scholarly journals Effect of aluminium toxicity on the development of poplar (Populus tremula L. x P. alba L.) cultured in vitro

2014 ◽  
Vol 68 (4) ◽  
pp. 245-250 ◽  
Author(s):  
Krystyna Bojarczuk
Keyword(s):  
Aluminium Toxicity ◽  
Inhibitory Effect ◽  
Populus Tremula ◽  
Aluminium Chloride ◽  
Adventitious Bud ◽  
Aluminium Sulphate ◽  
Low Concentrations ◽  
The Media ◽  
High Concentrations

Adventitious bud cultures were established using vegetative buds from selected clones of poplar (<em>Populus tremula</em> L. x <em>P</em>. <em>alba</em> L.) as initial explants. For multiplication of shoots a modified Murashige and Skoog medium (MS) was used. Aluminium salts (aluminium sulphate and aluminium chloride) were added to the media. It was found that the pH of the medium had no effect on the development of cultures at low concentrations of nutrients (1/2 or 1/4 MS). Low concentrations of aluminium (Al 25mg•dm<sup>-3</sup> supplied as aluminium sulphate, Al 15 mg•dm<sup>-3</sup> as aluminium chloride) had no inhibitory effect on shoot development but decreased regeneration of adventitious roots. High concentrations of aluminium inhibited the development of shoots and roots, especially in a medium at pH 4.5. Microcuttings rooted in the highest percentage and formed the strongest rooting system on 1/4 strength MS medium at pH 4.5. It was found that there was no difference between the rooting of shoots excised from cultures cultivated with or without A1 in this medium at pH 5.5.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Ticlopidine Selectively Inhibits Human Platelet Responses to Adenosine Diphosphate

1991 ◽  
Vol 66 (06) ◽  
pp. 694-699 ◽  
Author(s):  
Marco Cattaneo ◽  
Benjaporn Akkawat ◽  
Anna Lecchi ◽  
Claudio Cimminiello ◽  
Anna M Capitanio ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Clot Retraction ◽  
Fibrinogen Binding ◽  
Low Concentrations ◽  
Binding Inhibition ◽  
High Concentrations ◽  
Formalin Fixed

SummaryPlatelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrihogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPIIb/IIIa monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their K d were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.

HIGH CONCENTRATIONS OF HEPARIN ARE MORE INHIBITORY TO PLATE- AGGREGATION IN-VITRO THAN ARE LOW MOLECULAR WEIGHT HEPARINS AND HEPARINOIDS AT THE SAME CONCENTRATION

1987 ◽  
Author(s):  
H Messmore ◽  
B Griffin ◽  
J Seghatchian ◽  
E Coyne
Keyword(s):  
Molecular Weight ◽  
Heparan Sulfate ◽  
Dermatan Sulfate ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Low Molecular Weight ◽  
Low Concentrations ◽  
High Concentrations ◽  
Induced Aggregation

Other investigators have shown that heparin in the usual therapeutic range (0.1-0.5 units/ml) has an enhancing effect on ADP aggregation and an inhibitory effect on collagen and thrombin induced aggregation. The effects of low molecular weight heparin (LMWH)and heparinoids (dermatan sulfate, heparan sulfate) on platelet aggregation have not been as extensivelystudied. We have utilized citrated platelet rich plasma (3.2%citrate-whole blood 1:9) drawn in plastic and adjusted to a final platelet count of 250,000/ul. A Bio-Data 4 channgl aggregometer was utilized with constantstirring at 37 C. The reaction was allowed to run for 20 minutes. Platelet rich plasma was supplemented 1:9 with saline or heparin and various agonists were then added ifno aggregation occurred. ADP, collagen, thrombin, ristocetin and serum from patients with heparin inudced thrombocytopenia (HIT) were utilized as agonists. Heparin was substituted at concentrations of 0.1 to 500 units per ml and various LMWH and heparinoids were substituted in equivalent anti-Xa or gravimetric concentrations. At low concentrations no inhibitory effect on any ofthe agonists was observed with any of the heparins or heparinoids. At concentrations of heparin of 100 u/ml or greater, all agonists were inhibited. At equivalent concentrations of five different LMWH (Cy 216, Cy 222, Pk 10169, Kabi 2165 and pentasaccharide) inhibition did notoccur at all or at very high concentions only. Dermatan sulfate and heparan sulfate inhibited only at high concentrations. HIT serum could not aggregate platelets with dermatan sulfate or pentasaccharide atany concentrations, but it was a good agonist with the other heparins and heparinoids.

scholarly journals A proteinaceous organic matrix regulates carbonate mineral production in the marine teleost intestine

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Kevin L. Schauer ◽  
Christophe M. R. LeMoine ◽  
Adrian Pelin ◽  
Nicolas Corradi ◽  
M. Danielle McDonald ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Organic Matrix ◽  
Magnesium Content ◽  
Inhibitory Effect ◽  
Marine Teleost ◽  
Low Concentrations ◽  
The Matrix ◽  
Mineral Production ◽  
High Concentrations

AbstractMarine teleost fish produce CaCO3in their intestine as part of their osmoregulatory strategy. This precipitation is critical for rehydration and survival of the largest vertebrate group on earth, yet the molecular mechanisms that regulate this reaction are unknown. Here, we isolate and characterize an organic matrix associated with the intestinal precipitates produced by Gulf toadfish (Opsanus beta). Toadfish precipitates were purified using two different methods, and the associated organic matrix was extracted. Greater than 150 proteins were identified in the isolated matrix by mass spectrometry and subsequent database searching using anO. betatranscriptomic sequence library produced here. Many of the identified proteins were enriched in the matrix compared to the intestinal fluid, and three showed no substantial homology to any previously characterized protein in the NCBI database. To test the functionality of the isolated matrix, a micro-modifiedin vitrocalcification assay was designed, which revealed that low concentrations of isolated matrix substantially promoted CaCO3production, where high concentrations showed an inhibitory effect. High concentrations of matrix also decreased the incorporation of magnesium into the forming mineral, potentially providing an explanation for the variability in magnesium content observed in precipitates produced by different fish species.

scholarly journals Effect of aluminium on in vitro rooting of birch (Betula pendula Roth.) and poplar (Populus tremula L. x P. alba L.) microcuttings

2014 ◽  
Vol 69 (4) ◽  
pp. 251-255 ◽  
Author(s):  
Krystyna Bojarczuk
Keyword(s):  
Adventitious Roots ◽  
Betula Pendula ◽  
In Vitro Cultures ◽  
Populus Tremula ◽  
Aluminium Chloride ◽  
Ms Medium ◽  
Aluminium Sulphate ◽  
Rooting Medium ◽  
Negative Effect

Poplar (<em>Populus tremula</em> L. x <em>P. alba</em> L.) and birch (<em>Betula pendula</em> Roth.) microcuttings obtained from in vitro cultures on media with aluminium (Al+) or without aluminium (Al-) were rooted in perlite saturated with a liquid 1/4 MS medium. Aluminium was added to the rooting medium in the form of aluminium sulphate or aluminium chloride. In the control, i.e. in the medium without aluminium, Al+ and Al- shoots usually developed similarly. Addition of aluminium to the rooting medium had a negative effect on the development of adventitious roots. Poplar and birch shoots obtained from cultures on media with aluminium (AI+) were distinguished by a greater tolerance of aluminium in the medium than shoots obtained from cultures on media without aluminium (A1-).

Azotaemic Inhibition of Organic Anion Transport in the Kidney of the Rat: Mechanisms and Characteristics

1971 ◽  
Vol 40 (2) ◽  
pp. 159-169 ◽  
Author(s):  
E. P. Orringer ◽  
F. R. Weiss ◽  
H. G. Preuss
Keyword(s):  
Rat Kidney ◽  
Organic Anion ◽  
Anion Transport ◽  
Renal Transport ◽  
Organic Anion Transport ◽  
Kidney Slices ◽  
Low Concentrations ◽  
The Media ◽  
High Concentrations

1. While azotaemic sera depressed the in-vitro Na-iodohippurate transport of rat kidney slices at any concentration, normal sera excited transport at low concentrations and depressed transport at high concentrations. The depression of transport by azotaemic sera was partially overcome by neomycin feeding in contrast to the depression by normal sera, which was not altered by neomycin feeding. 2. Plotting the reciprocal of sodium-iodohippurate accumulated by slices against the reciprocal of the media concentrations of sodium iodohippurate suggested that the depression of hippurate transport produced by normal and azotaemic sera was competitive in nature. 3. Normal sera slowed the efflux of Na-iodohippurate from kidney slices while azotaemic sera affected it very little. 4. The depression produced by normal and azotaemic sera and the stimulation produced by low concentrations of normal sera were seen with serum ultrafiltrates and dialysates, and after passage through cation exchange columns, but not anion exchange columns. 5. The effects on Na-iodohippurate accumulation by normal and azotaemic sera could be reproduced with metabolizable (lactate), and nonmetabolizable (hippurate) organic anions as well as combinations of these. 6. The implications of these observations on the altered renal transport of Na-iodohippurate produced by azotaemic and normal sera are discussed.

A biphasic effect of noradrenaline on renin release from rat juxtaglomerular cells in vitro is mediated by α1- and β-adrenoceptors

1992 ◽  
Vol 132 (1) ◽  
pp. 133-140 ◽  
Author(s):  
M. Takagi ◽  
K. Atarashi ◽  
H. Matsuoka ◽  
T. Sugimoto
Keyword(s):  
Dynamic Balance ◽  
Inhibitory Effect ◽  
Renin Release ◽  
Dependent Manner ◽  
Adrenergic Stimulation ◽  
Cortical Cells ◽  
Adrenoceptor Antagonist ◽  
Low Concentrations ◽  
High Concentrations

ABSTRACT The direct effect of noradrenaline on renin release from juxtaglomerular (JG) cells in vitro were investigated in a dynamic superfusion system of dispersed rat renal cortical cells. At low concentrations (1–100 nmol/l), noradrenaline stimulated renin release in a dose-dependent manner, while at higher concentrations (0·1–1 mmol/l) it inhibited renin release. The stimulatory effect of 0·1 μmol noradrenaline/l was completely blocked by a β-adrenoceptor antagonist, propranolol (0·1 μmol/l). When applied at concentrations of 1 μmol/l or 10 μmol/l, noradrenaline had no consistent effect on renin release, although 10 μmol noradrenaline/l had an inhibitory effect in the presence of propranolol (0·1 μmol/l). The inhibitory effect of noradrenaline (0·1 mmol/l) was converted to a stimulatory effect by the addition of an α1-adrenoceptor antagonist (bunazosin, 1 μmol/l), but was not altered by the addition of an α2-adrenoceptor antagonist (yohimbine, 1 μmol/l). These results indicate that low concentrations of noradrenaline directly stimulate renin release from JG cells by the activation of β-adrenoceptors, while high concentrations of nor-adrenaline inhibit renin release by the activation of α1-adrenoceptors. Accordingly, a dynamic balance may exist between β-adrenergic stimulation and α1-adrenergic depression of renin release. Journal of Endocrinology (1992) 132, 133–140

Aggregation of Cat Platelets in Vitro

1970 ◽  
Vol 23 (03) ◽  
pp. 601-620 ◽  
Author(s):  
Th. B Tschopp
Keyword(s):  
Adenosine Monophosphate ◽  
Blood Collection ◽  
Base Line ◽  
Reversible Aggregation ◽  
Low Concentrations ◽  
Irreversible Aggregation ◽  
High Concentrations ◽  
Two Phases ◽  
Improved Technique

SummaryAggregation of cat platelets in the citrated plasma is examined by means of Born’s absorptiometer. A marked tendency of the platelets of this species to spontaneous aggregation necessitated first of all the development of an improved technique of blood collection.A hypothesis according to which 5-HT is released from the platelets, explains the absence of oscillations on the base line of the absorptiometer, the absence of platelet swelling, when ADP is added, and the effect of stirring on the aggregation curves in cat PRP. The average volume of cat platelets amounts to 10.46 μ3 when directly fixed in the blood, when fixed from PRP to 12.17 μ3, when fixed from stirred PRP to 13.51 μ3.In low concentrations (0.3-2 μM) ADP produce reversible aggregation; in narrowly restricted, individually dissimilar mean concentrations irreversible aggregation in two phases and in high concentrations, irreversible aggregation in one phase. Like ADP serotonin produces 2 phase irreversible aggregation in concentrations of 3-10 μM, but unlike ADP, the aggregation velocity decreases again with high 5-HT concentrations (>100 μM). Adrenaline does not produce aggregation and it is likely that adenosine and adenosine monophosphate inhibit the aggregation by serotonin but not by ADP. Species differences in the aggregation of human, rabbit and cat platelets are discussed.

Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

1982 ◽  
Vol 47 (02) ◽  
pp. 150-153 ◽  
Author(s):  
P Han ◽  
C Boatwright ◽  
N G Ardlie
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Antiarrhythmic Drugs ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Second Phase ◽  
Ionophore A23187 ◽  
High Concentrations ◽  
Artery Disease

SummaryVarious cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic add whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregation induced by the ionophore A23187.

Functional Involvement of Thrombospondin in Platelet Aggregation Induced by Low Versus High Concentrations of Thrombin

1986 ◽  
Vol 55 (01) ◽  
pp. 136-142 ◽  
Author(s):  
K J Kao ◽  
David M Shaut ◽  
Paul A Klein
Keyword(s):  
Platelet Aggregation ◽  
Binding Sites ◽  
Inhibitory Effect ◽  
Activated Platelets ◽  
Low Concentrations ◽  
Platelet Binding ◽  
Functional Involvement ◽  
Thrombin Activation ◽  
Platelet Aggregates ◽  
High Concentrations

SummaryThrombospondin (TSP) is a major platelet secretory glycoprotein. Earlier studies of various investigators demonstrated that TSP is the endogenous platelet lectin and is responsible for the hemagglutinating activity expressed on formaldehyde-fixed thrombin-treated platelets. The direct effect of highly purified TSP on thrombin-induced platelet aggregation was studied. It was observed that aggregation of gel-filtered platelets induced by low concentrations of thrombin (≤0.05 U/ml) was progressively inhibited by increasing concentrations of exogenous TSP (≥60 μg/ml). However, inhibition of platelet aggregation by TSP was not observed when higher than 0.1 U/ml thrombin was used to activate platelets. To exclude the possibility that TSP inhibits platelet aggregation by affecting thrombin activation of platelets, three different approaches were utilized. First, by using a chromogenic substrate assay it was shown that TSP does not inhibit the proteolytic activity of thrombin. Second, thromboxane B2 synthesis by thrombin-stimulated platelets was not affected by exogenous TSP. Finally, electron microscopy of thrombin-induced platelet aggregates showed that platelets were activated by thrombin regardless of the presence or absence of exogenous TSP. The results indicate that high concentrations of exogenous TSP (≥60 μg/ml) directly interfere with interplatelet recognition among thrombin-activated platelets. This inhibitory effect of TSP can be neutralized by anti-TSP Fab. In addition, anti-TSP Fab directly inhibits platelet aggregation induced by a low (0.02 U/ml) but not by a high (0.1 U/ml) concentration of thrombin. In conclusion, our findings demonstrate that TSP is functionally important for platelet aggregation induced by low (≤0.05 U/ml) but not high (≥0.1 U/ml) concentrations of thrombin. High concentrations of exogenous TSP may univalently saturate all its platelet binding sites consequently interfering with TSP-crosslinking of thrombin-activated platelets.

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