A case of arteriovenous hemangioma associated with liver cirrhosis.
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Aged↗
Biomedical subjects
F Otsuka
Publications and source records attributed to F Otsuka.
Hemodialysis neutropenia correlates with a decreased filterability and an increase in the number of cytoplasmic actin filaments in peripheral blood neutrophils, which is preceded by a decrease in the number of surface expression of L-selectin.
In order to clarify the precise cellular mechanism of hemodialysis neutropenia, we examined the changes in the viscoelasticity of peripheral blood neutrophils using both the micropore and the microchannel filtration methods, and the changes in the neutrophil surface expression of Mac-1, L-selectin and sialyl Lewis X and the cytoplasmic expression of the actin filaments using a flow cytometric analysis during a dialysis session. Five patients with chronic renal failure were selected who showed a nadir leukocyte count in peripheral blood at 30 min after the initiation of the dialysis session. The neutrophil count also reached a nadir at 30 min and thereafter returned to almost the predialysis level by 180 min. Both the micropore filtration time and the microchannel passage time, which reflect the viscoelasticity of the peripheral blood neutrophils, correlated inversely with the neutrophil count. At the nadir of neutropenia, the neutrophils were observed to have become both adhesive and viscoelastic. The actin filaments in the neutrophil cytoplasm gradually increased in number from the start of dialysis, reaching a peak level at 30 min, and thereafter decreasing to predialysis levels. The Mac-1 expression continuously increased up from 30 min until the end of dialysis. The L-selectin expression first decreased at 15 min, but thereafter returned to predialysis levels within 60 min. The SLex expression did not change throughout the course of the session. These results thus indicated the neutrophil counts during a dialysis session to inversely correlate with the viscoelasticity of the neutrophils expressed by the micropore filtration time or microchannel passage time, which possibly depends on the contents of cytoplasmic actin filaments. In addition, the shedding of L-selectin from neutrophil surface may also be involved in the first step of hemodialysis neutropenia.
Actin Cytoskeleton↗
Giant insulinoma in a patient with multiple endocrine neoplasia-type I: a case report.
We report a case of giant cystic insulinoma constituting part of multiple endocrine neoplasia (MEN) type I. A 29-year-old Japanese man presented with a history of recurrent hypoglycemic attacks. Endocrine examination showed hyperinsulinemia discordant with hypoglycemia, and a giant cystic insulinoma (11 x 10 cm) located in the pancreatic tail was detected radiologically. Hyperprolactinemia due to pituitary adenoma and hyperparathyroidism due to parathyroid hyperplasia were also present. The insulinoma, prolactinoma and hyperplastic parathyroid gland were surgically removed. Fluorescent microsatellite analysis detected loss of heterozygosity (LOH) in chromosome 11q13 in DNA samples from all resected tissues but not from white blood cells. This is a rare case of MEN type I because of the giant cystic insulinoma and the evidence of common LOH detected in all MEN type I tissues.
Adult↗
An elderly patient with transient diabetes insipidus associated with lymphocytic infundibulo-neurohypophysitis.
We present the eldest case ever reported of central diabetes insipidus (DI) associated with infundibulo-neurohypophysitis. A 77-year old woman, who complained of recent development of excessive thirst, polyuria and polydipsia, was referred to our hospital. The daily urine volume was markedly increased to 6 L. DDAVP administration effectively reduced urine volume and increased urine osmolality. The loading test using high-osmolar sodium chloride showed impaired excretion of vasopressin discordant with plasma osmolar changes. The anterior pituitary function was normal. Pituitary magnetic resonance imaging (MRI) showed thickening of the pituitary stalk and a lack of high-intensity signal of the neurohypophysis on T1-weighted images, suggestive of lymphocytic infundibulo-neurohypophysitis. The thickness of pituitary stalk on MRI improved 6 months later. DI was controlled with DDAVP for 40 days. This was followed by stabilization of the daily urine volume to less than 2.5 L without DDAVP. Our case is the eldest case of central DI associated with infundibulo-neurohypophysitis. The rapid remission of pituitary changes on MRI provides an insight that spontaneously partial remission of central DI may occur, resulting in transient polyuria and polydipsia.
Aged↗
A case of idiopathic deep vein thrombosis improved with glucocorticoid therapy.
A healthy, middle-aged Japanese man with no family history of thrombotic disorders presented with acute abdominal pain due to ischemic colitis. Two months later, he developed left leg pain and swelling. A venogram of the lower limbs, computed tomography, and a scintigram of pulmonary blood flow revealed deep vein thrombosis of the left lower limb extending to the inferior vena cava and emboli of both pulmonary arteries with bilateral pleural effusions. The responsible coagulation disorder was not detected in this case. Since these thrombi were refractory to the thrombolytic therapy with urokinase and anticoagulant therapy with warfarin, prednisolone was chosen for the suppression of accompanying thrombophlebitis. Two months following the initiation of prednisolone (20 mg/day), the venous thrombosis, abnormal pulmonary shadows, and pleural effusions had completely resolved. This case demonstrates the successful treatment of idiopathic venous and pulmonary thrombosis with glucocorticoids.
Administration, Oral↗
Effect of continuous infusion of vasopressin on glomerular growth response in spontaneously hypertensive rats.
Vasopressin (VP) is thought to play an important role in the pressor and proliferative responses of renal glomeruli. We have utilized the spontaneously hypertensive rat (SHR) model to determine if glomerular proliferation is induced by chronic infusion of exogenous VP. SHR were continuously infused with 0.1 ng/kg/min VP (H-VP group), 1.0 ng/kg/min (H-VP group), or vehicle alone (control group) for fifteen days using osmotic minipumps, and the histological alterations and level of expression of platelet-derived growth factor B-chain (PDGF-B) and transforming growth factor (TGF)-beta1 mRNA were determined. We observed no significant differences in systolic blood pressure, heart rate, serum electrolytes, protein and creatinine among the three groups of rats, but urine volume was found to be significantly decreased, and urine osmolality significantly increased, in the H-VP group. Kidney weight was significantly higher in the H-VP and L-VP groups than in the control group, and glomerular diameter was higher in the H-VP group. When we measured mesangial injury score and cellularity in the glomeruli of these animals, we observed VP dose-dependent proliferative changes. In the immunofluorescence study, although we did not find an obvious difference in depositions of collagen types III, IV and VI, alpha-smooth muscle actin and PDGF-B among the groups, the collagen type I and TGF-beta1 increased in several glomeruli in the H-VP group. Reverse transcription polymerase chain reaction (RT-PCR) revealed no significant differences in the glomerular levels of PDGF-B mRNA among the three groups of rats, but the level of expression of TGF-beta1 mRNA was significantly higher in the L-VP and H-VP groups than in the control group. These findings suggest that VP may contribute to glomerular proliferation, and that VP may exert its effects in part through the induction of TGF-beta1 expression. These results also raise the possibility that blockade of VP receptors may be useful in the treatment of some forms of glomerular disease.
Animals↗
Congenital adrenal hyperplasia with normokalemic periodic paralysis.
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Adrenal Hyperplasia, Congenital↗
Effects of interferons on tumour necrosis factor alpha production from human keratinocytes.
Interferons (IFNs) have been reported to have pleiotrophic effects including the ability to induce the production of other cytokines in several cell types. Tumour necrosis factor alpha (TNF-alpha) is pro-inflammatory cytokine a known to be produced by a variety of cells including human keratinocytes. In the present study, we sought to determine the effects of IFNs on TNF-alpha production from human keratinocytes. IFN-gamma (50-100 ng/ml) induced TNF-alpha production dose dependently, but no induction of TNF-alpha was observed with IFN-alpha or IFN-beta. Since in the epidermis cytokines often work with in a cascade fashion and keratinocytes are a source of primary cytokine, IL-1 alpha, whether combined treatment with IFN-gamma and IL-1 alpha had a synergistic effect on TNF-alpha production was examined. Combined treatment with IFN-gamma (100 ng/ml) and IL-1 alpha (10 ng/ml) induced 2-3-fold higher level of TNF-alpha than IL-1 alpha alone. These results suggest that IFN-gamma is a positive regulator for the production of TNF-alpha from human keratinocytes and likely to increase skin inflammation.
Cells, Cultured↗
Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia.
A case of unilateral adrenocortical hyperplasia is presented. A 46-year-old woman with a 7-year history of hypertension and a 1-year-history of hypokalemia was diagnosed with primary aldosteronism. Computed tomography, magnetic resonance imaging, venous sampling and adosterol scintigraphy exhibited a functioning left adrenal mass. The plasma aldosterone concentration increased markedly when furosemide with upright posture and either captopril or adrenocorticotropin were administered. Plasma renin activity was suppressed below the detectable range. Aldosterone secretion displayed a circadian rhythm and was not suppressed by dexamethasone administration. The resected left adrenal mass was pathologically diagnosed as adrenocortical nodular hyperplasia. Unilateral adrenal hyperplasia involving the zona glomerulosa rarely has been reported, with varying and incompletely characterized hormonal characteristics. This case report and literature review suggest unilateral adrenal hyperplasia as a rare cause of hyperaldosteronism with characteristics intermediate between idiopathic hyperaldosteronism and aldosterone-producing adrenocortical adenoma, resembling the functional features of the adenoma more closely.
Adrenal Cortex↗
Renal c-fos expression induced by angiotensin II is enhanced in spontaneously hypertensive rats.
We compared the effect of a bolus injection of angiotensin II (Ang II) on the expression of protooncogene c-fos in the renal cortex and medulla of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of 5 ng/kg body weight of Ang II resulted in an immediate rise in systolic blood pressure (SBP) in both SHR and WKY rats. The percent rise in SBP was similar in both strains. Pretreatment with Ang II type 1 (AT1)-receptor antagonist, L-158,809 (1 mg/kg) abolished the pressor response in both strains. Competitive reverse transcription-polymerase chain reaction (RT-PCR) showed that administration of Ang II increased the expression of c-fos mRNA within 10 min in both the renal cortex and medulla of SHR significantly higher than WKY rats. Moreover, the enhanced c-fos mRNA expression due to Ang II was significantly suppressed by the pretreatment of L-158,809 in both strains. These findings indicate that c-fos expression in the kidney is mediated by AT1-receptors and that the renal c-fos response to exogenous Ang II was significantly augmented in SHR compared with WKY rats, suggesting that this hyperresponsiveness on renal AT1-action may partly contribute to the progression of renal injury in SHR.
Angiotensin II↗
Diffuse necrobiosis lipoidica diabeticorum associated with non-insulin dependent diabetes mellitus.
We report a case of diffuse necrobiosis lipoidica (NL) which first appeared on the legs and scrotum, before gradually spreading across the back and arms; the patient also suffered from diabetes mellitus, and the NL lesion began to disappear as the diabetes mellitus was controlled. The possible contribution of various glycation and glycoxidation products of collagen to the pathogenesis of NL is discussed.
Collagen↗
A novel donor splice site mutation in the C1 inhibitor gene of a patient with type I hereditary angioneurotic edema.
We studied the molecular genetic basis of a C1 inhibitor deficiency in a patient with type I hereditary angioneurotic edema using both the polymerase chain reaction and nucleotide sequencing. A single nucleotide change (T-->A) at the GT 5' donor splice recognition motif in the seventh intron of the C1 inhibitor gene was detected. A restriction site analysis of the C1 inhibitor gene in the patient's family indicated that this mutation is correlated with a decreased level of C1 inhibitor activity. A northern blot analysis demonstrated C1 inhibitor mRNA to have a normal size, but its contents were reduced by about 50% compared with a normal subject. As the donor splice site is essential for an excising of the intron during mRNA processing, aberrant mRNA splicing may cause a rapid degradation of the transcript, thus resulting in the onset of hereditary angioneurotic edema.
Adult↗
Cluster headache dependent upon octreotide injection.
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Adult↗
The anti-BRCA1 peptide antibody C-20 recognizes smooth muscle cells.
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Antibodies↗
Dispersion of regional wall motion abnormality in patients with long QT syndrome.
OBJECTIVE: To examine the left ventricular regional wall motion abnormality and to evaluate dispersion of this abnormality in patients with long QT syndrome. DESIGN: Left ventricular short axis images at basal and middle levels were recorded on videotape and digitised to reconstruct digitised M mode echocardiograms, from which left ventricular wall thickness curves were obtained. The wall thickening time (ThT) was defined as the period in which the instantaneous wall thickness exceeded 90% of the maximum wall thickness. ThT was measured at three segments in each of the septal and free wall sides of the left ventricle, a total of 12 segments. To examine the mechanical dispersion of the left ventricle, the difference between the maximum and minimum ThT of 12 segments in each subject was obtained. PATIENTS: Eight patients with congenital long QT syndrome (averaged QTc interval (SD) 509 (27) ms1/2) and 10 control subjects (QTc interval 397 (26) ms1/2) were examined. RESULTS: The averaged ThT values of the 12 segments pooled form all subjects were correlated with the QT intervals (r = 0.72, p < 0.005). Thus the averaged ThT in the long QT syndrome patients was longer than in the control subjects (p < 0.005). The segmental variation of ThT in the patients was greater than in the control subjects (p < 0.001). The dispersion of ThT in the patients was therefore larger than in control subjects (p < 0.005). However, the pattern of ThT variation in the patients varied according to the individual subject. CONCLUSIONS: There is not only electrical but also mechanical dispersion in the left ventricle of long QT syndrome patients. Regional assessment of ventricular wall motion may allow quantification of the spatial variation of wall motion abnormality.
Adolescent↗
Linkage and association of an interleukin 4 gene polymorphism with atopic dermatitis in Japanese families.
We examined linkage between markers at and near the IL4 gene and atopic dermatitis (AD) in 88 Japanese nuclear families. Affected sib pair analysis suggested linkage between the IL4 gene and AD (SPLINK lod=2.28). Transmission disequilibrium testing showed a significantly preferential transmission to AD offspring of the T allele of the -590C/T polymorphism of the IL4 gene (p=0.001). A case-control comparison suggested a genotypic association of the TT genotype with AD (odds ratio=1.88, p=0.01). Since the T allele was reported to be associated with increased IL4 gene promoter activity compared with the C allele, our data indicate that genetic differences in transcriptional activity of the IL4 gene influence AD predisposition, particularly in Japanese, because of a high frequency of the T allele.
Case-Control Studies↗
Effects of chronic inhibition of ACE and AT1 receptors on glomerular injury in dahl salt-sensitive rats.
To elucidate the contribution of the renin-angiontensin system (RAS) to glomerular injury in salt-sensitive hypertension, we investigated the chronic effects of the angiotensin I-converting enzyme inhibitor cilazapril and the angiotensin II type 1-receptor antagonist (AT1a) TCV-116 in Dahl-Iwai rats. Dahl salt-sensitive (S) rats receiving 8% salt diet for 6 wk were simultaneously treated with cilazapril (n = 6), TCV-116 (n = 6), or saline (n = 14). The 8% salt diet markedly increased systolic blood pressure (SBP), urinary protein, and N-acetyl-beta-glucosaminidase (NAG) excretion compared with 0.3% salt-treated S (n = 6) or salt-resistant (n = 6) rats. Although neither cilazapril nor TCV-116 reduced the elevated SBP, TCV-116 significantly lowered urinary protein and NAG excretion. Histologically, 8% salt treatment in S rats induced progressive sclerotic and proliferative glomerular changes, which were ameliorated by both drugs. TCV-116 increased the glomerular diameter. Immunofluorescence demonstrated the increased level of type III collagen in the mesangium of 8% salt-treated S rats, which was completely reversed by TCV-116. Competitive RT-PCR of mRNA extracted from the glomeruli revealed that 8% salt treatment significantly increased the levels of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor B-chain and that TCV-116 significantly reduced the levels of PCNA and transforming growth factor-beta1 (TGF-beta1). Thus, although the chronic RAS-inhibition in salt-sensitive hypertension exerted a histologically renoprotective effect by both ways without lowering blood pressure, the RAS inhibition due to AT1a had more beneficial advantages of reducing proteinuria and attenuating the levels of glomerular TGF-beta1 and extracellular matrix.
Acetylglucosaminidase↗
Angiokeratoma corporis diffusum associated with galactosialidosis.
We describe a 34-year-old Japanese man with generalized angiokeratomas and various neurological symptoms since childhood. A number of reddish papules were scattered over his entire body and were especially numerous on his elbows, knees, penis and scrotum. An electron-microscopic study revealed a number of vacuoles in the cytoplasm of the vascular endothelial cells. This finding suggests that the angiokeratomas resulted from an injury of the endothelial cells due to the storage of metabolic material. A laboratory examination demonstrated a deficiency of both the beta-galactosidase and neuramidase activity in his leukocytes and fibroblasts. A restriction site analysis of PCR-amplified genomic DNA revealed that the patient had an mRNA splicing junction mutation at the 5' donor splice site of the exon 7/intron 7 junction in the protective protein gene.
Adult↗