Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Thimerosal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2000

Role of phospholipase A(2) and myoendothelial gap junctions in melittin-induced arterial relaxation.

We have used preconstricted rings of rabbit superior mesenteric artery to investigate the contribution of phospholipase A(2) and gap junctional communication to endothelium-derived hyperpolarizing factor (EDHF)-type relaxations evoked by melittin, a polypeptide toxin known to mobilize arachidonic acid from the cell membrane. Arachidonyl trifluoromethyl ketone (30 microM), an inhibitor of the Ca(2+)-dependent phospholipase A(2), and Gap 27 (300 microM), a connexin-mimetic peptide which attenuates intercellular communication via gap junctions, both abolished the endothelium-dependent component of EDHF-type responses evoked by melittin in the presence of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 300 microM) and the cyclooxygenase inhibitor indomethacin (10 microM). By contrast, the sulfhydryl agent thimerosal (300 nM), which amplifies EDHF activity, potentiated nitric oxide (NO)/prostanoid-independent relaxations induced by melittin. Neither arachidonyl trifluoromethyl ketone nor thimerosal modulated relaxations evoked by the peptide toxin in the absence of L-NAME and indomethacin. We conclude that melittin evokes EDHF-type relaxations through activation of the endothelial Ca(2+)-dependent phospholipase A(2) followed by the transmission of a chemical and/or electrical signal via myoendothelial gap junctions. This mechanism of vasorelaxation may be negatively regulated by NO.

Animals↗
PubMed2002

A pilot scale evaluation of removal of mercury from pharmaceutical wastewater using granular activated carbon.

Thimerosal (an organic mercury compound) is widely used in the pharmaceutical industry and hospitals. This study examines the removal of mercury (thimerosal and Hg(II)) from a pharmaceutical wastewater using F-400 granular activated carbon (GAC) at bench and pilot scales. Bench scale dynamic column tests are conducted with 30, 60, 90 and 120 min empty bed contact times (EBCTs). The pilot scale study is conducted using two GAC columns-in-series each of 30 min EBCT. The capital and operational cost analysis for the treatment system is performed. Simultaneous removal of copper, turbidity, phenol, and color from the wastewater by the pilot scale system is also reported.

Anti-Infective Agents, Local↗
PubMed2003

Intracytoplasmic sperm injection of bovine oocytes with stallion spermatozoa.

Five experiments were designed to study the fertilizability and development of bovine oocytes fertilized by intracytoplasmic sperm injection (ICSI) with stallion spermatozoa. Experiment 1 determined the time required for pronuclear formation after ICSI. Equine sperm head decondensation began 3 h after ICSI; 42% were decondensed 6 h after ICSI. Male pronuclei (MPN) began to form 12 h after ICSI. Female pronuclei (FPN), however, formed as early as 6 h after ICSI. In Experiment 2, ionomycin, ionomycin plus 6-dimethylaminopurine (DMAP), and thimerosal were used to activate ICSI ova. None of the ICSI ova cleaved after treatment with thimerosal. Ionomycin activation after 24 and 30 h of oocyte maturation resulted in 29 and 48% cleavage rates, respectively. Ionomycin combined with DMAP resulted in 49, 6 and 3% cleavage, morula and blastocyst rates, respectively, when oocytes were activated after 24 h maturation. In Experiment 3, rates of cleavage (45-60%) and development to morulae (4-13%) and blastocysts (1-5%) stages following ICSI were not different (P>0.05) among three stallions. Treatment of stallion spermatozoa with ionomycin did not affect cleavage or development of ova fertilized by ICSI. The chromosomal constitution of blastocysts derived from ICSI was bovine, not bovine and equine hybrids. In Experiment 4, to make male and FPN form synchronously, colchicine and DMAP were used for 4 h to inhibit oocytes at metaphase during activation; 63% of oocytes were still at metaphase 8h after ICSI when treated with colchicine, and 50% of sperm nuclei were decondensed. About 18 h after ICSI, 21 and 50% male and FPN had formed, respectively, but cleavage rates were low, and only 1% developed to morulae. In Experiment 5, to test if capacitated equine sperm could fuse with the bovine oolemma, capacitated spermatozoa were injected subzonally (SUZI). Of the 182 SUZI oocytes, 49 (27%) contained extruded second polar bodies. After activation of oocytes with second polar bodies, 44, 22 and 15% developed to 2-, 4- and 8-cell stages, respectively, but development stopped at the 8-cell stage. None of the unactivated oocytes cleaved. In conclusion, equine spermatozoa can decondense and form MPN in bovine oocytes after ICSI, but subsequent embryonic development is parthenogenetic with only bovine chromosomes being found.

Adenine↗
PubMed1998

Intracellular calcium responses in bovine oocytes induced by spermatozoa and by reagents.

The objectives of the present study were to clarify and compare the characteristics of the transient rises in intracellular calcium concentrations ([Ca2+]i) induced either by spermatozoa or by stimulation with artificial activators in bovine oocytes. These transient rises in [Ca2+]i in oocytes matured in vitro were recorded with Ca2+ imaging using the Ca2+ indicator fura-2. During fertilization, a series of transient rises in [Ca2+]i was observed. The first Ca2+ response peaked at a concentration of 521 +/- 39 nM (n = 20) and lasted for 4 min, while the subsequent Ca2+ responses were significantly smaller and shorter, with a peak of 368 +/- 13 nM (n = 23) and a duration of 2 min. Injection of inositol 1,4,5- triphosphate (InsP3) into unfertilized oocytes caused a transient rise in [Ca2+]i in a dose-dependent manner. The maximum response was induced by 20 nA x 1 sec injection of InsP3. Thimerosal, a sulfhydryl reagent, induced the repetitive transient rises in [Ca2+]i. The peak and the duration of the rises in [Ca2+]i induced by InsP3 or thimerosal were smaller and shorter, respectively, than those of the first rise induced by spermatozoa. Ethanol and Ca2+ ionophore IA23187, which are general parthenogenetic activators of unfertilized oocytes, each induced a single transient rise in [Ca2+]i. The duration of the rise in [Ca2+]i by ethanol or Ca2+ ionophore was significantly longer than that by spermatozoa at fertilization, although the peaks were smaller. These results clarified the characteristics of the rises in [Ca2+]i induced by spermatozoa and by several artificial reagents, and showed that the first rise in [Ca2+]i induced by spermatozoa had a higher peak [Ca2+]i and a longer duration compared with each the subsequent rises in [Ca2+]i and the rises in [Ca2+]i induced by artificial reagents. These indicate that a mode like as the first rise in [Ca2+]i induced by spermatozoa is an effective trigger for artificial activation of oocytes.

Animals↗
PubMed1998

Mechanisms of calcium release and sequestration in eggs of Chaetopterus pergamentaceus.

Increases in the intracellular free calcium concentration are of great importance to the initiation of development in deuterostomes. Their involvement has not yet been clearly defined in protostomes. We used endogenous ligands (IP3, cADPR, ryanodine and NAADP) and pharmacological agents (thapsigargin [Tg], thimerosal, caffeine and heparin) to study smooth endoplasmic reticulum Ca2+ pump and release mechanisms in eggs of an annelid, Chaetopterus. Oocyte homogenates effectively sequestered Ca2+ and released it in response to IP3 in a concentration-dependent manner. Repeated additions of IP3 were unable to cause further release. Heparin inhibited Ca2+ release in response to IP3. The homogenates also released Ca2+ in response to thimerosal, and this release was sensitive to heparin. Two antibodies to IP3 receptors recognized an appropriate band in Chaetopterus egg lysates. These results indicate that the oocytes possess type-1 IP3-gated Ca2+ channels. Neither calcium itself, nor strontium, cADPR, ryanodine, caffeine nor NAADP released appreciable Ca2+. At low concentrations, Tg caused a slow release of Ca2+; at higher concentrations, it elicited a rapid release. Release of Ca2+ by Tg activated development. Since one theory of fertilization invokes the introduction of a Ca2+ releasing soluble protein into the egg upon sperm-egg fusion, we also tested whether soluble extracts of Chaetopterus sperm could stimulate Ca2+ release in Chaetopterus egg homogenates. There was no Ca2+ release when the sperm extract was added to the homogenate; however, homogenates exposed to sperm extract became refractory to IP3. Thus, Ca2+ release at fertilization in these oocytes occurs through IP3-gated channels.

Adenosine Diphosphate Ribose↗
PubMed1997

Effects of erythromycin on chemoattractant-activated human polymorphonuclear leukocytes.

1. Erythromycin (2-100 micrograms ml-1) produced a concentration-related inhibition of superoxide generation and elastase release induced by in vitro exposure of human polymorphonuclear leukocytes (PMNs) to the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP; 30 nM). 2. By contrast, erythromycin (100 micrograms ml-1) did not alter the leukotriene B4 production elicited by FMLP (30 nM; in the presence of thimerosal 20 microM) or the intracellular calcium changes promoted by FMLP (30 nM; in the absence or presence of thimerosal 20 microM). 3. These results indicate that by reducing chemoattractant-triggered release of oxidative and proteolytic mediators from human PMNs, erythromycin may have clinically useful antiinflammatory effects.

Anti-Inflammatory Agents↗
PubMed1996

Synergistic effects of inositol 1,3,4,5-tetrakisphosphate on inositol 2,4,5-triphosphate-stimulated Ca2+ release do not involve direct interaction of inositol 1,3,4,5-tetrakisphosphate with inositol triphosphate-binding sites.

We have previously found that for permeabilized L1210 cells, low micromolar concentrations of Ins(1,3,4,5)P4 added prior to Ins(2,4,5)P3 enhance the effects of suboptimal concentrations of Ins(2,4,5)P3 in causing Ca2+ release from InsP3-sensitive Ca2+ stores [Cullen, Irvine and Dawson (1990) Biochem J. 271, 549-553]. If this was due either to some conversion of added Ins(1,3,4,5)P4 into Ins(1,4,5)P3 by the 3-phosphatase, or to Ins(1,3,4,5)P4 acting as a weak (or partial) agonist on the InsP3 receptor it would be expected that,in the presence of thimerosal to sensitize the InsP3 receptor, the dose-response curve to Ins(1,3,4,5)P4 would be left-shifted by the same extent as that of Ins(1,4,5)P3. This was found not to be the case; the dose-response curve to Ins(1,3,4,5)P4 was not shifted at all by thimerosal. Furthermore, L-Ins(1,3,4,5)P4, which can displace radiolabelled D-Ins(1,3,4,5)P4 but not D-Ins(1,4,5)P3 from their respective high-affinity binding sites, mimicked the effects of D-Ins(1,3,4,5)P4 in enhancing the slow phase of Ins(2,4,5)P3-stimulated Ca2+ release. Ins(1,3,4,5)P4 caused an increase in magnitude of the slow phase of InsP3-stimulated Ca2+ release leaving the magnitude of the fast phase unaltered, in contrast to increasing Ins(2,4,5)P3 concentrations which increased the size of both phases. In addition, Ins(1,3,4,5)P4 decreased the rate constant for the slow phase of Ca2+ release. These findings point strongly to the conclusion that InsP4 is not working directly via the InsP3 receptor but indirectly via an InsP4 receptor.

Animals↗
PubMed2001

Developmental expression of the calcium release channels during early neurogenesis of the mouse cerebral cortex.

The developmental changes of intracellular calcium release channels of mouse neocortex were studied at the onset of neurogenesis, which occurs between embryonic days E11 and E17. The three main isoforms of the two families of intracellular calcium release channels, namely the inositol trisphosphate receptors (IP3R) and the ryanodine receptors (RyR), were detected by their transcripts in the cerebral hemispheres, as early as stage E11. The major isoforms of each family, IP3R-1 and RyR-2, were found at the protein level by Western blot analysis. Expression of these proteins increases progressively throughout brain development. Their localization in coronal sections of cortex has been observed by immunodetection from E12, and compared to the TuJ1 (anti-class III beta-tubulin antibody) neuronal specific labelling. The expression of both channels is greatly enhanced after E12, and both were seen to be present in most of the proliferative and neuronal cells of the slice. Between E12 and E13, there is a striking transition in the pattern of calcium release elicited by specific agonists of these channels, thimerosal for IP3R and caffeine for RyR. The signals induced by thimerosal were not zone-specific, while the observed calcium release signals induced by caffeine were predominantly restricted out of the ventricular zone. This zone-specific caffeine sensitivity is consistent with the main RyR localization immunodetected at E13. Our results indicate that there is a time lag of several days between the molecular detection of calcium release channels and their functional expression, around the time of neuronal differentiation. Altogether, they provide a molecular basis for analyzing the developmental modulation of calcium signals useful for neurogenesis progression.

Animals↗
PubMed2000

Intracellular pH increase accompanies parthenogenetic activation of porcine, bovine and murine oocytes.

Although an intracellular pH (pHi) increase at the time of fertilization is necessary for activation of the sea urchin egg, recent reports in the mouse and rat have indicated that there is not a pHi increase during fertilization or during 7% ethanol activation in the mouse. It has been suggested that mammals may have lost the need for a pHi increase at the time of fertilization and the present study reports significant pHi changes during parthenogenetic activation of porcine IVM oocytes, as well as pHi responses to activation in bovine and murine oocytes. Transient intracellular pH changes were found during porcine oocyte activation when using 7% ethanol and with 50 or 100 microM calcium ionophore (A23187). Treatment with 200 microM thimerosal resulted in an increase in pHi after a delay of approximately 12 min. Murine oocytes showed a significant increase during activation with 7% ethanol and A23187 as well as during prolonged exposure to thimerosal. Bovine oocytes exhibited an increase in pHi only when activated with 50 or 100 microM A23187. The final set of experiments aimed to determine whether the porcine oocyte has mechanisms to alleviate induced acidic and alkaline challenges. Both acidic (approximately 20 mM acetic acid) and alkaline (approximately 30 mM ammonium chloride) challenges caused significant changes in pHi that porcine IVM oocytes were capable of recovering from within 35 min. Future studies will focus on determining which of the mechanisms is producing the pHi increase at the time of parthenogenetic activation in the porcine oocyte.

Animals↗
PubMed1996

Threshold for inositol 1,4,5-trisphosphate action.

We developed a unidirectional 45Ca2+ efflux technique in which 60 cumulative doses of inositol 1,4,5-trisphosphate (InsP3), each lasting 6 s, were subsequently added to permeabilized A7r5 cells. This technique allowed an accurate determination of the threshold for InsP3 action, which was around 32 nM InsP3 under control conditions. The InsP3-induced Ca2+ release was characterized by an initial rapid phase, after which the normalized rate progressively decreased. The slowing of the release was associated with a shift of the threshold to higher InsP3 concentrations. Stimulatory concentrations of thimerosal (10 microM) shifted the threshold to 4.5 nM InsP3 and increased both the cooperativity and the maximal normalized rate of Ca2+ release. This low threshold was maintained when the thimerosal concentration was increased to inhibitory levels (100 microM) but then the effects on the cooperativity and on the normalized rate of Ca2+ release disappeared. Oxidized glutathione (5 mM) was much less effective in stimulating the release and did not have an effect on the threshold or on the cooperativity. ATP (5 mM) stimulated the release despite a shift in threshold toward higher InsP3 concentrations. Luminal Ca2+ did not affect the threshold for InsP3 action but stimulated the normalized release at each InsP3 concentration. The inhibitory effect of 10 microM free cytosolic Ca2+ was associated with a shift in threshold to higher InsP3 concentrations and a decreased cooperativity of the release process. We conclude that this novel technique of accurately measuring the threshold for InsP3 action under various experimental conditions has allowed us to refine the analysis of the kinetic parameters involved in the regulation of the InsP3 receptor.

Adenosine Triphosphate↗
PubMed1994

Regulation of intracellular calcium in the mouse egg: evidence for inositol trisphosphate-induced calcium release, but not calcium-induced calcium release.

Fertilization of the mammalian egg initiates transient and repetitive release of Ca2+ from intracellular stores. The mechanism by which these Ca2+ transients are produced is not completely known. We examined the role of two principal Ca2+ release mechanisms, inositol trisphosphate-induced Ca2+ release and Ca(2+)-induced Ca2+ release, in altering intracellular Ca2+ in the mouse egg. Microinjection of inositol 1,4,5-trisphosphate (IP3) transiently elevated intracellular Ca2+ and, at higher concentrations, produced repetitive Ca2+ transients. Addition of 100 microM thimerosal, a sulfhydryl reagent, caused repetitive Ca2+ transients. IP3 and thimerosal responses were inhibited by prior injection of heparin, a competitive antagonist of IP3-induced Ca2+ release. Addition of caffeine or injection of caffeine, ryanodine, or cyclic ADP-ribose, which are known to initiate or modulate Ca(2+)-induced Ca2+ release in sea urchin eggs and other cells, produced no change in intracellular Ca2+. The response to injection of Ca2+ was not altered by prior injection of ryanodine. The magnitude of the Ca2+ transients produced by injection of IP3 was not changed by prior injection of cyclic ADP-ribose or external caffeine. We found no evidence of Ca(2+)-induced Ca2+ release from ryanodine- or caffeine-sensitive stores. It is most likely that release of Ca2+ from intracellular stores in the mouse egg is dependent on IP3-induced Ca2+ release.

Adenosine Diphosphate Ribose↗
PubMed1982

The effect of ophthalmic preservatives on the healing rate of the rabbit corneal epithelium after keratectomy.

Most ophthalmic preparations contain preservatives. Some are toxic to healthy corneal epithelium or retard healing of corneas from which part or all of the epithelium has been removed leaving an intact basement membrane. In this paper, the effect of commonly used concentrations of benzalkonium chloride (BAC), thimerosal, and ethylenediaminetetracetic acid (EDTA) upon the healing of rabbit corneas after partial lamellar keratectomy is investigated. This model has not been used previously for a study of preservative toxicity. Thimerosal (0.004%), BAC (0.01%), or EDTA (0.1%) applied four times per day had no significant effect on the corneal healing or epithelial migration rates. A slight retardation occurred when BAC (0.01%) and EDTA (0.1%) were used together, while healing failed to occur as long as benzalkonium chloride (0.02%) was administered.

Animals↗
PubMed1984

Solution intolerance among users of four chemical soft lens care regimens.

The incidence of solution intolerance in 161 soft contact lens patients was about 33% in those using chlorhexidine plus thimerosal chemical disinfecting systems. Those who disinfected their lenses with systems based primarily on thimerosal developed intolerance in 5 to 8% of cases. A family history of allergy appears not to be significant.

Chlorhexidine↗
PubMed1997

Mercurochrome allergy. Immediate and delayed hypersensitivity.

We describe eight patients suffering from Mercurochrome allergy. Patch and prick tests were carried out with the following organic and inorganic mercury compounds: thimerosal, Mercurochrome, phenylmercuric acetate, phenylmercuric nitrate, metallic mercury, and mercuric chloride, and with sodium fluorescein. Two patients had an anaphylactic reaction a few minutes after application of Mercurochrome. The prick tests with Mercurochrome were positive and they were negative with the other tested products. All patch tests were negative. In the other six patients, the clinical picture was local eczema, and the patch tests were all positive with Mercurochrome and the inorganic mercuric derivatives. Positive patch tests with thimerosal were found only in two patients, and only one had a positive patch test with salts of phenylmercury. In four patients, the prick test with Mercurochrome, negative in immediate reading, gave a late eczematous reaction.

Adolescent↗
PubMed2000

Nitric oxide and thiol reagent modulation of Ca2+-activated K+ (BKCa) channels in myocytes of the guinea-pig taenia caeci.

The modulation of large conductance Ca2+-activated K+ (BKCa) channels by the nitric oxide (NO) donors S-nitroso-L-cysteine (NOCys) and sodium nitroprusside (SNP) and agents which oxidize or reduce reactive thiol groups were compared in excised inside-out membrane patches of the guinea-pig taenia caeci. When the cytosolic side of excised patches was bathed in a physiological salt solution (PSS) containing 130 mM K+ and 15 nM Ca2+, few BKCa channel openings were recorded at potentials negative to 0 mV. However, the current amplitude and open probability (NPo) of these BKCa channels increased with patch depolarization. A plot of ln(NPo) against the membrane potential (V) fitted with a straight line revealed a voltage at half-maximal activation (V0.5) of 9.4 mV and a slope (K) indicating an e-fold increase in NPo with 12.9 mV depolarization. As the cytosolic Ca2+ was raised to 150 nM, V0.5 shifted 11.5 mV in the negative direction, with little change in K (13.1 mV). NOCys (10 microM) and SNP (100 microM) transiently increased NPo 16- and 3. 7-fold, respectively, after a delay of 2-5 min. This increase in NPo was associated with an increase in the number of BKCa channel openings evoked at positive potentials by ramped depolarizations (between -60 and +60 mV). Moreover, this NOCys-induced increase in NPo was still evident in the presence of 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ; 10 microM), the specific blocker of soluble guanylyl cyclase. The sulfhydryl reducing agents dithiothreitol (DTT; 10 and 100 microM) and reduced glutathione (GSH; 1 mM) also significantly increased NPo (at 0 mV) 7- to 9-fold, as well as increasing the number of BKCa channel openings evoked during ramped depolarizations. Sulfhydryl oxidizing agents thimerosal (10 microM) and 4,4'-dithiodipyridine (4,4DTDP; 10 microM) and the thiol-specific alkylating agent N-ethylmaleimide (NEM; 1 mM) significantly decreased NPo (at 0 mV) to 40-50% of control values after 5-10 min. Ramped depolarizations to +100 mV evoked relatively few BKCa channel openings. The effects of thimerosal on NPo were readily reversed by DTT, while the effects of NOCys were prevented by NEM. It was concluded that both redox modulation and nitrothiosylation of cysteine groups on the cytosolic surface of the alpha subunit of the BKCa channel protein can alter channel gating.

Animals↗
PubMed1992

High sensitivity of glutamate uptake to extracellular free arachidonic acid levels in rat cortical synaptosomes and astrocytes.

By using both synaptosomes and cultured astrocytes from rat cerebral cortex, we have investigated the inhibitory action of arachidonic acid on the high-affinity glutamate uptake systems, focusing on the possible physiological significance of this mechanism. Application of arachidonic acid (1-100 microM) to either preparation leads to fast (within 30 s) and largely reversible reduction in the uptake rate. When either melittin (0.2-1 microgram/ml), a phospholipase A2 activator, or thimerosal (50-200 microM), which inhibits fatty acid reacylation in phospholipids, is applied to astrocytes, both an enhancement in extracellular free arachidonate and a reduction in glutamate uptake are seen. The two effects display similar dose dependency and time course. In particular, 10% uptake inhibition correlates with 30% elevation in free arachidonate, whereas inhibition greater than or equal to 60% is paralleled by threefold stimulation of arachidonate release. In the presence of albumin (1-10 mg/ml), a free fatty acid-binding protein, inhibition by either melittin, thimerosal, or arachidonic acid is prevented and an enhancement of glutamate uptake above the control levels is observed. Our data show that neuronal and glial glutamate transport systems are highly sensitive to changes in extracellular free arachidonate levels and suggest that uptake inhibition may be a relevant mechanism in the action of arachidonic acid at glutamatergic synapses.

Albumins↗
PubMed1992

Repetitive transients in intracellular Ca2+ in cultured human vascular smooth muscle cells.

Human uterine vascular smooth muscle cells have been isolated and maintained in culture. When these cells are exposed to bathing solutions with nominally zero sodium, using potassium, N-methyl-D-glucamine or Tris as substitutes, repetitive transient increases in intracellular calcium are observed. These transients are abolished when the calcium concentration of the bathing solution is reduced to nominally zero suggesting a role for extracellular calcium in the activation or maintenance of the transients. The hypothesis is proposed that the underlying mechanism involves a calcium influx through the reversed operation of a sodium-calcium exchange mechanism and the cyclical activation of calcium-induced calcium release from the sarcoplasmic reticulum. Noradrenaline (10(-6) M) and caffeine (20-30 mM) reversibly inhibited the transients. The inhibitory action of these agents could not be mimicked by dibutyryl cAMP suggesting that cAMP does not mediate the inhibition. Caffeine alone had no effect on resting calcium. Thimerosal (1-100 microM), an agent thought to activate a second type of calcium-induced calcium release mechanism activated repetitive transient increases in intracellular calcium which behave in a similar manner to those activated by sodium removal. These data are consistent with the presence of a thimerosal-activated calcium-induced calcium release mechanism in these cultured human cells. It is proposed that this mechanism is different from the calcium-induced calcium release mechanism, described in other cell types, which is activated by caffeine.

Bucladesine↗
PubMed1982

Selection for mercurial resistance in hospital settings.

The frequency of resistance to Hg2+ in 1980 to 1981 collections from Barnes Hospital, St. Louis, Mo., was only 2% for Staphylococcus aureus and 9% for Escherichia coli. The frequency of Hg2+ resistance in E. coli isolates from Jikei University Hospital, Tokyo, Japan, was 57% during 1972 to 1977 and decreased to 29% in 1979 to 1982; for S. aureus the frequency of Hg2+ resistance dropped from 36% in 1972 to 1977 to 10% in 1979 to 1982. Frequencies of resistances to cadmium (S. aureus) and arsenic (S. aureus and E. coli) remained approximately constant during this time. The decrease in frequency of mercurial resistance is attributed to the termination of the use of organomercurials (largely phenylmercury and thimerosal) in hospital liquid detergents and disinfectants. It is proposed that selection for mercurial resistance occurred within the hospital setting when there was widespread use of mercurials. The resistance patterns and phage types for each of four new mercurial-resistant S. aureus isolates from St. Louis were distinct, indicating that no single type of "hospital staph" predominates. Furthermore, resistance to thimerosal, merbromin, and methylmercury and the ability to volatilize 14C from [14C]methylmercury were found with the new isolates and never with previously known mercurial resistance plasmids in S. aureus.

Bacteria↗