Objective: To evaluate the practical effectiveness of confidential unit exclusion (CUE) in ensuring blood safety in Zhengzhou, analyze its application characteristics and existing problems, and provide a basis for optimizing blood safety management strategies. Methods: A retrospective analysis was conducted on CUE data handled by Henan Red Cross Blood Center from January 2019 to December 2024. Parameters such as the number of cases, demographic characteristics, reasons for exclusion, and time of report were statistically analyzed and compared with those of non-CUE. Results: From 2019 to 2024, the CUE reporting rate in Zhengzhou was 0.002 6% (40/1 547 666). CUE donors were predominantly male (65.00%, 26/40), aged 18-34 years (47.50%, 19/40), had college degree orabove (50.00%, 20/40), and were employees of enterprises or public institutions (32.50%, 13/40). Among the 40 CUE blood units, only one was reactive for anti-TP, while all others were qualified. The main reasons for CUE were recent vaccination (32.50%, 13/40), medical conditions unsuitable for donation (27.50%, 11/40), and high-risk sexual behavior (17.50%, 7/40). A total of 70.00% of reports occurred within 24 hours after donation, during which none of the corresponding blood units had been released; all units reported after more than 7 days had already been issued for clinical use, with no adverse transfusion reactions reported upon follow-up. Conclusion: The confidential unit exclusion program has played an active role in establishing a supplementary information feedback channel for blood donors. The procedure can be optimized by strengthening interactive communication and confirmation before donation, improving the accuracy of donors' self-assessment, and expanding convenient and rapid information-based reporting channels.

ObjectiveTo elucidate the mechanism by which total flavonoids of Abelmoschi Corolla （TFA） treat immunoglobulin A （IgA） nephropathy （IgAN） through serum metabolomics analysis. MethodsSPF-grade male SD rats were randomly assigned into six groups （n=10）： blank， model， low-dose TFA （TFA-L， 27 mg·kg^-1）， medium-dose TFA （TFA-M， 54 mg·kg^-1）， high-dose TFA （TFA-H， 108 mg·kg^-1）， and losartan potassium （LST， 4.5 mg·kg^-1） groups. The remaining five groups， excluding the blank group， were modeled with bovine serum albumin （BSA）， lipopolysaccharide （LPS）， and carbon tetrachloride （CCl₄）. Specifically， from weeks 1 to 10， BSA was administered via gavage every other day， and a mixture of castor oil and CCl₄ was injected subcutaneously once a week， with LPS injected into the tail vein at weeks 6 and 8. After successful modeling， each intervention group was administrated with the medication prepared with distilled water once daily by gavage for a continuous period of 4 weeks. The levels of 24-hour urinary total protein （24 h UP） and serum creatinine （SCr） were quantified by kits， and the serum IgA level was determined by enzyme-linked immunosorbent assay （ELISA）. Renal pathological changes were observed by hematoxylin-eosin （HE） staining and periodic acid-Schiff （PAS） staining. Renal IgA deposition was assessed by immunofluorescence （IF）. Endoplasmic reticulum （ER） stress was observed by transmission electron microscopy. Western blot and immunohistochemistry （IHC） were employed to detect the expression of ER stress-related factors. Non-targeted metabolomics was used to screen differential metabolites for analysis， and key metabolites arachidonic acid （AA）， prostaglandin E₂ （PGE₂）， and cyclooxygenase-2 （COX-2） were validated. ResultsCompared with the blank group， the model group showed increased 24-hour urine protein （24 h UP） and serum creatinine （SCr） levels （P<0.01）， obvious renal pathological damage， elevated serum IgA level （P<0.01）， increased renal AA and PGE₂ levels （P<0.01）， and up-regulated protein levels of COX-2， glucose-regulated protein 78 （GRP78）， phosphorylated eukaryotic initiation factor 2α （P-EIF2α）， activating transcription factor 4 （ATF4）， inositol-requiring enzyme 1α （IRE1α）， and spliced X-box binding protein 1 （XBP1s） in the renal tissue （P<0.05， P<0.01）. Compared with the model group， the intervention groups showed reductions in 24 h UP and SCr levels （P<0.05， P<0.01）， alleviated renal pathological injury， decreased serum IgA level （P<0.05， P<0.01）， and reduced renal AA and PGE₂ levels （P<0.01）. Western blot and IHC results showed that TFA reduced the levels of COX-2， GRP78， P-EIF2α， ATF4， IRE1α， and XBP1s in the renal tissue （P<0.05， P<0.01）. Metabolomics results indicated that 51 commonly differential metabolites were found among the normal， model， and TFA-M groups. TFA ameliorated IgAN by affecting metabolic pathways related to the biosynthesis of arachidonic acid and arginine through L-aspartic acid， prostaglandin 2α， leukotriene B₄， leukotriene D₄， among others. ConclusionTFA can regulate the arachidonic acid metabolism pathway， thereby modulating ER stress， reducing renal damage， and ameliorating IgA nephropathy.

Background and aims As a ferroptosis inducer, sorafenib, a first-line treatment for hepatocellular carcinoma (HCC), has a significant antitumor effect. Nonetheless, HCC patients frequently develop sorafenib resistance. Here, we investigated the impacts of progestagen-associated endometrial protein (PAEP), which controls sorafenib resistance and tumorigenesis in HCC. Furthermore, we investigated the function of PAEP and the underlying molecular mechanisms that cause HCC ferroptosis when sorafenib is applied. Methods Western blot analysis, cell proliferation, colony formation and animal experiments were performed to investigate the function of PAEP in sorafenib resistance and tumorigenesis in HCC. We detected the levels of reactive oxygen species, iron, and malondialdehyde and preformed transmission electron microscopy to investigate the relationship between PAEP and ferroptosis. Co-immunoprecipitation (co-IP) assay was performed to investigate the underlying molecular mechanisms of PAEP that cause HCC ferroptosis. Results PAEP was significantly overexpressed in HCC tissues, and this was associated with a poor clinical prognosis. PAEP silencing dramatically reduced HCC cells’ malignant phenotype. We found that sorafenib-induced ferroptosis was more sensitive to HCC cells with PAEP knockdown. Furthermore, the orthotopic cell line-derived xenograft mouse model results showed that sorafenib sensitivity can be effectively increased in vivo by PAEP knockdown. We determined that transferrin (TF) was a PAEP target using the String database, and we further supported this finding with Co-IP analysis. Additionally, on sorafenib-induced ferroptosis in HCC cells, TF partially reversed the effects of PAEP knockdown. Conclusions Our research indicates that PAEP may be a potential biomarker for predicting sorafenib resistance in HCC and disruption of PAEP expression may be a potential cancer-directed therapeutic option for HCC.

Objective:To investigate the mechanism of the synergistic anti-leukemia effect of the combination of Bcl-2 inhibitor venetoclax(VEN)and histone deacetylase(HDAC)inhibitor chidamide(CDM)in T-cell acute lymphoblastic leukemia(T-ALL).Methods:The effect of VEN combined with CDM on the proliferation of T-ALL CEM and MOLT-4 cell lines was detected by CCK-8 assay.And the effects on the cell cycle and apoptosis were detected by flow cytometry.Cell cycle protein and apoptosis-related protein expression were detected by Western blot.The key pathways of VEN combined with CDM in T-ALL were screened through network pharmacology analysis,and verifying them in T-ALL cell lines,T-ALL patient cells and public databases.Results:VEN combined with CDM displayed a synergistic effect on cell proliferation of CEM and MOLT-4 cells.In cell cycle experiment,VEN combined with CDM induced G0/G1 phase arrest in CEM and MOLT-4 cells.Western blot experiment showed that VEN combined with CDM could significantly downregulate the expression of cyclin E2 and CDK2 and upregulate the expression of p21Waf1/Cip1.In the apoptosis experiment,VEN combined with CDM could significantly induce the apoptosis of CEM and MOLT-4 cells.Western blot experiment demonstrated that VEN combined with CDM promoted endogenous apoptosis by downregulating Mcl-1 and upregulating Bax and cleaved caspase-3 protein levels.Network pharmacology analysis identified 10 hub genes.KEGG enrichment analysis revealed the cell cycle,PI3K-AKT signaling pathway,and its downstream FoxO signaling pathway were significantly enriched.GO enrichment analysis revealed the G1/S transition of mitotic cell cycle,cyclin-dependent protein kinase holoenzyme complex,and kinase activity were significantly enriched.Western blot experiment showed that VEN combined with CDM could significantly downregulate the protein level of PI3K,AKT,and p-AKT,and upregulate FoxO1 in CEM and MOLT-4 cells.In T-ALL patients,FoxO1 showed significantly lower expression compared to the normal donors,and the same result was verified in the GSE13159 and GSE26713 datasets.Conclusion:The combination of VEN and CDM exerts synergistic anti-leukemia effects by inhibiting cellular proliferation,inducing G0/G1,phase arrest and promoting apoptosis through PI3K/AKT/FoxO1 axis in T-ALL.

Dental implantology has developed rapidly for over half a century,since pure titanium(99.7％)dental cylindrical threaded implants were exploited and osseointegration was introduced in 1960s by Prof.Br?nemark.The long term retention rates of 10 years or more are over 95％.However,the biological complications jeopardize the long term effects of dental implant treatment seriously.The prevalence of dental implant biological complications varies greatly among different reports resulting from the disparities on the defini-tions of dental implant biological complications.After analyzing and summarizing the major opinions proposed internationally in recent years,the consensus for the definition of dental implant biological complications has been reached.Generally the dental implant biologi-cal implications can be classified into early stage(before restoration)biological complications and late stage(after restoration)biological complications.The early stage biological complications include acute and chronic infections,pain,soft tissue deficiency,and osseointegration failure,etc.The late stage complications include peri-implant diseases(peri-implant mucositis and peri-implantitis),soft tissue deficiency around implant,implant loosening and dropping off,etc.The various risk factors related to different dental implant biological complications,the strategies of the prevention and treatment for the dental implant biological complications have been discussed comprehensively,and the consensus has been reached.It is aimed to advocate the dentist to pay more attention to the early prevention of the biological implant complications,to promote more researches on the implant biological complications,and to help elevate the level of dental implantology in our country.

Objective To assess the therapeutic effect of acupuncture in depressive disorders based on current randomized controlled trials(RCTs).Method RCTs on acupuncture interventions for primary depression by searching databases including CNKI,Wanfang,VIP,Sinomed,PubMed,and Embase.Two researchers independently assessed the quality of the literature,extracted data according to the latest Cochrane Handbook for Systematic Reviews of Interventions,and cross-checked the data.Meta-analysis was performed using RevMan 5.4 software.Result A total of 52 studies were included,comprising 5277 patients.The meta-analysis results showed that acupuncture significantly improved depression symptoms as measured by the Hamilton Depression Rating Scale(HAMD)and reduced clinical inefficacy rates{HAMD-17:WMD=-2.35,95%CI[-3.04,-1.67],P<0.000 01;HAMD-24:WMD=-2.77,95%CI[-3.52,-2.03],P<0.000 01;HAMD(unspecified scale):WMD=-2.77,95%CI[-3.52,-2.03],P<0.000 01;Clinical inefficacy:RR=0.39,95%CI[0.33,0.47],P<0.000 01}.Additionally,acupuncture increased 5-HT levels(SMD=1.11,95%CI[0.67,1.55],P<0.000 01).In terms of safety,acupuncture did not increase the incidence of adverse events and reduced TESS scores{Adverse event incidence:RR=0.65,95%CI[0.47,0.89],P=0.007;TESS scores:WMD=-1.66,95%CI[-3.12,-0.20],P=0.03}.There is potential publication bias regarding clinical inefficacy and adverse events,necessitating cautious interpretation.Conclusion Based on the current evidence,acupuncture is an effective and safe treatment for depressive disorders.However,more high-quality RCTs are needed to further validate or refine these conclusions.

Lung cancer is one of the malignant tumours with the highest morbidity and mortality rates worldwide today, posing a major threat to human health. Accurate diagnosis and standardised treatment play a crucial role in improving the survival rate of lung cancer patients. In recent years, the rapid rise of artificial intelligence (AI) has brought about significant changes in the medical field, providing a new diagnostic and treatment model for lung cancer, and making a series of breakthroughs in lung cancer diagnostic imaging, pathological diagnosis, surgical oncology, radiotherapy, and drug development and treatment. This article introduces the current status of AI application in the field of lung cancer diagnosis and treatment, and extensively discusses the current challenges and future prospects, hoping to provide references and suggestions for future clinical practice.

Objective:To investigate the effects of galectin-3 (Gal-3) expression on lipopolysaccharide (LPS)-induced proliferation, migration, apoptosis, reactive oxygen species (ROS) and inflammatory cytokine production in human gingival fibroblasts (GF) as well as its mechanism, thus laying the foundation for an in-depth discussion of the regulatory role of Gal-3 in periodontitis and its mechanisms.Methods:Gingival tissues from 6 periodontally healthy subjects undergoing crown lengthening were collected at the Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University from December 2022 to December 2023. GFs were extracted and cultured by collagenase digestion. Lentivirals with multiplicity of infection (MOI) of 15, 20, 30, 40, 50, 60, 70, 80 were used to achieve knockdown and overexpression of Gal-3 gene in GFs, whose efficiencies of Gal-3 gene were detected by using immunofluorescence, real-time fluorescence quantitative PCR (RT-qPCR) and Western blotting. Negative control of knockdown (shNC)+LPS group, Gal-3 knockdown (shGal-3)+LPS group, negative control of overexpression (oeNC)+LPS group, and Gal-3 overexpression (oeGal-3)+LPS group were established, respectively. 5-Ethynyl-2′-deoxyuridine (EdU), Ki67 staining, scratch migration assay, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) technology, immunofluorescence assay and RT-qPCR were used to investigate the effects of Gal-3 on LPS-induced proliferation, migration, apoptosis, ROS, interleukin (IL)-6, IL-8 expression. The effects of Gal-3 knockdown on the expression of differential genes and the enrichment of signaling pathways in LPS-induced GFs were investigated by RNA sequencing (RNA-seq).Results:More than 80% of GFs were successfully transfected by shGal-3 MOI 40 and oeGal-3 MOI 70. Immunofluorescence results showed that the morphologies of GFs were normal after lentiviral transfection, and green fluorescence could be distributed in the cytoplasm, nucleus, and cell membrane. The results of RT-qPCR and Western blotting assay showed that the expressions of Gal-3 at the gene and protein levels in shGal-3 group (0.26±0.01, 0.26±0.03, respectively) were significantly lower than those in the shNC group (1.00±0.03, 1.00±0.09, respectively) ( P<0.001); the expressions of Gal-3 at the gene and protein levels in the oeGal-3 group (4.26±0.05, 3.94±0.34) were significantly higher than those in the oeNC group (1.00±0.00, 1.00±0.24, respectively) ( P<0.001). EdU, Ki67 experiments showed that the percentage of GFs proliferation was significantly lower in the shGal-3+LPS group [(16.99±1.79)%, (13.48±0.95)%, respectively] than in the shNC+LPS group [(33.86±3.84)%, (35.63±1.62)%, respectively] ( P<0.05), and the proliferation ratio of GFs was significantly increased in the oeGal-3+LPS group [(45.36±1.56)%, (45.83±1.50)%, respectively] compared to the oeNC+LPS group [(34.47±1.02)%, (33.66±3.14)%, respectively] ( P<0.05). The results of scratch migration assay showed that the migration ratio of GFs in shGal-3+LPS group significantly decreased compared to the shNC+LPS group [(25.07±0.01)% vs (57.84±0.00)%] ( P<0.001), whereas the oeGal-3+LPS group significantly facilitated the migration ratio of GFs compared to the oeNC+LPS group [(74.70±0.03)% vs (53.36±0.01)%] ( P<0.001). The results of TUNEL experiments showed that LPS stimulation with shGal-3 promoted apoptosis of GFs ( P<0.05), whereas oeGal-3 inhibited apoptosis of GFs ( P<0.001). Immunofluorescence experiments and RT-qPCR results showed that knockdown of Gal-3 significantly reduced ROS production, IL-6 and IL-8 expression levels at the gene level in GFs ( P<0.001), whereas overexpression of Gal-3 significantly increased the production of ROS and the expression of IL-6 and IL-8 at the gene level in GFs ( P<0.001). RNA-seq results showed that differential genes caused by Gal-3 knockdown under LPS conditions were significantly enriched in biological processes such as cellular response to type Ⅰinterferon in the Gene Ontology database and in the Kyoto Encyclopedia of Genes and Genomes database for NOD-like receptor, RIG-I like receptor and other signaling pathways. Conclusions:Gal-3 knockdown inhibited LPS-induced proliferation, migration, ROS, IL-6 and IL-8 production, and promoted apoptosis of GFs, while overexpression had the opposite effect. This process might be closely linked to the Janus kinase-signal transducer and activator of transcription pathway.

Objective:To analyze and summarize clinical phenotypic characteristics and genetic variations in patients with intellectual disability and pathogenic variations of the DYNC1H1 gene across 4 generations within a single family. Methods:Retrospective case analysis.Clinical data of a child with epilepsy and intellectual disability and her family members were collected from the Children′s Medical Center, Peking University First Hospital on December 2019.The child was followed up regularly.DNA was extracted from the peripheral blood of the child′s family members.Then whole-exome sequencing and Sanger sequencing were performed to identify the genetic variation type in the proband and her family members.The relationship between genotype and phenotype was further analyzed.Results:A total of 13 patients across 4 generations in the family had intellectual disability, and the proband also had drug-resistant epilepsy.The variation c. 13556C> A (p.A4519E) of the DYNC1H1 gene was confirmed by gene testing in 8 patients (no blood samples were obtained from the remaining patients). Conclusions:DYNC1H1 gene-related intellectual disability in most previously reported cases are caused by novel variations of this gene.In this study, a large family of 13 intellectual disability patients across 4 generations caused by a pathogenic mutation in the DYNC1H1 gene was summarized.The findings make precise genetic counseling possible for this family and provide a basis for further studies on the relationship between the genotype and phenotype of the DYNC1H1 gene.

This research investigated the contamination level,distribution of drug-resistant strains,and molecular epidemiologi-cal characteristics of Campylobacter,and further explored transmission pathways and prevention strategies.Cecum,chicken carcass,chicken product,and environmental samples,as well as swabs from workers'hands,were collected from a slaughterhouse in a large broiler group in the Jiaodong area between August 2023 and July 2024.Quantitative contamination assessment of Campylobacter in chicken carcasses and chicken products was performed.After microbial mass spectrometry identification,the representative strains of different links were selected for drug resistance testing and whole genome sequencing(WGS).On the basis of the sequencing results,the resistance genes,virulence genes,multilocus sequence typing(MLST),and phylogenetic characteristics of representative strains were analyzed.Homology comparisons were performed between isolates and strains from patients with diarrhea in the NCBI database.A total of 297 Campylobacter strains were isolated from 806 samples,and the overall detection rate was 36.85%.The detection rate of Campylobacter was highest in the evisceration process(47.33%),followed by the cutting process(35.64%).Overall,the Campylo-bacter detection rate first increased,then decreased,and subsequently increased.Drug sensitivity testing revealed that 90 isolates were resistant to nalidixic acid and ciprofloxacin,and 94.97%of isolates were resistant to tetracycline.WGS showed that both Campylo-bacter jejuni(C.jejuni)and Campylobacter coli(C.coli)carried many drug resistance and virulence genes.ST-14176 of C.jejuni was isolated for the first time herein.The predominant ST-8261 strain of C.jejuni and ST-860,ST-829,and ST-1586 strains of C.coli are known to cause human diarrhea.LOS expression genes associated with Guillain-Barré syndrome(GBS)were detected in both C.jejuni isolates from the slaughter chain and patients with GBS.Some strains exhibited close genetic relatedness to human-derived Campylo-bacter strains from the NCBI database.The detection rate of Campylobacter in the slaughterhouse first increased,then decreased,and subsequently increased,and the quantitative contamination level of each link was similar to the detection rate.Quantitative analysis of chicken carcasses/products revealed that the average bacterial load was highest in eviscerated carcasses(102.80 cfu/g),and the high-est amount of Campylobacter in chicken products reached 451.80 cfu/g.Abundant drug resistance genes and virulence genes were iden-tified,and the drug resistance genes were highly correlated with the drug resistance rate.Therefore,surveillance intensity and control measures for Campylobacter in slaughter processes should be strengthened.