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Biomedical subjects

A Noma

Publications and source records attributed to A Noma.

At least 145 records · Page 8Linked to original sources
PubMed1990

Inhibitory effect of acyclic retinoid (polyprenoic acid) on the secretion of alpha-fetoprotein in CCl4-treated rats.

A study was conducted to examine the inhibitory effect of acyclic retinoid (polyprenoic acid) on the secretion of alpha-fetoprotein (AFP) in rats with chronic liver damage induced by CCl4. Oral administration of the compound brought about a significant reduction of serum AFP levels at the time when liver cirrhosis was formed. Acyclic retinoid also decreased the activities of serum aminotransferases and ornithine carbamyl transferase, while it increased serum albumin levels, demonstrating the reduction of hepatic parenchymal damage. Significant negative correlation was observed between serum AFP and albumin levels. This cytoprotective effect of the retinoid on the parenchymal cell may well be related to the inhibition of the synthesis and/or secretion of AFP. No significant side effect was observed, despite a long-term administration of the compound. The present finding will provide a potential scope for the future use of acyclic retinoid for the treatment of chronic liver damage.

Animals↗
PubMed1990

[Evaluation of the commercial ELISA method for lipoprotein(a) determination and interference by plasminogen].

We evaluated the "Tint Eliza (Bio pool, Co., Sweden)", based on an ELISA, for the determination of serum lipoprotein(a) [Lp(a)], and the immunological interference by plasminogen on the assay. Results obtained by the present assay were compared with those by our polyclonal ELISA method. The standard curve for this assay was linear to 60 mg/dl of Lp(a). Correlation with results by our method (x) was excellent: y = 0.94x + 1.2 mg/dl (n = 46, r = 0.986, Syx = 2.3). Within-run CVs for the method were 7.3, 4.8 and 4.5% at mean Lp(a) concentration of 4.0, 11.4 and 38.6 mg/dl, respectively. Detection limits were 0.6 mg/dl for Lp(a) in 1:15, 606 diluted sample. Immunological cross-reactivity of anti-Lp(a) antibody used in the present assay was observed in the immunoblot with plasminogen. In recommended procedure the specificity of Lp(a) sufficed to distinguish the cross-reactivity of plasminogen. Mean and median values of 148 blood donors were 15.5 and 11.5 mg/dl, respectively, and were compared well with those by our method.

Apolipoproteins A↗
PubMed1989

Li+ inhibition of membrane current responses to epinephrine in guinea-pig ventricular cells.

Membrane currents of guinea-pig ventricular myocytes were recorded using the whole-cell voltage clamp method. The epinephrine-induced increase in Ca2+ current (2.9 +/- 0.5 times control) was reduced (1.8 +/- 0.3 times) by replacing Na+ with Li+ in the bathing solution. In addition, 0.5 microM epinephrine increased a time-independent membrane conductance in the Na+ external solution, having a reversal potential of -19 +/- 3 mV (epinephrine-induced current). In the Li+ external solution, however, 0.5 microM epinephrine failed to induce the epinephrine-induced current. The findings are consistent with the reported Li+ inhibition of GTP-binding protein and/or adenylate cyclase.

Animals↗
PubMed1989

Lipoprotein(a) in nonhuman primates. Presence and characteristics of Lp(a) immunoreactive materials using anti-human Lp(a) serum.

Lipoprotein(a) (Lp(a] immunoreactive materials were examined in serum samples from 77 nonhuman primates of 24 species by Ouchterlony's double diffusion procedure and an enzyme-linked immunosorbent assay (ELISA) using rabbit antisera to human Lp(a). The precipitates obtained with sera from orang-utan and chimpanzee formed reactions of complete identity with the Lp(a) precipitate with human serum. When sera from Old World monkeys and human subjects were tested in wells next to each other, spurs developed between the 2 precipitates, indicating that Lp(a)-like lipoproteins in Old World monkeys have partial identity with human Lp(a). Lp(a) immunoreactive materials were identified in association with lipids by means of fat staining of the precipitates. On the other hand, reactants which could be precipitated with anti-human Lp(a) sera were not detectable in prosimians and New World monkeys. These results suggest that serum Lp(a)-like lipoprotein is phylogenetically acquired in Old World monkeys. However, the possibility that the structures of serum Lp(a)-like lipoproteins in prosimians and New World monkeys are too different to react with anti-human Lp(a) sera cannot be ruled out.

Animals↗
PubMed1989

Transient changes of serum lipoprotein(a) as an acute phase protein.

Serum lipoprotein(a) (Lp(a)) was serially determined after acute attacks of myocardial infarction and after surgical operations. Acute phase proteins, such as C-reactive protein, alpha 1-acid glycoprotein, alpha 1-antitrypsin and haptoglobin, increased rapidly and markedly after the episodes. Initial values of serum Lp(a) concentrations were almost the same in both groups. Increases in serum Lp(a) levels were also observed during the first few days, with a return to the initial levels after more than 1 month. The periods for reaching maximal levels of acute phase proteins were similar in both groups of patients. On the contrary, the period required for Lp(a) to reach the maximal level in the myocardial infarction group was significantly longer than in the post-operative group. The present study suggests that Lp(a) has the characteristics of an acute phase reactant and may play an important role in recovery from tissue damage.

Acute-Phase Proteins↗
PubMed1989

Measurement of reversal potential of Na+-Ca2+ exchange current in single guinea-pig ventricular cells.

1. To identify the Na+- or Ca2+-induced current as Na+-Ca2+ exchange current and to determine the stoichiometry of the Na+-Ca2+ exchange, the reversal potential was measured in a wide range of external Na+ [( Na+]o) or Ca2+ [( Ca2+]o) concentrations. The Na+- or Ca2+-induced current was recorded in single ventricular cells enzymatically dispersed from guinea-pig hearts, using the technique of whole-cell voltage clamp combined with internal perfusion. 2. In the presence of 10-40 mM-Na+ and 55-803 nM-Ca2+ in the internal solution, an increase of [Ca2+]o from 0.1 to 0.5-20 mM or an increase of [Na+]o from 30 to 50-140 mM induced an extra current associated with an increase in membrane conductance. The reversal potential of these extra currents was determined from an intersection of the current-voltage (I-V) relations obtained in the absence and presence of a Na+-Ca2+ exchange blocker, Ni2+ (2 mM). 3. Ba2+ in the external solution failed to induce the extra current, but inhibited the background conductance having a reversal potential at around 0 mV. Thus, 1 mM-Ba2+ was added to all external solutions, so that a change in the background current was minimized during application of Ca2+ or Ni2+. 4. The relation between [Ca2+]o and amplitude of the Ca2+-induced current was examined in the presence and absence of Ni2+. Lineweaver-Burk analysis revealed that the action of Ni2+ on the extra current might be a mixed type of competitive and non-competitive inhibition. 5. During the application of Ca2+, the Ca2+-induced outward current decayed in a time-dependent manner, resulting in a shift of the I-V relations towards positive potentials. This current decay was inhibited by increasing the capacity of the internal Ca2+-buffer, using BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) or higher concentrations of EGTA. The result indicates that [Ca2+]i, at least under the cell membrane, changes due to ion fluxes through the Na+-Ca2+ exchange and that control of the ion concentrations within the cell is prerequisite for measuring the reversal potential of the Na+-Ca2+ exchange. 6. The shift of both the holding current and the I-V relations during stimulation of the exchange was suppressed, when the membrane potential was clamped at the equilibrium potential of 3Na+:1Ca2+ exchange.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Triple-barrel structure of inwardly rectifying K+ channels revealed by Cs+ and Rb+ block in guinea-pig heart cells.

1. The hypothesis that the inwardly rectifying K+ channel consists of a triple-barrel structure was investigated. Inward currents were recorded under the blocking effects of external Cs+ or Rb+ in the cell-attached configuration of the patch-clamp technique using single ventricular cells enzymatically isolated from guinea-pig hearts. 2. Cs+ (10-100 microM) or Rb+ (20-100 microM) added to the 150 mM-K+ pipette solution induced rapid open-blocked transitions in the inward open-channel currents. In about 20% of experiments the inward current showed two intermediate current levels equally spaced between the unit amplitude and the zero-conductance level. The current fluctuated between these four levels. In the remaining experiments no obvious sublevels were observed except spontaneous ones, whose amplitudes were not always equal to one-third or two-thirds of the unit amplitude. 3. In experiments showing sublevels, the probability that the open-channel current stayed at each level was measured at various concentrations of blockers and membrane potentials. In both Cs+ and Rb+ block, the distribution of the current levels showed reasonable agreement with the binomial theorem. This finding suggests that the inwardly rectifying K+ channel is composed of three equally conductive subunits and each subunit is independently blocked by Cs+ or Rb+. 4. The dwell-time histogram in each substate was well fitted with a single-exponential function. On the assumption of the binomial model, the blocking (mu) and unblocking (lambda) rate for Cs+ and Rb+ were calculated. The value of mu was linearly proportional to the concentration of the blocking ion at a given membrane potential and increased with hyperpolarization (e-fold increase with a change of -43.5 mV in the Cs+ block). lambda was almost independent of the concentration of the blocking ion and less dependent on the membrane potential than mu. 5. The open and blocked times were calculated in experiments showing no clear sublevels. The mean open time was almost equal to the mean dwell time at the full open level in experiments showing sublevels under the same conditions. On the other hand, the mean blocked time was about two or three times longer than the mean dwell time at the zero-conductance level measured in experiments with sublevels. These results may suggest that the instant one of the three subunits is plugged by blocking ions, the remaining two subunits are closed by unknown mechanisms. 6. Our results support the hypothesis that the cardiac inwardly rectifying K+ channel is composed of three equally conductive subunits.

Animals↗
PubMed1989

The Mg2+ block and intrinsic gating underlying inward rectification of the K+ current in guinea-pig cardiac myocytes.

1. The blockade by Mg2+ and intrinsic gating of the channel, which underlie the rectification of the inward rectifier K+ current, was investigated using the oil-gap voltage clamp method in isolated guinea-pig ventricular cells. 2. The inward rectifier K+ current was isolated by subtracting trans-gap currents recorded at an extracellular K+ concentration ([K+]o) of 0 mM from those obtained at 14 mM [K+]o in the presence of a given concentration of intracellular Mg2+ ([Mg2+]i). The reversal potential (V0) of the difference current was near the equilibrium potential for K+ (EK). 3. On repolarization across EK, the inward rectifier K+ current showed a rapid exponential increase. The time constant decreased with increasing hyperpolarization, but it was independent of both [Mg2+]i and the preceding depolarization. 4. When the pre-pulse potential was made progressively positive between V0-20 and V0 + 30 mV, the amplitude of the time-dependent component became larger and the preceding current jump decreased at any [Mg2+]i. With pre-pulses more positive than V0 + 40 mV, the time-dependent component started from almost the zero current level at 2 microM [Mg2+]i. At higher [Mg2+]i (350, 500 and 3000 microM), however, the time-dependent component became smaller as the pre-pulse potential was made more positive than V0 + 40 mV. 5. When the membrane was depolarized from a potential of full activation at 2 microM [Mg2+]i, the initial jump in the outward current was ohmic and was followed by an exponential decay. The time-dependent component of the inward current, recorded on repolarization after increasing durations of the preceding depolarization, developed as the outward current decayed. The time constants of both processes were in good agreement. 6. At 500 microM [Mg2+]i, the outward current on depolarization was instantaneously rectified. The time-dependent component recorded on repolarization developed with prolongation of the pre-pulse with a time course slower than at 2 microM [Mg2+]i. The envelope time course became slower as the potential of the depolarization became more positive. 7. Lowering the temperature from 23 to 15 degrees C slowed the time-dependent current with an apparent Q10 of about 3.5 at V0. 8. Based on the experimental data, kinetic parameters were estimated for a model of Mg2+ block, which well simulated the inward-going rectification of the K+ current. 9. It is concluded that the instantaneous inward rectification on depolarization is due to the Mg2+ block at physiological [Mg2+]i.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Kinetics of ATP-sensitive K+ channel revealed with oil-gate concentration jump method.

Kinetics for gating the ATP-sensitive K+ channel was studied by exposing the inside-out patch to instantaneous changes in the intracellular concentration of ATP ( [ATP]i) using the oil-gate concentration jump technique in guinea pig ventricular cells. The closing time course of the channel after increasing [ATP]i was exponential with a time constant (tau), which decreased with increasing [ATP]i. The linear 1/tau - [ATP]i relation revealed two different binding (closing) rate constants (mu) of 51.7 and 5.6 mM-1.s-1 and predicted a common unbinding (opening) rate constant (lambda) of 3.2 s-1. A variable latent period was observed before channel opening when [ATP]i was decreased. The mechanism of latency is not clear. Once the channel started to open at the change lowering [ATP]i, the opening time course was exponential. Measurements of the exponential tau obtained at 0 mM [ATP]i were divided into two groups with corresponding lambda of 2.8 and 20.1 s-1, respectively. The former agrees with the predicted value of 3.2 s-1, but in the latter case, tau for opening increased as [ATP]i was increased. This increase in tau was attributed to a decrease of lambda, which approached an asymptotic value of 3.2 s-1. We conclude that binding and unbinding of one molecule of ATP determine the gating of ATP-sensitive K+ channel. Different pairs of mu and lambda result in four types of gating patterns and practically two states of sensitivities to ATP.

Adenosine Triphosphate↗
PubMed1989

[Sequential changes in plasma lipoprotein(a) as acute phase protein after myocardial infarction and surgery group].

The plasma lipoprotein(a), apo AI, apo B, and acute phase proteins, were studied in 21 patients with myocardial infarction and in 11 patients after surgery. In the both groups, C-reactive protein showed a rapid increase, and alpha 1 acid glycoprotein, alpha 1 antitrypsin and lipoprotein(a) followed by a moderate increase and restored to normal values after one month. Lipoprotein(a) increased to a maximum on day 11 in the myocardial infarction group, and on day 8 in the surgery group. Only slight changes in apolipoprotein AI and B were noted. We speculate that lipoprotein(a) is an acute phase protein that plays an important roles in recovery from trauma. Recently it was reported that the amino acid sequence of apolipoprotein(a) is partly identical to that of plasminogen. This sequence suggests that lipoprotein(a) and plasminogen are related immunochemically. We examined by immunoblotting technique whether our antibody for lipoprotein(a) is influenced by a plasminogen in plasma. By enzyme-linked immunosorbent assay, it was found that the purity of plasminogen does not influence determination of lipoprotein(a).

Acute-Phase Proteins↗
PubMed1989

[A case of psoriasis vulgaris whose lipoprotein lipase activity decreased during treatment with etretinate].

Treatment with etretinate is known to be effective for patients with psoriasis. However, it has been reported that the administration of etretinate often generates side effects which disturb lipoprotein metabolism. In this study, 5 patients with psoriasis vulgaris were treated with etretinate (1 mg/kg/day), and the changes in serum lipids, apolipoprotein levels, and lipoprotein lipase (LPL) activity were observed. In 4 out of the 5 cases, the above determinations were within the normal range throughout the course. However, in the case of one 35-year old man, LPL activity markedly decreased on day 28 after the administration of etretinate and was restored when the administration was suspended. Furthermore, LPL activity decreased again when the administration was resumed. Therefore, it appeared that the decrease of LPL activity in this case was mainly due to the administration of etretinate.

Adult↗
PubMed1989

Sensitive, direct colorimetric assay for copper in serum.

We have developed a sensitive procedure for determination of serum copper by use of the color reagent 4-(3,5-dibromo-2-pyridylazo)-N-ethyl-N-sulfopropylaniline. After mixing serum sample and reagent, and incubating at 37 degrees C for 5 min, we measure the absorbance of the resulting chelate complex at 580 nm (molar absorptivity, 80,000 L.mol-1.cm-1). Results of the method varied linearly with copper concentration to at least 5 mg/L; the lower limit of detection was 0.1 mg/L. Within-run CVs were 1.6% and 3.3% for copper concentrations of 1.03 and 0.72 mg/L, respectively (n = 10 each). Between-run CV was 2.8% at 1.22 mg/L (n = 14). Results of the proposed method (y) correlated well with those determined by standard atomic absorption spectrophotometric techniques (x): y = 0.99x - 0.02 mg/L; Syx = 0.08; r = 0.977; n = 56. Iron, zinc, cadmium, cobalt, and lead do not interfere.

Aniline Compounds↗
PubMed1988

Enzyme-linked immunosorbent assay of lipoprotein(a) in serum and cord blood.

We have developed a new sensitive method for quantifying lipoprotein(a) (Lp(a] in human serum, using a 'sandwich' type noncompetitive enzyme-linked immunosorbent assay (ELISA). The solid-phase used was a polystyrene plate. The anti-Lp(a) antibody-enzyme conjugate was labelled by linking Fab' fragments to peroxidase (EC 1.11.1.7) by the maleimide method. The minimum detectable concentration was 0.5 ng/well. Routinely, the assay was carried out with 1,000-fold diluted serum, and Lp(a) was quantified between 4.0 and 500 mg/l. Within-run coefficients of variation (CVs) ranged from 3.5% to 10.4% and between-run CVs from 5.0% to 11.1%. Results by the ELISA were in good agreement with those by radial immunodiffusion (r = 0.955). The distribution of Lp(a) in serum from 820 healthy donors was highly skewed: mean 141.1 mg/l, medium 97.9 mg/l. In cord blood, the mean and median were 15.6 and 9.8 mg/l, respectively. This ELISA for Lp(a) has the advantages of being highly sensitive and specific, simple to perform, and does not use radioisotopes.

Adolescent↗