PRB颗粒填料对Cd^(2+)的吸附特征及其孔隙结构动态演变规律

以PRB复合颗粒填料(CGF)开展动态吸附试验,探究其对Cd^(2+)的动态吸附规律与主要影响因素;借助可视化手段与孔隙网络模型(PNM),探究吸附前后CGF的几何特征与孔隙结构演变规律,明确填料消蚀与孔隙堵塞的动态平衡关系。研究结果表明:当泵速为10 r/min、质量浓度为50 mg/L时CGF的平衡吸附量最大,达到了1.81 mg/g;泵速对穿透曲线的影响最大,且低流量更有利于CGF对Cd^(2+)的吸附。吸附后孔隙率提高了7.79%,分形维数最多下降了7.95%,孔隙堵塞对分形维数影响较大;CGF溶蚀降低了表面积与平均等效直径,但球度在1.4~1.6范围的颗粒占比提高到75.9%。吸附后平均配位数由10.43降低至8.65,降低了17.07%;同时参与配位的“棍体”与“球体”数量分别降低了43.28%与31.63%。CGF消蚀导致动态柱中部发生堵塞,降低了孔隙与喉道的连接,但并未出现“实质性”堵塞,PNM仍保持良好的连通性能。

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。

高级氧化-PRB修复填埋场复合污染地下水的可行性

以杭州市某生活垃圾填埋场一期地下水中复合污染的COD,NH_(4)^(+),Mn^(2+)为对象,联用了非均相Fenton氧化和渗透性反应墙(PRB),设计了活性炭(AC),生物炭(BC),BC+Fe_(3)O_(4)3种不同的氧化反应催化剂组合并将其兼做PRB氧化层活性填料,下游串联沸石吸附层.批试验和柱试验结果显示,H_(2)O_(2)可直接预氧化47%的COD.氧化层中COD在催化氧化和吸附共同作用下被削减;Mn^(2+)受多孔碳材料灰分释放影响先沉淀后溶解,然后被吸附;AC和BC表面的官能团-OH和-COOH参与了反应.吸附层中NH_(4)^(+)和Mn^(2+)与沸石离子交换引起了沸石骨架结构变化,且沸石表面的官能团-NH和-OH也参与了兜底吸附.BC+Fe_(3)O_(4)氧化层与沸石吸附层长度比为1:3的串联组合对三种污染物的去除率均较高,且PRB失效时间(即污染物出流浓度达到入流的10%且超过限值的时间)最迟,填料失效时的有效利用率最高,是最优工艺.

PRB技术在地下水污染修复中的应用

地下水作为人类的主要淡水资源,其质量直接影响人体健康和生态平衡。对于已经受到污染的地下水,如何有效、经济、快速地进行修复是环境科学及工程领域面临的重要问题。对PRB技术进行分析,利用试验了解地下水污染实际情况,通过合理运用PRB技术降低地下水污染物浓度,提高地下水污染修复效果。

Effects of elafibranor on liver fibrosis and gut barrier function in a mouse model of alcohol-associated liver disease

BACKGROUND Alcohol-associated liver disease(ALD)is a leading cause of liver-related morbidity and mortality,but there are no therapeutic targets and modalities to prevent ALD-related liver fibrosis.Peroxisome proliferator activated receptor(PPAR)α and δ play a key role in lipid metabolism and intestinal barrier homeostasis,which are major contributors to the pathological progression of ALD.Meanwhile,elafibranor(EFN),which is a dual PPARαand PPARδagonist,has reached a phase III clinical trial for the treatment of metabolic dysfunctionassociated steatotic liver disease and primary biliary cholangitis.However,the benefits of EFN for ALD treatment is unknown.AIM To evaluate the inhibitory effects of EFN on liver fibrosis and gut-intestinal barrier dysfunction in an ALD mouse model.METHODS ALD-related liver fibrosis was induced in female C57BL/6J mice by feeding a 2.5% ethanol(EtOH)-containing Lieber-DeCarli liquid diet and intraperitoneally injecting carbon tetrachloride thrice weekly(1 mL/kg)for 8 weeks.EFN(3 and 10 mg/kg/day)was orally administered during the experimental period.Histological and molecular analyses were performed to assess the effect of EFN on steatohepatitis,fibrosis,and intestinal barrier integrity.The EFN effects on HepG2 lipotoxicity and Caco-2 barrier function were evaluated by cell-based assays.RESULTS The hepatic steatosis,apoptosis,and fibrosis in the ALD mice model were significantly attenuated by EFN treatment.EFN promoted lipolysis and β-oxidation and enhanced autophagic and antioxidant capacities in EtOH-stimulated HepG2 cells,primarily through PPARαactivation.Moreover,EFN inhibited the Kupffer cell-mediated inflammatory response,with blunted hepatic exposure to lipopolysaccharide(LPS)and toll like receptor 4(TLR4)/nuclear factor kappa B(NF-κB)signaling.EFN improved intestinal hyperpermeability by restoring tight junction proteins and autophagy and by inhibiting apoptosis and proinflammatory responses.The protective effect on intestinal barrier function in the EtOH-stimulated Caco-2 cells was predominantly mediated by PPARδ activation.CONCLUSION EFN reduced ALD-related fibrosis by inhibiting lipid accumulation and apoptosis,enhancing hepatocyte autophagic and antioxidant capacities,and suppressing LPS/TLR4/NF-κB-mediated inflammatory responses by restoring intestinal barrier function.

Astrocytes dynamically regulate the blood-brain barrier in the healthy brain

The blood-brain barrier(BBB)(discovered and defined by Max Lewandowsky and Lina Stern,and not,as it is universally,and yet erroneously believed,by Paul Ehrlich(Verkhratsky and Pivoriunas,2023))that separates the nervous system from the circulation is evolutionarily conserved from arthropods to man.The primeval BBB of the invertebrates and some early vertebrates was made solely by glial cells and secured(in invertebrates)by septate junctions.

Rebuilding insight into the pathophysiology of Alzheimer’s disease through new blood-brain barrier models

The blood-brain barrier is a unique function of the microvasculature in the brain parenchyma that maintains homeostasis in the central nervous system.Blood-brain barrier breakdown is a common pathology in various neurological diseases,such as Alzheimer’s disease,stroke,multiple sclerosis,and Parkinson’s disease.Traditionally,it has been considered a consequence of neuroinflammation or neurodegeneration,but recent advanced imaging techniques and detailed studies in animal models show that blood-brain barrier breakdown occurs early in the disease process and may precede neuronal loss.Thus,the blood-brain barrier is attractive as a potential therapeutic target for neurological diseases that lack effective therapeutics.To elucidate the molecular mechanism underlying blood-brain barrier breakdown and translate them into therapeutic strategies for neurological diseases,there is a growing demand for experimental models of human origin that allow for functional assessments.Recently,several human induced pluripotent stem cell-derived blood-brain barrier models have been established and various in vitro blood-brain barrier models using microdevices have been proposed.Especially in the Alzheimer’s disease field,the human evidence for blood-brain barrier dysfunction has been demonstrated and human induced pluripotent stem cell-derived blood-brain barrier models have suggested the putative molecular mechanisms of pathological blood-brain barrier.In this review,we summarize recent evidence of blood-brain barrier dysfunction in Alzheimer’s disease from pathological analyses,imaging studies,animal models,and stem cell sources.Additionally,we discuss the potential future directions for blood-brain barrier research.

Numerical simulation on sand sedimentation and erosion characteristics around HDPE sheet sand barrier under different wind angles

For the safety of railroad operations,sand barriers are utilized to mitigate wind-sand disaster effects.These disasters,characterized by multi-directional wind patterns,result in diverse angles among the barriers.In this study,using numerical simulations,we examined the behavior of High Density Polyethylene(HDPE)sheet sand barriers under different wind angles,focusing on flow field distribution,windproof efficiency,and sedimentation erosion dynamics.This study discovered that at a steady wind speed,airflow velocity varies as the angle between the airflow and the HDPE barrier changes.Specifically,a 90°angle results in the widest low-speed airflow area on the barrier’s downwind side.If the airflow is not perpendicular to the barrier,it prompts a lateral airflow movement which decreases as the angle expands.The windproof efficiency correlates directly with this angle but inversely with the wind’s speed.Notably,with a wind angle of 90°,wind speed drops by 81%.The minimum wind speed is found at 5.1H(the sand barrier height)on the barrier’s downwind side.As the angle grows,the barrier’s windproof efficiency improves,extending its protective reach.Sedimentation is most prominent on the barrier’s downwind side,as the wind angle shifts from 30°to 90°,the sand sedimentation area on the barrier’s downwind side enlarges by 14.8H.As the angle grows,sedimentation intensifies,eventually overtakes the forward erosion and enlarges the sedimentation area.

Activation of the wnt/β-catenin/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia/reperfusion conditions

Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic stroke remain largely unknown.The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt/β-catenin pathway.Meanwhile,Wnt/β-catenin pathway activation by the pharmacological inhibito r,TWS119,relieved oxidative stress,increased the levels of cytochrome P4501B1(CYP1B1)and tight junction-associated proteins(zonula occludens-1[ZO-1],occludin and claudin-5),as well as brain microvascular density in cerebral ischemia rats.Moreove r,rat brain microvascular endothelial cells that underwent oxygen glucose deprivation/reoxygenation displayed intense oxidative stress,suppression of the Wnt/β-catenin pathway,aggravated cell apoptosis,downregulated CYP1B1and tight junction protein levels,and inhibited cell prolife ration and migration.Overexpression ofβ-catenin or knockdown ofβ-catenin and CYP1B1 genes in rat brain mic rovascular endothelial cells at least partly ameliorated or exacerbated these effects,respectively.In addition,small interfering RNA-mediatedβ-catenin silencing decreased CYP1B1 expression,whereas CYP1B1 knoc kdown did not change the levels of glycogen synthase kinase 3β,Wnt-3a,andβ-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivatio n/reoxygenation.Thus,the data suggest that CYP1B1 can be regulated by Wnt/β-catenin signaling,and activation of the Wnt/β-catenin/CYP1B1 pathway contributes to alleviation of oxidative stress,increased tight junction levels,and protection of the blood-brain barrier against ischemia/hypoxia-induced injury.

Feasibility Evaluation of Using Biochar-based Permeable Reactive Barrier for the Remediation of Mercury and Arsenic Composite Polluted Water Bodies

This study employed a modified biochar material to construct a permeable reactive barrier(PRB)for the treatment of water bodies polluted with mercury and arsenic.The experimental results demonstrated that the addition of goethite-modified biochar significantly enhanced the remediation efficiency of As(III),achieving a maximum removal rate of 100%.Conversely,pure biochar exhibited high efficiency in the removal of Hg(II),with a maximum removal rate approaching 100%.Furthermore,the pH level of the water significantly influenced the adsorption efficiency of heavy metal ions,with the optimal removal performance observed at a pH of 6.0.The PRB system demonstrated excellent removal rates under low concentrations of heavy metals.However,as the concentration increased,the remediation efficiency exhibited a slight decrease.In summary,the findings of this study provide compelling evidence for the use of modified biochar in the construction of PRBs for the remediation of mercury and arsenic-polluted water bodies.Furthermore,the study reveals the mechanism by which pH and heavy metal concentration influence remediation efficiency.

Post-acute ischemic stroke hyperglycemia aggravates destruction of the blood-brain barrier

Post-acute ischemic stroke hyperglycemia increases the risk of hemorrhagic transformation,which is associated with blood-brain barrier disruption.Brain microvascular endothelial cells are a major component of the blood-brain barrier.Intercellular mitochondrial transfer has emerged as a novel paradigm for repairing cells with mitochondrial dysfunction.In this study,we first investigated whether mitochondrial transfer exists between brain microvascular endothelial cells,and then investigated the effects of post-acute ischemic stroke hyperglycemia on mitochondrial transfer between brain microvascular endothelial cells.We found that healthy brain microvascular endothelial cells can transfer intact mitochondria to oxygen glucose deprivation-injured brain microvascular endothelial cells.However,post-oxygen glucose deprivation hyperglycemia hindered mitochondrial transfer and exacerbated mitochondrial dysfunction.We established an in vitro brain microvascular endothelial cell model of the blood-brain barrier.We found that post-acute ischemic stroke hyperglycemia reduced the overall energy metabolism levels of brain microvascular endothelial cells and increased permeability of the blood-brain barrier.In a clinical study,we retrospectively analyzed the relationship between post-acute ischemic stroke hyperglycemia and the severity of hemorrhagic transformation.We found that post-acute ischemic stroke hyperglycemia serves as an independent predictor of severe hemorrhagic transformation.These findings suggest that post-acute ischemic stroke hyperglycemia can aggravate disruption of the blood-brain barrier by inhibiting mitochondrial transfer.

Blood-brain barrier pathology in cerebral small vessel disease

Cerebral small vessel disease is a neurological disease that affects the brain microvasculature and which is commonly observed among the elderly.Although at first it was considered innocuous,small vessel disease is nowadays regarded as one of the major vascular causes of dementia.Radiological signs of small vessel disease include small subcortical infarcts,white matter magnetic resonance imaging hyperintensities,lacunes,enlarged perivascular spaces,cerebral microbleeds,and brain atrophy;however,great heterogeneity in clinical symptoms is observed in small vessel disease patients.The pathophysiology of these lesions has been linked to multiple processes,such as hypoperfusion,defective cerebrovascular reactivity,and blood-brain barrier dysfunction.Notably,studies on small vessel disease suggest that blood-brain barrier dysfunction is among the earliest mechanisms in small vessel disease and might contribute to the development of the hallmarks of small vessel disease.Therefore,the purpose of this review is to provide a new foundation in the study of small vessel disease pathology.First,we discuss the main structural domains and functions of the blood-brain barrier.Secondly,we review the most recent evidence on blood-brain barrier dysfunction linked to small vessel disease.Finally,we conclude with a discussion on future perspectives and propose potential treatment targets and interventions.

Adaptive Trajectory Tracking Control for Nonholonomic Wheeled Mobile Robots:A Barrier Function Sliding Mode Approach

The trajectory tracking control performance of nonholonomic wheeled mobile robots(NWMRs)is subject to nonholonomic constraints,system uncertainties,and external disturbances.This paper proposes a barrier function-based adaptive sliding mode control(BFASMC)method to provide high-precision,fast-response performance and robustness for NWMRs.Compared with the conventional adaptive sliding mode control,the proposed control strategy can guarantee that the sliding mode variables converge to a predefined neighborhood of origin with a predefined reaching time independent of the prior knowledge of the uncertainties and disturbances bounds.Another advantage of the proposed algorithm is that the control gains can be adaptively adjusted to follow the disturbances amplitudes thanks to the barrier function.The benefit is that the overestimation of control gain can be eliminated,resulting in chattering reduction.Moreover,a modified barrier function-like control gain is employed to prevent the input saturation problem due to the physical limit of the actuator.The stability analysis and comparative experiments demonstrate that the proposed BFASMC can ensure the prespecified convergence performance of the NWMR system output variables and strong robustness against uncertainties/disturbances.

微生物PRB技术修复石油烃污染地下水的室内实验研究

随着石油及石油产品的广泛使用,地下水石油烃污染日益加重。原位可渗透反应墙(PRB)技术是修复地下水污染的重要手段。基于室内PRB模拟柱实验,采用生物炭固定化石油烃降解菌作为PRB反应介质,探究了PRB装置的最适地下水流量,并初步考察了微生物PRB反应介质的性能。结果表明,微生物PRB装置的最适用地下水流量为6 mL/min,运行30 d对自配废水和实际污染场地地下水石油烃的去除率分别为88.41%和69.72%;随反应进行,出水pH无显著变化,氧化还原电位和溶解氧浓度降低。微生物PRB反应介质性能评价结果表明,该PRB反应介质对直链烷烃(C10~C25)的降解效果较好;对吸附后的固定化菌进行解吸,石油烃析出较为迅速,解吸量为53.66 mg/g。

Breaking the brain barrier:cell competition in neural development and disease

General information on cell competition:Social behaviors are the basis of biological life.Like species and populations,cell communities experience Darwinian ecological interactions,and in case space and nutrient availability are not uniform throughout the tissue,they begin to compete for ground occupancy.

Damage on intestinal barrier function and microbial detoxification of deoxynivalenol:A review

Deoxynivalenol(DON)is a mycotoxin that is produced by various species of Fusarium and is ubiquitous in food and feed.At low concentrations,it can cause metabolic disorders in animals and humans and,at high concentrations,it can lead to pathological changes in the body.The impact of DON on human/animal health and animal productivity has thus attracted a great deal of attention around the world.DON causes severe damage to the intestine,including compromised intestinal barrier,mucosal damage,weakened immune function,and alterations in gut microbiota composition.These effects exacerbate intestinal infections and inflammation in livestock and poultry,posing adverse effects on overall health.Furthermore,research into biological methods for DON detoxification is a crucial avenue for future studies.This includes the utilization of adsorption,enzymatic degradation,and other biological approaches to mitigate DON's impact,offering new strategies for prevention and treatment of DON-induced diseases.Future research will focus on identifying highly efficient detoxifying microorganisms or enzymes to reduce DON levels in food and feed,thereby mitigating its risks to both animals and human health.

Psychosocial and Socioeconomic Barriers to Treatment Adherence in Pediatric Atopic Dermatitis

Research Background: Atopic dermatitis (AD) is a chronic inflammatory skin condition in children that significantly impacts physical health and quality of life. Adherence to treatment regimens is crucial for effective disease management but is often hindered by various psychosocial and socioeconomic barriers. Parental mental health issues, family dynamics, financial constraints, and limited access to specialized care contribute to inconsistent treatment adherence, exacerbating the condition. Purpose/Aim: The aim of this study is to explore the multifaceted barriers to treatment adherence in children with AD and evaluate the effectiveness of current interventions targeting these challenges. The study seeks to identify strategies that can improve adherence and health outcomes by addressing psychosocial and socioeconomic factors. Method: The method involves a comprehensive review of existing literature on the impact of psychosocial and socioeconomic factors on treatment adherence in children with AD. The study also examines various interventions designed to address these barriers, including community support programs, family-centered interventions, financial aid, integrated care models, and telehealth solutions. Results: Results indicate that psychosocial barriers, such as parental anxiety and depression, significantly hinder effective disease management. Family dynamics, including poor communication and single-parent households, complicate adherence efforts. Socioeconomic factors, such as financial constraints and limited healthcare access, further impede adherence. Interventions that address these barriers show promise in improving treatment adherence and health outcomes. Community support programs and family-centered interventions enhance parental mental health and family communication. Financial aid programs and integrated care models help mitigate economic and logistical challenges. Telehealth solutions improve access to specialized care, particularly in underserved areas. Conclusion: The study concludes that a holistic approach integrating medical treatment with psychosocial and socioeconomic support is essential for managing pediatric AD effectively. Policy recommendations include increased funding for community support programs, expanded telehealth services, and the integration of social services with medical care. Addressing these barriers comprehensively can enhance treatment adherence and improve the quality of life for children with AD. Further research should focus on long-term outcomes and diverse populations to refine these interventions and ensure they meet the needs of all affected children.

Establishment of a chicken intestinal organoid culture system to assess deoxynivalenol‑induced damage of the intestinal barrier function

Background Deoxynivalenol(DON)is a mycotoxin that has received recognition worldwide because of its ability to cause growth delay,nutrient malabsorption,weight loss,emesis,and a reduction of feed intake in livestock.Since DON-contaminated feedstuff is absorbed in the gastrointestinal tract,we used chicken organoids to assess the DON-induced dysfunction of the small intestine.Results We established a culture system using chicken organoids and characterized the organoids at passages 1 and 10.We confirmed the mRNA expression levels of various cell markers in the organoids,such as KI67,leucine-rich repeat containing G protein-coupled receptor 5(Lgr5),mucin 2(MUC2),chromogranin A(CHGA),cytokeratin 19(CK19),lysozyme(LYZ),and microtubule-associated doublecortin-like kinase 1(DCLK1),and compared the results to those of the small intestine.Our results showed that the organoids displayed functional similarities in permeability compared to the small intestine.DON damaged the tight junctions of the organoids,which resulted in increased permeability.Conclusions Our organoid culture displayed topological,genetic,and functional similarities with the small intes-tine cells.Based on these similarities,we confirmed that DON causes small intestine dysfunction.Chicken organoids offer a practical model for the research of harmful substances.

Retinol is involved in the intestinal regeneration and strengthens the intestinal barrier during refeeding in broiler chickens

Fasting is typically used before feeding metabolizable energy assessment in broilers.Previous studies have shown that fasting cause atrophy of the intestinal villus.Whether fasting affects intestinal permeability during refeeding by altering barrier function and nutrient absorption is of concern.Here,23-d-old broilers were randomly assigned to 5 treatments,fasted for 0,12,24,36,and 48 h,respectively,and then refed for 2 d,to study the impact of different duration of fasting on the intestinal regeneration and barrier function during refeeding.Results showed that the intestinal morphology in fasted birds was recovered in 2 d of refeeding at most.As fasting durations increased,enterocytes per intestinal villus were linearly and quadratically increased(both P<0.05),whereas goblet cells per intestinal villus was linearly decreased(both P<0.05).Besides,the mRNA level of lysozyme was linearly decreased as fasting durations increased during refeeding(both P<0.05),while quadratically increased mucin 2 was observed only after 1 d of refeeding(P<0.05).Linear increase effects were observed for claudin 2 and zonula occludens-1with increased fasting durations after 1 d of refeeding(all P<0.05),and linear and quadratical effects were observed for claudin 2 at 2 d of refeeding(both P<0.05).Besides,we found that intestinal permeability to creatinine,4 and 70 kD dextran were linearly and quadratically decreased with increased fasting durations at 6 h and 1 d of refeeding(all P<0.05).Furthermore,jejunum proteomic from birds refed for 6 h showed that birds fasted for 36 h showed increased antimicrobial peptides and upregulated retinol metabolism when compared to the nonfasted birds(P<0.05).Further study showed that retinyl ester catabolism was inhibited during fasting and enhanced during refeeding.Results of intestinal organoid culture showed that retinol benefits the cell proliferation and enterocyte differentiation.In conclusion,the intestinal permeability to small and large molecules was decreased during refeeding by strengthening the intestinal barrier function,and the activated retinol metabolism during refeeding is involved in the intestinal regeneration and strengthens the intestinal barrier.

High-temperature corrosion of sintered RE_(2)Si_(2)O_(7)(RE=Yb and Ho)environmental barrier coating materials by volcanic ash

Rare-earth silicates are promising environmental barrier coatings(EBCs)that can protect SiC_(f)/Si C_(m)substrates in next-genera tion gas turbine blades.Notably,RE_(2)Si_(2)O_(7)(RE=Yb and Ho)shows potential as an EBC due to its coefficient of thermal expansion(CTE)compatible with substrates and high resistance to water vapor corrosion.The target operating temperature for next-generation tur bine blades is 1400°C.Corrosion is inevitable during adhesion to molten volcanic ash,and thus,understanding the corrosion behavior o the material is crucial to its reliability.This study investigates the high-temperature corrosion behavior of sintered RE_(2)Si_(2)O_(7)(RE=Yb and Ho).Samples were prepared using a solid-state reaction and hot-press method.They were then exposed to volcanic ash at 1400°C for 224,and 48 h.After 48 h of exposure,volcanic ash did not react with Yb_(2)Si_(2)O_(7)but penetrated its interior,causing damage.Meanwhile Ho_(2)Si_(2)O_(7)was partially dissolved in the molten volcanic ash,forming a reaction zone that prevented volcanic ash melts from penetrating the interior.With increasing heat treatment time,the reaction zone expanded,and the thickness of the acicular apatite grains increased The Ca:Si ratios in the residual volcanic ash were mostly unchanged for Yb_(2)Si_(2)O_(7)but decreased considerably over time for Ho_(2)Si_(2)O_(7).Th Ca in volcanic ash was consumed and formed apatite,indicating that RE^(3+)ions with large ionic radii(Ho>Yb)easily precipitated apatit from the volcanic ash.