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Biomedical subjects

M Komiyama

Publications and source records attributed to M Komiyama.

At least 73 records · Page 4Linked to original sources
PubMed1999

Venous angiomas with arteriovenous shunts: report of three cases and review of the literature

OBJECTIVE AND IMPORTANCE: In spite of recent recognition of the benign nature of venous angioma (VA), only limited information is available on the clinical features of VA with arteriovenous shunt (AVS). The purpose of this study was to elucidate the clinical profile of VA with AVS. CLINICAL PRESENTATION AND INTERVENTION: We describe three patients having a VA with AVS and review the clinical features of 31 patients reported in the literature, including our three patients. The patients included 12 women and 19 men, ranging in age from 18 to 54 years. Seven patients (22.6%) presented with intracranial hemorrhage, and none of 16 patients developed a new or recurrent hemorrhage (mean follow-up period, 11 months). Treatment was conservative in 14 patients, lobectomy or partial resection of the VA in 6, removal of hematoma in 4, operation only for coexisting aneurysm or arteriovenous malformation in 4, and not known in 3. The outcome was reported as good recovery in 19 patients, persistent neurological deficits in 2, death or deterioration not related to the VA in 3, and not known in 7. CONCLUSION: Although there remains some uncertainty as to the clinical features of VA with AVS, its prognosis seems to be essentially as benign as that of VA without AVS. Thus, conservative treatment is recommend except for patients with a large hematoma or with a coexisting arteriovenous malformation or a symptomatic, accessible cavernous angioma, which may be treated by surgical intervention. Further collection of data is required to establish definite treatment guidelines.

Journal Article↗
PubMed1999

Marked regional heterogeneity in venous oxygen saturation in severe head injury studied by superselective intracranial venous sampling: case report.

OBJECTIVE: Continuous monitoring of jugular venous oxygen saturation (SjvO2) is useful in the management of severe head injury. Abnormally high SjvO2 values can be caused by increased cerebral blood flow, decreased cerebral metabolism, brain death, contamination from extracerebral venous blood, or traumatic arteriovenous fistula. CLINICAL PRESENTATION: A 20-year-old man with severe head injury was diagnosed to have a traumatic dural carotid-cavernous sinus fistula on the day of trauma. Continuous left SjvO2 monitoring from Days 4 to 12 revealed oxygen saturation ranging between 85 and 98%. INTERVENTION: Superselective intracranial and extracranial venous sampling on Day 5 demonstrated marked regional heterogeneity in venous oxygen saturation as follows: superior sagittal sinus, 95 to 97%; straight sinus, 88%; right transverse sinus, 94%; left transverse sinus, 74%; right SjvO2, 95%; left SjvO2, 89%; the basilar plexus, 99%; right internal jugular vein, 98%; the left internal jugular vein, 94%. Extremely high oxygen saturation in the superior sagittal sinus and basilar plexus was attributed to severe brain damage and carotid-cavernous sinus fistula, respectively. CONCLUSION: Although jugular bulb oximetry is useful in the management of severe head injury, high oxygen saturation values should be interpreted with caution because they cannot show the intracranial heterogeneity of venous oxygen saturation.

Adult↗
PubMed1999

Gamma Knife radiosurgery for metastatic brain tumor: the usefulness of repeated Gamma Knife radiosurgery for recurrent cases.

Forty-one patients with a total of 193 metastatic brain tumors were treated because of new lesions or in a few cases because of tumor regrowth. The management involved two to four treatments with Gamma Knife radiosurgery (GKRS). The overall median survival was 15 months. The local control rate of tumors was 89% for the first treatment and 93% for repeated treatments. Symptomatic radiation-induced edema appeared in only two cases (4.9%). Patients with metastatic brain tumors who developed new lesions after GKRS were treated with GKRS alone for subsequent lesions. It was possible to control tumors for a long period with minimal side effects. As a result, we were able to maintain the quality of life of these patients, but, the effect of GKRS in controlling tumor regrowth seemed temporary.

Actuarial Analysis↗
PubMed1999

Myofibrillogenesis in the developing chicken heart: assembly of Z-disk, M-line and the thick filaments.

Myofibrillogenesis in situ was investigated by confocal microscopy of immunofluorescently labelled whole mount preparations of early embryonic chicken heart rudiments. The time-course of incorporation of several components into myofibrils was compared in triple-stained specimens, taken around the time when beating starts. All sarcomeric proteins investigated so far were already expressed before the first contractions and myofibril assembly happened within a few hours. No typical stress fibre-like structures or premyofibrils, structures observed in cultured cardiomyocytes, could be detected during myofibrillogenesis in the heart. Sarcomeric proteins like (&agr;)-actinin, titin and actin were found in a defined localisation pattern even in cardiomyocytes that did not yet contain myofibrils, making up dense body-like structures. As soon as the heart started to beat, all myofibrillar proteins were already located at their exact position in the sarcomere. The maturation of the sarcomeres was characterised by a short delay in the establishment of the pattern for M-line epitopes of titin with respect to Z-disk epitopes and the incorporation of the M-line component myomesin, which preceded that of myosin binding protein-C. Thus dense body-like structures, made up of titin, (&agr;)-actinin and actin filaments serve as the first organised complexes also during myofibrillogenesis in situ and titin functions as a ruler for sarcomere assembly as soon as its C termini have become localised. We suggest that assembly of thin and thick filament occurs independently during myofibrillogenesis in situ and that myomesin might be important for integrating thick filaments with the M-line end of titin.

Animals↗
PubMed1999

High incidence of persistent primitive arteries in moyamoya and quasi-moyamoya diseases.

This study investigated the incidences of persistent primitive arteries in patients with moyamoya disease, unilateral moyamoya disease, and quasi-moyamoya disease. Cerebral angiograms of 50 patients (39 moyamoya disease patients, 6 unilateral moyamoya disease patients, and 5 quasi-moyamoya disease patients) were retrospectively reviewed. There were 35 females and 15 males, aged from 3 to 63 years (mean 27.4 years). Persistent primitive carotid-basilar artery anastomoses were observed in three patients: primitive hypoglossal artery in one moyamoya disease patient, primitive trigeminal artery variant in one unilateral moyamoya disease patient, and an anastomosis between the accessory meningeal artery and the anterosuperior cerebellar artery in one quasi-moyamoya disease patient. The ophthalmic artery originated from the middle meningeal artery in three moyamoya and two quasi-moyamoya disease patients. The incidence of the persistent primitive arteries is significantly higher in patients with moyamoya disease (10.7%) and quasi-moyamoya disease (60%) than in patients with other disease (0.67%) (p < 0.001), so congenital factors may be important in the pathogenesis of moyamoya disease.

Adolescent↗
PubMed1999

Dual origin of the vertebral artery--case report.

A 27-year-old female presented with dual origin of the left vertebral artery. Twenty-six cases of this rare congenital vascular anomaly have been reported. In general, the medial leg of the dual origin of the vertebral artery enters a higher transverse foramen (usually the fifth or less frequently the fourth) than the lateral leg, which usually enters the sixth. Exceptions to this rule occur when the medial and lateral legs of the right vertebral artery enter the right seventh and sixth transverse foramina, respectively. This congenital vascular anomaly has diagnostic and therapeutic implications in any intervention involving the proximal vertebral artery.

Adult↗
PubMed1999

Transumbilical embolization of a congenital dural arteriovenous fistula at the torcular herophili in a neonate. Case report.

A neonate, in whom a congenital cerebral vascular anomaly had been diagnosed prenatally, exhibited progressive high-output congestive heart failure soon after birth. Cerebral angiography revealed a congenital dural arteriovenous fistula (AVF) with a huge dural lake located at the torcular herophili. In addition to the meningeal blood supply, an unusual pial blood supply from all cerebellar arteries was observed to feed the fistula. The patient was treated by repeated transarterial and transvenous embolization through the umbilical venous route. To the authors' knowledge, neither the existence of a congenital dural AVF at the torcular herophili presenting with an enormous pial blood supply or the technique of trans-umbilical venous intervention has been reported in the literature.

Arteriovenous Fistula↗
PubMed1999

Fusiform vertebral artery aneurysms as a cause of dissecting aneurysms. Report of two autopsy cases and a review of the literature.

Two autopsy cases of angiographically determined fusiform aneurysms of the vertebral arteries (VAs) are reported and the appropriate literature is reviewed to investigate the pathological characteristics of both fusiform and dissecting VA aneurysms and the pathogenesis of dissecting aneurysms. One patient had suffered a subarachnoid hemorrhage (SAH) due to dissection of a previously documented incidental fusiform aneurysm. The other patient had harbored incidental fusiform aneurysms coexistent with a ruptured aneurysm of the posterior inferior cerebellar artery. The location and pathological features of the aneurysms were similar in the two cases. The aneurysms in both cases displayed intimal thickening, disruption of the internal elastic lamina, and degeneration of the media. A mural hemorrhage and patchy calcification were also found in the case that included SAH. Based on their pathological investigation of these two cases and a review of reported cases, the authors propose that incidental fusiform aneurysms in the VAs are characterized by weakness in the internal elastic lamina and, therefore, have the potential to become dissecting aneurysms, resulting in a fatal prognosis. This suggests that long-term control of blood pressure is mandatory in patients with incidental fusiform aneurysms in the VAs.

Adult↗
PubMed1998

Trichothecene 3-O-acetyltransferase protects both the producing organism and transformed yeast from related mycotoxins. Cloning and characterization of Tri101.

Trichothecene mycotoxins such as deoxynivalenol, 4,15-diacetoxyscirpenol, and T-2 toxin, are potent protein synthesis inhibitors for eukaryotic organisms. The 3-O-acetyl derivatives of these toxins were shown to reduce their in vitro activity significantly as assessed by assays using a rabbit reticulocyte translation system. The results suggested that the introduction of an O-acetyl group at the C-3 position in the biosynthetic pathway works as a resistance mechanism for Fusarium species that produce t-type trichothecenes (trichothecenes synthesized via the precursor trichotriol). A gene responsible for the 3-O-acetylation reaction, Tri101, has been successfully cloned from a Fusarium graminearum cDNA library that was designed to be expressed in Schizosaccharomyces pombe. Fission yeast transformants were selected for their ability to grow in the presence of T-2 toxin, and this strategy allowed isolation of 25 resistant clones, all of which contained a cDNA for Tri101. This is the first drug-inactivating O-acetyltransferase gene derived from antibiotic-producing organisms. The open reading frame of Tri101 codes for a polypeptide of 451 amino acid residues, which shows no similarity to any other proteins reported so far. TRI101 from recombinant Escherichia coli catalyzes O-acetylation of the trichothecene ring specifically at the C-3 position in an acetyl-CoA-dependent manner. By using the Tri101 cDNA as a probe, two least overlapping cosmid clones that cover a region of 70 kilobase pairs have been isolated from the genome of F. graminearum. Other trichothecene biosynthetic genes, Tri4, Tri5, and Tri6, were not clustered in the region covered by these cosmid clones. These new cosmid clones are considered to be located in other parts of the large biosynthetic gene cluster and might be useful for the study of trichothecene biosynthesis.

Acetylation↗
PubMed1998

Serial MR observation of cortical laminar necrosis caused by brain infarction.

To examine the chronological changes characteristic of cortical laminar necrosis caused by brain infarction, 16 patients were repeatedly examined using T1-, T2-weighted spin-echo, T2*-weighted gradient echo, fluid attenuated inversion recovery (FLAIR) images, and contrast enhanced T1-weighted images at 1.0 or 1.5 T. High intensity cortical lesions were visible on the T1-weighted images from 2 weeks after ictus and became prominent at 1 to 3 months, then became less apparent, but occasionally remained at high intensity for 2 years. High intensity cortical lesions on FLAIR images became prominent from 1 month, and then became less prominent from 1 year, but occasionally remained at high intensity for 2 years. Subcortical lesions did not display high intensity on T1-weighted images at any stage. On FLAIR images, subcortical lesions initially showed slightly high intensity and then low intensity from 6 months due to encephalomalacia. Cortical lesions showed prominent contrast enhancement from 2 weeks to 3 months, but subcortical lesions were prominent from 2 weeks only up to 1 month. T2*-weighted images disclosed haemosiderin in 3 of 7 patients, but there was no correlation with cortical short T1 lesions. Cortical laminar necrosis showed characteristic chronological signal changes on T1-weighted images and FLAIR images. Cortical short T1 lesions were found not to be caused by haemorrhagic infarction.

Adult↗
PubMed1998

Differentiation of muscle-specific proteins in chicken somites as studied by immunofluorescence microscopy.

Fluorescence microscopy of chicken cervical somites revealed that muscle-specific proteins began to appear at stage 11 (Hamburger and Hamilton numbering), and the onset of the expression of all the proteins examined in the present study had occurred by stage 17. Muscle proteins were classified into six groups according to the stage of their appearance. Since all these proteins were expressed before emergence of nerve fibers in myotomes, switching-on of their synthesis does not seem to require neuronal influence. However, since isoproteins other than adult muscle types disappeared and diversification of muscle fiber types occurred coordinately with the clustering of acetylcholine receptors in cervical muscles, switching-off of the synthesis of the nonadult isoforms might have been accelerated by the formation of functional neuromuscular junctions. The absence of nebulin and C-protein in early stages seems to indicate that these proteins are not required for the initial assembly of myofilaments and/or myofibrils. Further, this absence might be considered to facilitate exchangeabilities of proteins in nascent myofibrils, thereby changing the isoforms to adult types.

Animals↗
PubMed1998

Subcellular localization of dystrophin and vinculin in cardiac muscle fibers and fibers of the conduction system of the chicken ventricle.

The subcellular localization of dystrophin and vinculin was investigated in cardiac muscle fibers and fibers of the conduction system of the chicken ventricle by immunofluorescence confocal microscopy. In ventricular cardiac muscle fibers, strong staining with antibody against dystrophin appeared as regularly arranged transverse striations at the sarcolemmal surface, and faint but uniform staining was seen in narrow strips between these striations. In fibers of the ventricular conduction system, the sarcolemma was stained uniformly with this antibody, but strong staining was found as regular striations in many areas and as scattered patches in other areas of the sarcolemma. These intensely stained striations and scattered patches of dystrophin were colocalized with those of vinculin. Because dystrophin striations were located at the level of Z bands of the underlying myofibrils, they were regarded as the concentration of this protein at costameres together with vinculin. In fibers of the conduction system, myofibrils were close to the sarcolemma where dystrophin and vinculin assumed a striated pattern, at some distance from the cell membrane where these proteins exhibited a patchy distribution, and distant from the sarcolemma where dystrophin was uniformly distributed. These data suggest that the distribution patterns of dystrophin reflect the degree of association between the sarcolemma and underlying myofibrils.

Amino Acid Sequence↗
PubMed1998

An additional variant of the persistent primitive trigeminal artery: accessory meningeal artery--antero-superior cerebellar artery anastomosis associated with moyamoya disease.

Persistent embryological carotid-basilar anastomoses are rare. There has been no report on persistent anastomosis between the accessory meningeal artery and the antero-superior cerebellar artery. We describe a 3-year-old boy with moyamoya disease manifesting such a congenital vascular anomaly, namely, a large anastomosis between the accessory meningeal artery and the antero-superior cerebellar artery associated with marked hypoplasia of the basilar artery. This persistent vascular anomaly is considered embryologically as an additional variant of the persistent primitive trigeminal artery, i.e., a "stapedo-trigemino-cerebellar" variant.

Basilar Artery↗
PubMed1998

Exchangeability of actin in cardiac myocytes and fibroblasts as determined by fluorescence photobleaching recovery.

Rhodamine (Rho)-labeled muscle and non-muscle actins were microinjected into cultured embryonic chicken cardiac myocytes and fibroblasts. After incorporation of the fluorescent actin analog into cellular structures, small areas of labeled structures were photobleached with a laser pulse, and fluorescence recovery (FR) was measured to determine the exchangeability of isoactins in these structures. With both Rho-muscle and Rho-non-muscle actins, the FR rate in any part of stress fibers was consistently faster than that observed in any part of myofibrils. Thus, although non-striated (proximal and terminal) portions of nascent myofibrils are similar in appearance and composition to stress fibers, our data clearly revealed differences in actin stability between these two structures. Further, although cardiomyocytes were incapable of discriminating between the incorporation of muscle and non-muscle actin isoforms into myofibrils, FR after photobleaching of Rho-muscle actin was faster than that of Rho-non-muscle actin in immature non-striated portions. This indicates that actin molecules in cardiac myofibrils cannot be readily exchanged by heterotypic non-muscle actin. Fluorescently labeled actin incorporated into non-striated (proximal and terminal) portions of myofibrils and terminal portions of stress fibers was found to be more stable than alpha-actinin. The relative stability of actin could facilitate the formation of nascent Z-bands of myofibrils and the reorganization of stress fibers at these portions.

Actinin↗
PubMed1998

Intracranial aneurysms in identical twins.

BACKGROUND: Though familial intracranial aneurysms are well documented, only a few cases of intracranial aneurysms in identical twins have been reported. CASE REPORT: Our patient, a 46-year-old woman, presented with a subarachnoid hemorrhage (SAH) due to a ruptured aneurysm. At the age of 36, her identical twin sister had also suffered SAH from a ruptured aneurysm. Both twins were treated successfully. CONCLUSION: The likelihood of the occurrence of an aneurysm may be higher for a twin whose identical twin has developed an aneurysm than for the general population. Therefore, it is reasonable to perform certain screening procedures for aneurysms on an asymptomatic twin when the other presents with SAH due to a ruptured aneurysm.

Diseases in Twins↗