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Biomedical subjects

H Ino

Publications and source records attributed to H Ino.

At least 19 recordsLinked to original sources
PubMed1992

Cardiac characteristics and postoperative courses in Cushing's syndrome.

To assess the cardiac characteristics and postoperative courses in patients with Cushing's syndrome, electrocardiography and echocardiography were performed to study 12 consecutive, unselected patients, and results were compared with those of essential hypertension and primary aldosteronism. Eleven patients had hypertension and 7 had diabetes mellitus. Before adrenalectomy, common electrocardiographic abnormalities consisted of high-voltage QRS complexes (10 patients) and negative T waves (7 patients). Echocardiograms showed left ventricular hypertrophy in 9 patients, and all the patients had evidence of asymmetric septal hypertrophy. In patients with left ventricular hypertrophy, the thickness of the interventricular septum ranged from 16 to 32 mm, whereas the ratio of the thickness of interventricular septum to that of the posterior wall ranged from 1.33 to 2.67. The interventricular septum in Cushing's syndrome was extremely thicker and asymmetric septal hypertrophy occurred more often than essential hypertension and primary aldosteronism. Nine patients could be followed up after operation. In these patients abnormal electrocardiographic findings had normalized, the thickness of interventricular septum had decreased and asymmetric septal hypertrophy had disappeared except in 1 patient. The reason why left ventricular hypertrophy in Cushing's syndrome is severe is still unknown. Because left ventricular hypertrophy is more severe and the frequency of asymmetric septal hypertrophy much greater in Cushing's syndrome than in essential and other secondary hypertension, it is thought that not only increased aortic pressure but excessive plasma cortisol may be etiologic factors in the progression of left ventricular hypertrophy in Cushing's syndrome.

Adrenal Gland Neoplasms↗
PubMed1992

Disproportionate hypertrophy of the interventricular septum and its regression in Cushing's syndrome. Report of three cases.

Three patients of Cushing's syndrome with severe disproportionate hypertrophy of the interventricular septum are reported. All three underwent adrenalectomy and the diagnosis of Cushing's syndrome was confirmed by the presence of adrenal adenoma. All three showed hypertension before the adrenalectomy and two remained hypertensive following adrenalectomy. Before the operations the electrocardiograms revealed inverted T waves in broad leads, and mechanocardiogram systolic and diastolic dysfunction. After the adrenalectomies, abnormal findings on electrocardiograms were normalized and septal hypertrophy was completely regressed. It appears that not only high aortic pressure but also excessive plasma cortisol may be an etiologic factor of the left ventricular hypertrophy in Cushing's syndrome.

Adrenalectomy↗
PubMed1992

[The functional significance of coronary collateral circulation during sudden coronary occlusion].

The functional significance of the coronary collateral circulation remains controversial. It has been suggested that collateral circulation possibly helps prevent myocardial ischemia. Seventeen target lesions in 15 patients were studied to determine the relationship between the extent of the coronary collateral circulation and the degree of ventricular dysfunction during percutaneous transluminal coronary angioplasty (PTCA). During the first balloon inflation, diastolic indices such as left ventricular end-diastolic pressure, max negative dP/dt and the time constant of early relaxation were measured immediately before and at 60 sec following balloon inflation. During the second inflation, the contralateral and ipsilateral collateral circulations were evaluated. The latter was graded as follows: 0 = none; I = filling of side branches only; II = partial filling of the epicardial segment; and III = complete filling of the epicardial segment. Following balloon inflation, a significant increase was noted in the time constant of early relaxation in patients with grade 0 collateral circulation (40 +/- 7 to 47 +/- 7 msec: p < 0.01) and grade II collateral circulation (52 +/- 12 to 56 +/- 13 msec: p < 0.05). The percent increase in the time constant of early relaxation of patients with grade 0 and I collateral circulations exceeded that of patients with grade II (p < 0.05) or grade III collateral circulation (p < 0.05). Left ventricular end-diastolic pressure was elevated in all groups during PTCA. There was no significant difference in the percent increase of left ventricular end-diastolic pressure (LVEDP) between the 4 groups. However, LVEDP before PTCA was higher in patients with grade III collateral circulation than in patients in the other groups. Max negative dP/dt did not change significantly in any group. In conclusion, collateral circulation helps prevent myocardial ischemia during acute coronary occlusion, which is most precisely shown by the time constant of early relaxation. The degree of this protective function of collateral circulation seems to vary.

Aged↗
PubMed1992

[Effects of MPTP on the mouse retina].

MPTP is known as a selective neurotoxin which destroys dopamine-containing neurons, and induces a model of Parkinson's disease. In the retina, MPTP acts on the amacrine cells which contain dopamine. In the present study, C57BL/6J mice were treated i.p. with MPTP (cumulative dose, 150 mg/kg), and the role of dopamine in the mouse retina was investigated electrophysiologically and immunohistochemically. ERGs were recorded before and 10, 30 and 50 days after MPTP injection. The amplitude of the oscillatory potentials was greatly reduced, and that of the b-wave to a lesser degree, while the a-wave was slightly reduced 10 days after injection. These ERG changes tended to return to the control level 50 days after injection. Immunohistochemical analysis showed that 10 days after MPTP injection the number of tyrosine hydroxylase positive amacrine cells was reduced by approximately 50%, and that these changes had lasted at least until 50 days after MPTP injection.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

Direct DNA sequencing from colony: analysis of multiple deletions of mitochondrial genome.

We have developed a rapid and efficient nucleotide sequencing technique, named the colony direct sequencing method, which combines both the conventional cloning method for picking up a single gene and the polymerase chain reaction (PCR) method for amplifying the gene directly from a colony. In the present study, the colony direct PCR product was used both for identification of the DNA insert and for nucleotide sequencing by an automated DNA analysis system. A nucleotide sequence of 300 to 400 bp could be determined within 13 h after picking the bacterial colonies on LB medium plates. We applied this method to sequencing of junctional regions of multiple deleted mtDNAs in two siblings with inherited recurrent myoglobinuria. Mitochondrial DNA fragments with deletions were amplified by PCR and then cloned into plasmids. Among 48 white colonies propagated on LB medium plates, nine different clones were identified by PCR directly from colonies. Determination of six different junctional sequences disclosed involvement of directly repeated sequences of 2 to 12 bp in length on each side of the deletions. We believe that the colony direct sequencing method will be a powerful tool in molecular genetics for identification of a single gene among polymorphic DNAs.

Adenosine Triphosphatases↗
PubMed1991

Patients with idiopathic cardiomyopathy belong to the same mitochondrial DNA gene family of Parkinson's disease and mitochondrial encephalomyopathy.

Comparison of total mitochondrial DNA sequences of patients with idiopathic (deleted or hypertrophic) cardiomyopathy with those of patients with Parkinson's disease and mitochondrial encephalomyopathies revealed distinct clustering of point mutations among patients. Furthermore, an inverse relation was found between the total number of base-substitution and life span of the patients. Among point mutations found in each patient, sequentially diverged six clusters consisting of 14, 10, 7, 1, 2, and 3 mutations, respectively, were detected. Five sub-clusters consisting of 2, 2, 11, 1, and 1 mutations, respectively, were detected. From each cluster, the patient's unique mutations were diverged with three types of the mutations specific for the disease. The divergence allowed construction of a phylogenetic tree which clearly indicated that patients with idiopathic cardiomyopathy belong to the same mitochondrial DNA gene family of Parkinson's disease and mitochondrial encephalomyopathies.

Adult↗
PubMed1991

Distinct clustering of point mutations in mitochondrial DNA among patients with mitochondrial encephalomyopathies and with Parkinson's disease.

The total sequence data for mitochondrial DNA (mtDNA) revealed distinct clustering of point mutations (pms) in mtDNA among one patient with myoclonus epilepsy with ragged-red fibers (MERRF), two patients with Parkinson's disease (PD), two patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and one patient with fatal infantile cardiomyopathy (FICM). Among 33 to 62 pms found in each patients, sequentially diverged five clusters of pms were detected and designated as C-1 to C-5. C-1, consisted of fourteen pms, existed in the MERRF patient, C-1 and C-2 (nine pms) in one PD patient, C-1 to C-3 (seven pms) in another PD patient, C-1 to C-4 (one pm) in one MELAS patient and C-1 to C-5 (three pms) in another MELAS patient and the FICM patient. From these clustering of pms, a phylogenetic tree of mitochondrial encephalomyopathies (ME) was constructed. This tree clearly indicated that the ME and PD patients are members of the same gene family, and the MELAS and FICM patients are each others' closest relative. Each patient's unique pms (14 to 28 pms) were detected and, from their characteristic features, the types of the mutations specific for the disease were classified as mit- + syn- for MERRF, mit- + p- for PD, and syn- + mit- for MELAS. An inverse relation was found between the total number of pms and life span of the MELAS and FICM patients.

Adolescent↗
PubMed1991

Mitochondrial DNA mutations in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).

The total sequences of mitochondrial DNA were determined in two patients with juvenile-onset mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) due to Complex I deficiency. Patients 1 and 2 had three and two unique point mutations, respectively, causing replacement of phylogenically conserved amino acids. A transition from G to A was found at nucleotide position 5601 in the alanine tRNA gene of Patient 2, and a transition from A to G was found at 3243 in the leucine (UUR) tRNA gene of both patients. The latter mutation located at the phylogenically conserved 5' end of the dihydrouridine loop of the tRNA molecule, and was present in two patients with adult-onset MELAS and absent in controls. These results indicate that a mass of mtDNA mutations including the A-to-G transition in the tRNA(Leu) gene is a genetic cause of MELAS.

Adolescent↗
PubMed1991

Undifferentiated carcinoma of the vulva mimicking epithelioid sarcoma.

We report an undifferentiated sweat gland carcinoma of the vulva in an 80-year-old woman. The tumor, which was located in the right labium majus, resembled an epithelioid sarcoma histologically; it had a granulomatous appearance with multiple tumor nodules containing epithelioid tumor cells. The tumor also contained rhabdoid cells; a large cluster of them showed histological features indistinguishable from those of a malignant rhabdoid tumor. Immunohistochemically, the tumor cells reacted not only for epithelial markers such as cytokeratins, EMA, and CEA, which are known to be expressed by epithelioid sarcoma, but also for CA125 and with monoclonal antibodies recognizing sweat gland structures--namely, EKH5 and EKH6. For comparison, two epithelioid sarcomas and two extrarenal malignant rhabdoid tumors were also studied. Of these tumors, only one extrarenal rhabdoid tumor reacted with EKH5, and none reacted for CA125. Electron-microscopic examination of the present tumor showed the presence of discontinuous basal laminae and tonofibril-like structures as well as primitive cell junctions and interdigitating filopodia. From these findings, we conclude that the tumor was an undifferentiated sweat gland carcinoma mimicking an epithelioid sarcoma. Findings in this case support the idea of the diverse histogenesis of extrarenal malignant rhabdoid tumors and indicate that electron microscopy is important for differentiating epithelioid sarcoma from skin adnexal carcinoma.

Aged↗
PubMed1991

Identification of a possible control element, Mt5, in the major noncoding region of mitochondrial DNA by intraspecific nucleotide conservation.

Nucleotide sequences throughout the whole major noncoding region of mitochondrial DNA of 18 subjects were determined. Previously identified control elements were classified into three groups according to the degree of intraspecific nucleotide conservations: strictly conserved elements (LSP, HSP, Mt3, Mt3 on H-strand, mtTF1-element for HSP), relatively conserved elements (CSB-III, Mt4 on H-strand, and mtTF1-element for LSP), and variable elements (TAS, CSB-I, CSB-II). Moreover, alignment of nucleotide conservations disclosed a stretch of conserved sequence (5'-ATGCTTACAAGCAAG-3', nucleotide number 16, 194-16,208, designated as Mt5 element) in the middle of the hypervariable segment. Nucleotide conservation of this element was not only intraspecific but also interspecific.

Base Sequence↗
PubMed1991

[Myoglobinuria caused by multiple deletions of mitochondrial DNA].

We report two brothers with inherited recurrent myoglobinuria associated with distinct morphological abnormalities of muscle mitochondria and multiple deletions of muscle mitochondrial DNA. Patient 1 (26 years old) and Patient 2 (21 years old) had recurrent episodes of myoglobinuria provoked by strenuous exercise or alcohol intake. Histochemistry of their biopsied limb muscles showed ragged-red fibers and cytochrome c oxidase-negative fibers as well as degenerating and regenerating fibers. Electron microscopy showed a pronounced accumulation of abnormal mitochondria containing paracrystalline inclusions and moderate increases of glycogen particles. Southern blot analysis revealed multiple deletions of mitochondrial DNA, some of which were common to both patients. By the primer shift polymerase chain reaction method, we detected multiple abnormal fragments indicating mitochondrial DNA deletions. Nucleotide sequencing of the deleted regions disclosed directly repeated sequences of 1 to 12 bp on each side of the deletions. Since the end points of mitochondrial DNA deletions were within 20 bp of the major non-coding region, probable mutations in this region contribute to the pathogenesis of multiple mitochondrial DNA deletions found in these patients. We propose that a defect of the mitochondrial energy-transducing system due to multiple mitochondrial DNA deletions is a novel genetic cause of inherited recurrent myoglobinuria.

Base Sequence↗
PubMed1990

Mode of blockade by MK-801 of N-methyl-D-aspartate-induced increase in intracellular Ca2+ in cultured mouse hippocampal neurons.

Microfluorometry with fura-2 was applied to study the action of the anticonvulsant (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) on N-methyl-D-aspartate (NMDA)-induced increase in intracellular Ca2+ concentration ([Ca2+]i) in cultured mouse hippocampal neurons. MK-801 caused a potent and long-lasting blockade of the NMDA-activated [Ca2+]i elevation in a selective manner, not affecting the [Ca2+]i rise induced by quisqualate or kainate. Blockade and recovery from the blockade by MK-801 showed use dependency; the degree of blockade was dependent on the presence of NMDA. The use-dependent onset of antagonism was, however, highly sensitive to the bath temperature. MK-801 applied in the absence of NMDA had no effect on the response to subsequent application of NMDA at 22 degrees C, whereas it reduced the subsequent response to NMDA significantly at 37 degrees C. MK-801 interacted with the receptor-ion channel complex even when Mg2+, which is considered to block the open channel, had already blocked the NMDA-induced [Ca2+]i. The recovery from blockade by MK-801 was not accelerated by the application of 10 mM Mg2+ for 5 min. These results suggest that MK-801 can gain access to its binding site in the absence of NMDA at physiological temperature, and that this binding site is distinct from that for Mg2+.

Animals↗
PubMed1990

Characterization of binding sites for spider toxin, [3H]NSTX-3, in the rat brain.

A group of spider toxins (JSTX, NSTX, argiopin, argiotoxin etc.) share a basic common structure and have been reported to block strongly quisqualate- and kainate-sensitive glutamate responses in vertebrate and invertebrate nervous systems. They are presumed to be potent antagonists of both quisqualate and kainate receptors and may serve as useful tools for characterizing these receptors. We report here the synthesis of tritium-labeled NSTX-3 and the characterization of its binding sites in the rat brain. We found that high- and low-affinity binding sites exist in the cerebellum (Kd = 7.75 and 202 nM, Bmax = 0.37 and 5.54 pmol/mg protein, respectively). Synthetic NSTX analogs strongly inhibited [3H]NSTX-3 binding in the cerebellum (IC50 = 10(-7)-10(-6) M), whereas competitive agonists of glutamate receptors (AMPA, quisqualate, NMDA, kainate, glutamate and aspartate) exhibited weak or no inhibitory effects.

Amino Acids↗