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Biomedical subjects

Y Bando

Publications and source records attributed to Y Bando.

At least 55 records · Page 3Linked to original sources
PubMed1996

Duck lymphoid organs: their contribution to the ontogeny of IgM and IgY.

The occurrence of mRNAs encoding mu, nu and nu(delta Fc) immunoglobulin heavy chains and lambda light chains in organs of duck embryos from 16 days of incubation and ducklings up to 74 days of age was assessed by Northern hybridization. The mu message was first detected in bursa of Fabricius and spleen at 16 days of incubation and in cervical lymph nodes at 23 days of incubation, but in other organs (bone marrow, buffy coat, Harderian gland, liver) not until 7 17 days after hatching; in general, the appearance of the lambda message paralleled that of mu. Messenger RNAs encoding one or both of the nu isoforms were first detected in cervical lymph nodes at 25 days of incubation, in spleen and bursa in 1-day-old ducklings, in Harderian gland, bone marrow and liver from 10 to 17 days post-hatching and in buffy coat from 46 days. In most organs, the nu(delta Fc) message was detected prior to the nu message and predominated during the experiment; Harderian gland expressed the nu(delta Fc) message exclusively. These results indicate that bursa of Fabricius, spleen and cervical lymph nodes play early roles in the development of B cells and the ontogeny of duck immunoglobulins while other lymphoid organs support the later differentiation of plasma cells, and that IgY and IgY(delta Fc) are probably not simultaneous products of the same plasma cells.

Animals↗
PubMed1994

Molecular weight analysis of cow's milk antigens in neonate sera.

Some food antigens (Ag) can be detected in serum immunoglobulin G (IgG) antibodies (Ab) following ingestion. These Ag may thus be essential for inducing the production of IgE or IgG antibodies, which may in turn lead to the onset of atopic diseases such as atopic dermatitis, allergic rhinitis and asthma. The molecular weights (MW) of these Ag have yet to be determined. To select samples for MW analysis of circulating food Ag, we measured the concentrations of cow's milk (CM) Ag in the sera of 88 neonates by radio-immunoassay. They were found present in 20 samples of the sera. Twelve of the samples were analyzed for Ag MW by immunoblotting. Several bands appeared for one of the samples. Their MW were < 13,000 and no native CM proteins could be detected.

Animals↗
PubMed1993

Immunocytochemical localization of inflammatory cytokines and vascular adhesion receptors in radicular cysts.

Odontogenic cysts are one of the commonest bone destroying lesions of the maxillofacial skeleton, with the inflammatory radicular cyst being the commonest jaw cyst. Explants of radicular cysts produce an interleukin-1-like activity which could explain the osteolysis seen with these tumours though the cellular source of this osteolytic activity is unknown. In the present study, cytokines with known inflammatory and osteolytic activity: interleukin-1 (IL-1), tumour necrosis factor (TNF), interleukin-6 (IL-6), and the chemotactic cytokine interleukin-8 (IL-8) have been localized immunocytochemically in radicular cysts. The cellular adhesion receptors ICAM-1 and ELAM-1 have also been immunolocalized. All specimens showed positive staining for IL-1 (alpha and beta) and IL-6, with these cytokines being located in epithelial and vascular endothelial cells. Only two specimens demonstrated TNF and IL-8 staining, which was located in macrophages. All specimens demonstrated ELAM-1 staining in endothelium and ICAM-1 staining in epithelium, endothelium and mononuclear cells. These findings show that radicular cysts contain two bone-modulating cytokines, IL-1 and IL-6, and that these appear to be synthesized mainly by the epithelial cells. Cysts also contain a proportion of activated blood vessels whose endothelial cells express the cellular adhesion receptors ICAM-1 and ELAM-1.

Alveolar Bone Loss↗
PubMed1993

Odontogenic cyst induction by periapical infection in rats.

The purpose of this study was to test the hypothesis that odontogenic cysts can be induced by periapical infection. Pulp extirpation and reaming beyond the root apices were performed in 53 lower first molars in 27 Sprague-Dawley rats. The cavities were left open to allow continuous contamination by oral bacteria. Animals were killed at 6 and more than 8 months after operation. Odontogenic cysts were found in association with 8/53 teeth in 6 animals. Histologically, cysts were observed around the lower incisors below the first molars. The cyst wall consisted of fibrous connective tissue with inflammation and was lined with keratinized squamous epithelium. The cyst cavity contained a mass of keratin and necrotic debris. These results support the hypothesis that inflammatory stimulation from the apices can cause cystic changes in the enamel epithelium of underlying teeth.

Animals↗
PubMed1993

Immunosuppressive factors detected during convalescence in a patient with severe serum sickness induced by carbamazepine.

We report on a patient with severe serum sickness induced by carbamazepine in whom anticarbamazepine IgG antibodies were detected in the serum. The T cells of the patient showed impairment of phytohemagglutinin-induced proliferation, and hypergammaglobulinemia was evident. The clinical features and immunological abnormalities were compatible with immunoblastic lymphadenopathy. Immunosuppressive factors were also detected in the patient. Their molecular weights ranged from 20,000 to 30,000 as evaluated by Sephadex G-200 gel filtration. Such immunosuppressive cytokines were not detected in other patients with carbamazepine allergy who did not develop the clinical manifestations of immunoblastic lymphadenopathy. These results suggest that the T cell functional deficiency of immunoblastic lymphadenopathy is induced by these immunosuppressive cytokines.

Carbamazepine↗
PubMed1993

Incomplete activation of lymphokine-producing T cells by alloantigenic intraocular tumours in anterior chamber-associated immune deviation.

We have examined by limit dilution analysis the frequency of several types of DBA/2-specific precursor cells found in the draining lymph nodes of BALB/c mice following anterior chamber or subconjunctival inoculations of P815 tumour cells. Assays for precursors of cytotoxic T cells (pTc) and T-helper cells [interleukin-2 (IL-2)- and IL-4-producing cells] were conducted periodically during a 6-month interval after injection of tumour cells. The results indicate that nodes of both sets of recipients contained primed P815-specific CD8+ pTc that were detectable within 2 weeks of tumour implantation, and persisted throughout the 6-month observation period. Early after tumour inoculation, but not thereafter, these CD8+ cells also secreted Il-2. By contrast, only lymph nodes from mice that received P815 cells into the subconjunctival space contained CD4+ cells that secreted both IL-2 and IL-4; eventually, IL-4-secreting cells formed the vast majority of P815-specific CD4+ cells in these mice. Lymph nodes of mice that received P815 cells in the anterior chamber contained CD4+ T cells that were clonally expanded, and secreted IL-2, but not IL-4. These IL-2-secreting cells proved to be short-lived and were not present 6 months after inoculation. It is proposed that the IL-2- and IL-4-secreting T cells found in lymph nodes of subconjunctival tumour recipients are in vivo homologues of Th0 cells, that these cells can mediate delayed hypersensitivity responses, and that they are the forerunners of, or are themselves, memory T cells. These data indicate that the failure of mice that receive P815 tumour cells in the anterior chamber to display antigen-specific delayed hypersensitivity results from an inability to convert antigen-activated, IL-2-only-secreting CD4+ T cells (pTh) into Th0 cells. These findings also imply that mice with anterior chamber-associated immune deviation (ACAID) fail to develop memory CD4+ T cells.

Animals↗
PubMed1992

[A case of pseudohypoparathyroidism (PHP) type II associated with Bartter's syndrome--restoration of phosphaturic response to parathyroid hormone (PTH) by treatment for hypopotassemia].

We report a case of PHP Type II whose phosphaturic response to PTH was restored by treatment for complicated Bartter's syndrome. A 34-year-old woman was admitted to our hospital in July 1990 because of tetanic convulsion. The physical examination showed normal blood pressure (118/62mmHg), round face without shortness of metacarpal bones and positive Trousseau's sign. Although renal function was normal, hypocalcemia (6.5mg/dl) and hyperphosphatemia (4.8mg/dl) in association with high levels of serum PTH (942pg/ml) and 1.25 (OH)2D3 (86pg/ml) were disclosed. Ellsworth-Howard test revealed that there was no increase in the urinary secretion of phosphate despite an increase in urinary cAMP excretion. On the other hand, hypopotassemia (2.5mEq/l) and metabolic alkalosis with high plasma renin activity (22.8ng/ml/hr) and aldosterone concentration (22.7ng/dl) were coexistent. Pressor response to angiotensin II infusion was blunted. Although no glomeruli were obtained by renal biopsy specimen, vacuolar degeneration on proximal tubules were noted. These findings indicated that she had PHP Type II associated with Bartter's syndrome. By administration of potassium (24mEq/day), spironolactone (50mg/day) and only small doses of 1 alpha-hydroxyvitamin D3 (0.5mg/day), serum levels of potassium as well as calcium were normalized and tetanic attacks disappeared. In March 1991, she was re-examined by Ellsworth-Howard test in order to clarify the effects of hypopotassemia on renal tubular response to PTH. Interestingly, phosphaturic response to PTH was restored, and the degree of increase in urinary cAMP excretion was 4 times as high as that on the first admission. These results suggest that hypopotassemia changes the response of renal proximal tubular cells to PTH, particularly such as reabsorption of phosphate and cAMP response, although it is possible that hypocalcemia may contribute to the blunted phosphaturic response to PTH. The mechanism of hypocalcemia seen in this case remains to be elucidated.

Adult↗
PubMed1992

Differences in ceramic-bone interface between surface-active ceramics and resorbable ceramics: a study by scanning and transmission electron microscopy.

The interface between bioactive ceramics and bone was studied by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The materials were apatite-wollastonite-containing glass ceramic (A-W.GC) as a representative surface-active ceramic, and calcite and beta-tricalcium phosphate (beta-TCP) as resorbable ceramics. Particles of these materials, ranging between about 100 microns and 300 microns in diameter, were implanted into rat tibiae, and specimens were prepared for observation at 8 weeks after implantation. Both SEM and TEM demonstrated that A-W.GC was bonded to bone through a thin Ca-P-rich layer consisting of fine apatite crystals apparently different from those of bone in shape, size, and orientation. Collagen fibers of the bone reached the surface of this layer, and chemical bonding between A-W.GC and the bone was speculated. Calcite and beta-TCP, on the other hand, made direct contact with the bone, and no apatite layer was present at the interface. The surfaces of the implants became rough due to degradation, and bone grew into the finest surface irregularities. However, we were unable to demonstrate any continuity of crystals between the resorbable implants and bone by high-resolution TEM. Accordingly, the bonding strength was considered to be mainly attributable to mechanical interlocking.

Animals↗
PubMed1992

A comparative study of ultrastructures of the interfaces between four kinds of surface-active ceramic and bone.

The interfaces between four kinds of surface-active ceramic and bone were studied by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) using undecalcified specimens. The materials were Bioglass-type glass (Bioglass), Ceravital-type glass-ceramic (KGS), apatite- and wollastonite-containing glass-ceramic (A-W.GC) and hydroxyapatite (HA). Particles of these materials, ranging between about 100 and 300 microns in diameter, were implanted into rat tibiae, and specimens were prepared for observation at 8 weeks after implantation. All materials were observed to bond to bone through a collagen-free layer consisting of fine apatite crystals distinct from those in bone. The crystals of this apatite layer and those of bone were intermingled at their interface, suggesting chemical bonding. In Bioglass, which had only a glassy phase, several tens of microns of the material surface had changed to such an apatite layer. In KGS and A-W.GC, which had macrocrystals in the glassy phase, an intervening apatite layer about 0.5 micron thick was observed between the materials and bone. Furthermore, fine apatite crystals were also observed among the macrocrystals near the surface of the materials. In HA, which had no glassy phase, an intervening apatite layer was much less distinct and sometimes absent. These differences were considered to be attributable to the differences in chemical composition, crystallization, and solubility of the materials.

Animals↗
PubMed1992

An immunodominant haptenic epitope of carbamazepine detected in serum from patients given long-term treatment with carbamazepine without allergic reaction.

An anticarbamazepine antibody was detected in the serum of a patient with severe carbamazepine-induced serum sickness. We found that the patient's T cells and IgG antibody recognized an epitope which appeared in subjects showing an allergic reaction, as well as that in subjects who showed no allergic reaction, after long-term carbamazepine therapy. These results show that an anti-carbamazepine immune response does not occur in the majority of subjects who undergo long-term carbamazepine therapy without developing allergic symptoms, although the immunodominant haptenic epitope of carbamazepine is present in their sera.

Carbamazepine↗