Wearable and Mobile Technologies for the Evaluation and Treatment of Obsessive-Compulsive Disorder: Scoping Review.

BACKGROUND: Smartphones and wearable biosensors can continuously and passively measure aspects of behavior and physiology while also collecting data that require user input. These devices can potentially be used to monitor symptom burden; estimate diagnosis and risk for relapse; predict treatment response; and deliver digital interventions in patients with obsessive-compulsive disorder (OCD), a prevalent and disabling psychiatric condition that often follows a chronic and fluctuating course and may uniquely benefit from these technologies. OBJECTIVE: Given the speed at which mobile and wearable technologies are being developed and implemented in clinical settings, a continual reappraisal of this field is needed. In this scoping review, we map the literature on the use of wearable devices and smartphone-based devices or apps in the assessment, monitoring, or treatment of OCD. METHODS: In July 2022 and April 2023, we conducted an initial search and an updated search, respectively, of multiple databases, including PubMed, Embase, APA PsycINFO, and Web of Science, with no restriction on publication period, using the following search strategy: ("OCD" OR "obsessive" OR "obsessive-compulsive") AND ("smartphone" OR "phone" OR "wearable" OR "sensing" OR "biofeedback" OR "neurofeedback" OR "neuro feedback" OR "digital" OR "phenotyping" OR "mobile" OR "heart rate variability" OR "actigraphy" OR "actimetry" OR "biosignals" OR "biomarker" OR "signals" OR "mobile health"). RESULTS: We analyzed 2748 articles, reviewed the full text of 77 articles, and extracted data from the 25 articles included in this review. We divided our review into the following three parts: studies without digital or mobile intervention and with passive data collection, studies without digital or mobile intervention and with active or mixed data collection, and studies with a digital or mobile intervention. CONCLUSIONS: Use of mobile and wearable technologies for OCD has developed primarily in the past 15 years, with an increasing pace of related publications. Passive measures from actigraphy generally match subjective reports. Ecological momentary assessment is well tolerated for the naturalistic assessment of symptoms, may capture novel OCD symptoms, and may also document lower symptom burden than retrospective recall. Digital or mobile treatments are diverse; however, they generally provide some improvement in OCD symptom burden. Finally, ongoing work is needed for a safe and trusted uptake of technology by patients and providers.

Development of a novel tool to predict pulmonary complications in trauma patients with and without chest injury.

BACKGROUND: Existing chest trauma scoring tools are often only applicable to patients with chest trauma. We sought to develop a novel Trauma Induced Pulmonary Event (TIPE) score to predict the risk of developing pulmonary complications in all adult trauma patients. METHODS: Multiple logistic regression models were created using the 2017 Trauma Quality Improvement Program (TQIP) to identify independent predictors of pulmonary complications in trauma patients. The weighted average and relative impact of each independent predictor was used to derive a TIPE score. We then validated the score using area under the receiver operating curve (AROC). RESULTS: A total of 22 independent predictors of pulmonary complications were identified. The TIPE score was derived with scores ranging from 0 to 43. Injury accounted for 74% of the total score while comorbidities and demographics made up 21% and 5%, respectively. The most important individual predictors were injuries to the spinal cord and bile ducts (both 4 points). The AROC for this was 0.844. DISCUSSION: TIPE is a novel scoring tool to help predict pulmonary complications in all trauma patients.

The Predictive Capacity of American Society of Anesthesiologists Physical Status (ASA PS) Score in Burn Patients.

Advances in burn care continues to improve survival rates and patient outcomes. There are several burn prognostic tools used to predict mortality and outcomes; however, none include patient comorbidities. We used the American Society of Anesthesiologists physical status score as a surrogate measure for comorbidities, and evaluated its role in predicting mortality and outcomes in adult burn patients undergoing surgery. A retrospective analysis was performed on data collected from a single burn center in the United States, which was comprised of 183 patients. We evaluated the American Society of Anesthesiologists physical status score as an independent predictor of mortality and outcomes, including intensive care unit (ICU) length of stay (LOS), hospital LOS, mechanical ventilator (MV) days, and complications. We compared the American Society of Anesthesiologists physical status score to other prognostic models which included the revised Baux score, Belgian Outcome in Burn Injury, and the Abbreviated Burn Severity Index. Our results demonstrated that the revised Baux and American Society of Anesthesiologists physical status scores could be used to determine the mortality risk in adult burn patients. The revised Baux was the best predictor of mortality, ICU LOS, and MV days, while the Abbreviated Burn Severity Index was the best predictor of total LOS.

Long Noncoding RNA CPR (Cardiomyocyte Proliferation Regulator) Regulates Cardiomyocyte Proliferation and Cardiac Repair.

BACKGROUND: The adult mammalian cardiomyocytes lose their proliferative capacity, which is responsible for cardiac dysfunction and heart failure following injury. The molecular mechanisms underlying the attenuation of adult cardiomyocyte proliferation remain largely unknown. Because long noncoding RNAs (lncRNAs) have a critical role in the development of cardiovascular problems, we investigated whether lncRNAs have any role in the regulation of cardiomyocyte proliferation and cardiac repair. METHODS: Using bioinformatics and initial analysis, we identified an lncRNA, named CPR (cardiomyocyte proliferation regulator), that has a potential regulatory role in cardiomyocyte proliferation. For in vivo experiments, we generated CPR knockout and cardiac-specific CPR-overexpressing mice. In isolated cardiomyocytes, we used adenovirus for silencing (CPR-small interfering RNA) or overexpressing CPR. To investigate the mechanisms of CPR function in cardiomyocyte proliferation, we performed various analyses including quantitative reverse transcription-polymerase chain reaction, Western blot, histology, cardiac function (by echocardiography), transcriptome analyses (microarray assay), RNA pull-down assay, and chromatin immunoprecipitation assay. RESULTS: CPR level is comparatively higher in the adult heart than in the fetal stage. The silencing of CPR significantly increased cardiomyocyte proliferation in postnatal and adult hearts. Moreover, CPR deletion restored the heart function after myocardial injury, which was evident from increased cardiomyocyte proliferation, improvement of myocardial function, and reduced scar formation. In contrast, the neonatal cardiomyocyte proliferation and cardiac regeneration were remarkably suppressed in CPR-overexpressing mice or adeno-associated virus serotype 9-CPR-overexpressing heart. These results indicate that CPR acts as a negative regulator of cardiomyocyte proliferation and regeneration. Next, we found that CPR targets minichromosome maintenance 3, an initiator of DNA replication and cell cycle progression, to suppress cardiomyocyte proliferation. CPR silenced minichromosome maintenance 3 expression through directly interacting and recruiting DNMT3A to its promoter cysteine-phosphate-guanine sites, as evident from decreased minichromosome maintenance 3 promoter methylation and increased minichromosome maintenance 3 expression in CPR knocked-down cardiomyocytes and CPR knockout mouse heart. These results were confirmed in CPR-overexpressing cardiomyocytes and CPR-overexpressing mouse heart. CONCLUSIONS: Together, our findings identified that CPR is a suppressor of cardiomyocyte proliferation and indicated that lncRNAs take part in the regulation of cardiomyocyte proliferation and cardiac repair. Our study provides an lncRNA-based therapeutic strategy for effective cardiac repair and regeneration.

LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.

Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H2O2 and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.

Mitochondrial protein 18 (MTP18) plays a pro-apoptotic role in chemotherapy-induced gastric cancer cell apoptosis.

One of the severe limitations of chemotherapy is the development of drug resistance. However, the mechanisms underlying chemotherapy resistance remain to be elucidated. Mitochondrial mediated apoptosis is a form of cell death induced by chemotherapy. Several chemotherapeutic agents have been shown to induce mitochondrial fission, and finally activate the apoptosis cascade in various cancer cells. Here, we report that the mitochondrial membrane protein 18 (MTP18) induced mitochondrial fragmentation in gastric cancer cells under doxorubicin (DOX) exposure. Upon over-expression of MTP18, a sub-cytotoxic dose of DOX could sensitize a significant number of cells to undergo mitochondrial fission and subsequent apoptosis. These findings suggest that MTP18 can enhance the sensitivity of gastric cancer cells to DOX. Mechanistically, we found that MTP18 enriched dynamic-related protein 1 (DRP1) accumulation in mitochondria and it was responsible for mediating DOX-induced signaling required for mitochondrial fission. Intriguingly, MTP18 expression was downregulated during DOX treatment. Thus, down-regulation of MTP18 expression could be one of the resistance factors interfering with DOX-induced apoptosis in gastric cancer cells.

Knockdown of Mtfp1 can minimize doxorubicin cardiotoxicity by inhibiting Dnm1l-mediated mitochondrial fission.

The long-term usage of doxorubicin (DOX) is largely limited due to the development of severe cardiomyopathy. Many studies indicate that DOX-induced cardiac injury is related to reactive oxygen species generation and ultimate activation of apoptosis. The role of novel mitochondrial fission protein 1 (Mtfp1) in DOX-induced cardiotoxicity remains elusive. Here, we report the pro-mitochondrial fission and pro-apoptotic roles of Mtfp1 in DOX-induced cardiotoxicity. DOX up-regulates the Mtfp1 expression in HL-1 cardiac myocytes. Knockdown of Mtfp1 prevents cardiac myocyte from undergoing mitochondrial fission, and subsequently reduces the DOX-induced apoptosis by preventing dynamin 1-like (Dnm1l) accumulation in mitochondria. In contrast, when Mtfp1 is overexpressed, a suboptimal dose of DOX can induce a significant percentage of cells to undergo mitochondrial fission and apoptosis. These data suggest that knocking down of Mtfp1 can minimize the cardiomyocytes loss in DOX-induced cardiotoxicity. Thus, the regulation of Mtfp1 expression could be a novel therapeutic approach in chemotherapy-induced cardiotoxicity.

Foxo3a inhibits mitochondrial fission and protects against doxorubicin-induced cardiotoxicity by suppressing MIEF2.

Doxorubicin (DOX) as a chemotherapeutic drug is widely used to treat a variety of human tumors. However, a major factor limiting its clinical use is its cardiotoxicity. The molecular components and detailed mechanisms regulating DOX-induced cardiotoxicity remain largely unidentified. Here we report that Foxo3a is downregulated in the cardiomyocyte and mouse heart in response to DOX treatment. Foxo3a attenuates DOX-induced mitochondrial fission and apoptosis in cardiomyocytes. Cardiac specific Foxo3a transgenic mice show reduced mitochondrial fission, apoptosis and cardiotoxicity upon DOX administration. Furthermore, Foxo3a directly targets mitochondrial dynamics protein of 49kDa (MIEF2) and suppresses its expression at transcriptional level. Knockdown of MIEF2 reduces DOX-induced mitochondrial fission and apoptosis in cardiomyocytes and in vivo. Also, knockdown of MIEF2 protects heart from DOX-induced cardiotoxicity. Our study identifies a novel pathway composed of Foxo3a and MIEF2 that mediates DOX cardiotoxicity. This discovery provides a promising therapeutic strategy for the treatment of cancer therapy and cardioprotection.