Allergic diseases are a class of important immune imbalance diseases that lack effective cures. Helminth-derived serine protease inhibitors (serpins) exert immunoregulatory effects similar to those of helminth, are controllable, have few side effects, and have great application potential in correcting unbalanced immune responses. However, the immune regulatory effects and mechanisms mediated by the enzyme inhibitory activity of helminth-derived serpins have not been investigated or clarified in previous studies. We obtained mutant serpin proteins with significantly reduced enzyme inhibitory activity by predicting and mutating the single key amino acid. The therapeutic effect of immunoregulation mediated by enzyme inhibitory activity of serpin on allergic inflammation was investigated based on an acute allergy model constructed in OVA-specific T-cell receptor transgenic C57BL/6 mice. Unlike the Trichinella spiralis-derived serpin (Ts-serpin), the mutant proteins showed significantly reduced inhibitory activity against the chymotrypsin and elastase. Meanwhile, the immunosuppressive ability of the mutant proteins was weakened and mutant protein intervention groups showed more severe allergic inflammation in the lungs. Additionally, enzyme inhibitory activity regulates the differentiation of macrophages and Treg cells to establish immune tolerance, which is the key to rapidly improving lung injury at the challenge and treatment stages of allergy. These findings suggest that the rapid regulatory properties of enzymatic reactions have great potential in the prevention and treatment of allergic inflammation.

Aging is a complex process marked by the gradual functional decline of an organism. It involves imbalances in cellular homeostasis and decreased organ regenerative capacity, causing a significant increase in chronic diseases and mortality. Aging involves a cascade of molecular events such as genomic instability, epigenetic remodeling, and metabolic dysfunction. Targeting key molecular nodes can effectively delay aging and age-related disease progression. Nur77, an NR4A nuclear receptor, is key to stress response, energy sensing, and inflammation regulation. This molecule assists in maintaining stem cell homeostasis, repairing mitochondrial dysfunction, and regulating autophagy and protein quality control, which are core aging events. However, a systematic analysis of the regulatory roles and synergistic effects of Nur77 within the aging network remains lacking. This review comprehensively describes the structure and function of Nur77, explores its role in age-related mechanisms and diseases, and discusses its potential as a diagnostic and therapeutic target. These insights support the development of novel anti-aging strategies based on the Nur77 signaling pathway.

AimThis study aims to evaluate the efficacy and safety of telitacicept addition to standard therapy in adults with relapsing lupus nephritis (LN).MethodsFrom 2021 to 2024, patients with relapsing LN were identified and divided into two groups based on telitacicept administration. Laboratory indicators, renal remission status, Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) scores, glucocorticoid dosages, and the incidence of renal flares were evaluated. Multivariate regression was used to assess the baseline predictors of complete renal remission (CRR) and adverse events (AEs) were recorded.ResultsCompared to the standard therapy group (n=20), the proportion of patients who achieved a CRR and the primary efficacy renal response were significantly increased in the telitacicept group (n=20) at 6, 9, and 12 months, while the reduction rates of 24-hour urinary protein from baseline at 1, 3, and 9 months were significantly higher. The telitacicept group showed notable improvement in treatment responses in the median SLEDAI-2K score and glucocorticoid dose. Multivariate Cox regression analysis revealed that add-on telitacicept was associated with achieving early CRR. At the end of the follow-up period, the cumulative relapse rate in the telitacicept group was significantly lower than that in the standard treatment group, with no increase in the incidence of AEs.ConclusionsAs an add-on therapy, telitacicept is associated with early disease remission in patients with relapsing LN with reduced disease activity, lower glucocorticoid dosage, and fewer relapses. It also showed a favorable safety profile.

BACKGROUND:With the acceleration of population aging, elderly patients with nephrotic syndrome (NS) demonstrate a distinct histopathological profile compared to younger cohorts. This study aimed to characterize the renal histopathological spectrum in elderly NS patients from 2014 to 2023. METHODS:Pathological data from 628 elderly NS patients (≥60 years) were retrospectively analyzed and compared with a control group of 1416 younger NS patients (18-59 years). Pathological diagnosis were classified according to the 1995 WHO revised criteria for glomerular diseases. Statistical analyses were performed using the chi-square test. RESULTS:A progressive increase in the proportion of elderly patients with NS was observed, rising from 28.9% in 2014 to 37.6% in 2023. Among 544 elderly patients with primary NS, idiopathic membranous nephropathy (IMN) was the predominant pathological type (66.7%, 363/544), followed by minimal change disease (MCD) (18.6%, 101/544). Among 84 elderly patients with secondary NS, renal amyloidosis was most frequent (29.8%, 25/84), followed by diabetic nephropathy (DN) (25.0%, 21/84). The incidence of IMN increased from 63% in 2014-2018 to 71.2% in 2019-2023, while the incidence of MCD decreased from 21.7% to 15.1%. The incidence of DN decreased significantly from 34.3% in 2014-2018 to 14.3% in 2019-2023. Elderly NS patients exhibited significantly more severe glomerulosclerosis, tubular atrophy, interstitial fibrosis, inflammatory infiltration, and arteriolar hyalinization than younger patients. CONCLUSIONS:Among biopsy-confirmed cases in the elderly patients, IMN represents the predominant etiology of primary NS, while renal amyloidosis emerges as the leading cause of secondary NS. Elderly patients with NS exhibit more severe glomerulosclerosis and tubulointerstitial pathology compared to younger individuals.

BackgroundThe occurrence of lupus nephritis is primarily caused by the dysfunction of the autoimmune system, leading to the deposition of immune complexes (ICs) in the kidneys and associated inflammatory responses. Lymphocyte-related parameters, including the platelet to lymphocyte ratio (PLR), neutrophil to lymphocyte ratio (NLR), and monocyte to lymphocyte ratio (MLR), have been confirmed in recent years as important novel indicators for several inflammatory diseases. However, it remains unclear whether lymphocyte-related parameters can serve as prognostic indicators for lupus nephritis (LN).MethodsThis study included a total of 143 LN patients, who were divided into several groups based on the optimal cutoff values of lymphocyte-related parameters. The primary endpoint was poor renal prognosis, and the patients’ prognosis was monitored through follow-up, recording the time at which patients reached the study endpoint. The predictive effect was evaluated using the area under the receiver operating characteristic curve (AUROC), Kaplan-Meier (K-M) curves, and Cox proportional hazards analysis.ResultsCompared with the healthy control group, the PLR, NLR, and MLR levels in the LN group were significantly higher (P < 0.05). Kaplan-Meier survival analysis showed that patients with high PLR, NLR, and MLR had poorer prognosis (P < 0.05). Univariate Cox regression analysis indicated that PLR (HR 1.002, 95% CI 1.000-1.004, P = 0.05) and NLR (HR 1.081, 95% CI 1.031-1.134, P = 0.001) were associated with kidney progression. Multivariate Cox regression analysis showed that only MLR (HR 5.861, 95% CI 1.515-22.665, P = 0.010) was an independent risk factor affecting the renal prognosis of LN patients, whereas PLR and NLR were not. Based on the cutoff value of MLR, patients were divided into two groups. In terms of general data, the high MLR group had a significantly higher mean arterial pressure compared to the low MLR group (P = 0.002). In terms of laboratory tests, the high MLR group had a significantly lower eGFR compared to the low MLR group (P = 0.001). In terms of renal pathology, the high MLR group showed statistically significant differences compared to the low MLR group in AI index, CI index, capillary endothelial cell proliferation, cellular/fibrous crescent formation, and interstitial inflammatory cell infiltration (P < 0.05).ConclusionMLR may serve as an independent risk factor for poor renal prognosis in SLE patients.

Immunoglobulin G4-related disease (IgG4-RD) is a rare, multisystemic fibro-inflammatory condition affecting various organs, including kidneys, lungs, nasal cavity, pancreas, salivary glands, and orbit. Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAVs) is a multi-systemic inflammatory vascular disease encompassing eosinophilic granulomatosis with polyangiitis (EGPA), microscopic polyangiitis (MPA), and granulomatosis with polyangiitis (GPA). It often overlaps with the organs or tissues affected by IgG4-RD. Clinically, some individuals with IgG4-RD are ANCA-positive, while some with AAV exhibit elevated IgG4 levels or IgG4-positive plasma cell infiltration, making these conditions difficult to distinguish. Reports have documented cases of overlap syndromes involving IgG4-RD and AAV, highlighting shared pathogenic mechanisms that may include macrophages, B cells, CD4+T cells, and inflammatory cytokines. However, the pathophysiological mechanism underlying these overlap syndromes remains unclear. This review examines potential pathophysiological links between IgG4-RD and AAVs (GPA/MPA) overlap syndromes.

Diabetic kidney disease (DKD) is a major diabetic microvascular complication that still lacks effective therapeutic drugs. Ferroptosis is a recently identified form of programmed cell death that is triggered by iron overload. It is characterized by unrestricted lipid peroxidation and subsequent membrane damage and is found in various diseases. Accumulating evidence has highlighted the crucial roles of iron overload and ferroptosis in DKD. Here, we review iron metabolism and the biology of ferroptosis. The role of aberrant ferroptosis in inducing diverse renal intrinsic cell death, oxidative stress, and renal fibrosis in DKD is summarized, and we elaborate on critical regulatory factors related to ferroptosis in DKD. Finally, we focused on the significance of ferroptosis in the treatment of DKD and highlight recent data regarding the novel activities of some drugs as ferroptosis inhibitors in DKD, aiming to provide new research targets and treatment strategies on DKD.

The survival rates of patients with hematological malignancies such as multiple myeloma have improved with advances in cancer treatment. However, the risk of cardiovascular disease associated with novel therapeutic agents, including proteasome inhibitors (PIs), is becoming increasingly evident. PIs act on proteasome peptidases, leading to cell cycle arrest or apoptosis. Carfilzomib (CFZ), an intravenously administered irreversible PI, exhibits pronounced cardiovascular toxicity that is characterized by heart failure, hypertension, arrhythmia, and ischemic heart disease (IHD). This review focuses on CFZ, details its applications in treating multiple myeloma, presents its potential mechanisms of cardiotoxicity and the incidence of cardiotoxic events, and provides recommendations for the evaluation and management of adverse cardiac events during the early treatment of patients with this drug.

Background Exosomes have recently been considered as major players in cell-cell communication. Milk-derived exosomes contained abundant genetic cargos and the potential biological functions in the synthesis of milk fat remain poorly understood. Milk fat percentage is a crucial trait that influences dairy quality and consumer preference. This study focused on the regulatory role of milk-derived exosomal miRNAs in lipid synthesis within BMECs. Results Initially, based on 17,838 DHI milk production performance data collected from January 2021 to February 2023, compared with early lactation , mid-lactation from 100 to 199 days, late lactation from 200 to 299 days, duration lactation the milk fat percentage (MFP) of late lactation (4.24±1.07%) significant higher than other stages. The milk protein percentage during this stage (3.43±0.36) is significantly higher compared to other stages. The heritability estimates for milk fat and milk protein percentage show a positive correlation. Subsequently, 10 cows with high MFP （5.96±0.26 ) and ten cows with low MFP (1.68±0.23) were selected during the late lactation stage, and milk samples were collected for further analysis. Milk-derived exosomes isolated via differential ultracentrifugation exhibited a spherical vesicle structure ranging in size from 50 to 150 nm and were enriched in exosome-specific protein markers CD9, CD81, and TSG101. Through miRNA-seq, 1320 differentially expressed miRNAs were identified including 496 up-regulated and 824 down-regulated miRNAs by high-throughput miRNA sequencing. Furthermore, the exosome uptake experiment revealed that upon BMECs, exosomes predominantly localized in the cytoplasm.The results of exosomal q-PCR demonstrated that miR-423-5p and miR-125b were significantly up-regulated and down-regulated in HMF_EXO and LMF_EXO groups, respectively. Conclusions Milk-derived exosomal miRNAs associated with lipid metabolism can provide preliminary insights into the effects of exosomes on lactation mechanisms and potentially identify biomarkers for distinguishing molecular markers and loci related to high or low milk fat content in dairy cattle.

Pyroptosis is a recently discovered type of lytic-programmed cell necrosis. The process involves cells assembling an inflammasome and cleaving gasdermin (GSDM) to trigger the release of pro-inflammatory cytokines that eventually induce inflammatory cell death. Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus, which leads to end-stage renal disease. Podocyte damage or loss is an important feature of diabetic kidney injury. Pyroptosis involvement in podocyte injury is closely associated with DN progression, manifesting as increased renal fibrosis, glomerulosclerosis, and tubular injury. The study aims to elucidate the mechanism of pyroptosis and summarize the pathways and potential inhibitors related to pyroptosis activation in DN podocytes. We undertook a search of bibliographic databases for peer-reviewed research literature on various aspects of pyroptosis. Multiple different pathways mediate podocyte pyroptosis to promote DN progression. Inhibition of pyroptosis can reduce podocyte damage and improve renal function in DN, suggesting that pyroptosis may help identify potential new therapeutic targets for DN treatment.

Abstract Background: Type 1 diabetes (T1D) has been associated with a higher risk of Ovarian cancer (OC), albeit the mechanisms underlying this association remain elusive. A better understanding of the relationship between T1D and OC may contribute to improved primary prevention of OC. We aimed to investigate the putative causal role of T1D on OC, and to identify the potentially mediatory effects of the usage of insulin product underlying this relationship. Methods: We performed a two-sample Mendelian randomization (MR) analysis using genetic variants associated with T1D and OC from genome-wide association studies. Then, a multivariable MR analysis was conducted to investigate whether T1DM has an independent effect on OC after adjusting for potential confounders. Finally, the mediating role of insulin product was subsequently explored using mediation analysis via two-step MR. Results: the MR estimated based on IVW method indicated a causal association between genetically determined T1D and Ovarian cancer (OC) (OR: 1.0006, 95% CI 1.0001em dash1.0011; P=0.0164). After adjusting for body mass index , Smoking , physical activity , age at menopause and age at menarche, respectively ,we found that a causal relationship between T1DM and OC was still statistically significant (OR>1, P<0.05) .The two-step MR analysis revealed that insulin product acted as a mediating moderator between the T1D and OC (mediated proportion, 1.07%). Conclusions: Our findings suggest that T1D may confer a risk effect to OC, mediated in part by therapeutic insulin product. Therefore, precise dosage of insulin product or an alternative to insulin in T1D patients have a profound significance in terms of the prevention of OC. Keywords: Type 1 diabetes (T1D), Insulin product ,Ovarian cancer (OC), Mendelian randomization (MR) ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study research was funded by The National Natural Science Foundation of China (Grant No. 82273479 to LZ) ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: JiLin University Ethics Committees I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors All data produced in the present work are contained in the manuscript All data produced are available online atGWAS summary data.

The excretory-secretory product (ESP) of Trichinella spiralis (T. spiralis) has antitumor activity. To explore the effect of ESP on liver cancer cells, tumor models were established with H22 cells and then infected with T. spiralis. The results showed that the growth of tumors in mice infected with T. spiralis was significantly inhibited. ESP from adult worms or muscle larvae were then incubated with H22 cells in vitro, and it was found that the ESP could inhibit cell proliferation and promote apoptosis. Subsequently, apoptosis-related proteins in stimulated H22 cells were evaluated, and ESP was found to induce cell apoptosis through the mitochondrial pathway. Additionally, Th-related cytokines were investigated in vivo, and the results showed that the levels of Th1 cytokines were significantly increased in the early stage of T. spiralis infection, while Th2 cytokines increased later than Th1 cytokines, implying that Th1 cytokines with antitumor effects may play a role in inhibiting tumor growth at early stage. In short, ESP can directly induce tumor cell apoptosis and indirectly inhibit tumor cell growth through the host immune system, which may be the antitumor mechanism of T. spiralis infection.

A complication of pediatric systemic lupus erythematosus (pSLE) is immune thrombocytopenia (ITP). Although corticosteroids and immunoglobulins are frequently used as preliminary treatments, some patients do not respond to them. Rituximab has been reported to be safe and effective in the treatment of pSLE complicated with refractory ITP. Research is currently underway to determine the optimal rituximab dose for these individuals. We report a case of a child with SLE-associated ITP (SLE-ITP) who was successfully treated with rituximab. Rituximab is likely the most viable therapeutic option for refractory SLE-ITP. Furthermore, a comprehensive review of the relevant literature was performed and a concise overview of the pathogenesis and available treatment modalities for pediatric patients diagnosed with SLE and concurrent ITP was provided.

异尖科线虫病(Anisakiasis)是一种重要的食源性人兽共患线虫病,主要因食用生的或未煮熟的含异尖科线虫Ⅲ期活的幼虫的海鱼而引起.本研究利用重组酶聚合酶扩增技术(RPA)建立了异尖科线虫RPA的检测方法,首先对东海沿海舟山、温州、宁波、平潭、嘉兴市的九种鱼体内获得的线虫进行分离鉴定,获得了派氏异尖线虫、简单异尖线虫、典型异尖线虫、宫脂线虫和对盲囊线虫,然后根据获得的五种线虫的ITS区设计特异性引物.结果显示:本研究建立的RPA方法可特异性扩增出异尖科线虫340 bp左右的目的基因片段,可特异性检测出异尖科线虫,而对阔节裂头绦虫、华支睾吸虫、东方次睾吸虫、棘颚口线虫检测结果为阴性;优化后在35℃、25 min即可完成检测,其灵敏度可达1 pg/μL,人工污染实验结果显示呈阳性.此方法操作简单、便捷,对现场快速检测具有重要的意义.

Objective: To elucidate the potential causality of leukocyte telomere length (LTL) with immune-mediated inflammatory diseases (IMIDs), we conducted a Mendelian randomization (MR) study.Methods: The genetically predicted causation between LTL and IMIDs was evaluated using a two-sample MR method. We analyzed 16 major IMIDs, which included systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), ulcerative colitis (UC), Crohn’s disease (CD), ankylosing spondylitis (AS), sicca syndrome (SS), rheumatoid arthritis (RA), type 1 diabetes (T1D), primary sclerosing cholangitis (PSC), idiopathic pulmonary fibrosis (IPF), atopic dermatitis (AD), sarcoidosis, hypothyroidism, hyperthyroidism, psoriasis, and childhood asthma. The random-effects inverse-variance weighted (IVW) method was performed as the main analytical approach in MR. Various sensitivity analyses, including MR-Egger, MR robust adjusted profile score (MR-RAPS), weighted median, MR pleiotropy residual sum and outlier (MR-PRESSO) methods, weighted mode, radial plot, and radial regression, were used to guarantee the robustness of the results and detect horizontal pleiotropy. Cochran’s Q value was calculated to check for heterogeneity, and the MR Steiger approach was used to test the causal direction.Results: The MR results indicated significant inverse associations of LTL with risks of psoriasis (OR: 0.77, 95% CI: 0.66–0.89, and p = 3.66 × 10−4), SS (OR: 0.75, CI: 0.58–0.98, and p = 0.03), RA (OR: 0.77, 95% CI: 0.68–0.88, and p = 9.85 × 10−5), hypothyroidism (OR: 0.84, 95% CI: 0.78–0.91, and p = 7,08 × 10−6), hyperthyroidism (OR: 0.60, 95% CI: 0.44–0.83, and p = 1.90 × 10−3), sarcoidosis (OR: 0.67, 95% CI: 0.54–0.83, and p = 2.60 × 10−4), and IPF (OR: 0.41, 95% CI: 0.29–0.58, and p = 4.11 × 10−7) in the FinnGen study. We observed that longer LTL was associated with an increased risk of AS susceptibility (OR: 1.51, 95% CI: 1.18–1.94, and p = 9.66 × 10−4). The results of the IVW method showed no causal relationship between TL and SLE (OR: 0.92, 95% CI: 0.62–1.38, and p = 0.69) in the FinnGen study; however, a significantly positive correlation was shown between LTL and SLE in another larger GWAS (OR: 1.87, 95% CI: 1.37–2.54, and p = 8.01 × 10−5).Conclusion: Our findings reveal that abnormal LTL has the potential to increase the risk of IMIDs. Therefore, it could be treated as a predictor and may provide new potential treatment targets for IMIDs. However, the change of LTL may not be the direct cause of IMIDs. Further studies should aim at the pathogenic mechanism or potential protective effects of LTL in IMIDs.

Objective We investigated the correlation between zinc levels and Nrf2 expression and potential effects on the clinicopathology of patients with diabetic nephropathy (DN). Methods We selected 30 patients with DN, diagnosed via renal biopsy at our hospital from March 2018 to November 2019, and enrolled 30 healthy individuals from a medical examination center as the control group. Patients with DN were divided into normal-zinc and low-zinc groups. We detected the levels of zinc, copper, and Nrf2 mRNA in their serum, and collected the clinical and pathological data of DN patients. Results Serum zinc level and Nrf2 mRNA expression were significantly decreased in patients with DN compared to those of healthy people ( P < 0.05). Of the 30 patients, 16 had low zinc (53.3%) and 14 had normal zinc levels (46.7%). There was no significant difference in the blood Nrf2 mRNA expression between the two groups ( P > 0.05). However, the expression of Nrf2 in the kidney tissue of the low-zinc group was significantly lower compared to the normal-zinc group ( P < 0.05). Diastolic blood pressure and copper levels were significantly higher in the low-zinc group ( P < 0.05). In contrast, body mass index, red blood cell count, Hb level, and the ratio of zinc to copper were significantly lower in the low-zinc group ( P < 0.05). The pathological classifications of the low-zinc group were more severe ( P < 0.05). Conclusion Patients with DN were more likely to have zinc deficiency and lower expression of Nrf2. Additionally, DN patients with zinc deficiency were prone to have more severe clinical and pathological manifestations.

Lupus nephritis (LN) is a significant cause of various acute and chronic renal diseases, which can eventually lead to end-stage renal disease. The pathogenic mechanisms of LN are characterized by abnormal activation of the immune responses, increased cytokine production, and dysregulation of inflammatory signaling pathways. LN treatment is an important issue in the prevention and treatment of systemic lupus erythematosus. Mesenchymal stem cells (MSCs) have the advantages of immunomodulation, anti-inflammation, and anti-proliferation. These unique properties make MSCs a strong candidate for cell therapy of autoimmune diseases. MSCs can suppress the proliferation of innate and adaptive immune cells, such as natural killer cells (NKs), dendritic cells (DCs), T cells, and B cells. Furthermore, MSCs suppress the functions of various immune cells, such as the cytotoxicity of T cells and NKs, maturation and antibody secretion of B cells, maturation and antigen presentation of DCs, and inhibition of cytokine secretion, such as interleukins (ILs), tumor necrosis factor (TNF), and interferons (IFNs) by a variety of immune cells. MSCs can exert immunomodulatory effects in LN through these immune functions to suppress autoimmunity, improve renal pathology, and restore kidney function in lupus mice and LN patients. Herein, we review the role of immune cells and cytokines in the pathogenesis of LN and the mechanisms involved, as well as the progress of research on the immunomodulatory role of MSCs in LN.

Diabetic kidney disease (DKD) is a serious microvascular complication of diabetes and is the leading cause of end-stage renal disease (ESRD). Persistent proteinuria is an important feature of DKD, which is caused by the destruction of the glomerular filtration barrier (GFB). Glomerular endothelial cells (GECs) and podocytes are important components of the GFB, and their damage can be observed in the early stages of DKD. Recently, studies have found that crosstalk between cells directly affects DKD progression, which has prospective research significance. However, the pathways involved are complex and largely unexplored. Here, we review the literature on cellular crosstalk of GECs and podocytes in the context of DKD, and highlight specific gaps in the field to propose future research directions. Elucidating the intricates of such complex processes will help to further understand the pathogenesis of DKD and develop better prevention and treatment options.

基于氨氮(N H+4-N)污染地下水内在生态恢复机制,利用生态安全型天然矿物材料火山渣负载地下水中土著氮细菌进行NH+4-N污染地下水净化特性研究.结果表明:火山渣负载土著氮细菌生物量约为2.12×107个/g;负载材料在去除地下水中NH+4-N时,可有效去除水化学因子,NH+4-N去除率为83.39％～98.84％,水化学因子去除能力从大到小依次为Fe2+,HCO-3,Ca2+,Mn2+,CO2-3,SO2-4,S2-,Mg2+,其中Fe2+,Mn2+,S2-,SO2-4一定程度上促进NH+4-N净化;CO2-3,HCO-3,Ca2+,Mg2+抑制NH+4-N净化;负载材料的微观结构在净化后表面变平滑,细小突起被覆盖.研究结果为氮污染地下水内在生态调控修复技术研发提供了实验依据.

在全面推进社会主义现代化建设浪潮中,社会各行业都需要提升基层党组织的工作质量,发挥基层党建对行业可持续发展的推动作用,而文化建设与党建工作之间存在耦合互动关系,推动党建工作与文化建设的协同发展,将有助于为行业注入创新动力,塑造行业人文底蕴,推动行业高质量发展.