Annals of translational medicine最新文献

Background and objective: Neurological disorders are a group of diseases involving motor, sensory, cognitive, and autonomic functions, among which stroke, Alzheimer's disease (AD), and Parkinson's disease (PD) are prevalent. Their management, especially in conditions with chronic courses or long-term sequelae, remains a substantial unmet need. With the growing comprehension of neuroscience, the development of digital technology, and the rising demand for quality of life, wearable devices offer a promising solution for disease management. The review aimed to evaluate the application and prospect of wearable devices in neurological disorders.

Methods: We conducted the review by searching papers on the application of wearable devices and wearable technology in neurology and neurological disorders using multiple databases. We summarized the present development status of wearable devices, and outlined the potential value and future direction for further research.

Key content and findings: Existing wearable devices for neurological diseases can be applied to diagnosis and follow-up, as an electronic biomarker detector capturing subtle and objective changes in motor, sensory, and cognitive function. The devices can also be utilized for treatment and rehabilitation, mainly through exoskeletons and brain-computer interface. The application of wearable devices in neurology currently faces several critical limitations, including technical bottlenecks in the detection of fine motor and sensory functions, a lack of industry standards, and a limited sample size.

Conclusions: This review demonstrates the potential of wearable technology in people with neurological disorders, enabling disease management and clinical trials outside clinical settings in the future. Nevertheless, further research is required to develop lighter, more user-friendly devices with various functions. It is believed that with increasing demand and technical support, wearable devices would have a promising range of applications.

[This corrects the article DOI: 10.21037/atm-21-2717.].

[This retracts the article DOI: 10.21037/atm-22-3118.].

[This corrects the article DOI: 10.21037/atm-20-5192.].

Background: Cerebral visual impairment (CVI) is the leading cause of pediatric visual impairment and results from brain-related injury or maldevelopment. Higher-order visual processing deficits are commonly reported and can include difficulties recognizing faces, which can adversely affect the development of communication and socialization skills. In this study, we aimed to measure face discrimination ability in CVI compared to controls using a rapid, self-administered, remote paradigm.

Methods: We quantified face discrimination ability with a Foraging Interactive D-prime (FInD) paradigm that measured the threshold distance between Basel Model Faces required for participants to report whether faces were of the same or different people. We measured face discrimination thresholds in 8 control and 8 CVI participants viewing forward-facing and tilted faces.

Results: Face discrimination thresholds were significantly higher for CVI than control participants [t(13)=-3.439, P=0.004]. Contrary to controls, CVI participants showed no significant difference between forward-facing and tilted faces [t₍₇₎=-1.355, P=0.22]. Importantly, visual acuity did not correlate with face discrimination performance in the CVI group for forward-facing (r=0.040, R²=0.002, P=0.93) or tilted faces (r=-0.100, R²=0.010, P=0.813). A follow-up experiment with control participants (N=23) manipulating digital blur confirmed that face discrimination ability is resilient to visual acuity differences [t₍₂₂₎=-11.291; P<0.001, d=4.152].

Conclusions: These findings quantify a face processing deficit in individuals with CVI and show that this impairment is independent of visual acuity. We hypothesize that while control participants can exploit point-wise comparisons between identical images, individuals with CVI possibly do not utilize this additional source of information.

Medial opening wedge high tibial osteotomy (MOWHTO) has gained popularity for treating patients with medial knee osteoarthritis. Bicortical screw fixation is conventionally preferred, but its mechanical advantage over monocortical fixation remains elusive clinically, and may have additional symptomatic hardware risks. Our study aimed to quantify mechanical differences between monocortical and bicortical distal screws construct in MOWHTO. Twenty artificial composite tibiae were used, with 10 specimens per arm. The first arm underwent MOWHTO with bicortical screw fixation throughout; the second arm incorporated two monocortical distal locking screws. Mechanical properties of specimens were evaluated with static compressive load-bearing till failure and cyclic fatigue strength testing. For quasi-static compression testing, monocortical specimens had a median ultimate load of 2.60 [interquartile range (IQR)=0.12] kN [mean ± standard deviation (SD) =2.59±0.15 kN], comparable to the bicortical group [median (IQR) =2.64 (0.46) kN, mean ± SD =2.56±0.33 kN]. Cyclic fatigue strength testing also demonstrated comparable maximal loads tolerated by both monocortical [median (IQR) =1.28 (0.08) kN, mean ± SD =1.33±0.12 kN] and bicortical [median (IQR) =1.28 (0.00) kN, mean ± SD =1.28±0.06 kN] specimens, as well as median number of cycles attained before failure. Mann-Whitney-U tests showed no statistically significant difference for all measured outcomes between monocortical and bicortical groups (P>0.05). Our study found monocortical fixation of the two distal-most screws in MOWHTO mechanically non-inferior to bicortical fixation. This supports monocortical fixation as an alternative technique for distal screw placement in MOWHTO.

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease associated with systemic inflammation and various comorbidities, including potential gallbladder disease. However, evidence linking RA to gallstones or cholecystectomy remains limited and inconsistent. This study assesses whether patients with RA are at higher risk of developing gallstones and undergoing cholecystectomy than individuals without RA.

Methods: Using data from the Korean National Health Insurance Service, we identified 54,910 individuals diagnosed with RA between 2010 and 2017. After applying separate exclusion criteria for the analyses of developing gallstones and undergoing cholecystectomy, we matched those patients in a 1:3 ratio based on age and sex to derive a control population without RA. The study participants were followed from 1 year after their RA diagnosis or corresponding index date (lag period) to Dec. 31, 2020. Cox regression analyses were performed to estimate hazard ratios of developing gallstones and undergoing cholecystectomy compared with the matched controls.

Results: We analyzed 46,523 patients with RA and 139,569 matched controls, with a follow-up period ranging from 3.5 to 7.3 years. During the follow-up, gallstone disease developed in 8.33% of patients with RA and 5.51% of the matched controls, corresponding to incidence rates of 15.69 and 10.09 per 1,000 person-years, respectively. The risk of incident gallstones was higher in the RA cohort than in the matched control group [adjusted hazard ratio (aHR) 1.58; 95% confidence interval (CI): 1.52-1.65, P<0.001]. During the same period, 1.24 % of patients with RA and 1.1% of the matched control group underwent cholecystectomy, for incidence rates of 2.27 and 2.0 per 1,000 person-years, respectively. Patients with RA appear to have a marginally elevated risk of undergoing cholecystectomy, compared with matched controls (aHR 1.15, 95% CI 1.05-1.27, P=0.04).

Conclusions: The risk of gallstone disease is higher in individuals with RA than in matched controls.

Background: Studies on light-elicited endothelial period circadian regulator 2 (PER2) mediated cardioprotection revealed a critical role of PER2/hypoxia inducible factor 1 alpha (HIF1A) regulated endothelial factor ANGPTL4 for endothelial barrier protection during myocardial ischemia and reperfusion injury (IRI). Based on these observations, we deepened our studies on light-elicited cardioprotective mechanisms.

Methods: All animal and human studies had Institutional Animal Care and Use Committee (IACUC) and Colorado Multiple Institutional Review Board (COMIRB) approval. To study myocardial IRI, an in-situ mouse model for myocardial IRI was used. To study light-elicited mechanisms during myocardial IRI, endothelial-specific Per2-deficient mice were treated with the PER2 enhancer nobiletin (NOB), with the HIF1A activator dimethyloxalylglycine (DMOG), or with recombinant ANGPTL4. To evaluate whether light could increase ANGPTL4 or decrease troponin levels in patients, we exposed patients undergoing elective spine surgery postoperatively for 5 days with intense light for 30 minutes at sunrise. Patient's plasma samples were tested for melatonin, ANGPTL4 and troponin levels using enzyme-linked immunosorbent assay (ELISA).

Results: The PER2 enhancer NOB or the HIF1A activator DMOG protected from myocardial IRI, which was abolished in endothelial-specific Per2-deficient mice. ANGPTL4 was able to overcome an endothelial Per2 deficiency and revealed protection during myocardial IRI in endothelial-specific Per2-deficient or control mice. Intense light therapy in patients undergoing non-cardiac surgery showed increased ANGPTL4 and decreased troponin plasma levels.

Conclusions: Our study demonstrates that only the PER2/HIF1A downstream target ANGPTL4 can overcome an endothelial Per2 deficiency. Moreover, we discovered that intense light therapy in patients following non-cardiac surgery can be used to increase plasma levels of the endothelial protective factor ANGTL4 and decrease troponin levels, an indicator of myocardial injury in non-cardiac surgery (MINS). Further research with larger, more diverse human cohorts and long-term follow-up is needed to validate these findings and develop targeted therapies.