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Biomedical subjects

J Itoh

Publications and source records attributed to J Itoh.

At least 73 records · Page 4Linked to original sources
PubMed1994

Management of acute leukemia during pregnancy: from the results of a nationwide questionnaire survey and literature survey.

In March, 1993, a questionnaire was sent to 362 gynecological and obstetric offices of national, prefectural and municipal hospitals and private university hospitals with 250 beds or more. Answers were collected from 260 institutions. Thus, this study analyzed 39 patients with acute leukemia during pregnancy collected by the questionnaires survey and 64 cases reported in the Japanese literatures during 1975-1993 (total 103 patients). The weeks of pregnancy were defined as the 1st (< 15th week), 2nd (16th-27th week), and 3rd (> 28th week) trimesters. The time of diagnosis of leukemia during pregnancy changed from 25% in the 2nd trimester and 62% in the 3rd trimester during 1975-1984 to 39% and 48% after 1985, respectively. After 1985, the remission rate was 72% in the questionnaire group and 75% in the group from literatures. There was no statistical difference. The 50% survival period was 12 months in the group during 1975-1984, but 25 months in the group after 1985. The survival was significantly longer in the patients whose induction therapy was started before delivery than in those treated after delivery. The results suggest that the treatment for acute leukemia during pregnancy should be initiated as soon as possible after the diagnosis of leukemia, with carefully selected regimens. It is important that the time of delivery should be selected considering the maternal and fetal conditions after consultation with an obstetrician.

Adult↗
PubMed1994

Clinical and immunohistochemical studies on TSH-secreting pituitary adenoma: its multihormonality and expression of Pit-1.

Eight patients with thyrotropin (TSH)-secreting pituitary adenoma are described. Serum TSH levels were inappropriately elevated in spite of elevated thyroid hormones. The serum-free glycoprotein alpha-subunit level was elevated in all the patients. The alpha-subunit to TSH molar ratio, a "tumor marker" for TSH-secreting adenoma, ranged from 1.06 to 6.16. All patients had macroadenoma and underwent transsphenoidal surgery. Light-microscopic indirect immunoperoxidase method applied on formalin-fixed paraffin-embedded specimens revealed alpha-subunit and TSH beta immunoreactivity in all adenomas. The proportion of TSH beta-positive cells ranged from 20% to 75% of adenoma cells. Six adenomas (75%) were associated with growth hormone (GH) and/or prolactine (PRL) immunoreactivity. By the double staining method, TSH beta and the alpha-subunit were frequently colocalized in the same cells, but some cells were found to contain either alpha-subunit or TSH beta. We also analyzed the localization of a pituitary-specific transcriptional factor, Pit-1, which has been suggested to play a role in functional differentiation toward growth hormone, prolactine, and TSH. All cases were positive for Pit-1 product using antibody against human Pit-1 synthesized peptide. Pit-1 product was localized in the nuclei of many adenoma cells and was frequently identified in cells that were positive for both TSH beta and growth hormone or prolactine. From our investigations, the role of Pit-1 in multidirectional differentiation during the development of TSH-secreting adenoma was suggested.

Adenoma↗
PubMed1994

Dynorphin A-(1-13) potently improves the impairment of spontaneous alternation performance induced by the mu-selective opioid receptor agonist DAMGO in mice.

The effects of i.c.v. injection of the mu-selective opioid receptor agonist DAMGO and the effects of its combination with the endogenous kappa-opioid receptor agonist dynorphin A-(1-13) on memory processes were examined in mice, using spontaneous alternation performance associated with working memory in a Y-maze. DAMGO (10 and/or 30 ng) impaired spontaneous alternation performance and increased total arm entries, which are considered to reflect locomotor activity. beta-Funaltrexamine (5 micrograms, i.c.v.), a mu-selective opioid receptor antagonist, almost completely antagonized the impairment of alternation performance induced by DAMGO (10 ng). Physostigmine (0.1 mg/kg, i.p.), a cholinesterase inhibitor, improved the DAMGO (10 ng)-induced impairment of alternation performance. Dynorphin A-(1-13) (1, 3 and 10 micrograms, i.c.v.) alone was without significant effects on alternation performance. On the other hand, dynorphin A-(1-13) (3 and 10 micrograms) significantly improved the impairment of spontaneous alternation performance induced by DAMGO (10 ng). The effects of dynorphin A-(1-13) (3 micrograms) on the DAMGO-induced impairment of spontaneous alternation were almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid receptor antagonist. The present results demonstrate that DAMGO impairs alternation performance by activating mu-opioid receptors, whereas dynorphin A-(1-13) attenuates the DAMGO-induced impairment of alternation performance through the mediation of kappa-opioid receptors. These findings suggest that mu- and kappa-opioid systems are fully involved in memory function and have opposite effects on spontaneous alternation performance as it is reflected by working memory in mice.

Analgesics↗
PubMed1994

Enhanced expression of transforming growth factor-beta s and transforming growth factor-beta type II receptor in the synovial tissues of patients with rheumatoid arthritis.

BACKGROUND: A growing body of evidences suggests that transforming growth factor-beta (TGF-beta) is produced in the synovial fluid of patients with rheumatoid arthritis (RA), and that TGF-beta is an important regulator in the course of the disease. Careful studies on the endogenous synthesis of TGF-beta as well as its receptors are therefore necessary to clarify the possible role of TGF-beta in RA. EXPERIMENTAL DESIGN: We examined the expressions of latent TGF-beta 1, -beta 2, and -beta 3, the latent TGF-beta 1-binding protein (LTBP) as well as TGF-beta type II receptor (TGF-beta RII) in the synovial biopsy tissues of 21 patients with RA by immunohistochemistry. Five specimens from these cases representing both active and chronic inactive stages were also examined for the corresponding mRNA by in situ hybridization. Northern blot analysis was performed on 3 synovial membranes taken from the RA patients together with a control synovium. RESULTS: Abundant LTBP, TGF-beta 1, and TGF-beta RII-positive cells as well as less intensively stained TGF-beta 2 and TGF-beta 3-positive cells were found in the synovial layer. These cells were positive for the histocompatibility antigen, HLA-DR. In lymphocyte aggregates, scattered cells positively labeled for LTBP and TGF-beta 1 were found. They stained in a reticular pattern that was similar to that demonstrated by an antibody against human dendritic cells, and also expressed HLA-DR. In situ hybridization revealed markedly increased signals for LTBP and TGF-beta RII mRNA in tissues with an active inflammatory process, when compared with tissues with less active inflammation. However, no clear differences in the levels of expression for any of the TGF-beta isoforms were found. Specimens with pronounced fibrosis, fibroblasts, and surrounding collagen fibers expressed positive immunoreactivities for all TGF-beta isoforms and LTBP. Northern blot analysis on 4 synovial tissues demonstrated positive signals for LTBP and TGF-beta 1 mRNA in all three RA patients in contrast to a normal control, which did not show any signals. An increased expression of TGF-beta RII mRNA was detected in the tissue from one of the patients. CONCLUSIONS: An abundant expression of TGF-beta 1 and LTBP, as well as TGF-beta RII was seen in most actively proliferating synovial intimal cells, and the level of the expression varied during the course of the disease. We conclude that TGF-beta is involved tightly in the regulation of the inflammatory process, and it is thus possible that the endogenous TGF-beta functions as a self-regulator that induces the remission periods.

Amino Acid Sequence↗
PubMed1993

Dopaminergic involvement in the improving effects of dynorphin A-(1-13) on scopolamine-induced impairment of alternation performance.

The present study was designed to clarify whether dopamine systems are involved in the effect of dynorphin A-(1-13), an endogenous kappa-opioid receptor agonist, on the scopolamine-induced impairment of spontaneous alternation performance related to working memory in mice. Sulpiride (10 and/or 30 mg/kg), a dopamine D2-selective antagonist, markedly improved the impairment of alternation performance and significantly reduced the increase in total arm entries (i.e. locomotor activity) induced by scopolamine (1 mg/kg). In contrast, SCH 23390 (0.01, 0.03 and 0.1 mg/kg), a dopamine D1-selective antagonist, did not influence the impairment of alternation performance, whereas it dose dependently reduced total arm entries in scopolamine-treated mice RU 24213 (1 mg/kg), a dopamine D2-selective agonist, almost completely reversed the improving effect of dynorphin A-(1-13) (3 micrograms) on the scopolamine-induced impairment of alternation performance and reduced total arm entries, although it was without effects on behavioral responses in normal mice. However, SKF 38393 (3 and 10 mg/kg), a dopamine D1-selective agonist, failed to change alternation performance or total arm entries in normal or scopolamine-treated mice. These findings suggest that the impairment of spontaneous alternation performance induced by scopolamine is improved by the blockade of dopamine D2 receptors. Furthermore, the improving effect of dynorphin A-(1-13) on the scopolamine-induced impairment of spontaneous alternation performance may be based upon the inhibition of dopaminergic activity through the mediation of kappa-opioid receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

U-50,488H, a kappa-opioid receptor agonist, markedly prevents memory dysfunctions induced by transient cerebral ischemia in mice.

Transient ischemia produced marked memory dysfunctions in mice on three different tasks, spontaneous alternation, elevated plus-maze and passive avoidance, as tested 1, 1-2, and 2-3 days after ischemic insult, respectively. U-50,488H, a kappa-opioid receptor agonist, administered 20 min before ischemic insult markedly prevented the impairment of spontaneous alternation, the prolongation of transfer latency in elevated-plus maze and the shortening of step-through latency in passive avoidance induced by transient ischemia. The protective effect of U-50,488H (30 mg/kg) on ischemia-induced memory dysfunctions observed in the three tasks was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid antagonist. Although U-50,488H (30 mg/kg) did not affect body temperature in sham mice, it blocked hypothermia induced by ischemic insult. These results suggest that the protective effect of U-50,488H on memory dysfunctions in ischemic mice is associated with the activation of kappa-opioid receptors and is not based upon hypothermia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Dynorphin A-(1-13) markedly improves scopolamine-induced impairment of spontaneous alternation performance in mice.

The effect of intracerebroventricular (i.c.v.) injection of dynorphin A-(1-13) on the memory process was examined in mice, using spontaneous alternation performance related to working memory in a Y-maze. Dynorphin A-(1-13) (1, 3 and 10 micrograms) influenced neither spontaneous alternation performance nor total arm entries, which are considered to reflect locomotor activity. In contrast, dynorphin A-(1-13) (3 and 10 micrograms) significantly improved the impairment of spontaneously alternation performance induced by scopolamine (1 mg/kg s.c.). Simultaneously, the scopolamine-induced increase in total arm entries was markedly attenuated by dynorphin A-(1-13) (10 micrograms). The effect of dynorphin A-(1-13) (3 micrograms) on the scopolamine-induced impairment of spontaneous alternation was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms i.c.v.), a kappa-selective opioid antagonist. These findings suggest that dynorphin A-(1-13) improves through the mediation of kappa-opioid receptors the scopolamine-induced impairment of spontaneous alternation performance associated with working memory.

Analysis of Variance↗
PubMed1993

Dynorphin A-(1-13) potently prevents memory dysfunctions induced by transient cerebral ischemia in mice.

The effect of dynorphin A-(1-13), an endogenous kappa-opioid receptor agonist, on memory dysfunctions induced by transient cerebral ischemia in mice was investigated by using three different tasks, namely, spontaneous alternation, elevated plus-maze performance, and passive avoidance behavior. Transient ischemia produced a marked memory dysfunction in mice, as assessed in the three tasks, which were carried out consecutively 1 to 3 days after the ischemic insult. The i.c.v. injection of dynorphin A-(1-13) before the ischemic insult potently prevented the impairment of spontaneous alternations, the prolongation of transfer latency in the elevated plus-maze and the shortening of step-through latency in the passive avoidance task induced by transient ischemia. Dynorphin A-(1-13) (10 micrograms), however, did not affect the body temperature of the sham-operated or the ischemic mice. The protective effect of dynorphin A-(1-13) (10 micrograms) on ischemia-induced memory dysfunctions observed in the three tasks was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid receptor antagonist. These results suggest that dynorphin A-(1-13) prevents memory dysfunctions in ischemic mice through the activation of kappa-opioid receptors.

Animals↗
PubMed1993

Cloning and cDNA sequence analysis of nephritogenic monoclonal antibodies derived from an MRL/lpr lupus mouse.

Production of IgG3 in MRL/Mp-lpr/lpr (MRL/lpr) lupus mice is one of the major factors to develop glomerulonephritis (GN) in these mice. To examine molecular characteristics of IgG3 responsible for GN in these mice, hybridoma clones producing IgG3 antibodies were prepared from one unmanipulated MRL/lpr mouse. Two clones, 2B11.3 and 7B6.8, were nephritogenic; that is, they caused severe glomerular lesions when injected to normal mice, moreover with a different histopathological manifestation. The 2B11.3 clone generated diffuse cell-proliferative lesions, while those induced by the 7B6.8 clone resembled wire loop lesions in human lupus nephritis. The cDNA sequence analysis of 7B6.8 antibody and the other IgG3 antibody, 1G3, non-nephritogenic, revealed that the C regions of the heavy and light kappa chains were completely the same between them. Furthermore, they were identical in deduced amino acid sequences to those from non-autoimmune BALB/c mice, indicating no allelic difference of Igh-8 between these two strains. The V regions of 2B11.3 and 7B6.8 antibodies were composed of different sets of VH, D, JH, Vk and Jk. Although both of the VH belonged to the J558 family, they seemed to use a different VH germline gene. These findings suggest that GN in MRL/lpr mice is generated by the expansion of clonally different B cells producing particular antibodies possibly with a different pathogenetic potency.

Amino Acid Sequence↗
PubMed1993

Differentiation of hematuria using a uniquely shaped red cell.

Although variously shaped urinary red cells have been reported in glomerulonephritic hematuria, no specific shapes with concrete definition have been proposed. This made morphological differentiation of hematuria vague and caused different results among different observers. To solve these problems and improve the diagnostic rate, we employed a uniquely shaped red cell, which only appeared in glomerulonephritic hematuria, as a probe for diagnosis. We studied 182 hematuria cases from 90 glomerulonephritic patients and 95 hematuria cases from 68 urological disease patients. Fresh urine was collected and observed by differential interference microscopy. The red cell, referred to as G1, has a distinctive doughnut-like shape with blebs and was highly specific for glomerulonephritic hematuria. Occurrence of G1 cells increased at lower pH an higher osmolality of urine. A presence of 5% or more G1 cells could be an indicator of glomerulonephritic hematuria. Specificity and sensitivity of this criterion were 100 and 73%. However, when only acidic concentrated urine (pH < or = 6.4, osmolality > or = 400 mosm/kg H2O) was used, the specificity and sensitivity increased to 100 and 99.2%, respectively. Glomerulonephritic and urological hematuria were correctly diagnosed by counting the urinary red cells with doughnut-like shape in acidic and concentrated urine. This method seems to be superior to others in diagnostic rate, simplicity and clarity.

Adolescent↗
PubMed1993

Induction of different types of glomerulonephritis by monoclonal antibodies derived from an MRL/lpr lupus mouse.

MRL/Mp-lpr/lpr(MRL/lpr) lupus mice develop glomerulonephritis in which the histopathological manifestations of the disease are characterized by diffuse cell-proliferative, crescentic, and/or wire loop-like lesions, resembling those of human lupus nephritis. Although these lesions are thought to be mediated by antibodies, little data is available to explain these regular variations in glomerular lesions induced by antibodies at the monoclonal level. We studied glomerular lesions of normal or severe combined immunodeficient mice injected with nephritogenic immunoglobulin G3-producing hybridoma clones (2B11.3 and 7B6.8), which we previously established from an unmanipulated MRL/lpr mouse. Both clones caused increased serum levels of immunoglobulin G3 with identical patterns over time and both induced glomerular deposits of immunoglobulin G3 and C3. However, 2B11.3 and 7B6.8 induced glomerular lesions that differed in their histopathological manifestations. The 2B11.3 clone generated cell-proliferative lesions associated with marked Mac-2-positive macrophage infiltrates, but the 7B6.8 clone induced lesions characterized by subendothelial hyaline deposits resembling wire loops. The latter was not associated with significant inflammatory cell infiltrates at any point throughout the progression of the lesion. Thus, our findings suggest that the histopathological variation in glomerulonephritis seen in MRL/lpr mice results from clonally expanded B cell clones that produce nephritogenic antibodies with different pathogenic potencies.

Animals↗
PubMed1992

Continuous recording of changes in intracranial pressure using interference echoes of ultrasonic wave: a preliminary report of practicality and clinical evaluation.

We attempted to examine intracranial pressure (ICP) noninvasively using probes receiving interference echoes of ultrasound from thin layers between the skull and the surface of the cerebrum. The reception of echo through bone flaps less than 5-mm thick was good. Normal adults (4) and patients (4) were examined by attaching ultrasound probes to the frontotemporal scalp. Recordings were performed during rest, Valsalva maneuver, hyperventilation, and pumping of a shunt-flushing device. Ultrasound recordings of ICP were compared with those of the scalp using two different time windows. The effect of scalp vessels on the ultrasound recordings of ICP was evaluated. The waves from a pressure transducer and the ultrasound probe were similar. This method was found to be useful for ICP recording.

Adolescent↗
PubMed1992

Tumor diagnosis by PET: potential of seven tracers examined in five experimental tumors including an artificial metastasis model.

The potential of seven tracers for the metabolic imaging of tumors by positron emission tomography was studied using five experimental tumor models. The tracers examined were 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG), 2-deoxy-2-[18F]fluoro-D-galactose (2-[18F]FdGal) and 2-deoxy-2-[18F]fluoro-L-fucose (2-[18F]FdFuc) for investigating energy metabolism. L-[methyl-11C]Methionine ([11C]Met) and 6-[18F]fluoro-L-fucose (6-[18F]FFuc) were used for assessing protein and glycoprotein synthesis, while [3H]thymidine ([3H]Thd) and 2-deoxy-5'-[18F]fluorouridine ([18F]FdUrd) were used to investigate nucleic acid metabolism. The highest mean uptake by the five different tumors was found for [3H]Thd, followed in order by [18F]FDG, [11C]Met, 2-[18F]FdGal, [18F]FdUrd, 2-[18F]FdFuc and 6-[18F]FFuc. The tumor-to-tissue uptake ratios indicated that the nucleosides, [11C]Met and 6-[18F]FFuc were better tracers in the brain region. All the tracers except for the fucose analogs were suitable for the thoracic region, while [11C]Thd and [18F]FDG were superior in the abdominal region. In comparison with the primary tumor model of Lewis lung carcinoma (3LL), [3H]Thd uptake in the artificial metastatic 3LL model showed the maximum enhancement, followed by [18F]FDG, [11C]Met and the other tracers. The [18F]FDG uptake correlated with the [3H]Thd uptake. [18F]FdUrd, 6-[18F]FFuc and 2-[18F]FdGal could be used for distinguishing different types of tumors. The combined use of these radiotracers can possibly allow the assessment of tumor metabolism, and this indicates the viability of tumors.

Animals↗
PubMed1992

Spinous process-splitting laminoplasty using hydroxyapatite spinous process spacer.

Between February 1986 and August 1989, 45 patients with cervical myelopathy were treated by spinous process-splitting laminoplasty. Hydroxyapatite intraspinous spacers were used to maintain the enlargement of the cervical spinal canal. The shape of this spacer is trapezoidal. After sagittal splitting of the spinous process, the spacer was inserted between the two halves and affixed with the wire. Histologic study showed there was good fusion between the spacer and bone. In all cases, good enlargement of the cervical spinal canal was achieved. Spacer displacement, wire breakage, and postoperative infection were not seen. There was no postoperative neurologic deterioration. Computed tomography showed that the width of the cervical spinal canal was maintained.

Animals↗
PubMed1992

Spontaneous development of pancreatitis in the MRL/Mp strain of mice in autoimmune mechanism.

MRL/Mp mice are known to have autoimmune disease-prone genetic background, which contributes to the development of a lethal autoimmune disease at an early age in association with the lymphoproliferative gene, lpr. In this study, we found that MRL/Mp mice, not bearing lpr (MRL/Mp-(+)/+), spontaneously developed pancreatitis at a late stage of life, which was histopathologically characterized by destruction of pancreatic acinar cells with mononuclear cell infiltration. In female 34-38-weeks-old mice the incidence of pancreatitis reached 74%, whereas the male mice developed the disease with a reduced incidence, at a later stage of life and with a reduced severity. Cell infiltrates in the affected lesions were composed predominantly of CD4+ cells and to lesser extent Mac-2+ macrophages. Adoptive transfer of the spleen cells obtained from pancreatitis-bearing female mice generated pancreatitis in female normal mice, but not in the male mice. Transfer of the serum of pancreatitis-bearing mice failed to induce any pancreatic lesions. These findings indicate that pancreatitis in MRL/Mp-(+)/+ mice may be mediated by cellular autoimmune mechanism. This may present a useful concept for analysis of the developmental mechanisms of human chronic pancreatitis in an aspect of autoimmunity.

Animals↗
PubMed1992

Application of two-color immunofluorescence staining to demonstration of T-cells and HLA-DR-bearing cells in rheumatoid synovitis.

We studied the localization of T-cells and HLA-DR antigen-bearing (DR+) cells in rheumatoid synovitis by employing an improved two-color immunofluorescent staining (TCIF) technique. With this technique we have successfully identified DR+ activated T-cells in the inflammatory synovium. T-cells expressed HLA-DR antigen when they were in contact with DR+ antigen-presenting cells (APC). In addition, activated T-cells showed characteristic distribution within the synovium: they were found around high endothelial venules, within lymphoid follicles, and in hyperplastic synovial lining, suggesting their involvement in the development of rheumatoid synovial lesions via interaction with synovial DR+ APC lineage cells. These findings may contribute to better understanding of the role of activated T-cells in the histogenesis of rheumatoid synovitis, a typical chronic inflammatory lesion.

Arthritis, Rheumatoid↗