Search PubMed⌕ Search

Biomedical subjects

N Hayashi

Publications and source records attributed to N Hayashi.

At least 181 records · Page 10Linked to original sources
PubMed2000

Three-dimensional ultrasound in embryo transfer.

OBJECTIVE: To examine the feasibility of using three-dimensional (3D) ultrasound (US) guidance in routine embryo transfer (ET) procedures. METHODS: Seventy-five ETs were performed using a 3D US scanner to locate the catheter tip in the uterine cavity. RESULTS AND CONCLUSION: Three-dimensional ultrasound could show the exact position of the tip of the catheter in the uterine cavity quickly enough in most cases. It should be used in ET for seeking an optimal transfer area in the uterine cavity to assist in achieving high success rates and less complications.

Catheterization↗
PubMed2000

Expression of T-cadherin (CDH13, H-Cadherin) in human brain and its characteristics as a negative growth regulator of epidermal growth factor in neuroblastoma cells.

In the present study, we first examined the expression of T-cadherin in human CNS by northern blot analysis, immunohistochemical staining, and in situ hybridization. Northern blot analysis demonstrated expression of T-cadherin in human adult cerebral cortex, medulla, thalamus, and midbrain. Immunohistochemical staining with a newly generated monoclonal antibody, designated MA-511, revealed strong expression of T-cadherin in neural cell surface membrane and neurites in adult cerebral cortex, medulla oblongata, and nucleus olivaris. Little or no expression of T-cadherin was found in spinal cord. We further examined T-cadherin expression in various developing nervous systems, and found that T-cadherin expression was lower in developing brain than in adult brain. In situ hybridization revealed that neural cells in medulla oblongata and nucleus olivaris, but not in spinal cord, possessed T-cadherin molecules. We transfected T-cadherin-negative TGW and NH-12 neuroblastoma cells with a T-cadherin cDNA-containing expression vector. T-cadherin-expressing neuroblastoma cells lost mitogenic proliferative response to epidermal growth factor. Epidermal growth factor is known to be required for proliferation of neural stem cells. This finding, together with those of the present study, suggests that T-cadherin functions as a negative regulator of neural cell growth.

Adult↗
PubMed2000

Probability of hepatocellular carcinoma of small hepatocellular nodules undetectable by computed tomography during arterial portography.

Recent advances in imaging modalities enable the identification of small hepatocellular nodules. Among the imaging techniques currently used for detecting hepatocellular carcinomas (HCC), computed tomography (CT) during arterial portography (CTAP) is one of the most sensitive techniques available for detecting hemodynamic change. Even so, well-differentiated HCCs that display only limited hemodynamic change, a feature shared with nonmalignant hepatocellular nodules, are not always detectable by CTAP. To improve our ability to distinguish well-differentiated HCCs from nonmalignant hepatocellular nodules, we have attempted to clarify how the characteristics of the nodules are shown by each imaging technique. We studied the imaging and pathological characteristics of 31 nodules (in 22 patients) detected by ultrasonography (US), but not by CTAP. Histological diagnoses were as follows: HCC, 17 of 31 nodules (55%); high-grade dysplastic nodules, 1 of 31 (3%); and nonmalignant nodules, 13 of 31 (42%). Neither digital substraction angiography (DSA) nor CT arteriography (CTA) were able to detect any of the nodules. Detection rates for plain CT were: 5 of 17 (29%) HCC, 1 of 1 (100%) high-grade dysplastic nodules, and 1 of 13 (8%) nonmalignant nodules. Detection rates for T1/T2-weighted magnetic resonance imaging (MRI) were: 4 of 17 (24%) HCC, 1 of 1 (100%) high-grade dysplastic nodules, and 3 of 13 (23%) nonmalignant nodules. Dynamic CT and dynamic MRI provided no additional information. In conclusion, there is some probability that hepatocellular nodules detected by US, but not by CTAP, are HCC. Presently, it is difficult to distinguish between benign nodules and malignant ones with these imaging techniques, and our findings indicate that biopsy may be advisable for nodules detected under these conditions.

Adult↗
PubMed2000

Clinical features in patients requiring reoperation after failed endoscopic procedures for hydrocephalus.

The aim of this study was to clarify the clinical features of patients at risk of secondary obstruction following endoscopic fenestration. Clinical notes and endoscopic findings for 15 patients treated with endoscopic procedures were retrospectively reviewed. Endoscopic third ventriculostomy (ETV) was performed as initial treatment in 4 patients with non-communicating hydrocephalus, including a neonate with myelomeningocele, and as an alternative to shunt revision in 4 patients. Two patients with non-communicating hydrocephalus caused by tumor or arachnoid cyst were also managed with third ventriculostomy. Four patients with loculated hydrocephalus underwent endoscopic septostomy. A child with an isolated fourth ventricle was treated with endoscopic aqueductoplasty. Of the 15 patients undergoing endoscopic procedure, 4 required reoperation. Of the 10 patients treated with ETV, only the neonate with myelomeningocele required a ventriculoperitoneal shunt because of failure of the initial procedure. Of the 4 patients treated with endoscopic septostomy, 2 children with loculated hydrocephalus following intraventricular hemorrhage (IVH) underwent a second septostomy. In a patient with an isolated fourth ventricle following posthemorrhagic hydrocephalus, recurrence was noted 8 months after the initial procedure. He underwent a second procedure using a stent implanted into the aqueduct to maintain CSF circulation. Sufficient stomal size or implantation of a stent may be required in the under-2-year age group with hydrocephalus accompanied by IVH and associated with myelomeningocele, in whom the risk of secondary obstruction may be high.

Adolescent↗
PubMed2000

Contrast-enhanced magnetic resonance imaging of the cranial nerves in patients with acoustic schwannoma: correlation with surgical findings.

Eighteen patients with acoustic schwannoma were examined on a 1.5-T magnetic resonance imaging (MRI) unit with precontrast and postcontrast T1-weighted spin-echo sequences. Each abnormality was assessed in terms of the size, location, extensions and signal intensity of the lesions. If a nerve was enhanced and was involved by the tumor around the fundus of the internal auditory canal (IAC), the nerve was interpreted to be the originating nerve. The postcontrast T1-weighted images revealed enhanced masses of the cerebellopontine angle and/or the IAC in all cases. In 11 of the 19 operated patients with shwannomas, the site of tumor origin (or origin nerve) was confirmed by surgery. In 2 of the 11 cases (18%), surgical findings coincided with the T1-weighted image findings. Facial nerve enhancement on the ipsilateral side of the tumor was noted in 10 cases (53%) and the contralateral facial nerve enhancement was demonstrated in 7 (70%). The enhancement of facial nerve associated with acoustic schwannoma was not correlated to the degree of nerve compression by the tumor. These results demonstrate that it was possible, although infrequent, to predict the site of origin of acoustic schwannoma before surgery in some patients. Improvement of the imaging matrix or multiplanar reconstruction techniques with three-dimensional data acquisition may make it possible to overcome the limitations of MRI.

Adult↗
PubMed2000

Antisense oligodeoxynucleotides to human inducible nitric oxide synthase selectively inhibit induced nitric oxide production by human vascular endothelial cells: an experimental study.

OBJECTIVE: To find out whether the antisense oligodeoxynucleotide designed against the complementary DNA to human inducible NO synthase (iNOS) would block the translation from iNOS mRNA to NO in human vascular endothelial cells. DESIGN: Prospective controlled study. SETTING: Research laboratory, Japan. MATERIAL: Cultured human vascular endothelial cells. INTERVENTIONS: Human vascular endothelial cells were cultured for 24 hours, and divided into two groups, one of which was exposed to antisense oligodeoxynucleotides and the other to sense oligodeoxynucleotides at 100, 200, 400 and 800 micromol/L, respectively, for 18 hours. They were then exposed to interferon-gamma (1000 units/ml) and recombinant human tumour necrosis factor alpha (500 units/ml) to stimulate NO production. Each experiment was repeated ten times. RESULTS: Clear bands expressing cDNA of iNOS mRNA were identified in agarose gels in all cultured cells in both groups. The mean nitrite concentration in the supernatants of cultured cells in the group with the addition of antisense oligodeoxynucleotides was significantly lower than that in the group with sense oligonucleotides added at 200, 400, and 800 micromol/L. CONCLUSION: These findings indicate that the antisense oligodeoxynucleotides inhibited the NO production dependently, by preventing only their translation but not the processing, before their transcription from DNA into iNOS mRNA.

Cells, Cultured↗
PubMed2000

Temporal changes of the apparent diffusion coefficients of water and metabolites in rats with hemispheric infarction: experimental study of transhemispheric diaschisis in the contralateral hemisphere at 7 tesla.

The purpose of the present study was to clarify the temporal changes of the apparent diffusion coefficients (ADCs) of cerebral metabolites during early focal ischemia using stimulated echo acquisition mode with short echo time at a 7 T magnet to assess the pathophysiology of the reduction in diffusion properties observed both in the ischemic cerebral hemisphere and in the contralateral hemisphere. The ADCs of metabolites in the infarcted hemisphere 1 hour and 3 hours after the onset of ischemia decreased with 25% and 29% for choline containing compounds (Cho), 16% and 26% for creatine and phosphocreatine (Cre), and 19% and 19% for N-acetylaspartate (NAA), respectively, compared with the ADC values 2 hours later in the contralateral hemisphere. There were decreases in the ADC of Cho, Cre, and NAA with 21%, 7%, and 18% 8 hours later, respectively, in the noninfarcted hemisphere, which suggested transhemispheric diaschisis in rats with focal cerebral ischemia. The present study proposed that the diffusion characteristics of the brain metabolites might offer new insights into circulatory and metabolic alteration in the cerebral intracellular circumstance.

Animals↗
PubMed2000

Reappraisal of biochemical hepatitis C activity in hemodialysis patients.

We reappraised biochemical hepatitis C activity in hemodialysis patients in comparison with normal controls. A total of 111 hemodialysis patients and 66 healthy volunteer blood donors with hepatitis C virus (HCV) infection were consecutively enrolled. Serum alanine aminotransferase (ALT) levels were normal (< or =45 U/L) in 103 (93%) hemodialysis patients and 34 (52%) donors (p < 0.001). HCV viremic levels were lower in the hemodialysis group (p = 0.044), with no difference in the HCV genotype prevalence. During two-year follow-up, 60 (67%) of 90 hemodialysis patients and 13 (26%) of 50 donors showed persistently normal ALT levels (p < 0.001). For hemodialysis patients, however, the upper normal limit of ALT activity was reset at 25 U/L corresponding to the mean + 2 x SD for the normalized ALT distribution in 400 control patients. The adjusted ALT levels were initially normal in 73 (66%) hemodialysis patients and persistently normal in 19 (21%). Thus, ALT levels were the same for the two groups. GB virus C (GBV-C)/hepatitis G virus (HGV) coinfection found only in the hemodialysis group (10/111) had no influence on the disease. A relationship was noted between low disease activity and female gender in both groups. These findings indicate that biochemical hepatitis C activity in hemodialysis patients is similar to that in normal controls and should be monitored based on adjusted ALT levels.

Alanine Transaminase↗
PubMed2000

Recombinant human interleukin-11 decreases severity of acute necrotizing pancreatitis in mice.

Interleukin (IL)-11 has anti-inflammatory activity in animal models of gut inflammation, endotoxemia, and radiation-induced thoracic injury. The aim of the present study was to investigate the protective role of IL-11 in a model of acute necrotizing pancreatitis in mice. Acute pancreatitis was induced by administration of seven intraperitoneal injections of cerulein (50 microg/kg) at hourly intervals. Lipopolysaccharide (LPS) was injected 5 hours after the first cerulein injection. Treatment with recombinant human IL-11 (rhIL-11) was started 30 minutes before the first cerulein injection and repeated 4 hours later. Serum levels of amylase, lipase, and tumor necrosis factor (TNF)-alpha were measured at the end of the experiments. The severity of pancreatitis was evaluated by histological scoring using a semiquantitative analysis of hematoxylin and eosin-stained sections of the pancreas. Competitive reverse transcription-polymerase chain reaction (RT-PCR) was performed to quantify the intrapancreatic TNF-alpha mRNA levels. Serum amylase and lipase levels progressively increased with a maximum reached between 8 and 11 hours. Treatment with rhIL-11 significantly decreased amylase and lipase levels at 6 and 8 hours. Serum TNF-alpha peaked at 6 hours and rapidly decreased thereafter. The elevation of serum TNF-alpha was markedly inhibited by treatment with rhIL-11. Histologically, treatment of rhIL-11 reduced the severity of pancreatic injury including edema, inflammatory cell infiltration, and hemorrhage at 6 hours. Intrapancreatic TNF-alpha mRNA levels were reduced by >50% in the rhIL-11-treated group at 6 hours. In conclusion, rhIL-11 decreased the severity of experimental pancreatitis early on but not later and inhibited the intrapancreatic TNF mRNA expression in vivo, suggesting that the protective effect of IL-11 during the early stage of acute pancreatitis may be mediated, at least in part, through modulation of TNF production.

Amylases↗
PubMed2000

Effect of troglitazone on exocrine pancreas in rats with streptozotocin-induced diabetes mellitus.

Abnormality of pancreatic exocrine secretion has been observed in patients with diabetes mellitus. Troglitazone is a novel insulin-sensitizing agent that improves hyperglycemia and hyperinsulinemia in insulin-resistant diabetes mellitus. We investigated the effect of troglitazone on exocrine pancreas in streptozotocin (STZ)-induced diabetic rats. Diabetes mellitus was induced by intraperitoneal injection of STZ (25 mg/kg), and then 0.2% troglitazone containing rat chow was given for 2 weeks. Control diabetic animals received normal rat chow for 2 weeks. Glucose tolerance tests were performed before and after the administration of troglitazone. Pancreas weight, enzyme, protein, and insulin contents in the pancreas were measured. For the exocrine secretory study, pure pancreatic juice was collected hourly. Plasma glucose concentrations stimulated by the oral administration of 2.5 g/kg glucose in the troglitazone-treated group were significantly lower than those in the control group, but not plasma insulin concentrations. Pancreas weight in diabetic rats was less than that in normal rats. Administration of troglitazone resulted in a significant increase in pancreas weight and amylase and trypsin output. However, protein and insulin contents were not affected by the treatment with troglitazone. Both basal and cholecystokinin (CCK-8; 26 pmol/kg/h) stimulated exocrine secretion in juice volume, amylase, and trypsin output were markedly decreased in diabetic rats, compared with those in normal rats. Impaired basal and CCK-stimulated pancreatic exocrine secretion in diabetic rats recovered to the normal levels when troglitazone was given. In conclusion, troglitazone might be effective to restore exocrine pancreatic insufficiency in STZ-diabetic rats.

Animals↗
PubMed2000

The binding of myristoylated N-terminal nonapeptide from neuro-specific protein CAP-23/NAP-22 to calmodulin does not induce the globular structure observed for the calmodulin-nonmyristylated peptide complex.

CAP-23/NAP-22, a neuron-specific protein kinase C substrate, is Nalpha-myristoylated and interacts with calmodulin (CaM) in the presence of Ca2+ ions. Takasaki et al. (1999, J Biol Chem 274:11848-11853) have recently found that the myristoylated N-terminal nonapeptide of CAP-23/NAP-22 (mC/N9) binds to Ca2+ -bound CaM (Ca2+/CaM). In the present study, small-angle X-ray scattering was used to investigate structural changes of Ca2+/CaM induced by its binding to mC/N9 in solution. The binding of one mC/N9 molecule induced an insignificant structural change in Ca2+/CaM. The 1:1 complex appeared to retain the extended conformation much like that of Ca2+/CaM in isolation. However, it could be seen that the binding of two mC/N9 molecules induced a drastic structural change in Ca2+/CaM, followed by a slight structural change by the binding of more than two but less than four mC/N9 molecules. Under the saturated condition (the molar ratio of 1:4), the radius of gyration (Rg) for the Ca2+/CaM-mC/N9 complex was 19.8 +/- 0.3 A. This value was significantly smaller than that of Ca2+/CaM (21.9 +/- 0.3 A), which adopted a dumbbell structure and was conversely 2-3 A larger than those of the complexes of Ca2+/CaM with the nonmyristoylated target peptides of myosin light chain kinase or CaM kinase II, which adopted a compact globular structure. The pair distance distribution function had no shoulder peak at around 40 A, which was mainly due to the dumbbell structure. These results suggest that Ca2+/CaM interacts with Nalpha-myristoylated CAP-23/NAP-22 differently than it does with other nonmyristoylated target proteins. The N-terminal amino acid sequence alignment of CAP-23/NAP-22 and other myristoylated proteins suggests that the protein myristoylation plays important roles not only in the binding of CAP-23/NAP-22 to Ca2+/CaM, but also in the protein-protein interactions related to other myristoylated proteins.

Amino Acid Sequence↗
PubMed2000

Significance of Fas antigen-mediated apoptosis in human fulminant hepatic failure.

OBJECTIVE: The aim of this study was to elucidate the role of apoptosis in human fulminant hepatic failure. We studied the expression of Fas antigen on liver tissues, Fas ligand in lymphocytes, and soluble Fas ligand in patients' serum. METHODS: On finding apoptotic cells in fulminant hepatic failure liver, we first examined them using the TUNEL method. Subsequently, the expression of Fas was studied by immunostaining. Simultaneously, Fas ligand presenting on both liver-infiltrated cells and peripheral lymphocytes was studied by reverse transcription-polymerase chain reaction, and soluble Fas ligand in sera was measured by ELISA. RESULTS: By using the TUNEL method, we first demonstrated that many apoptotic cells existed in fulminant hepatic failure but not in normal ones. Our immunohistochemistry study showed that many hepatocytes in fulminant hepatic failure strongly expressed Fas. In addition, Fas ligand on both liver-infiltrating lymphocytes and peripheral lymphocytes in fulminant hepatic failure patients was detected. The serum level of soluble Fas ligand was significantly increased in fulminant hepatic failure (mean value, 2.91 ng/ml in fulminant hepatic failure [n = 10], 1.62 ng/ml in acute hepatitis [n = 10], and 0.27 ng/ml in healthy controls [n = 10]). Furthermore, this serum level of sFas ligand was significantly associated with prothrombin time both in acute hepatitis and fulminant hepatic failure. CONCLUSIONS: The present results indicate that Fas-mediated apoptosis may be one of the triggers for the induction of fulminant hepatic failure.

Adult↗
PubMed2000

Significance of soluble TNF receptor-I in acute-type fulminant hepatitis.

OBJECTIVE: Fulminant hepatitis is associated with apoptosis of hepatocytes, which is mediated via Fas and tumor necrosis factor (TNF) receptors. The clinical significance of apoptotic factors and these receptors was investigated in fulminant hepatitis. METHODS: Serum levels of TNF-alpha, soluble TNF receptor-I and -II, soluble Fas antigen, and Fas ligand were measured. Then, the relationships between these parameters and the severity or prognosis of fulminant hepatitis were studied. RESULTS: Serum levels of TNF-alpha, soluble TNF receptor-I, and soluble TNF receptor-II were increased in acute-type fulminant hepatitis. In particular, soluble TNF receptor-I was significantly higher than in patients with subacute-type fulminant hepatitis, severe acute hepatitis, acute hepatitis, or healthy controls. The soluble TNF receptor-I level continued to increase or remained high in patients who died of acute-type fulminant hepatitis, and eight of nine patients had a level >10 ng/ml. In contrast, the soluble TNF receptor-I level remained <10 ng/ml in survivors. Soluble Fas and soluble Fas ligand levels tended to increase in all types of acute liver disease and were not specific to fulminant hepatitis. CONCLUSION: Our findings suggested that monitoring the soluble TNF receptor-I level may help to assess the prognosis of acute-type fulminant hepatitis and that TNF might be associated with massive hepatic necrosis.

Acute Disease↗
PubMed2000

[A recurrent case of amebic liver abscess seventeen years after the first occurrence].

A 49-year-old male who had been diagnosed as having amebic liver abscess when he was 32-year-old was admitted to our hospital with fever and watery diarrhea. Ultrasonography and CT examination demonstrated a solitary abscess in the right lobe of the liver. Cysts of Entamoeba histolytica were detected in the stool and an aspiration of the liver abscess looked like anchovy paste. Serum amebic antibody by the IFA method was positive and the case was diagnosed as amebic liver abscess. The patient was treated with metronidazole, and percutaneous transhepatic abscess drainage was performed. The liver abscess decreased remarkably in size and serum amebic antibody was negative after the treatment. Recurrence of amebic liver abscess is rare and we report this case with some literature.

Humans↗
PubMed2000

Identification of multiple transcription factors, HLF, FTF, and E4BP4, controlling hepatitis B virus enhancer II.

Hepatitis B virus (HBV) enhancer II (EnII) is a hepatotropic cis element which is responsible for the hepatocyte-specific gene expression of HBV. Multiple transcription factors have been demonstrated to interact with this region. In this study, the region from HBV nucleotides (nt) 1640 to 1663 in EnII was demonstrated to be essential for enhancer activity and to be another target sequence of putative transcription factors. To elucidate the factors which bind to this region, we used a yeast one-hybrid screening system and cloned three transcription factors, HLF, FTF, and E4BP4, from a human adult liver cDNA library. All of these factors had binding affinity to the sequence from nt 1640 to 1663. Investigation of the effects of these factors on transcriptional regulation revealed that HLF and FTF had stimulatory activity on nt 1640 to 1663, whereas E4BP4 had a suppressing effect. FTF coordinately activated both 3. 5-kb RNA and 2.4/2.1-kb RNA transcription in a transient transfection assay with an HBV expression vector. HLF, however, activated only 3.5-kb RNA transcription, and in primer extension analysis, HLF strongly stimulated the synthesis of pregenome RNA compared to precore RNA. Thus, FTF stimulated the activity of the second enhancer, while HLF stimulated the activity of the core upstream regulatory sequence, which affects only the core promoter, and had a dominant effect on the pregenome RNA synthesis.

Base Sequence↗
PubMed2000

A combinatorial code for gene expression generated by transcription factor Bach2 and MAZR (MAZ-related factor) through the BTB/POZ domain.

Bach2 is a B-cell- and neuron-specific transcription repressor that forms heterodimers with the Maf-related oncoproteins. We show here that Bach2 activates transcription by interacting with its novel partner MAZR. MAZR was isolated by the yeast two-hybrid screen using the BTB/POZ domain of Bach2 as bait. Besides the BTB/POZ domain, MAZR possesses Zn finger motifs that are closely related to those of the Myc-associated Zn finger (MAZ) protein. MAZR mRNA was coexpressed with Bach2 in B cells among hematopoietic cells and in developing mouse limb buds, suggesting a cooperative role for MAZR and Bach2 in these cells. MAZR forms homo- and hetero-oligomers with Bach2 through the BTB domain, which oligomers bind to guanine-rich sequences. Unlike MAZ, MAZR functioned as a strong activator of the c-myc promoter in transfection assays with B cells. However, it does not possess a typical activation domain, suggesting a role for it as an unusual type of transactivator. The fgf4 gene, which regulates morphogenesis of limb buds, contains both guanine-rich sequences and a Bach2 binding site in its regulatory region. In transfection assays using fibroblast cells, the fgf4 gene was upregulated in the presence of both MAZR and Bach2 in a BTB/POZ domain-dependent manner. The results provide a new perspective on the function of BTB/POZ domain factors and indicate that BTB/POZ domain-mediated oligomers of transcription factors may serve as combinatorial codes for gene expression.

Amino Acid Sequence↗
PubMed2000

Bax is downregulated in inflamed colonic mucosa of ulcerative colitis.

BACKGROUND AND AIMS: One form of epithelial cell injury in inflamed colonic mucosa in ulcerative colitis (UC) is reported to involve apoptosis of these cells. Bcl-2 family proteins Bax and Bcl-2 are the major regulators of apoptosis. The aim of this study was to elucidate the involvement of the Bax/Bcl-2 system in induction of apoptosis of the inflamed colonic epithelium in UC. METHODS: Colonic epithelium was isolated from colonic biopsy specimens. Expression of CD95, Bax, Bcl-xL, and Bcl-2 proteins was determined by western blotting. Bax gene expression was assessed by both reverse transcription-polymerase chain reaction (RT-PCR) followed by Southern hybridisation and a real time PCR assay. RESULTS: Equal levels of expression of CD95, Bcl-xL, and Bcl-2 proteins were noted in normal and UC colonic epithelia. Equal levels of expression of Bax protein and mRNA were noted in epithelia of normal colon and inactive UC. Levels of expression of Bax protein and mRNA were markedly reduced in inflamed UC colonic epithelium. CONCLUSIONS: Our study showed for the first time downregulation of Bax in inflamed colonic epithelium of UC. The Bax/Bcl-2 system did not seem to be involved in induction of apoptosis of epithelial cells in the inflamed colonic mucosa of UC.

Adult↗