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Biomedical subjects

N Imoto

Publications and source records attributed to N Imoto.

8 recordsLinked to original sources
PubMed1992

[A case of unilateral pulmonary edema associated rupture of mitral chordae tendineae].

A 57-year-old man was admitted with dyspnea and bloody sputum. The chest X-ray showed unilateral alveolar infiltration, and alveolar cell carcinoma was suspected. Physical examination showed orthopnea and a loud systolic murmur, and the echocardiogram showed mitral valve prolapse. A chest X-ray 4 days later revealed bilateral infiltration. The cardiac catheterization showed pulmonary congestion and the capillary wedge pressure revealed a prominent V wave. Papanicolaou's test of sputum was negative. These findings suggested heart failure due to mitral regurgitation rather than lung carcinoma. The patient underwent mitral valve replacement because of his refractoriness to the medical treatment. During the operation, the chordae tendineae of the anterior mitral leaflet was found to be completely ruptured. The mechanisms of unilateral pulmonary edema could not be ascertained, but the effect of posture and gravity was thought to be a possible mechanism.

Cardiac Catheterization↗
PubMed1991

A Japanese family with two types of muscular dystrophy: DNA analysis and the dystrophin test.

A unique Japanese family with both Fukuyama type congenital muscular dystrophy (FCMD) and Duchenne muscular dystrophy (DMD) is described. Four boys, all from the sixth generation of the same family, were afflicted with severe neuromuscular diseases beginning in early life, three of them presenting the typical phenotype of FCMD and one, that of DMD. Although DNA analysis by Southern blotting with complementary DNAs representing the whole of the dystrophin coding sequence detected neither gross deletions nor duplications, immunohistochemistry and Western blotting of the biopsied skeletal muscle with an antidystrophin monoclonal antibody (dystrophin test) showed that the approximately 400-kd dystrophin was expressed normally at the sarcoplasmic membrane of the FCMD phenotype patient but was completely absent in the DMD phenotype patient. From these results, it was presumed that two different childhood muscular dystrophies, FCMD and DMD, coexisted in this family. This unique case illustrates the efficacy of the dystrophin test in the differential diagnosis of the two diseases even when conventional means of diagnosis do not give definite answers and DNA analysis of the dystrophin gene is not informative.

Blotting, Southern↗
PubMed1991

[Two long-living brothers of dystrophin-related muscular dystrophy with an in-frame deletion of exon 3 of the dystrophin gene--clinical features and diagnosis].

Two long-living brothers of dystrophin-related muscular dystrophy with an in-frame deletion of exon 3 of the dystrophin gene were described. Weakness of the lower extremities and pseudohypertrophy of calf muscles began at the age of 2 years in the elder brother and 4 years in the younger brother, respectively. Clinical symptoms progressed rapidly and both of them lost ambulation and became wheelchair bound at the age of 11-12 years. However, the progression of the disease process slowed in late teens, and now at the age of 36 and 33 years, respectively, they do not have respiratory or cardiac insufficiency, although they are disabled severely. Southern blotting with the entire dystrophin cDNAs, cDNA 1-2a, 2b-3, 4-5a, 5b-7, 8, and 9-14, revealed a single deletion of exon 3 in the 2 brothers. The mother was shown to be a heterozygote for this mutation. The unique clinical features of these brothers were presumed due to the following 2 factors: (1) a single deletion of exon 3 is an in-frame deletion of the dystrophin gene, and (2) exon 3 corresponds to a unique domain of the dystrophin molecule; the amino-terminal region which is highly homologous to the actin-binding-region of alpha-actinin. We consider that these 2 brothers are compatible with the so-called frame-shift hypothesis of Duchenne/Becker muscular dystrophy (DMD/BMD) phenotype, although they are diagnosed DMD by the classification method based on the patients' age of becoming permanently wheelchair bound.

Adult↗
PubMed1986

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.

Acetylcholine↗
PubMed1985

Recurrent ectopic junctional tachycardia in Ebstein's anomaly. Case report of a 67-year-old man.

We reported the case of a 67-year-old man with Ebstein's anomaly, the oldest patient with this disease in Japan as far as we know. His condition was often accompanied by ectopic junctional tachycardia with isorhythmic AV dissociation, which made him complain of palpitation by elevating right intra-atrial pressure. Although enhanced automaticity was the most likely mechanism of this tachycardia, it was abruptly initiated and terminated by a single premature contraction. Because this interesting character can not be explained solely by the usual ideas of automaticity, we suggest that ectopic junctional tachycardia in the present case may somewhat resemble the phenomenon of triggered automaticity.

Aged↗
PubMed1980

[Changes of prostaglandin receptors in myometrium--interaction between steroids and prostaglandins--(author's transl)].

One of the most important actions of prostaglandins (PGs) is contraction of myometrium. On the other hand, the inhibitory action of progesterone(P) on myometrial contraction is well known. The purpose of this study is to elucidate the mechanism of uterine contraction, analyzing the interaction between PGs and steroids on the receptor level. 1) PG receptor in myometrium was increased after the administration of estradiol (E) into castrated rabbits and addition of P and E enhanced the increases of PG receptor. On the contrary, PGF2 alpha in myometrium was decreased by E, but addition of P and E recovered the decrease. 2) P receptor was increased after the injection of PG in the castrated rabbits, but E receptor showed no significant changes in its level. These results suggest that PG acts on myometrium partly through the changes of steroid hormone receptor and vice versa. 3) PGE1 and PGF2 alpha receptor in pregnant rabbits were increased 4 hours after castration. From these results, it becomes clear that the increase of PG receptor and PG synthesis play an important role in the onset of uterine contraction.

Animals↗