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Biomedical subjects

E Rios

Publications and source records attributed to E Rios.

At least 19 recordsLinked to original sources
PubMed2003

Ca2+ sparks and embers of mammalian muscle. Properties of the sources.

Ca2+ sparks of membrane-permeabilized rat muscle cells were analyzed to derive properties of their sources. Most events identified in longitudinal confocal line scans looked like sparks, but 23% (1,000 out of 4,300) were followed by long-lasting embers. Some were preceded by embers, and 48 were "lone embers." Average spatial width was approximately 2 microm in the rat and 1.5 microm in frog events in analogous solutions. Amplitudes were 33% smaller and rise times 50% greater in the rat. Differences were highly significant. The greater spatial width was not a consequence of greater open time of the rat source, and was greatest at the shortest rise times, suggesting a wider Ca2+ source. In the rat, but not the frog, spark width was greater in scans transversal to the fiber axis. These features suggested that rat spark sources were elongated transversally. Ca2+ release was calculated in averages of sparks with long embers. Release current during the averaged ember started at 3 or 7 pA (depending on assumptions), whereas in lone embers it was 0.7 or 1.3 pA, which suggests that embers that trail sparks start with five open channels. Analysis of a spark with leading ember yielded a current ratio ranging from 37 to 160 in spark and ember, as if 37-160 channels opened in the spark. In simulations, 25-60 pA of Ca2+ current exiting a point source was required to reproduce frog sparks. 130 pA, exiting a cylindric source of 3 microm, qualitatively reproduced rat sparks. In conclusion, sparks of rat muscle require a greater current than frog sparks, exiting a source elongated transversally to the fiber axis, constituted by 35-260 channels. Not infrequently, a few of those remain open and produce the trailing ember.

Animals↗
PubMed2003

Differences between patients with non-Hodgkin's lymphomas in a cohort of HIV/AIDS patients in Puerto Rico.

The close association between AIDS and non-Hodgkin's lymphoma (NHL) is well known. Few studies are available that evaluate the profile of NHL in a cohort of HIV-infected patients who reside in Puerto Rico. The present study was performed in a cohort of 2,843 HIV-infected patients followed in the Retrovirus Research Center at Bayamón, Puerto Rico, evaluated between January 1992 until December 2000. NHL prevalence was determined and differences between AIDS defining and non-AIDS defining NHL were evaluated with the Fisher and ANOVA test. NHL prevalence was 0.9%. Nine (33%) were AIDS-defining (AIDS-d) NHL and 18 (67%) were non-AIDS-d NHL. Both groups were similar in gender distribution and mean diagnosis age. The median CD4+ T cell count at diagnosis was below 150/mm3 in both groups. Injecting drug use was higher in AIDS-d NHL patients and Homo-Bisexual contact was higher in non-AIDS-d NHL patients. Death rate in the first year after the NHL was 67% in the AIDS-d group and 56% in the non-AIDS-d group. AIDS-d NHL incidence decreased after the implementation of combined antiretroviral therapy in the cohort, a finding not seen in the non-AIDS-d NHL. In summary the study detected low NHL prevalence, with high degree of immunological damage at the time of the lymphoma diagnosis. Conversely dissimilar response to the antiretroviral therapies was also perceived in the incidence of the two NHL groups.

Adult↗
PubMed2003

Recurrent pneumonia mortality risk in a HIV/AIDS Puerto Rican cohort.

Recurrent pneumonia (RP) within 12 months is one of the AIDS diagnosis criteria. To gain knowledge of RP infection in HIV-infected patients, we studied 145 RP cases detected in a cohort of 2,996 HIV patients in Puerto Rico between Jan. 1992-Dec. 2001. The RP prevalence was 4.8%; 77.2% were males and 62.1% were injecting drug users (IDU). At the time of RP diagnosis, the mean CD4+ T cell count was 93.8 cells/mm3, 59.3% were in antiretroviral treatment, 13% had received the pneumococcal vaccine and 84.8% had another AIDS related condition. Over 37% received two or more antiretroviral medications. The death rate in the first year after the RP diagnosis was 63.4%. A Cox proportional hazard analysis showed that CD4+ T cells <200/mm3 (p<0.05), history of toxoplasmosis (p<0.01), wasting syndrome (p<0.01), esophageal candidiasis (p<0.05) and lower number of antiretroviral medications (p<0.05) increased their mortality risk. The studied patients had a highly compromised immune system and a very low pneumococcal vaccination percent at the time of RP diagnosis. Low CD4+ T cells significantly increased the hazard and mortality risk of the cases studied. Antecedents of antiretroviral therapy in these patients ensure a better outcome with lower mortality. Efforts to increase the vaccination rate should reduce the RP incidence in our HIV-infected population.

Adult↗
PubMed1997

Regulation of skeletal muscle Ca2+ release channel (ryanodine receptor) by Ca2+ and monovalent cations and anions.

The effects of ionic composition and strength on rabbit skeletal muscle Ca2+ release channel (ryanodine receptor) activity were investigated in vesicle-45Ca2+ flux, single channel and [3H]ryanodine binding measurements. In <0.01 microM Ca2+ media, the highest 45Ca2+ efflux rate was measured in 0.25 M choline-Cl medium followed by 0.25 M KCl, choline 4-morpholineethanesulfonic acid (Mes), potassium 1,4-piperazinediethanesulfonic acid (Pipes), and K-Mes medium. In all five media, the 45Ca2+ efflux rates were increased when the free [Ca2+] was raised from <0.01 microM to 20 microM and decreased as the free [Ca2+] was further increased to 1 mM. An increase in [KCl] augmented Ca2+-gated single channel activity and [3H]ryanodine binding. In [3H]ryanodine binding measurements, bell-shaped Ca2+ activation/inactivation curves were obtained in media containing different monovalent cations (Li+, Na+, K+, Cs+, and choline+) and anions (Cl-, Mes-, and Pipes-). In choline-Cl medium, substantial levels of [3H]ryanodine binding were observed at [Ca2+] <0.01 microM. Replacement of Cl- by Mes- or Pipes- reduced [3H]ryanodine binding levels at all [Ca2+]. In all media, the Ca2+-dependence of [3H]ryanodine binding could be well described assuming that the skeletal muscle ryanodine receptor possesses cooperatively interacting high-affinity Ca2+ activation and low-affinity Ca2+ inactivation sites. AMP primarily affected [3H]ryanodine binding by decreasing the apparent affinity of the Ca2+ inactivation site(s) for Ca2+, while caffeine increased the apparent affinity of the Ca2+ activation site for Ca2+. Competition studies indicated that ionic composition affected Ca2+-dependent receptor activity by at least three different mechanisms: (i) competitive binding of Mg2+ and monovalent cations to the Ca2+ activation sites, (ii) binding of divalent cations to the Ca2+ inactivation sites, and (iii) binding of anions to specific anion regulatory sites.

Adenosine Monophosphate↗
PubMed1996

Identification of palmitoylation sites within the L-type calcium channel beta2a subunit and effects on channel function.

The hydrophilic beta2a subunit of the L-type calcium channel was recently shown to be a membrane-localized, post-translationally modified protein (Chien, A. J., Zhao, X. L., Shirokov, R. E., Puri, T. S., Chang, C. F., Sun, D. D., Rios, E., and Hosey, M. M. (1995) J. Biol. Chem. 270, 30036-30044). In this study, we demonstrate that the rat beta2a subunit was palmitoylated through a hydroxylamine-sensitive thioester linkage. Palmitoylation required a pair of cysteines in the N terminus, Cys3 and Cys4; mutation of these residues to serines resulted in mutant beta2a subunits that were unable to incorporate palmitic acid. Interestingly, a palmitoylation-deficient beta2a mutant still localized to membrane particulate fractions and was still able to target functional channel complexes to the plasma membrane similar to wild-type beta2a. However, channels formed with a palmitoylation-deficient beta2a subunit exhibited a dramatic decrease in ionic current per channel, indicating that although mutations eliminating palmitoylation did not affect channel targeting by the beta2a subunit, they were important determinants of channel modulation by the beta2a subunit. Three other known beta subunits that were analyzed were not palmitoylated, suggesting that palmitoylation could provide a basis for the regulation of L-type channels through modification of a specific beta isoform.

Amino Acid Sequence↗
PubMed1995

Roles of a membrane-localized beta subunit in the formation and targeting of functional L-type Ca2+ channels.

We report several unexpected findings that provide novel insights into the properties and interactions of the alpha 1 and beta subunits of dihydropyridine-sensitive L-type channels. First, the beta 2a subunit was expressed as multiple species of 68-72 kDa; the 70-72-kDa species arose from post-translational modification. Second, cell fractionation and immunocytochemical studies indicated that the hydrophilic beta 2a subunit, when expressed alone, was membrane-localized. Third, the beta 2a subunit increased the membrane localization of the alpha 1 subunit and the number of cells expressing L-type Ca2+ currents, without affecting the total amount of the expressed alpha 1C subunit. Expression of maximal currents in alpha 1C/beta 2a cotransfected cells paralleled the time course of expression of the beta subunit. Taken together, these results suggest that the beta subunit plays multiple roles in the formation, stabilization, targeting, and modulation of L-type channels.

Amino Acid Sequence↗
PubMed1989

Nonlinear charge movement in mammalian cardiac ventricular cells. Components from Na and Ca channel gating.

Intramembrane charge movement was recorded in rat and rabbit ventricular cells using the whole-cell voltage clamp technique. Na and K currents were eliminated by using tetraethylammonium as the main cation internally and externally, and Ca channel current was blocked by Cd and La. With steps in the range of -110 to -150 used to define linear capacitance, extra charge moves during steps positive to approximately -70 mV. With holding potentials near -100 mV, the extra charge moving outward on depolarization (ON charge) is roughly equal to the extra charge moving inward on repolarization (OFF charge) after 50-100 ms. Both ON and OFF charge saturate above approximately +20 mV; saturating charge movement is approximately 1,100 fC (approximately 11 nC/muF of linear capacitance). When the holding potential is depolarized to -50 mV, ON charge is reduced by approximately 40%, with little change in OFF charge. The reduction of ON charge by holding potential in this range matches inactivation of Na current measured in the same cells, suggesting that this component might arise from Na channel gating. The ON charge remaining at a holding potential of -50 mV has properties expected of Ca channel gating current: it is greatly reduced by application of 10 muM D600 when accompanied by long depolarizations and it is reduced at more positive holding potentials with a voltage dependence similar to that of Ca channel inactivation. However, the D600-sensitive charge movement is much larger than the Ca channel gating current that would be expected if the movement of channel gating charge were always accompanied by complete opening of the channel.

Animals↗
PubMed1987

A general procedure for determining the rate of calcium release from the sarcoplasmic reticulum in skeletal muscle fibers.

A general procedure for using myoplasmic calcium transients measured with a metallochromic indicator dye to calculate the time course of calcium release from the sarcoplasmic reticulum in voltage-clamped skeletal muscle fibers is described and analyzed. Explicit properties are first assigned to all relatively rapidly equilibrating calcium binding sites in the myoplasm so that the calcium content (CaF) in this pool of "fast" calcium can be calculated from the calcium transient. The overall properties of the transport systems and relatively slowly equilibrating binding sites that remove calcium from CaF are then characterized experimentally from the decay of CaF following fiber repolarization. The rate of calcium release can then be calculated as dCaF/dt plus the rate of removal of calcium from CaF. Two alternatives are assumed for the component of CaF that is due to fast binding sites intrinsic to the fiber: a linear instantaneous buffer or a set of binding sites having properties similar to thin filament troponin. Both assumptions yielded similar calcium release wave forms. Three alternative methods for characterizing the removal system are presented. The choice among these or other methods for characterizing removal can be based entirely on convenience since any method that reproduces the decay of CaF following fiber repolarization will give the same release wave form. The calculated release wave form will be accurate provided that the properties assumed for CaF are correct, that release turns off within a relatively short time after fiber repolarization, that the properties of the slow removal system are the same during and after fiber depolarization, and that possible spatial nonuniformities of free or bound calcium do not introduce major errors.

Animals↗
PubMed1987

Intramembrane charge movement in frog skeletal muscle fibres. Properties of charge 2.

1. Membrane currents were measured in cut skeletal muscle fibres voltage-clamped in a double Vaseline gap in solutions that had impermeant ions substituted for Na+, K+ and Cl-. The fibres were maintained at a holding potential of 0 mV. Pulses to positive voltages elicited outward currents that were proportional to voltage at all times; these were used to estimate linear capacitive currents, which in turn were used in the construction of non-linear current transients. 2. Large negative-going pulses elicited proportionally larger inward currents that decayed during the pulse with voltage-dependent kinetics. A portion of the non-linear current could be eliminated by solutions containing EGTA, as well as by large negative conditioning pulses of 200 ms or more. This portion was probably an inward Ca2+ current. 3. The non-linear current remaining in EGTA-containing solutions had characteristics of intramembrane charge movement ('charge 2'). This charge depended on voltage according to a two-state Boltzmann function of average parameters Qmax = 47.7 nC/microF, V = -115 mV, K = 21.5 mV (seven fibres). 4. The charge movement current transients were single-exponential decays (after a short rising phase) with time constants (tau) that depended on voltage (V). A single-barrier Eyring rate model described well the dependence of time constant on voltage. This fit permitted an independent estimate of a transition voltage, V, and a slope parameter K related to apparent valence of the mobile particle. The values of V and K that best fitted the kinetic data were close to the corresponding values estimated from the charge vs. voltage distribution. 5. Effective capacitance was measured by the transfer of capacitive charge by a small pulse superimposed on a variable pre-pulse. The capacitance was found to depend on pre-pulse voltage. The voltage dependence of the capacitance was as expected from the properties of charge 2 measured independently in the same fibres. 6. The presence of charge 2, defined as charge that moves in a very negative voltage range, was compared on the same fibres in a depolarized and a normally polarized (holding potential = -100 mV) situation. All fibres had less charge 2 at a holding potential of -100 mV (14 nC/microF average reduction). In these fibres charge 1, explored with pulses from -70 mV to 0 mV, was greater at a holding potential of -100 mV (18 nC/microF average increase).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

Simultaneous measurements of Ca2+ currents and intracellular Ca2+ concentrations in single skeletal muscle fibers of the frog.

The relationship between Ca2+ current amplitudes and myoplasmic Ca2+ transients was studied in single muscle fibers. Segments of muscle fibers were voltage-clamped in a double Vaseline gap chamber. Ca2+ transients were measured as an optical signal derived from the interaction between Ca2+ and the dye antipyrylazo III. The cells were maintained at -90 mV. Ca2+ currents were detected at pulse potentials to -50 mV, reached a maximum value at 0 mV, were reduced in size for larger depolarizations, and reversed at about 40 mV. Ca2+ transients were also detected at -50 Mv and progressively increased in size with larger pulse potentials up to 10 mV. Depolarizations to voltages greater than 10 mV did not further increase the size of the transient. The magnitude and time course of transients from 10 to 70 mV were almost identical Ca2+ fluxes into the myoplasm (Ca2+ input fluxes) were calculated from the Ca2+ transients applying a removal model. The size of the input fluxes increased with depolarization up to 0 mV. Between 0 and 70 mV the peak input flux slightly increased, while the flux measured at 200 ms remained unchanged. In conclusion, Ca2+ transients and input fluxes were not reduced during pulses to large positive potentials, even though a drastic reduction of Ca2+ current occurred at these potentials. These observations make it very unlikely that a voltage-dependent Ca2+ entry is the triggering signal for contraction.

Animals↗
PubMed1985

Use of a metallochromic indicator to study intracellular calcium movements in skeletal muscle.

The transient increase in free myoplasmic calcium concentration due to depolarization of a skeletal muscle fibre is the net result of the release of calcium from the sarcoplasmic reticulum (SR) and its simultaneous removal by binding to various sites and by reuptake into the SR. We review here procedures recently developed in this laboratory for empirically characterizing the calcium removal processes in voltage-clamped fibres and for using such characterization to determine the time course of SR calcium release during a depolarizing pulse.

Animals↗
PubMed1984

Time course of calcium release and removal in skeletal muscle fibers.

The transient increase in free myoplasmic calcium concentration due to depolarization of a skeletal muscle fiber is the net result of the release of calcium from the sarcoplasmic reticulum (SR) and its simultaneous removal by binding to various sites and by reuptake into the SR. We present a procedure for empirically characterizing the calcium removal processes in voltage-clamped fibers and for using such characterization to determine the time course of SR calcium release during a depolarizing pulse. Our results reveal a decline of the SR calcium release rate during depolarization that was not anticipated from simple inspection of the calcium transients.

Animals↗
PubMed1983

Measurement and modification of free calcium transients in frog skeletal muscle fibres by a metallochromic indicator dye.

Myoplasmic free calcium transients were monitored with the metallochromic indicator dye Antipyrylazo III (AP III) in single frog skeletal muscle fibres cut at both ends, stretched so as to minimize or eliminate contractile filament overlap and voltage clamped using a double-Vaseline-gap system (approximately 6 degrees C). The dye entered the central fibre segment by diffusion from the solution applied to the two cut ends. The diffusion coefficient of AP III was about 20 times lower in the fibre than in solution. This very slow diffusion was not due to binding of dye since the ratio of bound to free dye obtained from analysis of the diffusion was only about 0.45. For a given depolarizing pulse, the ratio of dye-related absorbance changes delta A at 720 and 550 nm was the same as that produced on adding calcium to dye in calibrating solution, indicating that these signals were due to changes in myoplasmic calcium. The delta A signals at 700 or 720 nm were used to monitor transient changes in concentration of calcium-dye complex [CaD2] and of free calcium [Ca] in the myofilament space. By applying the same pulse at different times during dye entry, it was observed that increasing dye concentrations [D]T produced the following effects: (a) [CaD2] was increased; (b) [Ca] was decreased at early times during a pulse; (c) a declining phase of [Ca] observed at late times during pulses was decreased and finally reversed to a slow rising phase at high [D]T; (d) the decay of [Ca] after the pulse was slowed. Analyses of the effects of [D]T on (a) the magnitude of [CaD2] at a given early time during the calcium release produced by pulses to a given voltage and on (b) the time constant for [Ca] decay after a pulse were both consistent with a calcium: dye stoichiometry of 1:2 in the fibre as found in calibrating solution. Analysis of the effect of [D]T on the [Ca] decay time constants also revealed the presence of intrinsic rapidly equilibrating myoplasmic calcium binding sites and provided the basis for obtaining estimates of the combined concentration [Ca] of free calcium plus calcium bound to such sites. Unlike the estimates of [Ca], these estimates of [Ca] are independent of the value of the calcium-dye dissociation constant.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

The inotropic memory of amphibian myocardium.

(1) Experimentally observed changes of contractile force induced by changes in the pattern of stimulation of frog ventricular myocardium were compared with predictions computed on the basis of a model for the contractile conditioning, proposed in a previous paper. (2) For this purpose, two functions (Potentiation and Inhibition) which describe in the model the effect of previous contractions, were determined experimentally. (3) It is shown that the model adequately predicts : force-frequency curve Inotropic Effect Curves at different basal frequencies, effect of the suppression of a contraction in a sequence of definite frequency, frequency-staircases, and strength-interval curves. (4) The formal characteristics of the model are discussed, and it is suggested that the potentiation mechanism results from the recirculation of activator calcium in two types of compartments, from which calcium passes to the myofilaments during the contractions or is lost to the exterior with first order kinetics during the rest period. Possible locations for these compartments are proposed. Various hypothesis on the nature of the inhibitory mechanism are considered.

Animals↗
PubMed1975

The inotropic memory of amphibian myocardium. I.-Identification of two stimultaneous mechanisms and statement of a model.

(1) The effects of previous contractions on the actual contractile strength is studied in strips of toad ventricle. The inotropic effect is quantified by superposing a conditioning contraction to a rhythm of definite frequency, its measure being the difference in strength between a rhythm contraction in the presence and in the absence of the conditioning one. (2) The inotropic effect is studied as a function of the interval between the actual and conditioning contractions. Depressed sections of the curve, associated to shortened action potentials, are detected and excluded. (3) The inotropic effect is always positive at low frequencies, but at higher frequencies and long intervals it becomes negative. (4)In high calcium concentration the inotropic effect is always negative and does not depend on frequency. Morever, the joint effect of two previous contractions is equal to the sum of the individual effects of each one. (5) The results are interpreted in terms of two independent elementary processes, one of which potentiates whereaas the other inhibits the strength of contraction. The former disappears in high calcium. Assuming some simple properties for these processes a mathematical expression has been achieved. This expression describes the inotropic effect of any sequence of contractions as a function of intervals involved.

Action Potentials↗
PubMed1975

Relationship of maternal and infant iron stores as assessed by determination of plasma ferritin.

Using plasma ferritin derminations, iron stores have been evaluated at the end of pregnancy in 26 women and followed sequentially in their healthy, full-term infants. It has been shown that the iron storage status of the mother does not affect the iron status of the infant. Determinations of plasma ferritin in the infants have demonstrated that by 6 months of age the iron status of the infant reflects the adequacy of the dietary intake of iron. In the absence of effective iron supplementation during the first six months, plasma ferritin levels fall to low levels, indicating the depletion of iron stores in the infant.

Adult↗