Establishing a three-generation family cohort enables the investigation of the effects of genetic, epigenetic, lifestyle, and parenting factors in the grandparental (F0) and parental (F1) generations on the growth, development, and disease onset and progression of the offspring (F2). It facilitates further exploration of the biological mechanisms underlying the impact of intergenerational factors on the health of the offspring (F2), providing evidence for the formulation of public health policies and measures related to child health management and infant and young child care. Currently, the development of multi-generational cohorts in China remains in a preliminary stage, with no systematic multi-generational research framework yet established. Drawing on prior evidence-based scientific research, existing cohort studies, and the practical experience of multidisciplinary experts in maternal and child health, this consensus defines the scope of three-generation family cohorts regarding their definition, significance, key technologies, and application scenarios. It provides technical recommendations for establishing relevant cohorts, aiming to support research areas such as the intergenerational transmission of childhood diseases, the maternal intrauterine environment, and the tracing of family rearing environments. This will facilitate the early prevention and control of diseases manifesting in childhood and adulthood, ultimately promoting the comprehensive and healthy development of children.

Functional dyspepsia （FD） is a prioritized disease category where traditional Chinese medicine （TCM） demonstrates distinct therapeutic advantages. The current western medicine treatment for FD is mainly based on proton pump inhibitors and prokinetic agents， with digestive enzymes， probiotics and antidepressants serving as adjuvant medication， yet such therapies still have certain limitations. TCM treatment for FD includes oral administration of Chinese herbal formulas and Chinese patent medicines， as well as external TCM therapies such as acupuncture and moxibustion， acupoint application， hot medicinal compress therapy， rubbing with ointment， medicinal iontophoresis， auricular acupoint therapy and tui na （Chinese medical massage）. The combined treatment of FD with integrated TCM and western medicine can significantly improve clinical effectiveness and reduce adverse reactions. The common mechanisms underlying the therapeutic effects of both TCM and western medicine revolve around the core pathological processes of FD， mainly focusing on restoring gastrointestinal motility， regulating the levels of brain-gut peptides， modulating intestinal microecology， and ameliorating inflammatory status. The differential mechanisms lie in the precise targeting feature of western medicine versus the holistic-regulating and multi-target characteristics of TCM， and the two approaches exert a synergistic effect to enhance efficacy. This paper proposes to leverage the advantages of TCM in holistic regulation and the strengths of western medicine in targeted treatment， so as to provide personalized and comprehensive treatment regimens for FD patients.

ObjectiveTo evaluate the feasibility of various strength levels of deep learning image reconstruction （DLIR） algorithms for improving non-contrast abdominal CT image quality at ultra-low radiation doses， by comparing ultra-low-dose DLIR images with low-dose filtered back projection （FBP） images. MethodsA prospective collection of 85 patients undergoing non-contrast abdominal CT scans was performed， and a self-controlled study method was employed to conduct low-dose （LD） group and ultra-low-dose （ULD） group scans. The LD group used a noise index of 10 and employed FBP for image reconstruction （LD-FBP group）. The ULD group used a noise index of 30 and employed DLIR at different levels （low， medium， high）， resulting in three subgroups of reconstructed images： ULD-DLIR-L， ULD-DLIR-M， and ULD-DLIR-H. For each group， CT values， standard devia-tion （SD）， signal-to-noise ratio （SNR）， and contrast-to-noise ratio （CNR） were measured and calculated for the liver， spleen， kidneys， aorta， psoas major， and subcutaneous fat. Effective dose （ED） was also recorded. Two radiologists independently performed subjective evaluations of image quality using a 5-point scale. ResultsCompared with the LD-FBP group， the ULD-DLIR-L group showed significantly lower SNR and CNR values in the liver， spleen， kidneys， aorta， and psoas major （P<0.001）， while the ULD-DLIR-H group exhibited significantly higher values （P<0.001）. The difference of SNR and CNR values for the ULD-DLIR-M group showed no statistically significant difference. For subjective evaluation， the scores of the ULD-DLIR-L and ULD-DLIR-M groups were lower than those of the LD-FBP group， while there was no statistically significant difference in scores between the ULD-DLIR-H group and the LD-FBP group. The ED value of the ULD group was approximately 88% lower than that of the LD group. ConclusionCompared with the LD-FBP group， the ULD-DLIR-H group significantly reduces SD values while increasing SNR and CNR values， effectively improving the image quality of non-contrast abdominal CT scans.

Metabolic-associated fatty liver disease (MAFLD) and osteoporosis (OP) are two very common metabolic diseases. A growing body of experimental evidence supports a pathophysiological link between MAFLD and OP. MAFLD is often associated with the development of OP. Rutaecarpine (RUT) is one of the main active components of Chinese medicine Euodiae Fructus. Our previous studies have demonstrated that RUT has lipid-lowering, anti-inflammatory and anti-atherosclerotic effects, and can improve the OP of rats. However, whether RUT can improve both fatty liver and OP symptoms of MAFLD mice at the same time remains to be investigated. In this study, we used C57BL/6 mice fed a high-fat diet (HFD) for 4 months to construct a MAFLD model, and gave the mice a low dose (5 mg·kg^-1) and a high dose (15 mg·kg^-1) of RUT by gavage for 4 weeks. The effects of RUT on liver steatosis and bone metabolism were then evaluated at the end of the experiment [this experiment was approved by the Experimental Animal Ethics Committee of Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences (approval number: IMB-20190124D₃03)]. The results showed that RUT treatment significantly reduced hepatic steatosis and lipid accumulation, and significantly reduced bone loss and promoted bone formation. In summary, this study shows that RUT has an effect of improving fatty liver and OP in MAFLD mice.

Objective To evaluate the role of distortion product otoacoustic emissions (DPOAE) testing in evaluating early hearing loss among noise-exposed workers. Methods A total of 174 noise-exposed workers in a metal shipbuilding enterprise were selected as the research subjects by the convenience sampling method. Pure tone audiometry (PTA), DPOAE and the level of noise exposure were conducted on the workers. The rank correlation analysis was used to analyze the correlation between DPOAE amplitude and PTA threshold. The multilevel model was used to analyze the effects of gender, age, noise exposure intensity, cumulative noise exposure (CNE), hearing loss classification and PTA threshold on DPOAE results. Results At the frequencies of 0.50, 1.00, 2.00, 3.00, 4.00, 6.00 and 8.00 kHz, the DPOAE amplitude was negatively correlated with the PTA threshold (rank correlation coefficients were -0.12, -0.48, -0.47, -0.18, -0.23, -0.44, -0.19, respectively, all P<0.01). At the most frequencies, DPOAE amplitude was negatively correlated with age and CNE (all P<0.05). The results of multilevel model analysis showed that there were significant differences in DPOAE amplitudes at certain frequencies across gender, age, noise intensity, CNE, and hearing loss classification (all P<0.05). Significant differences in DPOAE responses were found among different CNE and hearing loss groups (all P<0.01). Conclusion DPOAE testing can objectively reflect the hearing status of noise-exposed workers and could be considered for inclusion in routine hearing monitoring to facilitate early detection of noise-induced hearing loss.

In recent years, the worldwide incidence rate of peripheral arterial and aortic diseases has increased year by year, significantly increasing the cardiovascular mortality and incidence rate of the whole population. In the past, peripheral arterial and aortic diseases were often more prone to missed diagnosis and delayed treatment compared to coronary artery disease. The 2024 ESC guidelines for the management of peripheral arterial and aortic diseases for the first time combines peripheral arterial and aortic diseases, integrating and updating the 2017 guidelines for peripheral arterial disease and the 2014 guidelines for aortic disease. The aim is to provide standardized recommendations for the management of systemic arterial diseases, ensuring that patients can receive coherent and comprehensive diagnosis and treatment, thereby improving prognosis. This article interprets the main content of the guideline in order to provide reference and assistance for the clinical diagnosis and treatment of peripheral arterial and aortic diseases in China at the current stage.

GPR126, also known as ADGRG6, is one of the most deeply studied aGPCRs. Initially, GPR126 was thought to be a receptor associated with muscle development and was primarily expressed in the muscular and skeletal systems. With the deepening of research, it was found that GPR126 is expressed in multiple mammalian tissues and organs, and is involved in many biological processes such as embryonic development, nervous system development, and extracellular matrix interactions. Compared with other aGPCRs proteins, GPR126 has a longer N-terminal domain, which can bind to ligands one-to-one and one-to-many. Its N-terminus contains five domains, a CUB (complement C1r/C1s, Uegf, Bmp1) domain, a PTX (Pentraxin) domain, a SEA (Sperm protein, Enterokinase, and Agrin) domain, a hormone binding (HormR) domain, and a conserved GAIN domain. The GAIN domain has a self-shearing function, which is essential for the maturation, stability, transport and function of aGPCRs. Different SEA domains constitute different GPR126 isomers, which can regulate the activation and closure of downstream signaling pathways through conformational changes. GPR126 has a typical aGPCRs seven-transmembrane helical structure, which can be coupled to Gs and Gi, causing cAMP to up- or down-regulation, mediating transmembrane signaling and participating in the regulation of cell proliferation, differentiation and migration. GPR126 is activated in a tethered-stalk peptide agonism or orthosteric agonism, which is mainly manifested by self-proteolysis or conformational changes in the GAIN domain, which mediates the rapid activation or closure of downstream pathways by tethered agonists. In addition to the tethered short stem peptide activation mode, GPR126 also has another allosteric agonism or tunable agonism mode, which is specifically expressed as the GAIN domain does not have self-shearing function in the physiological state, NTF and CTF always maintain the binding state, and the NTF binds to the ligand to cause conformational changes of the receptor, which somehow transmits signals to the GAIN domain in a spatial structure. The GAIN domain can cause the 7TM domain to produce an activated or inhibited signal for signal transduction, For example, type IV collagen interacts with the CUB and PTX domains of GPR126 to activate GPR126 downstream signal transduction. GPR126 has homology of 51.6%-86.9% among different species, with 10 conserved regions between different species, which can be traced back to the oldest metazoans as well as unicellular animals.In terms of diseases, GPR126 dysfunction involves the pathological process of bone, myelin, embryo and other related diseases, and is also closely related to the occurrence and development of malignant tumors such as breast cancer and colon cancer. However, the biological function of GPR126 in various diseases and its potential as a therapeutic target still needs further research. This paper focuses on the structure, interspecies differences and conservatism, signal transduction and biological functions of GPR126, which provides ideas and references for future research on GPR126.

Objective: To analyze the serological characteristics of anti-Mur antibodies and investigate the distribution frequency of the Mur antigen among voluntary blood donors in Shiyan, thereby providing a basis for guiding clinical transfusion and establishing a Mur blood type database. Methods: ABO blood grouping of donors and patients was performed using an automated blood typing analyzer and the gel card method, respectively. Unexpected antibody screening and identification were performed using the saline, tube anti-human globulin, and polybrene methods. The specificity of anti-Mur antibodies was confirmed using Fisher's exact probability test. Plasma treated with 2-mercaptoethanol was used to distinguish IgM and IgG antibodies. IgM and IgG anti-Mur titers were determined by the saline tube method and the anti-human globulin tube method, respectively, at 4℃, room temperature, and 37℃. A total of 1 659 donor red blood cell samples were initially screened for the Mur antigen phenotype using three samples of human-derived anti-Mur plasma by the micro-tube method. Donors who tested positive for Mur antigen were further tested by the direct antiglobulin test (DAT); those with negative results were confirmed for Mur antigen by the gel card and polybrene methods. Results: Three blood samples were identified to contain mixed IgG and IgM anti-Mur antibodies. The titers of both IgM and IgG anti-Mur antibodies were highest at 4℃, intermediate at room temperature, and lowest at 37℃. The positive frequency of the Mur antigen among voluntary blood donors in Shiyan was 1.99% (33/1 659). Conclusion: anti-Mur antibodies were detected in both blood donors and patients in our region. The Mur antigen shows a certain distribution frequency among voluntary blood donors in Shiyan. Screening for the Mur blood type and establishing a corresponding database could enhance transfusion safety.

Objective:To investigate the effect of the stress-induced protein sestrin 3(SESN3)on tumor proliferation and the sensitivity to endocrine therapy in hormone receptor-positive(HR+)breast cancer(BC)and its mechanism.Methods:The cancer genome atlas(TCGA)database was used to analyze the expression level of SESN3 in breast cancer tissue and paracancerous tissue.The clinical samples of breast cancer tissue and paracancerous tissue were collected,and immunohistochemistry(IHC)microarray was used to vali-date the expression of SESN3.Western blot was used to measure the protein expression level of SESN3 in BC cell lines with different pathological subtypes.HR+BC cell lines were used to establish the models of SESN3 overexpression and knockdown,and cell counting kit-8(CCK-8)assay and colony formation assay were used to assess the proliferative capacity of cells;Western blot was used to ana-lyze cell cycle alterations;a subcutaneous xenograft mouse model was used to validate the effect of SESN3 on proliferation in vivo.The bioinformatics analysis and Western blot were used to investigate the downstream mechanisms of SESN3 in regulating proliferation.Results:The analysis of TCGA database and clinical samples showed that the expression of the SESN3 gene in BC tissue was signifi-cantly lower than that in paracancerous tissue,and the patients with high SESN3 expression had a longer progression-free survival time.Compared with the other subtypes of BC cell lines,the HR+BC cells lines MCF-7 and T-47D had a relatively high expression level of SESN3.MCF-7 and T-47D cell lines were used to establish the cell models of knockdown(MCF-7KD and T-47DKD)and overexpres-sion(MCF-7OE and T-47DOE),and compared with the control group,MCF-7KD and T-47DKD cells showed increases in proliferative capacity and the proportion of cells arrested in the G2 and M phases.In vivo tumorigenesis experiments showed a significant increase in tumor growth in mice in the MCF-7KD group.The bioinfor-matics analyses showed a significant negative correlation between the mammalian Target of Rapamycin(mTOR)signaling pathway and SESN3 expression,and Western blot validation showed a significant increase in the expression of mTOR in MCF-7KD and T-47DKD cells,as well as reductions in the protein expression levels of autophagy-related genes.Subsequently,we further confirmed that the knockdown of MCF-7 and T-47D cells led to a decreased sensitivity to endocrine therapy.In addition,MCF-7、T-47D、MCF-7KD、and T-47DKD cell lines were treated with the mTOR inhibitor everolimus(EVE),and there was a significant reduction in proliferative capac-ity in the MCF-7KD group and the T-47DKD group;since the mTOR pathway reduced the sensitivity to endocrine therapy by reducing cell apopto-sis,there was a significant increase in the sensitivity to endocrine therapy with tamoxifen(TAM).Conclusion:The inte-grated database analysis,clinical sample validation,and in vivo/in vitro experimental models show that SESN3 inhibits the proliferation of HR+BC cells via the mTOR pathway and enhances the sensitivity to endocrine therapy.