[Pseudolymphoma of the liver].
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Diagnosis, Differential↗
Biomedical subjects
Y Tanabe
Publications and source records attributed to Y Tanabe.
Release of endogenous ATP from the caudal artery in rats with arteriosclerosis.
Noradrenaline significantly increased (by a prazosin-sensitive mechanism) the overflow of ATP and its metabolites from the caudal arteries of rats treated with excess vitamin D2 and a high-cholesterol diet (arteriosclerotic rats), although the amount of the overflow was smaller than that in the normal rats. The arteries from the arteriosclerotic rats showed a marked increase in the calcium content and there was a significant negative correlation between the noradrenaline-induced overflow of ATP and the arterial calcium content. These findings indicate that ATP release from arteriosclerotic rat caudal arteries mediated by alpha 1-adrenoceptors is impaired in proportion to the extent of arterial calcification.
Adenosine Diphosphate↗
[Evaluation of bone marrow by opposed phase T1-weighted images and enhanced MR imaging].
We investigated bone marrow in a control group, cases of aplastic anemia and post-irradiation patients by examining T1-weighted (T1WI), short TI inversion recovery (STIR), opposed phase T1WI (op-T1WI) and Gd-DTPA enhanced op-T1WI images obtained by 0.5T MRI. Bone marrow was classified into four types based on MR findings. Normal marrow showed low intensity on op-T1WI and STIR images without enhancement (I). Fatty marrow, which showed high intensity on T1WI and op-T1WI images was observed in aplastic anemia and post-irradiation patients (II). Hematopoietic marrow (III) showed low intensity on op-T1WI and enhanced, while active hematopoietic marrow (IV) revealed high intensity on both STIR and op-T1WI images and was enhanced following Gd-DTPA infusion. Aplastic anemia of moderate grade included types II, III and IV. Enhanced MR was needed to differentiate between types I and III since both types showed low intensity on op-T1WI images. Furthermore, type IV was considered as hyperplastic compared with type III. Enhanced MR and op-T1WI images were useful in evaluating hematopoiesis of bone marrow.
Adolescent↗
Behavior of a falling paper.
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Journal Article↗
A new point mutation at nucleotide pair 3291 of the mitochondrial tRNA(Leu(UUR)) gene in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
A new point mutation at nucleotide pair 3291 in the mitochondrial tRNA-Leu(UUR) gene was found in a Japanese MELAS patient. The nucleotides at the mutated site were evolutionarily invariant from humans through sea urchins. The mutant genomes were detected in a heteroplasmic fashion in muscle and blood cells of the proband by means of PCR-RFLP. Among 46 MELAS, 5 MERRF, 23 CPEO and 55 normal controls examined, this is the only patient with the mutation. This is the third mutation associated with MELAS in addition to nucleotides at 3243 and 3271. All three mutations occurred within the tRNA-Lue(UUR) region indicating that the tRNA alteration is responsible for the MELAS phenotype.
Animals↗
A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA.
BACKGROUND: Several families have been described in which a mutation of mitochondrial DNA, the substitution of guanine for adenine (A-->G) at position 3243 of leucine transfer RNA, is associated with diabetes mellitus and deafness. The prevalence, clinical features, and pathophysiology of diabetes with this mutation are largely undefined. METHODS: We studied 55 patients with insulin-dependent diabetes mellitus (IDDM) and a family history of diabetes (group 1), 85 patients with IDDM and no family history of diabetes (group 2), 100 patients with non-insulin-dependent diabetes mellitus (NIDDM) and a family history of diabetes (group 3), and 5 patients with diabetes and deafness (group 4) for the mutation. We also studied the prevalence and characteristics of diabetes in 39 patients with a syndrome consisting of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes who were known to have the mutation and 127 of their relatives (group 5). RESULTS: We identified 16 unrelated patients with diabetes associated with the A-->G mutation: 3 patients from group 1 (6 percent), 2 patients from group 3 (2 percent), 3 patients from group 4 (60 percent), and 8 patients from group 5 (21 percent). We also identified 16 additional subjects who had diabetes and the mutation among 42 relatives of the patients with diabetes and the mutation in groups 1, 2, 3, and 4 and 20 affected subjects among the 127 relatives of the patients in group 5. Diabetes cosegregated with the mutation in a fashion consistent with maternal transmission, was frequently (in 61 percent of cases) associated with sensory hearing loss, and was generally accompanied by impaired insulin secretion. CONCLUSIONS: Diabetes mellitus associated with the A-->G mutation at position 3243 of mitochondrial leucine transfer RNA represents a subtype of diabetes found in both patients with IDDM and patients with NIDDM in Japan.
Adolescent↗
Floor plate and motor neuron induction by vhh-1, a vertebrate homolog of hedgehog expressed by the notochord.
The differentiation of distinct cell types in the ventral neural tube depends on local inductive signals from the notochord. We have isolated a vertebrate homolog of the Drosophila segment polarity gene hedgehog (hh) from zebrafish and rat, termed vhh-1. vhh-1 is expressed in the node, notochord, floor plate, and posterior limb bud mesenchyme. Each of these cell groups has floor plate inducing activity, suggesting that the vhh-1 gene may encode a floor plate-inducing molecule. Widespread expression of rat vhh-1 in frog embryos leads to ectopic floor plate differentiation in the neural tube. In vitro tests for the signaling functions of vhh-1 demonstrate that COS cells expressing the rat vhh-1 gene induce floor plate and motor neuron differentiation in neural plate explants. vhh-1 may, therefore, contribute to the floor plate and motor neuron inducing activities of the notochord.
Amino Acid Sequence↗
Constitutive expression of TNF-alpha and -beta genes in mouse embryo: roles of cytokines as regulator and effector on development.
1. Using the RT/PCR method, we examined mRNA expression of several inflammatory factors in mouse embryos during mid-late embryonal development. mRNAs of tumor necrosis factor (TNF)-alpha, TNF-beta, their receptors (TNF-RI, TNF-RII), transforming growth factor (TGF)-beta, were expressed constitutively in most of the embryonic tissues. 2. While mRNAs of other factors, interleukin (IL)-1 alpha, IL-1 beta, IL-3, IL-6, granurocyte-colony stimulating factor (G-CSF), leukaemia inhibitory factor (LIF), and interferon (IFN)-gamma were only limitedly expressed. 3. The mRNAs of several complement components (C2, C3, C4, C5) and receptors (CR1, CR2) were also detected. Among them, the expression of C3 and CR1 were prominent. These results strongly support our idea that inflammation-like system play an important role to regulate embryogenesis.
Animals↗
Enhanced production of tumour necrosis factor alpha (TNF-alpha) by its precursor on the cell surface of primed THP-1 cells.
To clarify the biological significance of tumour necrosis factor alpha (TNF-alpha) precursor, we analysed its expression at the primed and triggered stages using human monocyte-like cell line THP-1. To prime them, THP-1 cells were treated with either recombinant human interferon gamma (rIFN-gamma) or recombinant human tumour necrosis factor alpha (rTNF-alpha). At the primed stage, transient accumulation of TNF-alpha, mRNA and a small amount of 26-KDa TNF-alpha precursor was observed, and the precursor molecule was located on the cell surface. Following treatment of the primed cells with bacterial lipopolysaccharide (LPS), augmentation of transcription of TNF-alpha mRNA and production of a larger amount of TNF-alpha precursor were observed followed by secretion of a larger amount of mature TNF-alpha (17-KDa) than secreted by the unprimed cells (triggered stage). This suggests that with priming THP-1 cells might be changed to a stage where they are ready for production of a larger amount of TNF-alpha at the triggered stage. When either primed or unprimed THP-1 cells were pretreated with anti-TNF-alpha antibody, augmentation of TNF-alpha production by primed THP-1 cells was specifically suppressed, suggesting that TNF-alpha precursor itself may play an important role in the enhancement of TNF-alpha production by the primed macrophages after treatment with LPS.
Cell Line↗
Clinical evaluation and bacterial survey in infants and young children with diarrhoea in the Santa Cruz district, Bolivia.
Clinical and laboratory studies on a total of 211 of infants and young children admitted to the National Santa Cruz General Hospital for various types of diarrhoea during 1991-1992 are described. A peak cluster was observed in children aged 1 year of which 80 per cent were acute diarrhoea and the remaining 20 per cent were prolonged or chronic diarrhoea. The major bacterial pathogen was enteropathogenic Escherichia coli. Other bacterial pathogens such as Klebsiella, Shigella, Cholera, etc., were detected. Ascaris, E. histolytica, Giardia and Ankylostoma were also detected. Many of the patients infected with enteropathogenic E. coli showed elevated serum titre to these bacterial antigens. Most of the detected E. coli and Shigella revealed that they were resistant to ampicillin, trimethoprim/sulfamethoxazole, and erythromycin, and some were resistant to gentamycin and chloramphenicol in vitro tests. It was difficult to make a diagnosis by clinical diagnosis alone for cholera of the el Tor Ogawa type. The detection of faecal leukocytes seems to be an useful predictor for diagnosis of invasive diarrhoea with mucobloody stools. Faecal pH and erythrocytes did not seem to be reliable diagnostic predictors. Fourteen cases (7 per cent) died of diarrhoeal disease. Many of them had complications with marked dehydration, hypoelectrolytaemia, malnutrition and infections, and rapid deterioration within 10 days despite rehydration therapy. Timely rapid rehydration and restoration of electrolytes followed by suitable management of complications are necessary.
Age Distribution↗
Central nervous system abnormalities in chromosome deletion at 11q23.
Two Japanese pediatric patients with terminal deletion of the long arm of chromosome 11 are described. Both had the morphological abnormalities of the 11q deletion syndrome, such as prominent epicanthal folds, broad flat nasal bridge with short, upturned nose, short philtrum with carp-shaped mouth, cardiac anomalies and nonprogressive moderate psychomotor developmental delay. Patient 1 is the first case to be reported with 11q deletion with serial magnetic resonance (MR) examinations of cerebral white matter. The initial MR imaging studies demonstrated multiple areas of T1 and T2 prolongation in the cerebral white matter in both patients at the ages of 2 5/12 and 2 1/12 years, respectively. A second MR imaging, performed 1 year after the first in Patient 1, demonstrated slight improvement of the lesions. Neither patient showed clinical deterioration. These results suggest that the lesions were caused by delayed myelination, rather than by demyelination. It is suggested that an unknown factor which is important for myelination is located on the long arm of chromosome 11: perhaps the neural cell adhesion molecule (NCAM).
Abnormalities, Multiple↗
A comparative magnetic resonance imaging study of the corpus callosum in neurologically normal children and children with spastic diplegia.
To determine the extent of brain damage in children with spastic diplegia, we analyzed the true midsagittal magnetic resonance imaging findings for the corpus callosum in 43 children with spastic diplegia and in 69 neurologically normal children. In the normal children, the thicknesses of the genu, midbody, splenium and the entire corpus callosum were found to increase with age, while the ratios of the thickness of the splenium and of the midbody to the length were constant, regardless of age. Both ratios were significantly reduced in diplegic children and the ratio for the splenium was highly correlated with the extent of motor impairment. Assessment of the morphometric changes in the corpus callosum using magnetic resonance imaging may contribute to the determination of the extent of brain damage in diplegic children.
Adolescent↗
MRI changes and deficits of higher brain functions in preterm diplegia.
Forty-one preterm children (29 with spastic diplegia and 12 without motor deficits) who had a normal verbal IQ were studied to clarify the clinical significance of neuroanatomical abnormalities disclosed by T1-weighted and T2-weighted magnetic resonance imaging (MRI). Both types of images clearly showed abnormalities in the frontal corona radiata of the children with spastic diplegia, while there were no abnormalities in the children without motor deficits. We compared the T1-weighted imaging findings with deficits of higher brain functions, evaluated by the performance subtests of the Wechsler Intelligence Scale. Thinning of the parietal and/or occipital white matter was noted in children with visuospatial cognitive deficits. Thus, MRI may be helpful in confirming early clinical suspicions of visuospatial cognitive deficits as well as motor deficits in preterm children, especially those with spastic diplegia.
Brain↗
Effect of digoxin on exercise performance in mildly symptomatic patients with idiopathic dilated cardiomyopathy and sinus rhythm.
The purpose of this investigation was to evaluate the effect of digoxin on aerobic performance in mildly symptomatic patients with congestive heart failure and sinus rhythm. Ten patients (8 men and 2 women) with idiopathic dilated cardiomyopathy (ejection fraction 17 to 33%, mean 27 +/- 4%) who were stable and mildly symptomatic with maintenance digoxin and diuretic therapy were studied. All patients underwent maximal symptom-limited ergometer exercise with analysis of respiratory gases during maintenance digoxin therapy, 4 weeks after digoxin withdrawal, and 4 weeks after digoxin readministration. Exercise capacity was assessed by peak oxygen uptake and anaerobic threshold. Serum digoxin concentration was 1.0 to 1.8 (mean 1.3 +/- 0.2) ng/ml during digoxin therapy, and less than the detectable level after digoxin withdrawal. No patients showed clinical deterioration after digoxin withdrawal. Peak oxygen uptake after digoxin withdrawal (23.7 +/- 3.0 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (23.8 +/- 2.5 ml/kg/min) or after digoxin readministration (24.1 +/- 2.9 ml/kg/min). The anaerobic threshold after digoxin withdrawal (14.9 +/- 2.5 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (15.0 +/- 2.1 ml/kg/min) or after digoxin readministration (14.9 +/- 2.2 ml/kg/min). No differences in heart rate and diastolic blood pressure were observed during exercise, but systolic blood pressure during exercise was significantly higher with digoxin therapy (p < 0.05). These results suggest that digoxin has no effect on aerobic performance in mildly symptomatic patients with idiopathic dilated cardiomyopathy and sinus rhythm.
Adult↗
Clinical and angiographic characteristics of patients with multivessel coronary spasm in variant angina. Significance of progressive course of angina and disease activity.
The purpose of this study was to investigate the incidence of multivessel coronary spasm and compare the clinical characteristics between patients with and without multivessel coronary spasm. In variant angina, it is controversial whether coronary hyperreactivity to vasoconstrictor stimuli is localized to a segmental lesion in only one coronary artery. Moreover, the clinical characteristics of patients with multivessel coronary spasm have never been investigated. Sixty-three patients (51 men and 12 women; mean age, 56 years; range 35-72 years) with variant angina and documented ST-segment elevation during a spontaneous attack underwent spasm provocation testing with selective intracoronary injection of ergonovine. All but 4 patients who experienced spontaneous attacks during cardiac catheterization had induced coronary spasm associated with ST-segment elevation and chest pain. Multivessel coronary spasm was found in 27 (43%) of 63 patients. By univariate analysis, a high frequency of angina (> or = 3 times/week), occurrence of a spontaneous attack within 24 hours after withdrawal of medication, a long history of angina and a progressive course of angina were significantly associated with multivessel coronary spasm. Multivariate analysis indicated a positive correlation between multivessel coronary spasm and progressive angina. Multivessel coronary spasm was found in 43% of patients with variant angina. Patients with multivessel coronary spasm have some unique clinical features. These results may increase the understanding of the pathophysiology and natural course of variant angina.
Adult↗
Distribution of substance P-containing and catecholaminergic nerve fibers in the rabbit carotid body: an immunohistochemical study in combination with catecholamine fluorescent histochemistry.
The distribution of substance P (SP)-immunoreactive nerve fibers in the rabbit carotid body was studied in combination with catecholamine autofluorescence images of sections where SP immunoreactivity was confirmed. Immunoreactivity for SP was found in nerve fibers distributed in the parenchyma of the carotid body. No glomus cells with SP immunoreactivity were observed in the carotid body. On comparing the distribution of SP-immunoreactive fibers with the catecholamine autofluorescence image in a single section, most SP fibers appeared associated with the fluorescent glomus cells, and were located around clusters of them. These results support the suggestion that SP fibers in the cat and rat carotid bodies are involved in chemosensory mechanisms. Furthermore, a survey of the present results and previous ones reported by other workers indicates that SP may be an essential neuropeptide in chemoreceptor organs in most vertebrates from amphibians on upwards evolutionally. In addition, the courses of some catecholaminergic fibers precisely agreed with those of some SP fibers. This suggests that certain sympathetic nerve fibers also contain SP.
Animals↗
Delayed cerebral ischemia manifesting as peduncular hallucinosis after aneurysmal subarachnoid hemorrhage--three case reports.
Three cases of peduncular hallucinosis occurred in patients with aneurysmal subarachnoid hemorrhage. All patients underwent early clipping of the ruptured aneurysms of the anterior circulation. Several days after onset of subarachnoid hemorrhage, the patients complained of vivid visual hallucinations associated with abnormal sleep-waking rhythms, suggesting a diagnosis of peduncular hallucinosis. The hallucinations disappeared with administration of an increased dose of dobutamine. These findings indicated that peduncular hallucinosis might be a manifestation of delayed cerebral ischemia after subarachnoid hemorrhage. No other possible cause of neurological deficits such as hydrocephalus, cerebral infarcts, or metabolic encephalopathies was identified. Damage to the ascending reticular activating system has been implicated in the pathogenesis of peduncular hallucinosis. Cerebral vasospasm in the perforating arteries of the ascending reticular activating system was probably the cause of the hallucinosis in our patients.
Adult↗
Angina-linked syncope and lack of calcium antagonist therapy predict cardiac arrest before definitive diagnosis of vasospastic angina.
BACKGROUND: Several prognostic factors have been identified in patients with vasospastic angina; however, factors that would predict potentially fatal cardiac arrest during the period between the onset of angina and its definitive diagnosis remain unknown. We investigated the predictive value of the clinical findings that are available when a patient is hospitalized after a cardiac arrest but before a definitive diagnosis of vasospastic angina is made. METHODS: We compared the clinical findings in 11 patients who experienced cardiac arrest before vasospastic angina was definitively diagnosed (group I) with 81 patients with vasospastic angina without cardiac arrest (group II). The definitive diagnosis of vasospastic angina was made on the basis of results of coronary spasm provocation test or ECGs during spontaneous attacks, or both. RESULTS: The incidence of angina-linked syncope was significantly higher in group I than in group II (six out of 11 versus nine out of 81, P < 0.005). Significantly fewer group I patients were receiving calcium antagonists than group II patients (three out of 11 versus 63 out of 81, P < 0.005). Serious arrhythmias were significantly more common in group 1 than in group II (seven out of 11 versus 12 out of 81, P < 0.005). Logistic regression analysis of the eight clinical variables available when first seen in the hospital indicated that angina-linked syncope and the lack of calcium antagonist therapy were independently related to risk of cardiac arrest. CONCLUSIONS: From the clinical findings available, a history of angina-linked syncope and lack of calcium antagonist therapy were found to be independent predictors of cardiac arrest before a definitive diagnosis had been made. Patients who have suspected vasospastic angina may benefit from early treatment with calcium antagonists if they have a history of angina-linked syncope.
Aged↗