These results obtained using standard colorimetry support the hypothesis that the use of color filters does not cause CVDs to have a perception similar to that of a normal observer.BACKGROUND AND OBJECTIVE Accurate retinal vessel segmentation is often considered to be a reliable biomarker of diagnosis and screening of various diseases, including cardiovascular diseases, diabetic, and ophthalmologic diseases. Recently, deep learning (DL) algorithms have demonstrated high performance in segmenting retinal images that may enable fast and lifesaving diagnoses. To our knowledge, there is no systematic review of the current work in this research area. Therefore, we performed a systematic review with a meta-analysis of relevant studies to quantify the performance of the DL algorithms in retinal vessel segmentation. METHODS A systematic search on EMBASE, PubMed, Google Scholar, Scopus, and Web of Science was conducted for studies that were published between 1 January 2000 and 15 January 2020. We followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) procedure. The DL-based study design was mandatory for a study's inclusion. Two authors independently screened al promising, especially for those countries with limited access to healthcare. More compressive studies and global efforts are mandatory for evaluating the cost-effectiveness of DL-based tools for retinal disease screening worldwide.Age-related hearing loss (ARHL) is an irreversible, progressive neurodegenerative disorder and is presently untreatable. Previous studies using animal models have suggested mitochondrial damage and programmed cell death to be involved with ARHL. Thus, we further investigated the pathophysiologic role of mitochondria and necroptosis in aged C57BL/6J male mice. Aged mice (20 months old) exhibited a significant loss of hearing, number of hair cells, neuronal fibers, and synaptic ribbons compared to young mice. Ultrastructural analysis of aged cochleae revealed damaged mitochondria with absent or disorganized cristae. Aged mice also showed significant decrease in cochlear blood flow, and exhibited increase in gene expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) and the pseudokinase mixed-lineage kinase domain-like (MLKL). Immunofluorescence (IF) assays of cytochrome C oxidase I (COX1) confirmed mitochondrial dysfunction in aged cochleae, which correlated with the degree of mitochondrial morphological damage. IF assays also revealed localization and increased expression of RIPK3 in sensorineural tissues that underwent significant necroptosis (inner and outer hair cells and stria vascularis). Selleckchem FK506 Together, our data shows that the aging cochlea exhibits damaged mitochondria, enhanced synthesis of proinflammatory cytokines, and provides new evidence of necroptosis in the aging cochlea in in vivo.Oral mucositis is a toxic side effect of non-surgical cancer treatments chemotherapy and radiotherapy, which strongly impair quality of life and can not only cause strong pain, but also lead to problems with basic physiological needs as eating and swallowing. Development of oral mucositis is associated with type, dosage, and schedule of radiation or chemotherapy and other factors related to patients. Management of oral mucositis is a valid problem, requiring topical application of anesthetics, coating agents, cryotherapy, low level laser therapy, pharmacological methods as usage of keratinocyte growth factors, supplementation of vitamins, and a proper diet. Another approach to oral mucositis measurement includesphotobiomodulation, which brings analgesic and anti-inflammatory effects.Although oral mucositis is a general health issues, the role of proper dental care is essential. It should include elimination of all potential sources of mucosal injury and microorganisms inhabiting theoral cavity through oral hygiene education,professional management ofdental plaque,and treatment of the caries and periodontium, which are necessary to reduce the risk of inflammation in the oral cavity. This paper describes the possibilities of monitoring oral mucositis,taking into account the latest therapeutic achievements.At least half of human immunodeficiency virus (HIV)-infected individuals suffer from a wide range of cognitive, behavioral and motor deficits, collectively known as HIV-associated neurocognitive disorders (HAND). The molecular mechanisms that amplify damage within the brain of HIV-infected individuals are unknown. Recently, we described that HIV augments the opening of connexin-43 (Cx43) hemichannels in cultured human astrocytes, which result in the collapse of neuronal processes. Whether HIV soluble viral proteins such as gp120, can regulate hemichannel opening in astrocytes is still ignored. These channels communicate the cytosol with the extracellular space during pathological conditions. We found that gp120 enhances the function of both Cx43 hemichannels and pannexin-1 channels in mouse cortical astrocytes. These effects depended on the activation of IL-1β/TNF-α, p38 MAP kinase, iNOS, cytoplasmic Ca2+ and purinergic signaling. The gp120-induced channel opening resulted in alterations in Ca2+ dynamics, nitric oxide production and ATP release. Although the channel opening evoked by gp120 in astrocytes was reproduced in ex vivo brain preparations, these responses were heterogeneous depending on the CA1 region analyzed. We speculate that soluble gp120-induced activation of astroglial Cx43 hemichannels and pannexin-1 channels could be crucial for the pathogenesis of HAND.In preeclampsia, widespread maternal endothelial dysfunction is often secondary to excessive generation of placental-derived anti-angiogenic factors, including soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), along with proinflammatory cytokines such as tumour necrosis factor-α (TNF-α) and activin A, understanding of which offers potential opportunities for the development of novel therapies. The antimalarial hydroxychloroquine is an anti-inflammatory drug improving endothelial homeostasis in lupus. It has not been explored as to whether it can improve placental and endothelial function in preeclampsia. In this in vitro study, term placental explants were used to assess the effects of hydroxychloroquine on placental production of sFlt-1, sEng, TNF-α, activin A, and 8-isoprostane after exposure to hypoxic injury or oxidative stress. Similarly, human umbilical vein endothelial cells (HUVECs) were used to assess the effects of hydroxychloroquine on in vitro markers of endothelial dysfunction.