scholarly journals Heat treatment induces an increase in intracellular cyclic AMP content in human epidermoid A-431 cells

1991 ◽  
Vol 276 (3) ◽  
pp. 683-689 ◽  
Author(s):  
J G Kiang ◽  
Y Y Wu ◽  
M C Lin
Keyword(s):  
Heat Treatment ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
G Proteins ◽  
Phosphodiesterase Inhibitors ◽  
Metabolic Inhibitors ◽  
Thermally Induced ◽  
Heat Treated ◽  
Atp Breakdown ◽  
In Cells

The basal level of intracellular cyclic AMP (cAMPi) in A-431 cells incubated at 37 degrees C in Na(+)-containing Hanks solution is 2086 +/- 139 fmol/10(6) cells. When cells are exposed to 45 degrees C for 10 min, cAMPi increases by 40 +/- 4%, and then returns to basal levels within 30 min. Incubating cells in Ca(2+)-free or Mg(2+)-free Hanks solution has no effect on the heat-induced increase in cAMPi, but the increase is inhibited by acid-loading cells to intracellular pH 7.0 or 6.8. In unheated cells, cAMPi increases by 16 +/- 8%, 53 +/- 7%, or 39 +/- 8%, when incubated with isobutyl-1-methylxanthine (1 mM), Ro 20-1724 (0.5 mM), or theophylline (1 mM) respectively. However, heat treatment further elevates cAMPi in cells treated with phosphodiesterase inhibitors, indicating that heat treatment and phosphodiesterase inhibitors elevate cAMPi by a different pathway(s). Heat treatment increases adenylate cyclase activity 2.5-fold. When forskolin (150 microM), an adenylate cyclase stimulator, is applied to cells, the basal cAMPi increases 28 +/- 6-fold compared with controls. Subsequent heating of these cells lowers cAMPi levels to 7.0 +/- 0.5 times that in control cells. This decrease is prevented by pretreatment with pertussis toxin (30 ng/ml, 24 h), suggesting that G-proteins are involved in the process of heat-induced cAMPi increase. 2-Deoxy-D-glucose (10 mM), NaN3 (10 mM) and 2,4-dinitrophenol (1 mM) also increase cAMPi in A-431 cells. However, application of these metabolic inhibitors to cells before heat treatment does not result in cAMPi levels greater than that observed in cells with heat alone. Similar observations are obtained in heat-treated cells previously exposed to adenosine, but not to AMP or ADP. These data are the first to suggest that thermally induced increase in cAMPi is due to a combination of activation of adenylate cyclase and G-proteins, and an increase in adenosine owing to ATP breakdown caused by hyperthermia.

Effect of Heat Treatment on the Microstructure and Property of TiAl Alloys Prepared by Gas Atomization Powders

2013 ◽  
Vol 747-748 ◽  
pp. 497-501
Author(s):  
Na Liu ◽  
Zhou Li ◽  
Guo Qing Zhang ◽  
Hua Yuan ◽  
Wen Yong Xu ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Heat Treatment Temperature ◽  
Tial Alloy ◽  
Lamellar Microstructure ◽  
Treatment Temperature ◽  
Gas Atomization ◽  
Thermally Induced ◽  
Heat Treated ◽  
Fine Duplex ◽  
Step Heat Treatment

Powder metallurgical TiAl alloy was fabricated by gas atomization powders, and the effect of heat treatment temperature on the microstructure evolution and room tensile properties of PM TiAl alloy was investigated. The uniform fine duplex microstructure was formed in PM TiAl based alloy after being heat treated at 1250/2h followed by furnace cooling (FC)+ 900/6h (FC). When the first step heat treatment temperature was improved to 1360/1h, the near lamellar microstructure was achieved. The ductility of the alloy after heat treatment improved markedly to 1.2% and 0.6%, but the tensile strength decreased to 570MPa and 600MPa compared to 655MPa of as-HIP TiAl alloy. Post heat treatment at the higher temperature in the alpha plus gamma field would regenerate thermally induced porosity (TIP).

scholarly journals Resensitization of hepatocyte glucagon-stimulated adenylate cyclase can be inhibited when cyclic AMP phosphodiesterase inhibitors are used to elevate intracellular cyclic AMP concentrations to supraphysiological values

1988 ◽  
Vol 249 (2) ◽  
pp. 543-547 ◽  
Author(s):  
G J Murphy ◽  
M D Houslay
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Phosphodiesterase Inhibitor ◽  
Phosphodiesterase Inhibitors ◽  
Maximal Effect ◽  
Cyclic Amp Phosphodiesterase ◽  
Dose Dependent Fashion ◽  
Independent Process ◽  
Pre Treatment ◽  
Dose Dependent

Treatment of intact hepatocytes with glucagon led to the rapid desensitization of adenylate cyclase, which reached a maximum around 5 min after application of glucagon, after which resensitization ensued. Complete resensitization occurred some 20 min after the addition of glucagon. In hepatocytes which had been preincubated with the cyclic AMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), glucagon elicited a stable desensitized state where resensitization failed to occur even 20 min after exposure of hepatocytes to glucagon. Treatment with IBMX alone did not elicit desensitization. The action of IBMX in stabilizing the glucagon-mediated desensitized state was mimicked by the non-methylxanthine cyclic AMP phosphodiesterase inhibitor Ro-20-1724 [4-(3-butoxy-4-methoxylbenzyl)-2-imidazolidinone]. IBMX inhibited the resensitization process in a dose-dependent fashion with an EC50 (concn. giving 50% of maximal effect) of 26 +/- 5 microM, which was similar to the EC50 value of 22 +/- 6 microM observed for the ability of IBMX to augment the glucagon-stimulated rise in intracellular cyclic AMP concentrations. Pre-treatment of hepatocytes with IBMX did not alter the ability of either angiotensin or the glucagon analogue TH-glucagon, ligands which did not increase intracellular cyclic AMP concentrations, to cause the rapid desensitization and subsequent resensitization of adenylate cyclase. It is suggested that, although desensitization of glucagon-stimulated adenylate cyclase is elicited by a cyclic AMP-independent process, the resensitization of adenylate cyclase can be inhibited by a process which is dependent on elevated cyclic AMP concentrations. This action can be detected by attenuating the degradation of cyclic AMP by using inhibitors of cyclic AMP phosphodiesterase.

Heat-induced and other chemical changes in commercial UHT milks

2005 ◽  
Vol 72 (4) ◽  
pp. 442-446 ◽  
Author(s):  
Anthony J Elliott ◽  
Nivedita Datta ◽  
Boka Amenu ◽  
Hilton C Deeth
Keyword(s):  
Heat Treatment ◽  
Bovine Serum Albumin ◽  
Bovine Serum ◽  
Room Temperature ◽  
Whey Proteins ◽  
Thermally Induced ◽  
Heated Milk ◽  
Heat Treated ◽  
Induced Changes ◽  
Β Lactoglobulin

The properties of commercial directly and indirectly heated UHT milks, both after heating and during storage at room temperature for 24 weeks, were studied. Thermally induced changes were examined by changes in lactulose, furosine and acid-soluble whey proteins. The results confirmed previous reports that directly heated UHT milks suffer less heat damage than indirectly heated milk. During storage, furosine increased and bovine serum albumin in directly heat-treated milks decreased significantly. The changes in lactulose, α-lactalbumin and β-lactoglobulin were not statistically significant. The data suggest that heat treatment indicators should be measured as soon as possible after processing to avoid any misinterpretations of the intensity of the heat treatment.

scholarly journals Platelet adenylate cyclase and phospholipase C are affected differentially by ADP-ribosylation. Effects on thrombin-mediated responses

1988 ◽  
Vol 252 (1) ◽  
pp. 297-300 ◽  
Author(s):  
H S Banga ◽  
R K Walker ◽  
L K Winberry ◽  
S E Rittenhouse
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Phospholipase C ◽  
G Protein ◽  
G Proteins ◽  
Pertussis Toxin ◽  
Marked Decrease ◽  
Human Platelets ◽  
Adp Ribosylation

Thrombin stimulates phospholipase C and inhibits adenylate cyclase in human platelets. We have studied the effect of purified S1 monomer, the ADP-ribosylating subunit of pertussis toxin, on these receptor-coupled G-protein-dependent activities. ADP-ribosylation of a 41 kDa protein is associated with a marked decrease in the ability of thrombin to inhibit cyclic AMP formation, but has little effect on phospholipase C. Therefore adenylate cyclase and phospholipase C appear to be modulated by different G-proteins.

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

Effect of Some Metabolic Inhibitors on Vinblastine-Induced Ribosomal-Granular Material Complexes

1971 ◽  
Vol 29 ◽  
pp. 548-549
Author(s):  
Awtar Krishan ◽  
Dora Hsu
Keyword(s):  
Granular Material ◽  
Rna Synthesis ◽  
Culture Medium ◽  
Actinomycin D ◽  
Metabolic Inhibitors ◽  
Protein And Rna Synthesis ◽  
Apparent Reduction ◽  
Plant Alkaloids ◽  
In Cells

Cells exposed to antitumor plant alkaloids, vinblastine and vincristine sulfate have large proteinacious crystals and complexes of ribosomes, helical polyribosomes and electron-dense granular material (ribosomal complexes) in their cytoplasm, Binding of H3-colchicine by the in vivo crystals shows that they contain microtubular proteins. Association of ribosomal complexes with the crystals suggests that these structures may be interrelated.In the present study cultured human leukemic lymphoblasts (CCRF-CEM), were incubated with protein and RNA-synthesis inhibitors, p. fluorophenylalanine, puromycin, cycloheximide or actinomycin-D before the addition of crystal-inducing doses of vinblastine to the culture medium. None of these compounds could completely prevent the formation of the ribosomal complexes or the crystals. However, in cells pre-incubated with puromycin, cycloheximide, or actinomycin-D, a reduction in the number and size of the ribosomal complexes was seen. Large helical polyribosomes were absent in the ribosomal complexes of cells treated with puromycin, while in cells exposed to cycloheximide, there was an apparent reduction in the number of ribosomes associated with the ribosomal complexes (Fig. 2).

Effect of a Complex Heat Treatment on the Structure of 300M Steel

1981 ◽  
Vol 39 ◽  
pp. 312-313
Author(s):  
R. Padmanabhan ◽  
W. E. Wood
Keyword(s):  
Heat Treatment ◽  
Metal Carbides ◽  
Austenite Grain Size ◽  
300M Steel ◽  
Heat Treated ◽  
Strain Fracture ◽  
Prior Austenite Grain Size ◽  
Short Time ◽  
Final Tempering ◽  
Similar Yield

Intermediate high temperature tempering prior to subsequent reaustenitization has been shown to double the plane strain fracture toughness as compared to conventionally heat treated UHSLA steels, at similar yield strength levels. The precipitation (during tempering) of metal carbides and their subsequent partial redissolution and refinement (during reaustenitization), in addition to the reduction in the prior austenite grain size during the cycling operation have all been suggested to contribute to the observed improvement in the mechanical properties. In this investigation, 300M steel was initially austenitized at 1143°K and then subjected to intermediate tempering at 923°K for 1 hr. before reaustenitizing at 1123°K for a short time and final tempering at 583°K. The changes in the microstructure responsible for the improvement in the properties have been studied and compared with conventionally heat treated steel. Fig. 1 shows interlath films of retained austenite produced during conventionally heat treatment.

“In vitro” and in Animal Model Studies on a Double Virus- Inactivated Factor VIII Concentrate

1995 ◽  
Vol 74 (03) ◽  
pp. 868-873 ◽  
Author(s):  
Silvana Arrighi ◽  
Roberta Rossi ◽  
Maria Giuseppina Borri ◽  
Vladimir Lesnikov ◽  
Marina Lesnikov ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Animal Model ◽  
Factor Viii ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Virus Inactivation ◽  
Enveloped Viruses ◽  
Model Studies ◽  
Heat Treated

SummaryTo improve the safety of plasma derived factor VIII (FVIII) concentrate, we introduced a final super heat treatment (100° C for 30 min) as additional virus inactivation step applied to a lyophilized, highly purified FVIII concentrate (100 IU/mg of proteins) already virus inactivated using the solvent/detergent (SID) method during the manufacturing process.The efficiency of the super heat treatment was demonstrated in inactivating two non-lipid enveloped viruses (Hepatitis A virus and Poliovirus 1). The loss of FVIII procoagulant activity during the super heat treatment was of about 15%, estimated both by clotting and chromogenic assays. No substantial changes were observed in physical, biochemical and immunological characteristics of the heat treated FVIII concentrate in comparison with those of the FVIII before heat treatment.

The Increased Sensitivity of Platelets to Prostacyclin in Marathon Runners

1984 ◽  
Vol 51 (03) ◽  
pp. 385-387 ◽  
Author(s):  
Clive J Dix ◽  
David G Hassall ◽  
K Richard Bruckdorfer
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Platelet Rich Plasma ◽  
Marathon Runners ◽  
Inhibition Of Platelet Aggregation ◽  
Increased Sensitivity ◽  
Membrane Bound

SummaryPlatelet-rich plasma was obtained 24 hr after the race ended from athletes who ran in the London marathon. The platelets were only marginally less sensitive to adrenaline than were those of non-runners using conventional aggregation tests. However, the runners’ platelets were much more sensitive to inhibition by prostacyclin, a prostaglandin synthesized by endothelial cells. It appeared that this effect was due to a greater activity in the platelets of the membrane-bound adenylate cyclase enzyme which generates intracellular cyclic AMP. Cyclic AMP production is known to be stimulated by prostacyclin and to cause the inhibition of platelet aggregation. The results indicate another possible protective effect of exercise against cardiovascular disease which is independent of the known changes in lipoprotein concentrations previously observed in athletes.

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