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Biomedical subjects

A Noma

Publications and source records attributed to A Noma.

At least 91 records · Page 5Linked to original sources
PubMed1994

Serum lipid and apolipoprotein levels in patients with psoriasis.

Although there have been extensive studies of serum lipid levels in psoriasis, the data are conflicting. In the present study, 38 male psoriatic patients and 40 age-matched male control subjects were studied. In addition, a 75 g oral glucose tolerance test (OGTT) was performed in 28 patients and 28 age-matched control subjects, in order to exclude subjects with abnormal OGTT values from the study. Twenty-two patients and 26 control subjects had normal OGTT values. There was a tendency for psoriatic patients with normal glucose tolerance to have increased triglyceride levels, but this was not statistically significant. Total cholesterol and high-density lipoprotein-cholesterol levels in patients were normal. However, serum apo B (P < 0.005), C-II (P < 0.005) and C-III (P < 0.005) levels in patients were significantly elevated compared with control subjects. When control subjects and patients with abnormal OGTT values were also included, a significant increase in triglyceride and apo E levels, and a significant decrease in the apo A-I level were observed in psoriatic patients. These findings suggest that psoriasis per se is associated with increases in apo B, C-II and C-III levels, but that this does not profoundly affect lipid levels. The abnormal lipoprotein metabolism may be related to the high incidence of atherosclerosis in psoriasis.

Adult↗
PubMed1994

Etretinate administration reduces serum propeptide of type I procollagen level in patients with psoriasis.

The serum carboxyterminal propeptide of type I procollagen (PICP) level in 26 patients with psoriasis was significantly lower than in control subjects (124 +/- 47 and 224 +/- 78 ng/ml, respectively; P < 0.001). The patients were divided into two groups, those treated with etretinate and untreated patients. PICP levels in the treated group were significantly lower than those in the untreated group (P < 0.001), but there was no difference between the control and untreated groups. In addition, there was a negative correlation between PICP levels and the serum etretinate concentration in treated patients (r = -0.622, P < 0.05). There was no difference between procollagen type III aminoterminal propeptide (PIIIP) levels in patients and controls, nor was there any significant difference between etretinate-treated and untreated patients. In cell culture studies, etretinate dose-dependently (from 10(-9) to 10(-5) M) decreased the PICP concentration in the medium of fibroblasts from both healthy subjects and patients. In osteoblast cell culture, PICP levels were reduced only in a high concentration of etretinate (10(-5) M). However, no change was observed in preadipose cells. Our in vivo and in vitro observations indicated that psoriasis per se did not affect either serum PICP or PIIIP levels, but that etretinate had an inhibitory effect on collagen synthesis by fibroblasts. Hence, the administration of etretinate to psoriatic patients is, at least in part, responsible for the reduction of serum PICP levels in these patients.

Adult↗
PubMed1994

Increase of the delayed rectifier K+ and Na(+)-K+ pump currents by hypotonic solutions in guinea pig cardiac myocytes.

To investigate the membrane current changes induced by membrane stretching, single guinea pig ventricular myocytes were superfused with solutions of various osmolarities, and the whole-cell current was recorded by the patch-clamp technique. The application of 70% and 130% osmolar bath solutions increased and decreased the amplitude of delayed rectifier K+ current (IK), respectively, whereas no obvious change was observed in the L-type Ca2+ current or the inward rectifier K+ current. When the Na(+)-K+ pump current (Ipump) was recorded by the use of high-Na+ (> 35 mmol/L) pipette solutions, Ipump was also increased and decreased by the superfusion of hypotonic and hypertonic solutions, respectively, in approximately half of the cells. An increase of the Ipump was also observed in the absence of external Na+, excluding a possibility that the enhancement of Ipump was secondary to an elevation of cytosolic Na+. In most cells that did not show the increase of Ipump, the hypotonic superfusion induced a gradual activation of Cl- current. The hypertonic superfusion did not cause any consistent change in the membrane Cl- conductance. Since the response of IK was observed in all experiments, its mechanism was studied. We failed to observe marked changes in the kinetic and conductance properties of IK in the hypotonic solution. The involvements of either the protein kinases or Ca2+ were also ruled out as major mechanisms underlying the IK response.

Animals↗
PubMed1994

Autonomic regulation of cardiac chloride current.

The cellular mechanism of autonomic regulation of the catecholamine-induced chloride current (ICl) was investigated by recording the whole-cell current in isolated guinea-pig ventricular cells. The beta-adrenergic and related stimulations such as adrenaline, isoprenaline, forskolin, or internal application of cyclic AMP (cAMP), induced the ICl. Acetylcholine (ACh) depressed the responses of ICl induced by the beta-adrenergic stimulation or forskolin, which was followed by a transient overshoot of the ICl response upon washing out ACh. ACh failed to interfere with ICl induced by cAMP, and the pretreatment of myocytes with pertussis toxin (PTX) abolished the inhibitory effect of acetylcholine. Intracellular application of cGMP, which levels are known to be elevated by the muscarinic stimulation, enhanced ICl activated by submaximal doses of isoprenaline. In the absence of agonists, cGMP failed to induce ICl. Thus, the antagonistic interaction between the beta-adrenergic stimulation and the muscarinic stimulation is at the membrane level, most probably via PTX-sensitive GTP-binding proteins. cGMP might contribute to the post-ACh rebound phenomenon by facilitating the beta-stimulation.

1-Methyl-3-isobutylxanthine↗
PubMed1994

[Lipoprotein (a)].

Lipoprotein (a) [Lp (a)] is a low density lipoprotein (LDL) disulfide-linked to apolipoprotein (a) [apo (a)] and considered to be an independent risk factor for atherosclerotic cardiovascular disease. Apo (a) has a high homology with plasminogen, which has stimulated a lot of interest in the mechanism of atherogenicity and thrombogenicity of this lipoprotein. Recent advances in this mechanism were reviewed. We are still unclear about the physiological role of Lp (a). This research aspect must receive attention in the future. Furthermore, the most pressing need is for drugs that will lower serum Lp (a) concentrations.

Arteriosclerosis↗
PubMed1994

[Changes in serum h-HGF levels after living-related liver transplantation].

It is well known that prognosis is very poor in patients with severe hepatic insufficiency such as congenital biliary atresia and fulminant hepatitis. The liver transplantation is only effective therapy for these patients and living-related liver transplantation is becoming popular in Japan. We observed the changes in serum human hepatocyte growth factor (h-HGF) levels of the recipients during the operation in 3 cases of congenital atresis and one of fulminant hepatitis. Serum h-HGF values in these patients reached the maximal levels (5-10-fold compared to the base line values) at the phase of portal or hepatic artery anastomosis during the operation. These observations suggest that the increase of h-HGF in the recipient is derived from the following three origins. (1) Wash outed h-HGF from the liver of the donor. (2) Induced h-HGF from other organs than the liver of the recipient. (3) The decreased catabolism of h-HGF in recipient due to total hepatectomy.

Adolescent↗
PubMed1993

Fast and slow blockades of the inward-rectifier K+ channel by external divalent cations in guinea-pig cardiac myocytes.

The present patch-clamp study shows that external Mg2+, Ca2+ and Sr2+ decrease the unit amplitude of inward current through the inward-rectifier K+ channel in a concentration-dependent manner. Sr2+ produces a voltage-dependent flickering block as well, and the fractional electrical distance between the external orifice and the Sr2+ binding site (delta) is 0.73. The decrease of unit amplitude is reversible and voltage independent while it does not increase the noise level on the open-channel current. Unit current decreased by Mg2+ or Ca2+ has a longer mean open time, which is inversely proportional to the unit amplitude. External Mg2+ does not decrease the amplitude of unit outward current. A surface potential shift, measured using voltage-dependent Cs+ block (delta = 1.60), failed to explain the current decrease. Therefore, we conclude that (1) the external divalent cations cause an extremely fast channel block, which appears as a decreased amplitude of the unit current on the recording system; (2) the blocking site (fast site) is present near the external orifice of the channel, and it is separate from the blocking site (slow site) to which Cs+ and Sr2+ bind.

Animals↗
PubMed1993

Gating properties of ATP-sensitive K+ channels in the heart.

Using a concentration jump technique (oil-gate method), the rate of closure or opening of the ATP-sensitive K+ channel was measured in response to varying the ATP concentration. The inside-out patch was prepared from dissociated ventricular cells of guinea-pig heart. The opening of the channel on jump to ATP-free solutions from various ATP concentrations showed a variable latent period before the almost exponential rise of the mean channel current. The mechanism of latency is not clear. On reapplying ATP, the channel closed without any obvious delay, and the time course was well fitted with a single exponential curve. The reciprocal time constant was proportional to the ATP concentration. The closing rate was explained by assuming a 1:1 binding stoichiometry and a rate constant of 51.7 or 5.6 mM-1s-1.

Adenosine Triphosphate↗
PubMed1993

Compensatory increase in intestinal apolipoprotein A-IV mRNA levels in the experimental nephrotic rat.

Using experimental nephrotic rats, we investigated the potential feedback regulation of apolipoproteins (apos) at their hepatic and intestinal synthetic sites. Nephrotic syndrome (NS) was induced in rats by puromycin aminonucleoside (PAN) with a single intraperitoneal injection (120 mg/kg). In nephrotic rats, we observed a 60% reduction in serum apo A-IV levels despite a 3.4-fold increase in jejunum and a 1.5-fold increase in ileum apo A-IV mRNA levels, although hepatic apo A-IV levels were unchanged compared with those in pair-fed control rats. A strikingly positive correlation was observed between daily urinary excretion of apo A-IV and its mRNA levels in jejunum (r = .856, P < .01; n = 10) and ileum (r = .710, P < .05; n = 10). On the other hand, nephrotic rats had an 8.2-fold increase in serum apo A-I level associated with a 4.6-fold increase in hepatic and a small but significant increase in jejunum apo A-I mRNA levels. Compared with the fractional catabolic loss of albumin or apo A-IV, that of apo A-I was small and suggests a diminished level of glomerular filtration, leading to a further elevation in serum apo A-I level. Barring nonspecific effects of PAN, these data suggest that reduction of serum apo A-IV level due to urinary loss may directly upregulate mRNA levels in the small intestine. Alternatively, it may be the result of an effective filtration of a serum component unassociated with lipoproteins that normally and site-specifically reduces apo A-I and apo A-IV mRNA transcription.

Albumins↗
PubMed1993

The ATP-sensitive K+ channel.

A small conductance K+ channel, that is inactivated by ATP, was recently found in the inner membrane of rat liver mitochondria (Inoue et al., 1991). This finding clearly indicates that a variety of K+ channels, showing ATP-sensitivity, are widely distributed. ATP is an important compound in view of its participation in oxidative phosphorylation and as the source of high-energy phosphate for nearly every energy-requiring reaction in the cell. Therefore, it is easy to speculate that transducing the ATP concentration within a cell into an electrical signal is vital for most living cells. The opening of the ATP-sensitive K+ channel by a decrease in the ATP level shifts the membrane potential in a negative direction and in general depresses cell function. The closing of the channel by an increase in ATP depolarizes the membrane and enhances membrane excitability. It might be speculated that a sequence of amino acids common for the binding site of ATP is preserved and combined with different types of K+ channels, so that the gating with ATP is quite similar between different K+ channels, but the conductance properties are different. The large variability in the value of K1/2ATP in the same cells or between different tissues might be due to modulation of the reaction of ATP and the binding site. These ideas will be substantiated by clarifying the molecular structure of the ATP-sensitive K+ channel in the near future. The molecular mechanisms for the selective channel blockers, sulfonylureas, and for the K+ channel openers should also be clarified.

Adenosine Triphosphate↗
PubMed1993

Intercellular adhesion molecule-1 on cultured human melanoma cells: influence of cytokines.

Adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and its counter-receptor, lymphocyte function associated antigen-1 (LFA-1), play very important roles in immune responses. In this study, the effects of cytokines on cultured human melanoma cells (MMG2) were examined, especially focussing on the expression of ICAM-1 on MMG2 and lymphocyte adhesion to MMG2. Both the expression of ICAM-1 and HLA-DR on MMG2 increased after treatment with IFN-gamma. ICAM-1 expression began to increase earlier than HLA-DR expression. TNF-alpha and IL-1 beta also increased the expression of ICAM-1 on MMG2. However, these cytokines did not increase the expression of HLA-DR. IFN-gamma had a dose dependent effect on lymphocyte adhesion to MMG2. Pretreatment of IFN-gamma treated MMG2 with 84H10 (anti-ICAM-1 antibody) or pretreatment of lymphocytes with either SPV-L7 (anti-LFA-1 alpha antibody) or IOT10 (anti-LFA-1 beta antibody) inhibited the lymphocyte adhesion to MMG2. These results suggest that ICAM-1 molecules induced on melanoma cells by IFN-gamma can interact with LFA-1 molecules on lymphocytes.

Antigens, CD↗
PubMed1993

Suppressive effects of elimination diets on T cell responses to ovalbumin in hen's egg-sensitive atopic dermatitis patients.

We investigated the effect of elimination diets on T cell responses to ovalbumin (OA) in hen's egg-sensitive atopic dermatitis (AD) patients. The proliferative responses of both peripheral blood mononuclear cells (PBMCs) and T cells with monocytes to OA decreased after elimination diets, but those to Candida albicans or phytohemagglutinin (PHA) did not decrease after elimination diets. The proliferative responses of CD4+ T cells with monocytes to OA decreased after elimination diets. In these patients, clinical symptoms of AD improved. These results indicate that T cells, especially CD4+ T cells, respond to food antigens in food-specific lymphocyte responses, and that elimination diets may be able to initiate reduction of the responsiveness of food-sensitive T cells, especially CD4+ T cells. Moreover, the surface marker phenotypes of the T cells responding to OA were analysed. Our results showed that CD4+CD45RA+ T cells tended to increase. The increase in circulating CD4+CD45RA+ T cells might function as systemic suppression against immune responses in the skin.

Adolescent↗
PubMed1993

Quantification of exponential Na+ current activation in N-bromoacetamide-treated cardiac myocytes of guinea-pig.

1. The activation kinetics of the Na+ current was investigated in single ventricular cells of the guinea-pig heart using an improved oil-gap voltage clamp method. The inactivation of the current was removed by an intracellular application of N-bromoacetamide (NBA) for less than 1 min. Although the NBA treatment slightly decreased the peak amplitudes (81.7 +/- 13.4% of control, n = 15), the Na+ current remained stable after the removal of inactivation. 2. On depolarization, the activation of Na+ current took an exponential time course after the capacitive current decreased to 5% of its peak amplitude (40-100 microseconds after the pulse onset). The time course of deactivation, recorded on repolarization from 1.2 ms depolarization, was also a single exponential. 3. The time constants of activation and deactivation were almost identical when compared at a given test potential within a range of -50 to -30 mV. These findings indicate that the cardiac Na+ current activation is determined by m1 kinetics, or one rate-limiting step. 4. At potentials negative to -60 mV, the deactivation was complete, and its time constant decreased e-fold per 20.3 +/- 1.8 mV hyperpolarization (n = 7). 5. The degree of steady-state activation (m(infinity)) was fitted to a Boltzmann equation with a slope factor of 7.4 +/- 0.3 mV and a half-maximum potential of -33.3 +/- 0.8 mV (n = 8). 6. Rate constants for the rate-limiting activation step between a closed state and an open state (alpha m, beta m), were determined from m(infinity) and tau m over a potential range between -100 and +50 mV. On a logarithmic scale, beta m-1 was a linear function of the membrane potential over the range -100 and -30 mV. 7. Fitting the newly determined activation kinetics to the rising phase of the action potential indicated that the activation kinetics in the present study is relevant to the physiological action potential. The density of the Na+ channels thus obtained was 1075 +/- 186 pF-1 (n = 6). 8. The measurements in the NBA-treated Na+ current were compared with those obtained without treatment.

Acetamides↗
PubMed1993

Turnover rate of the cardiac Na(+)-Ca2+ exchanger in guinea-pig ventricular myocytes.

1. Single guinea-pig ventricular myocytes were voltage clamped using the whole-cell configuration of the patch-clamp technique and membrane current generated by the Na(+)-Ca2+ exchange mechanism recorded. 2. Rapid increases in cytosolic free calcium ([Ca2+]i) evoked by flash photolysis of either nitr-5 or DM-nitrophen resulted in current relaxations, arising from a redistribution of exchanger carrier conformations induced by the changes in [Ca2+]i. 3. Relaxation time constants were temperature dependent with a temperature coefficient over a 10 degrees C range (Q10) of approximately 3 and also voltage dependent, decreasing on hyperpolarization for membrane potentials in the range +40 to -80 mV. 4. The experimental results are consistent with consecutive exchange models having electrogenic Na+ translocation steps, together with a site density and turnover rate similar to that for the Na(+)-K+ pump.

Animals↗
PubMed1993

Ion channels in the luminal membrane of endothelial cells of the bull-frog heart.

Ion channels in the luminal membrane of intact endothelial cells of the bull-frog atrium were examined with single channel recordings. A class of outwardly rectifying channels and at least two types of ohmic channels were recorded without any stimulation by vasoactive substances. The slope conductances of the outwardly rectifying channel measured at potentials positive to and negative to the reversal potential were 36.4 +/- 8.8 and 7.5 +/- 2.2 pS, respectively (n = 35). This channel was a cation channel with poor selectivity between K+ and Na+ (PNa/PK = 1.04 +/- 0.08, n = 3). The open probability and mean open time increased as the membrane was depolarized. The two ohmic channels had single channel conductances of 175.3 +/- 17.7 (n = 21) and 9.5 +/- 1.8 pS (n = 11), respectively. The 175pS channel also failed to discriminate between K+ and Na+. Its open probability was voltage-independent. Internal Ca2+ affected none of the channels examined. The luminal membrane may have a population of ion channels different from the abluminal membrane. These characteristics were different from those so far described in the cultured endothelial cells from mammalian blood vessels.

Animals↗
PubMed1993

[Analyses of ventricular arrhythmias in patients with progressive systemic scleroderma (PSS) by ambulatory electrocardiography].

Disorder of cardiac conduction and automaticity have been widely reported in patients with progressive systemic scleroderma (PSS). In the present study, ventricular arrhythmias were monitored by 24-hour ambulatory electrocardiographic recording (Holter monitor) in 30 female patients with PSS and 20 apparently healthy female controls. The following results were obtained: 1) In the waking state, 8 cases of 30 patients showed grade III, IVA or IVB of ventricular arrhythmias, according to Lown's classification. On the other hand, ventricular arrhythmias, such as grade III, IVA or IVB, were not observed in the control group. 2) In the patient group, grade IVA arrhythmias were observed during defecation, driving or light working, and grade IVB were during defecation, urination, light working or sleeping. These results suggest that it is important to examine arrhythmias by Holter monitors in patients with PSS.

Adult↗