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Biomedical subjects

Y Aida

Publications and source records attributed to Y Aida.

At least 73 records · Page 4Linked to original sources
PubMed1995

Identification of a new bovine MHC class II DRB allele by nucleotide sequencing and an analysis of phylogenetic relationships.

Three overlapping cDNA clones coding for the bovine major histocompatibility complex (MHC) class II DR beta chain were isolated. A clone NR1 encoded a primary translated product of 266 amino acids, 29 of which were deduced to form a signal peptide and 237 to form the mature polypeptide. The protein predicted from this cDNA appeared to have all the features expected of an expressed MHC class II molecule. Comparison of the sequences and construction of a phylogenetic tree revealed that NR1 represents a BoLA-DRB3 gene and not a BoLA-DRB1 or BoLA-DRB2 pseudogene. NR1 and ovine sequences exhibited the greatest overall similarity among sequences from various mammalian species, followed by the equivalent human sequences. Indeed, the bovine allele was more closely related to certain ovine alleles than to other bovine alleles. A large number of replacement substitutions were identified when beta 1 domains encoded by NR1 and each of the 36 distinct BoLA-DRB3 alleles were compared, and most of the allelic variations were found in regions that are commonly polymorphic in DRB sequences from different species and correspond to the predicted antigen-recognition site. Thus, the predicted structure of the unique NR1 allele for BoLA-DRB3 further confirms the overall conservation of the product of this locus, as previously established from studies in rodent and man.

Alleles↗
PubMed1995

Lipopolysaccharide-inactivating activity of neutrophils is due to lactoferrin.

Neutrophils can inactivate lipopolysaccharide (LPS), thereby blocking the ability of LPS to prime fresh neutrophils for enhanced fMLP-triggered release of superoxide. Here we show that inactivation of LPS by neutrophils was primarily due to lactoferrin. A time course for inactivating LPS showed that neutrophils (5 million/ml) took 30 min to inactivate 10 ng/ml LPS. Mononuclear cells could not inactivate LPS under the same conditions. Experiments with radioactive LPS showed that inactivated LPS remained in the medium and was not taken up or destroyed by the neutrophils during inactivation. Inactivated LPS still gelled Limulus lysate and primed monocytes. Cell-free medium from neutrophil suspensions also inactivated LPS. A single LPS-inactivating factor was purified from medium by heparin-agarose chromatography. SDS-PAGE showed a single band at 80 kDa, which was identified as lactoferrin by immunoblotting. Antilactoferrin immunoglobulin G removed the LPS-inactivating activity from purified lactoferrin and cell-free medium. Surprisingly, even purified neutrophil lactoferrin required 30 min to inactivate LPS, indicating inherently slow binding of lactoferrin to LPS.

Culture Media↗
PubMed1995

An analogue of lipid A and LPS from Rhodobacter sphaeroides inhibits neutrophil responses to LPS by blocking receptor recognition of LPS and by depleting LPS-binding protein in plasma.

When incubated with lipopolysaccharide (LPS) in the presence of plasma, neutrophils become primed for enhanced release of superoxide in response to triggering by formyl-Met-Leu-Phe (fMLP). The effect of LPS on phagocytes is inhibited by a synthetic lipid A precursor, LA-14-PP (lipid IVa) or by LPS from Rhodobacter sphaeroides (Rs). We studied the mechanisms by which LA-14-PP or Rs-LPS inhibited LPS-induced responses. When neutrophils were exposed to LA-14-PP or Rs-LPS for 3 min and then to Escherichia coli-LPS, the antagonists inhibited priming for superoxide release, and also blocked up-regulation of CD11b and adherence. This inhibition was dependent on plasma, was not overcome by higher amounts of E. coli-LPS or plasma, and was not observed at 0 degrees C, suggesting that E. coli-LPS was not able to interact with its receptor or other cellular recognition molecule in neutrophils that had been exposed to the antagonists. The alternative possibility that LA-14-PP or Rs-LPS depleted a plasma cofactor, resulting in inhibition of priming, was investigated by using LPS from Porphyromonas gingivalis (Pg) and Bordetella pertussis (Bp). These LPS primed neutrophils in a plasma-dependent and CD14-dependent manner, but were not blocked by LA-14-PP or Rs-LPS. When sub-optimal concentrations of plasma were exposed to LA-14-PP or Rs-LPS, and then mixed with Pg-LPS or Bp-LPS, followed by incubation with neutrophils, priming and up-regulation of CD11b were inhibited, and this inhibition was overcome by increasing the concentration of plasma. Binding of LPS-binding protein (LBP) in plasma to immobilized E. coli-LPS was inhibited by pre-incubation of plasma with LA-14-PP or Rs-LPS. Together with the result that treatment of plasma with anti-LBP antibody abolished the cofactor activity of plasma, these results indicated that LA-14-PP and Rs-LPS depleted LBP from plasma, resulting in inability of LPS to act on neutrophils. Thus LA-14-PP and Rs-LPS inhibited the action of LPS on neutrophils by at least two mechanisms, blocking of LPS receptor recognition and depletion of the cofactor LBP.

Acute-Phase Proteins↗
PubMed1995

The effect of AL0671, a novel potassium channel opener, on potassium current in rat aortic smooth muscle cells.

1. We evaluated the mechanism of activation by AL0671, a novel potassium channel opener, of potassium current in rat aortic smooth muscle cells. 2. Under conditions of whole cell recording, AL0671 (1-1000 microM) markedly increased potassium current with a Hill coefficient of 2 and dissociation constant of 1.5 x 10(-4) M. This activation was completely inhibited by intracellular ATP. 3. Under inside-out patch conditions, the ATP-sensitive K+ channels (KATP) treated with AL0671 (100 microM) showed prolongation of the slower open time component and shortening of the slower closed time component without modification of channel conductance.

Animals↗
PubMed1995

Lipopolysaccharides from periodontal pathogens prime neutrophils for enhanced respiratory burst: differential effect of a synthetic lipid a precursor IVA (LA-14-PP).

When neutrophils are incubated with bacterial lipopolysaccharide (LPS), they become primed for enhanced release of superoxide anion (O2-) in response to stimulation by FMLP. We investigated the human neutrophil-priming activity of LPS from the periodontal pathogens, Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi) and Actinobacillus actinomycetemcomitans (Aa) in comparison with that of LPS from Escherichia coli (E. coli). The optimum conditions for LPS to prime neutrophils were assessed for every LPS and found to be as follows: Neutrophils were incubated with LPS in the presence of 10% heat-inactivated plasma and 1 mM EDTA at 37 degrees C for 30 min and then stimulated with 1 microM FMLP at 37 degrees C for 7 min. Under these conditions, half-maximum priming was observed at 6.2 ng/ml Pg-LPS, 45 ng/ml Pi-LPS, 1.5 ng/ml Aa-LPS and 1.5 ng/ml E. coli-LPS. The priming activity of each LPS was neutralized by polymyxin B. Anti-CD14 monoclonal antibody inhibited priming by all LPS. The priming by Aa-LPS and E. coli-LPS was inhibited by LA-14-PP, a synthetic lipid A precursor IVA, but that by Pg-LPS and Pi-LPS was not. Priming by tumor necrosis factor alpha was not affected by polymyxin B, anti-CD14 antibody or LA-14-PP. Gelation of Limulus amebocyte lysate occurred at 10 pg/ml Pg-LPS, 30 pg/ml Pi-LPS, 3 pg/ml Aa-LPS and 3 pg/ml E. coli-LPS. Thus LPS from different periodontal pathogens primed neutrophils with different efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggregatibacter actinomycetemcomitans↗
PubMed1995

Immunohistologic studies on subpopulations of lymphocytes in cattle with enzootic bovine leukosis.

The distribution of subpopulations of lymphocytes in lymph nodes and tumors from cattle with enzootic bovine leukosis (EBL) was examined by immunohistochemistry using a panel of monclonal antibodies against leukocyte differentiation molecules of EBL. The lesions in lymph nodes could be divided into three types based on the extent of infiltration and proliferation of neoplastic cells with provirus and differential expression of leukocyte differentiation molecules. The number of B-B2+, sIgM+ cells was reduced in frequency in follicles during the neoplastic cell proliferation. CD4- and CD8-positive alpha/beta T cells and gamma/delta T cells positive for WC1 (workshop cluster designation) were also reduced in frequency in areas infiltrated with neoplastic cells. Almost all neoplastic cells were B-B2- and IgM-positive. However, there were a few B-B2- and/or IgM-negative cells or cells stained faintly in all cases. WC1+ cells were not observed in tumor tissues. However, CD4+ and CD8+ cells were observed throughout tumor tissues, suggesting a role for these cells in tumor immunity.

Animals↗
PubMed1995

Phenotypic analysis of neoplastic cells from calf, thymic, and intermediate forms of bovine leukosis.

Immunohistochemistry and flow cytometric analysis were used with monoclonal antibodies to examine the phenotype of neoplastic cells from cattle with sporadic bovine leukosis (three cases of calf form, two cases of thymic form, and three cases of intermediate form). Three cases of calf form and two cases of intermediate form were positive for B cell lineage in immunohistologic examination and in flow cytometric analysis for B-B2+, sIgM+, and major histocompatibility class II+. Two cases of thymic form and one case of intermediate form were CD2+, CD5+, CD6+, and CD8+ in immunohistologic examination and in flow cytometric analysis. The results show that neoplastic cells develop from B and T cell lineages in sporadic bovine leukosis.

Animals↗
PubMed1995

The antagonistic effects of khellactones on platelet-activating factor, histamine, and leukotriene D4.

Khellactones of Peucedanum praeruptorum DUUN., including praeruptorins A (= Pd-Ia, 2) and B (= Pd-II,11), had an antagonistic effect specifically on platelet aggregation induced by platelet activating factor (PAF) among various aggregating agents examined, and represent a new class of PAF antagonists. We examined the effects of twenty compounds on PAF-induced platelet aggregation and on histamine- and leukotriene D4 (LTD4)-induced contractions in isolated guinea pig ileum. Compounds 2, (+/-)-cis-3',4'-diacetylkhellactone (3), (+/-)-cis-4'-acetyl-3'-crotonoylkhellactone (5), (+/-)-cis-4'-acetyl-3'-tetrolylkhellactone (6), (+/-)-cis-4'-acetyl-3'-tigloylkhellactone (7), (+/-)-cis-4'-acetyl-3'-(2"-methylbutyryl)khellactone (8), (+/-)-cis-3',4'-ditigloylkhellactone (10), and 11 all strongly inhibited PAF-induced platelet aggregation. (+/-)-cis-4'-Acetyl-3'-(2"-methyl-2"-dodecenoyl)khellactone (9), (+/-)-cis-4'-ethyl-3'-tigloylkhellactone (13), (+/-)-cis-4'-ethyl-3'-[N-(2"-triethylammonio)ethylcarbamoyl] khellactone iodide (16), (+/-)-trans-3',4'-diacetylkhellactone (18), (+/-)-trans-4'-acetyl-3'-crotonoylkhellactone (19), (+/-)-trans-4'-acetyl-3'-valerylkhellactone (20), (+/-)-trans-4'-acetyl-3'-isovalerylkhellactone (21), and (+/-)-trans-4'-acetyl-3'-tigloylkhellactone (22) were weakly inhibitory. Most of the compounds exhibited noncompetitive antagonist actions on histamine- and LTD4-induced contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

A new class III antiarrhythmic drug, MS-551, blocks the inward rectifier potassium channel in isolated guinea pig ventricular myocytes.

We have studied the effects of MS-551 on the inward rectifier potassium channel (IK1) in isolated guinea-pig ventricular myocytes by use of whole-cell and single-channel recording techniques. MS-551 (5 microM) blocked the IK1 current. The percent blockade of the peak and steady-state IK1 current by MS-551 was constant at each test potential. In contrast 50 microM MS-551 failed to block either the sodium or the calcium current. Under cell-attached patch conditions, MS-551 reduced the open probability of IK1 channel activity by prolonging the interburst interval without changing either the unitary amplitude or the equilibrium potential. The blockade of IK1 was concentration-dependent. MS-551 did not change either the mean open time or mean closed time within a burst. Extracellular acidification (pH 6.4) strongly attenuated the effect of MS-551 on the open probability of IK1 channel activity when compared with its effect at pH 7.4. In summary, our results demonstrated that MS-551 blocked the IK1 channel. The neutral form of this drug molecules may penetrate the cardiac cell membrane via a hydrophobic pathway to block the steady-state IK1 current by reduction of open probability.

Animals↗
PubMed1995

[Cell proliferative activities of cholangiofibrosis induced in rats treated with bromodichloromethane].

To clarify whether bromodichloromethane (BDCM)-induced cholangiofibrosis progresses to cholangiocarcinoma, further morphological examinations were performed on the livers obtained from our previous experiment. The livers of Wistar rats fed diet containing 2200, 550, 140 or 0 ppm of microencapsulated BDCM up to 24 months were examined at months 6, 12, 18, and 24. The liver sections were stained with H-E, PAS and Azan, and were subjected to immunostaining using antiproliferating cell nuclear antigen (PCNA) monoclonal antibody for determination of the PCNA labeling index of bile duct epithelia, as well as silver staining for nucleolar organizer regions (AgNORs). At month 6, the severity of hyperplasia of atypical bile duct epithelia in the 2200 ppm group was marked, their PCNA labeling index being highest (68.5). The number of bile ducts gradually decreased, and the severity of fibrosis became more marked, with prolongation of the treatment. The PCNA labeling index in hyperplastic bile ducts in this group also decreased to 31.5 at month 24. The number of AgNORs in the nuclei of bile duct epithelia in the 2200 ppm group was highest at month 6, but decreased thereafter. The present study suggests that the possibility of the progression from cholangiofibrosis to neoplastic lesions is extremelly low.

Administration, Oral↗
PubMed1994

Cloning of cDNAs and the molecular evolution of a bovine MHC class II DRA gene.

Two overlapping cDNA clones coding for bovine major histocompatibility complex (MHC) class II antigen DRA chain were isolated and characterized. The full-length cDNA clone, MR1, encoded a primary translated product of 253 amino acids, 24 of which were deduced to be a signal peptide and 229 which formed a mature polypeptide. The amino acid sequences deduced from this clone resembled those of class II A molecules from other species in both size and structure, but no potential consensus site of N-linked glycosylation comparable to those in the human, mouse, rat and swine proteins was found in the alpha 2 domain, as well as ovine and equine DRA molecules. Comparison of amino acid sequences encoded by class II A genes among several species and a dendrogram constructed from these data places the DRA gene and the DQA/DYA genes on two distinct branches of a phylogenetic tree, with bovine DRA and ovine DRA being most similar on the DRA branch.

Amino Acid Sequence↗
PubMed1994

Bovine leukemia virus induces CD5- B cell lymphoma in sheep despite temporarily increasing CD5+ B cells in asymptomatic stage.

To investigate bovine leukemia virus (BLV)-induced leukemogenesis, we infected sheep with BLV and used flow-cytometric and immunohistological analysis to characterize the phenotypic alterations in lymphocytes from peripheral blood and lymph nodes taken from the animals with lymphoma at various stages. In sheep at the asymptomatic stage, depending on the extent of progression of the disease, the proportions of CD2(+)-, CD4(+)-, CD8(+)-, and gamma delta TCR(+)-T cells that coexpressed CD5 decreased, but CD5+ sIgM+ cells as well as CD5- sIgM+ cells increased for a period. The number of CD5+ B cells, however, rapidly decreased in the lymphoma stage. On the other hand, neoplastic lymphocytes appeared to be a monoclonal population derived from a single cell with surface phenotypes of sIgM+, B-cell-specific molecule B2+, major histocompatibility complex (MHC) class II+, OvCD5-, OvCD2-, OvCD4-, OvCD8-, gamma delta TCR-, which suggests that only CD5- B cells proliferate clonally when the disease proceeds to the lymphoma stage. Thus, rapid decrease of CD5+ B cells may be used as a marker of lymphoma stage. To identify the BLV provirus in the CD5- B and CD5+ B cells throughout the course of disease, each fraction of CD5- B and CD5+ B cell was sorted from the peripheral blood by flow cytometry and nested double polymerase chain reaction was performed. In BLV-infected but healthy sheep, BLV integrated both CD5- B and CD5+ B cells. In lymphoma, however, BLV provirus was detected only in CD5- B cells but not in CD5+ B cells. Therefore it appears that a disappearance of BLV-infected CD5+ cells is one of the critical events leading to CD5- B cell lymphoma in sheep. This is in contrast to the BLV-induced lymphoma in cattle which shows CD5+ phenotype.

Animals↗
PubMed1994

Immunohistochemical expression of manganese superoxide dismutase in hepatocellular carcinoma, using a specific monoclonal antibody.

The expression of manganese superoxide dismutase (Mn-SOD) was studied immunohistochemically, using a specific monoclonal antibody, in surgically resected hepatocellular carcinoma (HCC) and noncancerous tissues from 47 patients (2 with well-differentiated HCC, 36 with moderately differentiated HCC, 8 with poorly differentiated HCC, and 1 with undifferentiated carcinoma). Cancer cells in 44 patients (93.6%) were positive for Mn-SOD. The staining pattern of cancer cells was mostly homogeneous in well-differentiated HCC, whereas it was heterogeneous in poorly differentiated HCC. Moreover, strongly positive immunoreactivity was observed in noncancerous liver tissues in all patients, especially in normal hepatocytes surrounding HCC, regenerative small hepatocytes in the tumor boundary, and mononuclear inflammatory cells in the necroinflammatory lesions. The positive immunoreactivity for Mn-SOD in patients with HCC appears to reflect increased production of the enzyme protein.

Adult↗
PubMed1994

Acute, subchronic and chronic toxicity studies of a synthetic antioxidant, 2,2'-methylenebis(4-methyl-6-tert-butylphenol) in rats.

General toxicity studies on 2,2'-methylenebis(4-methyl-6-tert-butylphenol) (MBMBP) were conducted using male and female Wistar rats. LD50 values were greater than 5 g/kg BW by oral administration for both sexes. Diarrhea was observed until 5 days. In the subchronic test, rats were fed diet containing MBMBP at 0, 0.12, 0.6 or 3.0% for 12 weeks. Severe suppression of body weight gain was observed in both sexes of 0.6 and 3.0% groups. Death accompanied by hemorrhage from nasal cavity was observed in 0.6 and 3.0% males and 3.0% females. Dose-dependent toxicity to the liver in both sexes was observed in blood chemical analysis. Histopathologically, testicular atrophy and decrease of spermatogenesis were dose- and time-dependently observed in all treated males. Atrophy of ovaries was evident in 0.6 and 3.0% females. Thymus atrophy and bone marrow hypoplasia were observed in both sexes of 0.6 and 3.0% groups. In the chronic test, rats were fed diet containing MBMBP at 0, 0.01, 0.03 and 0.1% for 18 months. Body weight gain was only suppressed in both sexes receiving 0.1%. Histopathologically, testicular atrophy and decrease of spermatogenesis were apparent in 0.1% males. No neoplastic response by MBMBP administration was noted. NOAEL was concluded to be 0.03% in the diet (12.7 mg/kg BW/day for male rats and 15.1 mg/kg BW/day for female rats).

Administration, Oral↗