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Biomedical subjects

Tsuneo Morishima

Publications and source records attributed to Tsuneo Morishima.

At least 37 records · Page 2Linked to original sources
PubMed2005

Delirious behavior in children with influenza: its clinical features and EEG findings.

The clinical characteristics and electroencephalogram (EEG) findings in delirious behavior in children with influenza were studied in order to differentiate it from influenza-associated encephalitis/encephalopathy. Fifteen consecutive children with delirious behavior associated with influenza were investigated. Their clinical courses were investigated using medical records. EEG was obtained during the delirious behavior, when possible. The body temperature during the delirious behavior was 39.0 degrees C or higher in 13 children. A subtle reduction of consciousness was observed in 10 children. Seizures were observed in five children. EEG revealed some mildly abnormal findings in 13 children, including mild slowing of the background activity, insertion of semirhythmic high voltage slow waves, and appearance of relatively high voltage semirhythmic theta waves. The EEG findings normalized after the delirious behavior had disappeared. EEG revealed transient and mild abnormalities in children with delirious behavior but without encephalitis/encephalopathy, and thus might be useful for diagnostic evaluation in such condition.

Adolescent↗
PubMed2005

Ganciclovir therapy for congenital cytomegalovirus infection in six infants.

BACKGROUND: Congenital cytomegalovirus (CMV) infection is common, and its morbidity rate is high. Ganciclovir (GCV) treatment has been used for congenital CMV infection, but there are few reports on viral loads associated with GCV therapy. METHODS: A real-time PCR assay was used to monitor viral load in 6 cases of symptomatic CMV infection that received GCV therapy. Initially GCV was given at a dose of 5-12 mg/kg/d for 2-7 weeks. In 2 cases, additional doses were given as symptoms returned. RESULTS: After GCV administration, active signs of chorioretinitis, thrombocytopenia and anemia disappeared or improved in all cases. During GCV therapy, viral loads decreased while patients improved clinically and increased again when GCV therapy was stopped. Although CMV DNA continued to be detectable for a long period, clinical findings did not always worsen. In 2 cases, an improvement of hearing loss was observed. CONCLUSION: GCV therapy transiently suppresses the CMV concentrations. Subsequent increases of viral titers do not appear to be correlated with the clinical course or neurologic outcome.

Cytomegalovirus↗
PubMed2005

Association of cytomegalovirus with infantile hepatitis.

Infantile hepatitis is occasionally seen in apparently healthy children. In most cases, the etiology of the infection is uncertain. However, cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus-6 (HHV-6), human herpesvirus-7 (HHV-7), human parvovirus B19, and TT virus (TTV) are considered to be associated with hepatitis in children. The objective of this study was to investigate the correlations between these viruses and infantile hepatitis. Twenty-six children from 1 to 24 months old (median age, 7 months) who had liver dysfunction of unknown etiology were enrolled in this study. Plasma samples were examined by a real-time PCR assay for CMV, EBV, HHV-6, HHV-7, parvovirus B19, and TTV DNA. The DNA of CMV was detected in the plasma of four patients (15.4%) and was detected significantly more often in the patient group than in the control group. The CMV-infected patients were 1 to 3 months old, which was significantly younger than the remaining patients. The serological findings did not always correlate with the results of the real-time PCR assay. The DNA of TTV was detected in four patients (15.4%), while human parvovirus B19 DNA was detected in three (11.5%). However, the detection frequencies of these viral DNAs were not significantly different from those in the control groups, and some of these patients had co-infections. These results indicate that CMV might be one of the major pathogens responsible for infantile hepatitis; however, serological tests have limited utility for the diagnosis of CMV infection in young children.

Alanine Transaminase↗
PubMed2005

Apoptosis under hypercytokinemia is a possible pathogenesis in influenza-associated encephalopathy.

BACKGROUND: Influenza-associated encephalopathy is reported to be frequent in Japan and East Asia. No evaluating markers except interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha and no likely pathological mechanism for the disease have yet been elucidated. METHODS: In this study, influenza-associated encephalopathy was defined by clinical symptoms, and the use of an anti-influenza antibody test and/or influenza antigen detection kits, as well as computed tomography and/or magnetic resonance imaging. The levels of proinflammatory cytokines, acute phase proteins, endothelial markers and cytochrome c were compared in sera from 11 patients with and 42 without encephalopathy. RESULTS: Cytochrome c concentration in sera from patients with encephalopathy was markedly increased compared with that from patients without encephalopathy and normal controls. Although levels of several other proinflammatory cytokines and acute phase proteins such as TNF-alpha and IL-8 were also elevated in patients with influenza virus infection, the difference between those with and without encephalopathy, though significant, was less dramatic. The mean serum concentration of cytochrome c in 11 patients with encephalopathy, consisting of four deceased, four with and three without residual central nervous system sequelae, was 26.7 +/- 19.5 ng/mL on admission. In contrast, cytochrome c levels in 42 patients without encephalopathy were 0.3 +/- 0.7 ng/mL. CONCLUSION: The present results indicate that cytochrome c is a useful marker to follow patients with influenza-associated encephalopathy and suggest that an apoptosis of cells in several organs including the cerebrum and liver under the influence of hypercytokinemia is a possible mechanism of the disease.

Apoptosis↗
PubMed2005

Unique maternal deletion of 15q in a patient with some symptoms of Prader-Willi syndrome.

BACKGROUND: Human chromosome 15q11-q13 is a critical region for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and most of the genes are under the condition of imprinting mechanism. PWS results from the loss of expression of paternally expressed genes and AS of maternally expressed genes. In this study molecular studies about a patient with congenital anomalies and mental retardation are analyzed. METHODS: Highly polymorphic microsatellite markers were analyzed by PCR. These markers exist within 15q11-q13 and distal to 15q13. RESULTS: Only the maternal D15S986 locus within 15q11-q13 was deleted and other markers were biallelic. CONCLUSIONS: The result of maternal small region deletion in this patient is different from the typical PWS with paternal chromosome deletion and it suggests that nearby the deleted region there exists a gene (genes) which is not imprinted but needs biallelic expression.

Adolescent↗
PubMed2005

Virological aspects of Epstein-Barr virus infections.

Epstein-Barr virus (EBV) is usually maintained in an asymptomatic and latent form by the host immune system, and primarily by EBV-specific cytotoxic T cells (CTLs). However, EBV has been linked to several refractory diseases such as EBV-associated hemophagocytic syndrome(EBV-AHS) and chronic active EBV infection (CAEBV). In these ectopic diseases, EBV infects T/NK cells, causing severe immunodeficiency with a very high EBV load. In recent years, the laboratory procedure to assess these types of EBV infections has been improved. In particular, real-time polymerase chain reaction (PCR) has been used to quantify the EBV load, and the MHC: peptide tetramer assay has been used to quantitate EBV-specific CTLs; these tests have been employed for the management of the illnesses associated with EBV infection. Here, we have reviewed the recent progress in the clinical application of these assays. The pathogenesis of EBV-infected T/NK cells, and the host immune response to infection, including the roles carried out by innate immunity and inflammatory cytokines, are likely to be revealed in the future.

DNA, Viral↗
PubMed2005

Usefulness of helical computed tomography in diagnosing pulmonary vein stenosis in infants.

We investigated the usefulness of helical computed tomography(CT)in the morphological diagnosis of pulmonary vein stenosis, particularly that in infants and small children. In total, 20 helical CT examinations were performed in 10 post-operative cases of Total Anomalous Pulmonary Venous Drainage(TAPVD), 3 cases of single right ventricle, and 1 case of single left ventricle. In all cases, distinct morphological imaging was possible. Pulmonary vein stenosis could be categorized into three types: (1)stenosis from the anastomosis of the common pulmonary vein (CPV)-the left atrium (LA) to the peripheral pulmonary vein; (2) stenosis only at the anastomosis of CPV-LA; and (3) stenosis due to compression by nearby organs. Coronal views by multiplanar reconstruction (MPR) provided morphological information along the up-down direction of the body axis. Morphological diagnosis of pulmonary vein stenosis is important in deciding prognosis and therapeutic regimens, and helical CT was considered useful for such diagnosis in our 14 young patients.

Child, Preschool↗
PubMed2005

HHV-6 and seizures.

Human herpes virus-6 (HHV-6) is a ubiquitous virus, but one that can induce various neurological diseases. Recently, several seizures have been reported as new HHV-6-associated diseases based on virological analysis. Neonates who are perinatally infected with HHV-6 can develop afebrile seizures, which are considered to be exanthem subitum (ES) in the neonatal period. Infants with ES also tend to develop atypical febrile seizures. After primary infection, HHV-6 commonly establishes latency in the central nervous system (CNS) and sometimes reactivates in the hippocampus, causing limbic encephalitis and temporal lobe epilepsy. These HHV-6-associated CNS diseases due to virus reactivation can occur in both immunocompromised and immunocompetent hosts. This article summarizes HHV-6-associated seizures during childhood.

Encephalitis↗
PubMed2004

Quantitative analysis of Epstein-Barr virus (EBV)-specific CD8+ T cells in patients with chronic active EBV infection.

To clarify the pathogenesis of chronic active Epstein-Barr virus (EBV) infection, EBV-specific CD8+ T cells were enumerated, by use of human leukocyte antigen (HLA)-A*2402-restricted tetramers, in 8 patients with chronic active EBV infection, 10 patients with infectious mononucleosis, and 16 EBV-seropositive healthy control subjects. In most of the patients with chronic active EBV infection, EBV-specific CD8+ T cells were not detected. Of note, latent membrane protein 2-specific CD8+ T cells were not detectable in any patients with chronic active EBV infection. In contrast, EBV-specific CD8+ T cells were detected in patients with infectious mononucleosis and in healthy control subjects. Low frequencies of EBV-specific CD8+ T cells may be one of the immunological features of chronic active EBV infection.

Adolescent↗
PubMed2004

Analysis of cytokine levels and NF-kappaB activation in peripheral blood mononuclear cells in influenza virus-associated encephalopathy.

BACKGROUND: Influenza virus-associated encephalopathy (IE) is suggested to be a proinflammatory cytokine-related disease. METHODS: We measured the concentrations of interleukin-6 (IL-6), TNF-alpha, soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma, IL-2, IL-4, and soluble E-selectin (sE-selectin) in serum and CSF during the acute stage in 30 children with IE, 20 with influenza virus-associated febrile seizures (IFS), and 39 with influenza virus infection without complications (Flu). Moreover, the activation of transcription factor NF-kappaB in peripheral blood mononuclear cells (PBMC) of 5 children with IE was examined. RESULTS: The serum IL-6, sTNFR1, and IL-10 levels in the IE group with a poor prognosis (Group A) were significantly higher than those in the IE group without sequelae in IE (Group B), IFS, and Flu. In particular, the serum levels of IL-6, sTNFR1, and IL-10 in 5 deceased patients were markedly higher. The CSF IL-6 levels in Group A were significantly higher than those in Group B and IFS. Flow cytometric analysis revealed that NF-kappaB activation in PBMC in Group A was higher than that in Group B, IFS, and Flu. CONCLUSION: We suggest that cytokines are produced by PBMC in IE, and that the levels of serum IL-6, sTNFR1, and IL-10, CSF IL-6, and NF-kappaB activation in PBMC are useful indicators of the severity of the disease.

Adolescent↗
PubMed2004

Evaluation of systemic inflammatory responses in neonates with herpes simplex virus infection.

Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity. To investigate the pathogenesis of neonatal HSV infection, we examined inflammatory responses and markers of apoptosis in patients with neonatal HSV infection. Concentrations of inflammatory cytokines and markers of apoptosis were significantly higher in patients with disseminated HSV infection and were correlated with HSV load. It appears that the immunopathological damage that results from host responses to viral infection leads to organ dysfunction in patients with neonatal HSV infection.

Apoptosis↗
PubMed2004

Hemiconvulsion-hemiplegia syndrome and primary human herpesvirus 7 infection.

We report a case of hemiconvulsion-hemiplegia (HH) syndrome. An 18-month-old female infant had a hemiconvulsion followed by left hemiplegia. Magnetic resonance imaging immediately after the onset of hemiplegia showed high intensity in the right hemisphere in diffusion-weighted images (DWI), while T1- and T2-weighted images were normal. Single photon emission computed tomography showed hypoperfusion of the right hemisphere in the acute phase. Virological analyses proved primary human herpesvirus 7 (HHV-7) infection. DWI are useful for the early evaluation of HH syndrome. Vascular disorders due to HHV-7 infection may have been related to the development of HH syndrome in this patient.

Cerebral Cortex↗
PubMed2004

Influenza-associated acute encephalopathy in Japanese children in 1994-2002.

We addressed the incidence of influenza-associated acute encephalopathy, which is distinct from Reye syndrome, in children in Japan. Eighty-nine children with a mean age of 3.8 years were reported to have developed this disease during eight influenza seasons (December 1994-April 2002) in Hokkaido, Japan. None of them had received aspirin. Most of the patients rapidly became comatose with or without convulsions with a mean interval of 1.7 days from the onset of fever to the onset of central nervous system symptoms. Thirty-three (37.1%) patients died and 17 (19.1%) patients had neurological sequelae. A total of 53 (59.6%) cases were proved to have an influenza virus infection. Interleukin-6 and tumor necrosis factor-alpha were markedly elevated in serum and cerebrospinal fluid samples from two patients who died after a rapid, fulminant course. A post-mortem examination of one fatal case revealed vasogenic brain edema with generalized vasculopathy, suggesting that the generalized impairment of vascular endothelial cells caused by highly activated cytokines plays a central role in the pathophysiology of this disease. We conclude that influenza-associated acute encephalopathy may be an underestimated syndrome and is another reason to promote vaccination against influenza in infants and younger children.

Acute Disease↗
PubMed2004

Extraordinary changes in excitatory amino acid levels in cerebrospinal fluid of influenza-associated encephalopathy of children.

The correlation between the glutamate-glutamine cycle and nitric oxide (NO) production in the central nervous system (CNS) of a new type of influenza-associated encephalopathy in children is discussed. When measurements of several amino acids and NOx (nitrite/nitrate) levels in the cerebrospinal fluid (CSF) using HPLC-fluorescence and -UV methods, respectively, were made. the CSF glutamate levels of patients with the new type of encephalitis were significantly lower, and both glutamine and NOx levels were significantly higher than those of the control group and the patients of the meningitis group. Results indicate that the turnover rate of glutamate in CNS, particularly in the brain, increases in the influenza-associated encephalopathy. The high mortality in the disease may correlate with the hyperactivity of supra-spinal glutamate neurons and the subsequent high activity levels of NOx in CNS.

Brain Diseases↗
PubMed2004

Comparison of real-time and nested PCR assays for detection of herpes simplex virus DNA.

We performed a real-time PCR assay to detect herpes simplex virus (HSV) DNA, and compared it prospectively with a nested PCR assay in 164 clinical samples (109 cerebrospinal fluid and 55 sera) from patients suspected of having neonatal HSV infection or HSV encephalitis. In 25 of 164 samples, HSV DNA was detected by the nested PCR assay. All samples positive for HSV DNA in the nested PCR assay were also positive in the real-time PCR assay, and all but two samples negative for HSV DNA in the nested assay were negative in the real-time assay. The real-time PCR assay thus had a sensitivity of 100% and a specificity of 99%, when compared with the nested assay. Sequential assays in a case of disseminated HSV showed that a decrease in HSV DNA paralleled clinical improvement. Quantification of HSV DNA by real-time PCR was useful for diagnosing and monitoring patients with HSV encephalitis and neonatal HSV infection.

Cerebrospinal Fluid↗
PubMed2004

Serial changes of intrathecal viral loads evaluated by chemiluminescence assay and nested PCR with aciclovir treatment in herpes simplex virus encephalitis.

OBJECTIVE: We assessed the potential for estimating the effects of antiviral therapy on the clearance of intrathecal herpes simplex virus (HSV) antigens as evaluated by the chemiluminescence assay (CL) and on that of intrathecal HSV-DNA as evaluated by the nested polymerase chain reaction (PCR) in serial patients with herpes simplex virus encephalitis (HSVE). METHODS: The materials comprised serial cerebrospinal fluid (CSF) samples from 18 patients with HSVE. All patients were diagnosed as having HSVE retrospectively based on the detection of intrathecal HSV antigens by the CL, that of HSV-DNA by the nested PCR, and also serological confirmation of intrathecal antibody production. The relationships between the days of aciclovir therapy and serial HSV viral loads as evaluated by the CL and nested PCR in the serial CSFs were assessed. RESULTS: The serial intrathecal viral loads evaluated by the CL and nested PCR declined after the commencement of aciclovir administration in all patients. The serial alterations of the intrathecal viral load evaluated by the CL in each patient were similar to those of the intrathecal viral load evaluated by the nested PCR. The initial and maximum viral loads evaluated by the CL and nested PCR showed a wide distribution in the CSF samples taken from the patients with poor and good outcomes. Differences in the means of the viral loads in the CSF samples taken from the patients between a poor outcome and a good outcome were not evident. A transient increase of viral load as evaluated by these two methods was noted in the same 4 patients. The viral loads in these 4 patients also declined in the subsequent CSF samples. The outcome of these 4 patients was good in one patient and poor in the others. CONCLUSION: Evaluation of intrathecal viral antigens by the CL has a potential for estimating the effects of antiviral therapy, as does evaluation of the intrathecal HSV-DNA by the nested PCR. The intrathecal viral loads evaluated by CL and nested PCR were not a predictor of outcome in HSVE.

Acyclovir↗
PubMed2004

[Influenza-associated encephalopathy].

Infection with influenza viruses produces a spectrum of clinical responses, ranging from upper respiratory illness to central nervous system (CNS) involvement. Recently, the number of reports of influenza-associated encephalopathy in Japan has increased. During the winters of 1997-1998 and 1998-1999, when epidemics of type A influenza (H3N2) occurred, many pediatricians reported cases of influenza-associated encephalitis or encephalopathy in children. The prominent indicators of influenza-associated encephalopathy are the abrupt onset of seizures and coma within a few days of developing a high-grade fever. These patients often develop multi-organ failure and have high morbidity and mortality. The pathogenesis of influenza-associated encephalopathy remains unclear. Because not all patients with influenza develop encephalopathy, infection with the influenza vieus is necessary, but not sufficient, for the development of influenza-associated encephalopathy. Viral RNA is rarely detected in the cerebrospinal fluid (CSF), and the presence of viral antigen in the brain has not been proven. Pathological findings, including the lack of detectable viral antigen and inflammatory cells in brain tissues, suggest that direct viral invasion and inflammation are unlikely to be causes of this disease. In influenza-associated encephalopathy, serum and CSF concentrations of several proinflammatory cytokines and cytokine receptors--such as interleukin (IL)-6, IL-1beta, and soluble tumor necrosis factor (TNF) receptor-1 (sTNF-R1)--are elevated and are related to the clinical severity of the disease. Moreover, the damage of vascular endothelial cells has been shown. Using SNPs, molecular analysis of whole genome of the patients are now on going.

Brain Diseases↗