Endogenous Mobilization Research Articles

Estimating the Effect of a Change in Insurance Pricing Regime on Accidents with Endogenous Mobility

In this paper, we estimate the impact of introducing a bonus-malus system on the probability of having automobile accidents, taking into account contract duration or the client mobility between insurers. We show that the new incentive scheme reduces accident rates of all policyholders when contract duration is taken into account, but does not

Testing for Asymmetric Employer Learning

Recent evidence suggests that employers acquire more precise information about a worker’s productivity the more time he or she spends in the labor market. The following question arises: Is learning symmetric, that is, do all employers have the same information about workers’ productivity, or is learning asymmetric, that is, does the current employer have superior information about workers’ productivity? This article develops a learning model with endogenous mobility that nests both learning hypotheses. It then proposes new tests for asymmetric employer learning. Overall, learning appears to be mostly symmetric, except possibly when the employees involved are college graduates.

APOBEC3G and HIV-1: Strike and counterstrike

APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. This restriction is counteracted by the HIV-1 virion infectivity factor (Vif) protein, whose activity culminates in depletion of A3G from infected cells. In the absence of Vif, viruses encapsidate A3G, which acts in part to mutate viral DNA formed during reverse transcription upon subsequent infection of a new cell. Cellular A3G also functions as a post-entry restriction factor for HIV in resting CD4 T cells, where it resides in a low molecular mass form. Unfortunately, this barrier is forfeited when CD4 T cells are activated because A3G is recruited into inactive high molecular mass ribonucleoprotein complexes. In addition to restricting HIV, A3G and related deaminases may counter other retroviruses and protect the cell from endogenous mobile retroelements. Understanding A3G complex assembly and its interplay with HIV Vif may make possible future development of a new class of HIV therapeutic agents.

Amide proton transfer imaging of human brain tumors at 3T

Amide proton transfer (APT) imaging is a technique in which the nuclear magnetization of water-exchangeable amide protons of endogenous mobile proteins and peptides in tissue is saturated, resulting in a signal intensity decrease of the free water. In this work, the first human APT data were acquired from 10 patients with brain tumors on a 3T whole-body clinical scanner and compared with T1- (T1w) and T2-weighted (T2w), fluid-attenuated inversion recovery (FLAIR), and diffusion images (fractional anisotropy (FA) and apparent diffusion coefficient (ADC)). The APT-weighted images provided good contrast between tumor and edema. The effect of APT was enhanced by an approximate 4% change in the water signal intensity in tumor regions compared to edema and normal-appearing white matter (NAWM). These preliminary data from patients with brain tumors show that the APT is a unique contrast that can provide complementary information to standard clinical MRI measures.

APOBEC3G and HIV-1: Strike and counterstrike

APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. This restriction is counteracted by the HIV-1 virion infectivity factor (Vif) protein, whose activity culminates in depletion of A3G from infected cells. In the absence of Vif, viruses encapsidate A3G, which acts in part to mutate viral DNA formed during reverse transcription upon subsequent infection of a new cell. Cellular A3G also functions as a post-entry restriction factor for HIV in resting CD4 T cells, where it resides in a low molecular mass form. Unfortunately, this barrier is forfeited when CD4 T cells are activated because A3G is recruited into inactive high molecular mass ribonucleoprotein complexes. In addition to restricting HIV, A3G and related deaminases may counter other retroviruses and protect the cell from endogenous mobile retroelements. Understanding A3G complex assembly and its interplay with HIV Vif may make possible future development of a new class of HIV therapeutic agents.

Clinical and therapeutical implications of EPC biology in atherosclerosis

Bone marrow-derived circulating endothelial progenitor cells have been succesfully used to enhance angiogenesis after tissue ischemia. The role of endothelial progenitor cells in endothelial cell homeostasis and their putative role in atherogenesis have been recently investigated. Cardiovascular risk factors negatively influence endothelial progenitor cell number and function while vasculoprotection e.g. by statins, estrogens and physical activity may be partly mediated by progenitor cells. Endogenous mobilization or injection of ex-vivo generated endothelial progenitor cells is associated with an enhanced reendothelialization, an improvement of endothelial function and reduced athersclerotic burden. In contrast, endothelial progenitor cells may promote plaque angiogenesis in animal models and may negatively influence plaque development and stability. However, in humans with coronary atherosclerotic disease, endothelial progenitor cells are a novel risk prdictor for cardiovascular mortality and morbidity. In this review we focus on the role of circulating endothelial progenitor cells in endothelial cell repair mechanisms at the vascular wall and their potentially protective and therapeutic role in atherosclerotic disease.

Facilitation through Buffer Saturation: Constraints on Endogenous Buffering Properties

Synaptic facilitation (SF) is a ubiquitous form of short-term plasticity, regulating synaptic dynamics on fast timescales. Although SF is known to depend on the presynaptic accumulation of Ca 2+, its precise mechanism is still under debate. Recently it has been shown that at certain central synapses SF results at least in part from the progressive saturation of an endogenous Ca 2+ buffer (Blatow et al., 2003), as proposed by Klingauf and Neher (1997). Using computer simulations, we study the magnitude of SF that can be achieved by a buffer saturation mechanism (BSM), and explore its dependence on the endogenous buffering properties. We find that a high SF magnitude can be obtained either by a global saturation of a highly mobile buffer in the entire presynaptic terminal, or a local saturation of a completely immobilized buffer. A characteristic feature of BSM in both cases is that SF magnitude depends nonmonotonically on the buffer concentration. In agreement with results of Blatow et al. (2003), we find that SF grows with increasing distance from the Ca 2+ channel cluster, and increases with increasing external Ca 2+, [Ca 2+] ext, for small levels of [Ca 2+] ext. We compare our modeling results with the experimental properties of SF at the crayfish neuromuscular junction, and find that the saturation of an endogenous mobile buffer can explain the observed SF magnitude and its supralinear accumulation time course. However, we show that the BSM predicts slowing of the SF decay rate in the presence of exogenous Ca 2+ buffers, contrary to experimental observations at the crayfish neuromuscular junction. Further modeling and data are required to resolve this aspect of the BSM.

Genomic localization of endogenous mobile CACTA family transposons in natural variants of Arabidopsis thaliana.

The differentiation between gene-rich and transposon-rich (gene-poor) regions is a common feature of plant genomes. This may be due to preferential integration of transposons into gene-poor regions or may be due to purifying selection against transposon insertion into gene-rich regions. We examined the distribution of a low-copy-number mobile subfamily of Arabidopsis CACTA transposons in the genomes of 19 natural variants (ecotypes) of A. thaliana, and compared that to the pattern of integrations induced in the laboratory by mutation of the DDM1 (Decrease in DNA Methylation) gene. Sequences similar to mobile CACTA1 copies were distributed among the ecotypes and showed high degrees of polymorphism in genomic localization. Despite the high level of polymorphism, the copy number was low in all the ecotypes examined, and the elements were localized preferentially in pericentromeric and transposon-rich regions. This contrasts with the pattern of transposition induced by the ddm1 mutation, in which the range of integration sites is less biased and the copy number frequently increases. Based on these observations, we discuss the possible contribution of natural selection and chromatin structure to the distribution of transposons.

Metabolite comparisons and the identity of nutrients translocated from symbiotic algae to an animal host

Dinoflagellate algae of the genus Symbiodinium in symbiosis with marine animals release much of their photosynthetic carbon to the animal host. The compounds translocated to the host ('mobile compounds') were investigated by metabolite comparison as follows: a substrate was identified as a candidate mobile compound when comparable profiles of metabolites were generated from host metabolism of this substrate (supplied exogenously) and the endogenous mobile compounds. When the sea anemone Anemonia viridis was incubated with NaH14CO2 under photosynthesizing conditions, most of the radioactivity in the animal tissue was recovered from the low-molecular-mass fraction and distributed in the ratio 1:2:1 between the neutral, acidic and basic sub-fractions. Prominent 14C-labelled compounds included glucose, malate and glucose-6-phosphate. When the symbiosis was incubated with 14C-labelled glucose plus succinate or fumarate (but none of eight other substrate combinations tested), the 14C-labelled metabolites closely matched those obtained with NaH14CO2. These data suggest that glucose and succinate/fumarate (or metabolically allied compounds) may be important photosynthetic compounds transferred from the Symbiodinium cells to the tissues of A. viridis. Metabolite comparisons can be applied to study nutritional interactions in symbioses involving photosynthetic algae and, with appropriate modification, other associations between microorganisms and plants or animals.

Barriers to mobility in the Europe's Civil Aviation Markets:theory and new evidence

A questionnaire-based survey is applied to investigate the perception of mobilitybarriers by European airline managers. Whilst the liberalisation of Europe's airline markets removed regulatory mobility barriers, we find that mobility impediments still appear to exist. Potential entrants moreover, perceive some mobility barriers as significantly more effective than others. The perceived effectiveness of a particular mobility barrier varies considerably among airline managers. We also provide an overview of previous studies on the contestability hypothesis and the effectiveness of endogenous (strategic) mobility barriers. Our results support earlier findings for the U.S. to the effect that barriers to mobility are perceived to exist and matter. Whilst our results are clearly subjective, as they are based on the perceptions of managers, we believe such perceptions matter as they inform managerial actions. In this sensewe believe our results are of value.

Dynamics of intracellular calcium in hair cells isolated from the semicircular canal of the frog

Changes in cytosolic free Ca2+concentration ([Ca2+]i) were monitored optically in hair cells mechanically isolated from frog semicircular canals using the membrane-impermeant form of the Ca2+-selective dye Oregon Green 488 BAPTA-1 (OG, 100μM). Cells stimulated by depolarization under whole-cell voltage clamp conditions revealed Ca2+entry at selected sites (hotspots) located mostly in the lower (synaptic) half of the cell body. [Ca2+]iat individual hotspots rose with a time constant τ1∼70ms and decayed with a bi-exponential time-course (τ2∼160, τ3∼2500ms) following a 160ms depolarization to −20mV. With repeated stimulation [Ca2+]iunderwent independent amplitude changes at distinct hotspots, suggesting that the underlying Ca2+channel clusters can be regulated differentially by intracellular signalling pathways. Block by nifedipine indicated that the L-type Ca2+channels are distributed at different densities in distinct hotspots. No diffusion barrier other than the nuclear region was found in the cytosol, so that, during a prolonged depolarization (lasting up to 1s), Ca2+was able to reach the cell apical ciliated pole. The effective Ca2+diffusion constant, measured from the progression of Ca2+wavefronts in the cytosol, was ∼57mmμm2/s. Our results indicate that in these hair cells, buffered diffusion of Ca2+proceeds evenly from the source point to the cell interior and is dominated by the diffusion constant of the endogenous mobile buffers.

Oleate acutely stimulates the secretion of triacylglycerol by cultured rat hepatocytes by accelerating the emptying of the secretory compartment.

The acute effects of addition of oleate on the rate of triacylglycerol (TAG) secretion by cultured rat hepatocytes were studied by monitoring the use of endogenous (14C-prelabeled) acyl moieties and exogenous (3H-labeled) oleate for the synthesis of secreted TAG simultaneously. Inclusion of exogenous oleate in the medium stimulated the secretion of the endogenous 14C-labeled acyl moieties by 55-100%. To find out whether the stimulation was due to increased endogenous TAG mobilization or an increased rate of processing of TAG within the endoplasmic reticulum (ER) secretory machinery, use was made of the inhibition of apolipoprotein B (apoB) synthesis (but not degradation) by Ca2+ mobilization from the ER. Inhibition of apoB synthesis stopped entry of acyl moieties (from endogenous and exogenous sources) into the secretory pathway. However, even when entry of acyl moieties into the secretory pathway was totally inhibited, exogenous oleate was still able to stimulate (twofold) the secretion [14C]TAG, indicating that oleate stimulates the emptying of prelabeled TAG from the secretory compartment at a point distal to apoB synthesis and nascent particle formation. These data indicate that exogenous oleate, besides providing additional acyl moieties for incorporation into secreted TAG, stimulates the secretion of endogenous TAG in a manner (i) that is independent of effects on apoB synthesis and/or degradation and (ii) that involves the enhanced processing of TAG resident within the ER secretory pathway.

The spatial relationship between Ca2+channels and Ca2+-activated channels and the function of Ca2+-buffering in avian sensory neurons

In order to learn about the endogenous Ca2+-buffering in the cytoplasm of chick dorsal root ganglion (DRG) neurons and the distance separating the ryanodine receptor Ca2+release channels (RyRs) from the plasma membrane, we monitored the amplitude and time course of Ca2+-activated Cl–currents (lCl(Ca)) in protocols that manipulated Ca2+-buffering. lCl(Ca)was activated by Ca2+influx via voltage-gated Ca2+channels or by Ca2+release via RyRs activated by 10mM caffeine. lCl(Ca)was measured in neurons at 20°C and 35°C using the amphotericin perforated patch technique that preserves endogenous Ca2+-buffering, or at 20°C in neurons dialyzed with pipette solutions designed to replace the endogenous Ca2+buffers. The amplitude of lCl(Ca)activated by Ca2+influx or Ca2+at 20°C was similar in the amphotericin neurons and neurons dialyzed with an ‘unbuffered’ pipette solution containing 10mM citrate and 3mM ATP as the only Ca2+binding molecules. Thus, endogenous mobile Ca2+buffers are relatively unimportant in chick DRG neurons. Warming the neurons from 20°C to 35°C increased the amplitude and the rate of deactivation of lCl(Ca)consistent with an increased rate of Ca2+buffering by fixed endogenous Ca2+-buffers. Dialysis with 2mM EGTA/0.1μM free Ca2+reduced the amplitude and increased the rate of deactivation of lCl(Ca)activated by Ca2+influx and abolished lCl(Ca)activated by Ca2+release. Dialysis with 2mM BAPTA/0.1μM free Ca2+abolished lCl(Ca)activated by Ca2+influx or release. Dialysis with 42mM HEEDTA/0.5μM free Ca2+caused the persistent activation of lCl(Ca). Calculations using a Ca2+-diffusion model suggest that the voltage-gated Ca2+channels and the Ca2+-activated Cl–channels are separated by 50–400nm and that the RyRs are more than 600nm from the plasma membrane.

Vitamin A status and postnatal dexamethasone treatment in bronchopulmonary dysplasia.

Vitamin A (retinol) plays an important role in epithelial regeneration during recovery from lung injury in bronchopulmonary dysplasia (BPD). Dexamethasone is used in the postnatal treatment of very low birth weight (VLBW) neonates with BPD. To test the hypothesis that the vitamin A status is critical for the beneficial pulmonary response to dexamethasone, we performed a prospective cohort study in which we characterized the changes in plasma concentrations of vitamin A and retinol-binding protein (RBP) in response to dexamethasone, and correlated these changes with the pulmonary outcome. VLBW neonates (birth weight <1350 g, gestational age <31 weeks, postnatal age >10 days), who had presumptive diagnosis of severe BPD and need for high ventilatory support (fraction of inspired oxygen >/=.6, mean airway pressure >/=7 cm H(2)O), were treated with a seven-day course of dexamethasone (.5 mg/kg/d x 2 days,.25 mg/kg/d x 2 days,.1 mg/kg/d x 3 days). Plasma concentrations of vitamin A and RBP were determined sequentially at baseline, and during and after dexamethasone treatment. Pulmonary response to dexamethasone was graded daily using a composite ventilation score. The changes in plasma vitamin A and RBP concentrations were compared between infants with a positive (beneficial) pulmonary response to dexamethasone and those with a negative response. Among 23 infants studied, 13 showed a positive pulmonary response to dexamethasone, as indicated by successful weaning from supplemental oxygen and mechanical ventilation, whereas 10 showed a negative response. A significant, yet short-term, increase in plasma concentrations of both vitamin A and RBP was observed in most infants treated with dexamethasone. The plasma vitamin A and RBP responses to dexamethasone tended to be higher in infants with a positive pulmonary response than in those with a negative response. Accounting for gender, a vitamin A response with each 10.0 microg/dL increment in plasma vitamin A concentration was associated with a 60% increase in the odds favoring a positive pulmonary response to dexamethasone. Postnatal dexamethasone treatment in VLBW neonates with BPD induces a significant, yet short-term, increase in plasma concentrations of both vitamin A and RBP. This increase probably results from endogenous mobilization of vitamin A from the liver. Our data suggest that the beneficial pulmonary response to dexamethasone in infants with BPD is influenced, at least in part, by the vitamin A status, and that gender plays a role in this response.vitamin A, dexamethasone, bronchopulmonary dysplasia.

Transmitter release modulation in nerve terminals of rat neocortical pyramidal cells by intracellular calcium buffers.

1. Dual whole-cell voltage recordings were made from synaptically connected layer 5 (L5) pyramidal neurones in slices of the young (P14-P16) rat neocortex. The Ca2+ buffers BAPTA or EGTA were loaded into the presynaptic neurone via the pipette recording from the presynaptic neurone to examine their effect on the mean and the coefficient of variation (c.v.) of single fibre EPSP amplitudes, referred to as unitary EPSPs. 2. The fast Ca2+ buffer BAPTA reduced unitary EPSP amplitudes in a concentration dependent way. With 0.1 mM BAPTA in the pipette, the mean EPSP amplitude was reduced by 14 +/- 2.8% (mean +/- s.e.m., n = 7) compared with control pipette solution, whereas with 1.5 mM BAPTA, the mean EPSP amplitude was reduced by 72 +/- 1.5% (n = 5). The concentration of BAPTA that reduced mean EPSP amplitudes to one-half of control was close to 0.7 mM. 3. Saturation of BAPTA during evoked release was tested by comparing the effect of loading the presynaptic neurone with 0.1 mM BAPTA at 2 and 1 mM [Ca2+]o. Reducing [Ca2+]o from 2 to 1 mM, thereby reducing Ca2+ influx into the terminals, decreased the mean EPSP amplitude by 60 +/- 2.2% with control pipette solution and by 62 +/- 1.9% after loading with 0.1 mM BAPTA (n = 7). 4. The slow Ca2+ buffer EGTA at 1 mM reduced mean EPSP amplitudes by 15 +/- 2.5% (n = 5). With 10 mM EGTA mean EPSP amplitudes were reduced by 56 +/- 2.3 % (n = 4). 5. With both Ca2+ buffers, the reduction in mean EPSP amplitudes was associated with an increase in the c.v. of peak EPSP amplitudes, consistent with a reduction of the transmitter release probability as the major mechanism underlying the reduction of the EPSP amplitude. 6. The results suggest that in nerve terminals of thick tufted L5 pyramidal cells the endogenous mobile Ca2+ buffer is equivalent to less than 0.1 mM BAPTA and that at many release sites of pyramidal cell terminals the Ca2+ channel domains overlap, a situation comparable with that at large calyx-type terminals in the brainstem.

Phospholipase A2-Mediated Activation of Phospholipase D in Rat Heart Sarcolemma

The effect of phospholipase A2(PLA2)-dependent release of unsaturated fatty acids (FA) on phospholipase D (PLD) function was examined in purified sarcolemmal (SL) membranes isolated from rat heart. PLD hydrolytic activity was determined by measuring either [14C] phosphatidic acid formation from exogenous [14C] phosphatidylcholine (PtdCho) or [3H] choline release from prelabelled SL Ptd[3H]choline. SL membranes with endogenous [3H] PtdCho that were prelabelled with [3H] myristic acid were used for testing PLD transphosphatidylation activity. Exogenouscis-unsaturated FA, arachidonate and oleate, significantly enhanced the [3H] choline formation at 50 and 100μm, respectively; their effect was maximal at 250μmand declined at higher concentrations. Use of melittin (which stimulates membrane-bound PLA2, thus releasing FA) or exogenous PLA2reproduced the stimulatory effect of added arachidonate and oleate. Under melittin, PLA2-dependent FA release was strongly correlated (r=0.99) to the PLD-dependent phosphatidic acid formation. Arachidonate- or melittin-enhanced PLD transphosphatidylation activity confirmed the augmented catalytic rate of PLD by these agents. Melittin-evoked PLD activation was completely blocked by 1μmE-6-(bromomethylene) tetrahydro-3-(1-naphthalenyl)-2H-pyran-2-one, a selective inhibitor of Ca2+-independentvCa2+-dependent PLA2, thus indicating that PLD stimulation under melittin occurred via PLA2. Activity measurement and Western blotting studies revealed the presence of a Ca2+-independent, high molecular weight (110 kDa) PLA2in the SL membrane, and its immunoprecipitation by monoclonal antibodies significantly reduced the melittin-related PLD stimulation. These results suggest that Ca2+-independent PLA2and subsequent endogenous mobilization ofsn-2 unsaturated FA modulate PLD activity in heart SL membranes. This event may occur in physiological conditions via hormonal stimulation of membranal PLA2as well as in heart diseases characterized by PLA2pathological dysfunction.

Analytical steady-state solution to the rapid buffering approximation near an open Ca2+ channel

We derive an analytical steady-state solution for the Ca2+ profile near an open Ca2+ channel based on a transport equation which describes the buffered diffusion of Ca2+ in the presence of rapid stationary and mobile Ca2+ buffers (Wagner and Keizer, 1994). This steady-state rapid buffering approximation gives an upper bound on local Ca2+ elevations such as Ca2+ puffs or sparks when conditions for the validity of the rapid buffering approximation are met and is an alternative to approximations that assume that mobile buffers are unsaturable. This result also provides an analytical estimate of the cytosolic Ca2+ domain concentration ([Ca2+]d) near a channel pore and shows the dependence of [Ca2+]d on moderate concentrations of endogenous mobile buffer, Ca2+ indicator dye, and bulk cytosolic Ca2+. Assuming a simple relationship between [Ca2+]d and the lumenal depletion domain of an intracellular Ca2+ channel, lumenal and cytosolic Ca2+ profiles are matched to give an implicit analytical expression for the effect of bulk lumenal Ca2+ on [Ca2+]d.

Pre- and postsynaptic whole-cell recordings in the medial nucleus of the trapezoid body of the rat.

1. Simultaneous whole-cell recordings in a rat brain slice preparation are described from presynaptic terminals (calyces of Held) and postsynaptic somata which form an axosomatic synapse in the medial nucleus of the trapezoid body (MNTB). 2. Presynaptic action potentials evoked suprathreshold excitatory postsynaptic potentials (EPSPs). The minimum synaptic delay was around 0.4 ms at 36 degrees C and 0.9 ms at 23-24 degrees C. The amplitude of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor-mediated component of the excitatory postsynaptic currents (EPSCs) was 2-13 nA (at -80 mV). 3. Current-voltage relations showed that presynaptic Ca2+ channels were of the high voltage-activated type. 4. A single action potential evoked a presynaptic fluorescence transient that decayed with a time constant of 0.3-0.7 s, depending on the concentration (60-200 microM) of the Ca2+ indicator Calcium Green-5N (CG-5N). The peak amplitude of the [Ca2+]i transient was severalfold larger in the terminal than in the preterminal axon. 5. EPSC peak amplitudes were stable for more than 30 min after establishing the whole-cell configuration in the presynaptic terminal when the pipette contained 50 microM BAPTA. In contrast, with 1 mM BAPTA, peak amplitudes of EPSCs were reduced to one-third. 6. Trains of presynaptic action potentials evoked EPSCs with progressively smaller amplitudes. Little change was observed in the depression when the terminals were dialysed with 50 microM BAPTA, whereas depression was reduced with 1 mM BAPTA. 7. In low (1 mM) [Ca2+]o, facilitation instead of depression of EPSCs was observed. 8. The effects of presynaptic BAPTA suggest that the endogenous mobile Ca2+ buffer capacity of giant presynaptic terminals in the MNTB is lower than in other terminals of fast transmitting synapses.

Rapid Aequorin Loading into Platelets in the Presence of DMSO - Characteristics of the Responses (Changes in Light Transmission and in Calcium) to Various Agonists

We have looked at different parameters which could modify platelet behaviour during and after aequorin loading in the presence of DMSO. There is a decreased platelet reactivity in response to ADP, PAF and A-23,187 which appears to be mainly due to the exposure to EGTA during washing and loading and the 1 ml volume of the test suspension. All the studied agonists (including PMA) which elicit aggregation are able to induce an intracellular Ca2+ change detected with the aequorin probe. By contrast, epinephrine alone induces neither aggregation nor Ca2+ rise, but potentiates the responses to ADP. Different consecutive phases in Ca2+ changes after stimulation with ADP, PMA and A-23,187 can be evidenced. In the presence of external Ca2+, the second component of the Ca2+ change evoked with ADP is dependent on aggregation and the subsequent TXA2 synthesis. When the external medium is Ca2+ depleted, the two Ca2+ peaks induced by ADP disappear whereas a Ca2+ rise persists (endogenous mobilization) with the other agonists, being independent of TXA2 and ADP release. Ca2+ mobilization parallels activation with A-23,187 but not with low concentrations of thrombin.

Effects of Diets of Homogeneous Saturated Triglycerides on Cholesterol Balance in Rats

The effects of a diet of 10% homogeneous triglycerides of 12 to 18-carbon chain saturated fatty acids on cholesterol absorption and turnover were studied in rats. Cholesterol absorption was successively significantly less in rats fed tristearin than in groups fed tripalmitin, trimyristin and trilaurin. Lesser fatty acid absorption may explain the differences in part, since cholesterol absorption was significantly correlated with fat absorption. Cholesterol removal from plasma was fastest in rats fed tristearin. Plasma cholesterol levels were increased with the trilaurin diet although the rate of cholesterol accumulation in lymph after gavage was slower with trilaurin. Lymph triglycerides were highest with trilaurin and trimyristin diets perhaps indicating endogenous mobilization of triglyceride for lipoprotein formation. Lymph triglycerides were, however, decreased with tristearin. Sterol turnover (production, absorption plus synthesis) was increased with tristearin or trilaurin by kinetic or balance methods.