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Biomedical subjects

Akinori Hoshika

Publications and source records attributed to Akinori Hoshika.

At least 19 recordsLinked to original sources
PubMed2007

Usefulness of indomethacin for patent ductus arteriosus in full-term infants.

The aim of this retrospective study was to evaluate the effectiveness of indomethacin therapy for patent ductus arteriosus (PDA) in full-term infants. The patients were 41 full-term infants with a PDA birth weight (BW) > or =2500 g and a gestational age (GA) > or =37 weeks. The echocardiographic evaluation and medical management of PDA in these infants was similar to that for PDA in low-birth-weight infants. Indomethacin (0.2-0.25 mg/kg/dose) was given intravenously at 12-24-hour intervals within 23 days of birth. Of the 41 infants, 12 showed complete closure, and 13 showed improvement of clinical symptoms. These 25 infants were classified as the responder group (61%). The other 16 infants, who did not show improvement in clinical symptoms, were classified as the nonresponder group. Statistical analysis revealed no difference between the two groups regarding GA, BW, Apgar score at 1 minute, minimum diameter of the DA before treatment, the average age at the initiation of treatment, and DA flow pattern. No severe adverse reactions were observed in any infant. Indomethacin therapy appears to be an effective medical treatment option for PDA in full-term symptomatic infants prior to considering surgical treatment.

Cyclooxygenase Inhibitors↗
PubMed2006

Association and synergistic interaction between promoter variants of the DRD4 gene in Japanese schizophrenics.

Recent association studies suggest that polymorphisms in the promoter and exon 1 upstream region of the dopamine D4 receptor (DRD4) gene play a functional role in the development of common psychiatric illnesses, although there are also conflicting results. In this study, we re-sequenced this region to identify all genomic variants, and tested them for association with schizophrenia. A total of 570 Japanese schizophrenic cases with matched controls were studied by genotyping all identified/validated common polymorphisms (-1106T>C, -906T>C, -809G>A, -616G>C, -521T>C, -376C>T, -291C>T and 12-bp repeat) and a known microsatellite (120-bp tandem duplication) in the upstream region. A single nucleotide polymorphism (SNP) -809G>A in the promoter region was found to be significantly associated with disease (P=0.018 and 0.032 for allelic and genotypic comparisons, respectively), although not surviving after Bonferroni correction. Logistic regression analysis showed that a combination of the four polymorphisms, -809G>A, -616G>C, -291C>T and the 12-bp repeat, conferred a susceptibility to schizophrenia. These results suggest that the upstream variants have a primary functional effect in the etiology of schizophrenia in the Japanese population.

Exons↗
PubMed2006

Combined treatment of steroids and cyclosporine in Kimura disease.

Kimura disease is a rare but distinctive chronic eosinophilic inflammatory disorder that is characterized by tumor-like lesions in the soft tissue and lymph nodes of the head and neck or parotid gland. Recently, many immunopathogenetic features of underlying T lymphocytes and related cytokines have been noted in Kimura disease. However, few previous studies have investigated the serial levels of cytokines in children. In this report we describe an 11-year-old Japanese boy with relapsing Kimura disease. Before the diagnosis of Kimura disease, the patient had a swelling on his left neck. Steroids were effective, but the tumor relapsed within a few months as the steroids were tapered. He was treated with steroids and cyclosporine. This treatment was done by measuring serial levels of serum soluble interleukin-2 receptor, interleukin-4, interleukin-5, and eosinophil cationic protein. These results suggest the activation of T-helper cells and T-helper 2 cytokines, that after activated B cells and eosinophilic infiltration play an important role in Kimura disease, and that cyclosporine suppresses the activity of this disease.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed2006

Diagnostic and predictive value of CSF d-ROM level in influenza virus-associated encephalopathy.

The aim of this study was to assess the validity of serum and CSF oxidative status of patients with IE in their initial stage through the d-ROM (Diacron-Reactive Oxygen Metabolites, Italy) test, compared to those with other neurological diseases. The study was conducted on the following four groups: (1) influenza virus-associated encephalopathy (IE, n = 8), including four patients showing neurological sequelae or mortal; (2) influenza virus-associated febrile seizures (IFS, n = 11); (3) febrile convulsion (FC, n = 10): (4) enterovirus-associated encephalopathy (EE, n = 4), including one patient with neurological sequelae. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and the FC groups but not in the EE group. In addition, general laboratory findings such as leukocytes, platelets, C-reactive protein, aspartate aminotransferase, creatinine, creatinine kinase and LDH, including interleukin-6 (IL-6), were analyzed in each group. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and FC groups but not in the EE group. As for the serum d-ROM levels and general laboratory findings, with the exception of CSF IL-6 levels in IE, no significant differences were detected compared with the other groups. In patients with IE, the CSF d-ROM levels could be a valid predictive biomarker of the severity, and oxidative stress may be related to the pathogenesis of IE.

Biomarkers↗
PubMed2006

Primary biomarkers in cerebral spinal fluid obtained from patients with influenza-associated encephalopathy analyzed by metabolomics.

In order to search for the specific biomarkers of patients with influenza-associated encephalopathy this article analyzed all metabolites in cerebrospinal fluid (CSF) by using metabolome analysis. In all metabolites, the peaks of two molecular weights, 246.0092 and 204.0611, were significantly higher than those in other diseases including influenza without convulsion (p < .05). The peak of a molecular weight 228.0247 in all of the patients except one was less than that in other patients. These results indicate that the new metabolites detected in CSF would be primary markers for the diagnosis of influenza-associated encephalopathy.

Biomarkers↗
PubMed2006

IFN-alpha sensitizes daudi B lymphoma cells to anti-IgM induced loss of mitochondrial membrane potential through activation of c-Jun NH(2)-terminal kinase.

Interferon-alpha (IFN-alpha) regulates multiple biologic functions, including antiviral activity, immune regulation, cell differentiation, and cell survival or death, in a variety of cell types. We and others have recently demonstrated that IFN-alpha induces cell death through activation of c-Jun NH(2)-terminal kinase (JNK) in human Daudi B lymphoma and U266 myeloma cells. Moreover, the IFN-alpha-induced signaling pathway has been shown to cross talk with the antigen receptor-mediated signaling cascade. In the present study, we examined whether IFN-alpha affects cell death after engagement of membrane immunoglobulin (mIg) using anti-IgM. Daudi cells pretreated with low concentrations of IFN-alpha (25 or 250 U/mL) for 24 h were stimulated with anti-IgM (1-10 microg/mL) for 24 h. The cells were assayed for JNK activation, mitochondrial membrane potential (DeltaPsim) by Western blotting, and DiOC(6) staining, respectively. The IFN-alpha-primed Daudi cells showed an increased sensitivity to subsequent stimulation with anti-IgM, as assessed by JNK activation and DeltaPsim. Moreover, Daudi cells overexpressing the constitutively active or dominant-negative form of JNK were substantially susceptible or resistant to anti-IgM-induced DeltaPsim, respectively, compared with cells overexpressing the control vector alone. Taken together, these results indicate that IFN-alpha renders Daudi B lymphoma cells susceptible to anti-IgM-induced apoptosis, probably through upregulation of JNK activation.

Antibodies, Anti-Idiotypic↗
PubMed2005

Diagnosis and evaluation of febrile infants under 4 months of age in Japan by using RT-PCR for enterovirus.

OBJECTIVES AND METHODS: In order to establish an effective management for febrile infants under 4 months of age we analysed the causes of fever by using bacterial work up and a highly sensitive RT-PCR method during a 3-year-period. From February 1998 to January 2001, 263 infants under 4 months of age were admitted to our hospital because of fever (>38.0 degrees C) and enrolled in this study. RESULTS: Eighty-nine cases (33.8%) were diagnosed as lower respiratory infections, and 62 (23.5%) as urinary tract infections. Aseptic meningitis was found in 35 cases (13.2%) and fever of unknown origin in 22 (8.3%). Sepsis and purulent meningitis were found in three and two infants, respectively. Aseptic meningitis was the most common disease in infants below 30 days. Aseptic meningitis and fever of unknown origin revealed no seasonable tendency. Twelve cases out of 20 tested infants with aseptic meningitis showed positive results for enterovirus in CSF. CONCLUSION: Clinicians should consider age, sex and seasons when evaluating and treating infants with fever. Previously lumbar puncture, urinalysis and chest X-ray were recommended to avoid useless assays. These results also revealed that RT-PCR is a useful and significant assay to establish an exact diagnosis in very young infants.

Bacterial Infections↗
PubMed2005

Analysis of correlation between serum D-serine levels and functional promoter polymorphisms of GRIN2A and GRIN2B genes.

D-Serine is an endogenous coagonist that increases the opening of N-methyl-D-aspartate (NMDA)-type glutamate receptor channels. We previously reported a reduction of D-serine serum levels in schizophrenia, supporting the disease hypothesis of NMDA receptor-mediated hypo-neurotransmission. The serum levels of D-serine are thought to reflect brain d-serine content. It is important to understand whether there is a direct link between the altered D-serine levels and NMDA receptor expression in vivo or whether these are independent processes. Two polymorphisms are known to regulate the expression of NMDA receptor subunit genes: (GT)(n) (rs3219790) in the promoter region of the NR2A subunit gene (GRIN2A) and -200T > G (rs1019385) in the NR2B gene (GRIN2B). These polymorphisms are also reported to be associated with schizophrenia. Therefore, we examined the correlation between these two polymorphisms and d-serine serum levels in mentally healthy controls, schizophrenics and the combined group. We observed no significant genotype-phenotype correlations in any of the sample groups. However, analyses of larger sample numbers and the detection of additional polymorphisms that affect gene expression are needed before we can conclude that NMDA receptor expression and serum levels of d-serine, if involved in schizophrenia pathophysiology, are independent and additive events.

Adult↗
PubMed2005

A case of Reye syndrome with rotavirus infection accompanied with high cytokines.

We report on a 23-month-old boy with a rare complication of rotavirus gastroenteritis. He was diagnosed as acute encephalopathy with DIC accompanied with high levels of cytokines. The liver pathology also revealed mild infiltration and fatty changes. He was suspected to be suffering from a cytokine storm followed by Reye syndrome.

Anticonvulsants↗
PubMed2005

Nitrite/nitrate (NOx) and zinc concentrations in influenza-associated encephalopathy in children with different sequela.

NOx (NO2 and NO3) in CSF obtained from 22 patients with influenza-associated encephalopathy were higher than those of a control group. Within the different prognosis, there were no significant differences in NOx levels. By analyzing the serum obtained from patients infected with influenza, including encephalopathy, with others, the serum zinc levels did show marked differences between them. Four out of eleven patients with influenza-associated encephalopathy showed low zinc levels below the normal range. However, there were no significant differences in the zinc levels between the group with sequela and without sequela. These results indicate that the increase of NOx levels detected in influenza-associated encephalopathy relates to the low zinc levels, and both low molecules might play an important role for the cause of encephalopathy.

Brain Damage, Chronic↗
PubMed2005

Efficacy of plasma exchange and methylprednisolone pulse therapy on influenza-associated encephalopathy.

Patients with a new type of influenza-associated encephalopathy with high mortality are increasing in Japan and the United States. We present three patients treated with methyprednisolone pulse treatment and plasma exchange to remove cytokines, and all three patients recovered without severe sequela. IL-6 decreased dramatically after the start of the plasma exchange and methyprednisolone. Therefore when influenza-associated encephalopathy is actually diagnosed, steroid pulse therapy should be started at an early stage, and when signs of DIC and/or MOF appear, plasma exchange is recommended to remove the cytokines and NOx.

Brain Diseases↗
PubMed2005

Beta-catenin interacts with the FUS proto-oncogene product and regulates pre-mRNA splicing.

BACKGROUND & AIMS: beta-Catenin is a downstream effector of the Wnt signaling pathway and is believed to exert its oncogenic function by activating T-cell factor (TCF)/lymphoid enhancer factor (LEF) family transcriptional factors. However, it is still uncertain whether the diverse effects of beta-catenin are caused solely by aberrant gene transactivation. In this study, we used a proteomics approach to obtain further insight into the functional properties of nuclear beta-catenin. METHODS: The protein assembly of a native beta-catenin-containing complex in nuclear extracts from a colorectal cancer cell line, DLD-1, was identified using immunoprecipitation and mass spectrometry. RESULTS: beta-Catenin physically interacted with fusion (FUS)/translocated in liposarcoma (TLS) and various RNA-binding proteins. The expression of FUS/TLS was closely associated with the accumulation of beta-catenin and with the undifferentiated status of intestinal epithelial cells. The transient transfection of FUS suppressed beta-catenin-evoked gene transactivation of TCF/LEF, and beta-catenin transfection affected the splicing pattern of the E1A minigene and induced a novel splicing variant of estrogen receptor (ER)-beta exerting a dominant-negative activity. CONCLUSIONS: Human cancer expresses a large variety of alternatively spliced messenger RNA (mRNA), but the precise molecular mechanisms responsible for cancer-related alternative splicing are largely unknown. In this study, we demonstrated the interaction of beta-catenin with FUS/TLS and other RNA-binding proteins involved in the regulation of pre-mRNA splicing. Certain mRNA splicing abbreviations seen in human cancers may be induced by the activation of the Wnt signaling pathway.

Alternative Splicing↗
PubMed2005

Methylation status of the p15 and p16 genes in paediatric myelodysplastic syndrome and juvenile myelomonocytic leukaemia.

Aberrant DNA methylation is frequently observed in adults with myelodysplastic syndrome (MDS), and is recognized as a critical event in the disease's pathogenesis and progression. This is the first report to investigate the methylation status of p15 and p16, cell cycle regulatory genes, in children with MDS (n = 9) and juvenile myelomonocytic leukaemia (JMML; n = 18) by using a methylation-specific polymerase chain reaction. The frequency of p15 hypermethylation in paediatric MDS was 78% (7/9), which was comparable to that in adult MDS. In contrast, p15 hypermethylation in JMML was a rare event (17%; 3/18). In JMML, clinical and laboratory characteristics including PTPN11 mutations and aberrant colony formation were not different between the three patients with hypermethylated p15 and the others. Aberrant methylation of p16 was not detected in children with either MDS or JMML. Since p15 and p16 genes were unmethylated in two children with JMML, in whom the disease had progressed with an increased number of blasts, a condition referred to as blastic crisis, we infer that the aberrant methylation of these genes is not responsible for the progression of JMML. The results suggest that demethylating agents may be effective in most children with MDS and a few patients with JMML.

Adolescent↗
PubMed2005

Expression pattern of keratin subclasses in pancreatoblastoma with special emphasis on squamoid corpuscles.

Expression patterns of keratins (K), both simple epithelia-type (K7, K8, K18, K19) and complex/stratified epithelia-type (K1, K4, K5/6, K10, K13, K14, K15, K16, K17), and epithelial membrane antigen (EMA) were immunohistochemically studied in six pancreatoblastomas (PBL). In all six tumors, areas with overt acinar differentiation (AA), solid areas without any specific differentiation (SO), and squamoid corpuscles (SC) were diffusely positive for K8, K18, and K19. The AA and SO in all the tumors were diffusely positive for K7, but the SC were negative or displayed only scattered reactivity for K7. In three tumors, the AA and the SC showed scattered reactivity for K5/6. No reactivity for other complex/stratified epithelia-type K was found in any of the examined tumor. All tumors were reactive for EMA with consistent predominancy in the SC. Ultrastructurally, well-developed desmosome-tonofilament complexes were only partially observed in tumor cells comprising the SC. These results implied that (i) the SC usually lack a character of complete squamous metaplasia; and (ii) the SC have a characteristic phenotype (K8/K18/K19/EMA-positive, K7-negative or scatteredly positive) that can potentially be useful to delineate the SC in PBL.

Child↗
PubMed2005

Effects of rapid rewarming on cerebral nitric oxide production and cerebral hemodynamics after hypothermia therapy for kainic acid-induced seizures in immature rabbits.

BACKGROUND: The aim of the present study was to investigate whether rapid rewarming after hypothermia therapy during seizures alters the endogenous nitric oxide (NO) production in and around hippocampus, cortical cerebral blood flow (cCBF), and mean arterial blood pressure (MABP) in immature rabbits. METHODS: The hypothermic rabbits (rectal temperatures, 33 degrees C) were given kainic acid (KA; 12 mg/kg, i.v; at 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then either rewarming (RW; 33-37 degrees C) was started (KA[+]RW[+] group, n = 7) or cooling was continued (KA[+]RW[-] group, n = 7) for another 60 min (at the end 120 min). In the KA(-)RW(+) group (n = 5), 0.5 mL normal saline was given (at time 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then rewarming to 37 degrees C was started with observation for another 60 min (at the end 120 min). NO production in and around hippocampus was continuously measured by an NO-selective electrode, cCBF by laser Doppler flowmetry, cortical electroencephalogram (EEG), rectal and cerebral temperatures, and MABP during the experiment. Comparisons were made of these parameters between the values at 60 min and 120 min after the KA administrations. RESULTS: KA administration induced abnormal discharges in both KA(+)RW(+) and KA(+)RW(-) groups at the same degree. The KA(+)RW(+) group had a significant increase in %NO, and significant decreases in %cCBF and MABP after rapid rewarming, compared with before rewarming. In the KA(+)RW(-) group, there were no significant changes in %NO, %cCBF, and MABP between values at 60 and 120 min. These changes after rapid rewarming in the KA(+)RW(+) group were different from those with only elevation in brain temperature from 33 to 37 degrees C without seizures (KA[-]RW[+] group). CONCLUSIONS: These results suggest that rapid rewarming after hypothermia therapy induces an increase in the NO production in and around hippocampus and the decreases in cCBF and MABP during seizures in immature rabbits.

Animals↗