Variant angina due to deficiency of intracellular magnesium

A 51-year-old man was diagnosed as having variant angina by documentation of typical ST elevation during anginal attack and also by showing coronary arterial spasm (#2 and #12) during hyperventilation on coronary arteriography. Large quantities of calcium blocking agents and nitrates could not improve his symptoms. Lack of intracellular magnesium was suspected from a daily excretion of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). After hourly infusion of magnesium sulfate (80 mEq), coronary spasm could not be induced by ergonovine.     

包头地区918例儿童不同年龄阶段4种矿物质元素水平变化趋势及差异性比较

目的 了解包头地区0～12岁不同年龄段儿童全血中锌、铁、镁、铜4种矿物质元素营养水平及变化趋势。方法 0~12岁健康体检的儿童中随机抽样918例, 利用SPSS 16.0软件包进行统计分析。结果 4个年龄阶段Zn、Fe均有较高的缺乏率;随年龄的增长, 锌元素水平逐渐增加, 铁元素水平整体呈上升趋势, 6岁后上升更加明显;Cu和Mg元素缺乏率较低;镁元素水平随年龄增长呈上升趋势; 0～6岁间儿童体内铜元素的水平变化不明显, 6岁后含量明显下降。结论 包头地区儿童4种矿物质元素的缺乏顺位依次为:锌、铁、铜、镁;儿童4种矿物质元素诊断标准应按年龄阶段划分。     

火焰原子吸收光度法测定复方电解质注射液中钠、钾、镁离子

目的 建立复方电解质注射液中钠、钾、镁离子的定量测定方法。方法 采用原子分光光度法,钠、钾离子以氯化铯为掩蔽剂,镁离子以氧化镧为掩蔽剂,钠、钾、镁3种离子分别于589、766.5、285.2 nm处进行测定。结果 钠、钾、镁3种离子线性关系良好。平均回收率分别为99.8%、100.7%、99.4%。结论 本方法简便、快捷、准确,可用于复方电解质注射液中钠、钾、镁离子的定量测定。     

维拉帕米联合门冬氨酸钾镁治疗阵发性室上性心动过速27例的疗效观察

目的 总结维拉帕米及门冬氨酸钾镁治疗阵发性室上性心动过速（PSVT）的疗效.方法 对用维拉帕米及门冬氨酸钾镁治疗PSVT 27例的资料进行分析.结果 27例PSVT经静脉注射维拉帕米及静脉滴注门冬氨酸钾镁治疗后,25例心动过速终止并转为窦性心律,复律成功92.6%,多数病例于3~15 min心动过速终止并复律,未见明显不良反应.结论 维拉帕米联合门冬氨酸钾镁治疗PSVT简便易行,疗效确切安全,转复率高,无明显不良反应.     

From the Cover: Tonoplast CBL–CIPK calcium signaling network regulates magnesium homeostasis in Arabidopsis

Although Mg²⁺ is essential for a myriad of cellular processes, high levels of Mg²⁺ in the environment, such as those found in serpentine soils, become toxic to plants. In this study, we identified two calcineurin B-like (CBL) proteins, CBL2 and CBL3, as key regulators for plant growth under high-Mg conditions. The Arabidopsis mutant lacking both CBL2 and CBL3 displayed severe growth retardation in the presence of excess Mg²⁺, implying elevated Mg²⁺ toxicity in these plants. Unexpectedly, the cbl2 cbl3 mutant plants retained lower Mg content than wild-type plants under either normal or high-Mg conditions, suggesting that CBL2 and CBL3 may be required for vacuolar Mg²⁺ sequestration. Indeed, patch-clamp analysis showed that the cbl2 cbl3 mutant exhibited reduced Mg²⁺ influx into the vacuole. We further identified four CBL-interacting protein kinases (CIPKs), CIPK3, -9, -23, and -26, as functionally overlapping components downstream of CBL2/3 in the signaling pathway that facilitates Mg²⁺ homeostasis. The cipk3 cipk9 cipk23 cipk26 quadruple mutant, like the cbl2 cbl3 double mutant, was hypersensitive to high-Mg conditions; furthermore, CIPK3/9/23/26 physically interacted with CBL2/3 at the vacuolar membrane. Our results thus provide evidence that CBL2/3 and CIPK3/9/23/26 constitute a multivalent interacting network that regulates the vacuolar sequestration of Mg²⁺, thereby protecting plants from Mg²⁺ toxicity.Plants absorb essential mineral nutrients from the soil and translocate them to different organs for specific physiological processes. Most of these minerals are in the ionic forms and require a wide array of transporters to move them across the cell membranes and sort them into subcellular compartments (1). Although plants rely on a sufficient supply of mineral nutrients for proper growth and development, an excess of minerals often causes toxicity to plant cells. To adapt to the constantly changing availability of minerals in the environment, plants have evolved mechanisms that enhance ion uptake under low-nutrient conditions and sequester excessive ions in the vacuole when external levels are high. Such mechanisms enable plant cells to maintain a steady level of each nutrient ion, namely, ionic homeostasis. At the molecular level, this homeostasis entails the coordinated functions of a large number of regulatory molecules that constitute elaborate signaling networks to control the affinities and activities of numerous ion transporters. In these signaling networks, Ca²⁺ serves as a central messenger (2). A number of external ionic stresses can evoke stimulus-specific cellular Ca signals that are represented by the distinct spatiotemporal patterns of Ca²⁺ fluxes between cytosol and Ca²⁺ stores (3, 4). These “Ca²⁺ signatures” can be detected and relayed into diverse downstream signaling events by plant Ca²⁺-sensor proteins that manifest conformational changes upon binding Ca²⁺ and subsequently regulate the function of target proteins (5–7).Calcineurin B-like (CBL) proteins are a group of Ca²⁺ sensors that physically and functionally interact with a family of plant-specific protein kinases designated as “CBL-interacting protein kinases” (CIPKs) (8). Interaction between CBLs and CIPKs is mediated by the regulatory C-terminal region of CIPKs and is required for full activation of the kinase activity (9–11). Although CIPKs appear to be soluble in the cytosol, CBL proteins are largely associated with the cellular membranes through their N-terminal motifs that are subject to lipid modifications (12). Some CBLs, such as CBL1, -4, -5, and -9, are anchored to the plasma membrane through myristoylation and acylation at their N-terminal region (13). Other CBLs including, CBL2, -3, and -6, are localized to the vacuolar membrane via the N-terminal tonoplast targeting sequence that contains multiple cysteine residues subject to S-acylation (14, 15). It has been suggested that the dynamic localization of CIPKs is determined by their specific CBL partners, resulting in alternative CBL–CIPK complexes at either the plasma membrane or the tonoplast (16–18).Growing evidence has highlighted the CBL–CIPK regulatory pathways in plant responses to environmental stresses in general and ionic stresses in particular (19). In the Ca²⁺-dependent salt overly sensitive (SOS) pathway, the Ca sensor CBL4/SOS3 (20) and the protein kinase CIPK24/SOS2 (21) form a functional module to regulate the Na⁺/H⁺ exchanger SOS1 at the plasma membrane, thus facilitating Na⁺ extrusion under salt stress (22). Another CBL protein, CBL10/SCaBP8, was identified as a shoot-specific partner of CIPK24 in salt stress adaptation (16, 23, 24). In response to limited K⁺ supply, the Ca sensors CBL1 and CBL9 positively regulate CIPK23 and recruit the kinase to the plasma membrane, which in turn activates the K⁺ channel AKT1 for optimal K⁺ nutrition (25–27). Interestingly, the CBL1/9–CIPK23 module also regulates nitrate (NO₃⁻) uptake and sensing processes by phosphorylating the dual-affinity NO₃⁻ transporter CHL1 (28). A recent study shows that CIPK23, in complex with CBL1 or CBL9, could trigger the opening of the S-type anion channel SLAC1 or SLAH3 through its phosphorylation in a Ca-dependent manner (29).Ionic homeostasis is regulated mainly by ion transport across the plasma membrane and vacuolar membrane (tonoplast). Although CBL–CIPK signaling modules are well recognized as playing a critical role in the transport of several minerals across the plasma membrane, very little is known about the possible function of vacuolar CBL–CIPK complexes. Our recent work revealed a highly redundant role for tonoplasts CBL2 and CBL3 in plant development and ion homeostasis that is correlated with the regulation of vacuolar H⁺-ATPase (V-ATPase) activity (14). In this study, we describe a novel function of CBL2 and CBL3 in the regulation of Mg²⁺ homeostasis through a V-ATPase–independent pathway in Arabidopsis. Downstream of CBL2 and CBL3 are four functionally redundant CIPKs that are recruited to the tonoplast by interacting with CBL2 and CBL3. Our results thus build a CBL–CIPK network at the tonoplast that regulates vacuolar sequestration to detoxify excessive Mg²⁺ in plant cells.     

The Impact of Graphene and Diatomite Admixtures on the Performance and Properties of High-Performance Magnesium Oxychloride Cement Composites

A high-performance magnesium oxychloride cement (MOC) composite composed of silica sand, diatomite powder, and doped with graphene nanoplatelets was prepared and characterized. Diatomite was used as a 10 vol.% replacement for silica sand. The dosage of graphene was 0.5 wt.% of the sum of the MgO and MgCl₂·6H₂O masses. The broad product characterization included high-resolution transmission electron microscopy, X-ray diffraction, X-ray fluorescence, scanning electron microscopy and energy dispersive spectroscopy analyses. The macrostructural parameters, pore size distribution, mechanical resistance, stiffness, hygric and thermal parameters of the composites matured for 28-days were also the subject of investigation. The combination of diatomite and graphene nanoplatelets greatly reduced the porosity and average pore size in comparison with the reference material composed of MOC and silica sand. In the developed composites, well stable and mechanically resistant phase 5 was the only precipitated compound. Therefore, the developed composite shows high compactness, strength, and low water imbibition which ensure high application potential of this novel type of material in the construction industry.     

慢性腹泻患者结肠镜检查肠道准备方法的临床研究

目的探讨慢性腹泻患者在行结肠镜检查前的肠道准备方法。方法回顾性分析2017年3月-2018年3月行结肠镜检查的慢性腹泻患者,共119例。其中,37例患者(A组)于结肠镜检查前4 h开始口服复方聚乙二醇电解质散(PGEP)139.12 g(2 000 ml);42例患者(B组)于检查前4 h口服PGEP 208.68 g(3 000 ml);另外40例患者(C组)检查前4 h服用PGEP 104.34 g(1 500 ml),检查前2 h口服50.00%硫酸镁(MgSO_4)50 ml,再饮用温开水500 ml,至排泄液似清水样。应用Boston肠道准备量表(BBPS)评分,并对肠腔内气泡进行评分,比较3组患者肠道准备有效性、耐受性及安全性。结果 C组的进镜时间和退镜时间明显短于A组和B组;C组的BBPS评分明显高于A组和B组;C组的肠腔内气泡评分明显低于A组和B组;C组的肠道准备接受率、再次肠道准备接受率明显高于A组及B组;C组的总体不良反应评分明显低于A组及B组;差异均有统计学意义(P 0.05)。结论慢性腹泻患者采用PGEP联合MgSO_4进行结肠镜检查前肠道准备,其有效性、耐受性及安全性好。     

生物可降解镁合金支架研究现状

目前介入治疗中主要以金属永久性支架为主,这类支架存在血栓形成和再狭窄的问题.生物可降解镁合金支架开始成为关注的焦点和热点,它理论上克服了永久性支架的缺点,是未来支架发展方向之一.相信在不久的将来,生物可降解镁合金支架在许多疾病中都将得到广泛应用.     

Post-ischemic administration of nimodipine following focal cerebral ischemic-reperfusion injury in rats alleviated excitotoxicity, neurobehavioural alterations and partially the bioenergetics

The present study focuses on the temporal calcium significance in middle cerebral artery occluded (2 h ischemia)-reperfused (70 h reperfusion) rats treated with nimodipine (NM) through concurrent measurements of excitotoxicity, bioenergetics and neurobehavioural paradigms. Further, the suitable therapeutic time window of calcium channel antagonism in stroke was also ascertained. NM (5 mg/kg, i.p.) was administered at pre (30 min before the induction of ischemia), during (1 h following occlusion of MCA) and post-ischemic (3 h after begin of reperfusion) states. The magnitude of neuroprotection in terms of excitotoxicity (glutamate, glutamine synthetase, Na⁺K⁺ATPase), bioenergetics (ATP, NAD⁺) and neurobehavioural paradigms (neurological score and open field exploratory behaviour) were measured and compared to ensure the therapeutic time-window of NM in stroke. Middle cerebral artery occlusion-reperfusion (MCAO/R) was found to elevate glutamate, glutamine synthetase levels and deplete Na⁺K⁺ATPase activity in the vehicle treated group (IR group). Significant decrease in bioenergetics such as ATP and NAD⁺ levels was also observed. Further, IR group demonstrated grievous oxidative stress (increase in lipid peroxidation, protein carbonyl content, nitrite/nitrate levels and decrease in superoxide dismutase and glutathione levels) along with anxiogenic behaviour, neurological deficits and neuronal damage and decreased nuclear to cytoplasm ratio in CA1 hippocampal region. Post-ischemic NM administration reversed the excitotoxicity, neurobehavioural and histopathological alterations significantly, but it restored bioenergetics level in MCAO/R rats only partially.These findings were further confirmed with the combination treatment (CT) of post-ischemic NM and pre-ischemic memantine (MN) administration, since MN showed protective effect in the pre-ischemic administration (Babu and Ramanathan, 2009). The failure of NM to forefend the neurodegeneration on pre- and during-ischemic administration suggests that the initial phase damages in ischemic-reperfusion (IR) might be mediated through other mechanism(s) such as glutamergic overstimulation or reverse operation of glutamate transporters. From the present study, it is concluded that calcium plays a crucial role in post-ischemic status and the suitable therapeutic time window of calcium antagonism is the post-ischemic state.