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Biomedical subjects

T Aramaki

Publications and source records attributed to T Aramaki.

At least 19 recordsLinked to original sources
PubMed2000

A variant form of Churg-Strauss syndrome: initial temporal non-giant cell arteritis followed by asthma--is this a distinct clinicopathologic entity?

The clinical manifestations of the classical vasculitis syndromes are extraordinarily heterogenous with considerable overlap among them. Recently, several cases of unusual presentation of the vasculitis syndromes have been reported. We describe a patient who initially manifested with temporal arteritis and Raynaud's phenomenon and subsequently developed bronchial asthma, ie, a case of an atypical form of Churg-Strauss syndrome (allergic angiitis and granulomatosis) and discuss whether this case is a distinct clinicopathological entity.

Adult↗
PubMed2000

Effects of SSM (specific substance maruyama) on HBe antigen-positive chronic hepatitis B -clinical efficacy and modulation of cytokines.

Twenty-three patients with HBe antigen-positive chronic hepatitis B were treated with capitalite first letters Maruyama (SSM). HBe antigen turned negative in 15 patients. The levels of various cytokines in pre- and post-treatment frozen serum samples from six patients whose HBe antigen turned negative and from five whose HBe antigen did not were examined. Reduction of serum interleukin (IL) -10 level to below 20 pg/ml was observed after SSM treatment in four of the six patients whose HBe antigen turned negative. SSM was found to stimulate the production of interferon (IFN) -gamma in peripheral blood cells from two healthy volunteers. This stimulatory effect was confirmed in 12 out of 24 healthy volunteers. SSM augmented the production of IFN-gamma in eight out of 10 patients with chronic hepatitis B and nine of 10 with hepatitis C. These results demonstrate for the first time that SSM stimulates the production of IFN-gamma in human peripheral blood cells and also suggest that treatment of HBe antigen-positive chronic hepatitis B patients with SSM leads to the clearance of HBe antigen and normalization of serum aspartate aminotransferase levels through inhibition of IL-10 and stimulation of IFN-gamma.

Adult↗
PubMed2000

[Pediatric cataract surgery with posterior capsulorrhexis and optic capture of the intraocular lens].

We evaluated the result of the pediatric cataract surgery with optic capture. The intraocular lens (IOL) optic is subluxated to the vitreous body side through the posterior continuous curvilinear capsulorrhexis (PCCC). Five eyes with congenital or developmental cataracts were treated with phacoemulsification and IOL implantation, and then PCCC and optic capture was done. Three of the cases were bilateral and one case was unilateral. All cases have remained in good condition without secondary fibrous membrane formation, which influences visual acuity, and transparency of the posterior capsule was maintained in the visual axis area. We found one case of anterior capsule contraction. Long-term follow up should be continued.

Capsulorhexis↗
PubMed1999

Evidence for norepinephrine-activated Ca2+ permeable channels in guinea-pig hepatocytes using a patch clamp technique.

To determine whether the hepatocyte plasma membrane possesses a Ca2+ channel. we applied a patch clamp technique to isolated guinea-pig hepatocytes. In a cell-attached configuration, using an internal pipette solution of 110 mM BaCl2 or CaCl2, we observed sporadic inward single channel currents (Po = 0.004 +/- 0.002, n = 6) at various membrane potentials. The unit amplitude was 0.60 +/- 0.15 pA (n = 6) at resting membrane potential. The single channel conductance was 20.4 +/- 4.6 pS (n = 6) and this channel showed no rectification and no voltage dependence. Bay K 8644, a dihydropyridine Ca2+ channel activator, did not affect this channel activity. Although norepinephrine in the pipette solution did not activate this channel, its external application increased channel activity. These observations suggest that guinea-pig hepatocytes possess Ca2+ permeable channels that differ from the voltage-operated Ca2+ channels found in excitable cells and that such channels are responsible for the agonist-stimulated Ca2+ entry in hepatocytes.

Animals↗
PubMed1999

Ultrastructural changes and immunohistochemical localization of nitric oxide synthase, advanced glycation end products and NF-kappa B in aorta of streptozotocin treated Mongolian gerbils.

To evaluate the relationship among the induction of nitric oxide synthase (NOS), advanced glycation end products (AGEs) and NF-kappa B for vascular damage in hyperglycemia, we injected Mongolian gerbils intravenously with 150 mg/kg streptozotocin (STZ) and observed over the next one year the resulting aortic changes by immunohistochemical and electron microscopical techniques. After STZ treatment, hyperglycemia was confirmed and body weight transiently decreased. Morphological observation revealed no remarkable changs in vascular endothelial cells or vascular smooth muscle cells in the aorta at one week after STZ administration. After 4 weeks increased collagen fibrils were observed in the pericellular spaces of media. At one year after STZ administration, increased collagen fibrils and thickened elastic fibers were found around the vascular smooth muscle cells with vacuolization and increased cytoplasmic organellae compared with non-treated animals of the same age. Immunohistochemically endothelial constitutive NOS (ecNOS) was localized in the endothelium of the aorta of Mongolian gerbils. At one year after STZ administration, the reaction products of iNOS, AGEs and NF-kappa B in vascular endothelial cells and smooth muscle cells were much more greatly increased than at one week and 4 weeks. After STZ administration, the localization of NOS, AGEs and NF-kappa B was observed in the aorta, which suggests these factors play important roles in the pathogenesis of vasculopathy in diabetes mellitus.

Animals↗
PubMed1998

Nitric oxide production and energy state in the heart after endotoxin administration.

To evaluate nitric oxide (NO) production and the energy state of the heart after endotoxin administration, Wistar rats were injected i.p. with 10 mg/kg Escherichia coli lipopolysaccharide (endotoxin). Morphologic changes, plasma nitrite concentration, expression of inducible NO synthase (iNOS), and cardiac energy state, as reflected by several metabolites, were observed chronologically 0 (control), 4, 6 and 8 h after endotoxin administration. Electrocardiography (ECG) demonstrated arrhythmia after endotoxin administration. Biochemically, NO production increased in blood and iNOS increased in the heart. The amount of myocardial beta-ATP measured by 31P magnetic resonance spectroscopy (31P-MRS) increased transiently and then decreased. This transient increase might be a hyperdynamic response to endotoxin administration. At 4 and 6 h after endotoxin administration, pH measured by 31P-MRS was slightly decreased, but this decline was not statistically significant. On the other hand, the amount of lactate in heart samples increased in the 1H magnetic resonance spectra (1H-MRS). Ultrastructurally, in cardiovascular tissue, intracytoplasmic organelles were observed to be injured in blood vessels and cardiomyocytes associated with mast cell infiltration. These results suggest significant metabolic and morphologic abnormalities in the heart after endotoxin administration.

Animals↗
PubMed1998

Immunohistochemical and morphometric evaluations of coronary atherosclerotic plaques associated with myocardial infarction and diabetes mellitus.

Immunohistochemical and morphometrical studies were performed to elucidate the specificity of atherosclerosis in the descending branch (the segments 5 and 6) of the left coronary artery associated with acute myocardial infarction (AMI) in the anterior wall of the heart and non-insulin-dependent diabetes mellitus (NIDDM). The NIDDM without AMI group showed diffuse intimal thickening with smooth muscle cells, combined with much more intense immunostaining of tenascin than the non diabetic groups. The AMI without NIDDM group showed atheromatous thickening with decreased smooth muscle cells, a large number of macrophage and TUNEL-positive cells compared with the groups without AMI. However, the AMI with NIDDM group revealed atherosclerotic lesion with decreased smooth muscle cells, increased macrophages and TUNEL positive cells associated with the increased localization of tenascin and TGF-beta1 compared with the control. These findings suggest that the specificity of coronary atherosclerosis in diabetic patients may be the extensive atherosclerotic changes associated with increased tenascin. In AMI with NIDDM, increased TGF beta1 may induce apoptosis in the atheroma and coronary dysfunction, contributing to the development of acute myocardial infarction.

Actins↗
PubMed1997

Effects of the alpha-/beta-blocking agent carvedilol on hepatic and systemic hemodynamics in patients with cirrhosis and portal hypertension.

To enhance the portal hypotensive effect of nonselective beta-blockers, combinations of vasoactive agents with different mechanisms should be considered. The effect of carvedilol (CAS 72956-09-3, Artist), and alpha-/beta-blocking agent, on hepatic and systemic hemodynamics in 10 patients with portal hypertension was evaluated. After administration of carvedilol, the hepatic venous pressure gradient (HVPG) decreased from 15.9 +/- 3.2 mmHg to 13.3 +/- 4.0 mmHg (mean +/- SD) at 60 min (-15%) and to 12.9 +/- 3.0 mmHg at 90 min (-17%, p < 0.05). However, only 5 patients showed a decrease of HVPG by more than 20% at 60 or 90 min. The estimated hepatic blood flow (EHBF) was not significantly reduced. In contrast, heart rate (-8%, p < 0.05), mean arterial pressure (-10%, p < 0.01), and cardiac index (CI) (-8%, p < 0.05) were all reduced at 90 min, while total systemic vascular resistance was not altered. The reduction of HVPG was significantly correlated with the decrease of CI (r = 0.6415, p < 0.05). The portal hypotensive effect of carvedilol may mainly result from a reduction of CI. However, because of the greater reduction of HVPG than that of CI, other additive actions were suggested.

Adrenergic alpha-Antagonists↗
PubMed1995

Activation of the plasma membrane chloride channel by protein kinase C in isolated guinea-pig hepatocytes.

1. To assess the nature of the underlying mechanism of noradrenaline-induced increase of Cl- conductances in hepatocytes, macroscopic and unitary currents through noradrenaline-induced Cl- channels were examined in enzymatically isolated guinea-pig hepatocytes using whole-cell, cell-attached and excised inside-out configurations of the patch-clamp technique. 2. When K+ conductances were blocked and the intracellular Ca2+ concentration ([Ca2+]i) was set at 0.1 microM, bath application of noradrenaline activated the time-independent membrane currents under whole-cell voltage-clamp conditions. The current was similarly activated by phorbol ester (PMA), an activator of protein kinase C (PKC), while a specific protein kinase C inhibitor, H-9, reversed PMA activation of the current. The inactive phorbol ester, 4 alpha-phorbol 12-myristate, 13-acetate (alpha PMA), failed to activate the channel. 3. The reversal potential of the PMA-activated current shifted by approximately 60 mV per 10-fold change in the external Cl- concentration, indicating that the current was Cl- selective. Bath application of 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) partially inhibited both the noradrenaline- and PMA-induced currents. 4. In single channel recordings from cell-attached patches, bath application of noradrenaline or PMA induced unitary current activity, the averaged slope conductance of which was 10.1 +/- 1.5 pS (mean +/- S.D.; n = 12) in the noradrenaline-induced current and 9.7 +/- 1.3 pS (n = 7) in the PMA-induced current. The open time distribution was moderately well fitted by a single exponential function with mean open lifetime of 88.5 +/- 10.6 ms (n = 10), while at least two exponentials were required to fit the closed time distributions with a time constant for the fast component of 24.4 +/- 5.8 ms (n = 10) and for the slow component of 316.9 +/- 49.2 ms (n = 10). 5. Bath application of purified PKC to excised inside-out patches activated the channel. The PKC selective inhibitor, PKC(19-36), and DIDS inhibited the PKC-activated channel. 6. These results suggest that PKC can phosphorylate the channel protein or a related structure leading to the activation of Cl- channels in guinea-pig hepatocytes.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Portal and systemic hemodynamic responses to a very low dose of nitroglycerin in cirrhotic patients with portal hypertension.

Portal and systemic hemodynamic responses to a very low dose of nitroglycerin were studied in patients with portal hypertension and cirrhosis, and compared with those to a high dose of this compound. A 0.15 mg dose of nitroglycerin was given sublingually to 10 patients (LDG), and 0.3 mg to another 10 (HDG). Hemodynamic measurements were performed by means of hepatic venous and right cardiac catheterization before and 5 min after nitroglycerin administration. The wedged hepatic venous pressure decreased after dosing by 7.9% (p < 0.01) in LDG, and by 15.3% (p < 0.01) in HDG. Hepatic blood flow with ICG did not change in either group. In LDG, azygos blood flow remained unchanged, in contrast to a significant decrease by 10.1% (p < 0.05) in HDG. Mean arterial pressure fell by 3.6% (p < 0.05) in LDG and by 18.6% (p < 0.01) in HDG. Cardiac index did not change in LDG, but decreased by 11.4% (p < 0.05) in HDG. In both groups, mean pulmonary arterial pressure and pulmonary capillary wedge pressure fell significantly by the same amount. In HDG, a significant correlation between changes in wedged hepatic venous pressure and azygos blood flow (r = 0.70, p < 0.05) was observed. This suggested that splanchnic vasoconstriction mediated by a high-pressure, rather than a low-pressure, baroreceptor reflex was the main contributor to a decrease in portal venous blood flow, resulting in a reduction in wedged hepatic venous pressure; whereas a slight but significant fall of wedged hepatic venous pressure induced by a very low dose of nitroglycerin might have been due to venodilatation in the portal system and the hepatic vascular bed. These data suggest that, even with a very low dose of nitroglycerin, partial improvement of the hepatic circulation can be expected with minimal change in the systemic circulation in patients with cirrhosis and portal hypertension.

Female↗