Cerclage methods can be useful for initial reduction of displaced medial plates in acetabular fractures. These methods reduce operation time and blood loss as compared with other methods.

Regulation of differentiation potential of human mesenchymal stem cells by intracytoplasmic delivery of coactivator-associated arginine methyltransferase 1 protein using cell-penetrating peptide.

Recent studies suggest that epigenetic modifications, such as DNA methylation and histone modification, can alter the differentiation potential of stem cells or progenitor cells. Specifically, coactivator-associated arginine methyltransferase 1 (CARM1) is known to act as a coactivator for various transcription factors and to regulate gene expression by chromatin remodeling through histone methylation. Here, for the first time, we have used direct protein delivery of CARM1 using cell-penetrating peptide (CPP) to regulate the differentiation potential of human mesenchymal stem cells (hMSCs). Immunofluorescence showed that the CPP-CARM1 protein is successfully delivered into the nuclei of hMSCs. Further experiments using immunofluorescence and Western blotting showed that the delivered CARM1 protein can effectively methylate the arginine 17 residue of histone H3 in both bone marrow (BM)- and adipose-derived (AD)-hMSCs, thus suggesting that the CARM1 protein delivered by the CPP system is biologically active in hMSCs. Chromatin immunoprecipitation (ChIP) assay and genome-wide gene expression profiling supported the result that delivered CARM1 protein can cause chromatin remodeling through histone methylation. Finally, the CPP-CARM1 protein efficiently elevated the differentiation efficiency of BM-hMSCs and AD-hMSCs into adipogenic, osteogenic, and myogenic cell lineages in vitro. Altered expression of critical genes after hMSC differentiation was reconfirmed by real-time reverse transcription polymerase chain reaction (qRT-PCR). Collectively, our results suggest that CPP-CARM1 can elevate the differentiation potential of hMSCs into various cell types, and that this system using CPP is a useful tool for exogenous protein delivery in clinical applications of cell-based therapy.

Cerebrospinal fluid pathways from cisterns to ventricles in N-butyl cyanoacrylate-induced hydrocephalic rats.

OBJECT: Cerebrospinal fluid typically enters the subarachnoid space from the ventricles via the fourth ventricular foramina. However, there is clinical evidence that CSF also flows in the opposite direction. Ventricular reflux of CSF from a cistern is a well-known phenomenon in radioisotope studies in patients with normal-pressure hydrocephalus. Additionally, the presence of ventricular blood in acute subarachnoid hemorrhage is frequently observed. The goal of this investigation was to examine the potential CSF pathways from cisterns to ventricles. The authors examined pathways in rat models in which they occluded the fourth ventricular outlets and injected a tracer into the subarachnoid space. METHODS: The model for acute obstructive hydrocephalus was induced using N-butyl cyanoacrylate (NBCA) in 10 Sprague-Dawley rats. After 3 days, cationized ferritin was infused into the lumbar subarachnoid space to highlight retrograde CSF flow pathways. The animals were sacrificed at 48 hours, and the brains were prepared. The CSF flow pathway was traced by staining the ferritin with ferrocyanide. RESULTS: Ferritin was observed in the third ventricle in 7 of 8 rats with hydrocephalus and in the temporal horn of the lateral ventricles in 4 of 8 rats with hydrocephalus. There was no definite staining in the aqueduct, which suggests that the ventricular reflux originated from routes other than through the fourth ventricular outlets. CONCLUSIONS: The interfaces between the quadrigeminal cistern and third ventricle and those between the ambient cistern and lateral ventricle appear to be potential sites of CSF reflux from cisterns to ventricles in obstructive hydrocephalus.

A distal fluted, proximal modular femoral prosthesis in revision hip arthroplasty.

Most reports on the use of modular femoral stems during revision surgery have involved short follow-up periods. The authors evaluated the clinical and radiographic performance of 59 patients fitted with a distal fix modular stem. The average follow-up period was 8.2 years. Average Harris hip score was improved from 47 to 87.6. Of 19 patients with trochanteric osteotomy, 4 had a displaced greater trochanter. Re-revision was performed in 5 patients, and 3 of these were for subsidence (of these 3, subsidence was associated with dissociation of the coupling part in 1 and with osteotomy nonunion in other 2 [proximal component only]). Modular distally fixed femoral stems were found to offer intraoperative flexibility, but to suffer from subsidence and intraoperative greater trochanter and metaphyseal femoral fractures.

2x2 photonic crystal fiber splitter based on silica-based planar lightwave circuits.

A 2x2 photonic crystal fiber (PCF) planar lightwave circuit (PLC) splitter, which splits optical power between two PCF channels, has been made by PCF-to-PLC connections. PCF array blocks were lithographically fabricated to have fiber V grooves and used to firmly hold PCFs and align them to the PLC splitter. The proposed splitter showed a rather flat splitting ratio over a wide wavelength range from 1250 nmto1750 nm. With the implemented splitter, we obtained a low excess loss of 1.6 dB, a low polarization-dependent loss of 0.1 dB, and a high return loss of 52 dB. The ultrabroadband operation of the proposed splitter is expected to find applications in optical performance monitoring, Ethernet passive optical networks, and biomedical optics including optical coherence tomography.

Accelerated rehabilitation after arthroscopic Bankart repair for selected cases: a prospective randomized clinical study.

PURPOSE: Increased stress within a certain limit enhances ligament healing and improves joint function. In this prospective randomized clinical trial, we compared the clinical results of early motion versus conventional immobilization after arthroscopic Bankart repair in a selected patient population. TYPE OF STUDY: Prospective randomized clinical trial. METHODS: We performed an arthroscopic Bankart repair using suture anchors in 62 patients with traumatic recurrent anterior instability of the shoulder. Patients were randomized into 2 groups; group 1 (28 patients; mean age, 28 years) was managed with 3 weeks of immobilization using an abduction sling and conventional rehabilitation program, and group 2 (34 patients; mean age, 29 years) was managed with an accelerated rehabilitation program that consisted of staged range of motion and strengthening exercises from the immediate postoperative day. Selection criteria were nonathletes with recurrent anterior shoulder dislocation and a classic Bankart lesion with a robust labrum limited to 1 cm from the midglenoid notch. The patients were followed up for a mean of 31 months (range, 27 to 45 months; standard deviation, 9 months). Analysis of outcome included pain scores at 6 weeks and at final follow-up evaluation, range of motion, return to activity, recurrence rate, patient satisfaction with each rehabilitation program, and shoulder scores assessed by the American Shoulder and Elbow Surgeons Shoulder Index, the rating system of the University of California at Los Angeles, and another scoring system. RESULTS: The recurrence rate was not different between the 2 groups (P =.842). None of the groups developed recurrent dislocation. Two patients from each group were positive for anterior apprehension signs. Patients who underwent accelerated rehabilitation resumed functional range of motion faster (P <.001) and returned earlier to the functional level of activity (P <.001). Accelerated rehabilitation decreased postoperative pain (P =.013), and more patients were satisfied with this program (P <.001). Shoulder scores, return to activity, pain score, and range of motion were not different between the 2 groups at the final follow-up evaluation (P >.05). CONCLUSIONS: Early mobilization of the operated shoulder after arthroscopic Bankart repair does not increase the recurrence rate in a selected group of patients. Although the final outcomes are approximately the same for both groups, the accelerated rehabilitation program promotes functional recovery and reduces postoperative pain, which allows patients an early return to desired activities.