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.

Objective To systematically review the studies on predictive models for delayed graft function (DGF) after kidney transplantation. Methods Databases including China Biology Medicine Database, China National Knowledge Infrastructure, Wanfang Database, VIP Database, PubMed, Web of Science and CINAHL were searched to collect studies on predictive models for DGF after kidney transplantation published from the establishment of each database to June 29, 2025. Two researchers screened the literatures according to the inclusion and exclusion criteria, evaluated the quality of the literatures using the prediction model risk of bias assessment tool (PROBAST), and conducted a meta-analysis of the common predictors of the models using R software. Results A total of 12 literatures were included, involving 14 predictive models with sample sizes ranging from 103 to 24 653 cases. Donor serum creatinine level, cold ischemia time, donor age and donor body mass index were the top four common predictors. All the predictive models were at high risk of bias and low in applicability. The results of meta-analysis showed that abnormal donor body mass index, advanced donor age, prolonged cold ischemia time and elevated donor serum creatinine level were all associated with an increased risk of DGF after transplantation (all P<0.01), but there was high heterogeneity among the studies. Fixed-effect model and random-effect model were used to re-pool the effect sizes separately. The results indicated that the fixed-effect model and random-effect model had good consistency in terms of donor body mass index, donor age and cold ischemia time, while there was a significant difference in the effect sizes of the two models for donor serum creatinine level. Conclusions The predictive models for DGF risk after kidney transplantation have good predictive performance, but the overall risk of bias is high. In the future, large-sample, multicenter and high-quality prospective clinical studies should be carried out to optimize the predictive models, so as to improve their predictive ability and clinical application value.

The blood-brain barrier （BBB） is a physical and biochemical barrier that precisely regulates brain homeostasis and plays a central role in controlling the transport of endogenous and exogenous drugs and related metabolites across the blood-brain interface. These functions of the BBB are mediated by its major components， including brain microvascular endothelial cells （BMECs）， tight junction protein complexes， and influx and efflux transporter proteins. One of the pathological features of ischemic stroke （IS） is BBB disruption， which plays an important role in the development of post-stroke brain injury and subsequent neurological dysfunction. Therefore， given the increasing incidence of IS， there is an urgent need to develop new therapeutic strategies to prevent BBB dysfunction and thereby protect injured brain tissue after IS. This study describes the pathological mechanisms by which BMEC injury after IS leads to BBB dysfunction and elucidates the association between BMECs and IS， including the regulation of apoptosis， autophagy， inflammatory responses， oxidative stress， neurotoxic effects， and cerebral edema. In addition， this article summarizes Chinese herbal medicines that may prevent and treat IS by targeting BMECs. These include monomeric compounds and single herbs such as flavonoids， glycosides， phenols， phthalides， terpenoids， and Styrax. Traditional Chinese medicine （TCM） compound formulas and preparations include oral formulations such as Buyang Huanwu decoction， Sailuotong， Naoxintong capsules， Dandeng Tongnao capsules， and Shexiang Tongxin dropping pills， as well as injectable preparations such as Tongluo Jiunao injection， Xingnaojing injection， Danshen polyphenolic acid for injection， Yiqi Fumai injection， and Shuxuetong injection. This study aims to explore the protective effects of TCM against IS through targeted regulation of BMEC function， providing new insights into the mechanisms of IS and endovascular therapeutic strategies.

In March 2024, three male and two female specimens of the genus Lispe were intercepted on cargo ships inbound for Wan Zai Port under Gongbei Customs. Based on morphological characteristics and molecular analysis, the specimens were identified as Lispe pumila. In this study, we describe the morphological features, diagnostic characteristics, and geographical distribution of L. pumila, with the aim of providing a reference for the identification of this species when intercepted at ports.

Background and aims The mechanism of cholestatic liver injury (CLI) is unclear, and effective therapies are lacking. While peroxisome proliferator-activated receptor alpha (PPARα) agonists show potential hepatoprotective effect and pyroptosis is implicated in hepatocellular damage, how PPARα activation mitigates lithocholic acid (LCA)-induced pyroptosis remains unknown. Methods The hepatoprotective effect of PPARα agonists was evaluated in a mouse model of intrahepatic cholestasis induced by LCA. Liver injury was assessed via serum biochemistry, hematoxylin and eosin and TUNEL staining, and electron microscopy. Pyroptosis pathways were analyzed using real-time quantitative polymerase chain reaction, Western blot, and co-immunoprecipitation. Results Combined morphological, histopathological, and biochemical analyses confirmed that PPARα activation protects against CLI. Compared with LCA treatment alone, PPARα activation significantly attenuated the elevation of serum lactate dehydrogenase (LDH), the increased TUNEL-positive cells, and the formation of hepatocyte membrane pores. Mechanistically, PPARα activation suppressed both NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis and apoptosis protease-activating factor-1 (APAF-1)/CASPASE-3/GSDME-mediated pyroptosis. Furthermore, PPARα agonist pretreatment inhibited activation of the nuclear factor-kappa B (NF-κB) and forkhead box O1 (FOXO1) signaling pathways. Conclusions PPARα protects against LCA-induced CLI by inhibiting both NLRP3 inflammasome-mediated pyroptosis associated with NF-κB and APAF-1/CASPASE-3/GSDME-mediated pyroptosis associated with the FOXO1 signaling pathway.

Objective:In order to clarify the ABO phenotype and genotype,and explore the molecular biological mechanism,serological detection,genotyping and gene sequencing were performed on an upper gastrointestinal hemorrhage patient with inconsistent forward and reverse ABO blood typing.Methods:ABO forward and reverse blood typing,H antigen identification,capillary centrifugation test and salivary substance detection were performed by classical serological method,moreover,polymerase chain reaction-sequence specific primer(PCR-SSP)was used for ABO genotyping,ABO gene 1-7 exons were sequenced by Sanger analysis in order to identify mutation.Results:Mixed field agglutination with anti-A,anti-AB and no agglutination with anti-A1 were appeared in the forward typing tests,agglutination with B cells but no agglutination with A1 cells and O cells were appeared in the reverse typing tests.3+agglutination strength was showed with anti-H.In capillary centrifugation experiment,erythrocyte after isolation in proximal part and distal end had same strength of agglutination with anti-A.Substances A and H were detected in saliva.The patient was assigned an A3 phenotype according to serological characteristics.Sequencing results of ABO gene 1-7 exons showed c.261delG,c.467C＞T,c.865A＞G,in which,865A＞G was the first discovered mutation,and this new mutation had been submitted to GenBank with accession number PP187306.Conclusion:A novel site mutation c.865A＞G is reported in this study,and this new mutation can result in a replacement of Met with Val at residue 289(p.Met289Val)and lead to an A3 phenotype.

Objective:To explore the changes in plasma lipoprotein associated phospholipase A2(Lp-PLA2)and silencing information regulatory protein 1(SIRT1)in patients with sepsis complicated with acute kidney injury(AKI)and their relationship with short-term prognosis.Methods:243 sepsis patients who received treatment in our hospital from May 2022 to May 2024 were prospective selected,including 80 sepsis patients with AKI(AKI group)and 163 sepsis patients without AKI(non AKI group),the plasma Lp-PLA2 and SIRT1 levels between the two groups were compared.They were divided into good prognosis group and poor prognosis group according to 28 d prognosis after admission in AKI group.The influencing factors of short-term prognosis in sepsis patients complicated with AKI were analyzed by multiple logistic regression model.The short-term prognostic value of plasma Lp-PLA2 and SIRT1 alone and in combination for sepsis complicated with AKI patients was analyzed using receiver operating characteristic(ROC)curve.Results:Compared with non AKI group,AKI group had higher Lp-PLA2 and lower SIRT1(P＜0.05).39 deaths within 28 d after admission in AKI group(poor prognosis group),41 cases survived(good prognosis group),with poor prognosis rate of 48.75％(39/80).Sequential organ failure assessment(SOFA)score,acutephysiology and chronic health evaluationⅡ(APACHEⅡ)score,creatinine(Scr),lactate dehydrogenase albumin ratio(LAR)in poor prognosis group were higher than those in good prognosis group,while procalcitonin(PCT)was lower than that in good prognosis group(P＜0.05).Compared with the good prognosis group,poor prognosis group had higher Lp-PLA2 and lower SIRT1 at admission(P＜0.05).Elevated SOFA score,elevated Scr,elevated APACHEⅡ score,and elevated plasma Lp-PLA2 were risk factors for poor prognosis in sepsis patients complicated with AKI(P＜0.05),while elevated plasma SIRT1 was a protective factor(P＜0.05).ROC curve analysis results showed that,the combined detection of plasma Lp-PLA2 and SIRT1 predicted a poor prognosis for sepsis patients with AKI with an area under the curve(AUC)of 0.935,which was better than the prediction of 0.813 and 0.858 for plasma Lp-PLA2 and SIRT1 alone.Conclusion:Sepsis complicated with AKI patients have elevated plasma Lp-PLA2 and decreased SIRT1,combined detection of the two can assist in predicting the risk of poor prognosis.

This study explored the effects and underlying mechanism of Raf kinase inhibitory protein(RKIP)on apoptosis in mast cells sensitized by Echinococcus granulosus cyst fluid.Bone marrow-derived mast cells(BMMCs)were isolated and cultured from RKIP knockout(KO)and wild-type(WT)C57BL/6 mice.Cells were divided into control and sensitized groups.The sensitized group was incubated for 24 h in RPMI1640 medium containing 10%serum from mice infected with E.granulosus,then activated for 3 h or 6 h with E.granulosus cyst fluid.The control group was incubated for 24 h in RPMI1640 medium,and then received an equal vol-ume of PBS.Cells and supernatants were collected for analysis.Flow cytometry was used to detect the expression of CD117 and FcεRⅠα on BMMCs.The levels of β-hexosaminidase,IL-4,and TNF-α in the supernatant were quantified with ELISA.Western blot analy-sis was used to assess expression changes in RKIP,apoptosis-related proteins,and pathway proteins in BMMC before and after sensi-tization.Flow cytometry analysis revealed that after 4 weeks of induction,the CD117 and FcεRⅠα double-positivity rates on both WT and KO BMMC exceeded 90%.ELISA indicated that the E.granulosus cyst fluid resulted in significantly greater β-hexosaminidase re-lease(F=16.88,P<0.05),and levels of IL-4(F=16.51,P<0.05)and TNF-α(F=9.78,P<0.05)in the KO sensitized group than the WT sensitized group.With respect to the WT control group,the WT sensitized group showed significantly down-regulated pro-tein expression levels of RKIP(F=8.20,P<0.05)and Bcl-2(F=101.40,P<0.01)after 3 h,but significantly up-regulated levels of p-PI3K(F=8.04,P<0.05),p-Akt(F=32.52,P<0.01),p-P65(F=13.29,P<0.05),and cleaved-caspase-3(F=46.34,P<0.01).With respect to the WT sensitized group,the KO sensitized group showed significantly up-regulated protein expression of p-PI3K(F=8.45,P<0.05),p-Akt(F=8.58,P<0.05),p-P65(F=11.02,P<0.05),and Bcl-2(F=84.50,P<0.001)after 3 h,but significantly down-regulated expression of cleaved-caspase-3(F=15.66,P<0.05).In conclusion,RKIP may inhibit the PI3K/Akt/NF-κB pathway,thereby inducing apoptosis in mast cells sensitized by E.granulosus cyst fluid.This process may help ease aller-gic reactions caused by mast cells in echinococcosis,thus offering a promising new approach for preventing and treating such reactions.

Objective:To establish an arsenic free fully automatic online digestion iodine analyzer detection method for urinary iodine (hereinafter referred to as the method).Methods:Based on the principle of iodine catalyzed antimony cerium redox reaction, a fully automatic online digestion iodine analyzer was used to determine the iodine content in urine. The effectiveness of the method in terms of detection limit, precision, accuracy (determination of urinary iodine primary standard reference materials GBW09108z and GBW09110f and spiked recovery experiment), and interference experiments was validated. The method was compared with the arsenic cerium catalytic spectrophotometry method recommended by the National Reference Laboratory for Iodine Deficiency Disorders.Results:The linear range of the method was 0 - 300 μg/L, with a correlation coefficient │ r│> 0.999 5. The qualitative and quantitative detection limits were 7.41 and 18.01 μg/L, respectively. The relative standard deviation ( RSD) of urine samples with different iodine concentrations ranged from 1.0% to 1.7%. The results of the determination of iodine concentrations in urine using standard substances GBW09108z and GBW09110f were within the given standard range, with RSD < 2.5%. The range of spiked recovery rates for urine samples with different iodine concentrations was 101.3% to 104.8%, with an overall average spiked recovery rate of 103.0%. The average concentration of the baseline iodine standard solution was determined to be 116.21 μg/L, and the relative error of the concentration determination with the addition of interfering substances was less than 5.0%. The comparison results showed that there was no statistically significant difference in the measurement results between the two methods ( t = - 0.06, P = 0.952). Conclusions:The method adopts automated detection, which is simple to operate, labor-saving, and does not require the use of arsenic trioxide. It has high precision and accuracy, and is suitable for detection of large quantities of samples.

Objective:To analyze the abdominal CT types, surgical methods, obstruction recurrence rate and postoperative chemotherapy rate in patients with recurrent ovarian cancer and malignant bowel obstruction (MBO).Methods:The clinical data of 43 patients with recurrent ovarian cancer and MBO from September 30, 2021 to December 31, 2024 in the Fourth Affiliated Hospital of Nanjing Medical University were retrospectively analyzed. Intestinal surgical plans were determined based on abdominal CT classification and intraoperative conditions. The imaging data, surgical conditions, occurrence of severe complications within 30 d after surgery and mortality within 30 d after surgery were recorded. The patients were followed up once a month until February 28, 2025, and the obstruction recurrence rate and chemotherapy rate were recorded.Results:Among the 43 patients, the abdominal CT types were as follows: 9 cases (20.9%) of isolated recurrence type, 25 cases (58.2%) of non-infiltrating proximal small intestine type, 8 cases (18.6%) of infiltrating proximal small intestine type, and 1 case (2.3%) of other types. Two patients underwent exploratory laparotomy; 41 patients completed the intended surgical treatment, including 5 cases of intestinal intubation ostomy, 2 cases of pull-through ostomy, 2 cases of bypass surgery, 26 cases of resection + ostomy, and 6 cases of resection + anastomosis. After surgery, 19 cases (43.2%) resumed partial enteral nutrition, and 16 cases (37.2%) achieved complete enteral nutrition. The incidence of severe postoperative complications within 30 d after surgery was 9.3% (4/43). Obstructive symptoms such as abdominal distension were relieved in 41 cases (95.3%). The mortality within 30 d after surgery was 7.0% (3/43), the obstruction recurrence rate was 7.0% (3/43), and the chemotherapy rate was 76.7% (33/43). By the end of follow-up, 7 patients were still alive.Conclusions:Recurrent ovarian cancer complicated by MBO is a high-risk disease. Identifying patients who may benefit can improve the relief rate of obstructive symptoms such as abdominal distension, reduce the obstruction recurrence rate, and increase the chemotherapy rate.