Sleep induced by the administration of melatonin (5-methoxyn-acetyltryptamine) to the hypothalamus in unrestrained cats.
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Animals↗
Biomedical subjects
N Yamaguchi
Publications and source records attributed to N Yamaguchi.
Novel leukemic lymphoma with probable derivation from immature stage of natural killer (NK) lineage in an aged patient.
A 66-year-old male patient was admitted with dyspnea; physical examination revealed petechiae and systemic lymphadenopathy. Laboratory findings showed leukemia. The blasts in the peripheral blood were negative for cytochemical myeloperoxidase, and had condensed nuclear chromatin with a nucleolus. The histological diagnosis of the biopsied neck lymph node was lymphoblastic lymphoma. The leukemia cells expressed CD2, CD6, CD7, CD13low, CD56, beta chain of IL-2 receptorlow (IL-2R beta), and HLA-DR antigens, but not other pan-T (CD5, CD3, CD4, and CD8); pan-B (CD10, CD19, CD20, and CD24); natural killer (NK) (CD16, CD57); or myeloid (CD33) antigens. Electronmicroscopy revealed convoluted nuclei with conspicuous nucleoli and peripherally condensed heterochromatin. Membrane-bound granules containing an electron dense matrix were observed in the cytoplasm, indicating the NK cell nature of the neoplastic cells. While terminal deoxynucleotidyl transferase (TdT) and cytoplasmic CD3 were not detected by immunofluorescence on fixed smears, Northern blot analysis revealed the gene expression of CD3 epsilon, CD3 zeta, and TdT. Gene rearrangement analysis revealed that the beta, gamma, and delta chains of T-cell receptor (TCR) and immunoglobulin heavy chain (IgH) were of germline genotype. While the overall interpretation of the phenotype and genotype was difficult, the derivation of an immature stage of NK lineage was strongly suggested, based predominantly on the electronmicroscopic features. Despite initially successful chemotherapy, the patient died 14 months after initial presentation.
Aged↗
Use of epithelial cell cultures for studies on the mechanism of transformation by chemical carcinogens.
Evidence is reviewed for and against four major theories of chemical carcinogenesis. The development of several normal and transformed epithelial cell lines which should be useful for the analysis of this problem is described. The detection of RNA viral particles in cells transformed with chemical carcinogens is a recurrent finding in studies from our own and other laboratories, but the significance of these particles in terms of the mechanism of chemical carcinogenesis remains to be determined. Finally, we have described the first mutants of chemically transformed epithelial cells which are temperature sensitive in the maintenance of the transformed phenotype. These mutants should be particularly useful for detecting the critical biochemical changes that distinguish a chemically induced tumor cell from its normal counterpart.
Carcinogens↗
Therapeutic ethanol injection of hepatocellular carcinomas undetectable by angiography and Lipiodol computed tomography.
Seven smaller than 2 cm in diameter hepatocellular carcinomas (HCC) undetectable by hepatic arteriography and computed tomography (CT) after intraarterial injection of iodized oil (Lipiodol CT) were diagnosed by ultrasonography-guided fine-needle biopsy in 6 patients. All lesions were treated by percutaneous ethanol injection (PEI) in 1-3 weekly intervals. No recurrences have been demonstrated after 7-15 months. The treatment of HCCs undetectable by angiography and Lipiodol CT presents a problem as transcatheter arterial embolization is considered ineffective due to poor vascularity. PEI appears to be an excellent treatment for these small HCCs.
Aged↗
Anomalous insertion of the superior or the inferior vena cava into the right atrium.
Three cases with anomalous insertion of the superior or inferior vena cava into the right atrium are presented. One case was a 25-year-old healthy man with anomalous low insertion of the right superior vena cava into the right atrium. The remaining two cases were infants with complex cardiac anomalies showing anomalous high insertion of the inferior vena cava into the right atrium. The congenital anomalies of the connection between the superior and the inferior vena cava and the right atrium are rare. Angiographic and computed tomographic findings of these anomalies were reported.
Adult↗
Superselective intraarterial chemotherapy in combination with irradiation: preliminary report.
Since 1984, a new method for the intraarterial administration of antineoplastic drugs, termed "superselective intraarterial chemotherapy," has been used in combination with simultaneous irradiation in the treatment of 49 patients with squamous cell carcinoma of the head and neck. Under the fluoroscope, a retrograde catheter is inserted into the superficial temporal artery and the tip is led selectively into the main feeding artery of the tumor. In our series of 49 patients, catheter-related complications occurred in only 12.5%. Forty-five patients (91.8%) completed more than 80% of the planned irradiation dosage. The therapeutic effect was excellent. The initial response rate was 100%. Systemic toxicity was uncommon, but local mucositis was frequent in the infused area. These results demonstrate that this new combined therapy is easy, safe, effective, and confers the highest possible initial response rate.
Adult↗
Endogenous atrial natriuretic factor after endopeptidase 24.11 inhibition by Thiorphan.
The neutral endopeptidase 24.11 (NEP) was shown to degrade atrial natriuretic factor (ANF) in kidney membranes. An infusion of Thiorphan (25 micrograms/min/kg x 90 min), a specific NEP inhibitor, induced an increase in plasma ANF (65 +/- 26 to 163 +/- 52 pg/ml), plasma renin activity and in norepinephrine concentrations at 50 minutes of infusion in conscious rabbits. The increase in plasma ANF was accompanied by a gradual decrease in renal blood flow, despite maintenance of a stable mean arterial pressure. In conclusion, Thiorphan infusion produced an increase in endogenous plasma ANF. However, it may also have affected other hormonal systems which may have contributed to the overall dynamic and hormonal profile documented.
Aldosterone↗
The prevalence of Rett syndrome in Fukui prefecture.
The present study was performed to estimate the prevalence of Rett syndrome in Fukui prefecture by sending questionnaires to special classes (classes for handicapped children in schools for normal children) and schools for mentally/physically handicapped children, and observing children suspected of having this syndrome on the basis of answers to the questionnaire. The subjects were girls aged 6-14 years who were attending 11 special classes and 7 schools for handicapped children. The prevalence of Rett syndrome was estimated to be 0.22 per 10,000 girls aged 6-14 years in Fukui prefecture, as of April 1, 1993. The prevalence noted in this study was lower than those found in previous studies in Japan and Western countries.
Adolescent↗
Ultrastructural fragility and type IV collagen abnormality of the anterior lens capsules in a patient with Alport syndrome.
PURPOSE: To investigate ultrastructural and immunohistological abnormalities of the lens capsules in a patient with Alport syndrome. METHODS: Two anterior lens capsules were obtained at phacoemulsification from a 43-year-old female patient with bilateral lenticonus who was affected by Alport syndrome. The right capsule was examined by transmission electron microscopy and the left capsule was stained with two monoclonal antibodies against the triple-helical domains of type IV collagen alpha2 and alpha5 chains. RESULTS: Numerous vertical dehiscences with many disrupted interdigitations were observed in the right anterior lens capsule. Decreased reactivity of monoclonal antibodies against type IV collagen alpha5 chain and normal reactivity against the alpha2 chain were shown in the left anterior lens capsule. CONCLUSION: The ultrastructural fragility of the anterior lens capsules in this patient with Alport syndrome appears to be associated with the abnormality of the type IV collagen molecules including the alpha5 chain.
Adult↗
Redox reaction of poly(ethylene oxide)-modified hemoglobin in poly(ethylene oxide) oligomers at 120 degrees C.
Human hemoglobin, modified with poly(ethylene oxide) with average molecular weight of 3500 (PEO-Hb) was dissolved in PEO200 (molecular weight of 200) containing 0.5 M KCl. A quasi-reversible redox reaction of the PEO-Hb was found in PEO oligomers by alternatingly changing the potential polarity (+/- 1.2 V vs Ag). The PEO-Hb showed redox reactions in PEO200 even at 120 degrees C. PEO modification was concluded to give the thermal stability in some extent. In phosphate buffer at 70 degrees C, the electrochemical redox reaction of native Hb was not observed spectroscopically, but that of PEO-Hb was detected. The most effective factor was, however, concluded to be the use of PEO oligomers as a solvent. The molecular motion of PEO oligomers should be milder than that of water at higher temperature. This lower molecular motion was suggested to keep the redox activity of PEO-Hb in the PEO oligomer at 120 degrees C. However, the PEO-Hb in PEO200 was stable in the oxidized form at 30 degrees C; it was reduced without giving potential at 120 degrees C. Cyclic voltammetry revealed that this autoreduction was attributed to the shift of redox potential with elevating temperature.
Electrochemistry↗
Antiepileptic effects under steady state of phenytoin serum levels produced in acute experiments.
The antiepileptic effects of phenytoin (PHT) were examined during steady-state serum levels. Experiments were conducted on 69 adult male rabbits weighing 2.5-3.5 kg. A steady state of one or two different PHT serum levels per rabbit was produced with intravenous (i.v.) injections of loading and infusion doses. A train of focal and generalized seizure discharges (SDs) induced by electrical stimulation was compared before and after dosing with PHT. The results showed that PHT levels of 10-40 micrograms/ml induce inhibitory effects, shortening the duration of neocortical focal SDs. The inhibitory effects paralleled the PHT levels and were proportionally related to epileptogenicity in individual neocortical areas. At serum levels under approximately 5-10 micrograms/ml, the spread of secondarily generalized SDs originating from neocortical focal SDs was suppressed more than the shortening of the duration of the primary focus. On the other hand, PHT showed no effects or only slight inhibitory effects on hippocampal SDs, and the SDs spread from them even at levels of 15-40 micrograms/ml. Electroshock (ES)-induced generalized SDs were slightly suppressed in duration at levels of 20-30 micrograms/ml. Moreover, both the focal and the generalized SDs were greatly prolonged at high serum levels (greater than 40 micrograms/ml), although such facilitative effects were rare. The clinical contributions of these results to PHT treatment in human epilepsy are discussed.
Animals↗
A new experimental model for drug studies: effects of phenobarbital and phenytoin on photosensitivity in the lateral geniculate-kindled cat.
Photosensitivity was acquired as a result of kindling in the lateral geniculate body (GL), and the GL-kindled cat pretreated with DL-allylglycine showed a stable level of photosensitivity. To test the usefulness as a model for the evaluation of anticonvulsant drugs, the effects of phenobarbital (PB) and phenytoin (PHT) on photosensitivity were studied in the GL-kindled cat under DL-allylglycine. PB (5 and 10 mg/kg intravenously, i.v.) completely suppressed photically induced seizures in most subjects at plasma concentrations of 7-16 micrograms/ml, and this anticonvulsant action persisted for at least 4 h after the injection. PHT (15 mg/kg, i.v.) at plasma concentrations of 9-15 micrograms/ml produced toxic signs, e.g., pupil dilatation, hypersalivation, and tachypnea. At this dose, PHT was inactive against photically induced myoclonus but prevented the elicitation of a generalized tonic-clonic convulsion. From these results showing that the effects of anticonvulsant drugs on photically induced seizures can be assessed in relation to plasma concentration and acute neurologic toxicity, we suggest that the GL-kindled cat is a potentially useful animal model of epilepsy for testing the efficacy of anticonvulsant drugs.
Allylglycine↗
PACAP enhances stimulation-induced norepinephrine release in canine pancreas in vivo.
The present study was to investigate whether pituitary adenylate cyclase activating polypeptide (PACAP) can modify norepinephrine (NE) release in response to pancreatic nerve stimulation in anesthetized dogs. Plasma catecholamine concentrations in aortic and superior pancreaticoduodenal (SPD) venous blood were determined by a high performance liquid chromatography method. SPD venous blood flow was measured with an electromagnetic flowmeter. Pancreatic nerves were directly stimulated for 1 min (2 ms, 12 V) at various frequencies at the level of the SPD artery. Various doses of PACAP1-27 (PACAP27) were locally infused into the pancreas through the SPD artery. Nerve stimulation significantly increased both SPD venous NE concentration and its output from the pancreas in a frequency-dependent manner. With PACAP27 alone, neither SPD venous NE concentration nor its output changed significantly following the local administration of PACAP27 at any dose tested. In the presence of PACAP27, however, the net increases in NE concentration and its output in response to nerve stimulation at 2 Hz were significantly enhanced in a dose-dependent manner. The enhanced NE responses to nerve stimulation by PACAP27 were thus significantly greater than those obtained from the group receiving either PACAP27 or stimulation alone. Increases in NE concentration and its output induced by local administration of tyramine were virtually abolished by desipramine, a neural amine uptake inhibitor. However, the NE response to tyramine was not diminished by PACAP27. The results indicate that PACAP27 enhances the stimulation-induced NE release in the pancreas, and that this facilitatory effect of PACAP27 does not result from an inhibition of the neural amine uptake mechanism. The study suggests that PACAP receptor-mediated mechanisms may be involved either directly or indirectly in the local modulation of neural NE release in the canine pancreas in vivo.
Adrenergic Uptake Inhibitors↗
Inhibition by nifedipine of endothelin-induced adrenal catecholamine secretion in anesthetized dogs.
The present study was conducted to investigate local effects of endothelin-1 (ET-1) on basal adrenal catecholamine (CA) secretion and underlying mechanisms of action of ET-1 in anesthetized dogs. ET-1 was locally administered to the left adrenal gland through a catheter inserted into the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by an HPLC-electrochemical method. The local infusions (1 min, 0.5 mL/min) of ET-1, in doses of 0.01, 0.1, and 1.0 microgram/mL, resulted in a dose-dependent increase in epinephrine secretion, rising from an initial basal value of 6.9 +/- 1.4 ng.min-1 x g-1 to maximum values of 7.6 +/- 1.5, 81.1 +/- 38.3*, and 680.9 +/- 107.6* ng.min-1 x g-1 (*p < 0.05, n = 7), respectively. Neither mean arterial pressure nor plasma CA levels in aortic blood altered following ET-1 infusions. A similar dose-dependent increase in norepinephrine output was also observed with ET-1. Following the initial peak observed during infusion with the highest dose of ET-1, the output of both epinephrine and norepinephrine remained significantly elevated over a period of 30 min. This ET-1-induced, long-lasting increase in adrenal CA output was abolished by nifedipine (100 micrograms/mL) similarly administered 10 min before ET-1 infusion. The results indicate that ET-1 directly enhances the basal secretion of CA from dog adrenal medulla in vivo. The study suggests that the ET-1-induced increase in adrenal CA secretion is, at least in part, mediated by the opening of dihydropyridine-sensitive L-type calcium channels at the level of adrenal medullary chromaffin cells.
Adrenal Glands↗
Humoral immune response in Japanese acute hepatitis patients with hepatitis C virus infection.
The humoral immune response to acute infection by hepatitis C virus (HCV) is not yet perfectly clear in terms of immunoglobulin (Ig) response, diversity of HCV antigen, and the relation with hepatitis severity and antibody response. Serum IgM and IgG anti-HCV levels in patients with HCV and either acute hepatitis (AH) or fulminant hepatitis (FH) were investigated; the diversity of HCV antigen was investigated by RIBA test III. Of 22 AH patients, 12 (54.5%) were positive for IgM anti-HCV, mainly reacting to HCV core protein. The mean interval until the appearance of IgM anti-HCV after onset was 24.1+/-26.2 days. IgG anti-HCV mainly reacted to both core and NS-3 antigen, appearing 42.6+/-42.1 days after onset. From a serial study of 15 AH patients, it was considered that in seven AH patients (46. 7%), the IgM response would precede the IgG response. In another two AH patients, IgM anti-HCV was not detected during the acute disease phase. Of 48 chronic hepatitis patients with HCV-RNA, 40 patients were positive for IgM anti-HCV. Therefore, IgM anti-HCV was useful for diagnosis in some of the AH patients, but it was difficult to use for distinguishing between acute and chronic infection. All four FH patients with HCV-RNA were positive for both IgM and IgG antibody to HCV at onset. Their antibody titres were higher than those of AH patients. These results suggested that, as in FH due to HBV, FH due to HCV could induce strong and rapid humoral immunity.
Adolescent↗
Non-Alzheimer dementia with status spongiosus and neuronal cell loss showing unusual perineuronal structures and point mutation at 129 codon of prion protein.
The subject presented with intellectual decline followed by progressive muscle weakness of the bilateral upper limbs when he was 60 years old. He had a point mutation (methionin-valine) at 129 prion protein codon. He died at the age of 63 and necropsy revealed bilateral frontal lobe atrophy. The frontal cortex showed neuronal cell loss in layers II and III with spongiform change. Reusche silver impregnation technique for beta-peptide combined with ubiquitin immunostaining revealed perineuronal structures encircling degenerated neurons and ubiquitin-immunoreactive (IR) dot-like deposits. They were distributed particularly in the temporal neocortex and entorhinal cortex. They differed from either classic senile or diffuse plaque by the absence of amyloid core in the center and of amyloid fibrils. Ubiquitin-IR materials were also found as neuronal inclusions in the hippocampal granular cells. Nigral degeneration and neuronal loss in the hypoglossal nerve nucleus and in the anterior horn of the spinal cord were also found and spinal cord motoneurons had Bunina body inclusions. The clinical features and pathological findings were consistent with non-Alzheimer dementia with status spongiosus and neuronal cell loss. The unusual perineuronal structures found in our case might be a specific cellular pathology of dementia of the frontal lobe type.
Cell Death↗
Borrelia burgdorferi-seropositive chronic encephalomyelopathy: Lyme neuroborreliosis? An autopsied report.
A 36-year-old Japanese woman presented with progressive cerebellar signs and mental deterioration of subacute course after her return from the USA. Her serum antibody to spirochete Borrelia burgdorferi was significantly elevated. A necropsy 4 years after her initial neurological signs revealed multifocal inflammatory change in the cerebral cortex, thalamus, superior colliculus, dentate nucleus, inferior olivary nucleus and spinal cord. The lesions showed spongiform change, neuronal cell loss, astrocytosis and proliferation of activated microglial cells. The internal capsule was partially vacuolated and the spinal cord, notably at the thoracic level, was demyelinated and cavitated in the lateral funiculus. Microglial cells aggregated within and around the spongiform lesions and microglial nodules were present in the medulla oblongata. Use of Warthin-Starry stain demonstrated silver-impregnated organisms strongly suggesting B. burgdorferi in the central nervous tissues. The dentate nucleus and inferior olivary nucleus showed the most advanced lesions with profound fibrillary gliosis. Occlusive vascular change was relatively mild, and fibrous thickening of the leptomeninges with lymphocyte infiltrates was localized in the basal midbrain. The ataxic symptoms were due to the dentate and olivary nucleus lesions and mental deterioration was attributable to the cortical and thalamic lesions. Spongiform change, neuronal cell loss, and microglial activation are characteristic pathological features in the present case. The cerebellar ataxia and subsequent mental deterioration are unusual clinical features of Lyme neuroborreliosis. Spirochete B. burgdorferi can cause focal inflammatory parenchymal change in the central nervous tissues and the present case may be an encephalitic form of Lyme neuroborreliosis.
Adult↗
Age-related changes in nerve growth factor receptor immunoreactive neurons in the magnocellular basal forebrain system in rat brain--an immunocytochemical and morphometric study.
Morphometrical changes with aging in nerve growth factor receptor (NGFR) immunoreactive neurons in the basal forebrain were studied in juvenile and aged rat brains by means of NGFR immunohistochemistry. The nucleus basalis of Meynert (NBM) had cell loss and atrophy of NGFR immunoreactive neurons, and the horizontal nucleus of diagonal band of Broca (HNDB) showed only atrophy of these neurons. The medial septal nucleus and vertical nucleus of diagonal band of Broca had no significant change. Neuropil NGFR immunostaining was reduced in its intensity in the aged rats. As nerve growth factor is synthesized in the target areas and retrogradely transported to the nerve cell body within the basal forebrain and NGFR immunoreactive neurons are largely cholinergic ones, degeneration of NGFR-positive neurons in the basal forebrain may be related to a decreased cholinergic activity. The degeneration of the dendrites of NGFR-immunoreactive neurons were reported to be extensively found in the basal forebrain nuclei, in contrast, degeneration of the cell body of NGFR-immunoreactive neurons was confined to those in the NBM and HNDB in the present study. These findings suggest that atrophic changes in the dendrites precede those in the cell bodies of NGFR-immunoreactive neurons.
Aging↗