Olfactory receptors (ORs) form the largest superfamily of G protein-coupled receptors (GPCRs). Traditionally recognized for their role in the nasal olfactory epithelium, where they mediate the sense of smell, accumulating evidence has firmly established their ectopic expression in non-olfactory tissues, including the intestine, lungs, and kidneys. The intestine, as the primary site for nutrient digestion and absorption, harbors a highly complex chemical environment. To adapt to this environment, the gut employs a sophisticated network of “chemosensors” to monitor luminal contents and maintain homeostasis. Among these sensors, intestinal ORs have emerged as crucial functional components, serving as a molecular bridge that connects environmental chemical signals—such as food-derived odorants—to specific physiological responses. This discovery has significantly deepened our understanding of how dietary flavors and compounds influence intestinal physiology at the molecular level. This review systematically summarizes the expression profiles, ligand classification, and biological functions of ORs within the gastrointestinal tract. Studies indicate that intestinal ORs exhibit distinct spatial distribution patterns across different gut segments and display cell-type specificity, particularly within enterocytes and enteroendocrine cells. These receptors function as versatile sensors capable of recognizing a wide variety of ligands, including exogenous dietary components, gut microbiota metabolites such as short-chain fatty acids, and endogenous small molecules like azelaic acid. Upon activation by specific ligands, intestinal ORs trigger intracellular signaling cascades, primarily involving the AC-cAMP-PKA pathway or calcium influx channels. A major focus of this review is to elucidate the molecular mechanisms by which these receptors regulate the secretion of gut hormones. Activation of specific ORs in enteroendocrine cells has been shown to stimulate the release of hormones such as glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and serotonin (5-HT), thereby modulating systemic energy metabolism, glucose homeostasis, and gastrointestinal motility. Furthermore, the review addresses the critical roles of ORs in immune regulation and pathology. Evidence suggests that specific ORs contribute to the maintenance of intestinal immune homeostasis and may offer protection against inflammation. Beyond their involvement in inflammatory responses, ORs such as Olfr78 have been shown to regulate the differentiation and function of intestinal endocrine cells. Similarly, Olfr544 has been demonstrated to alleviate intestinal inflammation by remodeling the gut microbiome and metabolome. These findings collectively suggest that specific ORs hold promise as therapeutic targets for mitigating intestinal inflammation and maintaining gut homeostasis. Additionally, the review explores the emerging role of ORs in cancer. Although OR expression is often downregulated in tumor tissues compared to normal mucosa, activation of specific ORs by certain ligands can inhibit tumor cell proliferation and migration and induce apoptosis via pathways such as MEK/ERK and p38 MAPK. Conversely, other receptors, such as OR7C1, may serve as biomarkers for cancer-initiating cells. In conclusion, intestinal ORs represent a vital component of the gut’s sensory network. The review also discusses the translational potential of these findings. By elucidating the precise pairing relationships between dietary components and specific ORs, novel therapeutic strategies could be developed. Intestinal ORs may thus emerge as promising targets for nutritional and pharmacological interventions in metabolic diseases, inflammatory bowel diseases, and malignancies.

BackgroundThe middle school stage represents a crucial period for the development of borderline personality features. Negative parenting styles and emotional regulation strategies are associated with the formation of borderline personality features. However， the moderating role of emotional regulation strategies between negative parenting styles and borderline personality features among middle school students remains unclear. ObjectiveTo explore the moderating influence of emotional regulation strategies in the relationship between negative parenting styles and borderline personality features among middle school students， and to provide references for the intervention of borderline personality features. MethodsIn October 2023， a total of 5 965 middle school students from three middle schools in Nanning， Guangxi Zhuang Autonomous Region were selected by cluster sampling， and assessed by the Borderline Personality Features Scale for Children （BPFS-C）， the Egna Minnen Barndoms Uppfostran （EMBU）， and the Emotion Regulation Questionnaire-Chinese Revised Version （ERQ-CRV）. Pearson correlation analysis was used to test the correlation between the scores of each scale， and the model 1 of the Process macro program was used to conduct the moderating effect test. ResultsA total of 5 572 middle school students （93.41%） completed this study， and 1 388 of them （24.91%） were identified as having high borderline personality features. The BPFS-C score of middle school students was positively correlated with the score of the negative parenting style dimension of EMBU （r=0.367， P<0.01）， negatively correlated with the score of the cognitive reappraisal dimension of ERQ-CRV （r=-0.168， P<0.01）， and positively correlated with the score of the expression inhibition dimension of ERQ-CRV （r=0.344， P<0.01）. Cognitive reappraisal played a negative moderating effect between negative parenting styles and borderline personality features （β=-0.072， 95% CI： -0.104–-0.041， P<0.01）， while expressive suppression played a positive moderating effect （β=0.076， 95% CI： 0.055–0.097， P<0.01）. ConclusionCognitive reappraisal strategy may help mitigate the negative influence of negative parenting styles on middle school students' borderline personality features， while expressive suppression may exacerbate the harm of negative parenting styles to the borderline personality features of middle school students.

Osteoporosis is a systemic disease, and epidemiological projections indicate that by 2050, approximately 23.43% of the Chinese population over 50 years of age will be affected. Given the poor prognosis associated with osteoporosis, the exploration of safe and effective natural products is of considerable significance. Studies investigating the chemical constituents of traditional Chinese medicine in cellular and/or animal models have demonstrated bone-protective effects. Although most of these compounds lack clinical data, they hold considerable potential as lead candidates for drug development. In-depth study of the structure-activity relationship of these natural products not only contributes to elucidating the mechanisms of action but also provides a theoretical basis for the development of novel antiosteoporosis therapies. This review summarizes natural products with potential antiosteoporotic effects reported between 2020 and 2024. Overall, plant-derived natural compounds exhibit antiosteoporotic effects by regulating bone remodeling, inflammation, and oxidative stress, highlighting their promise as multitarget therapeutic candidates.

ObjectiveTo investigate whether intestinal deficiency of lanosterol synthase （LSS）， a key enzyme in cholesterol synthesis， influences the progression of metabolic dysfunction-associated steatotic liver disease （MASLD） by regulating intestinal cholesterol absorption and immune response. MethodsLSS heterozygous knockout （LSS^+/-） mice and wild-type （WT） controls were generated using CRISPR/Cas9 technology and fed either a high-fat diet （HFD） or regular chow （CHOW）. The model was validated by genotyping. Hepatic steatosis was assessed by HE and oil red O staining. Immunohistochemistry was used to detect the localization and expression of NPC1L1 and CD36 proteins in the intestine. Western blot analysis was performed to measure JNK phosphorylation and TLR4 protein levels in intestinal tissues. Real-time quantitative polymerase chain reaction （qPCR） was employed to examine the mRNA expression of TLR4 and IL-6. ResultsLSS^+/- mice were successfully validated by genotyping and reduced intestinal LSS protein expression. HE and oil red O staining of liver sections showed that， compared with WT mice fed a CHOW diet， WT mice fed a HFD exhibited a marked increase in hepatic lipid vacuoles. In contrast， compared with HFD-fed WT mice， HFD-fed LSS^+/- mice displayed significantly attenuated hepatic lipid deposition and reduced serum ALT levels （P<0.05）. Immunohistochemical analysis revealed that， compared with WT mice， the expression of the cholesterol absorption protein NPC1L1 in the intestinal villi of LSS^+/- mice was downregulated under both CHOW and HFD conditions （P_HFD<0.001）. Conversely， the expression of the fatty acid transporter CD36 was upregulated in the intestines of LSS^+/- mice （P_CHOW<0.05， P_HFD<0.01）. Western blot analysis demonstrated that， compared with WT mice， TLR4 protein expression in the intestines of LSS^+/- mice significantly increased under both CHOW and HFD conditions （both P<0.05）. JNK phosphorylation level was significantly elevated in LSS^+/- mice under CHOW condition （both P<0.05）. Under HFD condition， total JNK protein expression increased， but its phosphorylation level showed no significant change. qPCR analysis showed that， compared with WT mice， the mRNA levels of TLR4 （P_CHOW<0.01， P_HFD<0.000 1） and IL-6 （P_CHOW<0.001， P_HFD<0.01） were significantly upregulated in the intestines of LSS^+/-mice. ConclusionLSS deficiency counteracts hepatic lipid deposition by orchestrating a synergistic reprogramming involving restricted intestinal cholesterol absorption， enhanced fatty acid utilization， and activation of immune pathways， suggesting intestinal LSS as a potential therapeutic target of MASLD.

With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

Objective Inflammatory myofibroblastic tumor (IMT) is a rare condition. This report summarizes the characteristics of IMT in order to strengthen clinicians' understanding of this disease. Case Presentation A 59-year-old female patient presented with intermittent right flank and abdominal pain with fever for 1 month, and a right renal mass detected 3 weeks ago. The highest body temperature during the course of the illness was 39℃. She received symptomatic antiinfective treatment at another hospital for 2 weeks, and the symptoms were alleviated. Enhanced CT of the lower abdomen strongly suggested a right renal carcinoma, with multiple small lymph nodes in the peritoneal cavity and retroperitoneum. MRI indicated a neoplastic lesion in the right kidney, with suspicion of chromophobe cell carcinoma. Laparoscopic partial right nephrectomy was performed under general anesthesia, and the procedure was successful. Postoperative pathology showed that there was significant localized infiltration of lymphocytes and formation of lymphoid follicles, and the lymph nodes showed chronic inflammation. The final diagnosis was IMT. In the follow-up of 3 months, no tumor recurrence was observed. Conclusion IMT has a high misdiagnosis rate. When imaging findings are atypical for renal cell carcinoma, IMT should be suspected. The preferred treatment is laparoscopic partial nephrectomy.

OBJECTIVE To investigate the protective effect of Yishen tongluo formula on high glucose-induced injury in renal tubular epithelial cells and its impact on the silence information regulator 3 （SIRT3）-adenosine monophosphate-activated protein kinase （AMPK）/peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）/carnitine palmitoyltransferase 1A （CPT1A） signaling pathway. METHODS Human renal tubular epithelial cells HK-2 were used as the subject. The cells were divided into a normal glucose group （NC group）， a high glucose group （HG group）， a high glucose+low-dose Yishen tongluo formula group [HG+L group， 0.5 mg/mL （calculated by crude drugs）]， and a high glucose+high-dose Yishen tongluo formula group [HG+H group， 1.0 mg/mL （calculated by crude drugs）]. Except for the NC group， cells in all other groups were cultured under high glucose conditions （30 mmol/L）， and cells in the HG+L and HG+H groups were simultaneously treated with the corresponding mass concentrations of medicinal liquid. Cell viability was assessed at 0， 24， and 48 h post-incubation， and reactive oxygen species （ROS） level， adenosine triphosphate （ATP） content， and the expression of molecules related to the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway were measured after 48 h of incubation. RESULTS Compared with the NC group， the HG group showed significantly reduced cell viabilities （at 24 and 48 h） and ATP content， along with significantly elevated ROS levels （ P ＜0.05）. Additionally， the protein expressions of SIRT3， PGC-1α and CPT1A， as well as the mRNA expressions of PGC-1α and CPT1A， and the phosphorylation level of AMPK protein were all significantly downregulated or decreased（ P ＜0.05）. Compared with the HG group， the aforementioned indicators were significantly improved in both HG+L and HG+H groups， with the improvement being more pronounced in the HG+H group （ P ＜0.05）. CONCLUSIONS The Yishen tongluo formula can improve high-glucose-induced damage to renal tubular epithelial cells； its action may be related to activating the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway， improving mitochondrial energy metabolism， and alleviating oxidative stress.

OBJECTIVE To investigate the protective effect of Yishen tongluo formula on high glucose-induced injury in renal tubular epithelial cells and its impact on the silence information regulator 3 （SIRT3）-adenosine monophosphate-activated protein kinase （AMPK）/peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）/carnitine palmitoyltransferase 1A （CPT1A） signaling pathway. METHODS Human renal tubular epithelial cells HK-2 were used as the subject. The cells were divided into a normal glucose group （NC group）， a high glucose group （HG group）， a high glucose+low-dose Yishen tongluo formula group [HG+L group， 0.5 mg/mL （calculated by crude drugs）]， and a high glucose+high-dose Yishen tongluo formula group [HG+H group， 1.0 mg/mL （calculated by crude drugs）]. Except for the NC group， cells in all other groups were cultured under high glucose conditions （30 mmol/L）， and cells in the HG+L and HG+H groups were simultaneously treated with the corresponding mass concentrations of medicinal liquid. Cell viability was assessed at 0， 24， and 48 h post-incubation， and reactive oxygen species （ROS） level， adenosine triphosphate （ATP） content， and the expression of molecules related to the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway were measured after 48 h of incubation. RESULTS Compared with the NC group， the HG group showed significantly reduced cell viabilities （at 24 and 48 h） and ATP content， along with significantly elevated ROS levels （ P ＜0.05）. Additionally， the protein expressions of SIRT3， PGC-1α and CPT1A， as well as the mRNA expressions of PGC-1α and CPT1A， and the phosphorylation level of AMPK protein were all significantly downregulated or decreased（ P ＜0.05）. Compared with the HG group， the aforementioned indicators were significantly improved in both HG+L and HG+H groups， with the improvement being more pronounced in the HG+H group （ P ＜0.05）. CONCLUSIONS The Yishen tongluo formula can improve high-glucose-induced damage to renal tubular epithelial cells； its action may be related to activating the SIRT3-AMPK/PGC-1α/CPT1A signaling pathway， improving mitochondrial energy metabolism， and alleviating oxidative stress.

BACKGROUND: Recent studies have shown that sodium-glucose cotransporters-2 (SGLT2) inhibitors significantly improve major adverse cardiovascular events in heart failure with preserved ejection fraction (HFpEF) patients, but the exact mechanism is unknown. Ferritinophagy is a special form of selective autophagy that participates in ferroptosis. In this study, we aimed to investigate whether ferritinophagy was activated during the occurrence of HFpEF, and whether canagliflozin (CANA) could inhibite ferritinophagy. METHODS: We reared Dahl salt-sensitive (DSS) rats on a high-salt diet to construct a hypertensive HFpEF model, and simultaneously administered CANA intervention. Then we detected indicators related to ferritinophagy. RESULTS: The expression of nuclear receptor coactivator 4 (NCOA4), as well as microtubule-associated proteins light chain 3 (LC3), Bcl-2 interacting protein 1 (Beclin-1) and p62, were upregulated in HFpEF rats, accompanied by the downregulation of ferritin heavy chain 1 (FTH1), upregulation of mitochondrial iron transporter sideroflexin1 (SFXN1) and increased reactive oxygen species (ROS) production. Above changes were diminished by CANA. CONCLUSION Ferritinophagy is activated in HFpEF rats and then inhibited by CANA, leading to HFpEF benefits. The inhibition of ferritinophagy could provide new prospective targets for the prevention and treatment of HFpEF, and provide new ideas for investigating the mechanism of cardiovascular benefit of SGLT2 inhibitors.