Calcium uptake by sarcoplasmic reticulum from nerve-intact and standard skeletal muscle grafts

A freely grafted rat soleus muscle exhibits a decrease in velocity and capacity of SR calcium uptake. This deficit is not prevented by maintaining neural connections (nerve-intact graft) during grafting. Thus the greater mechanical capability of nerve-intact grafts, relative to standard grafts, is not accompanied by any enhancement of the SR tubules.     

Satellite cells in the regenerated and regrafted skeletal muscles of rats

Summary Soleus (SOL) muscles were grafted into extensor digitorum longus (EDL) muscle beds (EDL-first-graft). Sixty days later, some mature EDL-first-grafts were regrafted into their own beds (EDL-second-grafts). Fully regenerated muscle fibers and satellite cells were observed in both types of mature grafts. The ratios of satellite cell nuclei per total nuclei (myonuclei and satellite cell nuclei) were 4.81±0.47% for EDL-2nd graft, 4.26±0.51% for EDL-1st-graft, 4.30±0.33% for control SOL, and 3.30±0.18% for control EDL. It is thought that satellite cells are required for the repeated activity of muscle fiber regeneration. The persistance of satellite cells in EDL-second-grafts suggests that satellite cells are not depleted during the first grafting, making second-grafts possible.     

Hyperprolactinemia and estrogen-induced rhythms in LH and prolactin release in the ovariectomized rat

Summary Short-term (9 days) hyperprolactinemia induced by pituitary grafts reduced basal plasma LH levels in ovariectomized rats whereas long-term (31 days) grafts increased basal LH levels. Although long-term grafts inhibited estradiol-induced prolactin surges, hyperprolactinemia had no effect on the LH surge. It is concluded that the estrogen-treated ovariectomized rat is not suitable for studying the effects of hyperprolactinemia on LH release.     

Hyperprolactinemia and estrogen-induced rhythms in LH and prolactin release in the ovariectomized rat

Short-term (9 days) hyperprolactinemia induced by pituitary grafts reduced basal plasma LH levels in ovariectomized rats whereas long-term (31 days) grafts increased basal LH levels. Although long-term grafts inhibited estradiol-induced prolactin surges, hyperprolactinemia had no effect on the LH surge. It is concluded that the estrogen-treated ovariectomized rat is not suitable for studying the effects of hyperprolactinemia on LH release.     

Calcium release from frog sarcoplasmic reticulum by an imidazolyl reagent

Calcium is released from the isolated heavy sarcoplasmic reticulum (SR) of frog skeletal muscle upon application of 0.1-1 mM diethylpyrocarbonate (DEP, an imidazolyl reagent). The Ca-ATPase activity of SR was suppressed by 20% in the presence of 1 mM DEP. More than 1 mM of free magnesium ion or 5 microM ruthenium red eliminated the effect of DEP on calcium release but not on Ca-ATPase activity. A plausible site of DEP action is on the calcium channel.     

Calcium release from frog sarcoplasmic reticulum by an imidazolyl reagent

Summary Calcium is released from the isolated heavy sarcoplasmic reticulum (SR) of frog skeletal muscle upon application of 0.1–1 mM diethylpyrocarbonate (DEP, an imidazolyl reagent). The Ca-ATPase activity of SR was suppressed by 20% in the presence of 1 mM DEP. More than 1 mM of free magnesium ion or 5 M ruthenium red eliminated the effect of DEP on calcium release but not on Ca-ATPase activity. A plausible site of DEP action is on the calcium channel.     

Ensemble Forecasting for Complex Time Series Using Sparse Representation and Neural Networks

Based on the concept of ‘decomposition and ensemble’, a novel ensemble forecasting approach is proposed for complex time series by coupling sparse representation (SR) and feedforward neural network (FNN), i.e. the SR‐based FNN approach. Three main steps are involved: data decomposition via SR, individual forecasting via FNN and ensemble forecasting via a simple addition method. In particular, to capture various coexisting hidden factors, the effective decomposition tool of SR with its unique virtues of flexibility and generalization is introduced to formulate an overcomplete dictionary covering diverse bases, e.g. exponential basis for main trend, Fourier basis for cyclical (and seasonal) features and wavelet basis for transient actions, different from other techniques with a single basis. Using crude oil price (a typical complex time series) as sample data, the empirical study statistically confirms the superiority of the SR‐based FNN method over some other popular forecasting models and similar ensemble models (with other decomposition tools). Copyright © 2016 John Wiley & Sons, Ltd.     

Biochemical events associated with rapid cellular damage during the oxygen-and calcium-paradoxes of the mammalian heart

Summary The O_2– and Ca²⁺-paradoxes have a number of features in common and it is suggested that release of cytosolic proteins in both paradoxes is initiated by the activation of a sarcolemma NAD(P)H dehydrogenase which can generate a transmembrane flow of H⁺ and e^– and also oxygen radicals or recox cycling which damage ion channels and membrane proteins (phase I). Entry of Ca²⁺ through the damaged ion channels then exacerbates the damage by further activating this system, either directly or indirectly, and the redox cycling and/or oxygen radicals cause further damage to integral and cytoskeletal proteins of the sarcolemma resulting in microdamage to the integrity of the membrane (phase II) and the consequent release or exocytosis of cytoplasmic proteins and, under specialised condition, the blebbing of the sarcolemma. The system may be primed either by removal of extracellular Ca²⁺ or by raising [Ca²⁺]_i by a variety of measures, these two actions being synergistic. The system is initially activated in the Ca²⁺-paradox by the membrane perturbation associated with removal of extracellular Ca²⁺; prolonged anoxia in the metabolically active cardiac muscle causes a depletion of the ATP supply, particularly in the absence of glucose, and hence a rise in [Ca²⁺]_i in phase I of the oxygen paradox with the consequent activation of the NAD(P)H oxidase at the sarcolemma. Oxygen radicals are probably generated in both paradoxes and may have a partial role in the genesis of damage, but are not essential in the Ca²⁺-paradox which continues under anoxia. Massive entry of Ca²⁺ also activates an intracellularly localised dehydrogenase (probably at the SR) which produces myofilament damage by redox cycling.     

Increases in frequency of sister chromatid exchange following tumor grafts in different immunocompetent hosts]

Measurement of sister chromatid exchanges (SCEs) frequency of inbred Rat or nu/nu Mice bone marrow cells, following tumour grafts, have been developed. Increase of SCEs was observed in hosts which present or not metases and with reduced survival rates after malignant tumour grafts. These results suggest a remote control of tumoral tissue by a diffused matter effect.     

Calcium and sodium distribution and movements in smooth muscle

Electron probe microanalysis (EPMA) has been used to study the subcellular distribution of Ca, Na, K, Cl, and Mg in smooth muscle. The EPMA results indicate that the sarcoplasmic reticulum (SR) is the major intracellular source and sink of activator Ca: norepinephrine decreases the Ca content of the junctional SR in portal vein smooth muscle. Mitochondria do not play a significant role in regulating cytoplasmic free Ca2+, but mitochondrial Ca content can be altered to a degree compatible with suggestions that fluctuations in matrix Ca contribute to the control of mitochondrial metabolism. The rise in total cytoplasmic Ca during a maintained, maximal contraction is very much greater than the rise in free Ca2+, and is probably in excess of the known binding sites available on calmodulin and myosin. Cell Ca is not increased in normal cells that are Na-loaded. The non-Donnan distribution of Cl is not due to compartmentalization, but reflects high cytoplasmic Cl. Na-loading of smooth muscle in K-free solutions is temperature dependent, and may exhibit cellular heterogeneity undetected by conventional techniques. The total cell Mg is equivalent to approximately 12 mM, and less than 50% of it can be accounted for by binding to ATP and to actin. Mitochondrial monovalent cations in smooth muscle are relatively rapidly exchangeable.     

Calcium and sodium distribution and movements in smooth muscle

Summary Electron probe microanalysis (EPMA) has been used to study the subcellular distribution of Ca, Na, K. Cl, and Mg in smooth muscle. The EPMA results indicate that the sarcoplasmic reticulum (SR) is the majorintracellular source and sink of activator Ca: norepinephrine decreases the Ca content of the junctional SR in portal vein smooth muscle. Mitochondria do not play a significant role in regulating cytoplasmic free Ca²⁺, but mitochondrial Ca content can be altered to a degree compatible with suggestions that fluctuations in matrix Ca contribute to the control of mitochondrial metabolism. The rise intotal cytoplasmic Ca during a maintained, maximal contraction is very much greater than the rise in free Ca²⁺, and is probably in excess of the known binding sites available on calmodulin and myosin. Cell Ca is not increased in normal cells that are Na-loaded. The non-Donnan distribution of Cl is not due to compartmentalization, but reflects high cytoplasmic Cl. Na-loading of smooth muscle in K-free solutions is temperature dependent, and may exhibit cellular heterogeneity undetected by conventional techniques. The total cell Mg is equivalent to approximately 12 mM, and less than 50% of it can be accounted for by binding to ATP and to actin. Mitochondrial monovalent cations in smooth muscle are relatively rapidly exchangeable.     

Calcium-induced calcium release mechanism in vascular smooth muscles — assessments based on contractions evoked in intact and saponin-treated skinned muscles

Summary This article was concerned with the role of Ca in triggering the contraction in vascular smooth muscles. Whenever Ca influx is activated, this Ca does not directly activate the contractile proteins, but rather triggers the release of Ca from the SR to activate calmodulin. This release of Ca by Ca is dependent on the amount of Ca stored within the cells.Voltage dependent Ca influx activated by excess concentrations of K, electrical depolarization and Ca spikes is required to produce the contraction through activation of the Ca-induced Ca release mechanism. The elucidation of the contribution of the P-I response for Ca mobilization through activation of receptors under physiological conditions hopefully will lend support to our hypothesis.     

Calcium-induced calcium release mechanism in vascular smooth muscles--assessments based on contractions evoked in intact and saponin-treated skinned muscles

This article was concerned with the role of Ca in triggering the contraction in vascular smooth muscles. Whenever Ca influx is activated, this Ca does not directly activate the contractile proteins, but rather triggers the release of Ca from the SR to activate calmodulin. This release of Ca by Ca is dependent on the amount of Ca stored within the cells. Voltage dependent Ca influx activated by excess concentrations of K, electrical depolarization and Ca spikes is required to produce the contraction through activation of the Ca-induced Ca release mechanism. The elucidation of the contribution of the P-I response for Ca mobilization through activation of receptors under physiological conditions hopefully will lend support to our hypothesis.     

Inductions cérébrales et médullaires chez les Oiseaux

Summary Two grafts of the Hensen's node, one young (stage 3) and the other older (stage 5+), were implanted into area opaca of the same blastoderm. The hosts were at stages 2, 3 and 4. The young grafts always elicited the formation of the brain. On the contrary, old grafts only induce very small spinal cords. Moreover, the frequency of spinal cord induction is lowest in the oldest hosts.     

Anandamide induces cell death independently of cannabinoid receptors or vanilloid receptor 1: possible involvement of lipid rafts

Anandamide triggers various cellular activities by binding to cannabinoid (CB1/CB2) receptors or vanilloid receptor 1 (VR1). However, the role of these receptors in anandamide-induced apoptosis remains largely unknown. Here, we show that SR141716A, a specific inhibitor of cannabinoid receptor (CB1-R), did not block anandamide-induced cell death in endogenously CB1-R expressing cells. In addition, CB1-R-lacking Chinese hamster ovary (CHO) cells underwent cell death after anandamide treatment. SR144528, a specific inhibitor of CB2-R also failed to block anandamide-induced cell death in HL-60 cells. Capsazepine, a specific antagonist of VR1 could not prevent anandamide-induced cell death in constitutively and endogenously VR1 expressing PC12 cells. Moreover, anandamide noticeably triggered cell death in VR1-lacking human embryonic kidney (HEK) cells. In contrast, methyl-beta cyclodextrin (MCD), a membrane cholesterol depletor, completely blocked anandamide-induced cell death in a variety of cells, including PC12, C6, Neuro-2a, CHO, HEK, SMC, Jurkat and HL-60 cells. MCD also blocked anandamide-induced superoxide generation, phosphatidyl serine exposure and p38 MAPK/JNK activation. Thus, our data imply a novel role for of membrane lipid rafts in anandamide-induced cell death.     

Engineering of arteries in vitro

This review will focus on two elements that are essential for functional arterial regeneration in vitro: the mechanical environment and the bioreactors used for tissue growth. The importance of the mechanical environment to embryological development, vascular functionality, and vascular graft regeneration will be discussed. Bioreactors generate mechanical stimuli to simulate biomechanical environment of arterial system. This system has been used to reconstruct arterial grafts with appropriate mechanical strength for implantation by controlling the chemical and mechanical environments in which the grafts are grown. Bioreactors are powerful tools to study the effect of mechanical stimuli on extracellular matrix architecture and mechanical properties of engineered vessels. Hence, biomimetic systems enable us to optimize chemo-biomechanical culture conditions to regenerate engineered vessels with physiological properties similar to those of native arteries. In addition, this article reviews various bioreactors designed especially to apply axial loading to engineered arteries. This review will also introduce and examine different approaches and techniques that have been used to engineer biologically based vascular grafts, including collagen-based grafts, fibrin-gel grafts, cell sheet engineering, biodegradable polymers, and decellularization of native vessels.     

Depression of spontaneous and ionophore-induced neurotransmitter release by Salmonella.

Exposure of frog neuromuscular junctions to heat-killed, lyophilized Salmonella typhimurium (SR 11) produces an early increase in spontaneous transmitter release followed by depression of release and blockade of the obligatory release usually induced by ionophore X537A.     

Prolongation of the survival of skin grafts in mice by PUVA treatment

The combined application of psoralen and UVA radiation to skin grafts induced a prolongation of the survival time of the grafts in mice. This was observed using the H-Y barrier, an allogeneic barrier without H-2 disparities, and a strong H-2 incompatible barrier. The effect is probably due to a reduction of antigen-presenting cells, or to other, unknown mechanisms.     

Prolongation of the survival of skin grafts in mice by PUVA treatment

Summary The combined application of psoralen and UVA radiation to skin grafts induced a prolongation of the survival time of the grafts in mice. This was observed using the H-Y barrier, an allogeneic barrier without H-2 disparities, and a strong H-2 incompatible barrier. The effect is probably due to a reduction of antigen-presenting cells, or to other, unknown mechanisms.     

Enhanced calcium accumulation related to increased protein phosphorylation in cardiac sarcoplasmic reticulum induced by cyclic 3′, 5′-AMP or isoproterenol

Zusammenfassung Die cAMP-abhängige Inkorporation von³²P in das sarkoplasmatische Reticulum (SR) wurde im Zusammenhang mit Ca-Akkumulation in Kontrollherzen und in Herzen 2 h nach in vivo Verabreichung von 7,5 mg/kg Isoproterenol gemessen und gezeigt, dass die Katecholamine den intrazellulären Kalziumtransport in vitro sowie in vivo über die cAMP-stimulierte und PK-abhängige Phosphorylierung einer Proteinfraktion des SR regulieren.