Mobile Phone-Supported Physiotherapy for Frozen Shoulder: Feasibility Assessment Based on a Usability Study.

BACKGROUND: Patients with frozen shoulder show limited shoulder mobility often accompanied by pain. Common treatment methods include physiotherapy, pain medication, administration of corticosteroids, and surgical capsulotomy. Frozen shoulder often lasts from months to years and mostly affects persons in the age group of 40 to 70 years. It severely reduces the quality of life and the ability to work. OBJECTIVE: The objective of this study was to evaluate the feasibility of a mobile health (mHealth) intervention that supports patients affected by "stage two" frozen shoulder. Patients were supported with app-based exercise instructions and tools to monitor their training compliance and progress. These training compliance and progress data supplement the patients' oral reports to the physiotherapists and physicians and can assist them in therapy adjustment. METHODS: In order to assess the feasibility of the mHealth intervention, a pilot study of a newly developed app for frozen shoulder patients was conducted with 5 patients for 3 weeks. The main function of the app was the instruction for exercising at home. Standardized questionnaires on usability such as System Usability Scale (SUS) and USE (Usefulness, Satisfaction, and Ease of use), and Technology Acceptance Model-2 (TAM-2) were completed by the study participants at the end of the study. Additionally, a nonstandardized questionnaire was completed by all patients. The correctness of the exercises as conducted by the patients was assessed by a physiotherapist at the end of the study. The mobility of the shoulder and pain in shoulder movement was assessed by a physiotherapist at the start and the end of the study. RESULTS: The pilot study was successfully conducted, and the app was evaluated by the patients after 3 weeks. The results of the standardized questionnaires showed high acceptance (TAM-2) and high usability (SUS) of the developed app. The overall usability of the system as assessed by the SUS questionnaire was very good (an average score of 88 out of 100). The average score of the TAM-2 questionnaire on the intention to further use the app was 4.2 out of 5, which indicated that most patients would use the app if further available. The results of the USE questionnaires highlighted that the patients learned how to use the app easily (an average score of 4.2 out of 5) and were satisfied with the app (an average score of 4.7 out of 5). The frequency of app usage and training was very high based on patient reports and verified by analysis of the usage data. The patients conducted the exercises almost flawlessly. CONCLUSIONS: Our results indicate the feasibility of the mHealth intervention, as the app was easy to use and frequently used by the patients. The app supported the patients' physiotherapy by providing clear exercising instructions.

Training of carbohydrate estimation for people with diabetes using mobile augmented reality.

BACKGROUND: Imprecise carbohydrate counting as a measure to guide the treatment of diabetes may be a source of errors resulting in problems in glycemic control. Exact measurements can be tedious, leading most patients to estimate their carbohydrate intake. In the presented pilot study a smartphone application (BE(AR)), that guides the estimation of the amounts of carbohydrates, was used by a group of diabetic patients. METHODS: Eight adult patients with diabetes mellitus type 1 were recruited for the study. At the beginning of the study patients were introduced to BE(AR) in sessions lasting 45 minutes per patient. Patients redraw the real food in 3D on the smartphone screen. Based on a selected food type and the 3D form created using BE(AR) an estimation of carbohydrate content is calculated. Patients were supplied with the application on their personal smartphone or a loaner device and were instructed to use the application in real-world context during the study period. For evaluation purpose a test measuring carbohydrate estimation quality was designed and performed at the beginning and the end of the study. RESULTS: In 44% of the estimations performed at the end of the study the error reduced by at least 6 grams of carbohydrate. This improvement occurred albeit several problems with the usage of BE(AR) were reported. CONCLUSIONS: Despite user interaction problems in this group of patients the provided intervention resulted in a reduction in the absolute error of carbohydrate estimation. Intervention with smartphone applications to assist carbohydrate counting apparently results in more accurate estimations.

Mitochondrial phosphate-carrier deficiency: a novel disorder of oxidative phosphorylation.

The mitochondrial phosphate carrier SLC25A3 transports inorganic phosphate into the mitochondrial matrix, which is essential for the aerobic synthesis of adenosine triphosphate (ATP). We identified a homozygous mutation--c.215G-->A (p.Gly72Glu)--in the alternatively spliced exon 3A of this enzyme in two siblings with lactic acidosis, hypertrophic cardiomyopathy, and muscular hypotonia who died within the 1st year of life. Functional investigation of intact mitochondria showed a deficiency of ATP synthesis in muscle but not in fibroblasts, which correlated with the tissue-specific expression of exon 3A in muscle versus exon 3B in fibroblasts. The enzyme defect was confirmed by complementation analysis in yeast. This is the first report of patients with mitochondrial phosphate-carrier deficiency.

Reduced respiratory control with ADP and changed pattern of respiratory chain enzymes as a result of selective deficiency of the mitochondrial ATP synthase.

The F(o)F(1)-ATPase, a multisubunit protein complex of the inner mitochondrial membrane, produces most of the ATP in mammalian cells. Mitochondrial diseases as a result of a dysfunction of ATPase can be caused by mutations in mitochondrial DNA-encoded ATPase subunit a or rarely by an ATPase defect of nuclear origin. Here we present a detailed functional and immunochemical analysis of a new case of selective and generalized ATPase deficiency found in an Austrian patient. The defect manifested with developmental delay, muscle hypotonia, failure to thrive, ptosis, and varying lactic acidemia (up to 12 mmol/L) beginning from the neonatal period. A low-degree dilated cardiomyopathy of the left ventricle developed between the age of 1 and 2 y. A >90% decrease in oligomycin-sensitive ATPase activity and an 86% decrease in the content of the ATPase complex was found in muscle mitochondria. It was associated with a significant decrease of ADP-stimulated respiration of succinate (1.5-fold) and respiratory control with ADP (1.7-fold) in permeabilized muscle fibers, and with a slight decrease of the respiratory chain complex I and compensatory increase in the content of complexes III and IV. The same ATPase deficiency without an increase in respiratory chain complexes was found in fibroblasts, suggesting a generalized defect with tissue-specific manifestation. Absence of any mutations in mitochondrial ATP6 and ATP8 genes indicates a nuclear origin of the defect.

Severe depletion of mitochondrial DNA in spinal muscular atrophy.

Spinal muscular atrophy (SMA) is a neuromuscular disorder in childhood leading to a dramatic loss of muscle strength. Functional investigations with high-resolution polarography and enzyme measurements of the respiratory chain revealed lowered activities in muscle tissue of SMA patients. To gain a better understanding of this low energy supply we analyzed the amount of mitochondrial DNA (mtDNA) in skeletal muscle of 20 unrelated children with genetically proven SMA and 31 controls. Quantitative Southern blot analysis revealed a severe and homogeneous decrease in the content of muscle mtDNA in relation to nuclear DNA in SMA patients (90.3+/-7.8%), whereas by immunofluorescence no decrease in the number of mitochondria was detected. In addition, a two- to threefold reduction of the nuclear-encoded complex II (succinate dehydrogenase) activity was detected in SMA muscle tissue. Western blot analysis showed a significant reduction of both mitochondrial- and nuclear-encoded cytochrome c oxidase subunits. Our results indicate that mtDNA depletion in SMA is a consequence of severe atrophy, and has to be differentiated by measurement of complex II from an isolated reduction of mtDNA as found in patients with mitochondriocytopathies and the so-called mtDNA depletion syndrome.