Developing a Motion Sensor-Based Game to Support Frozen Shoulder Rehabilitation in Older Adults through a Participatory Design Approach.

Objective: Although some serious games have been developed for physical therapy, little work has been conducted through a participatory design approach. Therefore, a game prototype was developed, which involved related stakeholders in the design process. Materials and Methods: The iterative participatory design process was adopted with the input of 18 patients with frozen shoulder symptoms, 4 health professionals, 2 game designers, and 5 researchers in an iterative process to design, test, and evaluate the game prototype. In total, 17 patients participated in the interviews to explore their needs and desires for a serious game. The health professionals participated in the interviews to understand the medical requirement and experience pertaining to frozen shoulder and were included in the workshop to give feedback on the game prototype. At the conclusion of the iterative design process, a Kinect-based prototype game with three levels was used for a case study with one patient who was diagnosed with frozen shoulder and has been receiving medical treatment in the hospital. Results: Based on the outcomes derived from data collected among diverse stakeholders, the prototype game underwent iterative development by the team and was assessed by a participant with frozen shoulder symptoms. Findings revealed that the participant demonstrated enhanced shoulder mobility and a reduction in pain intensity, despite the lack of significant improvement for health-related quality of life. Nevertheless, the participant reported a positive experience with the prototype game. Conclusion: This study underscores the importance of involving diverse stakeholders in the development process to create more effective and user-centric serious games for rehabilitation. The participatory approach, exemplified by the prototype game, demonstrates potential improvements in both user experience and overall effectiveness during the rehabilitation process.

Decompressive Cranioplasty (Osteoplastic Hinged Craniectomy): A Novel Technique for Increased Intracranial Pressure-Initial Experience and Outcome.

BACKGROUND: We redesigned decompressive craniectomy and cranioplasty procedures to decrease the inherent risk of complications. This novel technique, called decompressive cranioplasty, not only may decrease the complication rate but also may improve the cosmetic result, obviate the need for artificial skull implant, and increase the decompressive volume compared with traditional craniectomy. METHODS: In decompressive cranioplasty, the Agnes Fast craniotomy was adopted without cutting the temporalis muscle from the underlying bone flap. After opening the dura with or without removal of intracranial hematomas, duraplasty was performed with an intracranial pressure monitor inserted. Four miniplates were bent into a "Z" shape, and the vascularized bone flap was elevated approximately 1.2-1.5 cm above the outer cortex of the skull and fixed with the miniplates. Subsequent cranioplasty was done with a mini-incision on the miniplate sites and reshaping of the miniplate to align the outer cortex of the bone flap. RESULTS: We successfully performed decompressive cranioplasty in 3 emergent cases-2 traumatic subdural hematomas and 1 malignant middle cerebral artery infarction. Postoperative brain computed tomography demonstrated adequate decompression in all cases. Cosmetic outcome was excellent, and there was no temporal hallowing. Mastication function was not affected. At 6-month follow-up, there was no bone flap shrinkage and no hydrocephalus. CONCLUSIONS: Decompressive cranioplasty is a safe and effective method in the management of patients with brain edema and intracranial hypertension. It is simple to perform and may reduce the morbidity associated with traditional decompressive craniectomy and subsequent cranioplasty.

A Meta-analysis of Clinical Effects of Low-level Laser Therapy on Temporomandibular Joint Pain.

[Purpose] Temporomandibular joint (TMJ) pain is a symptom of TMJ disease. Low-level laser therapy (LLLT) is often used in the clinical treatment of TMJ pain. The aim of this study was to review the effective parameters of LLLT for TMJ pain. [Methods] This study was a systematic review in which electronic databases were searched for the period of January 2005 to January 2010. We selected reports of randomized controlled trials and calculated the effect size (ES) of the pain relief to evaluate the effect of LLLT. [Results] Seven reports are found to meet the inclusion criteria and discussed. Based on the calculation results, the pooled ES was -0.6, indicating a moderate effect of pain relief. In addition, the dosages and treatments with wavelengths of 780 and 830 nm can cause moderate and large pain relief effects. [Conclusion] Use of LLLT on the masticatory muscle or joint capsule for TMJ pain had a moderate analgesic effect. The optimal parameters for LLLT to treat TMJ pain have not been confirmed. However, our results can be a vital clinical reference for clinical physicians in treatment of patients with TMJ pain.

Activity of the hypoxia-activated prodrug, TH-302, in preclinical human acute myeloid leukemia models.

PURPOSE: Acute myeloid leukemia (AML) is an aggressive hematologic neoplasm. Recent evidence has shown the bone marrow microenvironment in patients with AML to be intrinsically hypoxic. Adaptive cellular responses by leukemia cells to survive under low oxygenation also confer chemoresistance. We therefore asked whether therapeutic exploitation of marrow hypoxia via the hypoxia-activated nitrogen mustard prodrug, TH-302, could effectively inhibit AML growth. EXPERIMENTAL DESIGN: We assessed the effects of hypoxia and TH-302 on human AML cells, primary samples, and systemic xenograft models. RESULTS: We observed that human AML cells and primary AML colonies cultured under chronic hypoxia (1% O2, 72 hours) exhibited reduced sensitivity to cytarabine-induced apoptosis as compared with normoxic controls. TH-302 treatment resulted in dose- and hypoxia-dependent apoptosis and cell death in diverse AML cells. TH-302 preferentially decreased proliferation, reduced HIF-1α expression, induced cell-cycle arrest, and enhanced double-stranded DNA breaks in hypoxic AML cells. Hypoxia-induced reactive oxygen species by AML cells were also diminished. In systemic human AML xenografts (HEL, HL60), TH-302 [50 mg/kg intraperitoneally (i.p.) 5 times per week] inhibited disease progression and prolonged overall survival. TH-302 treatment reduced the number of hypoxic cells within leukemic bone marrows and was not associated with hematologic toxicities in nonleukemic or leukemic mice. Later initiation of TH-302 treatment in advanced AML disease was as effective as earlier TH-302 treatment in xenograft models. CONCLUSIONS: Our results establish the preclinical activity of TH-302 in AML and provide the rationale for further clinical studies of this and other hypoxia-activated agents for leukemia therapy.

Cycling exercise with functional electrical stimulation improves postural control in stroke patients.

The aim of this study is to determine whether short term functional electrical stimulation (FES)-assisted cycling training can affect the postural control of stroke patients, and whether the application of FES can enhance the effect of cycling training. 20 stroke patients were randomly assigned to the FES-cycling group (FES-CG) or the cycling group (CG). Measurements were completed before and immediately after each 20 min training sessions. The measurements included a balance test (to quantify the postural control ability), a Hoffmann's reflex/motor response ratio (H/M ratio) test and a pendulum test (to quantify the muscle tone). In the balance test, some parameters in all directions exhibited significant intervention effects between the FES-CG group and the CG group. The H/M ratios (p=.014; .005, FES-CG and CG respectively) and relaxation index (p=.005; .047, FES-CG and CG respectively) revealed significant difference between FES-CG and CG group. The change ratios of directional control in the forward direction and H/M ratio revealed significant difference (p=.022; .015) between FES-CG and CG among subjects with higher muscle tone. The stroke subjects' postural control was improved while their muscle tone was reduced after the 20 min cycling training program both with and without FES. We conclude that cycling training, with or without FES may reduce spasticity in stroke patients. The application of FES in cycling exercise was shown to be more effective in stroke patients with higher muscle tone.

Apoptosis induced by t10,c12-conjugated linoleic acid is mediated by an atypical endoplasmic reticulum stress response.

Conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis, in part by inducing apoptosis of preneoplastic and neoplastic mammary epithelial cells. The current study focused on the mechanism by which apoptosis is induced. In TM4t mammary tumor cells, trans-10,cis-12 (t10,c12)-CLA induced proapoptotic C/EBP-homologous protein (CHOP) concurrent with the cleavage of poly(ADP-ribose) polymerase. Knockdown of CHOP attenuated t10,c12-CLA-induced apoptosis. Furthermore, t10,c12-CLA induced the cleavage of endoplasmic reticulum (ER)-resident caspase-12, and a selective inhibitor of caspase-12 significantly alleviated t10,c12-CLA-induced apoptosis. Using electron microscopy, we observed that t10,c12-CLA treatment resulted in marked dilatation of the ER lumen. Together, these data suggest that t10,c12-CLA induces apoptosis through ER stress. To further explore the ER stress pathway, we examined the expression of the following upstream ER stress signature markers in response to CLA treatment: X-box binding protein 1 (XBP1) mRNA (unspliced and spliced), phospho-eukaryotic initiation factor (eIF) 2 alpha, activating transcription factor 4 (ATF4), and BiP proteins. We found that t10,c12-CLA induced the expression and splicing of XBP1 mRNA as well as the phosphorylation of eIF2 alpha. In contrast, ATF4 was induced modestly, but not significantly, and BiP was not altered. In summary, our data demonstrate that apoptosis induced by t10,c12-CLA is mediated, at least in part, through an atypical ER stress response that culminates in the induction of CHOP and the cleavage of caspase-12.