[en] Neuroblastoma is the second most common paediatric cancer. It develops from undifferentiated simpatico-adrenal lineage cells and is mostly sporadic; however, the aetiology behind the development of neuroblastoma is still not fully understood. Intracellular calcium ([Ca"2"+]_i) is a secondary messenger which regulates numerous cellular processes and, therefore, its concentration is tightly regulated. This review focuses on the role of [Ca"2"+]_i in differentiation, apoptosis and proliferation in neuroblastoma. It describes the mechanisms by which [Ca"2"+]_i is regulated and how it modulates intracellular pathways. Furthermore, the importance of [Ca"2"+]_i for the function of anti-cancer drugs is illuminated in this review as [Ca"2"+]_i could be a target to improve the outcome of anti-cancer treatment in neuroblastoma. Overall, modulations of [Ca"2"+]_i could be a key target to induce apoptosis in cancer cells leading to a more efficient and effective treatment of neuroblastoma

[en] High precision computer controlled tracings of bright Ca⁺-mottles were performed during 1974 and 1975 at the Locarno Observatory of Gottingen to study solar differential rotation and to search for giant cell circulation pattern. The method consists of measuring the position of 5-15 bright Ca⁺- mottles with respect to the center of the solar disc every 10 to 15 min during 4h every day. From a linear least square fit of the observed positions the solar-latitude and longitude were computed for the beginning and the end of the daily 4h observation period. From this the components in latitude and longitude of the proper motions were derived which result from the differential rotation, possible giant cell circulation and the small scale random walk of these features. (Auth.)

[en] In this study, the roles of ABA-cADPR-Ca²⁺ and ABA-IP3-Ca²⁺ signaling pathways in UV-B-induced isoflavone accumulation in soybean sprouts were investigated. Results showed that abscisic acid (ABA) up regulated cyclic ADP-ribose (cADPR) and inositol 1,4,5-trisphosphate (IP3) levels in soybean sprouts under UV-B radiation. Furthermore, cADPR and IP3, as second messengers of UV-B-triggered ABA, induced isoflavone accumulation by up-regulating proteins and genes expression and activity of isoflavone biosynthetic-enzymes (chalcone synthase, CHS; isoflavone synthase, IFS). After Ca²⁺ was chelated by EGTA, isoflavone content decreased. Overall, ABA-induced cADPR and IP3 up regulated isoflavone accumulation which was mediated by Ca²⁺ signaling via enhancing the expression of proteins and genes participating in isoflavone biosynthesis in soybean sprouts under UV-B radiation. - Highlights: • UV-B-induced cADPR and IP3 synthesis was mediated by ABA. • cADPR and IP3 were involved in UV-B-ABA-induced isoflavone accumulation. • cADPR and IP3-induced isoflavone accumulation may be mediated by Ca²⁺. • ABA, cADPR, IP3 and Ca²⁺ could activate proteins expression of CHS and IFS.

[en] Simultaneous observations of fine structure photospheric features at several wavelengths are described. The observations, which include regions near disk center and at the limb, were obtained using a narrow band calcium filter and selected wavelengths in Mg b₁, the red wing of Hα and the Hα continuum using the Universal Birefringent Filter of the Sacramento Peak Observatory. From the disk-center series it is concluded that bright point structures seen in calcium are cospatial with the Hα filigree and are related in origin. The limb photographs confirm that the calcium network is cospatial with the white light faculae. However, in regions of good seeing it is clear that even at the limb the calcium network patterns consist of individual bright points which are essentially the same as those seen near disk center. Thus it is concluded that the white light faculae, the Hα filigree and the calcium bright points are different manifestations of the same photospheric features. (orig.)

[en] Bioactuators are an attractive alternative for mechanical components of MEMS devices. We propose a flow-switching device active to calcium ion based on bioactuator of Vorticella. We develop a fundamental procedure for immobilization of Vorticella in a microfluidic chamber and control of contraction and extension of stalks. Cells were trapped in microfluidic chambers and allowed to adhere. After treatment of cells, stalks were contracted and extended by injecting solutions. Flow speed changed during the motion. Our developed method presents a strategy for application of bioactuator.

[en] TNF-α has been shown to be involved in cardiac dysfunction during ischemia/reperfusion injury; however, no information regarding the status of TNF-α production in myocardial injury due to intracellular Ca²⁺-overload is available in the literature. The intracellular Ca²⁺-overload was induced in the isolated rat hearts subjected to 5 min Ca²⁺-depletion and 30 min Ca²⁺-repletion (Ca²⁺-paradox). The Ca²⁺-paradox hearts exhibited a dramatic depression in left ventricular developed pressure, a marked elevation in left ventricular end diastolic pressure, and more than a 4-fold increase in TNF-α content. The ratio of cytosolic to homogenate nuclear factor-κB (NFκB) was decreased whereas the ratio of phospho-NFκB to total NFκB was increased in the Ca²⁺-paradox hearts. All these changes due to Ca²⁺-paradox were significantly attenuated upon treating the hearts with 100 μM pentoxifylline. These results suggest that activation of NFκB and increased production of TNF-α may play an important role in cardiac injury due to intracellular Ca²⁺-overload

[en] We examined the contractile responsiveness of rat thoracic aortas under pressure overload after long-term suprarenal abdominal aortic coarctation (lt-Srac). Endothelium-dependent angiotensin II (ANG II) type 2 receptor (AT_2R)-mediated depression of contractions to ANG II has been reported in short-term (1 week) pressure-overloaded rat aortas. Contractility was evaluated in the aortic rings of rats subjected to lt-Srac or sham surgery (Sham) for 8 weeks. ANG I and II levels and AT_2R protein expression in the aortas of lt-Srac and Sham rats were also evaluated. lt-Srac attenuated the contractions of ANG II and phenylephrine in the aortas in an endothelium-independent manner. However, lt-Srac did not influence the transient contractions induced in endothelium-denuded aortic rings by ANG II, phenylephrine, or caffeine in Ca"2"+-free medium or the subsequent tonic constrictions induced by the addition of Ca"2"+ in the absence of agonists. Thus, the contractions induced by Ca"2"+ release from intracellular stores and Ca"2"+ influx through stored-operated channels were not inhibited in the aortas of lt-Srac rats. Potassium-elicited contractions in endothelium-denuded aortic rings of lt-Srac rats remained unaltered compared with control tissues. Consequently, the contractile depression observed in aortic tissues of lt-Srac rats cannot be explained by direct inhibition of voltage-operated Ca"2"+ channels. Interestingly, 12-O-tetradecanoylphorbol-13-acetate-induced contractions in endothelium-denuded aortic rings of lt-Srac rats were depressed in the presence but not in the absence of extracellular Ca"2"+. Neither levels of angiotensins nor of AT_2R were modified in the aortas after lt-Srac. The results suggest that, in rat thoracic aortas, lt-Srac selectively inhibited protein kinase C-mediated activation of contraction that is dependent on extracellular Ca"2"+ entry

[en] Ca"2"+ pumps are important players in smooth muscle contraction. Nevertheless, little information is available about these pumps in the vas deferens. We have determined which subtype of sarco(endo)plasmic reticulum Ca"2"+-ATPase isoform (SERCA) is expressed in rat vas deferens (RVD) and its modulation by calmodulin (CaM)-dependent mechanisms. The thapsigargin-sensitive Ca"2"+-ATPase from a membrane fraction containing the highest SERCA levels in the RVD homogenate has the same molecular mass (∼115 kDa) as that of SERCA2 from the rat cerebellum. It has a very high affinity for Ca"2"+ (Ca_0_._5 = 780 nM) and a low sensitivity to vanadate (IC_5_0 = 41 µM). These facts indicate that SERCA2 is present in the RVD. Immunoblotting for CaM and Ca"2"+/calmodulin-dependent protein kinase II (CaMKII) showed the expression of these two regulatory proteins. Ca"2"+ and CaM increased serine-phosphorylated residues of the 115-kDa protein, indicating the involvement of CaMKII in the regulatory phosphorylation of SERCA2. Phosphorylation is accompanied by an 8-fold increase of thapsigargin-sensitive Ca"2"+ accumulation in the lumen of vesicles derived from these membranes. These data establish that SERCA2 in the RVD is modulated by Ca"2"+ and CaM, possibly via CaMKII, in a process that results in stimulation of Ca"2"+ pumping activity

[en] In clause the mechanism of sorption of ions of calcium by macromolecules of pectin is opened. Is shown, that the linkage of ions of calcium descends on acid bunches of pectin, and process carries cooperative character

[en] The survival of Dictyostelium cells depends on their ability to efficiently chemotax, either towards food or to form multicellular aggregates. Although the involvement of Ca²⁺ signaling during chemotaxis is well known, it is not clear how this regulates cell movement. Previously, fish epithelial keratocytes have been shown to display transient increases in intracellular calcium ([Ca²⁺]_i) that are mediated by stretch-activated calcium channels (SACs), which play a role in retraction of the cell body [J. Lee, A. Ishihara, G. Oxford, B. Johnson, and K. Jacobson, Regulation of cell movement is mediated by stretch-activated calcium channels. Nature, 1999. 400(6742): p. 382-6.]. To investigate the involvement of SACs in Dictyostelium movement we performed high resolution calcium imaging in wild-type (NC4A2) Dictyostelium cells to detect changes in [Ca²⁺]_i. We observed small, brief, Ca²⁺ transients in randomly moving wild-type cells that were dependent on both intracellular and extracellular sources of calcium. Treatment of cells with the SAC blocker gadolinium (Gd³⁺) inhibited transients and decreased cell speed, consistent with the involvement of SACs in regulating Dictyostelium motility. Additional support for SAC activity was given by the increase in frequency of Ca²⁺ transients when Dictyostelium cells were moving on a more adhesive substratum or when they were mechanically stretched. We conclude that mechano-chemical signaling via SACs plays a major role in maintaining the rapid movement of Dictyostelium cells