scholarly journals Extensive release of methane from Arctic seabed west of Svalbard during summer 2014 does not influence the atmosphere

2016 ◽  
Vol 43 (9) ◽  
pp. 4624-4631 ◽  
Author(s):  
C. Lund Myhre ◽  
B. Ferré ◽  
S. M. Platt ◽  
A. Silyakova ◽  
O. Hermansen ◽  
...  
Keyword(s):  
Extensive Release

Properties of Washed Human Platelets

1977 ◽  
Vol 37 (02) ◽  
pp. 291-308 ◽  
Author(s):  
Raelene L Kinlough-Rathbone ◽  
J Fraser Mustard ◽  
Marian A Packham ◽  
Dennis W Perry ◽  
Hans-Joachim Reimers ◽  
...  
Keyword(s):  
Major Effect ◽  
Human Platelets ◽  
Immune Serum ◽  
Immune Serum Globulin ◽  
Serum Globulin ◽  
Platelet Adherence ◽  
Low Concentrations ◽  
Induced Aggregation ◽  
Extensive Release ◽  
Protein Free Medium

SummaryWe have shown previously that washed human platelets resuspended in Tyrode solution containing albumin and apyrase maintain their disc shape and their ability to aggregate upon the addition of low concentrations of ADP, providing fibrinogen is added to the suspending medium. We have now examined their responses to other aggregating and release-inducing agents. Collagen, arachidonate, thrombin, immune serum globulin, the ionophore A 23, 187 and phytohaemagglutinin from Phaseolus vulgaris caused aggregation and release of granule contents. The response to adrenaline was variable. Serotonin caused the platelets to change shape but no aggregation or release occurred. Addition of a small amount of plasma was necessary for ristocetin-induced aggregation. Polylysine caused immediate platelet-to-platelet adherence with little or no release of granule contents. Responses to collagen or thrombin were greater in a modified medium containing magnesium but no calcium; in this medium, aggregation caused by ADP or polylysine was followed by the release of granule contents whereas these agents caused aggregation without release in a medium with both calcium and magnesium. When protein was omitted from the suspending medium, platelet aggregation in response to ADP was variable. In this medium, collagen and thrombin caused more extensive release than in the albumin-containing medium. Aggregation by polylysine was accompanied by release and extensive lysis in the protein-free medium. Thus, the composition of the final resuspending medium has a major effect on the responses of washed human platelets to aggregating agents.

scholarly journals CYTOLOGICAL AND PHARMACOLOGICAL OBSERVATIONS ON THE RELEASE OF HISTAMINE BY MAST CELLS

1954 ◽  
Vol 100 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Don W. Fawcett
Keyword(s):  
Mast Cells ◽  
Peritoneal Fluid ◽  
Appreciable Amount ◽  
Fluid Solution ◽  
Tyrode Solution ◽  
Morphological Effect ◽  
Liberation Of Histamine ◽  
To Come ◽  
Histamine Liberator ◽  
Extensive Release

Experimental solutions known to affect mast cells or to cause liberation of histamine from the tissue were introduced into the peritoneal cavity of rats. Samples of the peritoneal fluid were withdrawn at intervals afterward and assayed for histamine and the condition of the mast cells was subsequently ascertained by microscopic examination of stained spreads of the mesenteries. Intraperitoneal injection of distilled water caused osmotic disruption of the mast cells and the appearance of an appreciable amount of histamine in the peritoneal fluid. Injection of Tyrode solution alone was not particularly damaging to the mast cells and little or no histamine was released. Injection of Tyrode solution containing compound 48/80 resulted in extensive release of granules from mast cells and the appearance of large amounts of histamine in the fluid. Solution of 48/80 failed however to cause histamine release when injected into rats whose subserosal mast cells had previously been destroyed. A series of increasing doses of compound 48/80 had a graded morphological effect upon mast cells and resulted in a graded increase in the amount of histamine that appeared in the peritoneal fluid. It is unlikely therefore that this compound acts by simply lysing the plasma membrane. It is concluded that mast cells in the rat are extraordinarily rich in histamine which is liberated under conditions which cause mast cells to release their granules. The histamine set free by the potent histamine liberator, compound 48/80, appears to come principally from the tissue mast cells.

A PLASMA FACTOR FROM A PATIENT WITH A BLEEDING TENDENCY CAUSES PLATELET SECRETION IN THE ABSENCE OF EXTRACELLULAR CALCIUM

1987 ◽  
Author(s):  
S R Cockbill ◽  
S Heptinstall ◽  
H B Burmester
Keyword(s):  
Protein A ◽  
Ion Exchange Resin ◽  
Bleeding Tendency ◽  
Clotting Factors ◽  
Platelet Suspension ◽  
Normal Platelet ◽  
Plasma Factor ◽  
Extensive Release ◽  
Platelet Secretion

A woman with a history of bruising and bleeding but with a normal platelet count and normal clotting factors, had platelets that appeared grey when stained and viewed under the microscope. Unlike the grey-platelet syndrome, the abnormality was only evident when the blood had been collected into EDTA andnot when citrate or heparin was used as anticoagulant. When we examined the EDTA-blood further we found that large quantities of beta-thromboglobulin andserotonin (5HT) were present in the plasma with only small quantities in the platelets. Hie reverse was the case for blood collected into citrate or heparin. LDH (a cytoplasmic marker) levels in EDTA-plasma were not raised.Platelet-rich plasma (PRP) was prepared from blood collected into heparin and labelled with ^-4C-5HT. Incubating the PRP with EDTA (4mM) or EGTA (3mM, sufficient to chelate all the plasma calcium but not the magnesium) caused extensive release of 14C-5HT from the platelets. When Ca++ was removed by passing the PRP through an ion-exchange resin, extensive 14C-5HT release also occurred. Hie release reaction induced by exposing the platelets to a low-Ca++ environment could be prevented by agents that increase cAMP levels.In a series of cross-over experiments, we discovered that the platelet secretion that occurred on removing Ca++ was caused by a plasma factor. Platelets from a healthy donor which had been labelled with 14C-5HT were resuspended in the patient's heparinised plasma. Incubating the platelet suspension with EGTA resulted in extensive release of 14C-5HT. Heparinised plasma from the patient was also passed through a column of Protein A-Sepharose to remove the immunoglobulin fraction. EGTA-challengof control platelets resuspended in the eluted plasma did not cause any release of 14C-5HT, suggesting that the plasma factor responsible may be an immunoglobulin.We have yet to discover whether this new abnormality (that on initial investigation could be confused with the grey-platelet syndrome) has any relevance to the in vivo bleeding situation in the patient in whom it was discovered.

Deaggregation of In Vitro-Degranulated Human Platelets: Irreversibility of Aggregation May Be Agonist-Specific Rather Than Related to Secretion Per Se

1987 ◽  
Vol 58 (03) ◽  
pp. 899-904 ◽  
Author(s):  
Joan E Bauman ◽  
H Joachim Reimers ◽  
J Heinrich Joist
Keyword(s):  
Proteolytic Enzymes ◽  
Human Platelets ◽  
Prolonged Incubation ◽  
Gentle Agitation ◽  
Other Substances ◽  
Irreversible Aggregation ◽  
Per Se ◽  
Extensive Release ◽  
Dependent Interaction

SummaryBased on studies with thrombin, it has been proposed that human platelets exposed to strong release-inducing agents undergo irreversible aggregation and cannot be deaggregated without the use of proteolytic enzymes. We tested the hypothesis that irreversible human platelet aggregation occurs as a result of thrombin-specific platelet alterations rather than induction of the release reaction per se. Washed human platelets were exposed to either thrombin (THR) or the aminophospholipid N-(7-Nitro- 2,1,3-benzoxydiazol-4-yl) phosphatidylserine (NBD-PS) for 20 seconds. Both agents caused similarly extensive release of platelet dense- and α-granule contents. After neutralization of thrombin and NBD-PS, and addition of PGE1 and apyrase, the platelets were sedimented, resuspended and incubated at 37° C with gentle agitation. Single, disc-shaped, degranulated platelets which were recovered in both systems were capable of aggregation in response to a second exposure to aggregating and release- inducing stimuli. Deaggregation was more rapid, more extensive, and more reproducible with NBD-PS- than with THR-degranulated platelets. Platelets exposed to thrombin for longer than 20 seconds showed a progressive loss of deaggregability which was not observed after prolonged incubation with NBD-PS. These findings do not support the concept that extensive secretion per se causes irreversible aggregation of human platelets. Instead it appears that formation of irreversible linkages between platelets involves the specific, time-dependent interaction of THR with platelets, released fibrinogen and possibly one or more other substances secreted from platelets.

Total Stromal Fraction (TSF) - Fortified Adipose tissue-derived Stem Cells Source: An Emerging Regenerative Realm Against COVID-19 Induced Pulmonary Compromise

Coronaviruses ◽  
2021 ◽  
Vol 02 ◽  
Author(s):  
Madhan Jeyaraman ◽  
Sathish Muthu ◽  
Rashmi Jain ◽  
Ajay SS ◽  
Neha Garg ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Distress Syndrome ◽  
Signs And Symptoms ◽  
Lung Damage ◽  
Cell Based Therapy ◽  
Co Morbidity ◽  
Seasonal Flu ◽  
Systemic Manifestations ◽  
Extensive Release ◽  
Specific Antiviral Therapy

: The inception of the COVID-19 pandemic has jeopardized humanity with markedly dampening of worldwide resources. The viral infection may present with varying signs and symptoms, imitating pneumonia and seasonal flu. With a gradual course, this may progress and result in the deadliest state of acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Moreover, following recovery from the severe brunt of COVID-19 infection, interstitial portions of alveoli have been found to undergo residual scarring and further to have compromised air exchange. Such alterations in the lung microenvironment and associated systemic manifestations have been recognized to occur due to the extensive release of cytokines. The mortality rate increases with advancing age and in individuals with underlying co-morbidity. Presently, there is no availability of specific antiviral therapy or any other definitive modality to counter this progressive worsening. However, we believe principles and advancing cell-based therapy may prove fruitful in subjugating such reported worsening in these patients. This article reviews eminent knowledge and relevant advancements about the amelioration of lung damage due to COVID-19 infection using adipose tissue-derived – total stromal fraction (TSF).

Phthalocyanine 4 photodynamic therapy-induced apoptosis of mouse L5178Y-R cells results from a delayed but extensive release of cytochrome c from mitochondria

2001 ◽  
Vol 165 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Song-Mao Chiu ◽  
Helen H. Evans ◽  
Minh Lam ◽  
Anna-Liisa Nieminen ◽  
Nancy L. Oleinick
Keyword(s):  
Photodynamic Therapy ◽  
Cytochrome C ◽  
Induced Apoptosis ◽  
Extensive Release

Extensive Release. Excessive Storage

Lysosomes ◽  
1989 ◽  
pp. 319-361
Author(s):  
Eric Holtzman
Keyword(s):  
Extensive Release

Deaggregation of Human Platelets Aggregated by Thrombin

1985 ◽  
Vol 53 (01) ◽  
pp. 042-044 ◽  
Author(s):  
R L Kinlough-Rathbone ◽  
D W Perry ◽  
M A Packham ◽  
J F Mustard
Keyword(s):  
Antithrombin Iii ◽  
Human Platelets ◽  
The Other ◽  
Release Reaction ◽  
Fibrinogen Receptor ◽  
Extensive Release

SummaryHuman platelets that have undergone the release reaction do not deaggregate readily. We examined conditions under which washed human platelets can be deaggregated after they have undergone an extensive release reaction induced by thrombin (1 or 5 U/ml). To make fibrinogen receptors unavailable, either CP/ CPK (or apyrase) was used to remove released ADP, or PGEi was used to increase cAMP. Chymotrypsin was used to digest proteins that might link platelets, and heparin to interact with released proteins and interfere with their binding to platelets and to each other. Individually, none of these caused deaggregation; heparin did not inhibit the effect of thrombin because no antithrombin III was present. Platelets exposed to thrombin (1 U/ ml) which was neutralized at 90 sec by hirudin, could be deaggregated by combinations of CP/CPK (or apyrase) and chymotrypsin, or PGE1 and chymotrypsin. When a higher concentration of thrombin was used (5 U/ml) these combinations caused platelets to deaggregate only when heparin was added before thrombin induced the release reaction. Thus, when extensive release occurs three mechanisms may come into play to link human platelets: one that requires the fibrinogen receptor; a heparin-sensitive reaction that may involve the binding of released proteins; and a linkage that can be disrupted only by proteolysis, providing the other two mechanisms are also inhibited.

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