Alginate is an important natural biopolymer and metal ion-induced gelation is one of its most significant functional properties. Alginate-based hydrogels crosslinked with metal ions are commonly utilized in the food, biomedical, tissue engineering, and environment fields. The process of metal ion-induced alginate gelation has been the subject of thorough research over the last few decades. This review aims to summarize the mechanisms of alginate hydrogels induced by different cations (primarily including Ca²⁺, Ba²⁺, Cu²⁺, Sr²⁺, Fe²⁺/Fe³⁺, and Al³⁺). Metal ion-induced alginate gelation shows different preferences for α-L-guluronic acid (G), β-D-mannuronic acid (M), and GM blocks. Some metal ions can also selectively bind to the carboxyl groups of guluronic acid. The properties and applications of these alginate-based hydrogels are also discussed. The primary objective of this review is to provide useful information for exploring the practical applications of alginate.

Blockade of synaptic activity induces homeostatic plasticity, in part by stimulating synthesis of all-transretinoic acid (RA), which in turn increases AMPA receptor synthesis. However, the synaptic signal that triggers RA synthesis remained unknown. Using multiple activity-blockade protocols that induce homeostatic synaptic plasticity, here we show that RA synthesis is activated whenever postsynaptic Ca²⁺entry is significantly decreased and that RA is required for upregulation of synaptic strength under these homeostatic plasticity conditions, suggesting that Ca²⁺plays an inhibitory role in RA synthesis. Consistent with this notion, we demonstrate that both transient Ca²⁺depletion by membrane-permeable Ca²⁺chelators and chronic blockage of L-type Ca²⁺-channels induces RA synthesis. Moreover, the source of dendritic Ca²⁺entry that regulates RA synthesis is not specific because mild depolarization with KCl is sufficient to reverse synaptic scaling induced by L-type Ca²⁺-channel blocker. By expression of a dihydropyridine-insensitive L-type Ca²⁺channel, we further show that RA acts cell autonomously to modulate synaptic transmission. Our findings suggest that, in synaptically active neurons, modest “basal” levels of postsynaptic Ca²⁺physiologically suppress RA synthesis, whereas in synaptically inactive neurons, decreases in the resting Ca²⁺levels induce homeostatic plasticity by stimulating synthesis of RA that then acts in a cell-autonomous manner to increase AMPA receptor function.

Background: The growing applications of nanotechnologic products, such as quantum dots (QDs), increase the likelihood of exposure. Furthermore, their accumulation in the bioenvironment and retention in cells and tissues are arousing increasing worries about the potentially harmful side effects of these nanotechnologic products. Previous studies concerning QD cytotoxicity focused on the reactive oxygen species produced by QDs. Cellular calcium homeostasis dysregulation caused by QDs may be also responsible for QD cytotoxicity. Meanwhile the interference of QDs with voltage-gated sodium channel (VGSC) current (INa) may lead to changes in electrical activity and worsen neurotoxicologic damage. Objective: We aimed to investigate the potential for neurotoxicity of cadmium selenium QDs in a hippocampal neuronal culture model, focusing on cytoplasmic calcium levels and VGSCs function. Methods: We used confocal laser scanning and standard whole-cell patch clamp techniques. Results: We found that a) QDs induced neuron death dose dependently; b) cytoplasmic calcium levels were elevated for an extended period by QD treatment, which was due to both extracellular calcium influx and internal calcium release from endoplasmic reticulum; and c) QD treatment enhanced activation and inactivation of INa, prolonged the time course of activation, slowed INa recovery, and reduced the fraction of available VGSCs. Conclusion: Results in this study provide new insights into QD toxicology and reveal potential risks of their future applications in biology and medicine.

Background: Attention deficit/hyperactivity disorder (ADHD) and lead exposure are high-prevalence conditions among children. Objective: Our goal was to investigate the association between ADHD and blood lead levels (BLLs) in Chinese children, adjusting for known ADHD risk factors and potential confounding variables. Methods: We conducted a pair-matching case–control study with 630 ADHD cases and 630 non-ADHD controls 4–12 years of age, matched on the same age, sex, and socioeconomic status. The case and control children were systematically evaluated via structured diagnostic interviews, including caregiver interviews, based on the Diagnostic and Statistical Manual of Mental Disorders, 4th ed., revised criteria (DSM-IV-R). We evaluated the association between BLLs and ADHD using the Pearson chi-square test for categorical variables and the Student t-test for continuous data. We then performed conditional multiple variables logistic regression analyses with backward stepwise selection to predict risk factors for ADHD. Results: There was a significant difference in BLLs between ADHD cases and controls. ADHD cases were more likely to have been exposed to lead during childhood than the non-ADHD control subjects, with adjustment for other known risk factors [children with BLLs ≥ 10 μg/dL vs. ≤ 5 μg/dL; OR = 6.0; 95% confidence interval (CI) = 4.10–8.77, p < 0.01; 5–10 μg/dL vs.≤ 5 μg/dL, OR = 4.9; 95% CI = 3.47–6.98, p < 0.01]. These results were not modified by age and sex variables. Conclusions: This was the largest sample size case–control study to date to study the association between BLLs and ADHD in Chinese children. ADHD may be an additional deleterious outcome of lead exposure during childhood, even when BLLs are < 10 μg/dL.