原子吸收分光光度法测定硬脂酸钙中的钙

用原子吸收分光光度计测定了硬脂酸钙中的钙,确定了仪器的最佳工作条件.测定结果表明方法线性良好,r=0.999 9,加标回收率为98.9%～101.7%,相对标准偏差0.37%;测定结果与行业标准一致.操作简单易行,可以满足实际工作需要,并可对同一样品溶液进行其他元素的测定,更适合于成批样品的例行分析.     

Dysregulation of Astrocyte–Neuronal Communication in Alzheimer’s Disease

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.     

A Trend to the Production of Calcium Hydroxide and Precipitated Calcium Carbonate with Defined Properties

In this paper, production of precipitated calcium carbonate (PCC) with required particle size and morphological structure, along with its dependence on technological parameters and the properties of Ca(OH)₂, is discussed. The effect of the reaction environment on the kinetics of CaO hydration and the formation of crystals in water suspension was established. A remarkable difference in the system's restoration ability after stirring was observed. The hydration process is initially controlled by a kinetic mechanism, followed by a diffusion‐controlled process. The dissolution speed of lime hydrated to suspension is eight times higher than that of lime hydrated to powder. Particles of hydrated lime appeared in various forms.     

DOT1L Methyltransferase Regulates Calcium Influx in Erythroid Progenitor Cells in Response to Erythropoietin

Erythropoietin (EPO) signaling plays a vital role in erythropoiesis by regulating proliferation and lineage-specific differentiation of murine hematopoietic progenitor cells (HPCs). An important downstream response of EPO signaling is calcium (Ca²⁺) influx, which is regulated by transient receptor potential channel (TRPC) proteins, particularly TRPC2 and TRPC6. While EPO induces Ca²⁺ influx through TRPC2, TRPC6 inhibits the function of TRPC2. Thus, interactions between TRPC2 and TRPC6 regulate the rate of Ca²⁺ influx in EPO-induced erythropoiesis. In this study, we observed that the expression of TRPC6 in KIT-positive erythroid progenitor cells was regulated by DOT1L. DOT1L is a methyltransferase that plays an important role in many biological processes during embryonic development including early erythropoiesis. We previously reported that Dot1l knockout (Dot1l^KO) HPCs in the yolk sac failed to develop properly, which resulted in lethal anemia. In this study, we detected a marked downregulation of Trpc6 gene expression in Dot1l^KO progenitor cells in the yolk sac compared to the wild type (WT). The promoter and the proximal regions of the Trpc6 gene locus exhibited an enrichment of H3K79 methylation, which is mediated solely by DOT1L. However, the expression of Trpc2, the positive regulator of Ca²⁺ influx, remained unchanged, resulting in an increased TRPC2/TRPC6 ratio. As the loss of DOT1L decreased TRPC6, which inhibited Ca²⁺ influx by TRPC2, Dot1l^KO HPCs in the yolk sac exhibited accelerated and sustained elevated levels of Ca²⁺ influx. Such heightened Ca²⁺ levels might have detrimental effects on the growth and proliferation of HPCs in response to EPO.     

Nutritional Calcium Supply Dependent Calcium Balance,Bone Calcification and Calcium Isotope Ratios in Rats

Serum calcium isotopes (δ^44/42Ca) have been suggested as a non-invasive and sensitive Ca balance marker. Quantitative δ^44/42Ca changes associated with Ca flux across body compartment barriers relative to the dietary Ca and the correlation of δ^44/42Ca_Serum with bone histology are unknown. We analyzed Ca and δ^44/42Ca by mass-spectrometry in rats after two weeks of standard-Ca-diet (0.5%) and after four subsequent weeks of standard- and of low-Ca-diet (0.25%). In animals on a low-Ca-diet net Ca gain was 61 ± 3% and femur Ca content 68 ± 41% of standard-Ca-diet, bone mineralized area per section area was 68 ± 15% compared to standard-Ca-diet. δ^44/42Ca was similar in the diets, and decreased in feces and urine and increased in serum in animals on low-Ca-diet. δ^44/42Ca_Bone was higher in animals on low-Ca-diet, lower in the diaphysis than the metaphysis and epiphysis, and unaffected by gender. Independent of diet, δ^44/42Ca_Bone was similar in the femora and ribs. At the time of sacrifice, δ^44/42Ca_Serum inversely correlated with intestinal Ca uptake and histological bone mineralization markers, but not with Ca content and bone mineral density by µCT. In conclusion, δ^44/42Ca_Bone was bone site specific, but mechanical stress and gender independent. Low-Ca-diet induced marked changes in feces, serum and urine δ^44/42Ca in growing rats. δ^44/42Ca_Serum inversely correlated with markers of bone mineralization.     

钙硅比对水化硅酸钙加速碳化的影响

废弃水泥石、钢渣等碳酸化固定CO2不仅可以缓解温室效应还可以实现废弃物的再利用,同时制备出性能优良的建材制品。为了研究废弃水泥石矿物组成的碳酸化机理,探讨了钙硅比对水化硅酸钙加速碳化的影响。结果表明:随着钙硅比增加,水化硅酸钙(C-S-H)碳化率逐渐降低,高钙硅比的C-S-H具有相对粗大的孔结构使得早期的碳化速率增加;碳化产物中文石、球霰石、方解石在不同钙硅比时所占比例不同,钙硅比≤0.67时文石占较大比例,钙硅比≥1.00时方解石为主要碳化产物,钙硅比=0.83时球霰石含量最大;加速碳化条件下形成的碳酸钙分解温度分成两部分,在400~620℃范围内文石和球霰石都分解,方解石在650~800℃范围内分解。     

The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca²⁺ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca²⁺ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca²⁺ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca²⁺ in both mitochondria and cytoplasm, thereby regulating cellular Ca²⁺ homeostasis. Mitochondrial Ca²⁺ transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca²⁺ homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca²⁺ and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca²⁺ regulation helps diagnosis and therapy.     

Fatty Acid Synthesis in Glial Cells of the CNS

Fatty acids (FAs) are of crucial importance for brain homeostasis and neural function. Glia cells support the high demand of FAs that the central nervous system (CNS) needs for its proper functioning. Additionally, FAs can modulate inflammation and direct CNS repair, thereby contributing to brain pathologies such Alzheimer’s disease or multiple sclerosis. Intervention strategies targeting FA synthesis in glia represents a potential therapeutic opportunity for several CNS diseases.     

Crosstalk between Neuron and Glial Cells in Oxidative Injury and Neuroprotection

To counteract oxidative stress and associated brain diseases, antioxidant systems rescue neuronal cells from oxidative stress by neutralizing reactive oxygen species and preserving gene regulation. It is necessary to understand the communication and interactions between brain cells, including neurons, astrocytes and microglia, to understand oxidative stress and antioxidant mechanisms. Here, the role of glia in the protection of neurons against oxidative injury and glia–neuron crosstalk to maintain antioxidant defense mechanisms and brain protection are reviewed. The first part of this review focuses on the role of glia in the morphological and physiological changes required for brain homeostasis under oxidative stress and antioxidant defense mechanisms. The second part focuses on the essential crosstalk between neurons and glia for redox balance in the brain for protection against oxidative stress.     

亚硫酸钙和硫酸钙混合物共沉淀实验研究

亚硫酸钙和硫酸钙的沉淀物是钙基脱硫的必然产物,目前对于这两者的沉淀缺乏研究。文章用亚硫酸钠、硫酸钠和氯化钙溶液配制亚硫酸钙和硫酸钙的混合溶液,分别研究了25、45、55℃下,钙离子浓度为0．04M时,不同比例的亚硫酸钙和硫酸钙过饱和溶液的共沉淀过程中各离子的浓度变化,并探讨了温度、硫酸钙对亚硫酸钙沉淀晶型、热力学参数的影响。试验结果表明,在低浓度条件下,经过50h可沉淀完全,亚硫酸钙和硫酸钙共沉淀时形成混晶。混晶中硫酸根离子占了总比例20％,并得到了亚硫酸钙和硫酸钙共沉淀时的溶度积,从溶度积中求得沉淀过程的焓变。硫酸根离子的存在提高了钙离子平衡浓度,容易结垢,同时硫酸根离子的存在大大减小了亚硫酸根的离子浓度,不利于脱硫,因此必须控制双碱法过程中的氧化率在20％以下。     

分光光度法测定钙制剂中微量钙

通过吸光强度值可定量地确定元素离子的浓度值,因此选择合适的显色剂成为方法的关键.利用钙指示剂与钙的显色反应,确定最佳操作条件以后,指示剂在水相中与钙络合,无需萃取,便可准确快速测定;对于微量钙的测定,分光光度法显示出较高的灵敏度,具有稳定性好,准确度高,试剂和仪器廉价,操作简便快速等优点.     

Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia

Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We examined contractility, mitochondrial function, and intracellular calcium transients (ICTs) in muscles of mice throughout the life span to define their sequential relationships. We performed these same measures and analyzed neuromuscular junction (NMJ) morphology in mice with postnatal deletion of neuronal Sod1 (i-mn-Sod1^-/- mice), previously shown to display accelerated age-associated muscle loss and exacerbation of denervation in old age, to test relationships between neuronal redox homeostasis, NMJ degeneration and mitochondrial function. In control mice, the amount and rate of the decrease in mitochondrial NADH during contraction was greater in middle than young age although force was not reduced, suggesting decreased efficiency of NADH utilization prior to the onset of weakness. Declines in both the peak of the ICT and force were observed in old age. Muscles of i-mn-Sod1^-/- mice showed degeneration of mitochondrial and calcium handling functions in middle-age and a decline in force generation to a level not different from the old control mice, with maintenance of NMJ morphology. Together, the findings support the conclusion that muscle mitochondrial function decreases during aging and in response to altered neuronal redox status prior to NMJ deterioration or loss of mass and force suggesting mitochondrial defects contribute to sarcopenia independent of denervation.     

Axonal Injuries Cast Long Shadows: Long Term Glial Activation in Injured and Contralateral Retinas after Unilateral Axotomy

Background: To analyze the course of microglial and macroglial activation in injured and contralateral retinas after unilateral optic nerve crush (ONC). Methods: The left optic nerve of adult pigmented C57Bl/6 female mice was intraorbitally crushed and injured, and contralateral retinas were analyzed from 1 to 45 days post-lesion (dpl) in cross-sections and flat mounts. As controls, intact retinas were studied. Iba1⁺ microglial cells (MCs), activated phagocytic CD68⁺MCs and M2 CD206⁺MCs were quantified. Macroglial cell changes were analyzed by GFAP and vimentin signal intensity. Results: After ONC, MC density increased significantly from 5 to 21 dpl in the inner layers of injured retinas, remaining within intact values in the contralateral ones. However, in both retinas there was a significant and long-lasting increase of CD68⁺MCs. Constitutive CD206⁺MCs were rare and mostly found in the ciliary body and around the optic-nerve head. While in the injured retinas their number increased in the retina and ciliary body, in the contralateral retinas decreased. Astrocytes and Müller cells transiently hypertrophied in the injured retinas and to a lesser extent in the contralateral ones. Conclusions: Unilateral ONC triggers a bilateral and persistent activation of MCs and an opposed response of M2 MCs between both retinas. Macroglial hypertrophy is transient.     

Neuronal and Glial Communication via Non-Coding RNAs: Messages in Extracellular Vesicles

Extracellular vesicles (EVs) have been increasingly recognized as essential players in cell communication in many organs and systems, including the central nervous system (CNS). A proper interaction between neural cells is fundamental in the regulation of neurophysiological processes and its alteration could induce several pathological phenomena, such as neurodegeneration, neuroinflammation, and demyelination. EVs contain and transfer complex molecular cargoes typical of their cells of origin, such as proteins, lipids, carbohydrates, and metabolites to recipient cells. EVs are also enriched in non-coding RNAs (e.g., microRNAs, lncRNAs, and circRNA), which were formerly considered as cell-intrinsic regulators of CNS functions and pathologies, thus representing a new layer of regulation in the cell-to-cell communication. In this review, we summarize the most recent and advanced studies on the role of EV-derived ncRNAs in the CNS. First, we report the potential of neural stem cell-derived ncRNAs as new therapeutic tools for neurorepair. Then, we discuss the role of neuronal ncRNAs in regulating glia activation, and how alteration in glial ncRNAs influences neuronal survival and synaptic functions. We conclude that EV-derived ncRNAs can act as intercellular signals in the CNS to either propagate neuroinflammatory waves or promote reparative functions.     

电石渣制备超细碳酸钙的工艺研究

研究了以电石渣为原料,在无表面活性剂的条件下,利用间歇鼓泡碳化法制备超细碳酸钙的工艺条件.利用正交实验确定出优化工艺条件：Ca（OH）2质量分数4%、CO2体积分数60%、碳化温度10℃、搅拌速度1000r/min.产物的纯度98.5%,粒度0.98μm,白度95,钙回收率为90.2%.XRD与TEM表征显示,产物是纯净的方解石型CaCO3,产物微粒的平均一次粒径约为50nm.     

改性碳酸钙在聚氯乙烯中的应用研究

研究了一种改性碳酸钙在聚氯乙烯(PVC)中的应用情况。研究结果表明,这种经JL G0 1型改性剂(Modifier)改性的碳酸钙与普通碳酸钙相比,颗粒以原生粒子状态均匀分布,不团聚,其中部分以纳米粒子状态存在,因此填充于聚氯乙烯(PVC)硬质、软质制品中,不仅能改善体系的加工性能,而且赋予制品较好的物理机械性能,达到增韧补强的效果     

生产活性钙联产医药级碳酸钙新工艺

介绍了生产活性钙联产医药级碳酸钙新工艺 ,和其它方法相比 ,该工艺生产成本低、设备投资少、生产周期短 ,适应于工业化生产。     

碳酸钙产品及其展望

介绍几种碳酸钙产品:轻质碳酸钙、重质碳酸钙、活性碳酸钙、纳米碳酸钙,并且从理化性质、制备方法、颗粒形状以及应用等方面对重质碳酸钙与轻质碳酸钙进行了比较,并对轻质碳酸钙、重质碳酸钙、纳米碳酸钙三者的生产工艺以及发展前景作了简单介绍。