Biomedical subjects

L Sjödin

Publications and source records attributed to L Sjödin.

At least 19 recordsLinked to original sources

PubMed2001

[Hepatitis B outbreak in a day care center affected several families. It could have been prevented by vaccination of all children].

An outbreak of hepatitis B originating in a family day nursery affected several children with Somali background. The transmission chain was confirmed by sequence analysis of the S gene. In Africa hepatitis B is often spread horizontally among children of pre-school age, a pattern of transmission that was retained in this outbreak. To limit the outbreak 126 children in the nursery and 50 members of staff had to be vaccinated. The total cost for this intervention was estimated to about 300,000 SEK. Considering the great number of immigrants in Sweden from areas highly endemic for hepatitis B the inclusion of vaccination in the general child immunisation program seems to be the most cost effective measure for long term prevention not only of hepatitis B transmission among children but also of venereal spread in early adulthood.

Child Day Care Centers↗

PubMed2000

Caffeine inhibits a low affinity but not a high affinity mechanism for cholecystokinin-evoked Ca2+ signalling and amylase release from guinea pig pancreatic acini.

Caffeine has been found to inhibit the formation and action of Ca2+-mobilizing inositol 1,4,5-trisphosphate (IP3) in pancreatic acinar cells. The aim of the present study was to investigate the effects of caffeine on cytoplasmic Ca2+ concentrations ([Ca2+]i) and amylase release in response to different agonists. [Ca2+]i was determined by cytofluorometry using fura-2 as indicator and amylase release with a substrate reagent. Stimulation with low concentrations of carbachol or cholecystokinin octapeptide (CCK-8) induces [Ca2+]i oscillations whereas higher concentrations cause sustained elevation of [Ca2+]i. The less efficacious agonists pilocarpine and CCK-JMV-180 evoke oscillations only. Caffeine inhibited carbachol-induced elevation of [Ca2+]i and amylase responses in a competitive manner, abolishing the responses to low and incompletely inhibiting the responses to high concentrations of the agonist. Also, the [Ca2+]i elevations by pilocarpine were abolished by caffeine. The effects on CCK-8-induced elevation of [Ca2+]i and amylase secretion were paradoxical, the caffeine inhibition being more pronounced at high than at low concentrations of CCK-8. This enigma was further emphasized by moderate effects of caffeine on the responses to CCK-JMV-180. The results indicate that carbachol, pilocarpine and high concentrations of CCK-8 elicit IP3-mediated responses and that CCK-JMV-180 and low concentrations of CCK-8 elevate [Ca2+]i and stimulate amylase release by another signal transduction mechanism.

Amylases↗

PubMed1998

The beta-gal interferon assay: a new, precise and sensitive method.

Cells of a human glioblastoma line were stably transfected with a glial fibrillary acidic protein (GFAP) promoter sequence/lacZ reporter gene. Following this modification, they produced Escherichia coli beta-galactosidase constitutively in amounts that could be measured through their conversion of an added fluorophore into a product readily estimated by fluorimetry. Human interferons (IFN) selectively and in a dose-dependent manner reduce the formation of beta-galactosidase in this system. We have used it as the basis for a novel assay that is sensitive (4-40 pg/ml), precise, completed in 30 h, and applicable to both type I and type II human IFNs. Statistical analysis showed interassay relative standard deviations ranging from 5% to 11%, and most individual assays revealed potencies with limits of error within 85%-115%. Neither partially trypsin-digested IFN nor the other cytokines and mitogens we tested reacted in this system, except for tumor necrosis factor-alpha (TNF-alpha). The high selectivity was further shown by the loss of response to IFN in the presence of the appropriate specific anti-IFN or anti-IFN-gamma receptor antibodies.

Biological Assay↗

PubMed1997

Cholecystokinin-JMV-180 and pilocarpine are potent inhibitors of cholecystokinin and carbachol actions on guinea pig pancreatic acinar cells.

The release of amylase and the elevation of cytoplasmic Ca2+ concentration ([Ca2+]i) in response to cholecystokinin-octapeptide (CCK-8), the cholecystokinin analogue JMV-180, the stable choline ester carbamylcholine (carbachol) and the muscarinic agonist pilocarpine were studied in guinea-pig pancreatic acinar cells. The maximal amylase and [Ca2+]i responses to JMV-180 and pilocarpine were 12-15% of the corresponding responses to CCK-8 and carbachol. The amylase and [Ca2+]i responses to maximal concentrations of CCK-8 and carbachol were inhibited in concentration-dependent manners by JMV-180 and pilocarpine, respectively. In individual acinar cells, JMV-180 and pilocarpine like low concentrations of CCK-8 and carbachol caused oscillations of [Ca2+]i. The sustained [Ca2+]i responses to maximal concentrations of CCK-8 and carbachol were transformed into oscillatory responses during simultaneous exposure to JMV-180 and pilocarpine, respectively. Maximal concentrations of JMV-180 and pilocarpine did not cause homologous or heterologous desensitization of the [Ca2+]i responses but inhibited desensitization evoked by maximal concentrations of CCK-8 or carbachol. JMV-180 and pilocarpine acted as weak, partial agonists exhibiting effective inhibition of the acinar cell responses to full agonists. The effects appeared to be best explained by interactions with two forms of the respective receptor with JMV-180 and pilocarpine acting as partial agonists for one state of the receptor and as antagonist for the second state.

Amylases↗

PubMed1997

Cytoplasmic Ca2+ gradients evoked by acetylcholine and peptides in pancreatic acinar cells of the guinea-pig.

Cytoplasmic Ca2+ levels ([Ca2+]i) in guinea-pig pancreatic acinar cells stimulated with acetylcholine (ACh) as well as cholecystokinin octapeptide (CCK-8), its analogue CCK-JMV-180, bombesin and substance P (SP) have been compared by confocal Ca2+ imaging. We found that at intermediate and high concentrations all agonists evoked [Ca2+]i waves emanating from the secretory pole of the cell. The [Ca2+]i gradients evoked by ACh and SP were often unidirectional whereas CCK-8- and bombesin-elicited [Ca2+]i responses consisting of [Ca2+]i waves were normally followed by a secondary phase with reversed [Ca2+]i gradients. At low agonist concentrations the [Ca2+]i responses appeared diffuse or localized to the granular part of the cells. The lag times to the [Ca2+]i rises were shorter in response to ACh and SP than for other peptides. Thus, we found that agonists induced different spatio-temporal patterns of Ca2+ waves in pancreatic acinar cells of the guinea-pig. The reactions evoked by SP and bombesin resembled those evoked by ACh and CCK-8, respectively.

Acetylcholine↗

PubMed1996

In vitro bioassay for human erythropoietin based on proliferative stimulation of an erythroid cell line and analysis of carbohydrate-dependent microheterogeneity.

The human erythroleukemia cell line TF-1 was employed for the determination of proliferative stimulation induced by recombinant human erythropoietin (rhEpo). Potencies of various intact and sugar-trimmed rhEpo preparations were estimated using the International Standard for Human r-DNA-derived Epo (87/684) as a reference for activity. The cellular response was measured in a multi-channel photometer using a colorimetric microassay, based on the metabolism of the tetrazolium dye 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide to formazan, by viable cells. The linear part of the log dose-response relationship encompassed 2.5-90 pM and activity of rhEpo preparations was measured at doses between 3 and 60 pM. The assay was designed as a parallel line test, using three or four concentrations for potency determinations, which fulfills pharmacopoeial requirements for assay validity. Inter-assay relative standard deviation varied between 4.1% and 12.6% and most assays revealed potencies with limits of error within 87-113%. In order to acquire an additional means for an efficient probing of physiologically relevant features of rhEpo, a luminiscence-dependent Western detection system, based on a combined isoelectric focusing/sodium dodecyl sulphate-polyacrylamide gel electrophoresis separation, was established. As opposed to conventional electrophoresis the two dimensional approach enabled the disclosure of minor truncations in the rhEpo-attached glycan moieties using picomolar quantities of the hormone. Moreover, the separated isoforms of rhEpo were quantified by computer-assisted densitometry and compared with the 87/684 standard. Accordingly, results obtained by the cellular response were balanced against the general pattern observed and the relative amounts of separated rhEpo isomers as determined by the quantitative Western analysis. The method described should be suitable for potency assessments of pharmaceutical formulations of rhEpo.

Antibodies↗

PubMed1996

Resin modified glass ionomer cements. In vitro microleakage in direct class V and class II sandwich restorations.

Microleakage of conventional chemically cured and resin modified glass ionomer cements (GIC), a compomer and a composite resin was studied in vitro in direct class V and class II GIC/composite sandwich fillings. None of the restorative techniques investigated completely resisted microleakage at both the occlusal and gingival margins. The dentinal gingival margins exhibited the highest leakage pattern. The compomer and the resin modified GIC showed a better seal than the chemically cured GIC's. The use of a liner as separating agent between composite resin and GIC in the class II sandwich fillings did not improve the seal. The results suggest that the initial bond obtained immediately after light curing of the resin modified GIC's is stronger than that for chemically cured GIC's. The contradictory results of dye leakage studies reported in the literature are discussed and in vivo evaluations are suggested necessary to predict clinical performance.

Composite Resins↗

PubMed1995

In vitro bioassay with enhanced sensitivity for human granulocyte colony-stimulating factor.

A method for the determination of human granulocyte colony-stimulating factor (hG-CSF) activity, based on stimulation of cellular proliferation, was developed using a subclone of the murine myeloid leukemia cell line NFS-60, with an improved sensitivity for hG-CSF, as indicator. The optimal range for quantitative analysis of hG-CSF was about 4-60 pg ml-1. The stimulatory effect was measured by a colorimetric microassay: the optical density of formazan, which is produced by viable cells from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), was obtained by reading plates in a multi-channel photometer. The assay was designed as a five-dose parallel line test, employing three or four doses for potency determinations, which fulfil pharmacopoeial requirements for assay validity. Inter-assay relative standard deviation (RSD) varied between 5.2 and 12.0%. Most assay experiments revealed potencies within limits of error of 90-110% and the mean index of precision value was 0.057. The recently developed yeast cell-derived International Standard (88/502) served as a reference for activity of rhG-CSF. Specificity of the assay was demonstrated by absence of response upon exposure to a panel of biomolecules, including recombinant human interleukin-3, and by the suppression of growth stimulation in the presence of neutralizing anti hG-CSF antibodies. Potency readings of unglycosylated rhG-CSF were dependent on pH of assay medium with higher relative activities observed at pH 6.6 than at 7.4. Moreover, SDS-PAGE analysis of the carbohydrate-deficient preparation, following incubation at physiological pH, revealed several high molecular weight rhG-CSF bands and decreased monomeric form. The method described was found suitable for potency assessments of pharmaceutical formulations of hG-CSF.

Animals↗

PubMed1994

Rapid down-regulation of substance P binding to guinea-pig pancreatic acinar cells during homologous desensitization.

Binding of 125I-labelled peptides, cytoplasmic Ca2+ concentration ([Ca2+]i) and amylase release were studied in guinea-pig pancreatic acinar cells during exposure to substance P (SP), and cholecystokinin octapeptide (CCK-8). Pre-incubation of cells at 22 degrees C with 0.03 nM to 1 microM SP for 10 min or at 37 degrees C for 5 min followed by acid or neutral washes reduced subsequent binding of 125I-Bolton-Hunter reagent-labelled SP (125I-BH-SP) in a biphasic manner by up to 95%. Incubation at 4 degrees C eliminated high-affinity binding of 125I-BH-SP and concentrations of SP above 1 nM were required for inhibition of subsequent tracer binding. Pre-incubation of cells at 37 degrees C with 1 nM to 1 microM CCK-8 for 10 min followed by neutral washes reduced subsequent binding of 125I-BH-CCK-8 by up to 65%. In cell suspensions, the [Ca2+]i response to SP was gradually reduced by pre-exposure to increasing agonist concentrations from 0.2 to 20 nM. Pre-incubation with high SP concentrations for 10 min caused profound reduction of subsequent amylase responses to SP, whereas secretion was little affected in corresponding experiments with CCK-8. Down-regulation of receptor binding is not important during short exposure to CCK-8, but it is a pronounced and rapid phenomenon during SP exposure, which explains tachyphylaxis of [Ca2+]i and amylase responses.

Amylases↗

PubMed1994

Down-regulation of bombesin binding to guinea-pig pancreatic acinar cells during homologous desensitization.

1. [125I]-Tyr4-bombesin exhibited saturable binding to pancreatic acinar cells. 2. Preincubation of cells at 37 degrees C with 0.03 nM-1 microM-bombesin for 10 min followed by acid or neutral washes reduced subsequent binding of [125I]-Tyr4-bombesin in a concentration-dependent manner by up to 90%. 3. In cell suspensions, bombesin raised the cytoplasmic Ca2+ concentration ([Ca2+]i) and the [Ca2+]i response was reduced by pre-exposure to the agonist. 4. In individual superfused cells, bombesin at 1 nM normally caused a large [Ca2+]i transient followed by sustained [Ca2+]i oscillations. The cells exhibited a variable degree of desensitization when subsequently exposed to higher agonist concentrations. 5. Preincubation with bombesin for 10 min caused a concentration-related reduction of subsequent amylase responses to bombesin. 6. Down-regulation of receptor binding is a rapid phenomenon during bombesin exposure explaining, at least partially, tachyphylaxis of [Ca2+]i and amylase responses.

Amylases↗

PubMed1994

Supramaximal inhibition of cholecystokinin-induced pancreatic amylase release involves desensitization to cytoplasmic Ca2+.

BACKGROUND: Cholecystokinin (CCK) is a major stimulant of pancreatic enzyme secretion. The dose-response relationship for CCK-induced secretion is bell-shaped, with a characteristic supramaximal inhibition. The mechanism for this inhibition has now been studied. METHODS: The kinetics of amylase release and the changes of the cytoplasmic Ca2+ concentration ([Ca2+]i) were recorded during stimulation of guinea-pig pancreatic acinar cells with different concentrations of cholecystokinin octapeptide (CCK-8) and the Ca2+ ionophore ionomycin. RESULTS: Individual cells reacted with [Ca2+]i oscillations at 10(-11)-10(-10) M CCK-8 and with an initial peak followed by a sustained suprabasal level at 10(-9)-10(-8) M of the agonist. The latter response was also seen in suspensions of acinar cells at all tested concentrations of CCK-8 and at 10(-6)-10(-5) M of ionomycin. With increases of extracellular Ca2+ from 0.5 to 5.0 mM there was a rise of [Ca2+]i during exposure to 10(-9)-10(-8) M CCK-8 or 10(-5) M ionomycin but a paradoxical decrease at lower concentrations of CCK-8 or ionomycin. A dose-dependent increase of amylase release was seen at CCK-8 concentrations from 10(-11) to 10(-9) M. At 10(-9)-10(-8) M CCK-8 secretion was characterized by an initial peak followed by a sustained phase. Whereas the initial peak of secretion remained unaffected by increasing CCK-8 from 10(-9) to 10(-8) M, the sustained phase was inhibited (supramaximal inhibition). Increasing extracellular Ca2+ from 0.5 to 5.0 mM transiently enhanced secretion in response to 10(-9) M but lacked effect during supramaximal inhibition of secretion by 10(-8) M CCK-8. CONCLUSIONS: Both initial and sustained CCK-8-stimulated amylase release increase with [Ca2+]i. However, supramaximal inhibition of secretion was not due to a decrease of [Ca2+]i but was characterized by desensitization to the stimulatory effect of [Ca2+]i.

Amylases↗

PubMed1992

Development and validation of a bioassay for interleukin-2.

A reliable and precise method for the determination of IL-2 activity, based on stimulation of CTLL cell proliferation, was developed. Cells were incubated with different concentrations of IL-2 for 24 h in microtiter plates. The stimulatory effect was measured on a plate-reading spectrophotometer by reading the optical density of formazan, which is produced by viable cells from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The bioassay was designed as a four-dose parallel line test, fulfilling pharmacopoeial requirements for assay validity, and the inter-assay relative standard deviation (RSD) for a group of four experiments was 2.6%. The International Standard for human IL-2 and the Reference Reagent for Recombinant DNA-derived IL-2 were employed for potency determinations. The method was found suitable for potency assessments of pharmaceutical formulations of IL-2.

Animals↗

PubMed1992

Binding of epidermal growth factor to receptors in preparations of enriched porcine parietal cells and inhibition of aminopyrine uptake.

Preparations of isolated porcine gastric cells, enriched in parietal cells, were used to study binding of epidermal growth factor (EGF) to receptors and subsequent inhibition of [14C]aminopyrine uptake. EGF in concentrations from 10(-10) to 10(-7) M inhibited aminopyrine uptake stimulated by 10(-5) M histamine with an IC50 of 3 x 10(-10) M. [125]EGF bound in a saturable and specific manner to sites on cells in preparations containing 40-90% parietal cells. Mean apparent dissociation constant for the sites was 1.6 x 10(-9) M, with an average number of approximately 20,000 sites per cell. Endocytosis of ligand by parietal cells was limited, amounting to 10-20% of bound EGF after 1 h of incubation at 37 degrees C. Occupation of a fraction of the receptors caused a maximal reduction by 40% of aminopyrine uptake in histamine-stimulated cells, suggesting the occurrence of spare receptors. The results indicate the existence of specific receptors for EGF on porcine parietal cells exerting a regulatory influence on acid secretion.

Aminopyrine↗

PubMed1992

Cholecystokinin-induced inhibition of endocytosis of receptor-bound substance P in pancreatic acinar cells.

Association of 125I-Bolton-Hunter labelled substance P (125I-BH-SP) to suspended pancreatic acinar cells of the guinea pig was studied. Cellular association at 37 degrees C and 22 degrees C was inhibited by cholecystokinin octapeptide (CCK-8) in concentrations from 10(-9) to 10(-6)M, whereas another pancreatic secretagogue, carbachol, was uneffective. The CCK induced inhibition disappeared at low temperatures. CCK-8 mainly interfered with internalization of 125I-BH-SP into acinar cells. Increased extracellular Ca2+ and the Ca2+ ionophores A23187 and ionomycin reduced association of 125I-BH-SP to cells whereas extracellular Ca2+ chelation with EGTA had the opposite effect. However, extra- and intracellular Ca2+ chelation did not affect the degree of CCK-induced reduction of 125I-BH-SP association to acinar cells but eliminated the effect of the calcium ionophore ionomycin. Three agents known to interfere with receptor recycling, namely monensin, methylamine and ammonium chloride reduced cell-associated 125I-BH-SP. In a series of experiments, the cytoplasmic calcium concentrations ([Ca2+]i) during exposure to these three agents, to the CCK-8-analogue caerulein and to ionomycin were determined. In all cases, [Ca2+]i was raised. The results indicate that endocytosis of receptor-bound 125I-BH-SP is regulated by CCK and that the endocytotic process is influenced by calcium.

Animals↗

PubMed1992

A selective and potent antagonist of substance P receptors on pancreatic acinar cells.

CP-96,345 [(2S, 3S) cis-2-(diphenylmethyl)-N-((2-methoxyphenyl)-methyl)-1- azabicyclo[2.2.2]octan-3-amine] belongs to a new class of nonpeptide antagonists of the substance P (SP) receptor. The effects of this compound on [125I]-labelled Bolton-Hunter substance P ([125I]-BH-SP) binding and cytoplasmic Ca2+ ([Ca2+]i) responses of pancreatic acinar cells have now been studied. IC50 of CP 96,345 for binding of [125I]-BH-SP and for SP-induced (3 x 10(-9) M) rise of [Ca2+]i were about 10(-9) M. CP-96,345 neither affected binding of [125I]-labelled Bolton-Hunter cholecystokinin octapeptide ([125I]-BH-CCK-8) nor the [Ca2+]i responses to CCK-8, carbamylcholine or bombesin. The CP-96,345-induced inhibition of [Ca2+]i responses to SP appeared reversible after withdrawal of the antagonist and was overcome by increasing the concentration of the agonist. CP-96,345 was consequently a specific and potent competitive antagonist for SP receptors on pancreatic acinar cells.

Animals↗

PubMed1991

Calcium oscillations in guinea-pig pancreatic acinar cells exposed to carbachol, cholecystokinin and substance P.

1. Cytoplasmic Ca2+ ([Ca2+]i) responses were studied in guinea-pig pancreatic acinar cells during stimulation with cholecystokinin octapeptide (CCK-8), substance P (SP) and carbachol. 2. Individual cells exhibited [Ca2+]i responses to all three agonists. 3. In the absence of external Ca2+, all the agonists initiated [Ca2+]i peaks which, particularly at high agonist concentrations, rapidly declined. 4. SP induced repetitive monophasic [Ca2+]i transients which started from basal [Ca2+]i even after elevation of the external Ca2+ concentration. 5. CCK-8 triggered similar oscillations, which particularly at high agonist concentration or after elevating external Ca2+ became superimposed upon a sustained elevation of [Ca2+]i. 6. Carbachol-induced oscillations were more complex with [Ca2+]i transients superimposed on slower waves. 7. At high carbachol concentrations or elevation of external Ca2+ the slow waves fused into a sustained increase of [Ca2+]i. 8. The protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate attenuated the agonist-induced [Ca2+]i responses, and this effect was reversed by the PKC activator staurosporine. 9. The results indicate that oscillations of [Ca2+]i induced by SP, CCK-8 and carbachol involve intracellular mobilization of Ca2+. 10. CCK-8 and carbachol also cause a rise of [Ca2+]i by a mechanism more directly dependent on the presence of extracellular Ca2+. 11. In the case of carbachol the latter component is subject to oscillatory control. 12. The transition from oscillatory [Ca2+]i to sustained increase may be associated with inhibition of amylase release.

Animals↗

PubMed1991

Binding of epidermal growth factor (EGF) to a cultured human glioma cell line.

We have studied binding of 125I-EGF to the human malignant glioma cell line U-343 MG aCl2:6, which is planned to be used as a model system in studies of toxic effects of EGF conjugates. Special care has been taken to fulfil the requirements for a correct Scatchard analysis of binding parameters. Binding as a function of time, temperature and pH was investigated as well as dissociation and internalization of bound EGF. The stability of EGF during incubation was also determined. After binding to the receptor, EGF is rapidly internalized and degraded at physiological temperature. We found that binding experiments should be performed at 4 degrees C, since at this temperature practically no internalization took place, whereas dissociation occurred. From displacement experiments using increasing concentrations of unlabelled EGF competing with 125I-EGF for binding, binding parameters were calculated using a computerized, nonlinear, least-squares regression analysis of binding data. We found that EGF bound to a class of high affinity receptors with an apparent dissociation constant KD of about 4 x 10(-10) M. The mean number of receptors was 25,000 per cell. In experiments where receptors were saturated with 125I-EGF an additional class of low affinity receptors was detected. This had an apparent KD of 1 x 10(-8) M with a mean receptor number per cell of 780,000. We also noticed enhanced dilution-induced dissociation of bound 125I-EGF in the presence of excess unlabelled EGF, suggesting negative cooperativity.

Cell Count↗

PubMed1990

Stimulation of pancreatic amylase release is associated with a parallel sustained increase of cytoplasmic calcium.

The kinetics of the changes in the cytoplasmic Ca2+ concentration (Ca2+i) and amylase release were measured in fura-2-loaded pancreatic acinar cells and perifused pancreatic acini, respectively. Cholecystokinin octapeptide (CCK-8) and its amphibian analogue caerulein induced similar dose-related increases of Ca2+i and amylase secretion with threshold concentrations of 2-6 x 10(-12) M, and maximal effects at 2 x 10(-10) M. The action of CCK/caerulein on Ca2+i was complex and similar to that of carbachol and bombesin with a prompt several-fold increase within seconds followed by a gradual decline over more than 5 min to a new sustained suprabasal level. The kinetics of amylase release in response to CCK and carbachol correlated with the changes in Ca2+i. Additions of the antagonists N2,O2-dibutyrylguanosine 3':5'-cyclic monophosphate and atropine after 30 min of CCK-8 and carbachol stimulation, respectively, were associated with prompt lowerings of Ca2+i and inhibitions of amylase secretion. The patterns observed with substance P (SP) and eledoisin were different with high concentrations (10(-8)-10(-7) M) giving monophasic increases of Ca2+i and amylase release. An initial stimulation of cells with a high dose of CCK eliminated the Ca2+i response to further stimulation with CCK, carbachol, bombesin and SP, whereas cells subjected to initial stimulation with SP responded to subsequent exposure to CCK with prolonged elevation of Ca2+i. The data indicate that stimulation with CCK, carbachol and bombesin may be associated with intracellular mobilization of calcium from more than one pool, and that an increase of Ca2+i is involved even in threshold stimulation of amylase release.

Amylases↗