The role of regulatory T cells in vitiligo and therapeutic advances: a mini-review.

BACKGROUND: Regulatory T cells (Tregs) play vital roles in controlling immune reactions and maintaining immune tolerance in the body. The targeted destruction of epidermal melanocytes by activated CD8+T cells is a key event in the development of vitiligo. However, Tregs may exert immunosuppressive effects on CD8+T cells, which could be beneficial in treating vitiligo. METHODS: A comprehensive search of PubMed and Web of Science was conducted to gather information on Tregs and vitiligo. RESULTS: In vitiligo, there is a decrease in Treg numbers and impaired Treg functions, along with potential damage to Treg-related signaling pathways. Increasing Treg numbers and enhancing Treg function could lead to immunosuppressive effects on CD8+T cells. Recent research progress on Tregs in vitiligo has been summarized, highlighting various Treg-related therapies being investigated for clinical use. The current status of Treg-related therapeutic strategies and potential future directions for vitiligo treatment are also discussed. CONCLUSIONS: A deeper understanding of Tregs will be crucial for advancing Treg-related drug discovery and treatment development in vitiligo.

A cross-sectional study: correlation of forehead morphology and dentoskeletal malocclusion in Chinese people.

BACKGROUND: The lateral profile is an important indicator of facial attractiveness. This study explored the general characteristics of the forehead profile and protrusion, and their relationship with related factors in structure and development. METHODS: Four hundred fourteen Chinese participants in the Yangtze River Delta region were involved. Including 206 males (17.15 ± 7.68 years old) and 208 females (18.35 ± 8.06 years old); 94 children (8.54 ± 2.21 years old, ranging from 4 to 12 years old), 166 adolescents (14.83 ± 1.50 years old, ranging from 13 to 17 years old), and 154 adults (25.52 ± 4.89, 18 years or older). The frontal section of the forehead was used to explore its shape. The straight distance between the vertical line of the FH plane through the nasal root point and its parallel line, which is tangential to the forehead, indicates the forehead prominence. Frontal sinus width was measured using the method described by Mahmood. RESULTS: The general shape of the forehead was straight and slightly bulged near the eyebrow arch in males but rounder in females. The average forehead protrusion in males was higher than that in females in adults. Significant differences in forehead protrusion between the dentoskeletal classifications and growth phases were notable. Frontal protrusion significantly correlated with frontal sinus depth, especially in males, adults, Class I, and those whose convex points were located in the lower section of the forehead. CONCLUSIONS: Age, race, and sex affect the forehead protrusion and frontal sinus width. Forehead protrusion may be an indicator of dentoskeletal deformities in the early stage. And dentoskeletal deformities may impair the correlation between the frontal sinuses and forehead protrusion during development. TRIAL REGISTRATION: This retrospective, cross-sectional study was reviewed and approved by the Research Ethical Committee (T2020008), and registered at ClinicalTrial.gov with an identified number (ChiCTR2100041913).

CNN-Siam: multimodal siamese CNN-based deep learning approach for drug‒drug interaction prediction.

BACKGROUND: Drug‒drug interactions (DDIs) are reactions between two or more drugs, i.e., possible situations that occur when two or more drugs are used simultaneously. DDIs act as an important link in both drug development and clinical treatment. Since it is not possible to study the interactions of such a large number of drugs using experimental means, a computer-based deep learning solution is always worth investigating. We propose a deep learning-based model that uses twin convolutional neural networks to learn representations from multimodal drug data and to make predictions about the possible types of drug effects. RESULTS: In this paper, we propose a novel convolutional neural network algorithm using a Siamese network architecture called CNN-Siam. CNN-Siam uses a convolutional neural network (CNN) as a backbone network in the form of a twin network architecture to learn the feature representation of drug pairs from multimodal data of drugs (including chemical substructures, targets and enzymes). Moreover, this network is used to predict the types of drug interactions with the best optimization algorithms available (RAdam and LookAhead). The experimental data show that the CNN-Siam achieves an area under the precision-recall (AUPR) curve score of 0.96 on the benchmark dataset and a correct rate of 92%. These results are significant improvements compared to the state-of-the-art method (from 86 to 92%) and demonstrate the robustness of the CNN-Siam and the superiority of the new optimization algorithm through ablation experiments. CONCLUSION: The experimental results show that our multimodal siamese convolutional neural network can accurately predict DDIs, and the Siamese network architecture is able to learn the feature representation of drug pairs better than individual networks. CNN-Siam outperforms other state-of-the-art algorithms with the combination of data enhancement and better optimizers. But at the same time, CNN-Siam has some drawbacks, longer training time, generalization needs to be improved, and poorer classification results on some classes.

Triglyceride-glucose index in the prediction of clinical outcomes after successful recanalization for coronary chronic total occlusions.

BACKGROUND: Triglyceride-glucose index (TyG) has been widely used to predict cardiovascular outcomes. However, it remains unclear whether TyG holds prognostic significance for patients with coronary chronic total occlusions (CTO). Thus, our study aimed to evaluate the predictive accuracy and prognostic value of TyG in individuals who underwent successful percutaneous coronary intervention (PCI) for CTO. METHODS: A total of 331 consecutive patients with ≥ 1 successful CTO-PCI were included. The baseline and angiographic data were acquired. The duration of follow-up ranged from 32 to 79 months, with a median of 44 months and an interquartile range of 39 to 67 months. The primary outcome measured was the occurrence of major adverse cardiac and cerebrovascular events (MACCE), including mortality, target vessel revascularization, recurrent myocardial infarction, and stroke. RESULTS: After controlling for confounders, multivariate Cox regression analysis revealed that TyG remained statistically significant, regardless of being a continuous or categorical variable. In the partially adjusted regression model, the Hazard ratio (95%CI) for MACCE was 2.54 (1.12-5.79) in tertile 3 and 1.61 (1.22-2.12) per SD increase in the TyG.Kaplan-Meier survival analysis demonstrated significant differences in MACCE-free survival rates across tertiles of the TyG, as indicated by the log-rank test (p = 0.001). ROC analysis was conducted to evaluate the predictive ability of TyG for MACCE, resulting in an AUC of 0.677. CONCLUSION: The TyG index demonstrates independent predictive capabilities for MACCE in patients who have undergone successful CTO-PCI. These findings suggest that TyG holds the potential as a valuable tool in risk stratification and the identification of patients who may benefit from early intervention in the management of CTO.

Identification of the Shared Gene Signatures and Biological Mechanisms in Hyperplastic Enlarged Lobular Units and Breast Cancer.

Breast cancer is a common cancer worldwide. Hyperplastic enlarged lobular units (HELUs) are common changes in the breasts of adult women. HELUs may be closely related to the occurrence and development of breast cancer. In this study, genes that are commonly contained in the expression profiles of the genomes of the two diseases and have significant differences in expression before and after the respective diseases were identified. Various enrichment analyses were performed according to the expression levels of these differentially expressed genes. Furthermore, LASSO regression analysis was performed on the differentially expressed genes to identify genes significantly related to survival. The optimal risk model for the survival of patients with breast cancer was established, and the accuracy of the model was verified on multiple data sets. A gene combination containing 17 genes was ultimately determined to be an independent prognostic factor. Kaplan‒Meier survival analysis demonstrated the good performance of this risk model. The study found that Shared Gene Signatures and Biological Mechanisms in Hyperplastic Enlarged Lobular Units and Breast Cancer, screened 17 important Shared Gene Signatures of Hyperplastic Enlarged Lobular Units which are closely related to the survival of breast cancer patients through machine learning, and established a prognosis model with high-accuracy, which is worthy of further exploration.

Response of human periodontal ligament to orthodontic force using superb microvascular imaging.

INTRODUCTION: Remodeling of the periodontal ligament (PDL) during orthodontic tooth movement is closely related to the vascularity of the PDL, which has not been thoroughly investigated in humans. This study aimed to measure the width and vascular parameters of human PDL using superb microvascular imaging for the first time. METHODS: Patients aged 18-25 years were selected for participation. The intervention was randomly allocated from the maxillary canines to the first molars on both sides using 50 g or 150 g of force. The width and vascular parameters of the PDL were measured using superb microvascular imaging at different time intervals (baseline, 30 minutes, and 1, 3, 7, and 14 days). RESULTS: Before the intervention, the width of the PDL ranged from 0.14 to 0.25 mm, and the vascular index ranged from 9.40% to 13.54%. After applying orthodontic forces, the cervical and middle PDL widths increased. The vascular index decreased slightly in 30 minutes, decreased to a minimum value after 1 day, increased to the maximum in 3-7 days, and returned to baseline values in 14 days. The values of other vascular parameters showed similar trends. CONCLUSIONS: The width and vascular parameters of the PDL changed slightly after force application, underwent changes in the period of reconstruction for 3-7 days, and eventually returned to baseline in 14 days.

Effect of water temperature on reproductive performance and offspring quality of rare minnow, Gobiocypris rarus.

Water temperature plays a significant role in the reproductive processes of temperate fishes. In the present study, the effects of water temperature on the reproductive performance and offspring quality of rare minnow (Gobiocypris rarus) were evaluated by cultured parent fish at different temperature (18～30℃) in a 2-month trial. The results revealed that rare minnows could spawn continuously within the range from 18℃ to 30℃, and these at 24℃ and 27℃ spawned every 3-4 days. Batch size of rare minnow increased with increasing water temperature, while egg production increased with increasing water temperature and then decreased at 30℃. High water temperature (30℃) had significantly adverse effects on fertilization rate and hatching rate (P<0.05). It was found that the oocyte growth at 18℃, 21℃, and 30℃ were slower than those at 24℃ and 27℃. Histologic analysis further showed that low temperature (18℃ and 21℃) slowed down vitellogenesis and oocyte maturation, while high temperature (30℃) had suppressive effects on oocyte maturation and ovulation. Based on present results, it was concluded that 24-27℃ was optimal breeding temperature for rare minnows and water temperature higher than 30℃ resulting from climate change would pose a threat to its wild populations.

NAcM-OPT protects keratinocytes from H2O2-induced cell damage by promoting autophagy.

This study aimed to investigate the protective effect of NAcM-OPT, a small molecule inhibitor of defective in cullin neddylation 1 (DCN1), on H2O2-induced oxidative damage in keratinocytes. Immortalized human keratinocytes (HaCaT cells) were treated with NAcM-OPT and exposed to oxidative stress. CCK-8 assays were used to measure cell viability. The mGFP-RFP-LC3 dual fluorescent autophagy indicator system was utilized to evaluate changes in autophagic flux. Western blotting was used to measure the expression of the autophagy-related proteins LC3 and Beclin 1. Keratinocytes were treated with the autophagy activator rapamycin, and HaCaT cell supernatant was added to PIG1 cells (immortalized human melanocytes), followed by evaluation of tyrosinase (TYR) expression via qRT-PCR. NAcM-OPT increased cell viability and cell proliferation. Furthermore, this molecule promoted autophagic flux through increased expression of autophagy-related proteins under H2O2-induced oxidative stress. Additionally, rapamycin increased the mRNA levels of TYR in PIG1 cells. Moreover, NAcM-OPT alleviated mitochondrial damage, restored mitochondrial function, and upregulated the expression of NFE2L2, HO1, NQO1, and GCLM. Importantly, NAcM-OPT also increased epidermal thickness, follicle length, and melanin synthesis under oxidative stress in vivo. These findings suggest that NAcM-OPT may be a promising small molecule antioxidant drug for the treatment of vitiligo.

Application of multi-omics techniques to androgenetic alopecia: Current status and perspectives.

The rapid advancement of sequencing technologies has enabled the generation of vast datasets, allowing for the in-depth analysis of sequencing data. This analysis has facilitated the validation of novel pathogenesis hypotheses for understanding and treating diseases through ex vivo and in vivo experiments. Androgenetic alopecia (AGA), a common hair loss disorder, has been a key focus of investigators attempting to uncover its underlying mechanisms. Abnormal changes in mRNA, proteins, and metabolites have been identified in individuals with AGA, and future developments in sequencing technologies may reveal new biomarkers for AGA. By integrating multiple omics analysis datasets such as genomics, transcriptomics, proteomics, and metabolomics-along with clinical phenotype data-we can achieve a comprehensive understanding of the molecular underpinnings of AGA. This review summarizes the data-mining studies conducted on various omics analysis datasets as related to AGA that have been adopted to interpret the biological data obtained from different omics layers. We herein discuss the challenges of integrative omics analyses, and suggest that collaborative multi-omics studies can enhance the understanding of the complete pathomechanism(s) of AGA by focusing on the interaction networks comprising DNA, RNA, proteins, and metabolites.

Variation in placentophagy in golden snub-nosed monkeys (Rhinopithecus roxellana) reflects nutritional constraints.

Golden snub-nosed monkeys show inconsistent frequency of placentophagy between wild and captive populations, with almost all births in the wild but around half of the births in captivity accompanied by the female's consumption of placenta. This aligns with nutritional demands-driven placentophagy, as captive populations are generally under less nutritional constraints for breeding females than the wild population. Placentophagy is probably adaptive in the wild and under positive selection due to nutritional benefits to both mothers and infants.

Does diet or macronutrients intake drive the structure and function of gut microbiota?

Shift of ingestive behavior is an important strategy for animals to adapt to change of the environment. We knew that shifts in animal dietary habits lead to changes in the structure of the gut microbiota, but we are not sure about if changes in the composition and function of the gut microbiota respond to changes in the nutrient intake or food items. To investigate how animal feeding strategies affect nutrient intakes and thus alter the composition and digestion function of gut microbiota, we selected a group of wild primate group for the study. We quantified their diet and macronutrients intake in four seasons of a year, and instant fecal samples were analyzed by high-throughput sequencing of 16S rRNA and metagenomics. These results demonstrated that the main reason that causes seasonal shifts of gut microbiota is the macronutrient variation induced by seasonal dietary differences. Gut microbes can help to compensate for insufficient macronutrients intake of the host through microbial metabolic functions. This study contributes to a deeper understanding of the causes of seasonal variation in host-microbial variation in wild primates.

Pregnancy diagnosis and sex identification with urinary glycopatterns of two mammal species.

Glycome in urine could be promising biomarkers for detecting pregnancy diagnosis and sex noninvasively for animals, especially for rare species. We explore the applicability of grouping golden snub-nosed monkeys by sex or diagnosing pregnancy based on their urinary glycopatterns, which are determined via lectin microarray combining mass spectrometry analysis. Sprague-Dawley rats are used to verify whether this approach and whether the glycomic biomarkers can be generalized to other mammalian species. The results show that, for both species, lectin microarray combining mass spectrometry can distinguish individuals' pregnancy status and sex; significant differences are found in the types, amounts, and terminal modification of glycans between pregnant and non-pregnant females and between females and males. This indicates the approach could be generalized to other mammalian species to group sex and detect pregnancy, yet the glycopatterns appear to be species-specific and markers developed from one species may not be directly applicable to another.

Pharmacological Activation of GPR55 Improved Cognitive Impairment Induced by Lipopolysaccharide in Mice.

Our previous research found that activation of GPR55 can alleviate cognitive impairment induced by amyloid-beta 1-42 (Aß1-42) and streptozotocin in mice, but the role of GPR55 in the pathogenesis of cognitive impairment remains unknown. Here, we used a lipopolysaccharide (LPS) mouse model to further investigate the role and mechanism of O-1602, a GPR55 agonist, on cognitive dysfunction. ICR mice were treated with an intracerebroventricular (i.c.v.) injection of LPS, followed by cognitive function tests. The expression of GPR55, NF-κB p65, caspase-3, Bax, and Bcl-2 in the hippocampus was examined by Western blotting. Inflammatory cytokines and microglia were detected by ELISA kit and immunohistochemical analyses, respectively. The levels of MDA, GSH, SOD, and CAT were examined by assay kits. Furthermore, TUNEL-staining was used to detect neuronal apoptosis. Our results showed that i.c.v. injection of LPS in mice exhibited impaired performance in the behavior tests, which were ameliorated by O-1602 treatment (2.0 or 4.0 µg/mouse, i.c.v.). Importantly, we found that O-1602 treatment reversed GPR55 downregulation, decreased the expression of NF-κB p65, suppressed the accumulation of proinflammatory cytokines and microglia activation, increased the anti-inflammatory cytokines, and reduced the levels of MDA, increased the levels of GSH, SOD, and CAT in the hippocampus. In addition, O-1602 treatment also significantly reduced Bax and increased Bcl-2 expression as well as decreased caspase-3 activity and TUNEL-positive cells in the hippocampus. These observations indicate that O-1602 may ameliorate LPS-induced cognition deficits via inhibiting neuroinflammation, oxidative stress, and apoptosis mediated by the NF-κB pathway in mice.

Activation of GPR55 attenuates cognitive impairment and neurotoxicity in a mouse model of Alzheimer's disease induced by Aß1-42 through inhibiting RhoA/ROCK2 pathway.

The accumulation of amyloid-ß (Aß) peptides in the brain is considered to be the initial event in the Alzheimer's disease (AD). Neurotoxicity mediated by Aß has been demonstrated to damage the cognitive function. In the present study, we sought to determine the effects of O-1602, a specific G-protein coupled receptor 55 (GPR55) agonist, on the impairment of learning and memory induced by intracerebroventricular (i.c.v.) of Aß1-42 (400 pmol/mouse) in mice. Our results showed that i.c.v. injection of aggregated Aß1-42 into the brain of mice resulted in cognitive impairment and neurotoxicity. In contrast, O-1602 (2.0 or 4.0 µg/mouse, i.c.v.) can improve memory impairment induced by Aß1-42 in the Morris water maze (MWM), and novel object recognition (NOR) tests. Besides, we found that O-1602 reduced the activity of ß-secretase 1 (BACE1) and the level of soluble Aß1-42 in the hippocampus and frontal cortex. Importantly, O-1602 treatment reversed Aß1-42-induced GPR55 down-regulation, decreased pro-inflammatory cytokines, and the level of malondialdehyde (MDA), increased the levels of glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), as well as suppressed apoptosis as indicated by decreased TUNEL-positive cells, and increased the ratio of Bcl-2/Bax. O-1602 treatment also pronouncedly ameliorated synaptic dysfunction by promoting the upregulation of PSD-95 and synaptophysin (SYN) proteins. Moreover, O-1602 concurrently down regulated the protein levels of RhoA, and ROCK2, the critical proteins in the RhoA/ROCK2 pathway. This study indicates that O-1602 may reverse Aß1-42-induced cognitive impairment and neurotoxicity in mice by inhibiting RhoA/ROCK2 pathway. Taken together, these findings suggest that GPR55 could be a novel and promising target for the treatment of AD.

Activation of GPR55 attenuates cognitive impairment, oxidative stress, neuroinflammation, and synaptic dysfunction in a streptozotocin-induced Alzheimer's mouse model.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by cascading changes in cognition and behavior. G-protein-coupled receptor 55 (GPR55) has been used as a promising target for the treatment of diabetes, but its function in AD is unclear. The objective of this study was to investigate the neuroprotective effects of O-1602, a GPR55 agonist, on the streptozotocin (STZ)-induced AD mouse model. A single intracerebroventricular (i.c.v.) injection of STZ into the brains of mice significantly induced cognitive impairment. In contrast, O-1602 (2.0 or 4.0 µg/mouse, i.c.v.) can improve the cognitive dysfunction caused by STZ in the Morris water maze (MWM) and novel object recognition (NOR) tests. Importantly, O-1602 treatment reversed STZ-induced GPR55 down-regulation, reduced the activity of ß-secretase 1 (BACE1) and the level of Aß1-42, and abolished the up-regulation of acetylcholinesterase (AChE) activity in the hippocampus and frontal cortex. Besides, O-1602 markedly suppressed STZ-induced oxidative stress, characterized by decreased malondialdehyde (MDA) level, and increased the levels of glutathione (GSH), superoxide dismutases (SOD), and catalase (CAT), as well as attenuated neuroinflammation as indicated by decreased series of pro-inflammatory cytokines and microglia activation. O-1602 treatment also ameliorated synaptic dysfunction by promoting the up-regulation of PSD-95 protein in the STZ-treated mice. Our results suggest that O-1602 has potent neuroprotective effects against STZ-induced neurotoxicity. Meanwhile, these findings suggest that GPR55 might be a novel and promising target for the treatment of AD.

Sarcoptic mange is an emerging threat to biodiversity in the Qinling Mountains in China.

Sarcoptic mange, a disease caused by the burrowing mite Sarcoptes scabiei, is globally endemic and an emerging threat to wildlife. Although many studies have shown that wildlife diseases play key roles in biodiversity conservation, knowledge about sarcoptic mange is still insufficient. In this study, we aim to improve the understanding of the impacts of sarcoptic mange on wildlife populations, the mechanisms involved in its eco-epidemiology and the associated risks to public and ecosystem health by investigating mass death events in gorals and serows in the Qinling Mountains. We conducted interviews with practitioners and local people in the central Qinling Mountains. From the same locations, we collected 24 cutaneous samples from various animals and surveillance data from infrared cameras. Pathological, parasitological and microbiological examinations of the samples were performed. Mite-induced cutaneous lesions, mites and eggs were observed in samples from dead gorals and one dead serow but not in other species. Molecular analysis confirmed the mites to be S. scabiei and shared the same cox 1 genotype. The data obtained from the interviews and infrared cameras indicated that the death of wildlife was related to sarcoptic mange infection and that there had been a decrease in the goral population since the outbreak of the disease. We confirmed that sarcoptic mange was the major cause of the mass death events and may have spread from the western to eastern Qinling Mountains. Based on our findings, we propose several protection strategies to help preserve biodiversity in the Qinling Mountains.

Role of STAT-3 in regulation of hepatic gluconeogenic genes and carbohydrate metabolism in vivo.

The transcription factor, signal transducer and activator of transcription-3 (STAT-3) contributes to various physiological processes. Here we show that mice with liver-specific deficiency in STAT-3, achieved using the Cre-loxP system, show insulin resistance associated with increased hepatic expression of gluconeogenic genes. Restoration of hepatic STAT-3 expression in these mice, using adenovirus-mediated gene transfer, corrected the metabolic abnormalities and the alterations in hepatic expression of gluconeogenic genes. Overexpression of STAT-3 in cultured hepatocytes inhibited gluconeogenic gene expression independently of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha), an upstream regulator of gluconeogenic genes. Liver-specific expression of a constitutively active form of STAT-3, achieved by infection with an adenovirus vector, markedly reduced blood glucose, plasma insulin concentrations and hepatic gluconeogenic gene expression in diabetic mice. Hepatic STAT-3 signaling is thus essential for normal glucose homeostasis and may provide new therapeutic targets for diabetes mellitus.

Inhibition of GPR17 with cangrelor improves cognitive impairment and synaptic deficits induced by Aß1-42 through Nrf2/HO-1 and NF-κB signaling pathway in mice.

The accumulation of amyloid beta (Aß) in the brain is thought to be associated with cognitive deficits in Alzheimer's disease (AD). However, current methods to combat Aß neurotoxicity are still lacking. G protein-coupled receptor 17 (GPR17) has become a target for treating inflammation in brain diseases, but it is unclear whether it has a role in AD. Here, we investigated the effects of cangrelor, a GPR17 antagonist, on neurotoxicity and memory impairment induced by intracerebroventricular (i.c.v.) injection of Aß1-42 in mice. The behavior results showed that cangrelor (2.0 or 4.0 µg/mouse, i.c.v.) treatment reversed the deficits in memory and learning ability induced by Aß1-42 in mice. Importantly, we demonstrated for the first time that GPR17 expression in the hippocampus and frontal cortex is increased in response to Aß1-42 exposures. We also found that cangrelor treatment reduced the activity of ß-secretase 1 (BACE1) and the levels of soluble Aß1-42 in the hippocampus and frontal cortex. Meanwhile, cangrelor treatment suppressed oxidative stress induced by Aß1-42, as proved by reduced production of malondialdehyde (MDA), and increased glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), and promoted the expression of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1). Furthermore, cangrelor also suppressed Aß1-42-induced neuroinflammation, characterized by suppressed activation of microglia, decreased the levels of pro-inflammatory cytokines, and nuclear translocation of NF-κB p65, as well as ameliorated synaptic deficits by promoting the upregulation of synaptic proteins, and increasing the number of Golgi-Cox stained dendritic spines. These results suggest that cangrelor may reverse Aß1-42-induced cognition deficits via inhibiting oxidative stress, neuroinflammation, and synaptic dysfunction mediated by Nrf2/HO-1 and NF-κB signaling.

Biological applications of copper-containing materials.

Copper is an indispensable trace metal element in the human body, which is mainly absorbed in the stomach and small intestine and excreted into the bile. Copper is an important component and catalytic agent of many enzymes and proteins in the body, so it can influence human health through multiple mechanisms. Based on the biological functions and benefits of copper, an increasing number of researchers in the field of biomaterials have focused on developing novel copper-containing biomaterials, which exhibit unique properties in protecting the cardiovascular system, promoting bone fracture healing, and exerting antibacterial effects. Copper can also be used in promoting incisional wounds healing, killing cancer cells, Positron Emission Tomography (PET) imaging, radioimmunological tracing and radiotherapy of cancer. In the present review, the biological functions of copper in the human body are presented, along with an overview of recent progress in our understanding of the biological applications and development of copper-containing materials. Furthermore, this review also provides the prospective on the challenges of those novel biomaterials for future clinical applications.

cGAS-STING Signaling Pathway and Liver Disease: From Basic Research to Clinical Practice.

The cGAS-STING signaling pathway is an autoimmune inflammatory pathway that can trigger the expression of a series of inflammatory factors represented by type 1 interferon. Recent studies have found that the cGAS-STING signaling pathway played a significant role in liver physiology and was closely related to the progress of liver diseases. For example, activating the cGAS-STING signaling pathway could significantly inhibit hepatitis B virus (HBV) replication in vivo. Moreover, the cGAS-STING signaling pathway was also closely associated with tumor immunity in hepatocellular carcinoma (HCC). This review summarized the role of the cGAS-STING signaling pathway in several common liver diseases, especially the current application of the cGAS-STING signaling pathway in liver disease treatment, and prospected its future research, which provided a new idea for understanding and treating liver diseases.