Biomedical subjects
Y Ushio
Publications and source records attributed to Y Ushio.
Contrast-enhanced T1-weighted three-dimensional gradient-echo MR imaging of the whole spine for intradural tumor dissemination.
BACKGROUND AND PURPOSE: When evaluating intradural tumor dissemination in the spine, contrast-enhanced T1-weighted 2D spin-echo (2D-SE) images are frequently problematic because most of the lesions are very small. Our purpose was to compare 2D-SE images with 3D gradient-echo (3D-GE) postcontrast images to determine which technique is better for depicting intradural tumor dissemination. METHODS: Ten patients with and 10 without intradural tumor dissemination were examined prospectively with MR imaging. After contrast administration, all patients underwent sagittal imaging with 2D-SE and 3D-GE sequences. Subsequently, the 2D-SE, 3D-GE, and multiplanar reconstruction (MPR) images of the 3D-GE sequence were evaluated for image quality, lesion detectability, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) of the disseminated lesions. RESULTS: Although delineation of spinal cord from CSF was slightly poorer on the 3D-GE sequences than on the 2D-SE sequences, the difference was not significant. In the evaluation of image artifacts and contrast between spinal cord and CSF, there was no significant difference. In seven patients with nodular enhancement, the 3D-GE sequence detected 46 lesions and the 2D-SE sequence detected 36. With MPR, the greatest number of lesions (n = 51) was detected, and vascular enhancement was clearly distinguished. There was no difference in SNR and CNR of lesions between the 3D-GE and 2D-SE sequences. CONCLUSION: The contrast-enhanced 3D-GE technique offers advantages over 2D-SE imaging in detecting intradural tumor dissemination, especially when the MPR technique is applied. This technique should be used for detecting intradural tumor dissemination.
Pathophysiology and treatment of cerebral ischemia.
This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused "penumbra" tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6-12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative.
MR evaluation of radiation otomastoiditis.
PURPOSE: The purpose of this study was to evaluate the incidence of radiation otomastoiditis, on using T2-weighted magnetic resonance (MR) imaging, in relation to radiation fields, doses, intervals, and clinical symptoms after radiotherapy that included the temporal bone in the fields. METHODS AND MATERIALS: We performed follow-up MR examinations at various intervals after radiotherapy including the temporal bones for 270 ears of 114 patients with various diseases of the head and neck and intracranial regions. The middle ear and mastoid air cells on T2-weighted images were scored as follows; showing no high signal intensity, a local high signal intensity area, or a high signal intensity area occupying the entire middle ear and all mastoid air cells. The radiation fields as depicted on the lateral simulator films classed as anterior to the clival line, posterior to the clival line, or both. RESULTS: The incidence of radiation otomastoiditis depicted on T2-weighted MR images increased in the patients who had received irradiation doses of 50 Gy or more. In the patients with doses of less than 50 Gy, the incidence was 18% within 6 months following radiotherapy, 13% at between 6 and 12 months, and 8% after 12 months, whereas it was more than 50% at any period after radiotherapy in the patients with 50 Gy or more. The incidence of radiation otomastoiditis was quite high in the patients whose radiation fields included region both anterior and posterior to the clival line. CONCLUSION: The incidence of radiation otomastoiditis as demonstrated on T2-weighted MR images is increased at irradiation doses of 50 Gy or more. To reduce the incidence of severe radiation otomastoiditis, the irradiation fields of the temporal bone when the dose is 50 Gy or more should be limited to as small as possible. The clival line is considered to be a good landmark in reducing the irradiation field when doses of 60-70 Gy are delivered in curative radiotherapy.
Cloning and characterization of NE-dlg: a novel human homolog of the Drosophila discs large (dlg) tumor suppressor protein interacts with the APC protein.
We have cloned a cDNA for a novel human homolog of the Drosophila discs large (dig) tumor suppressor protein, termed NE-dlg (neuronal and endocrine dig). Northern blot analysis revealed that the gene is highly expressed in neuronal and endocrine tissues. Fluorescence in situ hybridization (FISH) and radiation hybrid mapping studies localized the NE-dlg gene to chromosome Xq13. We also found that the NE-dlg gene encoded a 100 kDa protein. Immunolocalization studies using an NE-dlg antibody showed that the protein tended to be expressed in non-proliferating cells, such as neurons, cells in Langerhans islets of the pancreas, myocytes of the heart muscles, and the prickle and functional layer cells of the esophageal epithelium. Proliferative cells, including various cultured cancer cell lines and basal cells in the esophageal epithelium, showed little expression of the NE-dlg protein. In addition, yeast two-hybrid screening and in vitro binding assays revealed that the NE-dlg interacted with the carboxyl-terminal region of the APC tumor suppressor protein. These data suggest that NE-dlg negatively regulates cell proliferation through its interaction with the APC protein.
Postnatal ontogeny of striatal-enriched protein tyrosine phosphatase (STEP) in rat striatum.
The present study was undertaken to examine developmental change in expression of striatal-enriched protein tyrosine phosphatase (STEP) in the postnatal striatum of rats. For this purpose, immunohistochemical staining and transimmunoblotting analyses were carried out using a cDNA-generated polyclonal antibody to the STEP with a molecular weight of 46 kDa. Immunostaining showed that in neonatal striatum STEP-immunoreactivity was found in discrete patches composed of many immature cells, which corresponded to the tyrosine hydroxylase-immunopositive "dopamine islands." With development there was an increase in staining intensity and in the number of positively reacting cells. By 4 weeks postnatally, STEP-immunoreactivity was almost homogeneously distributed throughout the striatum, as was seen at the adult stage. Immunoblotting analysis showed that STEP protein expression abruptly increased from 2 to 4 weeks postnatally when it reached the adult level. These findings suggest that STEP is involved in development and maturation of the striatal neurons.
GABA receptor agonist promotes reformation of the striatonigral pathway by transplant derived from fetal striatal primordia in the lesioned striatum.
Striatal lesions are known to cause the anterograde transneuronal degeneration of the substantia nigra pars reticulata (SNr) neurons in consequence to loss of GABAergic inhibitory striatonigral efferents. The present study was undertaken to examine whether long-term intraventricular administration of the GABA agonist muscimol could promote reformation of the striatonigral pathway arising from transplants by rescuing host SNr neurons from transneuronal death in rats with striatal ischemic lesions. Compared to nongrafted rats with striatal lesions, (i) a prominent axonal projection from the transplants to the ipsilateral substantia nigra, (ii) a significant increase in number of survived neurons in the ipsilateral SNr, and (iii) a significant reduction in number of apomorphine-induced turning behaviors were found in grafted animals with muscimol infusion, but not in those without muscimol administration. These findings suggest that preservation of the host target neurons for grafted cells may increase an efficacy of cerebral implants in establishment of the host-graft fiber connections, possibly, leading to functional restoration.
Initial and postoperative hyponatremia associated with pituitary adenoma: a case report.
This 67 year-old man experienced 3 episodes of symptomatic hyponatraemia. Radiological examination revealed a sellar lesion and the tumour was removed via the transsphenoidal route. Thereafter, he simultaneously developed intractable diabetes insipidus and serious hyponatraemia with persistent natriuresis. His level of atrial natriuretic peptide was not significantly elevated, however, his plasma aldosterone concentration was low. The oral administration of salt gradually improved his hyponatraemia as well as the coincident symptoms. By the administration of a mineralocorticoid, fludrocortisone acetate, we succeeded in maintaining his serum sodium level without salt replacement. We discuss the mechanism(s) and treatment of hyponatraemia associated with pituitary tumour.
Intracranial intraparenchymal schwannoma: report of three cases.
Intracranial intraparenchymal schwannomas are rare. We report three patients with an intracranial intraparenchymal schwannoma and discuss the clinical and neuroradiological aspects of this particular tumour. The patients were a 21-year-old male, a 64-year-old female and a 17-year-old male. The tumours were located in cerebrum in two patients and the cerebellum in one patient. Computerized tomography (CT) scans demonstrated a slightly high density area with homogeneous enhancement by contrast medium. Magnetic resonance imaging (MRI) showed slightly low signal intensity on the T1-weighted image, high or mixed signal intensity on the T2-weighted image and homogeneous enhancement by gadolinium diethylene triamine penta-acetic acid (Gd-DTPA). Radiological studies revealed cystic components in 2 of the 3 patients. All tumours were firm, well-demarcated, and completely removed. The diagnosis of schwannoma was derived from histological and immunohistochemical studies in all 3 cases; 2 cases were also examined by electron microscopy.
A paediatric patient with meningioma arising from the cavernous sinus wall.
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Dynamic MRI of meningiomas and schwannomas: is differential diagnosis possible?
We studied 23 patients with meningiomas and 14 with schwannomas using dynamic spin-echo (TR/TE 200/15 ms) MRI. Histologically the meningiomas were classified according to the 1993 WHO classification. Serial images were obtained every 30s for 210s after rapid injection of gadopentetate dimeglumine (0.1 mmol/kg). The contrast-enhancement ratio (CER) was divided into three patterns; a sharp rise with a peak within 60 s (A), a relatively rapid increase with a peak between 60 and 210s (B), a slow increase without a peak (C). The patterns were correlated with the histology of the tumors. The signal intensities of the tumours on T2-weighted images were also analyzed and correlated with the dynamic patterns. Meningiomas had more varied dynamic patterns than schwannomas. Almost half of the meningiomas showed pattern A, and one third pattern C. Of six meningiothelial meningiomas showed pattern A; all schwannomas and fibrous meningiomas showed pattern C. Various patterns were observed in transitional meningiomas. Of the 8 meningiomas showing pattern C, only one gave high signal on T2-weighted images, and could not be differentiated from the schwannomas. Thus, one third of meningiomas could not be differentiated from schwannomas by the dynamic contrast enhancement alone. However, when this was combined with the signal intensity on T2-weighted images, most meningiomas could be differentiated from schwannomas.
Differential distribution and expressions of collagens in the cerebral aneurysmal wall.
To investigate the role of collagens in the formation and rupture of cerebral aneurysms, we examined the distribution and synthesis of vascular collagens in the wall of normal human cerebral main trunks and of cerebral aneurysms using immunohistochemistry and in situ hybridization techniques. Fifteen cerebral aneurysmal walls were resected at operation; control cerebral main trunks were obtained from seven autopsy cases. Semiserial sections from the specimens were subjected to immunofluorescence and immunohistochemical staining with antibodies to collagen types I, III, IV, V, VI, desmin and alpha-smooth muscle actin. In addition, type III collagen mRNA was examined by in situ hybridization. Immunohistochemical study showed that all collagen types were grossly preserved in the aneurysmal wall, although the distribution patterns were different for each collagen. The distribution of major fibrillar collagen types I and III was more diffuse and homogeneous in the luminal layer of the aneurysmal wall than the media of the control artery, although the intensity of immunohistochemical staining was weaker in the abluminal layer of the aneurysmal wall than the adventitia of the control artery. Collagen types IV and V were distributed more sparsely in the luminal layer of the aneurysmal wall than the media of the control artery. Collagen type VI was noted in the luminal as well as the abluminal layer of the aneurysmal wall, whereas it was located exclusively in the adventitia of the control artery. In situ hybridization showed that the signal for collagen type III mRNA on fibroblastic and smooth muscle cells was higher in the aneurysmal walls than the control arteries, suggesting up-regulation of type III collagen transcription in the cerebral aneurysmal wall. The study of the distribution and synthetic regulation of various types of collagen in the aneurysmal wall may be essential for understanding the formation of the aneurysmal wall and its protection against enlargement or rupture.
Reoperation for recurrent malignant gliomas: what are your indications?
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Calcineurin in the adult rat hippocampus: different distribution in CA1 and CA3 subfields.
We examined the immunohistochemical regional distribution of calcineurin (Ca2+/calmodulin-dependent protein phosphatase) in the adult rat hippocampus, following various regional destruction. In the normal adult rat hippocampus, the calcineurin immunoreactivity showed a characteristic pattern. This protein phosphatase was detected in all layers of the CA1 subfield, including the cytoplasm of the pyramidal cells, whereas it was strongly evident in the stratum lucidum and moderately so in the cytoplasm of pyramidal cells in the CA3 subfield. Seven days after transient forebrain ischemia, which induced destruction of CA1 pyramidal cells, the calcineurin immunoreactivity decreased in all layers of the CA1 subfield, while the immunoreactivity for synapsin I, a marker of the presynaptic site, was preserved. Seven days after the intraventricular injection of kainate, which induced destruction of CA3 pyramidal cells, the calcineurin immunoreactivity in the stratum lucidum was preserved, although the immunostaining pattern of the stratum lucidum changed when CA3 pyramidal cells were destroyed. Seven days after mechanical destruction of the dentate gyrus and CA4 subfield, which induced destruction of mossy fibers, the calcineurin immunoreactivity in the stratum lucidum was lost, except in the far site of the stratum lucidum. In the CA1 subfield, calcineurin was mainly located in postsynaptic sites, while it was mainly located in the presynaptic sites in the mossy fibers of the CA3 subfield. The immunohistochemistry of adjacent sections with antibodies of microtubule-associated protein 2 and synapsin I, which are markers of postsynaptic and presynaptic sites respectively, supports these results. Thus, calcineurin has a different synaptical distribution in the rat hippocampus.
Continuous intraventricular drug infusion for the in vivo study of transneuronal degeneration in the striatonigral system of the rat.
Injuries to certain parts of the brain may induce neuronal death in distant areas innervated by the sites of the primary lesion. Such characteristic pathological changes, known as anterograde transneuronal degeneration, may occur at the next and more distant synaptic levels and play a part in the slow progression of some types of system degeneration. Delayed transneuronal degeneration of the substantia nigra pars reticulata (SNr) is one example of this form of cell death, and it occurs as a consequence of a neostriatal lesion caused by focal ischemia, Huntington's disease, or experimental axon-sparing injections of neurotoxin. Ever since the demonstration by Saji and Reis that the administration of GABA receptor agonist effectively prevented delayed transneuronal degeneration of the SNr, the degeneration of nigral reticulata cells has been attributed to the loss of striatal inhibition (Fig. 1A). The latter process severely upset the balance of membrane potential of nigral reticulata cells, producing an effect resembling excitotoxicity. In this report, we describe a continuous intraventricular MK-801 infusion technique that is useful in clarifying the role of glutamatergic action via N-methyl-D-aspartate (NMDA) receptor subclasses involved in exo-focal postischemic death of the SNr.
Ruptured distal accessory anterior cerebral artery aneurysm: case report.
OBJECTIVE AND IMPORTANCE: Accessory anterior cerebral artery (ACA), which is a type of median artery of anomalous triplicate ACA, is not rare, but aneurysmal formation is extremely rare. We report a rare case with ruptured aneurysm arising from a distal accessory ACA. We discuss the characteristics and causes of this type of aneurysm and classification of this anomaly. CLINICAL PRESENTATION: A 63-year-old man suddenly developed severe headache and then loss of consciousness and paraplegia. Computed tomography disclosed thick and diffuse subarachnoid hemorrhage and interhemispheric hematoma. Subsequent bleeding occurred 2 hours after the first hemorrhage. Cerebral angiography disclosed a saccular aneurysm arising from the distal accessory ACA. INTERVENTION: Neck clipping of the aneurysm was performed 22 hours after the second episode, using an interhemispheric approach. CONCLUSION: Although transient paraplegia occurred 8 days after onset, the patient recovered well after surgery without neurological deficit. The characteristics of the aneurysm arising from distal accessory ACA are considered similar to those of distal ACA aneurysm. There is, however, some confusion regarding the terminology of the anterior communicating artery complex anomalies, which we discuss.
Two distinct populations of primary cytotoxic cells infiltrating into allografted tumor rejection sites: infiltration of macrophages cytotoxic against allografted tumor precedes that of multiple sets of cytotoxic T lymphocytes with distinct specificity to alloantigens.
It has been reported that the rejection of tumor allografts is mainly mediated by cytotoxic T lymphocytes (CTLs). Here, we characterized the cytotoxic effector cells of C57BL/6 (B6; H-2b) mice infiltrating into the rejection site of the i.p. allografted Meth A fibrosarcoma (or P815 mastocytoma) cells of H-2d origin. Two types of cytotoxic cells (i.e., CD8+ CTLs and macrophages (M phi s)) were identified by flow cytometric fractionation of the infiltrates or by specific in vitro elimination of cells either with antibody (Ab)-coated beads or with an Ab-plus complement. Of particular interest, these effector cells showed distinct and unique target specificities. First, the CTLs were inactive against transplanted tumor (e.g., Meth A) cells, whereas they were cytotoxic against donor-related concanavalin A (Con A) blasts as well as CTLL-2 (H-2b) cells transfected with a class I gene of H-2d origin. A cold target competition assay suggested that the CTLs were composed of multiple sets of T cells, each of which specifically recognized different allo-antigens. Second, the M phi s lysed the allografted tumor cells but were inert toward the Con A blasts and the CTLL-2 transfectants. Unexpectedly, the infiltration of M phi s preceded the infiltration of CTLs by several days during the course of rejection. These results indicate that two distinct populations of unique cytotoxic cells (i.e., CTLs and M phi s) are induced in the allografted tumor rejection site, and that the infiltration of cytotoxic M phi s responsible for rejection precedes that of the CTLs cytotoxic against cells expressing donor-related allo-antigens.
Epidemiological study of primary intracranial tumours in elderly people.
The incidence of primary intracranial tumours in a well defined population of persons older than 70 years (elderly) who resided in Kumamoto prefecture was examined. During the period from 1989 to 1995, primary intracranial tumours were diagnosed in 271 elderly people; of these, 155 (57.2%) tumours were confirmed microscopically. In a mean population of 216,000 people over the age of 70 years, this yields an average annual incidence rate of 18.1 cases/100,000 population/year. The incidence was lower in men (15.2/100,000 population) than women (20.3/100,000 population). The age specific incidence/100,000/year was 23.2 for the 70-74 year age group, 18.1 for the 75-79 year age group, 15.1 for the 80-84 year age group, and 7.6 for persons older than 85 years. The most common tumours were meningiomas (50.6%), followed by malignant gliomas (13.3%), pituitary adenomas (12.9%), schwannomas (6.6%), malignant lymphomas (3.7%), and benign astrocytomas (3.7%).