Urolithiasis represents a prevalent clinical challenge marked by high recurrence rates and morbidity，with existing preventive strategies struggling to effectively curb its epidemic trajectory，thereby posing a significant threat to public health. The etiology of this condition is intricate，involving a complex network of interactions spanning classical supersaturation-crystallization theory，Randall’s plaque theory，and multifactorial elements such as cellular injury，inflammatory responses，metabolic derangements，the gut-kidney axis，immune dysregulation，and genetic predisposition. However，the critical mechanisms initiating stone formation and the early pathophysiological processes remain incompletely elucidated，constituting the core impasse in current preventive strategies. This review systematically synthesizes classical theories and cutting-edge advancements in urolithiasis etiology research，emphasizing the urgent need to integrate emerging technologies，including high-dimensional omics，advanced imaging modalities，and artificial intelligence，to dissect pivotal pathological nodes in early stone formation. Such interdisciplinary efforts are essential to overcome cognitive bottlenecks and ultimately achieve personalized，precision-based prevention strategies.

Objective To observe the effect of a Jianpi Huayu Jiedu formula on the NLRP3-mediated pyroptosis pathway in gastric precancerous lesion(GPL)associated with Helicobacter pylori(Hp)infection.Methods A GPL mouse model was prepared using Hp suspension gavage combined with Atp4a gene-deficient mice.The Jianpi Huayu Jiedu formula was administered as an intervention.Gastric mucosal tissue pathological damage was observed using hematoxylin and eosin(HE)staining.The presence of intestinal metaplasia(IM)was assessed using Alcian Blue-Periodic Acid Schiff(AB-PAS)staining.Ultrastructural changes in cell organelles were observed using transmission electron microscopy.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of gastrin-17(G-17),pepsinogen I(PGI),and proinflammatory cytokines IL-1β and IL-18.The expression of molecules related to the pyroptosis pathway was detected using Western blot and real-time quantitative PCR(RT-qPCR).Results Compared to the control group,Hp-related GPL mice exhibited gastric mucosal atrophy accompanied by IM and dysplasia.Damage to mitochondria and endoplasmic reticulum in parietal cells was observed.Levels of G-17,PGI,and proinflammatory cytokines IL-1β and IL-18 were elevated.The expression of molecules related to the pyroptosis pathway was increased.The Jianpi Huayu Jiedu formula significantly reduced gastric mucosal tissue pathological damage in GPL mice,decreased G-17 and PGI levels,mitigated inflammatory responses,and downregulated the expression of molecules related to the pyroptosis pathway.Conclusion The Jianpi Huayu Jiedu formula may exert its effects by inhibiting the NLRP3-mediated pyroptosis signaling pathway,thereby alleviating or even reversing the pathological damage of gastric mucosa in Hp-related GPL.

Objective To observe the effect of a Jianpi Huayu Jiedu formula on the NLRP3-mediated pyroptosis pathway in gastric precancerous lesion(GPL)associated with Helicobacter pylori(Hp)infection.Methods A GPL mouse model was prepared using Hp suspension gavage combined with Atp4a gene-deficient mice.The Jianpi Huayu Jiedu formula was administered as an intervention.Gastric mucosal tissue pathological damage was observed using hematoxylin and eosin(HE)staining.The presence of intestinal metaplasia(IM)was assessed using Alcian Blue-Periodic Acid Schiff(AB-PAS)staining.Ultrastructural changes in cell organelles were observed using transmission electron microscopy.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of gastrin-17(G-17),pepsinogen I(PGI),and proinflammatory cytokines IL-1β and IL-18.The expression of molecules related to the pyroptosis pathway was detected using Western blot and real-time quantitative PCR(RT-qPCR).Results Compared to the control group,Hp-related GPL mice exhibited gastric mucosal atrophy accompanied by IM and dysplasia.Damage to mitochondria and endoplasmic reticulum in parietal cells was observed.Levels of G-17,PGI,and proinflammatory cytokines IL-1β and IL-18 were elevated.The expression of molecules related to the pyroptosis pathway was increased.The Jianpi Huayu Jiedu formula significantly reduced gastric mucosal tissue pathological damage in GPL mice,decreased G-17 and PGI levels,mitigated inflammatory responses,and downregulated the expression of molecules related to the pyroptosis pathway.Conclusion The Jianpi Huayu Jiedu formula may exert its effects by inhibiting the NLRP3-mediated pyroptosis signaling pathway,thereby alleviating or even reversing the pathological damage of gastric mucosa in Hp-related GPL.

Urolithiasis represents a prevalent clinical challenge marked by high recurrence rates and morbidity，with existing preventive strategies struggling to effectively curb its epidemic trajectory，thereby posing a significant threat to public health. The etiology of this condition is intricate，involving a complex network of interactions spanning classical supersaturation-crystallization theory，Randall’s plaque theory，and multifactorial elements such as cellular injury，inflammatory responses，metabolic derangements，the gut-kidney axis，immune dysregulation，and genetic predisposition. However，the critical mechanisms initiating stone formation and the early pathophysiological processes remain incompletely elucidated，constituting the core impasse in current preventive strategies. This review systematically synthesizes classical theories and cutting-edge advancements in urolithiasis etiology research，emphasizing the urgent need to integrate emerging technologies，including high-dimensional omics，advanced imaging modalities，and artificial intelligence，to dissect pivotal pathological nodes in early stone formation. Such interdisciplinary efforts are essential to overcome cognitive bottlenecks and ultimately achieve personalized，precision-based prevention strategies.

Objective:To explore the mechanism of noise-induced hidden hearing loss by proteomics.Methods:In October 2022, 64 SPF male C57BL/6J mice were divided into control group and noise exposure group with 32 mice in each group according to random sampling method. The noise exposure group was exposed to 100 dB sound pressure level, 2000-16000 Hz broadband noise for 2 h, and the mouse hidden hearing loss model was established. Auditory brainstem response (ABR) was used to test the change of hearing threshold of mice on the 7th day after noise exposure, the damage of basal membrane hair cells was observed by immunofluorescence, and the differentially expressed proteins in the inner ear of mice in each group were identified and analyzed by 4D-Label-free quantitative proteomics, and verified by Western blotting. The results were statistically analyzed by ANOVA and t test. Results:On the 7th day after noise exposure, there was no significant difference in hearing threshold between the control group and the noise exposure group at click and 8000 Hz acoustic stimulation ( P>0.05) . The hearing threshold in the noise exposure group was significantly higher than that in the control group under 16000 Hz acoustic stimulation ( P<0.05) . Confocal immunofluorescence showed that the basal membrane hair cells of cochlear tissue in noise exposure group were arranged neatly, but the relative expression of C-terminal binding protein 2 antibody of presynaptic membrane in middle gyrus and basal gyrus was significantly lower than that in control group ( P<0.05) . GO enrichment analysis showed that the functions of differentially expressed proteins were mainly concentrated in membrane potential regulation, ligand-gated channel activity, and ligand-gated ion channel activity. KEGG pathway enrichment analysis showed that differentially expressed proteins were significantly enriched in phosphatidylinositol 3 kinase-protein kinase B (PI3K-Akt) signaling pathway, NOD-like receptor signaling pathway, calcium signaling pathway, etc. Western blotting showed that the expression of inositol 1, 4, 5-trisphosphate receptor 3 (Itpr3) was increased and the expression of solute carrier family 38 member 2 (Slc38a2) was decreased in the noise exposure group ( P<0.05) . Conclusion:Through proteomic analysis, screening and verification of the differential expression proteins Itpr3 and Slc38a2 in the constructed mouse noise-induced hidden hearing loss model, the glutaminergic synaptic related pathways represented by Itpr3 and Slc38a2 may be involved in the occurrence of hidden hearing loss.

Objective:To explore the mechanism of noise-induced hidden hearing loss by proteomics.Methods:In October 2022, 64 SPF male C57BL/6J mice were divided into control group and noise exposure group with 32 mice in each group according to random sampling method. The noise exposure group was exposed to 100 dB sound pressure level, 2000-16000 Hz broadband noise for 2 h, and the mouse hidden hearing loss model was established. Auditory brainstem response (ABR) was used to test the change of hearing threshold of mice on the 7th day after noise exposure, the damage of basal membrane hair cells was observed by immunofluorescence, and the differentially expressed proteins in the inner ear of mice in each group were identified and analyzed by 4D-Label-free quantitative proteomics, and verified by Western blotting. The results were statistically analyzed by ANOVA and t test. Results:On the 7th day after noise exposure, there was no significant difference in hearing threshold between the control group and the noise exposure group at click and 8000 Hz acoustic stimulation ( P>0.05) . The hearing threshold in the noise exposure group was significantly higher than that in the control group under 16000 Hz acoustic stimulation ( P<0.05) . Confocal immunofluorescence showed that the basal membrane hair cells of cochlear tissue in noise exposure group were arranged neatly, but the relative expression of C-terminal binding protein 2 antibody of presynaptic membrane in middle gyrus and basal gyrus was significantly lower than that in control group ( P<0.05) . GO enrichment analysis showed that the functions of differentially expressed proteins were mainly concentrated in membrane potential regulation, ligand-gated channel activity, and ligand-gated ion channel activity. KEGG pathway enrichment analysis showed that differentially expressed proteins were significantly enriched in phosphatidylinositol 3 kinase-protein kinase B (PI3K-Akt) signaling pathway, NOD-like receptor signaling pathway, calcium signaling pathway, etc. Western blotting showed that the expression of inositol 1, 4, 5-trisphosphate receptor 3 (Itpr3) was increased and the expression of solute carrier family 38 member 2 (Slc38a2) was decreased in the noise exposure group ( P<0.05) . Conclusion:Through proteomic analysis, screening and verification of the differential expression proteins Itpr3 and Slc38a2 in the constructed mouse noise-induced hidden hearing loss model, the glutaminergic synaptic related pathways represented by Itpr3 and Slc38a2 may be involved in the occurrence of hidden hearing loss.

Objective:To investigate the changes of serum Golgi protein 73 (GP73) expression and its clinical significance in breast cancer patients before and after radiotherapy.Methods:A total of 135 patients with primary breast cancer who were diagnosed and treated in Qingdao Hospital Affiliated to Shandong First Medical University Hospital from Aug. 2016 to Dec. 2017 were selected and received standard radiotherapy after surgery. Enzyme-linked immunosorbent assay (ELISA) was used to determine the content of GP73 in the serum of patients before and after radiotherapy, and the differences in the expression levels of GP73 before and after radiotherapy in patients with different molecular phenotypes, tumor stages, and pathological types were compared. Association between the expression of serum GP73 and clinical outcome before and after radiotherapy was analyzed.Results:The expression of GP73 in breast cancer patients was (117.69±33.57) mg/L before radiotherapy and (101.88±30.92) mg/L after radiotherapy, and the difference was statistically significant ( t=4.025, P<0.001) . Different molecular phenotypes were stratified and found that the expression of serum GP73 in patients with luminal A, luminal B, HER-2 overexpression, and triple negative after radiotherapy decreased compared with those before radiotherapy, but only the HER-2 overexpression type had statistically significant difference between before and after radiotherapy ( P<0.05) . Stratification according to different tumor stages showed that the expression of serum GP73 in patients with stage I, II, III and IV after radiotherapy was lower than that before radiotherapy, but only the patients with stage II, stage III, and stage IV were compared before and after radiotherapy, and the difference was statistically significant ( P<0.05) . Stratification according to different pathological types showed that the expression of serum GP73 in patients with invasive ductal carcinoma before and after radiotherapy was significantly lower in patients with invasive lobular carcinoma ( P<0.05) . In addition, the 1-year survival rate of the descending group was significantly higher than that of the ascending group, while the local recurrence rate and the occurrence of distant metastasis were significantly lower than those of the ascending group, and the difference was statistically significant ( P<0.05) . Conclusions:The expression level of serum GP73 in breast cancer patients after radiotherapy is significantly higher than that before radiotherapy, and it has a certain relationship with molecular phenotype, tumor stage, and pathological type. At the same time, the increase in serum GP73 expression after radiotherapy may be detrimental to the clinical outcome of patients.

Objective To study the visfatin level changes in patients with rheumatoid arthritis (RA), and to study the correlation of visfatin level and atherosclerosis in RA.Methods Fifty cases of patients were divided to the plaque group (33 cases) and plaque-free group (17 cases) according to the carotid intima media thickness checked by carotid ultrasonography.In addition, their blood lipid level, homeostasis model assessment of insulin resistance (HOMA-IR), rheumatoid factors (RFs), anti-CCP, visfatin etc.were measured.Fifty healthy people were set as the control group.The correlation between the visfatin level of RA patients and atherosclerosis was analyzed.The statistical analysis was carried out with independent t-test,analysis of variance, Spearman correlation analysis and multiple stepwise regression.Results The serum visfatin level of RA plaques group was obviously higher than that of the plaque-free group [(47±22) μg/L vs (34±19) μg/L, t=4.361, P＜0.01].The serum visfatin level of RA patients was positively correlated to HOMA-IR (r=0.567, P=0.001), RF (r=0.502, P=0.003), anti-cyclic peptide containing citrulline, (anti-CCP) (r=0.420, P=0.038) and carotid artery IMT (r=0.596, P=0.001).High-density lipoprotein-C (OR=1.009, P=0.020), HOMA-IR (OR=1.450, P=0.006), anti-CCP (OR=1.005, P=0.014) and visfatin (OR=0.971, P=0.008) were independent relevant factors affecting carotid artery IMT.Conclusion The serum visfatin level of RA patients is closely related to atherosclerosis.

Objective To discuss the correlation between the joint detection of BA,EMAb,ACA and unexplained recurrent spontaneous abortion(URSA).Methods Selected 144 URSA cases,166 SA(sporadic abortion)cases,188 normal pregnant women,and detected their BA,EMAb,ACA and statistical analysis of parallelism.Results Comparing URSA group with SA group and control group respectively,there were significant statistical difference between BA negative rate (74.31%, 25.30% and 50.53%),EMAb positive rate (35.42%,7.23% and 6.91%)and ACA positive rate (26.39%,5.42% and 5.32%)(χ2 = 19.344 ~ 74.180;P < 0.05;χ2 = 37.837 ~ 42.586,P < 0.05),(χ2 = 26.355 ~ 29.270,P < 0.05).URSA group’s BA,ACA and EMAb joint detection rate of positive (84.72%)was significantly higher than SA group and the con-trol group (χ2 =35.532~93.076,P <0.05).Conclusion There was a close relationship between the lack of BA,the genera-tion of EMAb,ACA and unexplained recurrent spontaneous abortion.Joint detection has important clinical significance in auxiliary diagnosis of unexplained recurrent spontaneous abortion and prognosis judgement.

Objective Discussing the correlation between joint detection of procalcitonin(PCT) ,hypersensitive c‐reactive protein (hs‐CRP) ,WBC and bronchopneumonia in children .Methods Choosing 89 bacterial infection bronchopneumonia children ,92 virus infection bronchopneumonia children ,90 mycoplasma infection bronchopneumonia children and 100 normal children ,detecting their PCT ,hs‐CRP ,WBC and statistical analysis of the level of parallelism .Results There is a positive correlation between bacterial in‐fection group′s PCT and hs‐CRP ,WBC(r=0 .807 ,0 .764 ,P<0 .05) .The joint detection of PCT ,hs‐CRP ,WBC positive rate in bac‐terial infection group is significantly higher than the rest group(P<0 .05) .Conclusion PCT ,hs‐CRP and WBC is a sensitive indica‐tor of bacterial infection .There is important clinical reference value in joint detection to the diagnosis of bacterial infection broncho‐pneumonia in children ,in dynamic monitoring the disease progression ,and in prognosis judgement .