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K Hongo

Publications and source records attributed to K Hongo.

At least 55 records · Page 3Linked to original sources
PubMed2000

Mechanisms associated with the negative inotropic effect of deuterium oxide in single rat ventricular myocytes.

Deuterium oxide (D2O) is known to cause a negative inotropic effect in muscle although the mechanisms associated with this response in cardiac muscle are not well understood. We studied the effects of D2O in single rat ventricular myocytes in order to characterise the mechanisms associated with its negative inotropic effect and to assess its possible use as an acute modulator of microtubules. D2O rapidly reduced the magnitude of contraction in rat ventricular myocytes, and there was some recovery of contraction in the presence of D2O. Colchicine, an agent known to depolymerise microtubules, did not modify the effect of D2O. D2O decreased the L-type Ca2+ current (ICa), measured under whole cell and perforated patch clamp conditions. Slowing of the time to peak and a delay in inactivation of ICa were observed. Intracellular calcium ([Ca2+]i) and sodium ([Na+]i) were measured using the fluorescent indicators fura-2 and SBFI, respectively. The fall in contraction upon exposure to D2O was not associated with a fall in the [Ca2+]i transient; this response is indicative of a reduction in myofilament Ca2+ sensitivity. Both the [Ca2+]i transient and [Na+]i increased during the partial recovery of contraction in the presence of D2O. We conclude that a decrease in the myofilament sensitivity for Ca2+ and a reduction in Ca2+ influx via ICa are principally responsible for the negative inotropic effect of D2O in cardiac muscle. We found no evidence to explain the negative inotropic effect of D2O in terms of microtubule proliferation. In addition we suggest that acute application of D2O is not a useful procedure for the investigation of the role of microtubules in excitation-contraction coupling in cardiac muscle.

Animals↗
PubMed2000

[Surgical treatments for 7 pituitary adenomas in multiple endocrine neoplasia type 1].

We analyzed 7 pituitary adenomas in patients with multiple endocrine neoplasia type 1 (MEN1). Their incidence was 1.6% among 450 patients with pituitary adenomas which had been treated surgically in our department between 1978 and 1999. The age, gender, symptoms, type of hormone secretion, pathological and operative findings in the MEN1 patients were not apparently different from those in the non-MEN1 patients. Incidence of non-functioning pituitary adenomas, however, was more frequently encountered in our series than that in previous reports among Caucasian people. One patient who had 5 previous operations for the MEN tumors died following postoperative subarachnoid hemorrhage. Four of the seven patients presented initial symptoms related to pituitary adenomas and increased serum Ca level was retrospectively recognized in three of the four at the time of treatment for the pituitary adenomas.

Adenoma↗
PubMed1999

Functional communications between the apical and equatorial domains of GroEL through the intermediate domain.

The Escherichia coli GroEL subunit consists of three domains with distinct functional roles. To understand the role of each of the three domains, the effects of mutating a single residue in each domain (Y203C at the apical, T89W at the equatorial, and C138W at the intermediate domain) were studied in detail, using three different enzymes (enolase, lactate dehydrogenase, and rhodanese) as refolding substrates. By analyzing the effects of each mutation, a transfer of signals was detected between the apical domain and the equatorial domain. A signal initiated by the equatorial domain triggers the release of polypeptide from the apical domain. This trigger was independent of nucleotide hydrolysis, as demonstrated using an ATPase-deficient mutant, and, also, the conditions for successful release of polypeptide could be modified by a mutation in the apical domain, suggesting that the polypeptide release mechanism of GroEL is governed by chaperonin-target affinities. Interestingly, a reciprocal signal from the apical domain was suggested to occur, which triggered nucleotide hydrolysis in the equatorial domain. This signal was disrupted by a mutation in the intermediate domain to create a novel ternary complex in which GroES and refolding protein are simultaneously bound in a stable ternary complex devoid of ATPase activity. These results point to a multitude of signals which govern the overall chaperonin mechanism.

Adenosine Triphosphate↗
PubMed1999

Vascular compression of the medulla oblongata by the vertebral artery: report of two cases.

OBJECTIVE AND IMPORTANCE: Compression of the medulla oblongata by a tortuous vertebral artery is rare. We report two patients with this lesion who were treated with vascular decompression of the vertebral artery. CLINICAL PRESENTATION: A 36-year-old man developed right hemiparesis with lower cranial nerve deficits, and a 47-year-old man developed left lower cranial nerve deficits and left cerebellar dysfunction. In both patients, magnetic resonance imaging revealed a tortuous vertebral artery compressing the medulla oblongata. INTERVENTION: In both patients, the compressed medulla oblongata was treated by detaching the vertebral artery from the medulla oblongata, shifting it, and anchoring it to the nearby dura mater. Postoperatively, both patients are asymptomatic and have returned to their previous jobs. CONCLUSION: Although compression of the medulla oblongata by a tortuous vertebral artery is rare, it can cause brainstem dysfunction. Magnetic resonance imaging clearly revealed the vascular compression in these patients. Surgical treatment was effective. The symptoms related to a tortuous vertebral artery and some techniques for surgical treatment are discussed. Awareness of this rare lesion is necessary to ensure appropriate treatment.

Adult↗
PubMed1998

Estimation of myofibrillar responsiveness to Ca2+ in isolated rat ventricular myocytes.

To estimate myofibrillar responsiveness to Ca2+, we used the relation between cell length and intracellular [Ca2+] ([Ca2+]i) during tetanic contractions of isolated ventricular myocytes. Enzymatically isolated rat ventricular myocytes were loaded with fura-2 AM (4 microM for 10 min) and excited alternately at 340 nm and 380 nm. The ratio (R) of fura-2 fluorescence at these wavelengths [F(340)/F(380), an index of [Ca2+]i] and cell length (L) were measured simultaneously. Following treatment with thapsigargin (0.2 microM), myocytes were stimulated at 10 Hz for 10 s to produce a tetanic contraction every min and an instantaneous plot of R vs L (R-L trajectory) was constructed. The R-L trajectory followed the same path during cell shortening and re-lengthening, suggesting that dynamic equilibrium between R and L was achieved during tetanus. Increasing the extracellular [Ca2+] from 1 to 8 mM extended the R-L trajectory without a substantial shift of the relation. The Ca2+-sensitizing thiadiazinone derivative, EMD57033 (1 microM), shifted the R-L trajectory to the left (sensitization of the myofibrils to Ca2+), whereas the non-selective phosphodiesterase inhibitor, 3-isobutyl-1-methylxantine (200 microM), shifted the R-L trajectory to the right (desensitization of the myofibrils to Ca2+), in agreement with previous results obtained using skinned preparations. We conclude that the R-L trajectory is useful for estimating the myofibrillar responsiveness to Ca2+ in isolated myocytes and may be beneficial for the evaluation of inotropic agents.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Different effects of gadolinium on I(KR), I(KS) and I(K1) in guinea-pig isolated ventricular myocytes.

1. Using the whole cell configuration of the patch clamp technique, we studied the potential blocking effects of gadolinium (1 microM to 1 mM) on potassium currents: I(KR), I(KS) and I(K1). The study was performed on guinea-pig isolated ventricular myocytes. 2. The background current, I(K1) was insensitive to Gd3+. Thus, we found that no obvious screening of surface charges was visible with concentrations of Gd3+ up to 100 microM. 3. By use of three different protocols: tail currents fitting, analysis of envelope of tails and electrophysiological dissection, we found that I(KR) was the only component of IK that was sensitive to Gd3+. The sensitivity was apparently different depending on the protocol used. 4. Comparison of the results obtained with the different protocols revealed that the rapid component of I(KR) is more sensitive to Gd3+ than the slow one. 5. Of the different protocols used to distinguish between I(KR) and I(KS), the electrophysiological dissection seems to be the more accurate.

Animals↗
PubMed1998

Chaperonin GroE-facilitated refolding of disulfide-bonded and reduced Taka-amylase A from Aspergillus oryzae.

The refolding characteristics of Taka-amylase A (TAA) from Aspergillus oryzae in the presence of the chaperonin GroE were studied in terms of activity and fluorescence. Disulfide-bonded (intact) TAA and non-disulfide-bonded (reduced) TAA were unfolded in guanidine hydrochloride and refolded by dilution into buffer containing GroE. The intermediates of both intact and reduced enzymes were trapped by GroEL in the absence of nucleotide. Upon addition of nucleotides such as ATP, ADP, CTP or UTP, the intermediates were released from GroEL and recovery of activity was detected. In both cases, the refolding yields in the presence of GroEL and ATP were higher than spontaneous recoveries. Fluorescence studies of intrinsic tryptophan and a hydrophobic probe, 8-anilinonaphthalene-1-sulfonate, suggested that the intermediates trapped by GroEL assumed conformations with different hydrophobic properties. The presence of protein disulfide isomerase or reduced and oxidized forms of glutathione in addition to GroE greatly enhanced the refolding reaction of reduced TAA. These findings suggest that GroE has an ability to recognize folding intermediates of TAA protein and facilitate refolding, regardless of the existence or absence of disulfide bonds in the protein.

Adenosine Triphosphate↗
PubMed1998

[Clinical evaluation of MRCP].

Recently, MRCP can be obtained with good spacial resolution within a few seconds using half fourier fast spin echo technique. From July 1995 to August 1997, 1000 patients suspected of having pancreatobiliary diseases were examined with MRCP. MRCP was performed with 1.5 T scanner using Fast Asymmetric Spin Echo sequence (FASE). Satisfactory images of the main pancreatic duct were obtained in 98%, of Santorini's duct in 90%, and of uncinate process branch in 83%. Pancreas divism was accurately diagnosed. In the patients with pancreatic ductal adenocarcinomas, MRCP depicted stenosis and proximal dilatation of the main pancreatic duct in 89%, and in the remaining patients no abnormalities were seen in the main pancreatic ducts because tumors were limited to side branches or Santorini's duct or distal end of the tail of the pancreas. Diagnosis of small pancreatic carcinomas (smallest lesion measured 10 mm in diameter) were feasible. In the patients with intraductal papillary neoplasms, dilatation of the main pancreatic duct and cystic dilatation of side branches were depicted, and polypoid lesions were detectable with source images. In the patients with serous cystadenomas, accumulation of the microcysts were visualized. In the patients with chronic pancreatitis, dilatation and stenosis of the main pancreatic duct, as well as side branch dilatation was depicted despite overestimation of the extent of the stenosis. Stones in the main pancreatic duct were well visualized as intraductal filling defects. In conclusion, MRCP is an effective imaging technique in the diagnosis of various pancreatic diseases.

Biliary Tract↗
PubMed1997

Gadolinium blocks the delayed rectifier potassium current in isolated guinea-pig ventricular myocytes.

The effect of Gd3+ on the delayed rectifier potassium current (IK) in single guinea-pig ventricular myocytes was tested using whole-cell patch-clamp techniques. It was found that Gd3+ blocked 70% of the IK tail current at a concentration of 100 microM. The EC50 was 24 microM. Action potential durations were, however, reduced, consistent with a predominant effect on depolarizing L-type Ca2+ current (Ica.L). In the presence of 5 microM nifedipine Gd3+ prolonged the action potential. Using carbon fibres to stretch cells we observed that 10 microM Gd3+ was not effective in reducing a large stretch-activated increase in resting calcium. Modelling studies using the OXSOFT HEART program suggest that this lack of response is influenced by blockade of repolarizing current but is best reproduced by additional blockade of Ca2+ extrusion via the Na(+)-Ca2+ exchanger. When Gd3+ is used as a blocker of stretch-activated channels its actions upon both Ica.L and IK must therefore be accounted for.

Action Potentials↗
PubMed1996

Changes in [Ca2+]i, [Na+]i and Ca2+ current in isolated rat ventricular myocytes following an increase in cell length.

Isolated rat ventricular myocytes were stretched using carbon fibres to investigate the mechanisms underlying the increase in contraction following stretch. 2. [Ca2+]i and [Na+]i were monitored using the fluorescent indicators fura-2 and sodium-binding benzofuran isophthalate, respectively. The L-type Ca2+ current was recorded simultaneously with contraction using the perforated patch-clamp technique. 3. Mechanical stretch caused an immediate increase in contraction, followed by a slow increase. Contraction was prolonged immediately after the stretch, but did not change during the slow phase. 4. The Ca2+ transient did not change immediately after the stretch. The slow increase in contraction was accompanied by an increase in the amplitude of the Ca2+ transient. However, diastolic [Ca2+]i did not change significantly following stretch. 5. [Na+]i did not change significantly either immediately, or during the slow increase in contraction, after the stretch. 6. The L-type Ca2+ current was not significantly altered either by mechanical loading of the cell with carbon fibres or by stretching the cell. 7. These results suggest that: (1) the rapid increase in contraction following a stretch is due to an increase in myofilament Ca2+ sensitivity rather than to changes in the L-type Ca2+ current or [Na+]i; and (2) a slow increase in the Ca2+ transient underlies the slow increase in contraction in isolated myocytes, but is not caused by either an increase in diastolic [Ca2+]i or a change in [Na+]i (and hence Ca2+ influx via Na(+)-Ca2+ exchange) or a change in myofilament Ca2+ sensitivity.

Animals↗
PubMed1996

Extradural extension of glioblastoma multiforme into the oral cavity: case report.

A rare case of glioblastoma multiforme with oral extension is presented in a 41-year-old female. She underwent two surgical treatments and both radiotherapy and chemotherapy for the right temporoparietal glioblastoma multiforme. A follow-up computed tomographic scan and magnetic resonance imaging demonstrated destruction of the temporal base and extradural extension of the tumor into the orbital, nasal, and oral cavities. This is the first report of the oral extension of glioblastoma multiforme. The mechanism for the extradural extension is discussed.

Adult↗
PubMed1996

Vasospastic angina in a patient with Fabry's disease who showed normal coronary angiographic findings.

It has been reported that coronary diseases in patients with Fabry's disease are induced by deposits in endothelial cells and coronary smooth muscle cells. Most of those are ischemia due to stenosis. This report describes a case of patient with Fabry's disease who showed severe vasospasms without coronary artery stenosis during acetylcholine loaded coronary angiography. In this case, a myocardial biopsy revealed that the deposits in the endothelial cells of the myocardial capillaries were lamellated appearance. Recently, it is reported that endothelial cell damage could be an important cause of coronary vasospasm. This case suggests that the some sort of functional disorder was induced by glyco-sphingolipid deposits in the coronary endothelial cells, and that this might have led to coronary artery spasms without the organic stenosis of coronary arteries.

Adult↗
PubMed1996

Influence of cisapride on the pharmacokinetics and antihypertensive effect of sustained-release nifedipine.

To investigate the clinical significance of interactions between cisapride and sustained-release nifedipine, we compared the plasma nifedipine concentration and blood pressure after administration of nifedipine alone (20 mg) with those obtained after administration of nifedipine cisapride (2.5 mg) in 20 patients with hypertension. The plasma nifedipine level was not altered by cisapride at one hour after administration, but was significantly increased at two (p < 0.01), three (p < 0.01), and four (p < 0.05) hours when compared with the level measured after nifedipine alone. Cisapride significantly decreased the mean blood pressure at three hours (p < 0.05) after administration of nifedipine. The acetaminophen method was used to determine gastric emptying time. The plasma concentration of acetaminophen at 45 minutes after administration was significantly increased by cisapride, suggesting that enhanced gastrointestinal motility might be the basis for the increase in the plasma nifedipine concentration. These results suggest that enhancement of the antihypertensive effect of nifedipine can occur when the drug is prescribed with cisapride, and that caution is needed when using such a combination therapy.

Aged↗
PubMed1995

The role of ATP hydrolysis in the function of the chaperonin GroEL: dynamic complex formation with GroES.

In order to understand the role of ATP hydrolysis of the chaperonin GroEL during protein folding, we have studied GroEL-GroES complex formation in the presence of ATP or ADP by using capillary electrophoresis and surface plasmon resonance. Capillary electrophoresis analysis showed that the GroEL 14-mer and GroES 7-mer formed a 1:1 complex in the presence of ATP. In the presence of ADP, both the association and dissociation rates of the complex were slower by about one order of magnitude than the rates in the presence of ATP at 25 degrees C. The implications of such a stable complex on the overall mechanism of chaperonin function are discussed.

Adenosine Diphosphate↗
PubMed1995

The mechanism underlying the cardiotoxic effect of the toxin from the jellyfish Chironex fleckeri.

We have investigated the mechanisms underlying the cardiac effects of the toxin from the box jellyfish Chironex fleckeri. Papillary muscles isolated from the hearts of ferrets and ventricular myocytes isolated from the hearts of ferrets and rats were used. Force, intracellular [Ca2+], and membrane potential were monitored in the papillary muscles; contraction, intracellular [Ca2+], intracellular [Na+], and membrane currents were monitored in the isolated myocytes. Application of the toxin to these preparations resulted in a large increase in intracellular [Ca2+] and the adverse symptoms of Ca2+ overload (aftercontractions, spontaneous contractions, a decrease in developed force, and an increase in resting force). The response of papillary muscles to the toxin was not inhibited by blockers of Ca2+ or Na+ channels or by inhibitors of the sarcoplasmic reticulum, Na+/K+ ATPase, or Na+/H+ exchange. The response to the toxin was, however, blocked by prior exposure to a solution which contained no Na+ and by Ni2+. In the isolated myocytes, as well as an increase in intracellular [Ca2+], the toxin also caused an increase in intracellular [Na+] and the appearance of a current which was inward at negative potentials and reversed at about -10 mV. These data can be explained by the toxin increasing Na+ influx into the cell. The increase in intracellular [Na+] will then increase intracellular [Ca2+] via the Na+/Ca2+ exchange mechanism, thus producing the observed Ca2+ overload.

Animals↗