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In this review, we discuss recent progress in DL-based RIQA models in general and the need for RIQA models tailored for ONH disorders. Finally, we propose suggestions for such models in the future.

Deep learning algorithms as tools for automated image classification have recently experienced rapid growth in imaging-dependent medical specialties, including ophthalmology. However, only a few algorithms tailored to specific health conditions have been able to achieve regulatory approval for autonomous diagnosis. There is now an international effort to establish optimized thresholds for algorithm performance benchmarking in a rapidly evolving artificial intelligence field. This review examines the largest deep learning studies in glaucoma, with special focus on identifying recurrent challenges and limitations within these studies which preclude widespread clinical deployment. We focus on the 3 most common input modalities when diagnosing glaucoma, namely, fundus photographs, spectral domain optical coherence tomography scans, and standard automated perimetry data. We then analyze 3 major challenges present in all studies defining the algorithm output of glaucoma, determining reliable ground truth datasetscoma, determining reliable ground truth datasets, and compiling representative training datasets.

Deep learning (DL) is a subset of artificial intelligence based on deep neural networks. It has made remarkable breakthroughs in medical imaging, particularly for image classification and pattern recognition. In ophthalmology, there are rising interests in applying DL methods to analyze optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA) images. Selleckchem DPCPX Studies showed that OCT and OCTA image evaluation by DL algorithms achieved good performance for disease detection, prognosis prediction, and image quality control, suggesting that the incorporation of DL technology could potentially enhance the accuracy of disease evaluation and the efficiency of clinical workflow. However, substantial issues, such as small training sample size, data preprocessing standardization, model robustness, results explanation, and performance cross-validation, are yet to be tackled before deploying these DL models in real-time clinics. This review summarized recent studies on DL-based image analysis modeldeploying these DL models in real-time clinics. This review summarized recent studies on DL-based image analysis models for OCT and OCTA images and discussed the potential challenges of clinical deployment and future research directions.

Most published systematic reviews have focused on the use of virtual reality (VR)/augmented reality (AR) technology in ophthalmology as it relates to surgical training. To date, this is the first review that investigates the current state of VR/AR technology applied more broadly to the entire field of ophthalmology.

PubMed, Embase, and CINAHL databases were searched systematically from January 2014 through December 1, 2020. Studies that discussed VR and/or AR as it relates to the field of ophthalmology and provided information on the technology used were considered. Abstracts, non-peer-reviewed literature, review articles, studies that reported only qualitative data, and studies without English translations were excluded.

A total of 77 studies were included in this review. Of these, 28 evaluated the use of VR/AR in ophthalmic surgical training/assessment and guidance, 7 in clinical training, 23 in diagnosis/screening, and 19 in treatment/therapy. 15 studies used AR, 61 used VR, and 1 used both. Most studies focused on the validity and usability of novel technologies.

Ophthalmology is a field of medicine that is well suited for the use of VR/AR. However, further longitudinal studies examining the practical feasibility, efficacy, and safety of such novel technologies, the cost-effectiveness, and medical/legal considerations are still needed. We believe that time will indeed foster further technological advances and lead to widespread use of VR/AR in routine ophthalmic practice.

Ophthalmology is a field of medicine that is well suited for the use of VR/AR. However, further longitudinal studies examining the practical feasibility, efficacy, and safety of such novel technologies, the cost-effectiveness, and medical/legal considerations are still needed. We believe that time will indeed foster further technological advances and lead to widespread use of VR/AR in routine ophthalmic practice.We identified a microRNA (miRNA) profile characterizing HIV lipodystrophy and explored the downstream mechanistic implications with respect to adipocyte biology and the associated clinical phenotype. miRNA profiles were extracted from small extracellular vesicles (sEV) of HIV-infected individuals with and without lipodystrophic changes and individuals without HIV, among whom we previously showed significant reductions in adipose Dicer expression related to HIV. miR-20a-3p was increased and miR-324-5p and miR-186 reduced in sEV from HIV lipodystrophic individuals. Changes in these miRNAs correlated with adipose Dicer expression and clinical markers of lipodystrophy, including fat redistribution, insulin resistance, and hypertriglyceridemia. Human preadipocytes transfected with mimic miR-20a-3p, anti-miR-324-5p or anti-miR-186 induced consistent changes in Ltbp2, Wisp2, and Nebl expression. Knockdown of Ltbp2 (Latent-transforming growth factor beta-binding protein 2) downregulated markers of adipocyte differentiation (Fabp4, Pparg, C/ebpa, Fasn, adiponectin, Glut4, CD36), and Lamin C, and increased expression of genes involved in inflammation (IL1β, IL6, and Ccl20). Our studies suggest a unique sEV miRNA signature related to dysregulation of Dicer in adipose in HIV. Enhanced miR-20a-3p or depletion of miR-186 and miR-324-5p may downregulate Ltbp2 in HIV leading to dysregulation in adipose differentiation and inflammation, which could contribute to acquired HIV lipodystrophy and associated metabolic and inflammatory perturbations.Myelofibrosis (MF) is a progressive chronic myeloproliferative neoplasm characterized by hyperactivation of JAK/STAT signaling and dysregulation of the transcription factor GATA1 in megakaryocytes (MKs). TGFβ plays a pivotal role in the pathobiology of MF by promoting bone marrow fibrosis and collagen deposition and by enhancing the dormancy of normal hematopoietic stem cells (HSCs). In this study, we show that MF MKs elaborated significantly greater levels of TGFβ1 than TGFβ2 and TGFβ3 to a varying degree, and evaluated the ability of AVID200 a potent TGFβ1/3 protein trap, to block the excessive TGFβ signaling. Treatment of human mesenchymal stromal cells (MSCs) with AVID200 significantly reduced their proliferation, decreased phosphorylation of SMAD2, and interfered with the ability of TGFβ1 to induce collagen expression. Moreover, treatment of MF mononuclear cells (MNCs) with AVID200 led to increased numbers of progenitor cells (PC) with wild type JAK2 rather than mutated JAK2V617F. This effect of AVID200 on MF PC was attributed to its ability to block TGFβ1-induced p57Kip2 expression and SMAD2 activation thereby allowing normal rather than MF PCs to preferentially proliferate, and form hematopoietic colonies. To assess the in vivo effects of AVID200, Gata1low mice, a murine model of MF, were treated with AVID200 resulting in the reduction in bone marrow (BM) fibrosis and an increase in BM cellularity. AVID200 treatment also increased the frequency and numbers of murine progenitor cells as well as short and long term HSCs.Collectively, these data provide the rationale for TGFβ1 blockade with AVID200 as a therapeutic strategy for MF patients.Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remains limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with non-failing or DCM pediatric patient serum activates the fetal gene program (FGP). Here we show that serum treatment with Proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating microRNAs, promote these pathological changes. Evaluation of the protein secretome showed that midkine (MDK) is up-regulated in DCM serum, and NRVM treatment with MDK activates the FGP. Changes in gene expression in serum-treated NRVMs, evaluated by next-generation RNA sequencing (RNA-Seq), indicates extracellular matrix remodeling and focal adhesion pathways are upregulated in pediatric DCM serum and serum-treated NRVMs, suggesting alterations in cellular stiffness. Cellular stiffness was evaluated by Atomic Force Microscopy, which showed an increase in stiffness in DCM serum-treated NRVMs. Of the proteins increased in DCM sera, secreted frizzled related protein 1 (sFRP1) was a potential candidate for the increase in cellular stiffness, and sFRP1 treatment of NRVMs recapitulated the increase in cellular stiffness observed in response to DCM-serum treatment. Our results show that serum circulating proteins promote pathological changes in gene expression and cellular stiffness, and circulating miRNAs are protective against pathological changes.A long-term high-salt intake (HSI) seems to accelerate cardiac aging and age-related diseases, but the molecular mechanism is still not entirely clear. Exercise is an effective way to delay cardiac aging. However, it remains unclear whether long-term exercise (LTE) can protect heart from aging induced by high-salt stress. In this study, heart CG2196(salt) specific overexpression (HSSO) and RNAi (HSSR) was constructed by using the UAS/hand-Gal4 system in Drosophila. Flies were given exercise and a high-salt diet intervention from 1 to 5 weeks of age. Results showed that HSSR and LTE remarkably prevented heart from accelerated age-related defects caused by HSI and HSSO, and these defects included a marked increase in heart period, arrhythmia index, malondialdehyde (MDA) level, salt expression, and dTOR expression, and a marked decrease in fractional shortening, SOD activity level, dFOXO expression, PGC-1α expression, and the number of mitochondria and myofibrils. The combination of HSSR and LTE could better protect the aging heart from the damage of HSI. Therefore, current evidences suggested that LTE resisted HSI-induced heart presenility via blocking CG2196(salt)/TOR/oxidative stress and activating dFOXO/PGC-1α. LTE also reversed heart presenility induced by cardiac-salt overexpression via activating dFOXO/PGC-1α and blocking TOR/oxidative stress.Mastitis is a disease that seriously threatens the health of the mammary gland after delivery. Pedunculoside (PE) is the main bioactive component of Aquifoliaceae. The purpose of this experiment is to explore the effects of PE on mastitis and its underlying mechanisms. Our research results showed that PE could significantly inhibit the increase in the levels of inflammatory mediators such as TNF-α, IL-6, IL-1β, MPO and iNOS during mastitis. Mechanism studies have found that PE could significantly inhibit the phosphorylation of AKT protein and binds to the ASP-184 site. Further research found that PE also inhibited the activation of AKT's downstream pro-inflammatory signals NF-κB and MAPK. In addition, PE effectively promote the expression of tight junction proteins occludin and claudin-3 during inflammation, maintaining the integrity of the blood-milk barrier. In summary, our research shows that PE inhibits the phosphorylation of AKT/NF-κB and MAPK signals; It also relieves mastitis by repairing the blood-milk barrier.