Shape- and size-controlled synthesis of single-crystalline maghemite (gamma-Fe2O3) nanocrystals are performed by utilizing a solution-based one-step thermolysis method. Modulating the growth parameters, such as the type and amount of capping ligands as well as the growth time, is shown to have a significant effect on the overall shape and size of the obtained nanocrystals and on the ripening process itself. The resulting shapes of the novel structures are diverse, including slightly faceted spheres, diamonds, prisms, and hexagons, all of which are in fact truncated dodecahedron structures with different degrees of truncation along the {111}, {110}, or {100} faces. Spherical nanocrystals are easily assembled into the three-dimensional superlattices, demonstrating the uniformity of these nanocrystals. The size-dependent magnetic properties are examined, and large hexagon-shaped gamma-Fe2O3 nanocrystals are shown to be ferrimagnetic at room temperature.
With a baton the general directs soldiers and the conductor musicians, and in the nanoworld the rodlike shape also means control, as this form enhances magnetic and coercive properties of crystalline aggregates. Also reported here is a tunable synthetic method, in which the overall shape of the crystal is determined by a balance of kinetically and thermodynamically controlled growth mechanisms. The graphic shows one example of the degree of ordering available in the crystalline through this method.
Background & Aims Pancreatitis is characterized by increased influx of Ca 2+ into acinar cells, by unknown mechanisms. Inhibitors of Ca 2+ influx channels could be effective in treating acute pancreatitis, but these have deleterious side effects that can result in death. We investigated the expression patterns and functions of acinar cell Ca 2+ channels and factors that regulate them during development of acute pancreatitis, along with changes in the channel inactivator store-operated calcium entry-associated regulatory factor (SARAF). We investigated whether SARAF is a target for treatment of acute pancreatitis and its status in human with pancreatitis. MethodsWe generated mice that expressed SARAF tagged with hemagglutinin, using CRISPR/Cas9 gene editing, and isolated acinar cells. We also performed studies with Saraf -/mice, Saraf zf/zf mice, mice without disruption of Saraf (control mice), and mice that overexpress fluorescently labeled SARAF in acinar cells. We analyzed interactions between stromal interaction molecule 1 (STIM1) and SARAF in HEK cells stimulated with carbachol using fluorescence resonance energy transfer microscopy and immunoprecipitation. Mice were given injections of caerulein or L-arginine to induce pancreatitis. Pancreatic tissues and blood samples were collected and levels of serum amylase, trypsin, tissue damage, inflammatory mediators, and inflammatory cells were measured.We performed quantitative polymerase chain reaction analyses of pancreatic tissues from 6 organ donors without pancreatic disease (controls) and 8 patients with alcohol-associated pancreatitis. ResultsPancreatic levels of Ca 2+ influx channels or STIM1 did not differ significantly between acinar cells from mice with vs. without pancreatitis. By contrast, pancreatic levels of Saraf messenger RNA 2 and SARAF protein initially markedly increased but then decreased during cell stimulation or injection of mice with caerulein, resulting in excessive Ca 2+ influx. STIM1 interacted stably with SARAF following stimulation of HEK or mouse acinar cells with physiologic levels of carbachol, but only transiently following stimulation with pathologic levels of carbachol, leading to excessive Ca 2+ influx. We observed reduced levels of SARAF messenger RNA in pancreatic tissues from patients with pancreatitis, compared with controls. SARAF knockout mice developed more severe pancreatitis than control mice after administration of caerulein or L-arginine, and pancreatic acinar cells from these mice had significant increases in Ca 2+ influx. Conversely, overexpression of SARAF in acini reduced Ca 2+ influx, eliminated inflammation, and reduced severity of acute pancreatitis. ConclusionsIn mice with pancreatitis, SARAF initially increases but is then degraded, resulting in excessive, pathological Ca 2+ influx by acinar cells. SARAF knockout mice develop more severe pancreatitis than control mice, whereas mice that express SARAF from a transgene in acinar cells develop less-severe pancreatitis. SARAF therefore appears to prevent pancreat...
The increasing of intracellular calcium concentration is a fundamental process for mediating osteoclastogenesis, which is involved in osteoclastic bone resorption. Cytosolic calcium binds to calmodulin and subsequently activates calcineurin, leading to NFATc1 activation, a master transcription factor required for osteoclast differentiation. Targeting the various activation processes in osteoclastogenesis provides various therapeutic strategies for bone loss. Diverse compounds that modulate calcium signaling have been applied to regulate osteoclast differentiation and, subsequently, attenuate bone loss. Thus, in this review, we summarized the modulation of the NFATc1 pathway through various compounds that regulate calcium signaling and the calcium influx machinery. Furthermore, we addressed the involvement of transient receptor potential channels in osteoclastogenesis.
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