管线钢精炼过程中夹杂物CaO和CaS的研究

通过现场取样进行电镜观察检测,研究了管线钢精炼过程中钢中大尺寸CaO和CaS复合夹杂物形貌、尺寸和成分,并结合钢液中Ca-O和Ca-S平衡曲线、CaO和CaS热力学分析,对其形成机理和形成原因进行了研究.实验结果表明：夹杂物可能是由于钙处理时喂入了过量硅钙线造成的.     

副产硫酸钙室温固相球磨制备氧化钙

以锰尾矿制备硫酸锰过程中副产硫酸钙为原料在室温下与碳酸氢铵进行固相球磨反应,制备出氧化钙的前驱体碳酸钙,然后将其煅烧得到氧化钙.分别考察了物料配比、球磨时间、球料质量比等因素对硫酸钙转化率的影响,采用X射线衍射和化学分析方法对产物进行了分析,并对室温固相球磨反应的机理进行了探讨.在物料配比(摩尔比)为3.5:1、球磨时间为40 min以及球料质量比为5:1时,硫酸钙的转化率可达到99.8%,将固相产物在1000℃热解1 h后所制备的氧化钙纯度为99.2%.室温球磨过程细化了反应物的颗粒尺寸,增加了反应物的接触面积,为引发反应提供了必要的能量,因此提高了化学反应的有效性.     

氧化应激降低鸡肉品质的作用机制研究进展

氧化应激会引发肉鸡的恐惧和躁动,造成生理代谢失调,这不仅会降低肉鸡肌肉pH值,增加滴水损失,导致鸡肉品质变差,而且还会降低加工特性。鸡肉品质下降的主要原因为：肌肉中的能量代谢平衡被打破,导致有氧呼吸减弱,无氧酵解增强,引起肌肉中乳酸的大量积累,导致肌肉pH值快速下降;钙离子代谢紊乱,引发肌细胞膜破损;线粒体结构和功能受损,导致线粒体外膜透化,促进凋亡因子释放至细胞质,激活内源性细胞凋亡途径。文章从肉鸡的能量代谢、钙离子代谢和细胞凋亡三个方面,本文深入介绍了氧化损伤的发生机制,在生产实践中寻求缓解肉鸡氧化应激的方法以提高鸡肉品质,促进肉鸡产业健康发展提供理论基础。     

Nanoengineering Calcium Peroxide-Based Site-Specific Delivery Platform to Efficiently Activate the cGAS-STING Pathway for Cancer Immunotherapy by Amplified Endoplasmic Reticulum Stress

Currently, the understanding of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway's involvement in efficient immunotherapy mainly revolves around the role of mitochondria or nucleus modulation. Nonetheless, the role of endoplasmic reticulum (ER) stress in activating the cGAS-STING mechanism to boost immunity against tumors remains essentially unexplored. Herein, novel findings demonstrating that ER stress can be used as a strategy for stimulating the cGAS-STING pathway, thereby augmenting the immune response against cancer, are presented. To accomplish this objective, ER-targeting p-methylbenzene sulfonamide-tailored IR780 (p-780) is synthesized and it is loaded into CaO₂ nanoparticles, which are further functionalized with distearoyl phosphoethanolamine-polyethylene glycol（DSPE-PEG）-biotin to form PEG/CaO₂@p-780 NPs. The disruption of calcium homeostasis, coupled with the heightened levels of reactive oxygen species (ROS) mediated by p-780, along with hyperpyrexia, collectively contributes to the amplification of endoplasmic reticulum (ER) stress. This cascade of events effectively triggers the cGAS-STING pathway and, in parallel, facilitates the degradation of the programmed cell death 1 ligand 1 (PD-L1) protein. In addition, oxygen released through CaO₂ decomposition is expected to promote p-780–mediated phototherapy, while reversing the immunosuppressive tumor microenvironment associated with hypoxia. Furthermore, DSPE-PEG-biotin facilitates tumor site-specific drug delivery through active targeting mediated by the biotin receptor. Collectively, PEG/CaO₂@p-780 nanoparticles successfully activate systemic antitumor immunity by enhancing ER stress.     

发挥资源优势,坚持循环经济,以高新技术打造西部大型氯碱基地

介绍了新疆天业(集团)有限公司利用资源丰富、地理位置独特等优势和国家政策的支持,按循环经济的发展理念,采用先进技术,建设大型氯碱生产基地的情况。     

描述微纳米多孔复合绝热材料的单元体传热模型

根据硬硅钙石-气凝胶复合绝热材料的微观结构特点,建立了描述材料内气固耦合导热的三维单元体传热模型.通过模型计算对硬硅钙石型硅酸钙、气凝胶及硬硅钙石-气凝胶复合绝热材料的导热系数进行了对比研究.结果表明:硬硅钙石型硅酸钙密度是影响复合绝热材料有效导热系数的关键因素,而气凝胶密度的影响不大;在高温下,复合绝热材料的导热系数要明显低于硬硅钙石型硅酸钙及二氧化硅气凝胶的导热系数.     

钙处理H13钢中夹杂物的转变

利用真空感应炉和扫描电镜等设备, 实验研究了钙处理对H13模具钢中夹杂物的影响, 并对钢中夹杂物的转变进行了热力学计算, 讨论了钙处理对夹杂物成分和结构的影响.结果表明:钙处理H13钢后, 夹杂物尺寸减小, 圆形度提高, 夹杂物面积比降低;夹杂物由钙处理前的Si O₂-Al₂O₃系夹杂物转变为Ca O-Si O₂-Al₂O₃- (MgO) 系夹杂物, 钢中Ca质量分数达到12×10^-6时, 夹杂物完全处于Ca O-Si O₂-Al₂O₃- (MgO) 相图的1400℃低熔点区以内;钢中高的T.O含量使Ca S不会在钙处理后形成, 钢中Ca/T.O的质量分数比达到0.3时, 复合夹杂物中的Al₂O₃将会完全消除; (Mn, Cr) S夹杂依附氧化物夹杂析出, Mn、Cr和S的偏析程度决定了复合氧硫化物夹杂的形貌.     

Whole Exome Sequencing Identifies a Heterozygous Variant in the Cav1.3 Gene CACNA1D Associated with Familial Sinus Node Dysfunction and Focal Idiopathic Epilepsy

Cav1.3 voltage-gated L-type calcium channels (LTCCs) are involved in cardiac pacemaking, hearing and hormone secretion, but are also expressed postsynaptically in neurons. So far, homozygous loss of function mutations in CACNA1D encoding the Cav1.3 α₁-subunit are described in congenital sinus node dysfunction and deafness. In addition, germline mutations in CACNA1D have been linked to neurodevelopmental syndromes including epileptic seizures, autism, intellectual disability and primary hyperaldosteronism. Here, a three-generation family with a syndromal phenotype of sinus node dysfunction, idiopathic epilepsy and attention deficit hyperactivity disorder (ADHD) is investigated. Whole genome sequencing and functional heterologous expression studies were used to identify the disease-causing mechanisms in this novel syndromal disorder. We identified a heterozygous non-synonymous variant (p.Arg930His) in the CACNA1D gene that cosegregated with the combined clinical phenotype in an autosomal dominant manner. Functional heterologous expression studies showed that the CACNA1D variant induces isoform-specific alterations of Cav1.3 channel gating: a gain of ion channel function was observed in the brain-specific short CACNA1D isoform (Cav1.3_S), whereas a loss of ion channel function was seen in the long (Cav1.3_L) isoform. The combined gain-of-function (GOF) and loss-of-function (LOF) induced by the R930H variant are likely to be associated with the rare combined clinical and syndromal phenotypes in the family. The GOF in the Cav1.3_S variant with high neuronal expression is likely to result in epilepsy, whereas the LOF in the long Cav1.3_L variant results in sinus node dysfunction.     

The STIM1/2-Regulated Calcium Homeostasis Is Impaired in Hippocampal Neurons of the 5xFAD Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common cause of age-related dementia. Neuronal calcium homeostasis impairment may contribute to AD. Here we demonstrated that voltage-gated calcium (VGC) entry and store-operated calcium (SOC) entry regulated by calcium sensors of intracellular calcium stores STIM proteins are affected in hippocampal neurons of the 5xFAD transgenic mouse model. We observed excessive SOC entry in 5xFAD mouse neurons, mediated by STIM1 and STIM2 proteins with increased STIM1 contribution. There were no significant changes in cytoplasmic calcium level, endoplasmic reticulum (ER) bulk calcium levels, or expression levels of STIM1 or STIM2 proteins. The potent inhibitor BTP-2 and the FDA-approved drug leflunomide reduced SOC entry in 5xFAD neurons. In turn, excessive voltage-gated calcium entry was sensitive to the inhibitor of L-type calcium channels nifedipine but not to the T-type channels inhibitor ML218. Interestingly, the depolarization-induced calcium entry mediated by VGC channels in 5xFAD neurons was dependent on STIM2 but not STIM1 protein in cells with replete Ca²⁺ stores. The result gives new evidence on the VGC channel modulation by STIM2. Overall, the data demonstrate the changes in calcium signaling of hippocampal neurons of the AD mouse model, which precede amyloid plaque accumulation or other signs of pathology manifestation.     

Activation of Piezo1 Increases Na,K-ATPase-Mediated Ion Transport in Mouse Lens

Lens ion homeostasis depends on Na,K-ATPase and NKCC1. TRPV4 and TRPV1 channels, which are mechanosensitive, play important roles in mechanisms that regulate the activity of these transporters. Here, we examined another mechanosensitive channel, piezo1, which is also expressed in the lens. The purpose of the study was to examine piezo1 function. Recognizing that activation of TRPV4 and TRPV1 causes changes in lens ion transport mechanisms, we carried out studies to determine whether piezo1 activation changes either Na,K-ATPase-mediated or NKCC1-mediated ion transport. We also examined channel function of piezo1 by measuring calcium entry. Rb uptake was measured as an index of inwardly directed potassium transport by intact mouse lenses. Intracellular calcium concentration was measured in Fura-2 loaded cells by a ratiometric imaging technique. Piezo1 immunolocalization was most evident in the lens epithelium. Potassium (Rb) uptake was increased in intact lenses as well as in cultured lens epithelium exposed to Yoda1, a piezo1 agonist. The majority of Rb uptake is Na,K-ATPase-dependent, although there also is a significant NKCC-dependent component. In the presence of ouabain, an Na,K-ATPase inhibitor, Yoda1 did not increase Rb uptake. In contrast, Yoda1 increased Rb uptake to a similar degree in the presence or absence of 1 µM bumetanide, an NKCC inhibitor. The Rb uptake response to Yoda1 was inhibited by the selective piezo1 antagonist GsMTx4, and also by the nonselective antagonists ruthenium red and gadolinium. In parallel studies, Yoda1 was observed to increase cytoplasmic calcium concentration in cells loaded with Fura-2. The calcium response to Yoda1 was abolished by gadolinium or ruthenium red. The calcium and Rb uptake responses to Yoda1 were absent in calcium-free bathing solution, consistent with calcium entry when piezo1 is activated. Taken together, these findings point to stimulation of Na,K-ATPase, but not NKCC, when piezo1 is activated. Na,K-ATPase is the principal mechanism responsible for ion and water homeostasis in the lens. The functional role of lens piezo1 is a topic for further study.