原子吸收光谱法测定糖尿病患者血清锌、镁、钙含量的研究

采用原子吸收光谱法测定了30例糖尿病患者血清锌、镁、钙的含量,并与30例正常人相比较。结果表明,其锌和镁较正常人为低(P<0.05),但钙与正常人无显著性差别。另外,本文还对锌、镁与糖尿病的关系进行了探讨。     

硫酸镁治疗新生儿重症肺炎的临床研究及对血气血镁的影响

目的　为探讨硫酸镁治疗新生儿重症肺炎的临床效果及对血气血镁的影响。方法　采用 96例新生儿重症肺炎患儿随机分成治疗组 4 8例 ,对照组 4 8例 ,治疗组加用硫酸镁 30～ 5 0mg/(kg·d)加入 5 %葡萄糖 2 0ml静滴 ,持续 1h ,疗程3～ 8d ,同时监测血气血镁。结果　治疗组总有效率 79.2 % ,对照组总有效率 5 0 .0 % (P <0 .0 1) ,硫酸镁在改善症状 ,消除肺部体征及缩短住院时间和提高治愈率等方面优于对照组 ,治疗组病死率下降 ,同时血气恢复正常优于对照组 ,血镁含量治疗前后无变化。结论　硫酸镁治疗新生儿重症肺炎疗效显著 ,未发现明显副作用。     

硫酸镁联合亚低温治疗对大鼠局灶性脑缺血的保护作用

目的　探讨硫酸镁对SD大鼠局灶性脑缺血损伤的保护作用。方法　将 4 0只大鼠随机分成模型对照组、硫酸镁治疗组、亚低温治疗组、硫酸镁联合亚低温治疗组。采用线栓法建立大鼠局灶性脑缺血模型。通过计算大鼠神经功能缺陷评分 ,测量脑梗死体积 ,观察神经元超微结构改变 ,评定硫酸镁联合亚低温治疗作用。结果各治疗组大鼠神经功能评分及脑梗死体积均显著低于对照组 (P <0 0 5 ) ,联合治疗组大鼠明显低于对照组 (P<0 0 1) ;联合治疗组神经元超微结构改变轻微。结论　硫酸镁联合亚低温治疗对大鼠局灶脑缺血有明显保护作用     

老人自发与黑发中铜、锰、铁、锌、镁含量的比较

本文用原子吸收光谱法测定了延边地区65岁～108岁健康老人110人头发中的铜、锰、铁、锌及镁的含量,比较了66人的白发与44人的黑发中这些元素的含量差异.结果表明,白发中的锰和镁的含量明显低于黑发,但铜、锌、铁的含量则无明显差异.这些差别在男性很明显,但在女性则不甚明显.     

Generation of the eosinophil chemotactic factor (ECF) from various cell types by melittin

The peptide melittin, the main constituent of bee venom is a potent stimulus for the generation of an eosinophil chemotactic factor (ECF) from human polymorphonuclear neutrophils, rat mast cells and rat peritoneal cells depleted in mast cells. Optimal EFC induction required a sublytic activation of the cells. With each cell type the kinetics of ECF generation were similar in that after an early rise in activity a steep fall off occurred at later times of incubation suggesting a mechanism of inactivation. The induction of ECF by melittin is increased in the presence of calcium. The polar portion of the melittin molecule (aminoacids 20–26) is responsible for the generation of the chemotactic activity. Other peptides of honey bee venom such as the mast cell degranulating peptide (MCD) or apamine do not initiate ECF release. It appears that melittin leads to ECF induction via the phospholipase A₂-arachidonic acid dependent pathway of cell activation. Our data suggests that the lipid mediator ECF can be obtained from phagocytes and mast cells thus indicating the interdependence of inflammatory reactions.     

Mg2+ reduces N-methyl-D-aspartate neurotoxicity in embryonic chick neural retina in vitro

N-Methyl-D-aspartate (NMDA) is a potent neurotoxin that affects cells in the inner layers of the embryonic chick retina exposed in vitro. After exposure of the embryonic day 12 neural retina to 0.5-10.0 mM NMDA for 30 min, 50-80% of the cells in the inner region of the inner nuclear layer and 50-100% of the cells in the ganglion cell layer were hypochromatic. When retinas were incubated with Mg2+ (0.5-10.0 mM) for 15 min and then incubated with Mg2+ and NMDA (0.5 mM) for 30 min, the NMDA effect in the inner layers was dramatically reduced but not abolished. Removal of Mg2+ before NMDA exposure produced retinas as seriously affected as retinas not exposed to Mg2+. Studying the effects of NMDA inhibitors, such as Mg2+, may help elucidate the mechanism of the cytotoxic events that occur in the retina in response to certain excitatory acidic amino acids.     

Magnesium depletion in patients on long-term chlorthalidone therapy for essential hypertension

Summary Sixty patients were treated for 1 year for essential uncomplicated hypertension, 30 with beta-blockers alone (BB) and 30 with BB and chlorthalidone (CTD). BB did not affect serum K⁺ or Mg⁺⁺. In the BB-group there was a statistically significant trend towards retention of Mg⁺⁺ in a loading test, but the effect was clinically marginal. BB + CTD reduced serum K⁺ and Mg⁺⁺ and caused significant Mg⁺⁺ depletion, as shown by the Mg⁺⁺ loading test. All the effects were highly significant and were clinically important. The metabolic perturbations due to CTD are potentially dangerous and make this drug unattractive as first choice treatment for hypertension.     

Mg2+ Transporters in Digestive Cancers

Despite magnesium (Mg²⁺) representing the second most abundant cation in the cell, its role in cellular physiology and pathology is far from being elucidated. Mg²⁺ homeostasis is regulated by Mg²⁺ transporters including Mitochondrial RNA Splicing Protein 2 (MRS2), Transient Receptor Potential Cation Channel Subfamily M, Member 6/7 (TRPM6/7), Magnesium Transporter 1 (MAGT1), Solute Carrier Family 41 Member 1 (SCL41A1), and Cyclin and CBS Domain Divalent Metal Cation Transport Mediator (CNNM) proteins. Recent data show that Mg²⁺ transporters may regulate several cancer cell hallmarks. In this review, we describe the expression of Mg²⁺ transporters in digestive cancers, the most common and deadliest malignancies worldwide. Moreover, Mg²⁺ transporters’ expression, correlation and impact on patient overall and disease-free survival is analyzed using Genotype Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) datasets. Finally, we discuss the role of these Mg²⁺ transporters in the regulation of cancer cell fates and oncogenic signaling pathways.     

Magnesium in Obesity,Metabolic Syndrome,and Type 2 Diabetes

Magnesium (Mg²⁺) deficiency is probably the most underestimated electrolyte imbalance in Western countries. It is frequent in obese patients, subjects with type-2 diabetes and metabolic syndrome, both in adulthood and in childhood. This narrative review aims to offer insights into the pathophysiological mechanisms linking Mg²⁺ deficiency with obesity and the risk of developing metabolic syndrome and type 2 diabetes. Literature highlights critical issues about the treatment of Mg²⁺ deficiency, such as the lack of a clear definition of Mg²⁺ nutritional status, the use of different Mg²⁺ salts and dosage and the different duration of the Mg²⁺ supplementation. Despite the lack of agreement, an appropriate dietary pattern, including the right intake of Mg²⁺, improves metabolic syndrome by reducing blood pressure, hyperglycemia, and hypertriglyceridemia. This occurs through the modulation of gene expression and proteomic profile as well as through a positive influence on the composition of the intestinal microbiota and the metabolism of vitamins B1 and D.     

Zinc Nutritional Status in a Series of Children with Chronic Diseases: A Cross-Sectional Study

Background: Zinc is an essential trace element for the normal growth and development of human beings. The main objective was to evaluate the nutritional status of zinc and its association with nutritional indicators in a series of children with chronic diseases. Methods: The prevalence of patients with dietary zinc deficiency or deficit zinc intake (<80% DRI: dietary reference intake) was analyzed through prospective 72 h dietary surveys, and serum zinc deficiency or hypozincemia (≤70 µg/dL in children under 10 years of age in both sexes and in females older than 10 years and <74 μg/dL in males older than 10 years) was measured through atomic absorption spectrophotometry. The participants were classified according to their nutritional status by body mass index (BMI). Results: Mean serum zinc level in obese (87 µg/dL), undernourished (85 µg/dL), and eutrophic children (88 µg/dL) were normal, but in the undernutrition (60% DRI) and eutrophic (67% DRI) groups the mean dietary zinc intake was low compared to that in the obesity group (81% DRI). There were different associations between nutritional parameters, dietary zinc intake, and serum zinc. All patients with hypozincemia had dietary zinc deficiency. Conclusions: In the whole series, 69% of participants showed a zinc intake lower than recommended and might be at high risk of zinc deficiency.