Search PubMed⌕ Search

Biomedical subjects

K Ohno

Publications and source records attributed to K Ohno.

At least 343 records · Page 19Linked to original sources
PubMed1996

[Morphological and clinical study of acoustic tumor with respect to enlargement of internal auditory canal: mechanism of bone destruction].

The mechanism of widening of the internal auditory canal (IAC) by an acoustic tumor is still unknown. Degree of IAC enlargement was expressed as "IAC ratio' calculated from the measurement of bilateral horizontal diameters from bone-imaging CT. Comparing IAC ratio to radiological findings of tumors, such as size, solidity, mode of attachment to pyramidal bone and the presence of ventricular dilatation, we found a positive correlation between the ratio and the volume of solid tumors (especially of smaller ones) and more marked destruction of IAC in association with ventricular dilatation. Preoperative degrees of hearing ability or facial nerve function didn't correlate with that of IAC enlargement. It is our hypothesis that the mechanism involved in the destruction of IAC is as follows: (1) The repeated strokes of the tumor caused by brain pulsation gradually erode the bony wall of IAC (especially, that of the posterior wall). The apparently less destruction of IAC in cases with mostly cystic large tumors might be due to the restriction of this pulsatile movement. (2) Increased CSF pressure on the site has some influence on the mechanism of bone erosion as also does solidity of the tumor.

Bone and Bones↗
PubMed1996

Magnetic resonance imaging and pathologic studies on lateral fluid percussion injury as a model of focal brain injury in rats.

In this study, morphologic changes in brain lesions initiated by moderate lateral fluid percussion injury in rats were investigated chronologically using high-resolution magnetic resonance imaging (MRI) and histopathologic methods. Rats were subjected to moderate fluid percussion injury (average 2.80 +/- 0.48 atmospheres) over the exposed dura overlying the right parietal cortex. MRI obtained in vivo were compared with corresponding pathologic findings at 1, 6, and 24 h and at 3, 6, 14 and 80 days after injury. T2-weighted images showed scattered low-signal intensity in the injured cortex within a few hours after injury, whereas histologic findings revealed intraparenchymal hemorrhages. T2-weighted images of the ipsilateral cerebral cortex and/or corpus callosum showed a high-signal-intensity area 4 h after injury. The high-signal-intensity area became largest in size between 6 and 24 h, then declined gradually, and almost disappeared 14 days after injury. Histologic examination revealed pyknosis, retraction of the cell body of neurons with vacuolated neuropil in the corresponding regions 6 and 24 h after injury, and cystic necrosis 14 days after injury. The location and extent of these pathologic changes were depicted accurately by MRI in vivo. In the hippocampus, pyknosis and retraction of the cell body of pyramidal neurons were observed on the injured side 24 h after injury, and the number of neurons in the CA1 and CA2-CA3 regions decreased significantly on the same side by 14 days after injury. It is concluded that morphologic changes in the brain following experimental traumatic brain injury in rats are detectable in vivo by high-resolution MRI, and that MRI may be useful for the evaluation of treatment effects in experimental brain injury.

Animals↗
PubMed1996

[Recovery from descending necrotizing mediastinitis and multiple organic failure after seven months of mechanical ventilation].

A 61-year-old man with a history of hypertension and diabetes mellitus had a tooth extracted. Nine days later, he was admitted to the hospital with complaints of high fever, dyspnea, and anterior chest pain. Physical examination revealed a drowsy man with a fever of 38.2 degrees C, blood pressure of 66/44 mmHg, and marked redness and swelling from the neck to anterior part of the chest. Laboratory examination indicated severe infection and multiple organ failure, consisting of cardiac, respiratory, renal, and hepatic failure, with disseminated intravascular coagulation. Chest X-ray and CT-scan films showed abscesses extending from the neck to the mediastinum, and bilateral pleural effusion. Immediately, he was treated with catecholamines, furosemide, mechanical ventilation with a high concentration of oxygen, continuous drainage, repeated skin incisions, and broad-spectrum antibiotics. In addition, steroid pulse therapy was administered for persistent respiratory failure. On the 28th hospital day, a fistula developed between the trachea and the mediastinum, and an intratracheal tube had to be inserted through the fistula. On the 212 th hospital day, after intravenous hyperalimentation, continuous intravenous insulin infusion, and administration of broad-spectrum antibiotics, catecholamines, and furosemide, the patient was weaned from mechanical ventilation. A restrictive ventilatory defect due to ankylosis and atrophy of underused muscles was noted after weaning, but the PaO2 was high with a low dose of oxygen (1 to 2 l/min), and 21 months later, the blood gases were normal while the patient was breathing room air. As of January, 1996, he was undergoing rehabilitation to promote his recovery from ankylosis, muscle atrophy, and speech dysfunction.

Catecholamines↗
PubMed1996

[Mediastinal thoracic duct cyst--a case report].

The patient, a 55-year-old asymptomatic man, was referred to our hospital in October 1995 for further investigation of a chest ++roentogenographic abnormality found during a "physical check-up". His chest X-ray showed a round shadow over the hilus of the left lung. Computed tomography revealed a homogeneous, low density mass bordering the esophagus, vertebral column, left lower pulmonary vein and descending aorta. Roentogenography after swallowing barium sulfate showed that the esophagus was compressed and displaced to the right in the anterior direction. Endoscopic ultrasound scan demonstrated a cystic mass. The preoperative findings were suggestive of an esophageal cyst or a thoracic duct cyst. On December 12, 1995, the patient was operated on. The mass was 2 x 3 x 6 cm in size, and was easily separated from the left pulmonary vein, esophagus and vertebral column by blunt and sharp dissection, but it was strongly adhered to the aorta. The wall of the cyst was incised and a chylous fluid was found inside. The mass was diagnosed as a thoracic duct cyst and was removed after clipping and cutting the thoracic duct above and below the cyst. Histopathological features of the wall of the cyst was that the luminal surface was lined by a monolayer of flat endothelium and composed of loose fibrous tissue with scattered bundles of smooth muscle. It differed from that of veins. The postoperative course was uneventful and he was discharged on the 12th postoperative day. Mediastinal thoracic duct cysts are rare and only 25 operated cases have been reported in the literature. We review and discuss these cases.

Humans↗
PubMed1996

Surgical approaches for treatment of ischaemic cerebral stroke other than moyamoya disease in children.

Ischaemic cerebral strokes in children are relatively uncommon. With the exception of patients with moyamoya disease, there is no effective treatment for these lesions. One potential approach is encephalo-duro-arterio-synangiosis (EDAS). This is a safe neurosurgical procedure that promotes spontaneous transdural anastomosis that may provide additional blood flow to ischaemic regions. We present eight children with ischaemic strokes other than moyamoya disease, and discuss surgical attempts to treat this entity. The mean age of the eight children was 3.6 years (range: 13 months to 9 years). All children presented with acute childhood hemiplegia. Ischaemic stroke had occurred in association with a head injury in three children, but without an apparent cause in five. Five children underwent stable xenon-enhanced computed tomography to evaluate cerebral blood flow and all but one patient underwent EDAS. One child with no angiographic abnormalities recovered to a normal neurological state without surgery. Following surgery, another child also fully recovered, and the remaining six children recovered with only a slight hemiparesis. Revascularization was observed on a follow-up angiogram in three children. Our surgical experiences suggest that revascularization is influenced by haemodynamic demand and recanalization of the occluded artery. We favour the use of indirect anastomosis (EDAS) for selected patients and suggest that chronic ischaemia probably contributes to surgical success.

Anastomosis, Surgical↗
PubMed1996

[A case of multiple pulmonary leiomyomatous hamartoma].

A 45-year-old woman with multiple pulmonary leiomyomatous hamartoma was reported. Multiple round shadows were observed in the chest X-ray film of mass examination. Retrospectively chest X-ray films revealed an increase in size and number of pulmonary nodules in three years. Metastatic pulmonary tumors were suspected. Primary site was unclear. Calcified myoma uteri was recognized. The pathological diagnosis under diagnostic thoracotomy was multiple leiomyomatous hamartoma. After ten months of medical castration using superactive analogue of LHRH (buserelin) by intranasal spray, chest X-ray film showed a slight decrease in size of nodular shadows in the right middle lung field.

Female↗
PubMed1996

[A case of enlarging rounded atelectasis difficult to distinguish from a pulmonary neoplasm].

A 55-year-old man with occupational exposure to asbestos presented with a chest roentgenographic abnormality that was found during a physical check-up. Computed tomography disclosed pleural thickening and a pulmonary mass in the left lower lobe. A fine-needle biopsy was done, but the presence of a malignant lesion was not confirmed. The patient was asymptomatic. He was observed closely, and 10 months later computed tomography showed that the mass had enlarged. A fine-needle biopsy was done again, but no evidence of malignancy was found. We suspected that it was rounded atelectasis, but could not rule out a neoplasm. An exploratory thoracotomy was done, and the histopathological findings showed that the mass was lung tissue with alveolar wall fibrosis that had resulted in thickening of the wall. The mass was diagnosed as rounded atelectasis. Rounded atelectasis requires no special treatment, but if the mass increases in size as in the case of this patient, an exploratory thoracotomy is required.

Diagnosis, Differential↗
PubMed1995

Deafferentiation-induced c-fos gene expression in subthalamic nucleus and substantia nigra reticulata is reduced by non-NMDA receptor antagonist.

Molecular events underlying the mechanism by which brain injury elicits delayed transneuronal degeneration of neurons remote from the site of initial injury are not well understood. In rats, acute injury of the caudate nucleus (CN) and globus pallidus (GP) by local injection of excitotoxic ibotenic acid (IA) or by transient forebrain ischemia resulted in delayed cell death of neurons in the substantia nigra reticulata (SNr). To elucidate the involvement of glutamate receptor mediated hyperactivity of neurons produced by loss of inhibitory inputs in this delayed degeneration of SNr neurons, the region-specific expression of an immediate early gene, c-fos, and the effect of glutamate receptor antagonists on the c-fos expression were examined by using immunocytochemical and in situ hybridization analysis. Following unilateral IA-injection into the CN and GP, a robust expression of c-fos mRNA and Fos protein was induced specifically in neurons of both subthalamic nucleus (STN) and SNr deafferented by the IA-lesions 36 h after IA-injection. The delayed expression of Fos-protein in SNr neurons lasted for 48 h longer than that in STN neurons. Following unilateral IA-injection confined to the CN, an intense but short-term expression of Fos-protein was exhibited only in neurons of the deafferented SNr. c-fos mRNA and Fos protein were not expressed in neurons of the substantia nigra compacta at any time points examined. The induction of c-fos mRNA and Fos protein in neurons of the STN and SNr following IA-lesions of the CN and GP was reduced markedly by non-NMDA receptor antagonist (GYKI52466), but not by NMDA receptor antagonist (MK-801). The region-specific c-fos expression implies that deprivation of inhibitory afferents (disinhibition) due to destruction of presynaptic neurons can induce increased activity of postsynaptic neurons. The effect of GYKI52466 on the c-fos gene expression in neurons of the deafferented STN and SNr suggests that activation of non-NMDA receptors may be involved in a pathophysiological cascade for the transneuronal degeneration of SNr neurons.

Afferent Pathways↗
PubMed1995

Silk gland factor-1 involved in the regulation of Bombyx sericin-1 gene contains fork head motif.

Silk gland factor-1 (SGF-1) regulates transcription of the Bombyx sericin-1 gene via interaction with the SA site. In this study, two related SGF-1 polypeptides of apparent molecular masses of 40 and 41 kDa were purified. Specific interaction of these proteins with the SA site was demonstrated by electrophoretic mobility shift and dimethyl sulfate methylation interference assays. The SGF-1 40-kDa protein was partially sequenced and characterized as a new member of the fork head/HNF-3 family. Several full-length cDNAs encoding the SGF-1 40-kDa and possibly also the 41-kDa proteins were cloned and sequenced. SGF-1 mRNA is expressed consistently with the presumed role of the SGF-1 protein product in regulating the sericin-1 gene. The SGF-1 protein contains putative transactivation domains. We conclude that the 40- and 41-kDa SGF-1 proteins affect transcription of the sericin-1 gene via binding to the SA site.

Amino Acid Sequence↗
PubMed1995

Tumor necrosis factor alpha differentially modulates the cellular response of rat hepatocytes in periportal- and pericentral-equivalent cultures.

Alterations of cellular functions induced by recombinant human tumor necrosis factor alpha (TNF alpha) were compared in rat hepatocytes cultured under either periportal-equivalent (10 nM insulin; 10 nM glucagon; 13% O2) or perivenous-equivalent conditions (10 nM insulin; 1 nM glucagon; 4% O2). TNF alpha induced a time- and dose-dependent increase in nitric oxide (NO) production and an acute phase response (inhibition of albumin secretion and elevation of alpha 2-macroglobulin production) under both culture conditions. NO production was more pronounced in periportal cultures, while the acute phase response was stronger in pericentral cultures. This suggests that NO production and the acute phase response are controlled by different pathways. After exposure to TNF alpha, DNA content was measured fluorimetrically and biochemically. A marked decrease in nuclear DNA content was found exclusively in pericentral cultures after an 8-h exposure, followed by an elevation of lactic dehydrogenase (LDH) release after a 12-h exposure. Aurintricarboxylic acid (100 microM), an inhibitor of endonuclease, significantly inhibited the TNF alpha-induced decrease in nuclear DNA content but only partially inhibited the LDH release. This indicates that the loss of nuclear DNA content in pericentral cultures is due to an activation of endonuclease and the resulting DNA fragmentation and does not correlate with NO production. Furthermore, the release of LDH seems to be only partially associated with DNA damage. Dexamethasone (100 nM) completely inhibited both TNF alpha-induced DNA fragmentation and the elevation of LDH release. The results clearly indicate that the toxicity of TNF alpha is influenced by the metabolic state of hepatocytes. Accordingly, the preferential perivenous cell injury observed after exposure to endotoxins in vivo seems to be due to a higher sensitivity of the pericentrally localized hepatocytes towards TNF alpha rather than a TNF alpha concentration gradient.

Animals↗
PubMed1995

Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit.

In a congenital myasthenic syndrome with a severe endplate myopathy, patch-clamp studies revealed markedly prolonged acetylcholine receptor (AChR) channel openings. Molecular genetic analysis of AChR subunit genes demonstrated a heterozygous adenosine-to-cytosine transversion at nucleotide 790 in exon 8 of the epsilon-subunit gene, predicting substitution of proline for threonine at codon 264 and no other mutations in the entire coding sequences of genes encoding the alpha, beta, delta, and epsilon subunits. Genetically engineered mutant AChR expressed in a human embryonic kidney fibroblast cell line also exhibited markedly prolonged openings in the presence of agonist and even opened in its absence. The Thr-264-->Pro mutation in the epsilon subunit involves a highly conserved residue in the M2 domain lining the channel pore and is likely to disrupt the putative M2 alpha-helix. Our findings indicate that a single mutation at a critical site can greatly alter AChR channel kinetics, leading to a congenital myasthenic syndrome. This observation raises the possibility that mutations involving subunits of other ligand-gated channels may also exist and be the basis of various other neurologic or psychiatric disorders.

Acetylcholine↗
PubMed1995

Healing of the medial collateral ligament after a combined medial collateral and anterior cruciate ligament injury and reconstruction of the anterior cruciate ligament: comparison of repair and nonrepair of medial collateral ligament tears in rabbits.

The optimal treatment for a combined injury of the medial collateral and anterior cruciate ligaments is controversial, and the question remains as to whether repair of the medial collateral ligament and reconstruction of the anterior cruciate ligament improves healing of the medial collateral ligament. We compared reconstruction of the anterior cruciate ligament with and without repair of the medial collateral ligament in a rabbit model of a combined injury of these two ligaments. The anterior-posterior translation and varus-valgus rotation of the knee, the structural properties of the femur-medial collateral ligament-tibia complex, and the mechanical properties of the midsubstance of the medial collateral ligament were evaluated immediately after surgery and at 6 and 12 weeks postoperatively. Repair of the medial collateral ligament led to significantly less varus-valgus rotation of the knee than did no repair, but the anterior-posterior translation of the knees in the repair and nonrepair groups were not significantly different at any study time. At 12 weeks, the cross-sectional area and ultimate load in the repair group were 60 and 53% greater, respectively, than in the nonrepair group. Among 12 specimens that were repaired (six specimens at 6 weeks and six specimens at 12 weeks), failure occurred within the midsubstance in four (two at each time period); in all of the specimens that were not repaired, failure occurred at the tibial insertion site. There was no significant difference between the modulus of the modulus of the midsubstance in the repaired and the nonrepaired medial collateral ligaments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Cell targeting for gene delivery: use of fusion protein containing the modified human receptor for ecotropic murine leukemia virus.

We have previously cloned a human gene (H13) homologous to the murine ecotropic retrovirus (E-MuLV) receptor, which, however, does not confer susceptibility to E-MuLV infection. The extracellular domain 3 (ECD3) of H13 contains amino acid residues critical for E-MuLV binding in that the modified H13 gene (mH13), substituted with amino acids from the actual receptor, has the ability to bind E-MuLV. Here we have expressed a fusion protein consisting of mH13/ECD3 and transforming growth factor-alpha in Escherichia coli and demonstrated its binding activity to both ecotropic AKR virus and the epidermal growth factor receptor expressed on the cell surface. Fusion proteins of mH13/ECD3 and ligands to cell surface molecules might be useful for specific cell targeting in E-MuLV-based gene delivery systems.

Amino Acid Sequence↗
PubMed1995

Transforming growth factor beta 1 preferentially induces apoptotic cell death in rat hepatocytes cultured under pericentral-equivalent conditions.

The cytotoxicity of transforming growth factor beta 1 (TGF beta 1) was assessed in rat hepatocytes cultured under periportal (PP)-or pericentral (PC)-equivalent conditions. TGF beta 1 induced a 5-fold greater DNA fragmentation and LDH release in PC cultures than in PP cultures. At low exposure level (1 ng/ml TGF beta 1), albumin secretion and mitochondrial activity (rhodamine-123 uptake) were selectively reduced in PP cultures, whereas the incidence of apoptotic cells in PC cultures was about 10-fold higher than that in PP cultures. The time profiles of TGF beta 1-induced apoptotic and necrotic events and the concentration-response relationship differed in PC and PP cultures. In PC cultures the early appearance of cells with apoptotic nuclei was not associated with DNA fragmentation nor with an increase in LDH release or impaired mitochondrial function. At a high exposure level (5 ng/ml TGF beta 1), again cells with apoptotic nuclei were much more strongly induced in PC cultures but DNA fragmentation, LDH release, and impairment of mitochondrial activity all increased in an exposure-time dependent manner in both PP and PC cultures. At this exposure level 48 and 72% of the apoptotic cells detected in PC cultures after continuous exposure for 24 hr were induced within an exposure of 1 and 4 hr, respectively. Aurintricarboxylic acid (50 microM), an inhibitor of endonucleases, significantly inhibited the appearance of apoptotic cells and the progression in apoptosis. Clearly, TGF beta 1 preferentially induced apoptotic cell death in hepatocytes with PC-equivalent metabolism at low exposure levels. High exposure levels or prolonged exposure periods produced both apoptosis and necrosis.

Animals↗