Using 5-fold cross-validation during training, the average AUCs of the DL models were approximately 0.99. In the external validation data set, the DL algorithm achieved an AUC of 0.99 with a sensitivity of 94.0% and a specificity of 99.3%. The DL algorithm's performance (with an accuracy of 0.95) in diagnosing referable horizontal strabismus was better than that of the resident ophthalmologists (with accuracy ranging from 0.81 to 0.85).
We developed and evaluated a DL model to automatically identify referable horizontal strabismus using primary gaze photographs. The diagnostic performance of the DL model is comparable to or better than that of ophthalmologists.
DL methods that automate the detection of referable horizontal strabismus can facilitate clinical assessment and screening for children at risk of strabismus.
DL methods that automate the detection of referable horizontal strabismus can facilitate clinical assessment and screening for children at risk of strabismus.Vascular dementia (VaD) is a neurodegenerative disease, with cognitive dysfunction attributable to cerebrovascular factors. At present, it is the second most frequently occurring type of dementia in older adults (after Alzheimer's disease). The underlying etiology of VaD has not been completely elucidated, which limits its management. Currently, there are no approved standard treatments for VaD. The drugs used in VaD are only suitable for symptomatic treatment and cannot prevent or reduce the occurrence and progression of VaD. This review summarizes the current status of pharmacological treatment for VaD, from the perspective of the molecular mechanisms specified in various pathogenic hypotheses, including oxidative stress, the central cholinergic system, neuroinflammation, neuronal apoptosis, and synaptic plasticity. As VaD is a chronic cerebrovascular disease with multifactorial etiology, combined therapy, targeting multiple pathophysiological factors, may be the future trend in VaD.Cartilage is a relatively simple connective tissue that plays a variety of roles in the human body, including joint support and protection, load bearing of the intervertebral discs, joint lubrication, formation of the external structure of the ears and nose and support of the trachea. The maintenance of cartilage homeostasis is therefore crucial. Cartilage-related diseases are difficult to diagnose and treat because their molecular and pathological mechanisms are not fully understood. Melatonin, which has a wide range of physiological effects, is an endocrine hormone mainly secreted by the pineal gland. Its biological effects include its antioxidant, antiaging, analgesic, and hypnotic effects and its ability to stabilize the circadian rhythm. In recent years, research on cartilage homeostasis and melatonin has been increasing, and melatonin has gradually been used in the treatment of cartilage-related diseases. Therefore, this article will briefly review the role of melatonin in cartilage homeostasis, including its anti-inflammatory effects and effects in protecting cartilage from damage by other factors and promoting chondrocyte growth and the expression of cartilage-related genes. Based on the above, the current status and future developmental direction of melatonin in the treatment of cartilage-related diseases are also discussed, demonstrating the broad prospects of melatonin in maintaining cartilage homeostasis and treating cartilage injury-related diseases.Sepsis is a form of life-threatening organ dysfunction caused by dysregulated host responses to an infection that can be partly attributed to immune dysfunction. https://www.selleckchem.com/products/H-89-dihydrochloride.html Although sepsis affects patients of all ages, elderly individuals display increased susceptibility and mortality. This is partly due to immunosenescence, a decline in normal immune system function associated with physiological aging that affects almost all cell types in the innate and adaptive immune systems. In elderly patients with sepsis, these alterations in immune cells such as endothelial cells, neutrophils, monocytes, macrophages, natural killer cells, dendritic cells, T lymphocytes, and B lymphocytes, are largely responsible for their poor prognosis and increased mortality. Here, we review recent studies investigating the events affecting both innate and adaptive immune cells in elderly mice and patients with sepsis, including alterations in their number, phenotype, and function, to shed light on possible new therapeutic strategies.Ferroptosis is a form of programmed cell death caused by production of reactive oxygen species and disequilibrium of iron homeostasis. Many chemical compounds and clinical drugs induce ferroptosis in normal and cancer cells, while peroxidation inhibitors, iron chelators, and antioxidants can block ferroptosis. Glutathione peroxidase 4, ferroptosis suppressor protein 1, nuclear factor erythroid 2-related factor 2, and system Xc- are the negative regulators of ferroptosis, whereas nicotinamide adenine dinucleotide phosphate oxidase, p53, mitochondria voltage-dependent anion channel, and cysteinyl-tRNA synthetase function as positive regulators. Ferroptosis plays important roles in pathogen infection and tumor immunology. Recent studies suggest that ferroptosis plays a vital role in the pathogenesis of cardiovascular diseases (CVDs), which seriously threaten human health. Potential therapies designed around ferroptosis may alter the pathological progression of CVDs. Therefore, we redacted an overview of the discovery of ferroptosis, its regulatory mechanisms, and its potential impact on CVDs treatment.Idiopathic inflammatory myopathies (IIMs) are chronic autoimmune disorders involving multiple organs, such as the muscle, skin, lungs and joints. Although the detailed pathogenesis of IIMs remains unclear, immune mechanisms have long been recognised as of key importance. Immune cells contribute to many inflammatory processes via intercellular interactions and secretion of inflammatory factors, and many studies have demonstrated the participation of a variety of immune cells, such as T cells and B cells, in the development of IIMs. Here, we summarise the current knowledge regarding immune cells in IIM patients and discuss their potential roles in IIM pathogenesis.Parkinson's disease (PD) ranks second among the most common neurodegenerative diseases, characterized by progressive and selective loss of dopaminergic neurons. Various cross-species preclinical models, including cellular models and animal models, have been established through the decades to study the etiology and mechanism of the disease from cell lines to nonhuman primates. These models are aimed at developing effective therapeutic strategies for the disease. None of the current models can replicate all major pathological and clinical phenotypes of PD. Selection of the model for PD largely relies on our interest of study. In this review, we systemically summarized experimental PD models, including cellular and animal models used in preclinical studies, to understand the pathogenesis of PD. This review is intended to provide current knowledge about the application of these different PD models, with focus on their strengths and limitations with respect to their contributions to the assessment of the molecular pathobiology of PD and identification of the therapeutic strategies for the disease.In keeping with its status as one of the major causes of disability and mortality worldwide, brain damage induced by cerebral arterial disease has been the subject of several decades of scientific investigation, which has resulted in a vastly improved understanding of its pathogenesis. Brain injury mediated by venous etiologies, however, such as cerebral, jugular, and vertebral venous outflow disturbance, have been largely ignored by clinicians. Unfortunately, this inattention is not proportional to the severity of cerebral venous diseases, as the impact they exact on the quality of life of affected patients may be no less than that of arterial diseases. This is evident in disease sequelae such as cerebral venous thrombosis (CVT)-mediated visual impairment, epilepsy, and intracranial hypertension; and the long-term unbearable head noise, tinnitus, headache, dizziness, sleeping disorder, and even severe intracranial hypertension induced by non-thrombotic cerebral venous sinus (CVS) stenosis and/or internal jugular venous (IJV) stenosis. In addition, the vertebral venous system (VVS), a large volume, valveless vascular network that stretches from the brain to the pelvis, provides a conduit for diffuse transmission of tumors, infections, or emboli, with potentially devastating clinical consequences. Moreover, the lack of specific features and focal neurologic signs seen with arterial etiologies render cerebral venous disease prone to both to misdiagnoses and missed diagnoses. It is therefore imperative that awareness be raised, and that as comprehensive an understanding as possible of these issues be cultivated. In this review, we attempt to facilitate these goals by systematically summarizing recent advances in the diagnosis and treatment of these entities, including CVT, CVS stenosis, and IJV stenosis, with the aim of providing a valid, practical reference for clinicians.Physical activity, together with its ameliorative effects on Parkinson's disease (PD) symptoms, remains a relatively unappreciated factor which may be beneficial for the treatment outcome. Contemporary evidence supports the positive effects of non-pharmacological approaches to PD symptom management, in particular the effects of the exercise on both, motor and non-motor symptoms. The aim of the study was to review the mechanisms of exercise-induced amelioration of PD symptoms. Methods Electronic databases (PubMed, Web of Science and Google Scholar) were searched using the following key words "Parkinson and physical activity" OR "Parkinson disease and exercise" OR "Parkinson disease and lifestyle factors" OR "Parkinson disease and longevity". A total of 97 studies which investigated PD genetics and various forms of exercise and their etiologic impact on PD were reviewed. The studies were subdivided into four topic groups 1) genetics of PD, 2) exercise and the brain, 3) physical activity and PD, 4) mind-body interventions, and discussed accordingly. Adequate levels of physical activity are associated with higher quality of life in PD patients. Physical activity may have protective and stimulatory effects for better functional efficiency in higher-level cognitive networks. It can also improve balance and motor functions by improving muscle strength. Given the etiologic evidence of the beneficial effects of physical activity on PD, albeit tentative, a concerted effort to elucidate the processes and outcomes of physical activity on ameliorating symptoms of PD must be undertaken.Currently, the world is challenged by the coronavirus disease 2019 (COVID-19) pandemic. Epidemiologists and researchers worldwide are invariably trying to understand and combat this precarious new disease. Scrutinizing available drug options and developing potential new drugs are urgent needs to subdue this pandemic. Several intervention strategies are being considered and handled worldwide with limited success, and many drug candidates are yet in the trial phase. Despite these limitations, the development of COVID-19 treatment strategies has been accelerated to improve the clinical outcome of patients with COVID-19, and some countries have efficiently kept it under control. Recently, the use of natural and traditional medicine has also set the trend in coronavirus treatment. This review aimed to discuss the prevailing COVID-19 treatment strategies available globally by examining their efficacy, potential mechanisms, limitations, and challenges in predicting a future potential treatment candidate and bridging them with the effective traditional Chinese medicine (TCM).