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Dive into the research topics where Hideo H. Itabashi is active.

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Featured researches published by Hideo H. Itabashi.


Journal of Clinical Investigation | 1992

The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat

Kwang Sik Kim; Hideo H. Itabashi; Peter Gemski; Jerald C. Sadoff; Richard L. Warren; Alan S. Cross

Although Escherichia coli strains possessing the K1 capsule are predominant among isolates from neonatal E. coli meningitis and most of these K1 isolates are associated with a limited number of 0 lipopolysaccharide (LPS) types, the basis of this association of K1 and certain 0 antigens with neonatal E. coli meningitis is not clear. The present study examined in experimental E. coli bacteremia and meningitis in newborn and adult rats whether or not the K1 capsule and/or O-LPS antigen are critical determinants in the development of meningitis. Rats received subcutaneously at K1 E. coli strain (018+K1+) or mutants lacking either the K1 capsule (018+K1-) or 0 side-chain (018-K1+). 12-24 h later, blood and cerebrospinal fluid (CSF) specimens were obtained for quantitative cultures. The isolation of E. coli from CSF was observed in both newborn and adult rats infected with K1+ strains regardless of LPS phenotype (018+ or 18-) who also developed a high degree of bacteremia (e.g., greater than 10(4) CFU/ml of blood). In contrast, none of the newborn and adult rats infected with 018+K1- and developing bacteremia of greater than 10(4) were found to have positive CSF cultures. These findings indicate that the presence of the K1 capsule and a high degree of bacteremia are key determinants in the development of E. coli meningitis, suggesting that there may be specific binding sites present in the brain which have an affinity for the K1 capsule and thus may be responsible for the entry of K1-encapsulated E. coli into the meninges.


Epilepsia | 2000

Status epilepticus-induced neuronal loss in humans without systemic complications or epilepsy.

Denson G. Fujikawa; Hideo H. Itabashi; Aiguo Wu; Steve Shinmei

Summary: Purpose: To determine the regional distribution of neuronal damage caused strictly by status epilepticus (SE) without systemic complications, underlying brain pathology, or a history of preexisting epilepsy.


The New England Journal of Medicine | 1975

Chronic Progressive Panencephalitis Due to Rubella Virus Simulating Subacute Sclerosing Panencephalitis

Marvin L. Weil; Hideo H. Itabashi; Natalie E. Cremer; Lyndon S. Oshiro; Edwin H. Lennette; Laurence Carnay

Late-onset chronic progressive panencephalitis developed in a 12-year-old boy with congenital rubella syndrome from whose brain rubella virus was isolated. Progressive dementia began at eight, and ataxia, choreiform movements, myoclonic seizures, and fine perimacular pigmentation appeared at 11 years of age. The cerebrospinal fluid was minimally pleocytotic and had a total protein of 156 mg per deciliter, of which 52 per cent was gamma globulin. Electroencephalography demonstrated generalized medium and occasional high-voltage slowing without burst suppression. The antibody titer to rubella virus (hemagglutination inhibition) was 1:8192 in serum and 1:256 in cerebrospinal fluid. Antibody titer to measles virus (complement fixation) was less than 1:8 in serum. Microscopical study of biopsied brain tissue at the age of 11 disclosed panencephalitis similar to subacute sclerosing panencephalitis, but with perivascular deposits and without inclusion bodies. Rubella virus was isolated from the brain by cocultivation with CV-1 cells.


Journal of the American Geriatrics Society | 1995

SPECT in dementia : clinical and pathological correlation

Stephen L. Read; Bruce L. Miller; Ismael Mena; Ronald C. Kim; Hideo H. Itabashi; Amy Darby

BACKGROUND: The clinical diagnosis of dementia continues to be flawed. Although the diagnosis of Alzheimers disease (AD) is better than 90% at research centers in highly selected patients, the diagnosis of patients with non‐AD dementias and atypical AD patients is poor. Single photon emission computed tomography (SPECT) is a functional imaging technique touted as a diagnostic technique for the degenerative disorders. However there have been few clinicopathological studies using SPECT.


Neurology | 1987

Upbeat nystagmus Clinicopathologic study of two patients

James R. Keane; Hideo H. Itabashi

Two patients had upward nystagmus on forward gaze before they died with acute caudal brainstem dysfunction. Bilateral dorsal paramedian damage in the rostral medulla, involving the perihypoglossal nuclei, was probably the critical lesion responsible for upbeat nystagmus.


Journal of General Virology | 1975

Isolation of rubella virus from brain in chronic progressive panencephalitis.

Natalie E. Cremer; Lyndon S. Oshiro; Marvin L. Weil; Edwin H. Lennette; Hideo H. Itabashi; L. Carnay

Rubella virus was isolated from the brain of a congenitally-infected, 12-year-old child in whom progressive mental and motor deterioration became evident at age 8 and 11 years respectively. The virus was initially isolated in a co-culture of CV-I cells with the trypsinized brain tissue; subsequently the culture of the brain tissue also showed evidence of rubella virus infection recognized by indirect fluorescent antibody technique (IFA) using anti-rubella virus antibody prepared in rabbits as intermediate serum. Both isolates interfered with infection of BSC-I cell lines by echovirus type II. The interfering virus was identified as rubella virus by IFA with the specific antiserum, and it is designated as the NTr strain of rubella virus. The complement fixing antibody titre to rubella virus in serum was I:256. The spinal fluid was anticomplementary. Rubella virus haemagglutinating antibody titre (HI) in serum was I:8196 and in the spinal fluid I:128. The HI antibody was of the IgG class. The corresponding HI titres to rubeola virus in serum and spinal fluid were I:8 and less than I:2 respectively.


Neurology | 1979

Computerized tomography in Central pontine myelinolysis

Thomas L. Anderson; Robin A. Moore; Verity Grinnell; Hideo H. Itabashi

We describe an autopsy-proven case of central pontine myelinolysis (CPM) with premortem computerized tomographic (CT) visualization of the lesion on two scans, performed with an interval of 2 weeks. This case demonstrates the capability of CT to support the clinical diagnosis of central pontine myeI.inolysis. Identification of the condition should facilitate prompt initiation-of aggressive supportive care.


Journal of Forensic Sciences | 1998

Subdural neomembranes and sudden infant death syndrome

Christopher Rogers; Hideo H. Itabashi; Uwamie Tomiyasu; Eva T. Heuser

Cranial dura maters of 36 consecutive infants with sudden infant death syndrome (SIDS) and 16 control infants coming to the Department of Coroner were examined microscopically to determine if subdural neomembranes are associated with cases submitted as SIDS. Thirty-one percent (31%) of the infants with SIDS and 13% of control infants had organizing subdural neomembranes (p > 0.05). Overall prevalence of organizing subdural neomembranes was 25% in the group examined. In all but two cases, birth trauma could be excluded as a cause of head trauma by aging neomembranes histologically. No association was found between type of delivery (vaginal or Cesarean) and presence of a subdural neomembrane. Subdural neomembranes are common in infants autopsied in a forensic setting, but they may be missed without a microscopic examination. Subdural neomembranes have no demonstrated association with SIDS.


Neurology | 1985

Locked‐in syindrome due to tentorial herniation

James R. Keane; Hideo H. Itabashi

A 28-year-old man had a chronic locked-in syndrome following tentorial herniation caused by an epidural hematoma. Postmortem examination revealed bilateral corticospinal tract degeneration caudal to the midbrain, with infarction of the right internal capsule just rostra1 to the cerebral peduncle and pressure necrosis of the pyramidal portion of the left cerebral peduncle.


Forensic Neuropathology#R##N#A Practical Review of the Fundamentals | 2007

Dating/aging of common lesionsin neuropathology

Hideo H. Itabashi; John M. Andrews; Uwamie Tomiyasu; Stephanie S. Erlich; Lakshmanan Sathyavagiswaran

This chapter summarizes the present understanding of dating/aging issues that may be encountered by the forensic neuropathology consultant, and to do this in a format that also highlights areas in which data are not sufficient to answer some frequently asked questions. Issues of timing of tissue responses receive more emphasis in forensic pathology than general pathology because timing conclusions based on histological studies may help to confirm or refute certain witness and advocate statements. In general pathology, etiologic and mechanistic issues understandably often take precedence over detailed timing of the earliest appearance, maximum expression, or longest duration of a given histological finding. For the consulting neuropathologist involved in forensic work, the question so often is usually not about “time of death” as it is about “time interval between central nervous system (CNS) insult and death.” This question is perhaps most often asked in the context of child abuse cases in an attempt by counsel to include or exclude involvement by a given caretaker. It can also occur in a variety of other scenarios. In this chapter, the dating/aging data are selected with criteria that reflect ones understanding of conceptual filters, or gradually evolving working hypotheses. These “timetables” continue to be revised as indicated, as additional data are collected and examined, and by reviewing pertinent publications that become available. More data must be gathered before a general consensus is likely to be reached in many of these parameters.

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Marvin L. Weil

University of California

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Edwin H. Lennette

United States Department of State

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James R. Keane

University of Southern California

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Kwang Sik Kim

University of California

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