5q-syndrome presenting as essential thrombocythemia: myelodysplastic syndrome or chronic myeloproliferative disorders?
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Adult↗
Biomedical subjects
K Toba
Publications and source records attributed to K Toba.
[Essential thrombocythemia in transformation to smouldering megakaryoblastic leukemia with myelofibrosis].
Leukemic transformation in essential thrombocythemia (ET) is rare. We describe a patient with ET which transformed to megakaryoblastic leukemia with myelofibrosis after treatment with melphalan for 8 years. His course after transformation smouldered for 20 months without antileukemic chemotherapy. A 61-year-old man was referred by a local doctor to Niigata University Hospital due to nasal bleeding in June 1984. Complete blood count (CBC) was as follows; hemoglobin 12.4 g/dl, platelets 268.8 x 10(4)/microliters, and white blood cells 11,900/microliters, with differentials of 39% PMN, 1% basophils, 2% eosinophils, 4% monocytes, and 13% lymphocytes. Bone marrow examination revealed hyperplasia of megakaryocytes without increase of reticulin fibers. Neutrophil alkaline phosphatase activity and karyotype of marrow cells were normal. ET was diagnosed. He was followed up by local doctor. The platelet count was controlled at a level of approximately 40 x 10(4)/microliters with melphalan for eight years. In January 1992 he developed pain in his lower extremities. He was admitted to our hospital on May 29, 1992. CBC was as follows; hemoglobin 8.9 g/dl, platelets 14.3 x 10(4)/microliters, and white blood cells 3,500/microliters, with differentials of 25% PMN, 5% monocytes, 28% lymphocytes, and 24% blasts. Bone marrow aspiration was unsuccessful and bone marrow biopsy revealed increases in fibroblasts and collagen fibers. Circulating blasts were positive for CD4, CD7, CD25, CD13, CD33, CD34, and HLA-DR and partly positive for CD41 and CD36. In ultrastructural cytochemistry blasts were positive for platelet peroxidase but negative for myeloperoxidase. Cytogenetic study revealed 46, XY, +der (1) t(1:7) (p11;q11) in all of five metaphases. He was diagnosed with megakaryoblastic leukemia accompanied by myelofibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Effect of an intracerebroventricularly administered vasopressin V1 antagonist on blood pressure and heart rate in deoxycorticosterone-salt hypertensive rats.
It is well known that peripheral vasopressin (VP) is essential for the development and maintenance of DOC-salt hypertension. It is, however, still unclear whether central VP is involved in this type of hypertension. Therefore, the aim of this study was to clarify the role of central VP in the regulation of blood pressure in DOC-salt hypertension. In order to examine this issue, three series of investigations were performed. First, a novel vasopressin V1 antagonist (OPC21268) was administered intravenously to DOC-salt hypertensive rats, and mean arterial blood pressure (MABP) and heart rate (HR) were recorded. Second, the concentration of VP in the perfusate of microdialysis of cerebrospinal fluid (CSF) was determined in DOC-salt hypertensive and control rats. Finally, intracerebroventricular (i.c.v.) administration of a V1 antagonist was performed in DOC-salt hypertensive rats to determine the central mechanism of hypertension. Intravenous administration of a V1 antagonist had no effect on MABP and HR. There was no difference in VP in the perfusate of CSF between DOC-salt hypertensive and control rats. I.c.v. administration of a V1 antagonist significantly decreased MABP and HR in a dose-dependent manner in DOC-salt hypertensive rats (P < 0.05-0.01). These results suggest that central VP is involved in the maintenance of DOC-salt hypertension, and the mechanism is, in part, mediated by upregulation of the V1 receptor.
Animals↗
Parathyroid hormone-related protein reduces cytosolic free Ca2+ level and tension in rat aortic smooth muscle.
The effect of parathyroid hormone-related protein (PTHrP) on cytosolic free Ca2+ level ([Ca2+]i) and tension in rat aortic smooth muscle was investigated with special reference to the role of production and action of cyclic AMP. Rat aortic spiral strip preparations without endothelium were treated with the acetoxymethyl ester of fura 2, and the ratio of fluorescences (R340/380), an index of [Ca2+]i, emitted from smooth muscle, was measured. The tension of the preparations was simultaneously measured. PTHrP-(1-34) produced concentration-dependent decreases both in the tension and in R340/380 increased by phenylephrine (10(-7) M). These effects were significantly inhibited by pretreatment with either PTHrP-(7-34) (10(-6) M), a PTHrP receptor antagonist, or with Rp diastereomer of adenosine cyclic 3',5'-phosphorothioate (RpcAMPS; 10(-4) M), a cyclic AMP-dependent protein kinase inhibitor. Dibutyryl cyclic AMP (10(-5)-10(-3.5 M) elicited effects similar to those of PTHrP-(1-34). PTHrP-(1-34) was found to significantly elevate aortic cAMP level, measured by specific radioimmunoassay, after 5 min incubation with PTHrP-(1-34). These results suggest that the decrease in [Ca2+]i is involved in the vasodilator action of PTHrP, and that the decreases both in tension and in [Ca2+]i might be attributed to cyclic AMP production stimulated by PTHrP.
Animals↗
Immunocytochemical detection of parathyroid hormone-related protein in vascular endothelial cells.
The expression of parathyroid hormone-related protein (PTHrP) in cultured endothelial cells derived from bovine carotid artery was immunocytochemically investigated. The cells showed positive immunoreactivity for PTHrP abundantly in cytoplasm. PTHrP-like immunoreactivity was found in all endothelial cells under investigation. Negative control prepared with non-immune rabbit serum or with the antiserum preabsorbed with PTHrP showed no significant staining, indicating the specificity for immunostaining. Addition of 10% fetal calf serum to serum-deprived endothelial cells did not significantly increase PTHrP-like immunoreactivity. These results suggest that endothelial cells express PTHrP constitutively and PTHrP may act as a new class of endothelium-derived relaxing factor.
Animals↗
The role of activation of the sympathetic nervous system in the central pressor action of calcitonin gene-related peptide in conscious rats.
The effects of intracerebroventricular (i.c.v.) administration of calcitonin gene-related (CGRP) on blood pressure and heart rate (HR), and the underlying mechanisms were studied in conscious rats. CGRP (0.1-3.0 nmol i.c.v.) increased mean arterial blood pressure (MABP) and HR. CGRP (3.0 nmol i.c.v.) also significantly increased both plasma norepinephrine and epinephrine concentrations. Pretreatment with 16.5 nmol i.c.v. CGRP(8-37), a specific CGRP receptor antagonist, significantly inhibited the i.c.v. CGRP (1.0 nmol)-induced increases in MABP and HR. Phenoxybenzamine inhibited the i.c.v. CGRP-induced increase in MABP, while propranolol suppressed the tachycardiac response to i.c.v. CGRP. Chemical sympathectomy by 6-hydroxydopamine inhibited the increases in MABP and HR produced by i.c.v. CGRP. These results suggest that the central pressor and tachycardiac effects of i.c.v. CGRP are mediated by catecholamine release due to stimulation of sympathetic nervous system activity, possibly via specific CGRP receptors in the central nervous system.
Animals↗
Role of central vasopressin in cardiovascular regulation: effect of dehydration and sex.
The present study was performed to evaluate the role of central vasopressin in cardiovascular regulation. First, a novel vasopressin V1 antagonist (OPC21268) was injected intracerebroventricularly in conscious rats. In water-deprived animals, the mean arterial blood pressure (MABP) and heart rate were significantly decreased compared with euhydrated control rats. There was, however, no significant difference in the concentration of vasopressin in the perfusate of cerebrospinal fluid between groups. Second, vasopressin was intracerebroventricularly injected in male and female homozygous Brattleboro rats. The increase in MABP was greater in males than in females. These results suggest that central vasopressin is involved in blood pressure regulation in pathophysiological states.
Animals↗
Central neural mechanism contributing to attenuation of angiotensin II-induced hypertension in rats on dietary calcium supplementation.
The effect of dietary calcium (Ca) supplementation on blood pressure (BP) and the central nervous system (CNS) mechanism underlying this effect were studied in angiotensin II (Ang II)-induced hypertensive rats. The effects of dietary Ca (0.5, 2, 4%) on systolic blood pressure (SBP), ionized Ca concentration (Ca++) in cerebrospinal fluid (CSF) and central norepinephrine (NE) turnover were investigated in male Wistar rats receiving subcutaneous infusion of Ang II (100 ng/min). Central NE turnover was studied by measuring 3-methoxy-4-hydroxyphenylglycol (MHPG) concentration in CSF with multiple electrode liquid chromatography. Ang II significantly increased SBP, and dietary Ca dose-dependently attenuated the increase. SBP inversely correlated with Ca++ and MHPG in CSF. Intracerebroventricular injection of CaCl2 more markedly reduced BP in Ang II-treated rats than that in control rats. These results suggest that modulation of central NE turnover possibly caused by the increase in CNS Ca++ is involved in the anti-hypertensive mechanism of dietary Ca supplementation in Ang II-induced hypertensive rats.
Angiotensin II↗
[The importance of the host nutritional and immune status on the prognosis of urinary tract infection in the elderly].
This study was performed to evaluate the role of the nutritional and immune status on the prognosis of urinary tract infections (UTI) in the elderly. 192 patients among the 790 inpatients were diagnosed as UTI. Age-related increase in the prevalence of UTI was accompanied with poor prognosis in the patients with hypoalbuminemia (< 2.6 g/dl) and lymphocytopenia (< 700/mm3). To study the immunologic basis for susceptibility to UTI in the aged further, we compared the T-cell functions between outpatients without serious disease and inpatients with chronic UTI. The absolute numbers of lymphocyte, OKT3 (pan T-cell marker), OKT4 (Helper/Inducer marker) and Interleukin (IL)-2 as well as serum albumin concentration were decreased in the patients with UTI. A prospective study was done to confirm that these nutritional and immunological changes become risk factors in the prognosis of UTI with long-term and low-dose chemotherapy. In the patients continued with bacteriuria (Non-responders, n = 6), serum albumin concentration and IL-2 production were significantly lower than the patients who became free from bacteriuria (Responders, n = 7). These results suggest that poor nutrition-related immune dysfunction contributes to the vulnerability of elderly patients to UTI and becomes risks for he prognosis of UTI.
Adult↗
[Peripheral neuropathy in large granular lymphocytic leukemia].
A 16-year old woman with LGL leukemia developed peripheral neuropathy. She showed virus-associated hemophagocytic syndrome (VAHS)-like signs including high fever, liver dysfunction, huge splenomegaly, hepatomegaly and pancytopenia. The presence of chronic active EB virus infection was proved by marked high titers for IgG and IgA antibodies to the Epstein-Barr viral capsid and early antigens and low titers of antibody to Epstein-Barr nuclear antigens. She showed dysesthesia and paresthesia of bilateral lower extremities with marked swelling and tenderness, and later developed muscular weakness and atrophy with areflexia of lower extremities. Findings of the central nervous system dysfunction were not observed except for the acceleration of jaw jerk. Pleocytosis and increased protein levels in the cerebrospinal fluid were found. Pulse therapy of methyl-prednisolone and high dose intravenous immunoglobulin therapy (20 g/day for 3 days) were effective for neurological findings. The increased neopterin in the cerebrospinal fluid suggested that peripheral neuropathy was caused by activated macrophages.
Adolescent↗
A rise of erythrocytes and platelets in a patient with myelodysplastic syndrome during the administration of G-CSF.
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Aged↗
Improved staining method for the simultaneous flow cytofluorometric analysis of DNA content, S-phase fraction, and surface phenotype using single laser instrumentation.
We have developed an improved technique for triple staining that permits the simultaneous flow cytofluorometric analysis of cell surface antigens, bromodeoxyuridine incorporation into DNA, and DNA quantification using 7-amino-actinomycin D. PHA-activated human peripheral blood lymphocytes were incubated with bromodeoxyuridine and stained for cell surface phenotype with phycoerythrin-labeled monoclonal antibodies. Stained cells were fixed serially with 1% paraformaldehyde and 45% ethanol. Fixed cells were sequentially stained with an anti-BrdUrd monoclonal antibody followed by a FITC-conjugated goat anti-mouse antibody and incubated with 7-amino-actinomycin D. Hypotonic buffer was employed for all procedures after fixation. Stained-fixed cells were analyzed by flow cytofluorometry for simultaneous green (525 nm), orange (570 nm), and red (greater than 650 nm) fluorescence. Utilizing this staining technique, we were able to analyze simultaneously cell phenotype, DNA synthesis, and total cellular DNA content with single laser excitation.
Antibodies, Monoclonal↗
Effect on vasopressin release of microinjection of cholinergic agonists into the rat supraoptic nucleus.
It is likely that central cholinergic pathways to the paraventricular and supraoptic nuclei participate in the control of vasopressin release. We have shown previously that this is due, in part, to activation of muscarinic, but not nicotinic, receptors in the paraventricular nucleus. There is, however, reason to believe that this cholinergic effect in the supraoptic nucleus may be the result of activation of nicotinic receptors. To test this possibility, we have studied in conscious unrestrained rats the effect of microinjection of muscarinic and nicotinic agonists into the supraoptic nucleus on vasopressin release, mean arterial blood pressure, and heart rate. Under ether anesthesia, a stainless steel guide cannula was placed in the supraoptic nucleus 5-7 days before the experiment, and femoral, arterial, and venous catheters were implanted 1 day before the experiment. Microinjection of nicotine into the supraoptic nucleus at doses of 1 and 10 micrograms resulted in transient increases in the plasma vasopressin concentration that were 7-fold and 11-fold greater, respectively, than control values at 3 min. There were also small transient increases in mean arterial blood pressure, but heart rate was unchanged. The microinjection of 2 and 20 ng of oxotremorine, a muscarinic agonist, into the supraoptic nucleus had no effect on the plasma vasopressin concentration, mean arterial blood pressure, or heart rate. These doses of oxotremorine were previously shown to have potent stimulatory effects on vasopressin release when microinjected into the paraventricular nucleus. These findings suggest that the central cholinergic stimulation of vasopressin release is due, in part, to activation of muscarinic receptors in the paraventricular nucleus and nicotinic receptors in the supraoptic nucleus.
Animals↗
Occurrence of ITP in a splenectomized patient.
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Aged↗
Effects of vasopressin on arterial blood pressure and cardiac output in male and female rats.
This study was performed to investigate further the mechanisms underlying the sexual dimorphism of the pressor responses to vasopressin. We have confirmed our earlier findings that the pressor response to graded infusions of vasopressin in conscious unrestrained male rats is similar to that in estrous females and greater than in diestrus, proestrus, and metestrus. This difference was due primarily to greater increases in total peripheral resistance (TPR) in males and estrous females, since there were no sex- or cycle-related differences in the vasopressin-induced reductions in cardiac output. Gonadectomy was without effect in males but, in females, increased blood pressure responses to vasopressin to levels found in males. Chronic treatment of ovariectomized rats with estradiol reduced pressor responsiveness to vasopressin; treatment with progesterone was without effect. These differences were also due to differences in TPR. It is concluded that the sex- and cycle-dependent differences in vasopressin-induced increases in blood pressure are due largely to attenuation of increases in TPR by estrogen.
Animals↗
Antihypertensive action of medullipin I given by mouth.
Perfusion of normal rat kidneys with 5% human albumin in a balanced salt solution bubbled with oxygen yielded medullipin I (Med I) in the renal venous effluent. The presence of Med I in the renal venous effluent has been established by thin-layer chromatography, by the type of vasodepressor effect when injected intravenously as a bolus into the hypertensive rat, by inhibition of the vasodepressor effect of the renal venous effluent by Tween 20 and SKF 525A (proadifen, inhibitor of cytochrome P-450), and by removal of the liver from the circulation (a procedure that inhibits extracted Med I). Med I so derived lowered blood pressure of spontaneously hypertensive rats when injected into the stomach by an indwelling tube or when given by mouth. The lowering of blood pressure was attended by no change in cardiac output and no change in heart rate. Med I given by mouth to the spontaneously hypertensive rat is a vasodilator that suppresses sympathetic tone, acting in the same way as Med I extracted from renal papillae and given intravenously. Importantly, the antihypertensive action was demonstrated in the spontaneously hypertensive rat, a model of hypertension considered to mimic idiopathic or essential hypertension of humans. Med I is a promising therapeutic agent for hypertension.
Administration, Oral↗
[Long-term single dose chemoprophylaxis of recurrent urinary tract infection in elderly female subjects].
To evaluate the efficacy of the single dose chemoprophylaxis of recurrent urinary tract infection (UTI) in the elderly, 20 female inpatients (mean age 81.4) who had one or more culture documented UTIs in the past 12 months were studied. They were randomly assigned to be treated for 6 months either with chemoprophylaxis (200 mg of norfloxacin) or conventional therapy (without any antimicrobials except when overt UTI occurred). After a 4 months of washout period, the protocols were exchanged with each other and next 6 months of trial was carried out. All cases were followed at least 4 months after the discontinuance of the chemoprophylaxis. The difference of efficacy between the two modalities was evaluated by periodical examinations of urine cultures, urinalysis and inflammatory markers. During chemo-prophylaxis, the frequency of the symptomatic UTI (bacteriuria greater than 10(4)/ml, pyuria greater than 5/HPF, CRP greater than +) was 0.267/patient.year which was significantly lower than during conventional therapy (2.97/patient.year, p less than 0.01). This prophylactic effect remained 4 months after the discontinuance of the drug. On the other hand, bacteriuria was persistent in more than half of patients with chemoprophylaxis. Minimal inhibitory concentration of norfloxacin for separated bacteria revealed that the resistant species steeply increased from 4 to 6 months after the beginning of chemoprophylaxia. These species disappeared 4 months after the drug was discontinued. Optimal durations of chemoprophylaxis and drug-holidays were discussed.
Aged↗
[Familial essential thrombocythemia in a daughter and mother].
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Aged↗