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As the burgeoning field of Artificial Intelligence (AI) continues to permeate the fabric of healthcare, particularly in the realms of patient surveillance and telemedicine, a transformative era beckons. This manuscript endeavors to unravel the intricacies of recent AI advancements and their profound implications for reconceptualizing the delivery of medical care. Through the introduction of innovative instruments such as virtual assistant chatbots, wearable monitoring devices, predictive analytic models, personalized treatment regimens, and automated appointment systems, AI is not only amplifying the quality of care but also empowering patients and fostering a more interactive dynamic between the patient and the healthcare provider. Yet, this progressive infiltration of AI into the healthcare sphere grapples with a plethora of challenges hitherto unseen. The exigent issues of data security and privacy, the specter of algorithmic bias, the requisite adaptability of regulatory frameworks, and the matter of patient acceptance and trust in AI solutions demand immediate and thoughtful resolution .The importance of establishing stringent and far-reaching policies, ensuring technological impartiality, and cultivating patient confidence is paramount to ensure that AI-driven enhancements in healthcare service provision remain both ethically sound and efficient. In conclusion, we advocate for an expansion of research efforts aimed at navigating the ethical complexities inherent to a technology-evolving landscape, catalyzing policy innovation, and devising AI applications that are not only clinically effective but also earn the trust of the patient populace. By melding expertise across disciplines, we stand at the threshold of an era wherein AI's role in healthcare is both ethically unimpeachable and conducive to elevating the global health quotient.
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Inteligência Artificial , Medicina de Precisão , Telemedicina , Inteligência Artificial/ética , Humanos , Medicina de Precisão/métodos , Atenção à SaúdeRESUMO
BACKGROUND: Diabetic foot ulcers (DFUs) are a common complication of diabetes, often leading to severe infections, amputations, and reduced quality of life. The current standard treatment protocols for DFUs have limitations in promoting efficient wound healing and preventing complications. A comprehensive treatment approach targeting multiple aspects of wound care may offer improved outcomes for patients with DFUs. The hypothesis of this study is that a comprehensive treatment protocol for DFUs will result in faster wound healing, reduced amputation rates, and improved overall patient outcomes compared to standard treatment protocols. AIM: To compare the efficacy and safety of a comprehensive treatment protocol for DFUs with those of the standard treatment protocol. METHODS: This retrospective study included 62 patients with DFUs, enrolled between January 2022 and January 2024, randomly assigned to the experimental (n = 32) or control (n = 30) group. The experimental group received a comprehensive treatment comprising blood circulation improvement, debridement, vacuum sealing drainage, recombinant human epidermal growth factor and anti-inflammatory dressing, and skin grafting. The control group received standard treatment, which included wound cleaning and dressing, antibiotics administration, and surgical debridement or amputation, if necessary. Time taken to reduce the white blood cell count, number of dressing changes, wound healing rate and time, and amputation rate were assessed. RESULTS: The experimental group exhibited significantly better outcomes than those of the control group in terms of the wound healing rate, wound healing time, and amputation rate. Additionally, the comprehensive treatment protocol was safe and well tolerated by the patients. CONCLUSION: Comprehensive treatment for DFUs is more effective than standard treatment, promoting granulation tissue growth, shortening hospitalization time, reducing pain and amputation rate, improving wound healing, and enhancing quality of life.
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Photobiomodulation (PBM) therapy uses light of different wavelengths to treat various retinal degeneration diseases, but the potential damage to the retina caused by long-term light irradiation is still unclear. This study were designed to detect the difference between long- and short-wavelength light (650-nm red light and 450-nm blue light, 2.55 mW/cm2, reference intensity in PBM)-induced injury. In addition, a comparative study was conducted to investigate the differences in retinal light damage induced by different irradiation protocols (short periods of repeated irradiation and a long period of constant irradiation). Furthermore, the protective role of PARP-1 inhibition on the molecular mechanism of blue light-induced injury was confirmed by a gene knockdown technique or a specific inhibitor through in vitro and in vivo experiments. The results showed that the susceptibility to retinal damage caused by irradiation with long- and short-wavelength light is different. Shorter wavelength lights, such as blue light, induce more severe retinal damage, while the retina exhibits better resistance to longer wavelength lights, such as red light. In addition, repeated irradiation for short periods induces less retinal damage than constant exposure over a long period. PARP-1 plays a critical role in the molecular mechanism of blue light-induced damage in photoreceptors and retina, and inhibiting PARP-1 can significantly protect the retina against blue light damage. This study lays an experimental foundation for assessing the safety of phototherapy products and for developing target drugs to protect the retina from light damage.
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Luz , Poli(ADP-Ribose) Polimerase-1 , Retina , Degeneração Retiniana , Animais , Poli(ADP-Ribose) Polimerase-1/metabolismo , Camundongos , Luz/efeitos adversos , Retina/efeitos da radiação , Retina/patologia , Degeneração Retiniana/etiologia , Degeneração Retiniana/metabolismo , Degeneração Retiniana/patologia , Degeneração Retiniana/prevenção & controle , Camundongos Endogâmicos C57BL , Lesões Experimentais por Radiação/patologia , Lesões Experimentais por Radiação/metabolismo , Modelos Animais de Doenças , Western Blotting , Masculino , Terapia com Luz de Baixa Intensidade , Luz AzulRESUMO
Few studies were performed on the impact of exposure to gaseous pollutants on the risk of knee osteoarthritis (KOA). We conducted this study to analyze the association between short-term exposure to gaseous pollutants and the risk of hospitalizations for KOA. A total of 2952 KOA hospitalizations derived from two hospitals in Hefei, and the relationship between gaseous pollutants and KOA hospitalizations was analyzed by a distributed lag non-linear model combined with a generalized linear model. We found that the decreased risk of hospitalizations for KOA were both related to exposure to NO2 (RR = 0.993, lag19 day) and O3 (RR = 0.984, lag0 day), while exposure to CO could increase the risk of hospitalizations for KOA (RR = 1.076, lag2 day). Stratified analyses suggested that the KOA patients < 65 years were more susceptible to O3 exposure, and the female, male, patients ≥ 65 years, and patients < 65 years were both more sensitive to CO exposure. Our findings demonstrated that exposure to NO2, O3 resulted in a decreased risk for KOA hospitalizations, and CO exposure might increase the risk of KOA hospitalizations.
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Poluentes Atmosféricos , Poluição do Ar , Poluentes Ambientais , Osteoartrite do Joelho , Humanos , Masculino , Feminino , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Dióxido de Nitrogênio , Exposição Ambiental/análise , Osteoartrite do Joelho/epidemiologia , China/epidemiologia , Material Particulado/análiseRESUMO
Microcystins (MCs) are the most widespread, frequently found, and seriously toxic cyanobacterial toxins in aquatic environments. Microcystin-leucine-arginine (MCLR) and microcystin-arginine-arginine (MCRR) are the most studied MCs. Normally, their levels are low and they coexist in the environment; however, they may also interact with each other. The developmental toxicity of MCLR in the presence of MCRR in the early life stage of zebrafish (from 2 to 120 h post fertilization) was investigated for the first time in this study. Our findings revealed that MCRR treatment marginally elevated thyroxine (T4) and 3,5,3'-triiodothyronine (T3) levels, whereas MCLR treatment alone resulted in a significant increase in T3 and T4 levels, indicating a cooperative effect. Furthermore, clear changes in the expression levels of genes involved in growth and development, accompanied by growth inhibition, were observed after co-treatment with MCRR and MCLR. In addition, zebrafish larvae subjected to MCRR and/or MCLR treatment showed increased levels of superoxide dismutase, glutathione, and malondialdehyde, and decreased levels of catalase in the MCRR + MCLR group, indicating oxidative stress and lipid peroxidation. Thus, we investigated the synergistic developmental toxicity of MCRR and MCLR during the early life stages of zebrafish development.
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Toxinas Marinhas , Microcistinas , Peixe-Zebra , Animais , Peixe-Zebra/metabolismo , Microcistinas/toxicidade , Larva , Arginina/metabolismoRESUMO
Under increasing anthropogenic pressure, species with a previously contiguous distribution across their ranges have been reduced to small fragmented populations. The critically endangered Yangtze finless porpoise ( Neophocaena asiaeorientalis asiaeorientalis), once commonly observed in the Yangtze River-Poyang Lake junction, is now rarely seen in the river-lake corridor. In this study, static passive acoustic monitoring techniques were used to detect the biosonar activities of the Yangtze finless porpoise in this unique corridor. Generalized linear models were used to examine the correlation between these activities and anthropogenic impacts from the COVID-19 pandemic lockdown and boat navigation, as well as environmental variables, including hydrological conditions and light levels. Over approximately three consecutive years of monitoring (2020-2022), porpoise biosonar was detected during 93% of logged days, indicating the key role of the corridor for finless porpoise conservation. In addition, porpoise clicks were recorded in 3.80% of minutes, while feeding correlated buzzes were detected in 1.23% of minutes, suggesting the potential existence of localized, small-scale migration. Furthermore, both anthropogenic and environmental variables were significantly correlated with the diel, lunar, monthly, seasonal, and annual variations in porpoise biosonar activities. During the pandemic lockdown period, porpoise sonar detection showed a significant increase. Furthermore, a significant negative correlation was identified between the detection of porpoise click trains and buzzes and boat traffic intensity. In addition to water level and flux, daylight and moonlight exhibited significant correlations with porpoise biosonar activities, with markedly higher detections at night and quarter moon periods. Ensuring the spatiotemporal reduction of anthropogenic activities, implementing vessel speed restrictions (e.g., during porpoise migration and feeding), and maintaining local natural hydrological regimes are critical factors for sustaining porpoise population viability.
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COVID-19 , Toninhas , Animais , Efeitos Antropogênicos , COVID-19/epidemiologia , COVID-19/veterinária , Controle de Doenças Transmissíveis , Lagos , Pandemias , Rios , ChinaRESUMO
The retinal pigment epithelium (RPE) is a highly specialized and polarized epithelial cell layer that plays an important role in sustaining the structural and functional integrity of photoreceptors. However, the death of RPE is a common pathological feature in various retinal diseases, especially in age-related macular degeneration (AMD) and diabetic retinopathy (DR). Mitophagy, as a programmed self-degradation of dysfunctional mitochondria, is crucial for maintaining cellular homeostasis and cell survival under stress. RPE contains a high density of mitochondria necessary for it to meet energy demands, so severe stimuli can cause mitochondrial dysfunction and the excess generation of intracellular reactive oxygen species (ROS), which can further trigger oxidative stress-involved mitophagy. In this review, we summarize the classical pathways of oxidative stress-involved mitophagy in RPE and investigate its role in the progression of retinal diseases, aiming to provide a new therapeutic strategy for treating retinal degenerative diseases. The role of mitophagy in AMD and DR. In AMD, excessive ROS production promotes mitophagy in the RPE by activating the Nrf2/p62 pathway, while in DR, ROS may suppress mitophagy by the FOXO3-PINK1/parkin signaling pathway or the TXNIP-mitochondria-lysosome-mediated mitophagy.
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Degeneração Macular , Epitélio Pigmentado da Retina , Humanos , Epitélio Pigmentado da Retina/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Mitofagia , Estresse Oxidativo/fisiologiaRESUMO
BACKGROUND: In addition to rescuing injured retinal ganglion cells (RGCs) by stimulating the intrinsic growth ability of damaged RGCs in various retinal/optic neuropathies, increasing evidence has shown that the external microenvironmental factors also play a crucial role in restoring the survival of RGCs by promoting the regrowth of RGC axons, especially inflammatory factors. In this study, we aimed to screen out the underlying inflammatory factor involved in the signaling of staurosporine (STS)-induced axon regeneration and verify its role in the protection of RGCs and the promotion of axon regrowth. METHODS: We performed transcriptome RNA sequencing for STS induction models in vitro and analyzed the differentially expressed genes. After targeting the key gene, we verified the role of the candidate factor in RGC protection and promotion of axon regeneration in vivo with two RGC-injured animal models (optic nerve crush, ONC; retinal N-methyl-D-aspartate, NMDA damage) by using cholera toxin subunit B anterograde axon tracing and specific immunostaining of RGCs. RESULTS: We found that a series of inflammatory genes expressed upregulated in the signaling of STS-induced axon regrowth and we targeted the candidate CXCL2 gene since the level of the chemokine CXCL2 gene elevated significantly among the top upregulated genes. We further demonstrated that intravitreal injection of rCXCL2 robustly promoted axon regeneration and significantly improved RGC survival in ONC-injured mice in vivo. However, different from its role in ONC model, the intravitreal injection of rCXCL2 was able to simply protect RGCs against NMDA-induced excitotoxicity in mouse retina and maintain the long-distance projection of RGC axons, yet failed to promote significant axon regeneration. CONCLUSIONS: We provide the first in vivo evidence that CXCL2, as an inflammatory factor, is a key regulator in the axon regeneration and neuroprotection of RGCs. Our comparative study may facilitate deciphering the exact molecular mechanisms of RGC axon regeneration and developing high-potency targeted drugs.
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Excessive light exposure can potentially cause irreversible damage to the various photoreceptor cells, and this aspect has been considered as an important factor leading to the progression of the different retinal diseases. AMP-activated protein kinase (AMPK) and the mammalian target of rapamycin (mTOR) are crucial intracellular signaling hubs involved in the regulation of cellular metabolism, energy homeostasis, cellular growth and autophagy. A number of previous studies have indicated that either AMPK activation or mTOR inhibition can promote autophagy in most cases. In the current study, we have established an in vitro as well as in vivo photooxidation-damaged photoreceptor model and investigated the possible influence of visible light exposure in the AMPK/mTOR/autophagy signaling pathway. We have also explored the potential regulatory effects of AMPK/mTOR on light-induced autophagy and protection achieved by suppressing autophagy in photooxidation-damaged photoreceptors. We observed that light exposure led to a significant activation of mTOR and autophagy in the photoreceptor cells. However, intriguingly, AMPK activation or mTOR inhibition significantly inhibited rather than promoting autophagy, which was termed as AMPK-dependent inhibition of autophagy. In addition, either indirectly suppressing autophagy by AMPK activation/ mTOR inhibition or directly blocking autophagy with an inhibitor exerted a significant protective effect on the photoreceptor cells against the photooxidative damage. Neuroprotective effects caused by the AMPK-dependent inhibition of autophagy were also verified with a retinal light injured mouse model in vivo. Overall, our findings demonstrated that AMPK / mTOR pathway could inhibit autophagy through AMPK-dependent inhibition of autophagy to significantly protect the photoreceptors from photooxidative injury, which may aid to further develop novel targeted retinal neuroprotective drugs.
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Proteínas Quinases Ativadas por AMP , Fármacos Neuroprotetores , Camundongos , Animais , Proteínas Quinases Ativadas por AMP/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Transdução de Sinais , Células Fotorreceptoras/metabolismo , Fármacos Neuroprotetores/farmacologia , Sirolimo/farmacologia , Autofagia , Mamíferos/metabolismoRESUMO
Importance: Glaucoma is the second leading cause of blindness in the world. The causal direction and magnitude of the association between blood cell traits and glaucoma is uncertain because of the susceptibility of observational studies to confounding and reverse causation. Objective: To explore whether there is a causal relationship of blood cell traits including white blood cell (WBC) count (WBCC) and its subtypes [basophil cell count (BASO), monocyte cell count (MONO), lymphocyte cell count (LYMPH), eosinophil cell count (EOS), neutrophil cell count (NEUT)], red blood cell (RBC) count (RBCC), red blood distribution width (RDW), platelet count (PLT), and plateletcrit (PCT) on glaucoma risk. Methods: A two-sample Mendelian randomization (MR) analysis was conducted. Genome-wide significant single nucleotide polymorphisms (SNPs) from published genome-wide association studies (GWAS) on human blood cell traits were utilized as exposure instruments and the dataset for outcome was from the GWAS summary data of glaucoma. In the univariable MR analysis, we examined the association between genetic evidence of blood cell traits and glaucoma. To further investigate the potential causal mechanisms underlying the observed association, we performed multivariable MR analysis with three models, taking into account the mediator effect of inflammation and oxidative stress. According to Bonferroni-corrected for the 10 exposures in 3 methods, the MR study yielded a statistically significant p-value of 0.0017. Results: Genetically BASO, PCT, LYMPH, and PLT were potentially positively associated with glaucoma in the European ancestry [BASO: Odds ratio (OR) = 1.00122, 95% confidence interval (CI), 1.00003-1.00242, p = 0.045; PCT: OR = 1.00078, 95% CI, 1.00012-1.00143, p = 0.019; LYMPH: OR = 1.00076, 95% CI, 1.00002-1.00151, p = 0.045; PLT: OR = 1.00065, 95% CI, 1.00006-1.00123, p = 0.030], There was insufficient evidence to support a causal association of MONO, NEUT, EOS, WBCC, RBCC and RDW (MONO: OR = 1.00050, p = 0.098; NEUT: OR = 1.00028, p = 0.524; EOS: OR = 1.00020, p = 0.562; WBCC: OR = 1.00008, p = 0.830; RBCC: OR = 0.99996, p = 0.920; RDW: OR = 0.99987, p = 0.734) with glaucoma. The multivariable MR with model 1, 2, and 3 demonstrated that BASO, PCT, LYMPH, and PLT were still potentially genetically associated with the risk of glaucoma. Conclusion: Our study reveals a genetic predisposition to higher LYMPH, BASO, PLT, and PCT are associated with a higher risk of glaucoma, whereas WBCC, MONO, EOS, NEUT, RBCC, and RDW are not associated with the occurrence of glaucoma. This finding also supports previous observational studies associating immune components with glaucoma, thus provide guidance on the predication and prevention for glaucoma.
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Purpose: The incidence of orbital blowout fractures (OBFs) is gradually increasing due to traffic accidents, sports injuries, and ocular trauma. Orbital computed tomography (CT) is crucial for accurate clinical diagnosis. In this study, we built an artificial intelligence (AI) system based on two available deep learning networks (DenseNet-169 and UNet) for fracture identification, fracture side distinguishment, and fracture area segmentation. Methods: We established a database of orbital CT images and manually annotated the fracture areas. DenseNet-169 was trained and evaluated on the identification of CT images with OBFs. We also trained and evaluated DenseNet-169 and UNet for fracture side distinguishment and fracture area segmentation. We used cross-validation to evaluate the performance of the AI algorithm after training. Results: For fracture identification, DenseNet-169 achieved an area under the receiver operating characteristic curve (AUC) of 0.9920 ± 0.0021, with an accuracy, sensitivity, and specificity of 0.9693 ± 0.0028, 0.9717 ± 0.0143, and 0.9596 ± 0.0330, respectively. DenseNet-169 realized the distinguishment of the fracture side with accuracy, sensitivity, specificity, and AUC of 0.9859 ± 0.0059, 0.9743 ± 0.0101, 0.9980 ± 0.0041, and 0.9923 ± 0.0008, respectively. The intersection over union (IoU) and Dice coefficient of UNet for fracture area segmentation were 0.8180 ± 0.0093 and 0.8849 ± 0.0090, respectively, showing a high agreement with manual segmentation. Conclusions: The trained AI system could realize the automatic identification and segmentation of OBFs, which might be a new tool for smart diagnoses and improved efficiencies of three-dimensional (3D) printing-assisted surgical repair of OBFs. Translational Relevance: Our AI system, based on two available deep learning network models, could help in precise diagnoses and accurate surgical repairs.
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Algoritmos , Inteligência Artificial , Tomografia Computadorizada por Raios X/métodosRESUMO
PURPOSE: Due to the inimitable anatomical structure of the eyeball and various physiological barriers, conventional ocular local administration is often complicated by apparent shortcomings, such as limited bioavailability and short drug retention. Thus, developing methods for sustainable, safe and efficient drug delivery to ocular target sites has long been an urgent need. This study briefly summarizes the barriers to ocular drug administration and various ocular drug delivery routes and highlights recent progress in ocular implantable sustained-release drug delivery systems (DDSs) to provide literature evidence for developing novel ocular implants for sustained drug delivery. METHODS: We conducted a comprehensive search of studies on ocular implantable sustained-release DDSs in PubMed and Web of Science using the following keywords: ocular, implantable and drug delivery system. More than 400 papers were extracted. Publications focused on sustained and controlled drug release were primarily considered. Experimental articles involving DDSs that cannot be implanted into the eye through surgeries and cannot be inserted into ocular tissues in solid form were excluded. Approximately 143 publications were reviewed to summarize the most current information on the subject. RESULTS: In recent years, numerous ocular sustained-release DDSs using lipids, nanoparticles and hydrogels as carriers have emerged. With unique properties and systematic design, ocular implantable sustained-release DDSs are able to continuously maintain drug release, effectively sustain the therapeutic concentration in target tissues, and substantially enhance the therapeutic efficacy. Nevertheless, few ocular implantable sustained-release DDSs have been available in clinical use. CONCLUSIONS: Ocular implantable sustained-release DDSs have become a new focus in the field of ocular drug development through unique designs and improvements in the materials of drug carriers, administration methods and dosage forms. With more ocular implantable sustained-release DDSs being commercialized, ocular therapeutics may be revolutionized.
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Sistemas de Liberação de Medicamentos , Olho , Humanos , Preparações de Ação Retardada/farmacologia , Preparações de Ação Retardada/uso terapêutico , Portadores de Fármacos/química , Portadores de Fármacos/farmacologia , Administração OftálmicaRESUMO
Retinitis pigmentosa (RP) is a group of genetic disorders resulting in inherited blindness due to the degeneration of rod and cone photoreceptors. The various mechanisms underlying rod degeneration primarily rely on genetic mutations, leading to night blindness initially. Cones gradually degenerate after rods are almost eliminated, resulting in varying degrees of visual disability and blindness. The mechanism of cone degeneration remains unclear. An understanding of the mechanisms underlying cone degeneration in RP, a highly heterogeneous disease, is essential to develop novel treatments of RP. Herein, we review recent advancements in the five hypotheses of cone degeneration, including oxidative stress, trophic factors, metabolic stress, light damage, and inflammation activation. We also discuss the connection among these theories to provide a better understanding of secondary cone degeneration in RP. Five current mechanisms of cone degenerations in RP Interactions among different pathways are involved in RP.
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Células Fotorreceptoras Retinianas Cones , Retinose Pigmentar , Humanos , Células Fotorreceptoras Retinianas Cones/metabolismo , Células Fotorreceptoras Retinianas Bastonetes/metabolismo , Retinose Pigmentar/genética , Retinose Pigmentar/metabolismo , Retinose Pigmentar/terapia , Cegueira/metabolismo , Estresse OxidativoRESUMO
Orbital and eyelid disorders affect normal visual functions and facial appearance, and precise oculoplastic and reconstructive surgeries are crucial. Artificial intelligence (AI) network models exhibit a remarkable ability to analyze large sets of medical images to locate lesions. Currently, AI-based technology can automatically diagnose and grade orbital and eyelid diseases, such as thyroid-associated ophthalmopathy (TAO), as well as measure eyelid morphological parameters based on external ocular photographs to assist surgical strategies. The various types of imaging data for orbital and eyelid diseases provide a large amount of training data for network models, which might be the next breakthrough in AI-related research. This paper retrospectively summarizes different imaging data aspects addressed in AI-related research on orbital and eyelid diseases, and discusses the advantages and limitations of this research field.
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Photobiomodulation (PBM) refers to the beneficial effect produced from low-energy light irradiation on target cells or tissues. Increasing evidence in the literature suggests that PBM plays a positive role in the treatment of retinal diseases. However, there is great variation in the light sources and illumination parameters used in different studies, resulting in significantly different conclusions regarding PBM's therapeutic effects. In addition, the mechanism by which PBM improves retinal function has not been fully elucidated. In this study, we conducted a narrative review of the published literature on PBM for treating retinal diseases and summarized the key illumination parameters used in PBM. Furthermore, we explored the potential molecular mechanisms of PBM at the retinal cellular level with the goal of providing evidence for the improved utilization of PBM in the treatment of retinal diseases.
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Terapia com Luz de Baixa Intensidade , Doenças Retinianas , Humanos , Terapia com Luz de Baixa Intensidade/métodos , Retina , Doenças Retinianas/radioterapia , NeurôniosRESUMO
Advancements in technology have resulted in increasing concerns over the safety of eye exposure to light illumination, since prolonged exposure to intensive visible light, especially to short-wavelength light in the visible spectrum, can cause photochemical damage to the retina through a photooxidation-triggered cascade reaction. Poly(ADP-ribose) polymerase-1 (PARP-1) is the ribozyme responsible for repairing DNA damage. When damage to DNA occurs, including nicks and breaks, PARP-1 is rapidly activated, synthesizing a large amount of PAR and recruiting other nuclear factors to repair the damaged DNA. However, retinal photochemical damage may lead to the overactivation of PARP-1, triggering PARP-dependent cell death, including parthanatos, necroptosis, and autophagy. In this review, we retrieved targeted articles with the keywords such as "PARP-1," "photoreceptor," "retinal light damage," and "photooxidation" from databases and summarized the molecular mechanisms involved in retinal photooxidation, PARP activation, and DNA repair to clarify the key regulatory role of PARP-1 in retinal light injury and to determine whether PARP-1 may be a potential marker in response to retinal photooxidation. The highly sensitive detection of PARP-1 activity may facilitate early evaluation of the effects of light on the retina, which will provide an evidentiary basis for the future assessment of the safety of light illumination from optoelectronic products and medical devices.
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Inibidores de Poli(ADP-Ribose) Polimerases , RNA Catalítico , Biomarcadores , DNA/metabolismo , Dano ao DNA , Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia , Retina/metabolismoRESUMO
Based on the service encounter perspective, this study combines theoretical foundations for such factors as service quality and the characteristics of the hospital service industry to develop a research model scale to investigate whether the quality of hospital services affects patients' perceptions of health service encounters, trust, and loyalty. Nowadays, with the advancement of medical technology, patients pay more attention to the quality of medical services and good service encounters provided by healthcare professionals in order to establish positive patient relationships; hospitals need to improve their own service quality and establish good patient trust relationships so that doctor-patient satisfaction and loyalty can be improved. In a review of related literature, this study found that most past studies focused on issues related of quality of medical services and patient satisfaction, but ignored those related to the relationship between medical service encounters and patient trust and loyalty, as well as the lack of scientific measurement markers for service encounters in the Chinese medical service industry. Therefore, this study uses the Service Encounter Perspective and Service Quality Theory Development Research Scale to collect and analyze data for a typical case of a Chinese tertiary hospital. Finally, this study explores the relationship between the four variables of service quality, service encounter, trust, and loyalty by means of a questionnaire and statistical analysis of the data. Finally, it is concluded that the higher the service quality of the hospital, the higher the customer trust, the higher the service encounter, and in the greater the doctor-patient loyalty.
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Qualidade da Assistência à Saúde , Confiança , Idoso , Doença Crônica , Hospitais , Humanos , Satisfação do PacienteRESUMO
Natural visible light is an electromagnetic wave composed of a spectrum of monochromatic wavelengths, each with a characteristic color. Photons are the basic units of light, and their wavelength correlates to the energy of light; short-wavelength photons carry high energy. The retina is a fragile neuronal tissue that senses light and generates visual signals conducted to the brain. However, excessive and intensive light exposure will cause retinal light damage. Within the visible spectrum, short-wavelength light, such as blue light, carries higher energy, and thus the retinal injury, is more significant when exposed to these wavelengths. The damage mechanism triggered by different short-wavelength light varies due to photons carrying different energy and being absorbed by different photosensitive molecules in the retinal neurons. However, photooxidation might be a common molecular step to initiate cell death. Herein, we summarize the historical understanding of light, the key molecular steps related to retinal light injury, and the death pathways of photoreceptors to further decipher the molecular mechanism of retinal light injury and explore potential neuroprotective strategies.
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Doenças Retinianas , Humanos , Retina/metabolismo , Doenças Retinianas/metabolismoRESUMO
Single-factor intervention, such as physical exercise and auditory and visual stimulation, plays a positive role on the prevention and treatment of Alzheimer's disease (AD); however, the therapeutic effects of single-factor intervention are limited. The beneficial effects of these multifactor combinations on AD and its molecular mechanism have yet to be elucidated. Here, we investigated the effect of multifactor intervention, voluntary wheel exercise, and involuntary treadmill running in combination with acousto-optic stimulation, on adult neurogenesis and behavioral phenotypes in a mouse model of AD. We found that 4 weeks of multifactor intervention can significantly increase the production of newborn cells (BrdU+ cells) and immature neurons (DCX+ cells) in the hippocampus and lateral ventricle of Aß oligomer-induced mice. Importantly, the multifactor intervention could promote BrdU+ cells to differentiate into neurons (BrdU+ DCX+ cells or BrdU+ NeuN+ cells) and astrocytes (BrdU+GFAP+ cells) in the hippocampus and ameliorate Aß oligomer-induced cognitive impairment and anxiety- and depression-like behaviors in mice evaluated by novel object recognition, Morris water maze tests, elevated zero maze, forced swimming test, and tail suspension test, respectively. Moreover, multifactor intervention could lead to an increase in the protein levels of PSD-95, SYP, DCX, NeuN, GFAP, Bcl-2, BDNF, TrkB, and pSer473-Akt and a decrease in the protein levels of BAX and caspase-9 in the hippocampal lysates of Aß oligomer-induced mice. Furthermore, sequencing analysis of serum metabolites revealed that aberrantly expressed metabolites modulated by multifactor intervention were highly enriched in the biological process associated with keeping neurons functioning and neurobehavioral function. Additionally, the intervention-mediated serum metabolites mainly participated in glutamate metabolism, glucose metabolism, and the tricarboxylic acid cycle in mice. Our findings suggest the potential of multifactor intervention as a non-invasive therapeutic strategy for AD to anti-Aß oligomer neurotoxicity.