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Biomedical subjects

Y Eishi

Publications and source records attributed to Y Eishi.

At least 19 recordsLinked to original sources
PubMed1995

Ultrastructural features of alveolitis in sarcoidosis.

Seventy-nine specimens of lung parenchyma from 61 patients with sarcoidosis were examined ultrastructurally with a focus on alveolitis, and they were compared with specimens of hypersensitivity pneumonitis (HP) and the percentage of lymphocytes in bronchoalveolar lavage fluid (BALF). Lymphocytes and monocytes were frequently observed in the capillary lumina, and these cells and macrophages were found in the interstitium of the alveolar walls in the specimens with alveolitis of sarcoidosis and HP. Increases in the percentage of lymphocytes in BALF correlated with the degree of alveolitis. Swelling and bleb formation of the endothelium of alveolar capillaries and changes in the capillary basement membrane were commonly found and were significantly increased in the specimens with alveolitis. The frequency of bleb formation was significantly higher in alveolitis of sarcoidosis than in that of HP. However, the changes in alveolar epithelium were not significant in sarcoidosis. Microvascular changes in alveolitis are not specific for sarcoidosis, but they are observed in other interstitial lung diseases. These alterations may play an important role in the development of pulmonary sarcoidosis.

Adult↗
PubMed1994

Paraneoplastic encephalo-myelo-ganglionitis: cellular binding sites of the antineuronal antibody.

The cellular binding sites of an antineuronal antibody were characterized in an autopsy case of the paraneoplastic encephalo-myelo-ganglionitis. A 61 year-old woman developed a subacute sensorimotor polyneuropathy and, later, multiple involvement of cranial nerves, disturbance of consciousness, and generalized seizure. An autopsy revealed a small cell lung carcinoma and neuropathological changes that included disseminated encephalitis, spinal anterior horn lesions, severe loss of dorsal root ganglion neurons, and secondary degeneration and loss of the nerve fibers in the spinal posterior column and peripheral nerves. The serum IgG from the patient contained antineuronal antibody(s) including an antibody to 35- to 37-kDa neuronal antigens called anti-Hu as demonstrated in Western blot. In immunohistochemical studies, the serum IgG immunostained neurons of the brains, spinal cords, and dorsal root ganglia of humans or rats. Confocal laser-scanning microscopy revealed binding of the patient's IgG in the neuronal nuclei and cytoplasm, but not in the nucleoli. In immunoelectron microscopic studies, immunolabelling with the IgG was found diffusely in the karyoplasm, excluding nucleoli, and in the cytoplasmic matrix between the cisternae of the reticulums, Golgi apparatus, and mitochondria. Encephalo-myeloganglionitis is a clinicopathological entity frequently associated with the presence of neoplasm and antineuronal antibody, however, the role of the antibody in the pathogenesis remains to be elucidated.

Autoantibodies↗
PubMed1994

Transferrin receptor in oral tumors.

The transferrin receptor (TfR) appears in vigorously proliferating cells. We did an immunohistochemical study of TfR in oral tissues and a quantitative analysis by flow cytometry of TfR in a cancer cell line after an anticancer drug treatment. TfR was found in the parabasal and basal layers of the normal epithelium, but rarely in benign tumors. Generally, in the malignant tumors, the poor prognostic cases showed strong staining regardless of the differentiation of the tumor. In the flow cytometric analysis, the amount of TfR decreased according to the reduction of the proliferative ability of cancer cells. These results suggest that TfR expression may be useful as a prognostic marker.

Adult↗
PubMed1994

[Seeking a causative agent of sarcoidosis].

Bacterial components (MDP and IT27 antigen), demonstrated in sarcoid granulomas, strongly suggest the causative agent of sarcoidosis to be derived from some bacteria but many kinds of bacteria are known to have these bacterial components. Our PCR detection of mycobacterial DNA could not demonstrate a significant contribution of M. tuberculosis to the pathogenesis. We then developed a monoclonal antibody to the causative agent by immunizing mice with a crude homogenate of the affected lymph nodes. Hybridized spleen cells were checked with ELISA and all the Ig-producing cell colonies were examined by immunostaining on paraffin sections of lymph nodes with sarcoidosis or tuberculosis. The established antibody (SG5) recognized some extrinsic antigens sequestrated in sarcoid granulomas, in a similar pattern of distribution to those of the bacterial component of MDP and the bacterial product of IT-27. Moreover, ELISA analysis of the SG5 antibody revealed a specific reactivity to culture supernatant of P. acnes. By the immunization of mice with a crude bacterial extract of P. acnes, we recovered one clone of hybridoma named PAB antibody, that possessed an identical reactivity to that of SG5 antibody, as far as examined by ELISA and immunohistochemistry. Furthermore, PCR detection of P. acnes DNA resulted in 92% (36/39) positive in the lymph nodes with sarcoidosis and 41% (12/29) in the control lymph nodes, with a significant difference (p < 0.001, by Fisher's Probability Test) between these two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Basic fibroblast growth factor (bFGF) receptors decrease with luteal age in rat ovarian luteal cells: colocalization of bFGF receptors and bFGF in luteal cells.

Ovarian growth factors have been implicated in the development and differentiation of corpus luteum. We have characterized both high and low affinity receptors for basic fibroblast growth factor (bFGF) in luteal cells and tissue throughout the life span of corpus luteum using gonadotropin-treated rat luteinized ovaries. Additionally, we determined bFGF location in luteal tissue. High affinity (Kd, approximately 0.2 nM) and low capacity (approximately 500-6000 sites/cell, depending on luteal ages) [125I] bFGF-binding sites (mol wt, 140 kilodaltons, determined by affinity labeling) were found on luteal cells. [125I]bFGF binding to luteal cells and corpus luteum membranes progressively decreased in binding capacity without affecting binding affinity as the age of corpus luteum advanced. bFGF receptor (flg) mRNA in luteinized ovaries decreased with the luteal age similar to the [125I]bFGF binding. In contrast, low affinity binding sites, identified as heparan sulfate proteoglycans, which were immunohistochemically visualized around luteal cells, did not appear to change with luteal age. The signals for heparan sulfate proteoglycans that were found only in granulosa, but not theca-interstitial, cells of follicles became intense during folliculogenesis. The functionality of the bFGF receptors was shown by tyrosine phosphorylation of 16.5- and 18-kilodalton proteins in luteal cells with the antiphosphotyrosine antibody. Immunohistochemistry localized bFGF to steroidogenic luteal cells, and immunoblotting displayed larger molecular forms of bFGF in luteal cells. These results suggest that the bFGF receptors may be associated with the development and differentiation of corpus luteum in an autocrine manner.

Animals↗
PubMed1991

Human autoantibody to Sertoli cells detected in healthy individuals.

Human autoantibody to Sertoli cells was detected in normal human sera. This IgM-type autoantibody was undetectable during the neonatal period and was found in 11.5% of 365 serum samples taken from adult healthy persons of both sexes. This human autoantibody to Sertoli cells exhibited quite the same target-organ specificity and multi-organ reactivity (salivary gland ductules, pancreatic intercalated duct, renal lower nephron, pituitary acidophilic cells) as those of the murine monoclonal autoantibody (IgM class) to Sertoli cells (TM-1: WHO registered code T43). The TM-1 monoclonal antibody could recognize testicular antigens with molecular weights of 67,000 and 23,000 in Sertoli cells, and had already been demonstrated capable of inducing murine experimental spermatogenic disturbance when administrated together with murine monoclonal autoantibody to seminiferous tubular basement membrane (TM-2: WHO registered code T44). These observations may suggest that human spermatogenic disturbance could be easily induced by the multi-organ reactive autoantibody to Sertoli cells even in healthy individuals under particular conditions where this autoantibody can be allowed to reach the target Sertoli cells across the barrier of seminiferous tubular wall by either autoantibody to seminiferous tubular basement membrane or other toxic damage.

Adolescent↗
PubMed1991

Developmental expression of autoimmune target antigens during organogenesis.

A common factor existing among autoimmune target antigens was sought in association with their developmental expression during organogenesis. Autoimmunity against a certain organ was experimentally induced in rats by deliberate immunization with whole tissue extract of the respective organ. Histopathological changes in a target organ of the immunized rats were recorded, and tissue specificity of the raised autoantibodies was immunohistologically examined with tissue sections of normal adult rats. These immune sera were also reacted with tissue sections of a target organ in each stage of organogenesis, and the time of first expression of the target antigen was determined for each immune serum. As a result, induced autoantibodies were directed only to a limited number of tissue antigens, such as thyroid follicular antigens [gestation day 17 (17 GD)], salivary ductal antigens (18 GD), anterior pituitary antigens (21 GD), gastric parietal cell antigens (22 GD), neural myelin antigens (2 days after birth), retinal photo-receptor cell antigens (3 days after birth) and testicular germ cell antigens (4 weeks after birth). They were first expressed on the day indicated in parentheses. Comparing with the development of the immune system, which was monitored by demonstrating CD4- and/or CD8-positive cells in the developing thymus and spleen, a common feature of these potential autoimmune target antigens was found to be that they were expressed either in parallel with, or after, but never before, the development of the immune system. This observation might suggest why only a limited number of self antigens can be autoimmune target antigens among the enormously large number of antigen determinants existing in the whole extract of each organ.

Animals↗
PubMed1991

Transferrin receptor expression in oral tumors.

Transferrin receptor expression in oral tumors was examined by staining with monoclonal antibody against the human transferrin receptor. The cells with positive reaction were recognized in the basal and parabasal layers of the normal epithelium. The staining was found in all the malignant tumors but not in the benign tumors. These results suggest that the immunohistochemical analysis of the transferrin receptor is useful for the diagnosis of oral malignant tumor in addition to the clinical and pathological examinations.

Antibodies, Monoclonal↗
PubMed1989

Adult pigment type (Peiffer) of sudanophilic leukodystrophy. Pathological and morphometrical studies on two autopsy cases of siblings.

Two autopsy cases of siblings with the adult pigment (Peiffer) type of sudanophilic leukodystrophy (SLD), which demonstrated the full-blown stage (case 1) and early stage (case 2) of demyelination, were examined. Numerous brown pigments deposited in demyelinated cerebral areas were characterized histochemically and ultrastructurally as lipofuscin and ceroid. Under the electron microscope formation of blebs due to myelin splitting associated with deposition of multilamellar myeloid bodies within them was a prominent feature in the demyelinated cerebral areas of case 2 as compared with case 1. However, various features of myelin degradation such as thinning, partial or complete circumferential myelin loss, and deposition of electron-dense material on the interperiodic lines were found in both cases. Blebs occurred in all layers of myelin, and axons were compressed by these blebs or the hydropically swollen inner lips of oligodendroglias. Oligodendroglias were relatively well preserved in the demyelinated and nondemyelinated areas in case 2, although the cytoplasm was hydropic. Many spheroids were present in demyelinated areas and were irregularly distributed in both cases. The peripheral nerves in case 1 presented essentially the same changes as those in the brain, although those in case 2 were not affected. Morphometrically, the results showed that hypomyelination was not the mechanism for this pigment type of SLD. One possible cause may be an accelerated ageing of the metabolic process of myelin turnover.

Astrocytes↗
PubMed1988

Splenic hemopoiesis of the platypus (Ornithorhynchus anatinus): evidence of primary hemopoiesis in the spleen of a primitive mammal.

The generation of blood cells has been observed in the spleen and in the bone marrow of the platypus. Hemopoiesis was found to be far more active in the spleen than in the bone marrow judging by the number of proliferating hemopoietic elements within a unit area of tissue from each organ. Granulocytes, erythroblasts, and megakaryocytes, with the related immature forms for each cell line, were noted in the spleen. In contrast, there were very few examples of immature forms of these cell lines and a complete absence of mature megakaryocytes in the bone marrow. These findings suggest that the spleen is the primary hemopoietic organ in the platypus. Since the platypus is one of two species representing the most primitive existing mammals, it seems likely that the spleen may be the primary hemopoietic organ in mammalian evolution.

Animals↗
PubMed1988

The relative contributions of immune system and target organ to variation in susceptibility of rats to experimental allergic thyroiditis.

Previous investigations of the cellular basis of genetic susceptibility to experimental allergic thyroiditis (EAT) in semi-allogeneic mice bearing thyroid grafts from resistant, parental strain donors have indicated that these grafts remain relatively resistant to EAT when this is induced in the susceptible bearer. It was concluded that genetic control of susceptibility to EAT is expressed in both the immune system and the thyroid gland. Our experiments in which thyroid grafts were transferred to fully allogeneic, but immunologically tolerant, recipient rats indicate that thyroid tissue from an EAT-resistant strain of rat becomes entirely susceptible when transplanted into a susceptible host. The differing susceptibility of thyroid grafts in semi-allogeneic and tolerant allogeneic hosts may result from restrictions on interaction between host lymphocytes and the graft in the former situation. The present findings call into serious doubt the proposition that genetically determined resistance to EAT is mediated, to any extent, at the level of the target organ.

Animals↗
PubMed1988

Peripheral neuropathy with predominantly motor manifestations in a patient with carcinoma of the uterus.

An autopsy case of a 56-year-old woman who had carcinoma of the corpus uteri and peripheral neuropathy with predominantly motor manifestations is described. The neurological abnormalities included subacute weakness of the limbs and loss of deep reflexes, which improved after the surgical removal of the uterine carcinoma. Neuropathologically, peripheral nerves mainly presented features of axonal degeneration with a mild loss of myelinated fibres. Anterior horns of the spinal cord showed central chromatolysis of the motor nerve cells and many spheroids without neuronal loss. Axonopathy of peripheral nerves was considered to be the main pathological process in this paraneoplastic syndrome.

Carcinoma↗
PubMed1988

PVG rats, resistant to experimental allergic thyroiditis, develop high serum levels of thyroglobulin after sensitization.

Following challenge with rat thyroglobulin and adjuvants, DA rats invariably develop the histological features of severe experimental allergic thyroiditis while the thyroid glands of PVG rats remain histologically normal. It has been reported previously that some PVG rats develop high titers of anti-thyroglobulin antibody when challenged despite apparent resistance to thyroiditis. In the present experiment, PVG rats consistently developed high serum levels of both antibody and thyroglobulin. Although release of thyroglobulin from the thyroid is usually considered an indication of damage to the gland, the thyroid remained completely normal in all challenged PVG rats.

Animals↗
PubMed1988

Regulation of experimental allergic thyroiditis.

The susceptibility to experimental allergic thyroiditis (EAT) of rats that had previously been immunized against thyroglobulin was examined. Challenge with thyroglobulin 5 weeks previously conferred strong resistance to the induction of EAT after exposure to a sensitization protocol that was otherwise highly effective. Resistance to induction of EAT could also be conferred by the inoculation of spleen cells from thyroglobulin-sensitized donors on the day of birth. Heavily irradiated spleen cells from sensitized donors were able to confer resistance on neonatal recipients, indicating that prolonged survival of the transferred cells was not required.

Animals↗
PubMed1988

An autopsy case of sarcoidosis followed up for 27 years, with special reference to pulmonary fibrosis.

An autopsy case of sarcoidosis followed up for 27 years in a 48-year-old woman with pulmonary fibrosis is presented. Chest roentgenography demonstrated an interstitial pneumonia-like pattern with gradual contraction of the upper lobes. Focal and extending fibrosis and hyalinization were observed in various organs including the lung, lymph nodes, heart and liver. Most of the fibrosis was thought to be derived from solitary or confluent granuloma, showing hyalinized nodular, stellate or band-like fibrosis. There was also another type of fibrosis, not derived from granuloma, manifested as fibrosing alveolitis in the lung, and diffuse fibrosis extending throughout the other organs. In the lymph nodes, chromogenic bodies (Hamazaki-Wesenberg bodies) were seen. The process of fibrosis and the significance of chromogenic bodies in cases of chronic sarcoidosis are discussed.

Female↗
PubMed1988

Acquisition of immunological self-recognition by the fetal rat.

Rats in which normal development of the thyroid gland had been interrupted by the injection of 131I during fetal life are liable to mount autoimmune responses against grafts of syngeneic thyroid tissue transplanted in adult life. Although autoimmune thyroiditis developed spontaneously in grafted tissue, the recipients' own thyroid glands remained free from autoimmune changes, showing only irradiation damage. Other syngeneic endocrine grafts transplanted to these rats were not susceptible to autoimmune attack. This experiment demonstrates that contact of self-determinants with the developing mammalian immune system is required if autoimmunity is to be prevented.

Animals↗
PubMed1985

Glycogen storage disease confined to the heart with deficient activity of cardiac phosphorylase kinase: a new type of glycogen storage disease.

The case of a male infant with marked deposition of glycogen, confined to the heart, is presented. Clinically, prominent cardiomegaly had been evident from immediately after birth until the infant's death due to heart failure. There were no significant clinical manifestations in other organs, including liver and skeletal muscle, during the clinical course. Autopsy revealed abnormal deposition of normally structured glycogen in the heart, but no deposition in the liver, skeletal muscle, or other systemic organs. This unusual pattern of glycogen deposition was also confirmed by measurement of the glycogen content of each organ. This is the first report of glycogen storage disease confined to the heart. Enzymatic analysis revealed no decrease in the activities of acid maltase, amylo-1,6-glucosidase, and phosphorylase in the heart or in the liver or skeletal muscle. However, phosphorylase kinase activity was not detectable in the heart, although high activity levels were observed in the liver and skeletal muscle. In this case the inborn error of metabolism responsible for the isolated deposition of glycogen in heart muscle may have been due to a deficiency of cardiac phosphorylase kinase.

Cardiomyopathies↗