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Biomedical subjects

A Noma

Publications and source records attributed to A Noma.

At least 55 records · Page 3Linked to original sources
PubMed1997

Existence of a low-threshold and sustained inward current in rabbit atrio-ventricular node cells.

Single myocytes were dissociated from the atrio-ventricular (AV) node of rabbit hearts. Spontaneous action potentials of the N or NH type were recorded from the fusiform AV node cells. Under whole-cell voltage clamp, these cells were characterized by the presence of hyperpolarization-activated cation current (I(f)), delayed rectifier K+ current (IK), and L-type Ca2+ current (ICa,L). After blocking I(f) and IK, depolarizing pulses from -80 mV revealed a sustained inward current, which was suppressed by 1 microM nicardipine. The activation threshold of the sustained inward current was around -60 mV and the maximum amplitude was 25.4 +/- 20.1 pA at -40 mV (n = 15). The current was also blocked by 1 microM verapamil. The sustained inward current was not decreased (125 +/- 32% of control, N = 5) by reducing [Ca2+]o from 1.8 to 0.1 mM, while it was nearly suppressed by depleting [Na+]o, differently from ICa,L. We concluded that the nicardipine-sensitive sustained inward current is largely attributable to Ist described in the rabbit sino-atrial node pacemaker cells. I(f) and Ist were not found in rod-shape AV node cells.

Action Potentials↗
PubMed1997

Temperature dependence of the inward rectifier K+ channel gating in guinea-pig ventricular cells.

Whole-cell and single-channel currents of the inward rectifier K+ channels from guinea-pig ventricular myocytes were recorded over the range between 5 and 37 degrees C. The conductance for inward currents was decreased by lowering the temperature with a Q10 of 1.28 (whole cell), or 1.41 (single channel) between 20 and 30 degrees C. The open probability of the channel at -100 mV remained high (> 0.9). The distribution of open times was single exponential at all temperatures, confirming a single open state. The entropy change (delta S) for the closing rate of the channel obtained from open-time distribution was -14.0 e.u. (cal/mol/K), and enthalpy change (delta H) was 11.9 kcal/mol. The configuration of closed-time distribution varied markedly by altering the temperature, and three exponentials were necessary to fit the histogram. The slowest component showed higher temperature dependency (delta S = 13.6 e.u. and delta H = 19.0 kcal/mol) than the other two faster components. By assuming a reduced model of C-O at 37 degrees C, the difference in Gibb's free energy (GOC) between the open and closed states was approximately 2 kcal/mol, and the height of the energy barrier for the C-O transition was estimated to be approximately 15 kcal/mol.

Animals↗
PubMed1996

Expression of activin A in human keratinocytes at early stages of cultivation.

Activins are members of the TGF-beta superfamily and are classified into 3 types: activin A, which consists of a homodimer of betaA, activin B, which consists of a homodimer of betaB, and activin AB, which consists of a heterodimer of betaAbetaB. We studied the expression of activin mRNAs by RT-PCR in normal human epidermis, cultured keratinocytes, and DJM-1 cells (a squamous cell carcinoma line). We could detect only activin A mRNA (betaA) in normal human epidermis. In cultured keratinocytes and DJM-1 cells, activin betaA mRNA was observed at 4 h but not at 96 h after plating. Activin A activity was detected in the conditioned medium of DJM-1 cells within 48 h. In addition, although follistatin mRNA was not observed in human epidermis in situ, it was transiently expressed in cultured cells at 4 h after plating. These findings suggest that the expression of these molecules in keratinocytes is associated with cell proliferation. In an in vitro tissue injury model, activin A was observed at the wound edge, where cell migration and proliferation may be activated. In DJM-1 cells cultured for 92 h, betaA mRNA was observed 4 h after injury treatment. These findings suggest that activin A acts as a potent inducer of proliferation in vitro, at least in keratinocytes.

Activins↗
PubMed1996

Impaired synthesis of retinol-binding protein and transthyretin in rat liver with bile duct obstruction.

To gain further insight into the protein metabolism in bile duct-obstruction, we examined the synthesis of retinol-binding protein (RBP) and transthyretin (TTR) in rats with common bile duct-ligation. In these rats, liver and plasma levels of RBP and TTR decreased markedly, whereas liver retinoid contents remained unchanged. Although there appeared no decrease in the total amount of RBP or TTR mRNA expressed in the liver, the subcellular distribution of these mRNAs changed from the membrane-bound polysome fraction to the membrane-unbound polysome fraction. This abnormal distribution recovered rapidly after biliary drainage, resulting in the subsequent recovery of the plasma RBP and TTR levels. These observations suggest that cholestasis inhibits the synthesis and secretion of RBP and TTR by disrupting the binding of their mRNAs to membrane-bound polysomes. Plasma levels of RBP and TTR might be sensitive indicators of the recovery of protein synthesis after biliary drainage in patients with obstructive biliary disorders.

Animals↗
PubMed1996

Reduction of intestinal apo A-IV mRNA levels in the cirrhotic rat.

In the present study, intestinal apo A-IV synthesis was investigated using a carbon tetrachloride (CCl4)-induced cirrhosis rat model. Triglyceride (TG) content in rat cirrhotic liver was increased markedly by 170% (P < 0.001) and apo B was increased by 20% (P < 0.05) compared with control levels. These results reflected the steatotic change in the liver. In contrast, TG levels in the small intestine of cirrhotic rats decreased significantly (P < 0.01). In addition, intestinal apo A-IV (jejunum P < 0.001; ileum P < 0.01) and its mRNA levels (jejunum P < 0.01; ileum P < 0.05) were also reduced. The decreased apo A-IV content in the jejunum was confirmed by immunohistochemical analysis. These results indicate that intestinal apo A-IV synthesis in cirrhosis is suppressed, at least under the condition of an overnight fast. Therefore, decreased intestinal apo A-IV synthesis may relate to the decreased ability to absorb fat in cirrhosis, but a fat-loading study will be necessary to confirm this hypothesis. It is unknown from the present study why serum apo A-IV level is not significantly decreased, despite a reduction in apo A-IV synthesis. The clearance of apo A-IV by the liver may be delayed or apo A-IV synthesis may be rather markedly enhanced during fat absorption in liver cirrhosis.

Animals↗
PubMed1996

Rapid method for detection of Coxiella burnetii antibodies using high-density particle agglutination.

A high-density particle agglutination test, using erythrocyte-sensitizing substance from phase II Coxiella burnetii adsorbed to high-density composite particles, was developed for rapid serodiagnosis of Q fever. The test was compared with the microimmunofluorescence test for sensitivity and specificity by using 3,036 human serum samples collected in Gifu Prefecture, Japan. An excellent agreement was found between the two tests for the acute-phase group and paired serum samples, but some discordant results were observed in the single-sample group. The sensitivity and specificity of the high-density particle agglutination test were both 100% in the former group and 81.6 and 99.9%, respectively, in the latter group. The test is a very promising tool for routine serodiagnosis of Q fever because of its simplicity, sensitivity, and specificity.

Agglutination Tests↗
PubMed1996

Effects of lipid administration on lymphatic apolipoprotein A-IV and B output and synthesis.

We examined the mesenteric lymphatic and portal venous transport of triglyceride (TG), free fatty acids (FFA), apolipoproteins (apo)A-IV and B in response to a bolus duodenal infusion of a TG-free control solution, and long-chain (18:1) and medium-chain (8:0) TG (LCT and MCT, respectively) emulsions in the rat. Additionally, intestinal and hepatic apo A-IV and apo B mRNA levels were also measured. Lymph apo A-IV, apo B (B-48), FFA, and TG output increased after LCT infusion, whereas only apo A-IV and FFA outputs increased after MCT infusion. On the other hand, portal FFA and apo A-IV transports increased at 15 min after MCT infusion but not after LCT infusion. Portal TG and apo B transports were not altered by either MCT or LCT infusion. Jejunal apo A-IV mRNA was increased after both MCT and LCT infusions. Hepatic apo A-IV mRNA levels increased only after MCT infusion. Conversely, neither LCT nor MCT had any effect on apo B mRNA levels in intestine or liver. These results indicate that apo A-IV is regulated by MCT absorption and that fatty acid reesterification and lipoprotein assembly are not prerequisite for such regulation. Conversely, it is likely that apo B-48 participates only in the formation and/or transport of chylomicrons after LCT absorption.

Animals↗
PubMed1996

Cell distension-induced increase of the delayed rectifier K+ current in guinea pig ventricular myocytes.

Single ventricular myocytes of guinea pig heart were distended by applying a positive pressure of 5 to 20 mm Hg in the pipette during the whole-cell voltage clamp. The amplitude of delayed rectifier K+ current (I(K)) was increased by approximately 1.5 times, whereas the inward rectifier K+ current was scarcely affected. The increase of I(K) was reversible by applying a negative pressure of -10 to -30 mm Hg accompanied by shrinkage of the inflated cell. This response of I(K) was largely attributed to the E-4031-insensitive component of I(K). The fully activated current amplitude, measured using long-lasting depolarizing pulses (> 30 seconds) to +60 mV, was increased by the cell distension. The activation time course of I(K) during the long pulse consisted of more than three exponential components, and the slowest time constant was decreased by the distension from control 20.2 +/- 7.7 seconds (n=4) to 7.6 +/- 1.6 seconds (n=5). We failed to detect an involvement of microtubules or microfilaments, protein kinase C, and Ca2+ in the inflation-mediated increase of I(K).

Action Potentials↗
PubMed1996

Ionic mechanisms of the cardiac pacemaker potential.

The experimental evidence so far described in the literature is reviewed to explain the ionic mechanisms underlying the cardiac pacemaker potential in the sinoatrial node cell. Following gating mechanisms underlie the slow diastolic depolarization of the SA node cells. The delayed rectifier K+ channels (mainly the rapidly activated component of the delayed rectifier K+ currents, which is blocked by E-4031) activated during the preceding action potential are deactivated during diastole. The inactivation of the L-type Ca2+ channel is removed during the early diastolic period and results in an increasing inward current, provided that the amplitude of the window component is of significant amplitude. Because of its sustained nature, the removal of inactivation of the sustained inward current Ist, also generates inward current. The negative membrane potential near the maximum diastolic potential activates the hyperpolarization-activated non-selective cation current, I(f). Finally, the L-type Ca2+ channel is activated at the late phase of diastole depolarization, resulting in the maximum rate of rise of the action potential. These time- and voltage-dependent changes in membrane conductance occur in the presence of a significant background conductance. During the slow diastolic depolarization, Ist and IK may be the major component in the inward and outward currents, respectively.

Action Potentials↗
PubMed1996

[Clinical significance of serum soluble interleukin-2 receptor (sIL-2R) determination in patients with rheumatoid arthritis].

It has been recently shown that soluble interleukin-2 receptor (sIL-2R) is related to the pathogenesis of autoimmune diseases. We determined serum levels of sIL-2R in patients with rheumatoid arthritis (RA). Fifty-three patients (3 males and 50 females from 35 to 70 years old) and sex- and age-matched 50 healthy subjects were included in this study. The sIL-2R concentrations positively correlated with Lansbury index of RA (r = 0.602, p < 0.01). There was a significant correlation between sIL-2R levels and the prevalence of CD3+.HLA-DR+ lymphocytes (r = 0.420, p < 0.01).

Adult↗
PubMed1996

The effects of the beta-adrenergic-blocking agents, timolol and carteolol, on plasma lipids and lipoproteins in Japanese glaucoma patients.

PURPOSE: To determine whether two topical beta-blockers, timolol and carteolol, differently affect plasma lipids and lipoproteins in normolipidemic Japanese patients with glaucoma. PATIENTS AND METHODS: Thirty-three normolipidemic patients with primary open-angle glaucoma or ocular hypertension were randomly allocated to and completed 16 weeks of bilateral treatment with 0.5% timolol, 1.0% carteolol, or 2.0% carteolol twice daily in a three-center, prospective study. Patients using any drugs affecting plasma lipids or with a history of beta-blocker use of hyperlipoproteinemia were excluded. Fasting blood lipids and lipoproteins, including total cholesterol, high-density lipoprotein cholesterol, triglyceride, and apoproteins, were measured three times before therapy was initiated. These measurements were repeated every 4 weeks during the treatment period. RESULTS: The level of high-density lipoprotein cholesterol significantly decreased in the timolol treatment group but did not change in the carteolol treatment groups. The ratio of total cholesterol minus high-density lipoprotein cholesterol to high-density lipoprotein cholesterol increased in the timolol treatment group. CONCLUSIONS: Topical beta-blockers do affect plasma lipids in Japanese patients with glaucoma. The effects of timolol are greater than those of carteolol.

Adrenergic beta-Antagonists↗
PubMed1996

[Subfractionation of serum high density lipoproteins and its clinical significance].

Serum concentrations of HDL subfractions, LpAI and LpAI:AII, were simultaneously determined simply, specifically and rapidly by use of rocket immunoelectrophoresis with the home-made gel plates. The method was reproducible, and the results correlated well with those obtained with Sebia's kits. The normal levels of LpAI were 57 +/- 13 mg/dl in males and 59 +/- 15 mg/dl in females. LpAI levels were significantly lower in patients with renal failure and atherosclerosis, and tended to decrease in hepatic diseases than those in normal subjects. The levels of LpAI:AII were also decreased in these three diseased groups. Decreases in LpAI levels were more slightly in patients with hepatic or renal diseases than those in LpAI:AII levels. On the contrary, decrease in LpAI level was more markedly in patients with atherosclerosis than that in the other subfraction. The results in the present study suggest that the determination of HDL subfractions will be useful for diagnosis of various diseases.

Adult↗