Alzheimer’s disease (AD) is a common neurodegenerative disease. The major problems that exist in the diagnosis of AD include the costly examinations and the high-invasive sampling tissue. Therefore, it would be advantageous to develop blood biomarkers. Because AD’s pathological process is considered tightly related to autophagy; thus, a diagnostic model for AD based on ATGs may have more predictive accuracy than other models. We obtained GSE63060 dataset from the GEO database, ATGs from the HADb and screened 64 differentially expressed autophagy-related genes (DE-ATGs). We then applied them to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses as well as DisGeNET and PaGenBase enrichment analyses. By using the univariate analysis, least absolute shrinkage and selection operator (LASSO) regression method and the multivariable logistic regression, nine DE-ATGs were identified as biomarkers, which are ATG16L2, BAK1, CAPN10, CASP1, RAB24, RGS19, RPS6KB1, ULK2, and WDFY3. We combined them with sex and age to establish a nomogram model. To evaluate the model’s distinguishability, consistency, and clinical applicability, we applied the receiver operating characteristic (ROC) curve, C-index, calibration curve, and on the validation datasets GSE63061, GSE54536, GSE22255, and GSE151371 from GEO database. The results show that our model demonstrates good prediction performance. This AD diagnosis model may benefit both clinical work and mechanistic research.

Cataracts are a serious complication of diabetes. In long-term hyperglycemia, intracellular Ca²⁺ concentration ([Ca²⁺]_i) and reactive oxygen species (ROS) are increased. The apoptosis of lens epithelial cells plays a key role in the development of cataract. We investigated a potential role for transient receptor potential vanilloid 2 (TRPV2) in the development of diabetic cataracts. Immunohistochemical and Western blotting analyses showed that TRPV2 expression levels were significantly increased in the lens epithelial cells of patients with diabetic cataracts as compared with senile cataract, as well as in both a human lens epithelial cell line (HLEpiC) and primary rat lens epithelial cells (RLEpiCs) cultured under high-glucose conditions. The [Ca²⁺]_i increase evoked by a TRPV2 channel agonist was significantly enhanced in both HLEpiCs and RLEpiCs cultured in high-glucose media. This enhancement was blocked by the TRPV2 nonspecific inhibitor ruthenium red and by TRPV2-specific small interfering (si)RNA transfection. Culturing HLEpiCs or RLEpiCs for seven days in high glucose significantly increased apoptosis, which was inhibited by TRPV2-specific siRNA transfection. In addition, ROS inhibitor significantly suppressed the ROS-induced increase of TRPV2-mediated Ca²⁺ signal and apoptosis under high-glucose conditions. These findings suggest a mechanism underlying high-glucose–induced apoptosis of lens epithelial cells, and offer a potential target for developing new therapeutic options for diabetes-related cataracts.

Light plays a direct crucial role in the switch between sleep and arousal and the regulation of physiology and behaviour, such as circadian rhythms and emotional change. Artificial lights, which are different from natural light sources with a continuous light spectrum, are composed of three single-colour lights and are increasingly applied in modern society. However, in vivo research on the mechanisms of blue light-regulated sleep and arousal is still insufficient. In this work, we detected the effects of inserting white or blue light for 1 h during the dark period on the wheel-running activity and sucrose preference of C57 mice. The results showed that blue light could induce delays in sleep and arousal-promoting responses. Furthermore, this lighting pattern, including blue light alone, induced depressive-like emotions. The c-fos expression in the blue light group was significantly higher in the arcuate hypothalamic nucleus (Arc) and significantly lower in the cingulate cortex (Cg) and anterior part of the paraventricular thalamic nucleus (PVA) than in the white light group. Compared with the white light group, the phospho-ERK expression in the paraventricular hypothalamic nucleus (PVN) and PVA was lower in the blue light group. These molecular changes indicated that certain brain regions are involved in blue light-induced response processes. This study may provide useful information to explore the specific mechanism of special light-regulated physiological function.

Diabetic foot is a major complication of diabetes. The bone transverse transport method could be applied in clinics for treatment, which could improve the metabolism of the tissues via lasting distraction forces. However, the process’ specific regulating mechanism is still unknown. Based on the notion that the healing of bones involves the recruitment of calcium ions, in this study, we established the model of tibial cortex transverse transport (TTT) on rats and then used tissue immunologic detection, such as the double fluorescent staining to explore the expression of the calcium channels’ calcium release-activated calcium modulator 1 (Orai1)/stromal interaction molecule 1 (STIM1), which belong to the store-operated calcium entry (SOCE) signaling pathways on the tissues around the bone transport area. By using the laser capture microdissection (LCM) tool, we acquired samples of tissues around the bone and endeavored to identify pivotal protein molecules. Subsequently, we validated the functions of key protein molecules through in vitro and in vivo experiments. After protein profile analysis, we found the differentially expressed key protein osteopontin (OPN). The in vitro experiments verified that, being stimulated by OPN, the migration, proliferation, and angiogenesis of human umbilical vein endothelial cells (HUVEC) were observed to be enhanced. The activation of Orai1/STIM1 might increase the activity of endothelial nitric oxide synthase (eNOS) and its effect on releasing nitric oxide (NO). Subsequently, the migration and proliferation of the HUVECs are improved, which ultimately accelerates wound healing. These signaling pathway was also observed in the OPN-stimulated healing process of the skin wound surface of diabetic mice. This study identifies the molecular biological mechanism of OPN-benefited the migration and proliferation of the HUVECs and provides ideas for searching for new therapeutic targets for drugs that repair diabetes-induced wounds to replace invasive treatment methods. The OPN is highly expressed in the tissues surrounding the TTT bone transfer area, which may possibly stimulate the activation of eNOS to increase NO release through the SOCE pathway mediated by Orai1/STIM1. This mechanism may play a significant role in the angiogenesis of diabetic foot's wounds promoted by TTT, providing new therapeutic strategies for the non-surgical treatment for this disease.