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Biomedical subjects

Y Hakamata

Publications and source records attributed to Y Hakamata.

At least 55 records · Page 3Linked to original sources
PubMed1995

Coexistent myelodysplastic syndrome and non-Hodgkin lymphoma. Report of a case and review of the literature.

The patients with a hematopoietic neoplasm can develop myelodysplastic syndrome following chemotherapy. We report herein a case of non-Hodgkin B-cell lymphoma and refractory anemia with ringed sideroblasts. Absence of the preceding chemotherapy establishes the true coincidence of the two disorders. We review 25 similar cases reported in the last 11 years and discuss the possible etiology of coexistence.

Aged↗
PubMed1995

Long-term high-colloid oncotic therapy for ischemic brain edema in gerbils.

BACKGROUND AND PURPOSE: We evaluated the effects of long-term administration of high-colloid oncotic pressure on ischemic brain edema in Mongolian gerbils. METHODS: Animals that exhibited stroke after 35 minutes of unilateral forebrain ischemia were used. The gerbils were divided into albumin- (1 g/kg body wt, 25% albumin; n = 30) and saline-injected (4 mL/kg; n = 30) groups. Both agents were administered intravenously every 12 hours starting immediately after the recirculation. Plasma colloid oncotic pressure, serum sodium and potassium concentrations, and brain water, sodium, and potassium content were measured 24, 48, and 72 hours after recirculation. RESULTS: Plasma colloid oncotic pressure at 24, 48, and 72 hours after recirculation was significantly higher in the albumin- (26.1 +/- 2.3 mm Hg) than in the saline-treated group (18.5 +/- 1.9 mm Hg; P < .01), and brain water content of the ischemic hemisphere was significantly lower in the albumin group (79.5%, 80.2%, and 80.5%, respectively) than in the saline group (80.9%, 81.6%, and 82.1%, respectively; P < .05) at all three time points. Brain sodium content at 24 hours was significantly lower in the albumin than in the saline group (P < .05), while brain potassium content at 24 and 48 hours was significantly higher in the albumin than in the saline group (P < .05). The changes in brain water and sodium plus potassium content, which were calculated from differences between the ischemic and nonischemic hemispheres, showed a significant correlation in both groups (P < .01), but there was no significant difference between the linear regression lines for both groups. CONCLUSIONS: Long-term high-colloid oncotic pressure was effective in treating ischemic brain edema, probably acting by diminishing the bulk flow through the disrupted blood-brain barrier and ameliorating the vasogenic edema.

Albumins↗
PubMed1994

Involvement of the brain type of ryanodine receptor in T-cell proliferation.

Cloning and sequence analysis of cDNA showed that the brain type of ryanodine receptor (RYR) is expressed in human Jurkat T-lymphocyte cells. Fura-2 measurements revealed that the RYR in T-cells functions as a ryanodine-sensitive, caffeine-insensitive Ca2+ release channel. Furthermore, ryanodine stimulated proliferation and altered the growth pattern of cultured human T-cells when added together with FK506.

Amino Acid Sequence↗
PubMed1994

Multiple types of ryanodine receptor/Ca2+ release channels are differentially expressed in rabbit brain.

The neuronal Ca2+ signal is induced by a rise in the intracellular free Ca2+ concentration ([Ca2+]i), and is thought to be important for higher brain function. Dynamic changes in [Ca2+]i are affected by the spatial distributions of various Ca(2+)-increasing molecules (channels and receptors). The ryanodine receptor (RyR) is an intracellular channel through which Ca2+ is released from intracellular stores. To define the contribution of neuronal Ca2+ signaling via the RyR channel, we examined RyR type-specific gene expression in rabbit brain by in situ hybridization histochemistry. The neuronal RyR was composed of three distinct types, two types dominant in skeletal (sRyR) and cardiac (cRyR) muscle, respectively, and a novel brain type (bRyR). sRyR was distinguished by its high level of expression in cerebellar Purkinje cells. cRyR was predominantly expressed throughout nearly the entire brain, and was characterized by its markedly high level of expression in the olfactory nerve layer, layer VI of the cerebral cortex, the dentate gyrus, cerebellar granule cells, the motor trigeminal nucleus, and the facial nucleus. bRyR expression was the least widely distributed throughout the brain, and was high in the hippocampal CA1 pyramidal layer, caudate, putamen, and dorsal thalamus. This investigation demonstrates that the heterogeneous distribution of neuronal RyRs may be implicated in distinct Ca(2+)-associated brain functions. Moreover, it should be noted that cRyR, a typical CICR channel, is distributed widely throughout the brain, suggesting that in a variety of cell types, the amplification of neuronal Ca2+ signals is functionally accompanied by a rise in [Ca2+]i, such as Ca2+ influx stimulated by neuronal activity. This widespread distribution of the neuronal RyR family indicates that Ca2+ signals via the intracellular stores should be considered in studies of neuronal Ca2+ dynamics.

Animals↗
PubMed1993

Repeated unilateral carotid occlusion in Mongolian gerbils: quantitative analysis of cortical neuronal loss.

To develop an experimental model which enables quantitative analysis of chronic neuronal loss in the cerebral cortex, repeated ischemic insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The effect of the time interval between the repeated ischemic insult on the survival rate of the animals and the amount of cortical neuronal loss were examined. The time course of the cortical neuronal damage in repeated ischemic insult was also studied. We repeated the occlusion four times; i.e., one 10-min and three 7-min occlusions (total 31 min of ischemia). The number of animals surviving for 3 weeks after the last ischemic insult was minimum (15.4%) for animals undergoing occlusions at 1-h intervals and maximum (100%) at 24- and 48-h intervals. The number of ischemic neuronal deaths was also dependent upon the time interval, and it was so pronounced as to allow analysis at intervals of 12 hr or 24 hr in the absence of infarction in the cortex. The number of neuronal deaths could not be determined for animals with occlusion at 1-h intervals due to the production of a large infarction, with which the 3-week survival rate was minimum. The temporal profile of cortical neuronal loss in the repeated ischemic insult at 24-h intervals indicated that the number of cortical neurons significantly decreased until 7 days after the start of the ischemic procedure. This model is useful for clarifying the pathophysiology of chronically developing ischemic neuronal death.

Animals↗
PubMed1993

Changes in cranial and rectal temperature, blood pressure and arterial blood gas during and after unilateral and bilateral forebrain ischemia in Mongolian gerbils.

Transient forebrain ischemia was produced by occluding the common carotid arteries, either unilaterally or bilaterally, in Mongolian gerbils under halothane anesthesia. After 20-min ischemia, the cranial temperature measured in the temporal muscle decreased compared to the preischemic level, the decrease being larger after the bilateral than after the unilateral occlusion. After recirculation, cranial temperature recovered promptly to the preischemic level in the unilateral group, while it was elevated to above the preischemic level in the bilateral group. The rectal temperature also decreased with a similar time course. During 30-min ischemia, the blood pressure of both groups increased to above the preischemic level, the increase being larger in the bilateral group than in the unilateral group. After recirculation, blood pressure of the unilateral group recovered promptly to the preischemic level, while that of the bilateral group decreased to below the preischemic level. When forebrain ischemia was produced immediately after cessation of halothane inhalation, blood pH, PaO2 or PaCO2 did not change significantly from the control level. However, these values showed larger variation in the bilateral group than in the unilateral group. Unilateral occlusion in preselected gerbils provided a good model of transient brain ischemia, giving rise to uniform experimental results.

Animals↗
PubMed1992

Primary structure and distribution of a novel ryanodine receptor/calcium release channel from rabbit brain.

The complete amino acid sequence of a novel ryanodine receptor/calcium release channel from rabbit brain has been deduced by cloning and sequence analysis of the cDNA. This protein is composed of 4872 amino acids and shares characteristic structural features with the skeletal muscle and cardiac ryanodine receptors. RNA blot hybridization analysis shows that the brain ryanodine receptor is abundantly expressed in corpus striatum, thalamus and hippocampus, whereas the cardiac ryanodine receptor is more uniformly expressed in the brain. The brain ryanodine receptor gene is transcribed also in smooth muscle.

Amino Acid Sequence↗
PubMed1991

Basic fibroblast growth factor-like substance in nuclei of male germ cells undergoing meiosis.

The presence of a basic fibroblast growth factor-like immunoreactive substance was demonstrated in the nuclei of germ cells at stages from spermatocyte to spermatid in adult rat testis by using immunohistochemistry with an antibody raised against a synthetic peptide corresponding to residues 1-10 of bovine basic fibroblast growth factor [1-146]. The fluorescence was very weak in the nuclei and cytoplasm of spermatogonia, Sertoli cells, and most of the interstitial compartments, except for capillary endothelial cells. This is the first study to demonstrate the presence of basic fibroblast growth factor-like immunoreactive material in the nuclei of haploid cells in vivo.

Animals↗
PubMed1988

A new male hypogonadism mutant rat (hgn/hgn): concentrations of testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in the serum and the responsiveness of accessory sex organs to exogenous T, FSH, human chorionic gonadotropin, and luteinizing hormone-releasing hormone.

To determine the etiology of male hypogonadism in a newly found mutant rat (hgn/hgn, with a single autosomal recessive trait), concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured, and the responsiveness of the urogenital organs, hypothalamus, and pituitary gland to testosterone (1 mg/kg s.c. for 7 days), FSH (0.3 AU/kg s.c. for 7 days), human chorionic gonadotropin (hCG) (40 IU/kg s.c. for 7 days), and luteinizing hormone-releasing hormone (LHRH) (0.5 or 5.0 micrograms/kg s.c. for 7 days) were tested. Treatment with testosterone only increased the weights of all of the accessory sex organs, whereas treatment with FSH, hCG, or LHRH did not. Levels of serum FSH and LH were extremely higher and testosterone was lower in hgn/hgn males than in normal males. Serum FSH and LH decreased to levels found in intact animals after treatment with testosterone, suggesting that hypothalamic responsiveness to exogenous testosterone is present in the hgn/hgn males. Thus, the status of the hgn/hgn males was indicated to be due to primary Leydig cell dysfunction.

Animals↗
PubMed1986

A 7-hydroxymethyl sulphate ester as an active metabolite of the carcinogen, 7-hydroxymethylbenz[a]anthracene.

7-Hydroxymethylbenz[a]anthracene (7-HBA) showed potent mutagenicity towards Salmonella typhimurium TA 98 in the presence of untreated rat liver cytosol fortified with the PAPS-generating system, sodium sulphate and ATP. No mutagenic activity was observed either when the cytosol was boiled or when sodium sulphate or ATP was omitted from the assay medium. A highly reactive sulphate ester of 7-HBA was isolated and identified from the medium. It had a half-life of 3.5 min at 37 degrees C and pH 7.4 in water and showed potent, intrinsic mutagenicity towards TA 98. The mutagenicity of 7-HBA sulphate was almost completely retarded in the presence of the cytosol and glutathione. From the biological systems containing glutathione a non-mutagenic and stable glutathione conjugate was isolated that was assigned as S-(benz[a]anthracen-7-yl)methylglutathione. 7-HBA sulphate covalently bound to calf thymus DNA and cytosolic proteins. A fluorospectroscopic study indicated that the carcinogen bound to the biomacromolecules through its 7-methylene group with loss of a sulphate anion as a leaving group.

Animals↗
PubMed1983

Complete nucleotide sequence of the human corticotropin-beta-lipotropin precursor gene.

The nucleotide sequence of an 8658-base-pair human genomic DNA segment containing the entire corticotropin-beta-lipotropin precursor gene has been determined, and some sequence features of the gene and its flanking regions have been analysed. The gene is composed of 7665 base pairs including two introns of 3708 and 2886 base pairs. Comparison of the 5'-flanking sequences of the human, bovine and mouse corticotropin-beta-lipotropin precursor genes reveals the presence of a highly conserved region, which contains sequences of 14-15 base pairs homologous with sequences located upstream of the mRNA start site of other glucocorticoid-regulated genes.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Transmigration of donor cells involved in the sciatic nerve graft.

INTRODUCTION: Recently, human hand transplantation in Europe has shown that motor function may be recovered in some cases. However, little is known about cell trafficking involved the graft nerve. We have succeeded to use green fluorescent protein transgenic (GFP-Tg) rats with various cells strongly expressing GFP in a model a long-term survival of limb graft. In this model, we found retrograde migration of GFP-positive donor cells through the sclatic nerve anastomosis. It is well known that cellular components in the peripheral nerve graft especially Schwann cells, play an important role in the axonal regeneration promoted by nerve grafting. However, it was difficult to distinguish the cellular component of the nerve graft from recipient cells. The purpose of this study was to evaluate the migration of donor origin cells to the recipient's nerve and to examine the contribution of these cells in axonal regeneration using a simplified model of sciatic grafting. METHODS: Nerve defects were created in recipient rats, using three experimental combinations: group 1: wild-type rats from GFP Tg rats; group 2: GFP Tg rats from wild-type rats; group 3: wild-type rats from GFP Tg rats whose nerve grafts had been pretreated by freeze-thawing cycles (representing an acellular graft). The sciatic nerve specimens were examined under excitation light at 1, 2, and 3 weeks after transplantation. RESULTS: GFP-positive area expanded clearly beyond the anastomosis both proximally and distally in group 1 and infiltrated into the middle of the null graft in group 2. On the contrary, freeze-thawing grafts donated GFP Tg rats lost GFP expression completely. Columns of GFP-positive cells were formed in the degenerated graft migrated into the recipient's nerve both ante- and retrograde. The S100-positive GFP-positive cells were considered to be graft-origin Schwann cells. The regenerating axons were accompanied with these double-positive cells in the recipient nerve. In conclusion, we have visualized the contribution of graft cells to axonal regeneration beyond a peripheral nerve anastomosis.

Animals↗
PubMedDate not supplied

A novel immunomodulator KRP-203 combined with cyclosporine prolonged graft survival and abrogated transplant vasculopathy in rat heart allografts.

To find more effective and less toxic immunosuppressive strategies in long-term treatment for organ transplantation patients, we examined the effects on rat heart allograft survival of a novel sphigosine-1-phosphate receptor agonist, KRP-203, combined with a subtherapeutic dose of cyclosporine (CsA). Rat heart transplantation was performed across a major histocompatibility complex-incompatible (DA to LEW) rat combination. KRP-203 alone showed little or no effect on heart allograft survival. In contrast, KRP-203 combined with a subtherapeutic dose of CsA led to prolonged allograft survival. Histologic analyses showed that the combination completely suppressed acute rejection, as characterized by allograft vasculopathy, mononuclear cell infiltration, and myocardial necrosis in the heart allografts. RT-PCR analysis showed that the allografts treated with CsA or KRP-203 alone showed no suppression of IL-10, IFN-gamma, and TNF-alpha mRNA expression, but when combined with a subtherapeutic dose of CsA it completely suppressed their mRNA expressions. Furthermore, the combination treatment reduced donor-specific antibody production. KRP-203 combined with a subtherapeutic dose of CsA synergistically prolonged rat heart allograft survival. The combination of CsA with KRP-203 may provide an option to prevent allograft rejection and reduce adverse effects.

Animals↗
PubMedDate not supplied

Composite tissue transplantation in rats: fusion of donor muscle to the recipient site.

UNLABELLED: Little information currently exists on the repair of muscular tissue at the site of an amputation stump. This study examined the healing process of muscular tissue following composite limb transplantation using transgenic rat models. METHODS: Green fluorescent protein (GFP) transgenic rats were used to study the process of connection of donor muscle with the recipient. A DsRed2/GFP double-reporter transgenic rat and an NCre transgenic rat were used to study cell fusion. These rats have the unique characteristic of changing red fluorescence to green fluorescence by Cre/LoxP recombination when cell-to-cell fusion occurs between the two transgenic strains. Orthotopic hind limb transplantation was performed in two combinations: GFP transgenic rat to Wild Wistar rat and DsRed2/GFP transgenic rat to NCre transgenic rat. RESULTS: We observed extension of donor-derived GFP(+) myofibers into recipient site a few weeks after limb transplantation. A histologic study of the DsRed2/GFP transgenic rat to the NCre transgenic rat combination showed that red myofibers of the DsRed2/GFP rat were partly replaced by green myofibers as a result of Cre-mediated recombination. PCR analysis detected both the recombined transgene (330 bp) and the nonrecombined gene (1420 bp) in muscle around the junction. These findings indicate that the muscles sutured between the amputation stumps fused with each other and that donor-recipient hybrid cells were formed at the muscle junction following limb transplantation. CONCLUSIONS: This basic information shows muscle fusion between donor and recipient at the site of composite tissue transplant using newly established transgenic rats.

Animals↗
PubMedDate not supplied

Efficiency of adenovirus-mediated gene transduction in heart grafts in rats.

AIM: We determined the characteristics of transgene expression of heart grafts following ex vivo gene transfer using an adenovirus vector. Transgene expression was assessed periodically in the same animals by a non-invasive bioimaging system. METHODS: Rat heterotopic heart transplantation was performed in a syngenic combination. We infused 1 x 10(9) plaque-forming units of adenovirus vectors containing firefly luciferase gene into the heart graft via the coronary artery, with preservation at 4 degrees C and transplanted into the cervix of the recipient. Transgene expression was periodically visualized and quantified by a noninvasive bioimaging system without sacrificing experimental animals. RESULTS: Transgene expression in the graft peaked at day 7 and then fell gradually. Transgene expression was also observed in the recipient liver. CONCLUSIONS: We have determined the time course of transgene expression in the heart graft. This constitutes important information about ex vivo gene therapy for heart grafts.

Adenoviridae↗