With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Peptide-based radiopharmaceuticals targeting integrin α5β1 show promise for precise tumor diagnosis and treatment. However, current peptide-based radioligands that target α5β1 demonstrate inadequate in vivo performance owing to limited tumor retention. The use of PEGylation to enhance the tumor retention of radiopharmaceuticals by prolonging blood circulation time poses a risk of increased blood toxicity. Therefore, a PEGylation strategy that boosts tumor retention while minimizing blood circulation time is urgently needed. Here, we developed a PEGylation-enabled peptide multidisplay platform (PEGibody) for PR_b, an α5β1 targeting peptide. PEGibody generation involved PEGylation and self-assembly. [⁶⁴Cu]QM-2303 PEGibodies displayed spherical nanoparticles ranging from 100 to 200 nm in diameter. Compared with non-PEGylated radioligands, [⁶⁴Cu]QM-2303 demonstrated enhanced tumor retention time due to increased binding affinity and stability. Importantly, the biodistribution analysis confirmed rapid clearance of [⁶⁴Cu]QM-2303 from the bloodstream. Administration of a single dose of [¹⁷⁷Lu]QM-2303 led to robust antitumor efficacy. Furthermore, [⁶⁴Cu]/[¹⁷⁷Lu]QM-2303 exhibited low hematological and organ toxicity in both healthy and tumor-bearing mice. Therefore, this study presents a PEGibody-based radiotheranostic approach that enhances tumor retention time and provides long-lasting antitumor effects without prolonging blood circulation lifetime. The PEGibody-based radiopharmaceutical [⁶⁴Cu]/[¹⁷⁷Lu]QM-2303 shows great potential for positron emission tomography imaging-guided targeted radionuclide therapy for α5β1-overexpressing tumors.

Inhibiting glutamine metabolism has been proposed as a potential treatment strategy for improving non-alcoholic steatohepatitis (NASH). However, effective methods for assessing dynamic metabolic responses during interventions targeting glutaminolysis have not yet emerged. Here, we developed a positron emission tomography (PET) imaging platform using l-[5-¹¹C]glutamine ([¹¹C]Gln) and evaluated its efficacy in NASH mice undergoing metabolic therapy with bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide (BPTES), a glutaminase 1 (GLS1) inhibitor that intervenes in the first and rate-limiting step of glutaminolysis. PET imaging with [¹¹C]Gln effectively delineated the pharmacokinetics of l-glutamine, capturing its temporal-spatial pattern of action within the body. Furthermore, [¹¹C]Gln PET imaging revealed a significant increase in hepatic uptake in methionine and choline deficient (MCD)-fed NASH mice, whereas systemic therapeutic interventions with BPTES reduced the hepatic avidity of [¹¹C]Gln in MCD-fed mice. This reduction in [¹¹C]Gln uptake correlated with a decrease in GLS1 burden and improvements in liver damage, indicating the efficacy of BPTES in mitigating NASH-related metabolic abnormalities. These results suggest that [¹¹C]Gln PET imaging can serve as a noninvasive diagnostic platform for whole-body, real-time tracking of responses of glutaminolysis to GLS1 manipulation in NASH, and it may be a valuable tool for the clinical management of patients with NASH undergoing glutaminolysis-based metabolic therapy.

The activation proteins released by fibroblasts in the tumor microenvironment regulate tumor growth, migration, and treatment response, thereby influencing tumor progression and therapeutic outcomes. Owing to the proliferation and metastasis of tumors, fibroblast activation protein (FAP) is typically highly expressed in the tumor stroma, whereas it is nearly absent in adult normal tissues and benign lesions, making it an attractive target for precision medicine. Radiolabeled agents targeting FAP have the potential for targeted cancer diagnosis and therapy. This comprehensive review aims to describe the evolution of FAPI-based radiopharmaceuticals and their structural optimization. Within its scope, this review summarizes the advances in the use of radiolabeled small molecule inhibitors for tumor imaging and therapy as well as the modification strategies for FAPIs, combined with insights from structure-activity relationships and clinical studies, providing a valuable perspective for radiopharmaceutical clinical development and application.

AIM:Fine particulate matter(PM2.5)is closely associated with airway hyper-responsiveness(AHR).However,the underlying mechanism by which PM2.5 leads to AHR is still unclear.This study aimed to investi-gate the respiratory effects of ambient PM2.5 exposure.METHODS:Forty mice were randomly divided into five groups:control group(intranasal saline),lipopolysaccharide(LPS)group(100 mg/L),PM2.5 low-dose group(0.003 5 mg/d),PM2.5 medium-dose group(0.007 mg/d),and PM2.5 high-dose group(0.014 mg/d).They were treated with intranasal in-stillation for 30 d.Lung function and tracheal contractile responses were evaluated using whole-body plethysmography and sensitive wire myograph.Inflammatory mediators in serum and oxidative stress parameters were detected using enzyme-linked immunosorbent assay(ELISA).Lung tissues were subjected to HE and Masson staining.RT-qPCR and Western blot were used to determine the expression of contractile receptors and the phosphorylation of the mitogen-activated protein kinase(MAPK)signal pathway.RESULTS:Intranasal instillation of PM2.5 significantly increased airway resistance in mice and enhanced tracheal contractility in response to carbachol.PM2.5 elevated levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,and IL-6 in serum.PM2.5 instillation also led to a decrease in glutathione peroxidase(GSH-Px)levels and an increase in malondialdehyde(MDA)levels.Lung tissue exhibited notable pathological changes,including inflammatory cell infiltration,hyperplasia of alveolar epithelial cells,and collagen deposition.Mechanistically,exposure to PM2.5 increased the expression of muscarinic M3 receptor mRNA and protein,as well as the phosphorylation of p-ERK1/2 and p-p38 proteins following PM2.5 instillation.CONCLUSION:Intranasal instillation of PM2.5 induced inflammation and oxidative stress,along with the activation of the extracellular signal-regulated kinase 1/2(ERK1/2)and p38 MAPK pathways,resulting in the upregulation of M3 receptor-induced AHR.

AIM:Fine particulate matter(PM2.5)is closely associated with airway hyper-responsiveness(AHR).However,the underlying mechanism by which PM2.5 leads to AHR is still unclear.This study aimed to investi-gate the respiratory effects of ambient PM2.5 exposure.METHODS:Forty mice were randomly divided into five groups:control group(intranasal saline),lipopolysaccharide(LPS)group(100 mg/L),PM2.5 low-dose group(0.003 5 mg/d),PM2.5 medium-dose group(0.007 mg/d),and PM2.5 high-dose group(0.014 mg/d).They were treated with intranasal in-stillation for 30 d.Lung function and tracheal contractile responses were evaluated using whole-body plethysmography and sensitive wire myograph.Inflammatory mediators in serum and oxidative stress parameters were detected using enzyme-linked immunosorbent assay(ELISA).Lung tissues were subjected to HE and Masson staining.RT-qPCR and Western blot were used to determine the expression of contractile receptors and the phosphorylation of the mitogen-activated protein kinase(MAPK)signal pathway.RESULTS:Intranasal instillation of PM2.5 significantly increased airway resistance in mice and enhanced tracheal contractility in response to carbachol.PM2.5 elevated levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,and IL-6 in serum.PM2.5 instillation also led to a decrease in glutathione peroxidase(GSH-Px)levels and an increase in malondialdehyde(MDA)levels.Lung tissue exhibited notable pathological changes,including inflammatory cell infiltration,hyperplasia of alveolar epithelial cells,and collagen deposition.Mechanistically,exposure to PM2.5 increased the expression of muscarinic M3 receptor mRNA and protein,as well as the phosphorylation of p-ERK1/2 and p-p38 proteins following PM2.5 instillation.CONCLUSION:Intranasal instillation of PM2.5 induced inflammation and oxidative stress,along with the activation of the extracellular signal-regulated kinase 1/2(ERK1/2)and p38 MAPK pathways,resulting in the upregulation of M3 receptor-induced AHR.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

In order to elucidate the therapeutic effect and mechanism of action of Zhengqing Fengtongning Sustained-release Tablets on knee osteoarthritis, this study created a knee osteoarthritis model using 0.2 mL 40 g·L~(-1) papain and randomly divided the rats into the model group, high-dose and low-dose groups of Zhengqing Fengtongning Sustained-release Tablets, and celecoxib group. All groups were given the drug for four weeks, with the diameter of their knee joint being measured during this period. Hematoxylin-eosin staining and Senna solid green staining were utilized to observe the pathology of knee joint tissue in SD rats. The initial therapeutic impact of Zhengqing Fengtongning Sustained-release Tablets on knee osteoarthritis in rats was assessed by monitoring the levels of interleukin-1β(IL-1β) and interleukin-6(IL-6) in the plasma. Using a combination of non-targeted metabolomics and 16S rRNA techniques, researchers determined the variations in endogenous molecules and intestinal flora in rats and identified potential biomarkers. The results showed that Zhengqing Fengtongning Sustained-release Tablets improved the diameter of knee joint swelling, ameliorated the pathological damage of cartilage tissue, and reduced the plasma levels of IL-1β and IL-6 in rats with knee osteoarthritis. Metabolomics analysis identified 22 potential biomarkers associated with the modulatory effects of Zhengqing Fengtongning Sustained-release Tablets, including 5-hydroxytryptamine, corticosterone, methylmalonic acid, and other biomarkers, which were mainly involved in eight metabolic pathways, including tryptophan metabolism, vitamin K metabolism, steroid synthesis, and so on. The results of intestinal flora showed a decrease in the diversity of intestinal flora in the model group, an increase in the diversity of intestinal flora, and an improvement in the microecology of intestinal flora. Significant differences were found in Lachnospiraceae＿NK4A136＿group, Helicobacter, Lactobacillus, Bacteroides, and Parabacteroides. Finally, the results of the combined analysis showed that 22 biomarkers were correlated with five genera. The above results indicate that Zhengqing Fengtongning Sustained-release Tablets can improve the tissue morphology and structure of knee joints, reduce the level of plasma inflammatory factors, regulate the diversity of intestinal flora, and balance the metabolic pathways of steroid synthesis, vitamin K metabolism, and tryptophan metabolism to exert a therapeutic effect on knee osteoarthritis.
Animals ; Drugs, Chinese Herbal/administration & dosage* ; Rats ; Rats, Sprague-Dawley ; Gastrointestinal Microbiome/drug effects* ; Osteoarthritis, Knee/genetics* ; Metabolomics ; Delayed-Action Preparations/administration & dosage* ; Male ; Tablets ; Humans ; Interleukin-1beta/blood* ; Interleukin-6/blood*

ObjectiveTo investigate the effect of Jingangwan on the expression of osteoclast， c-Jun N-terminal kinase（JNK）， p38 mitogen-activated protein kinase（p38 MAPK）， and interleukin-1（IL-1） in the osteoporosis model rats， explore the mechanism of Jingangwan in the treatment of osteoporosis， and determine the optimal dosing concentration of Jingangwan. MethodFifty-six rats of SPF grade were randomized into a blank group，a sham operation group，a model group， model group，high-， medium-， and low-dose Jingangwan groups （0.72， 0.36， 0.18 g·kg^-1·d^-1， ig），and an estradiol valerate group （0.009 g·kg^-1·d^-1， ig）， with eight rats in each group. The rats in the model group， the blank group， and the sham operation group received 3 mL of normal saline， respectively. Samples were collected 12 weeks after drug administration. The number of osteoclasts was observed by tartrate-resistant acid phosphatase （TRAP） staining. Serum levels of JNK， p38 MAPK， and IL-1 were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expression levels of p38 MAPK and JNK were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultThe TRAP staining results showed that compared with the model group， the estradiol valerate group and the Jingangwan groups could inhibit the formation of osteoclasts to different degrees. As revealed by ELISA results， compared with the model group and the sham operation group， the model group showed increased serum levels of p38 MAPK， JNK， and IL-1 （P<0.01）， while compared with the model group， all the groups with drug intervention showed decreased levels of p38 MAPK， JNK， and IL-1 （P<0.01）. The serum levels of JNK and IL-1 in the high-dose Jingangwan group were lower than those in the estradiol valerate group （P<0.05）. Real-time PCR results showed that compared with the blank group， the model group showed increased relative mRNA expression of p38 MAPK and JNK in the thighbone （P<0.01）， while compared with the model group， all the groups with drug intervention showed decreased relative mRNA expression of p38 MAPK and JNK in the thighbone （P<0.01）. ConclusionJingangwan can inhibit the formation of osteoblasts，reduce the diameter of the bone marrow cavity，improve bone quality，suppress the production of inflammatory factors，affect the metabolism of the MAPK signaling pathway，and blunt p38 MAPK and JNK activities to inhibit the differentiation and proliferation of osteoblasts and regulate bone metabolism， thereby preventing osteoporosis. Therefore，Jingangwan may be of application value in maintaining bone health and treating osteoporosis.