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Biomedical subjects

S Oda

Publications and source records attributed to S Oda.

At least 253 records · Page 14Linked to original sources
PubMed1993

Inhibitory effect of interleukin 4 on production of interleukin 6 by adult T-cell leukemia cells.

Freshly isolated leukemic cells from patients with adult T-cell leukemia (ATL) produce high levels of interleukin 6 (IL-6), which is suggested to play an important role in thrombocytosis, elevation of C-reactive protein, and hypercalcemia in ATL. In this study, we investigated the effects of T-cell growth factors such as interleukin 2 (IL-2) and interleukin 4 (IL-4) on IL-6 production by ATL cells in vitro. Although IL-2 and/or IL-4 enhanced the cell proliferation of freshly isolated ATL cells from seven of nine patients, IL-2 did not affect the IL-6 release in most cases. In contrast, another T-cell tropic factor, IL-4 markedly inhibited the release of IL-6 in the conditioned medium in all cases. This IL-4-mediated inhibition of IL-6 release was completely abrogated by the addition of anti-IL-4 monoclonal antibody. Time course experiments demonstrated that IL-4 reduced the secretion of IL-6 for a prolonged period of time (more than 72 h). By Northern analysis, IL-4 reduced the transcription level of IL-6 mRNA. Furthermore, by flow cytofluorometry with the use of anti-human IL-4 receptor monoclonal antibody, ATL cells showed the significant level of IL-4 receptor on their cell surfaces without any stimulation. These data suggest that IL-4 may play an important regulatory role in the production of IL-6 in ATL.

Aged↗
PubMed1993

Direct synaptic connections between thalamocortical axon terminals from the mediodorsal thalamic nucleus (MD) and corticothalamic neurons to MD in the prefrontal cortex.

A combined anterograde axonal degeneration with ibotenic acid and wheat germ agglutinin-horseradish peroxidase (WGA-HRP) retrograde tracing study revealed that some degenerating thalamocortical axon terminals from the mediodorsal thalamic nucleus (MD) directly formed asymmetrical synaptic contacts predominantly with dendritic spines of apical dendrites of WGA-HRP-labeled corticothalamic projection neurons to MD in the prelimbic cortex of the rat. This result suggests that there is a monosynaptic feedback loop from and to MD via deeper layer neurons in the prelimbic cortex.

Animals↗
PubMed1993

Rises of intracellular Ca2+ and pH mediate the initiation of sperm motility by hyperosmolality in marine teleosts.

Spermatozoa of marine teleosts, puffers and flounder, were completely quiescent when they were washed to remove electrolytic components of the seminal plasma and then diluted in nonelectrolyte solutions isotonic to the seminal plasma. Sperm motility was initiated upon dilution in hypertonic nonelectrolyte solutions. These observations suggest that sperm motility is suppressed by seminal osmolality and motility is triggered solely by the increase in external osmolality which occurs at natural spawning in hypertonic seawater. Extracellular Ca2+ had no influence on the osmolality-dependent initiation of sperm motility. However, sperm motility was initiated even in isotonic solution when Ca2+ was introduced into the sperm cells by Ca2+ ionophore. Intracellular Ca2+ increased at the osmolality-dependent initiation of sperm motility under Ca(2+)-free conditions. These results suggest that the release of Ca2+ from intracellular storage in response to the increase in external osmolality has a key role in the initiation of sperm motility. A transient increase in intracellular pH was also observed at the hyperosmolality-dependent initiation of sperm motility. Furthermore, initiation of sperm motility was induced even in isotonic solutions when intracellular pH increased by the treatment with ammonium salts. These results suggest that an increase in intracellular pH, as well as the rise in intracellular Ca2+, has an important role in the initiation of sperm motility in marine teleosts.

Acetates↗
PubMed1993

Obstructed migration of Purkinje cells in the developing cerebellum of the reeler mutant mouse.

It has been considered that cortical malformation in the brain of the reeler mutant mouse is due to a defect in the process of neuroblast migration during development. We examined the process of Purkinje cell migration in the cerebellar primordium of the reeler mutant immunohistochemically and electron-microscopically, employing a specific marker for Purkinje cells and markers for radial glia. To facilitate the recognition of the homozygote of the reeler mutation (r1) at the embryonic stage, we introduced the chromosome carrying the autosomal semi-dominant mutation, hammer-toe (Hm), by crossbreeding and backcross into the heterozygote of the reeler mutation, which is an autosomal recessive and located on the homologous chromosome. Using this double heterozygous strain (+/rl-Hm/+), the homozygote of rl can be selected from littermates by the normal appearance of the feet. Both the heterozygous rl embryos and non-carriers harbor the Hm locus and show the Hm phenotype as a deformity of the feet that can be recognized from the 15th day of gestation. In the cerebellar primordium of control mice, Purkinje cells migrated radially from the ventricular zone towards the cortex. In contrast, most of the migratory Purkinje cells remained in the intermediate zone, and their migration towards the cortex was obstructed in the cerebellum of the reeler mutant. A disorganized arrangement of both the processes and cell bodies of the radial glia was demonstrated in the cerebellar primordium of the reeler by labeling them with the antibody against tenascin, a neuron-glial adhesion molecule, and the monoclonal antibody 1D11, a marker for immature astroglia. Electron-microscopic observations revealed apposition of the migratory cells to the radially oriented glial processes in the intermediate zone of the control cerebellum. In contrast, the apposition of leading processes of the migratory neuroblasts to disorganized processes of the radial glia was observed in the intermediate zone of the reeler cerebellum. These findings suggest that the obstructed migration and disordered cortical alignment of Purkinje cells in the reeler cerebellum is due to dysgenesis and abnormal development of radial glia, resulting in disturbance of contact guidance in the process of Purkinje cell migration.

Animals↗
PubMed1993

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions.

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Akinetic Mutism↗
PubMed1993

Augmented central pressor action of magnesium in SHR.

This study attempted to determine whether central magnesium (Mg) influences the regulation of blood pressure (BP). An intracerebroventricular (icv) injection of a high Mg2+ solution (190.0 mEq/L, 10 microL), made by adding MgC12 to artificial cerebrospinal fluid, increased the mean BP in both conscious spontaneously hypertensive rats (SHR; n = 17, p < 0.001) and Wistar Kyoto rats (WKY; n = 8, p < 0.005). Spontaneously hypertensive rats showed a greater pressor response than WKY (+11.7 +/- 0.9 mm Hg versus +3.5 +/- 1.1 mm Hg, p < 0.001). This pressor response to Mg2+ given icv was dose-dependent in the range of Mg2+ concentration between 47.5 and 190.0 mEq/L in SHR. A high Mg2+ solution (190.0 mEq/L), made by adding MgSO4 given icv, also increased the mean BP in SHR (n = 7, p < 0.001) and WKY (n = 6, p < 0.01), whereas the high osmolarity solution (340 mOsm/kg H2O) given icv did not change the mean BP in either SHR or WKY. Also administered was a high Mg2+ solution icv after either hexamethonium bromide (Hx; 50 mg/kg intravenously) or arginine vasopressin antagonist (aAVP, (CH2)5Tyr(Me)AVP, 30 micrograms/kg i.v.). The pressor response to the high Mg2+ solution was abolished by arginine vasopressin antagonist both in SHR and WKY, although it was not canceled by Hx. A high Mg2+ solution administered icv caused a 3.5-fold increase in plasma arginine vasopressin concentration in SHR (n = 5, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Enhancing effect of interleukin-2 on production of parathyroid hormone-related protein by adult T-cell leukemia cells.

Leukemic cells from patients with adult T-cell leukemia (ATL) can produce a calcium-regulating protein, parathyroid hormone-related protein (PTHrP). Moreover, it has been reported that ATL cells produce some cytokines besides PTHrP and that these cells respond to the T-cell growth factors, interleukin-2 (IL-2) and interleukin-4 (IL-4). To elucidate whether PTHrP produced by ATL cells is regulated by IL-2 or IL-4, we investigated the in vitro effects of IL-2 and IL-4 on the release of PTHrP. IL-2 increased the release of PTHrP into the conditioned medium from leukemic cells in some, but not all, ATL patients; however, IL-4 did not affect the PTHrP release. PTHrP messenger RNA (mRNA) levels were increased in ATL cells cultured in the presence of IL-2. These data suggest that IL-2 plays a role in the regulation of hypercalcemia by enhancing the production of PTHrP in ATL patients.

Aged↗
PubMed1993

An HTLV-I carrier who developed CD4+ T-CLL expressed the IL-2 receptor beta chain alone without expressing the alpha chain.

We describe a case of T-chronic lymphocytic leukaemia (T-CLL) with monoclonal proliferation of CD3+4+8- T cell expressing the interleukin 2 receptor (IL-2R) beta chain without expressing the alpha chain. Southern blot analysis of T-cell receptor beta chain gene revealed rearranged bands. The serum antibody was positive against human T-cell lymphotropic virus type I (HTLV-1)-associated antigens, but monoclonal integration of proviral DNA was not detected in the leukaemic cells. In accordance with the expression of IL-2R beta chain, the leukaemic cells proliferated in response to exogenous IL-2 without prior stimulation. However, culture supernatants of these cells did not show IL-2 activity. Since the role of the IL-2R beta chain in freshly isolated cells from T-CLL patients is not well understood, detailed analysis of this case would give us valuable information on the role of IL-2/IL-2R system in the proliferation of the leukaemic T cells.

Aged↗
PubMed1993

Mental health in family members living with elders.

We assessed the mental health conditions of 217 subjects who took care of elders at home, using our depression scale by the surveillance of the elders living at home in Ibaraki Prefecture. An analysis was made on how depression in the caretakers was related with each item of demographical results of the caretakers and the elders living together at home, and with ADL, depression, dementia, personality change and the personality trait of the elders. Our study revealed that depression, personality change and the viscous character of the elders are three factors associated with depression in the female caretakers. Furthermore, we pointed out the necessity of an education campaign to provide the caretakers with information on the elders' personality and personality change for maintenance of the good mental health of the caretakers living with the elders.

Adolescent↗
PubMed1993

Interleukin-4 induces proliferation of adult T-cell leukemia cells.

To evaluate the effect of IL-4 on the growth of leukemic cells from adult T-cell leukemia (ATL) patients (ATL cells) and determine whether the IL-4 autocrine mechanism is involved in the growth of ATL cells, we studied the proliferative response of ATL cells, from 11 patients, cultured in the presence or absence of IL-4 in vitro. Leukemic cells from 10 of the 11 patients examined proliferated in response to both IL-2 and IL-4 in a dose-dependent manner. The proliferative response to IL-4 was higher than that obtained with IL-2 in 8 patients. The expression of the IL-2 receptor (IL-2R) alpha alpha-chain in leukemic cells from some patients was also enhanced by IL-4. The IL-4 receptor was demonstrated by flow cytometry on the surface of ATL cells. Neither IL-4-induced proliferation of ATL cells nor IL-4-induced IL-2R expression on ATL cells was inhibited by anti-Tac or anti-IL-2 antibody and, therefore, these effects of IL-4 are considered independent of endogenous IL-2 activity. However, IL-2 and IL-4 were undetectable in the culture supernatants of ATL cells from any patient by enzyme-linked immunosorbent assay. Interferon-gamma (IFN-gamma) partially inhibited IL-2 or IL-4-induced proliferation of ATL cells. These results suggest that leukemic cells from ATL patients proliferate by an IL-2 or IL-4 paracrine mechanism in lymphoid tissue in vivo and that IFN-gamma inhibits IL-2- or IL-4-induced proliferation of ATL cells.

Aged↗
PubMed1993

Proliferative activation of quiescent Rat-1A cells by delta FosB.

Fos and Jun transcription factors are induced during the normal course of the proliferative response of quiescent cells to serum or to growth factors. We have shown that delta FosB, an alternatively spliced form of FosB, is formed as rapidly as FosB in serum-stimulated Rat-1A cells. Although delta FosB lacks the C-terminal region of FosB carrying the transactivation function, constitutive expression of delta FosB transforms Rat-1A cells as does expression of FosB. The transforming ability of delta FosB suggests that delta FosB may lead to proliferative activation of quiescent cells without activating AP-1-responsive genes. To address this question, FosB or delta FosB was expressed as a fusion protein with the ligand binding domain of the human estrogen receptor (ER) in Rat-1A cells. After estrogen treatment, the fusion protein accumulates in nuclei and forms stable complexes with Jun proteins. We have shown that ER-delta FosB or to a lesser extent ER-FosB triggers quiescent Rat-1A cells to transit G1, initiate DNA replication, and ultimately undergo cell division at least once. Since ER-FosB, but not ER-delta FosB, induced expression of the AP-1-responsive transin/stromelysin gene, we concluded that the N-terminal region and the DNA binding domain of FosB or delta FosB itself have the potential to regulate cell proliferation and that the transactivation function carried by the C-terminal region of FosB is not essential for the proliferative activation of quiescent cells.

Animals↗
PubMed1993

Inhibitory effect of volatile fatty acids on GRF-induced GH secretion in sheep.

The effect of intravenous infusion of acetate, propionate and butyrate (0, 3, 10, 30 mumol kg-1 min-1 over 40 min) on the secretion of growth hormone (GH), insulin and glucagon in response to growth hormone-releasing factor (GRF) injection (0.25 micrograms/kg, 10 min after the onset of acid infusion) was determined in six sheep. The intravenous injection of GRF caused a marked increase in plasma GH at every dose of each acid. The GH response to GRF was unaffected by an intravenous infusion of acetate. The basal plasma levels of insulin, glucagon and glucose were unchanged by acetate infusion. The infusion of propionate markedly suppressed the GH response to GRF in a dose-dependent manner. Propionate produced increases in plasma insulin, glucagon and glucose concentrations. Butyrate infusion also caused a significant attenuation of GRF-induced GH secretion. Butyrate infusion stimulated the secretion of both insulin and glucagon and caused hyperglycemia. After cessation of the infusion of propionate or butyrate plasma GH tended to increase again. Plasma somatostatin concentrations, which were measured only for the highest dose of butyrate, were unchanged during acid infusion, but increased on discontinuing the infusion. It is concluded that propionate and butyrate suppress GH secretion, while stimulating the secretion of insulin and glucagon in sheep.

Acetates↗
PubMed1993

Angiotropic lymphoma of paranasal sinuses with initial symptoms of oculomotor nerve palsy.

A 78-year-old female was found to have angiotropic lymphoma, a rare fatal disease, with initial symptoms of oculomotor nerve palsy. A biopsy of the paranasal sinus mucosa showed that the small vessels were occupied by large mononuclear cells which upon immunohistochemical examination tested positive for pre B-cell markers. She felt a gradually increasing pain in her left thigh. Magnetic resonance imaging suggested the involvement of neoplastic cells in the left femoral bone marrow. Following chemotherapy treatment remission was achieved. Early diagnosis of angiotropic lymphoma appears very significant, as this disorder could be well controlled by systemic chemotherapy.

Aged↗
PubMed1993

Intracranial complications of hypervolemic therapy in patients with a delayed ischemic deficit attributed to vasospasm.

This investigation has revealed the frequency of various intracranial complications that may result from hypervolemic therapy for a delayed ischemic deficit following subarachnoid hemorrhage (SAH). Among 323 patients with SAH, 112 patients developed a delayed ischemic deficit, 94 of whom underwent hypervolemic therapy. Infarction due to vasospasm was found ultimately in 43 of these 94 patients. Twenty-six patients (28%) developed an intracranial complication during hypervolemic therapy: cerebral edema was aggravated in 18, and a hemorrhagic infarction developed in eight. In 13 of 18 patients with aggravation of edema, delayed ischemic deficit developed within 6 days after the SAH; at that time, a massive new infarction was found in four and edema in 10 patients. After hypervolemic therapy, the 18 patients with aggravation of edema deteriorated rapidly, and 14 of them died. In every case in which hemorrhagic infarction followed hypervolemic therapy, a new infarct was found on computerized tomography (CT) when the delayed ischemic deficit became apparent. Hemorrhagic infarction developed as the delayed ischemic deficit resolved, with one exception. In patients who sustained no complication from hypervolemia, the incidence of both massive new infarction and edema at the time when the delayed ischemic deficit was manifested was only 1%. In 44 of 68 patients who sustained no complication from hypervolemia, the delayed ischemic deficit was manifested on or after the 7th day following the SAH. This study suggests that hypervolemic therapy is contraindicated in a patient who is found to have a massive abnormality on CT at the time when a delayed ischemic deficit is manifested, especially when it occurs within 6 days after the SAH. To avoid hemorrhagic infarction, it is important to discontinue hypervolemic therapy as soon as the delayed ischemic deficit resolves.

Adult↗
PubMed1993

Synaptic organization and prefrontal corticothalamic termination in the mediodorsal thalamic nucleus of the cat.

The synaptic organization of the mediodorsal thalamic nucleus (MD) in the cat have been studied with the electron microscope, and correlated with the termination of the medial prefrontal corticothalamic afferents using the method of anterograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). The neuropil of MD was divided into glomerular and extraglomerular regions. A synaptic glomerulus was composed of a central dendrite and some different presynaptic profiles with astroglial ensheathment. The prevalent presynaptic elements in glomeruli were presynaptic dendrites (PSDs) that contained pleomorphic vesicles, and formed symmetric synaptic contacts and puncta adhaerentia junctions with central dendrites. One or two large terminals with round vesicles and asymmetric specializations (LR) also participated in glomerular formations. They were invariably presynaptic to central dendrites and PSDs. As terminals less frequently found within glomeruli, there were small-sized terminals with round vesicles and asymmetric synaptic junctions with PSDs. In the extraglomerular neurophils, small to medium-sized terminals with pleomorphic vesicles (SMP) were found besides the presynaptic profiles identified in glomerular regions. These SMP terminals formed axodendritic and axosomatic symmetric synapses. WGA-HRP injections into the medial prefrontal cortex resulted in anterograde labelings in not only SR but also LR presynaptic terminals. SR boutons made up the majority of labeled terminals, and they were found only in the extraglomerular neuropil. While labeled LR terminals were detected in the extraglomerular neuropil and synaptic glomeruli with less encounter. The results of the present study show that the synaptic organization in MD of the cat is similar to that in other thalamic relay nuclei and in MD of the monkey. Further, MD receiving two subsets of synaptic terminations from the prefrontal cortex might play a different functional role in regulating the neural circuit between MD and the prefrontal cortex in comparison with that in the sensory and motor thalamic nuclei that receive only SR terminals from the sensorimotor cortex.

Animals↗
PubMed1993

Enhancing effects of IL-2 on M-CSF production by human peripheral blood monocytes.

Monocytes have the capacity to produce granulopoietic factors such as M-CSF and G-CSF. Our findings here showed that interleukin-2 (IL-2), at a concentration of more than 0.05 ng/ml, led to a 12-fold increase in the production of M-CSF in the human peripheral blood mononuclear cells after 72 h incubation compared to the control culture. Even in purified monocyte cultures with added IL-2, a 3-fold increase in M-CSF production was observed at an IL-2 concentration of 50 ng/ml. The enhancing effect of IL-2 on M-CSF secretion was also observed when IL-2-stimulated non-phagocytic cell-conditioned medium was added to monocyte cultures. These results indicated that IL-2, both directly and indirectly, activated monocytes to enhance the production of M-CSF. In addition, the expression of IL-2 receptor (CD25) on monocytes was more enhanced in cultures containing IL-2 than in cultures without IL-2. On the other hand, IL-2 did not induce G-CSF production in purified monocytes. These in vitro results suggest that when IL-2 is used clinically, the various biological activities of M-CSF should also be taken into consideration.

Cells, Cultured↗