The Dynamics and Regulation of Mesenchymal Cell Fusion in the Sea Urchin Embryo

AbstractCell–cell fusion occurs in a wide variety of developmental contexts, yet the mechanisms involved are just beginning to be elucidated. In the sea urchin embryo, primary mesenchyme cells (PMCs) fuse to form syncytial filopodial cables within which skeletal spicules are deposited. Taking advantage of the optical transparency and ease of micromanipulation of sea urchin embryos, we have developed methods for directly observing the dynamics of PMC fusionin vivo.A fraction of the PMCs was labeled with fluorescent dextran and transfer of the dye to unlabeled PMCs was followed by time-lapse, fluorescence microscopy. Fusion was first detected about 2 h after PMCs began to migrate within the blastocoel. Fusion proceeded in parallel with the assembly of the PMC ring pattern and was complete by the early gastrula stage. The formation of a single, extensive PMC syncytium was confirmed by DiI labeling of fixed embryos. When single micromeres were isolated and cultured in unsupplemented seawater, they divided and their progeny underwent fusion. This shows that the capacity to fuse is autonomously programmed in the micromere–PMC lineage by the 16-cell stage. PMC transplantations at late embryonic stages revealed that these cells remain fusion-competent long after their fusion is complete. At late stages, other mesenchyme cells (blastocoelar cells) are also present within the blastocoel and are migrating and fusing with one another. Fusion-competent blastocoelar cells and PMCs come into contact but do not fuse with one another, indicating that these two cell types fuse by distinct mechanisms. When secondary mesenchyme cells convert to a skeletogenic fate they alter their fusogenic properties and join the PMC syncytium, as shown by transfer of fluorescent dextran. Our analysis has provided a detailed picture of the cellular basis and regulation of mesodermal cell fusion and has important implications regarding molecular mechanisms that underlie fusion

Thermal decomposition of foundry resins: A determination of organic products by thermogravimetry–gas chromatography–mass spectrometry (TG–GC–MS)

AbstractThe article presents the results of research on thermal decomposition of Ester-Cured Alkaline Phenolic No-Bake (ALPHASET) binders used in molding technology. In the ALPHASET system phenol-formaldehyde resin of resole type is cured with a liquid mixture of esters. Under the influence of the molten metal the thermal decomposition of the binder follows, resulting in the evolution of gases, often harmful, e.g. from benzene, toluene, ethylbenzene and xylenes (BTEX) or Polycyclic Aromatic Hydrocarbon (PAH) groups. The identification of gases evolved during the pyrolysis of the binders was carried out and their decomposition temperatures were determined using the Thermogravimetry–Gas Chromatography–Mass Spectrometry (TG–GC–MS) technique. The tests were subjected to two types of binders from different manufacturers. Among the products of pyrolysis there have been identified mainly benzene and its derivatives, and phenol and its derivatives. Compounds identified in pyrolytic gas are largely considered to be harmful to humans and the environment (some of the compounds are carcinogenic and mutagenic). The presented results of the TG–GC–MS measurements show that the applied analytic methods are feasible to perform a qualitative and also quantitative characterization of the binder samples

Zinc ferrite nanoparticles as perspective functional materials for applications in casting technologies

In this article it discuss on possible application of magnetic oxide nanoparticles, namely non-stoichiometric zinc ferrite nanoparticles as a functionalizing agent in foundry processes. Thermal analysis showed a weight loss of the sample at 1 273 K in an amount of 7,7 %, which is a result of the following processes taking place in different temperature ranges. Upon its thermal treatment Zn0,4Fe2,6O4 decomposes to zinc oxide and iron (III) oxide (first stage) and next to iron (II,III) oxide and oxygen (second stage). The degree of decomposition was expressed as Fe2+ / Fetotal. Mössbauer spectroscopy showed that the over 30 % of Fe3+ present in starting material was reduced to Fe2+

Thermal decomposition of foundry resins: A determination of organic products by thermogravimetry–gas chromatography–mass spectrometry (TG–GC–MS)

AbstractThe article presents the results of research on thermal decomposition of Ester-Cured Alkaline Phenolic No-Bake (ALPHASET) binders used in molding technology. In the ALPHASET system phenol-formaldehyde resin of resole type is cured with a liquid mixture of esters. Under the influence of the molten metal the thermal decomposition of the binder follows, resulting in the evolution of gases, often harmful, e.g. from benzene, toluene, ethylbenzene and xylenes (BTEX) or Polycyclic Aromatic Hydrocarbon (PAH) groups. The identification of gases evolved during the pyrolysis of the binders was carried out and their decomposition temperatures were determined using the Thermogravimetry–Gas Chromatography–Mass Spectrometry (TG–GC–MS) technique. The tests were subjected to two types of binders from different manufacturers. Among the products of pyrolysis there have been identified mainly benzene and its derivatives, and phenol and its derivatives. Compounds identified in pyrolytic gas are largely considered to be harmful to humans and the environment (some of the compounds are carcinogenic and mutagenic). The presented results of the TG–GC–MS measurements show that the applied analytic methods are feasible to perform a qualitative and also quantitative characterization of the binder samples

Mesenchymal cell fusion in the sea urchin embryo.

Mesenchymal cells of the sea urchin embryo provide a valuable experimental model for the analysis of cell-cell fusion in vivo. The unsurpassed optical transparency of the sea urchin embryo facilitates analysis of cell fusion in vivo using fluorescent markers and time-lapse three-dimensional imaging. Two populations of mesodermal cells engage in homotypic cell-cell fusion during gastrulation: primary mesenchyme cells and blastocoelar cells. In this chapter, we describe methods for studying the dynamics of cell fusion in living embryos. These methods have been used to analyze the fusion of primary mesenchyme cells and are also applicable to blastocoelar cell fusion. Although the molecular basis of cell fusion in the sea urchin has not been investigated, tools have recently become available that highlight the potential of this experimental model for integrating dynamic morphogenetic behaviors with underlying molecular mechanisms.</p

Thermal decomposition of foundry resins: A determination of organic products by thermogravimetry–gas chromatography–mass spectrometry (TG–GC–MS)

The article presents the results of research on thermal decomposition of Ester-Cured Alkaline Phenolic No-Bake (ALPHASET) binders used in molding technology. In the ALPHASET system phenol-formaldehyde resin of resole type is cured with a liquid mixture of esters. Under the influence of the molten metal the thermal decomposition of the binder follows, resulting in the evolution of gases, often harmful, e.g. from benzene, toluene, ethylbenzene and xylenes (BTEX) or Polycyclic Aromatic Hydrocarbon (PAH) groups. The identification of gases evolved during the pyrolysis of the binders was carried out and their decomposition temperatures were determined using the Thermogravimetry–Gas Chromatography–Mass Spectrometry (TG–GC–MS) technique. The tests were subjected to two types of binders from different manufacturers. Among the products of pyrolysis there have been identified mainly benzene and its derivatives, and phenol and its derivatives. Compounds identified in pyrolytic gas are largely considered to be harmful to humans and the environment (some of the compounds are carcinogenic and mutagenic). The presented results of the TG–GC–MS measurements show that the applied analytic methods are feasible to perform a qualitative and also quantitative characterization of the binder samples

Zinc ferrite nanoparticles as perspective functional materials for applications in casting technologies

In this article it discuss on possible application of magnetic oxide nanoparticles, namely non-stoichiometric zinc ferrite nanoparticles as a functionalizing agent in foundry processes. Thermal analysis showed a weight loss of the sample at 1 273 K in an amount of 7,7 %, which is a result of the following processes taking place in different temperature ranges. Upon its thermal treatment Zn_0,4Fe_2,6O₄ decomposes to zinc oxide and iron (III) oxide (first stage) and next to iron (II,III) oxide and oxygen (second stage). The degree of decomposition was expressed as Fe²⁺ / Fe_total. Mössbauer spectroscopy showed that the over 30 % of Fe³⁺ present in starting material was reduced to Fe²⁺

Sleep deprivation before stroke is neuroprotective: A pre-ischemic conditioning related to sleep rebound

BACKGROUND AND AIM: We have previously shown in a rat model of focal cerebral ischemia that sleep deprivation after stroke onset aggravates brain damage. Others reported that sleep deprivation prior to stroke is neuroprotective. The main aim of this study was to test the hypothesis that the neuroprotection may be related to an increase in sleep (sleep rebound) during the acute phase of stroke. METHODS: Male Sprague Dawley rats (n=36) were subjected to continuous polygraphic recordings for baseline, total sleep deprivation (TSD), and 24h after ischemia. TSD for 6h was performed by gentle handling and immediately followed by ischemia. Focal cerebral ischemia was induced by permanent occlusion of distal branches of the middle cerebral artery. Control experiments included ischemia without SD (nSD) and sham surgery with TSD (n=6/group). RESULTS: Shortly after stroke, the amount of slow wave sleep (SWS) and paradoxical sleep (PS) increased significantly (p<0.05) in the TSD/ischemia, resulting in an increase in the total sleep time by 30% compared to baseline, or by 20% compared with the nSD/ischemia group. The infarct volume decreased significantly by 50% in the TSD/ischemia compared to nSD group (p<0.02). Removal of sleep rebound by allowing TSD-rats sleep for 24h before ischemia eliminated the reduction in the infarct size. CONCLUSION PRESTROKE: Sleep deprivation results in sleep rebound and reduces brain damage. Sleep rebound may be causally related to the neuroprotection