Risk of hepatitis B virus reactivation in oncological patients treated with tyrosine kinase inhibitors:A case report and literature analysis

Hepatitis B virus(HBV)reactivation(HBVr)represents a severe and potentially life-threatening condition,and preventive measures are available through blood test screening or prophylactic therapy administration.The assessment of HBVr traditionally considers factors such as HBV profile,including hepatitis B surface antigen(HBsAg)and antibody to hepatitis B core antigen,along with type of medication(chemotherapy;immunomodulants).Nevertheless,consideration of possible patient’s underlying tumor and the specific malignancy type(solid or hematologic)plays a crucial role and needs to be assessed for decision-making process.

Overview of the immunological mechanisms in hepatitis B virus reactivation:Implications for disease progression and management strategies

Hepatitis B virus(HBV)reactivation is a clinically significant challenge in disease management.This review explores the immunological mechanisms underlying HBV reactivation,emphasizing disease progression and management.It delves into host immune responses and reactivation’s delicate balance,spanning innate and adaptive immunity.Viral factors’disruption of this balance,as are interac-tions between viral antigens,immune cells,cytokine networks,and immune checkpoint pathways,are examined.Notably,the roles of T cells,natural killer cells,and antigen-presenting cells are discussed,highlighting their influence on disease progression.HBV reactivation’s impact on disease severity,hepatic flares,liver fibrosis progression,and hepatocellular carcinoma is detailed.Management strategies,including anti-viral and immunomodulatory approaches,are critically analyzed.The role of prophylactic anti-viral therapy during immunosuppressive treatments is explored alongside novel immunotherapeutic interventions to restore immune control and prevent reactivation.In conclusion,this compre-hensive review furnishes a holistic view of the immunological mechanisms that propel HBV reactivation.With a dedicated focus on understanding its implic-ations for disease progression and the prospects of efficient management stra-tegies,this article contributes significantly to the knowledge base.The more profound insights into the intricate interactions between viral elements and the immune system will inform evidence-based approaches,ultimately enhancing disease management and elevating patient outcomes.The dynamic landscape of management strategies is critically scrutinized,spanning anti-viral and immunomodulatory approaches.The role of prophylactic anti-viral therapy in preventing reactivation during immunosuppressive treatments and the potential of innovative immunotherapeutic interventions to restore immune control and proactively deter reactivation.

Risk of hepatitis B virus reactivation in cancer patients undergoing treatment with tyrosine kinase-inhibitors

This editorial commented on an article in the World Journal of Gastroenterology titled“Risks of Reactivation of Hepatitis B Virus in Oncological Patients Using Tyrosine Kinase-Inhibitors:Case Report and Literature Analysis”by Colapietro et al.In this editorial,we focused on providing a more comprehensive exploration of hepatitis B virus reactivation(HBVr)associated with the usage of tyrosine kinase inhibitors(TKIs).It includes insights into the mechanisms underlying HBV reactivation,the temporal relationship between TKIs and HBV reactivation,and preventive measures.The aim is to understand the need for nucleos(t)ide analogs(NAT)and serial blood tests for early recognition of reactivation and acute liver injury,along with management strategies.TKIs are considered to be an intermediate(1%-10%)of HBVr.Current guidelines stipulate that patients receiving therapy with high or moderate risks of reactivation or recent cancer diagnosis must have at least tested hepatitis B surface antigen,anti-hepatitis B core antigen(HBc),and anti-hepatitis B surface antibody.Anti-HBc screening in highly endemic areas means people with negative tests should be vaccinated against HBV.Nucleoside or nucleotide analogs(NAs)like entecavir(ETV),tenofovir disoproxil fumarate(TDF),and tenofovir alafenamide(TAF)form the basis of HBV reactivation prophylaxis and treatment during immunosuppression.Conversely,lamivudine,telbivudine,and adefovir are generally discouraged due to their reduced antiviral efficacy and higher risk of fostering drug-resistant viral strains.However,these less effective NAs may still be utilized in cases where ETV,TDF,and TAF are not feasible treatment options.

Investigating the reactivation of historical landslides during the 2022 Luding M_(S)6.8 earthquake

On September 5,2022,a strong earthquake with a magnitude of MS6.8 struck Luding County in Sichuan Province,China,triggering thousands of landslides along the Dadu River in the northwest-southeast(NW-SE)direction.We investigated the reactivation characteristics of historical landslides within the epicentral area of the Luding earthquake to identify the initiation mechanism of earthquake-induced landslides.Records of the two newly triggered and historical landslides were analyzed using manual and threshold methods;the spatial distribution of landslides was assessed in relation to topographical and geological factors using remote sensing images.This study sheds light on the spatial distribution patterns of landslides,especially those that occur above historical landslide areas.Our results revealed a similarity in the spatial distribution trends between historical landslides and new ones induced by earthquakes.These landslides tend to be concentrated within a range of 0.2 km from the river and 2 km from the fault.Notably,both rivers and faults predominantly influenced the reactivation of historical landslides.Remarkably,the reactivated landslides are characterized by their small to medium size and are predominantly situated in historical landslide zones.The number of reactivated landslides surpassed that of previously documented historical landslides within the study area.We provide insights into the critical factors responsible for historical landslides during the 2022 Luding earthquake,thereby enhancing our understanding of the potential implications for future co-seismic hazard assessments and mitigation strategies.

Prevention of hepatitis B reactivation in patients with hematologic malignancies treated with novel systemic therapies:Who and Why?

The risk of reactivation in patients with chronic or past/resolved hepatitis B virus(HBV)infection receiving chemotherapy or immunosuppressive drugs is a wellknown possibility.The indication of antiviral prophylaxis with nucleo(t)side analogue is given according to the risk of HBV reactivation of the prescribed therapy.Though the advent of new drugs is occurring in all the field of medicine,in the setting of hematologic malignancies the last few years have been characterized by several drug classes and innovative cellular treatment.As novel therapies,there are few data about the rate of HBV reactivation and the decision of starting or not an antiviral prophylaxis could be challenging.Moreover,patients are often treated with a combination of different drugs,so evaluating the actual role of these new therapies in increasing the risk of HBV reactivation is difficult.First results are now available,but further studies are still needed.Patients with chronic HBV infection[hepatitis B surface antigen(HBsAg)positive]are reasonably all treated.Past/resolved HBV patients(HBsAg negative)are the actual area of uncertainty where it could be difficult choosing between prophylaxis and pre-emptive strategy.

Navigating the complex terrain of hepatitis B virus reactivation in the era of Bruton tyrosine kinase inhibitors

In this editorial,we offer a summary of the risk associated with hepatitis B reactivation(HBVr)in the setting of both solid and hematologic malignancies treated with Bruton tyrosine kinase(BTK)inhibitors,with insights derived from current studies.Furthermore,we emphasize the critical need for a framework regarding robust risk evaluation in patients undergoing such treatments.This framework is essential for identifying those at increased risk of HBVr,enabling healthcare providers to implement proactive measures to prevent reactivation and ensure the safe administration of BTK inhibitor therapy.

Reactivation of hepatitis B virus infection – an important aspect of multifaceted problem

In this editorial we comment on the article published in the recent issue of the W orld Journal of Gastroenterology.We focus specifically on the problem of occult hepatitis B virus(HBV)infection,that is a result of previous hepatitis B(PHB)and a source for reactivation of HBV.The prevalence of PHB is underestimated due to the lack of population testing programs.However,this condition not only com-plicate anticancer treatment,but may be responsible for the development of other diseases,like cancer or autoimmune disorders.Here we unveil possible mecha-nisms responsible for realization of these processes and suggest practical approa-ches for diagnosis and treatment.

CXCL10 Induces Lytic Reactivation of EBV through EXTL1

Epstein-Barr virus (EBV) infects over 90% of the global population, establishing latent infections in most individuals. Under specific conditions like inflammation and immune suppression, EBV can be reactivated, leading to the initiation and progression of related diseases. While inflammation is known to induce EBV reactivation, the precise mechanisms underlying this phenomenon remain unclear. Chemokine (C-X-C motif) ligand (CXCL10), a key inflammatory factor, plays a significant role in various infectious diseases. In this study, we investigated how CXCL10 levels regulate the transition between the latent and lytic replication phases of the EBV lifecycle using cell culture, Western blot, fluorescent quantitative PCR, immunofluorescence, and flow cytometric apoptosis assays. Our findings indicate that CXCL10 induces EBV transition from latency to lytic replication through its receptor CXCR3 by regulating the downstream effector, exostosis-like glycosyltransferase 1. Additionally, CXCL10 activates the JAK2/STAT3 pathway. This study confirms the role of CXCL10 in promoting EBV lytic replication, providing crucial insights into the pathogenic mechanisms of inflammation-triggered EBV reactivation.

Hepatitis B virus reactivation in patients treated with monoclonal antibodies

Hepatitis B virus(HBV)reactivation poses a significant clinical challenge,espe-cially in patients undergoing immunosuppressive therapies,including mono-clonal antibody treatments.This manuscript briefly explores the complex rela-tionship between monoclonal antibody therapy and HBV reactivation,drawing upon current literature and clinical case studies.It delves into the mechanisms underlying this phenomenon,highlighting the importance of risk assessment,monitoring,and prophylactic measures for patients at risk.The manuscript aims to enhance the understanding of HBV reactivation in the context of monoclonal antibody therapy,ultimately facilitating informed clinical decision-making and improved patient care.This paper will also briefly review the definition of HBV activation,assess the risks of reactivation,especially in patients treated with monoclonal antibodies,and consider management for patients with regard to screening,prophylaxis,and treatment.A better understanding of patients at risk can help clinicians provide optimum management to ensure successful patient outcomes and prevent morbidity.

考虑大规模风光分层接入的配电网多层协调无功优化方法

大量风光新能源分层、多点接入给配电网运行带来了电压越限等负面影响,增加了不同电压等级无功协同优化的难度。兼顾不同电压等级调节需求,从模型降维等值的角度,提出了基于等值模型的配电网多层协调无功优化方法。该方法分别针对含有无功调节设备及没有无功调节设备的两种台区系统,利用神经网络对大量台区相关运行数据进行训练得到台区拟合模型,形成不可控和可控两种类型的台区等值模型,并用这两类拟合模型分别代替两类台区系统的物理模型,使台区以数据驱动的方式参与配电网无功优化,形成馈线物理模型和台区拟合模型组成的单一电压等级物数混合优化调度模型。将原多层无功优化问题转换为单层系统优化问题,再对该单层系统无功优化调度问题进行求解。该方法可降低配电网系统优化计算规模,从而减小计算量,以无功优化数学模型与数据驱动方法相结合的方式,实现配电网馈线-台区多层协调无功优化。通过算例验证了所提方法对于解决分布式风光分层接入所导致电压越限问题的可行性、有效性和优越性,能够保障配电网的经济安全稳定运行。

自适应下垂系数的孤岛微电网无功均分策略

在孤岛微电网中,由于线路阻抗的不匹配,常常导致传统的下垂控制无法完成分布式电源(DG)之间无功功率的均分.为了消除DG之间的无功不均分,首先分析了传统下垂控制无法完成无功均分的原因,设计了可自适应调节的无功下垂系数,使无功下垂系数可以满足无功均分的条件,从而解决无功功率无法均分的问题.为了使无功均分控制器具有更高的灵活性和可靠性,设计了动态分布式观测器,并证明了其收敛性.动态分布式观测器可以使DG以分布式的方式更加灵活可靠地获取所需的信息.通过4个不同的算例对所提的控制策略进行验证,仿真结果验证了所提控制策略的优越性和有效性.

甘露醇对草菇继代菌株生产性状和ROS清除能力的影响

【目的】研究甘露醇对草菇继代菌株的生产性状和活性氧(ROS)清除能力的影响,探索一种简便、有效的草菇退化菌种复壮方法。【方法】以笔者课题组前期获得的组织分离继代菌株T6、T12、T19为试验菌株,T6为连续继代6次,T12为连续继代12次,T19为连续继代19次;草菇原种V844(T0)为商业栽培种。将传统马铃薯葡萄糖琼脂培养基(PDA)中的葡萄糖替换为等质量的甘露醇,进行菌丝生理性状测定;在栽培基质中添加甘露醇,测定子实体农艺学性状;以硝基四氮唑蓝(NBT)染色、超氧阴离子(O_(2))、过氧化氢(H_(2)O_(2))含量反映活性氧(ROS)积累;采用实时荧光定量PCR(RT-qPCR)测定抗氧化酶基因表达量;利用试剂盒测定抗氧化酶活力;通过菌丝染色法测定细胞核数量和线粒体膜电位;利用高效液相色谱仪(HPLC)测定菌丝能量指标。【结果】甘露醇处理对未退化菌株T0、T6的影响不显著,但能有效恢复草菇退化菌株T12、T19的生产性状和ROS清除能力。甘露醇使T12、T19的菌丝生长速度分别提高31.46%、20.99%,菌丝生物量分别提高97.33%、76.36%;使T12的生产周期缩短12.24%,生物学效率提高17.97%,恢复至T0水平;并使退化严重、失去出菇能力的T19重新长出子实体。同时,甘露醇使T12、T19的Cu/Zn超氧化物歧化酶基因(Cu/Zn-sod)相对表达量分别上调24.64%和61.54%,Mn-sod2相对表达量分别上调19.76%和267.09%,谷胱甘肽过氧化物酶基因(gpx)相对表达量分别上调25.67%和55.82%,并使SOD活力分别提高10.79%和72.32%,GPX活力分别提高16.98%和103.85%;使T12、T19中的ROS积累量显著降低,T12、T19中的O_(2)含量分别下降35.96%和41.62%,H_(2)O_(2)含量分别下降14.44%和18.26%;并使T12、T19的细胞核数目和线粒体膜电位显著增加;使T12、T19中的ATP含量分别提高17.08%和14.55%,EC值分别提高4.52%和0.92%。【结论】甘露醇能显著提高草菇退化菌株T12、T19的抗氧化能力和线粒体功能,并有效恢复其生产性状。

高空电磁脉冲晚期成分作用下500 kV变压器无功损耗仿真研究

高空电磁脉冲晚期成分(HEMP E3)效应会在变压器中性点与大地构成的回路中产生地磁感应电流(GIC),严重时会使变压器铁心半波饱和,进而导致励磁电流严重畸变、无功损耗急剧增加、局部过热和振动加剧等后果。为准确地分析电力变压器在HEMPE3作用下的无功损耗特性,该文搭建了HEMP E3对500 kV电力变压器作用的电磁暂态仿真模型,基于IEC 61000-2-9给出的标准HEMP E3波形,定量分析了感应电场幅值、上升时间、下降时间以及变压器带负载情况等对电力变压器的影响规律。分析结果表明,HEMP E3作用下500 kV变压器无功损耗与GIC呈正相关性,且无功损耗波形滞后于感应电场的变化;HEMP E3感应电场的下降时间对500 kV变压器无功损耗的影响远超上升时间;负载阻抗的阻值相同时,容性负载下的励磁电流和无功损耗幅值最大,感性负载下幅值最小。研究结果可为进一步评估HEMPE3对电力系统稳定性的影响提供重要依据。

考虑系统稳定边界的同步调相机励磁与升压变参数联合优化

现有提升调相机动态无功特性的参数优化方法侧重于电磁参数的优化,这给生产企业带来较高的工艺要求和较大的成本压力。针对该问题提出考虑系统稳定约束的调相机励磁系统及升压变参数联合优化方法,分析其对电磁参数优化的可替代性。首先,推导了基于Park模型下调相机的无功频域特性,与6阶实用模型下的无功频域特性对比,基于调相机的Park模型可提升调相机动态无功特性的分析精度。然后,提出根据调相机并网系统的稳定边界确定参数的优化区间,采用频域灵敏度方法确定重点参数,并基于人工鱼群算法进行参数优化。最后,通过仿真结果表明,励磁系统与升压变参数的联合优化,可获得与仅优化电磁参数时相近的调相机动态无功性能,验证了电磁参数优化的可替代性,从而降低调相机的制造成本,扩大同步调相机的应用场合和范围。

血清PCT、CRP及IL-4水平预测小儿支原体肺炎病情严重程度的价值

目的:探讨血清降钙素原(PCT)、C反应蛋白(CRP)及白细胞介素-4(IL-4)水平预测支原体肺炎患儿病情严重程度的价值。方法:选取2019年1月—2023年1月淮安市第二人民医院儿科收治的102例支原体肺炎患儿作为研究对象,根据病情将患儿分为轻症组59例和重症组43例。比较两组临床资料及基质细胞衍生因子(CXCL12)、γ干扰素(IFN-γ)、硫化氢(H_(2)S)、超氧化物歧化酶(SOD)、基质金属蛋白酶-9(MMP-9)、PCT、CRP及IL-4水平,多因素分析采取非条件logistic逐步回归分析,采用ROC曲线分析PCT、CRP及IL-4水平对重症支原体肺炎的预测价值。结果:两组性别、年龄、病程及CXCL12、IFN-γ、H_(2)S、SOD、MMP-9水平比较,差异无统计学意义(P>0.05);重症组PCT、CRP、IL-4水平显著高于轻症组,差异有统计学意义(P<0.05)。logistic逐步回归分析结果显示,PCT、CRP及IL-4为重症支原体肺炎独立危险因素(P<0.05)。ROC分析显示,PCT、CRP及IL-4预测重症支原体肺炎的曲线下面积分别为0.896、0.851、0.787。结论:血清PCT、CRP及IL-4水平均参与支气管肺炎患儿的病情进展,且可作为重症支气管肺炎的诊断指标。

富血小板纤维蛋白对难愈合创面炎症反应的影响

目的:研究富血小板纤维蛋白(Platelet-Rich Fibrin,PRF)对难愈合创面炎症反应的影响。方法:将2020年9月至2022年12月承德医学院附属医院烧伤整形科确诊的难愈合创面患者,完全随机分为PRF组、对照组,每组各20例,入院后均进行创面清创碘伏消毒,PRF组创面外敷PRF,隔日换药;对照组无菌敷料包扎换药治疗。于治疗前、治疗后第7天和第14天留取创面组织,进行HE染色来观察创面病理学变化;抽取静脉血分别检测白细胞(White Blood Cell,WBC)、C反应蛋白(C-Reac-tive Protein,CRP)和降钙素原(Procalcitonin,PCT)水平变化;创面组织进行CD34免疫组织化学染色,观察治疗前后创面血管化情况;通过流式细胞术比较治疗前与治疗后第7天患者血液中CD4^(+)T细胞与CD8^(+)T细胞水平变化以及CD4^(+)T/CD8^(+)T比值。结果:两组患者在性别、年龄和入院前病程的比较,差异均无统计学意义(P>0.05)。HE染色显示,在治疗前,两组患者创面均可见大量炎症细胞浸润,可见少量血管;治疗后第7天,PRF组的炎性细胞浸润减少,血管新生,治疗后第14天,PRF组炎性细胞明显减少,上皮增生,出现新生的皮肤附属器。WBC、CRP、PCT水平,治疗前差异无统计学意义(P>0.05),在治疗后的第7天和第14天时,炎症指标均下降,并且两组差异有统计学意义(P<0.05)。在治疗后第7、14天,PRF组CD34阳性表达细胞多于对照组,新生血管较多,创面上皮化出现也早于对照组。治疗前两组患者CD4^(+)T细胞、CD8^(+)T细胞和CD4^(+)/CD8^(+)比值无统计学意义(P>0.05);在治疗后第7天,两组患者的CD4^(+)T和CD4^(+)/CD8^(+)比值细胞均有上升,CD8^(+)T细胞均有下降,两组患者CD4^(+)T细胞、CD8^(+)T细胞及CD4^(+)/CD8^(+)比值比较具有统计学差异(P<0.05)。结论:PRF应用于难愈合创面,能减轻创面炎症反应,改善创面血液循环和免疫功能。

六味地黄丸治疗早发性卵巢功能不全模型小鼠的分子机制

背景:在临床上,大多数治疗早发性卵巢功能不全的方剂均以六味地黄丸为基础方演变而来,并且取得了较好的疗效。目前对六味地黄丸的实验研究大多为体内动物模型的形态学观察及生理生化指标的检测,而分子机制方面的研究报道较少。目的:探讨六味地黄丸治疗早发性卵巢功能不全的分子作用机制。方法:环磷酰胺120 mg/kg联合白消安12 mg/kg腹腔注射制备早发性卵巢功能不全小鼠模型,然后用六味地黄丸混悬液对早发性卵巢功能不全小鼠进行干预,干预12周采用ELISA法检测小鼠血清中促卵泡刺激素、促黄体生成素、雌激素、抗苗勒氏管激素、8-羟脱氧鸟苷、总抗氧化能力、活性氧水平;苏木精-伊红染色观察小鼠卵巢形态学改变;透射电镜观察小鼠卵泡颗粒细胞超微结构及颗粒细胞线粒体的凋亡情况;免疫组化法检测六味地黄丸对小鼠卵巢颗粒细胞中核受体转录辅激活因子(receptor gamma coactivator-1 alpha,PGC-1α)、线粒体转录因子A(mitochondrialtranscriptionfactorA,TFAM)的表达水平。结果与结论:①与模型组比较,实验组小鼠血清促卵泡刺激素、促黄体生成素、活性氧、8-羟脱氧鸟苷水平降低(P<0.05),雌激素、抗苗勒氏管激素、总抗氧化能力水平升高(P<0.05);②苏木精-伊红染色发现模型组小鼠卵巢组织中闭锁卵泡和黄体较多,个别可见次级卵泡,间质纤维化增生;实验组小鼠卵巢组织可见大量闭锁卵泡,黄体较少,边缘可见原始卵泡,次级卵泡较少,未见明显成熟卵泡;③透射电镜发现实验组小鼠卵巢颗粒细胞内细胞器较完整;④免疫组化结果显示,实验组小鼠卵巢组织PGC-1α的表达水平在第4周稍有升高至第8,12周无明显变化,与模型组有明显差异;实验组小鼠卵巢组织TFAM的表达水平在第4周时短暂升高,然后稍有所下降,但结果均与模型组有明显差异;⑤结果表明,六味地黄丸通过PGC-1α-TFAM-ROS信号通路在一定程度上抑制早发性卵巢功能不全小鼠卵巢颗粒细胞凋亡,从而改善卵巢的内分泌功能,提高机体抗氧化能力,减轻氧化应激损伤程度。

急性颅脑损伤患者CT评分变化及血清乳酸、NSE、CRP的相关性分析

目的探讨急性颅脑损伤(ACI)患者计算机断层扫描(CT)评分变化与血清乳酸(LA)、神经元特异性烯醇化酶(NSE)及C-反应蛋白(CRP)水平的关系及其对预后的预测价值。方法选取2020年1月—2022年1月东台市人民医院收治的50例急性颅脑损伤患者作为疾病组,根据患者治疗后格拉斯哥预后评分(GOS)分为预后良好组(32例)和预后不良组(18例);选取50例行健康体检受试者作为健康组。受试者工作特征曲线(ROC)评估血清乳酸、NSE、CRP水平与CT评分对急性颅脑损伤患者预后的评估价值。结果疾病组血清乳酸、NSE、CRP水平均高于健康组(P<0.05);预后不良组乳酸、NSE、CRP水平和CT评分均高于预后良好组;经Spearman相关分析,急性颅内损伤患者血清中乳酸、NSE、CRP水平与CT评分呈正相关(r=0.431、r=0.345、r=0.226,均P<0.05);ROC曲线分析显示,血清乳酸、NSE、CRP水平、CT评分联合预测急性颅内感染预后的曲线下面积(AUC)高于单一指标检测(P<0.05)。结论急性颅脑损伤患者CT评分与患者入院血清乳酸、NSE、CRP水平呈正相关,联合诊断对患者预后评估有一定价值。

计及IGBT结温约束的光伏高渗透配电网无功电压优化控制策略

光伏电源参与配电网无功电压调节是提升光伏高渗透配电网运行经济性和可靠性的有效手段,但光伏电源提供无功支撑会使得光伏电源IGBT最大结温升高、结温波动加剧,进而影响光伏电源和配电网的安全稳定运行。为此,该文提出一种计及IGBT结温约束的光伏高渗透配电网无功电压优化控制策略。首先,利用CatBoost算法计算IGBT结温,提高了IGBT结温计算效率,避免了传统结温算法对IGBT热模型参数的依赖;然后,建立考虑IGBT结温约束的有源配电网多目标无功优化模型,利用二分法求解IGBT结温约束下的光伏电源最大输出功率,实现了IGBT结温约束向二阶锥约束的转换;最后,利用IEEE33节点典型配电系统验证了所提策略在光伏高渗透配电网无功电压优化、光伏电源运行可靠性提升方面的有效性,并提出了综合考虑配电网网损、光伏电源可靠性的光伏电源IGBT结温限值整定原则。

固废基PRB复合颗粒填料对Cd^(2+)的吸附特性及净化机制

鉴于传统可渗透反应墙(PRB)填料价格昂贵,且易消蚀、钝化,本文以钢渣、脱硫石膏等固废材料制备了复合颗粒填料(CGF),探究CGF对Cd^(2+)的等温吸附与动力学特征,并结合浸水试验明确CGF的强度损失规律与散失特性。借助动态吸附试验探究不同条件下CGF的动态吸附规律,明确CGF对Cd^(2+)的净化机制。结果表明:CGF对Cd^(2+)的吸附过程受化学吸附与颗粒内扩散控制,符合PS-order模型与Langmuir模型。T3组CGF综合性能最好,吸附量达到8.12 mg/g,且28 d散失率最小,为4.98%,强度损失率为6.16%。Thomas模型可以很好地描述CGF的动态吸附行为,泵速对CGF的穿透曲线影响最大,且动态平衡吸附量qe随初始浓度、床层高度增加而提高。CGF通过水化反应、火山灰反应生成C-S-H凝胶、AFt等水化产物,在提供颗粒强度的同时又可通过共沉淀、离子置换等方式实现对Cd^(2+)的吸附。本文可为有色金属矿山污染场地的修复治理提供一种新思路。