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Biomedical subjects

K Fukushima

Publications and source records attributed to K Fukushima.

At least 199 records · Page 11Linked to original sources
PubMed1998

Dispersion of regional wall motion abnormality in patients with long QT syndrome.

OBJECTIVE: To examine the left ventricular regional wall motion abnormality and to evaluate dispersion of this abnormality in patients with long QT syndrome. DESIGN: Left ventricular short axis images at basal and middle levels were recorded on videotape and digitised to reconstruct digitised M mode echocardiograms, from which left ventricular wall thickness curves were obtained. The wall thickening time (ThT) was defined as the period in which the instantaneous wall thickness exceeded 90% of the maximum wall thickness. ThT was measured at three segments in each of the septal and free wall sides of the left ventricle, a total of 12 segments. To examine the mechanical dispersion of the left ventricle, the difference between the maximum and minimum ThT of 12 segments in each subject was obtained. PATIENTS: Eight patients with congenital long QT syndrome (averaged QTc interval (SD) 509 (27) ms1/2) and 10 control subjects (QTc interval 397 (26) ms1/2) were examined. RESULTS: The averaged ThT values of the 12 segments pooled form all subjects were correlated with the QT intervals (r = 0.72, p < 0.005). Thus the averaged ThT in the long QT syndrome patients was longer than in the control subjects (p < 0.005). The segmental variation of ThT in the patients was greater than in the control subjects (p < 0.001). The dispersion of ThT in the patients was therefore larger than in control subjects (p < 0.005). However, the pattern of ThT variation in the patients varied according to the individual subject. CONCLUSIONS: There is not only electrical but also mechanical dispersion in the left ventricle of long QT syndrome patients. Regional assessment of ventricular wall motion may allow quantification of the spatial variation of wall motion abnormality.

Adolescent↗
PubMed1998

Discharge characteristics of vestibular saccade neurons in alert monkeys.

We previously described a class of neurons, located in and around the interstitial nucleus of Cajal of the cat, that discharged during vestibular stimulation and before saccades. We called these neurons vestibular saccade neurons (VSNs). In the present study, we characterized similar neurons in the monkey. These neurons discharged before vertical saccades and during vertical vestibular stimulation as well as vertical smooth pursuit. Like cat VSNs, the discharge metrics of these VSNs were poorly related to saccade metrics and showed only occasional, weak sensitivity to eye position. They discharged most intensely (on-direction) for movements that were either upward or downward, and their on-directions were consistent during pitch and pursuit but not for eye position. For saccades, the correlation coefficient of number of spikes and vertical saccade size varied from 0.08 to 0.90 with a mean of approximately 0.6. The average sensitivity (i.e., slope) of the number of spikes and vertical saccade size linear regression was 0.3 +/- 0.2 spike/deg. Average correlations between peak discharge rate and peak saccade velocity and between burst duration and saccade duration were 0.5 and 0.4; sensitivities were 0.2 +/- 0.2 spike per s per deg/s and 0.6 +/- 0.5 ms/ms, respectively. Average vestibular sensitivities during 0.5 Hz, +/-10 degrees sinusoidal pitch while the animals suppressed their vestibular ocular reflex were 0.97 spike/s per deg/s for up VSNs and 0.66 spike/s per deg/s for down VSNs. The average static position sensitivity for the population of 39 VSNs tested was 0.55 spike/s per deg. The average gain for VSNs tested during 0.5 Hz, +/-10 degrees sinusoidal smooth pursuit tracking was 1.4 spike/s per deg/s. As we could not identify analogous neurons in the region of the monkey ponto-medullary junction, we conclude that horizontal on-direction VSNs do not exist in the monkey. We discuss a possible functional role for VSNs and similar neurons described in previous studies and conclude that these neurons are most likely involved with the process of neural integration (in a mathematical sense) of velocity-coded inputs from a variety of oculomotor subsystems and are not a pivotal element in saccade generation.

Action Potentials↗
PubMed1998

Neuronal responses related to smooth pursuit eye movements in the periarcuate cortical area of monkeys.

To examine how the periarcuate area is involved in the control of smooth pursuit eye movements, we recorded 177 single neurons while monkeys pursued a moving target in the dark. The majority (52%, 92/177) of task-related neurons responded to pursuit but had little or no response to saccades. Histological reconstructions showed that these neurons were located mainly in the posterior bank of the arcuate sulcus near the sulcal spur. Twenty-seven percent (48/177) changed their activity at the onset of saccades. Of these, 36 (75%) showed presaccadic burst activity with strong preference for contraversive saccades. Eighteen (10%, 18/177) were classified as eye-position-related neurons, and 11% (19/177) were related to other aspects of the stimuli or response. Among the 92 neurons that responded to pursuit, 85 (92%) were strongly directional with uniformly distributed preferred directions. Further analyses were performed in these directionally sensitive pursuit-related neurons. For 59 neurons that showed distinct changes in activity around the initiation of pursuit, the median latency from target motion was 96 ms and that preceding pursuit was -12 ms, indicating that these neuron can influence the initiation of pursuit. We tested some neurons by briefly extinguishing the tracking target (n = 39) or controlling its movement with the eye position signal (n = 24). The distribution of the change in pursuit-related activity was similar to previous data for the dorsomedial part of the medial superior temporal neurons (, indicating that pursuit-related neurons in the periarcuate area also carry extraretinal signals. For 22 neurons, we examined the responses when the animals reversed pursuit direction to distinguish the effects of eye acceleration in the preferred direction from oppositely directed eye velocity. Almost all neurons discharged before eye velocity reached zero, however, only nine neurons discharged before the eyes were accelerated in the preferred direction. The delay in neuronal responses relative to the onset of eye acceleration in these trials might be caused by suppression from oppositely directed pursuit velocity. The results suggest that the periarcuate neurons do not participate in the earliest stage of eye acceleration during the change in pursuit direction, although most of them may participate in the early stages of pursuit initiation in the ordinary step-ramp pursuit trials. Some neurons changed their activity when the animals fixated a stationary target, and this activity could be distinguished easily from the strong pursuit-related responses. Our results suggest that the periarcuate pursuit area carries extraretinal signals and affects the premotor circuitry for smooth pursuit.

Animals↗
PubMed1998

Downward gaze palsy caused by bilateral lesions of the rostral mesencephalon.

A 55-year-old man with diabetes mellitus developed diplopia and experienced difficulty in moving his eyes in the vertical plane, especially downward. Horizontal movement of each eye was normal with exotropia. Magnetic resonance imaging revealed small and high signals on both sides of the midbrain near the interstitial nucleus of Cajal (INC). Based upon the recent experimental evidence, we speculate that bilateral lesions involving the INC may have caused downward gaze palsy in our patient.

Blepharoptosis↗
PubMed1998

Retention mechanism of imidazoles in connective tissue. IV. Identification of a nucleophilic imidazolone metabolite in rats.

Formation of a nucleophilic 4(5H)(or 5(4H))-imidazolone structure has been postulated from in vitro studies to be one of the causative elements involved in the retention of drugs with imidazole moiety in connective tissue. To confirm this, we searched for the imidazolone-related metabolite in rats after intravenous dosing of 2-methylimidazole (2MI; 14C-labeled and unlabeled form, 3 and 300 micromol/kg body weight) as a model compound. The excreted urine, the major route of elimination of the compound, was collected and analyzed using the HPLC/MS system with a counterion effect for metabolite separation. 2-Methyl-4(5H)(or 5(4H))-imidazolone (2MIone) was identified as a urinary metabolite by chromatographic and mass-spectral inspection with the corresponding authentic standard. Pretreatment of rats with either SKF-525A (50 mg/kg, i.p.) or cimetidine (200 mg/kg, i.p.) significantly increased the excreted amount of 2MIone in urine and the irreversible binding of 2MI equivalents in the aortic tissue, whereas both factors were reduced by pretreatment with triethylenetetramine dihydrochloride (150 mg/kg/d for 5 d, s.c.). These results support the aforementioned deduction, and also raise the possibility that a cytochrome P450-independent, copper-related metabolic reaction might be involved in the imidazolone formation in vivo.

Animals↗
PubMed1998

Retention mechanism of imidazoles in connective tissue. II. Activation of imidazoles in cupro-ascorbate system for irreversible binding formation with aortic tissue in vitro.

In order to obtain an insight into the retention mechanism of drugs with imidazole moiety in the connective tissue, the in vitro characteristics of the interaction between 14C-labeled imidazoles (imidazole and its 2-methyl derivative) and slices of dog aorta were studied. We found that cupro-ascorbate-catalyzed oxidative reactions for the imidazoles led to their irreversible binding with connective tissue, and that, from a study using protein modifiers, the aldehydic function intrinsic to the tissue protein was involved in the binding formation. This characteristic in vitro was observed under physiological conditions, hence it can be extrapolated to the in vivo situation and could also give a clue to the nature of the retention of imidazole-containing drugs in connective tissue.

Animals↗
PubMed1998

Retention mechanism of imidazoles in connective tissue. III. Aldehyde adduct formation of a 4(5H)(or5(4H))-imidazolone product in vitro.

2-Methylimidazole (2MI), as well as imidazole, has been thought to undergo cupro-ascorbate (Cu-VC)-catalyzed oxidative transformation in vitro to become a reactive species capable of combining with aldehydes intrinsic to connective-tissue proteins. We attempted to seize the essence of the above reaction through obtaining the structural information of an aldehyde-bonding species. As major products from 2MI in the in vitro Cu-VC system, 2-hydroxymethylimidazole (2(OH)MI) and 2-methyl-4(5H)(or 5(4H))-imidazolone (2MIone) were identified by mass-spectral and chromatographic comparison with the corresponding authentic standards synthesized. The in situ addition of acetaldehyde or propionaldehyde as a simple protein-aldehyde model to the system resulted in the deducible formation of an aldol condensate, 2-methyl-4(or 5)-ethylidene-4(5H)(or 5(4H))-imidazolone (2MEIone) or its possible analogue with a propylidene moiety, respectively. The authentic compound of 2MIone directly reacted with acetaldehyde and easily afforded the products assignable to the isomers of 2MEIone through the ethylidene moiety at physiological pH and temperature, whereas neither 2MI or 2(OH)MI reacted at all. These results suggest that a 4(5H)(or 5(4H))-imidazolone product, although simply a monooxygenated form, is sufficiently reactive to give aldol condensation-typed covalent adducts with aldehydes, even under physiological conditions, probably having an activated methylene moiety in the ring structure. Based on the present results, we discussed the mechanism of the retention of imidazole-containing drugs in connective tissue.

Acetaldehyde↗
PubMed1998

Three-dimensional structure of mucosal and submucosal lymphatics in rat small intestine.

The organization of the lymphatic system in the rat ileum was investigated by the three-dimensional reconstruction using serial sections after dilatation of lymphatics. This method has an advantage to exclude possible artifacts in the conventional corrosion cast method. The villus possessed several lacteals and connected to each other by sinus. Two or three perpendicularly oriented lymphatics descended and led into the submucosal lymphatic network. In mucosa and submucosa, no valvular structure was detected. This study confirmed the voluminous lacteals and fine network structure of lymphatics in submucosa without valves, suggesting great potential to keep lymph and to drain soluble factors and cellular components.

Animals↗
PubMed1998

Ocular tilt reaction with vertical eye movement palsy caused by localized unilateral midbrain lesion.

A 60-year-old man developed diplopia and experienced difficulty moving his eyes. Vertical movement of each eye, including vestibulo-ocular reflex and smooth pursuit, was extremely limited. Horizontal eye movements were normal. His head position was tilted toward his left. There was 10 prism diopters of exotropia and 10 prism diopters of right hypertropia. Fundus photographs revealed a clockwise torsion of both eyes. These signs indicate leftward ocular tilt reaction. Magnetic resonance imaging showed a small area of an increased signal intensity localized in the midbrain dorsomedial to the red nucleus on the right side. Based on recent experimental evidence, it may be assumed that the unilateral lesion involving the right interstitial nucleus of Cajal most probably caused leftward ocular tilt reaction in our patient.

Cerebral Hemorrhage↗
PubMed1998

Contrast enhanced magnetic resonance imaging for femoral neck fracture.

Femoral head perfusion was evaluated in 29 patients after acute femoral neck fracture using contrast enhanced fat saturation magnetic resonance imaging. The patients were followed up with T1 and T2 weighted spin echo magnetic resonance imaging without fat saturation, which is suitable in detecting avascular necrosis. The mean interval from injury to the initial contrast enhanced fat saturation magnetic resonance imaging was 24.5 hours. The mean age at the time of injury was 69 years, and the mean followup was 26.9 months. Three distinct patterns of femoral head enhancement were recognized in the acute phase after fracture. When the whole femoral head was well enhanced (Type 3, n = 11), no avascular necrosis developed. In contrast, when the head showed no enhancement (Type 1, n = 6), avascular necrosis developed in all patients. In patients with partial enhancement (Type 2, n = 12), avascular necrosis developed in five patients. These data showed the current method provided an accurate prediction of the development of avascular necrosis in the patients with Type 1 and Type 3 enhancement. However, overall predictive value was 59% (17 of 29 patients) because of the uncertainty in the patients with partial enhancement (Type 2), and additional study is needed for this method to become routine in clinical use.

Adolescent↗
PubMed1998

[Lung abscess in a patient with Good's syndrome and pure red cell aplasia].

A 56-year-old man with pure red cell aplasia (PRCA), hypogammaglobulinemia and mediastinal tumor was admitted to our hospital with of dyspnea, high fever and general fatigue. Chest X-ray showed a large cavity with a niveau in the left lung. Biopsy of the mediastinal tumor revealed an epithelial cell-type thymoma. Lung abscess with Good's syndrome and PRCA was diagnosed. Antibiotics was administered, and percutaneous catheter drainage of the lung abscess was performed. He recovered and was discharged. Hypogammaglobulinemia in the case may have resulted from reduced production of gammaglobulin associated with a quantitative B-cell defect.

Agammaglobulinemia↗
PubMed1998

Effect of pibutidine hydrochloride on nitric oxide production in rat gastric mucosa.

This study examined the effect of pibutidine hydrochloride, a novel histamine H2 receptor antagonist (IT-066), on nitric oxide (NO) production in gastric mucosa by measuring nitrite and nitrate contents. IT-066 (0.3-3 mg/kg, p.o.) and NO donors, sodium nitroprusside (0.3 mg/kg, s.c.) and NOR3 (0.1 mg/kg, s.c.), increased the NO contents in gastric mucosa. Cimetidine (100 mg/kg, p.o.), ranitidine (30 mg/kg, p.o.) and famotidine (10 mg/kg, p.o.) did not significantly affect the NO production. Pretreatment with NG-nitro-L-arginine methyl ester (3 mg/kg, i.v.), a NO synthase inhibitor, decreased the level of IT-066 (3 mg/kg, p.o.)-stimulated NO production. These results suggest that IT-066 stimulated gastric mucosal NO production, and that endogenous NO may be implicated in the pharmacological effect of IT-066.

Animals↗
PubMed1998

Elevated serum levels of Trichosanthes japonica agglutinin-I binding alkaline phosphatase in relation to high-risk groups for hepatocellular carcinomas.

The N-linked sugar chain structures of human hepatic, intestinal, and placental alkaline phosphatases (ALPs) were studied comparatively by chromatography on various lectin columns in combination with digestion by several kinds of exoglycosidases. The sugar chain structures were organ specific. On the basis of these organ-specific structures, we investigated serum ALP using a Neu5Ac(alpha)2-->6Gal(beta)1-->4 GlcNAc-specific Trichosanthes japonica agglutinin-I (TJA-I)-Sepharose column to clarify whether the level of TJA-I-binding serum ALP activity can be used as an indicator to discriminate one form of chronic liver disease from another. Levels of TJA-I-binding ALP in serum were higher in cases of liver cirrhosis and hepatocellular carcinoma than in chronic hepatitis (P < 0.01). The levels of TJA-I-binding ALP in serum did not change significantly after transcatheter arterial embolization, and the amounts of TJA-I-binding ALP activity in noncancerous cirrhotic liver tissues were higher than those in cancerous liver tissues derived from hepatocellular carcinoma patients, indicating that the TJA-I-binding ALP is mainly derived from cirrhotic liver tissues rather than cancerous liver tissues. These results indicate that analysis of the levels of TJA-I-binding ALP in serum is clinically useful for differentiating liver cirrhosis from chronic hepatitis and that altered sugar chain expression in ALP occurs mainly in liver cirrhosis.

Alkaline Phosphatase↗
PubMed1997

Lectin-like characteristics of recombinant human interleukin-1beta recognizing glycans of the glycosylphosphatidylinositol anchor.

We found that 35S-labeled recombinant human interleukin-1beta (rhIL-1beta) binds phosphatidylinositol-specific phospholipase C-treated human placental alkaline phosphatase, phosphatidylinositol-specific phospholipase C-treated trypanosome surface variant glycoproteins, and urinary uromodulin immobilized on plates or immobilized on CNBr-activated Sepharose 4B. The interaction between rhIL-1beta and these glycoproteins was lectin-like, since it was inhibited in the presence of specific saccharides, i.e. mannose 6-phosphate or synthetic Ac-NH.CH2.CH2. PO4--->6Manalpha1-->(+/-2Manalpha1-->+/-6Manalpha1-->) propyl at about 1 microM. On the other hand, a wide variety of compounds including biantennary sugar chains derived from these glycoproteins as well as ethanolamine phosphate, inositol phosphate, mannose 6-sulfate, mannose 1-phosphate, glucose 6-phosphate, and mannitol 6-phosphate did not show any inhibitory effect at concentrations up to 1 mM. These results indicate that rhIL-1beta interacts with these glycoproteins via the mannose 6-phosphate diester of glycans on the glycosylphosphatidylinositol (GPI) anchor. Furthermore, when monolayers of polarized Madin-Darby canine kidney cells on polycarbonate filter membranes were incubated with 35S-rhIL-1beta in either the apical or basolateral chamber, 35S-interleukin-1beta was found to bind specifically to the apical membranes with a Ka value of 4.6 x 10(7) M-1, and the specific interaction was inhibited by 1 microM mannose 6-phosphate. Since the mannose 6-phosphate diester moiety exists only in the GPI glycans on plasma membranes, it was evident that interleukin-1beta can directly interact with the mannose 6-phosphate diester component of the intact glycan of GPI anchors on plasma membranes.

Alkaline Phosphatase↗