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Biomedical subjects

Y Abe

Publications and source records attributed to Y Abe.

At least 577 records · Page 32Linked to original sources
PubMed1994

The role of tumor necrosis factor receptors in cell signaling and the significance of soluble form levels in the serum.

Two types of tumor necrosis factor membrane receptors (TNF-R) have been identified, namely 55 and 75 kDa TNF-R. Soluble forms of these receptors are present in the human serum. Recent findings on the role of these two TNF-R in biological cell signaling and the clinical significance of the serum levels of soluble TNF-R (sTNF-R) were reviewed. It is not the uptake of TNF molecules into cells but rather the molecular capping of TNF-R on the cell membrane that initiates the biological activity of TNF. The 55 kDa TNF-R mediates major bioactivities of TNF, while the significance of 75 kDa TNF-R remains unclear. We herein suggest a new concept of the role of these two TNF-R: The 75 kDa TNF-R signal appeared to enhance that of 55 kDa TNF-R in the induction of ICAM-1 expression on HL-60 human promyelocytic leukemic cells. High serum levels of sTNF-R are reported in patients with malignancy, endotoxin shock, pneumonia, and autoimmune diseases. However, the source of elevated serum sTNF-R remains unclear. Studies on the clinical usefulness of serum sTNF-R levels as cancer and inflammation markers are now being carried out.

Cell Communication↗
PubMed1994

Growth factor from human milk: purification and characterization.

A protein (HPLC-P-1) purified from human milk induced the proliferation of IMR-90 cells (human fetal lung fibroblast cells, diploid) and was named milk growth factor (MGF). The human MGF (HPLC-P-1 fraction) showed a molecular size of 8 kDa on SDS-polyacrylamide gel electrophoresis (PAGE). The band on SDS-PAGE was also detected by Western blotting with anti-human MGF. However, this MGF showed two bands (MGF-S1 and MGF-S2) on 9.8% polyacrylamide native PAGE. The amino acid compositions of MGF-S1 and MGF-S2 were almost the same, but completely different from those of EGF, IGF-1 and TGF beta. The amino acid sequence of NH2-terminal of MGF was T.K.F.E.L.Y.Q.L.L.K.D.I. Neither EGF nor IGF-1 was detectable in the human MGF fraction by RIA. The effects of human MGF on IMR 90 cells (increases in cell number, incorporation of 3H-thymidine and DNA amount) were dose dependent. The activating effect on incorporation of 3H-thymidine (methyl-3H) was suppressed by anti-human MGF antibody in a dose-dependent manner. All these results indicate that MGF purified from human milk activates the growth of IMR-90 cells.

Amino Acids↗
PubMed1994

Staphylococcus aureus infection on experimental croton oil-inflamed skin in mice.

Staphylococcus aureus cells were inoculated on the surface of skin inflamed by application of croton oil in cyclophosphamide-treated mice. Skin specimens were taken at 1, 3, 6, 12, and 24 h inoculation and each specimen was examined by microscopy. The S. aureus cells which attached to the surface of the skin immediately after inoculation had invaded the horny layer within 1 h. The cells gradually penetrated deeper into the epidermis. Electron microscopy revealed fibril-like structures around the S. aureus cells and the cells which adhered to the horny layer and fibrin by means of Ruthenium red-positive, fibril-like structures. A combined application of 0.1% gentamicin ointment, 2% fusidic acid ointment, and clobetasol propionate ointment was more effective in decreasing the number of S. aureus cells in the lesions than was an application of clobetasol propionate ointment alone. However, a combined application of 0.1% gentamicin ointment and 2% fusidic acid ointment without clobetasol propionate ointment showed almost the same efficacy as that with clobetasol propionate ointment. Although povidone iodine killed S. aureus in vitro at a concentration of 0.01% (100 micrograms/ml) in 40 s, its in vivo efficacy was limited.

Animals↗
PubMed1994

Pre-B cells adhere to fibronectin via interactions of integrin alpha 5/alpha V with RGDS as well as of integrin alpha 4 with two distinct V region sequences at its different binding sites.

The present study aimed to develop an assay system capable of directly examining the adhesion of cells to each cell-binding site on fibronectin (FN) and to investigate molecular mechanisms underlying the pre-B cell-FN interaction. Treatment of culture plates with 3-(2-pyridyldithio) propionic acid N-hydroxysuccinimide ester and subsequently with dithiothreitol (DTT) allowed the plates to adsorb DTT-treated extracellular matrix (ECM) proteins as well as synthetic peptides containing cysteine at the N-terminal. These treatments produced culture plates coated with ECM proteins or peptides corresponding to its cell-binding sequences, i.e. three sites on FN termed RGDS, LDVP, and RGDV. Pre-B cells exhibited potent adhesiveness to FN-coated plates. Its FN binding was most efficiently inhibited by adding a combination of free forms of RGDS, LDVP, and RGDV peptides, indicating the involvement of these three cell-binding sites in the pre-B cell-FN interaction. In accordance with this, pre-B cells exhibited considerable and potent binding to the respective RGDS-, LDVP-, or RGDV-coated plates. Such binding was specific for the peptide used for coating, because each binding to a given peptide-coated plate was inhibited only by addition of a homologous free peptide. This assay system further demonstrated that the pre-B cell binding to RGDS was mediated by the alpha 5 and alpha v integrins, whereas the binding to LDVP and RGDV was mediated by the alpha 4 integrin. It was also shown that LDVP binding was inhibited by LDVP but not by RGDV and, likewise, RGDV binding was inhibited by RGDV but not by LDVP.2+ interaction involving complex molecular mechanisms.

Amino Acid Sequence↗
PubMed1994

Reduction of disulfide bonds in proteins by 2-aminothiophenol under weakly acidic conditions.

We developed a method for reducing disulfide bonds in proteins under weakly acidic conditions by use of 2-aminothiophenol. The disulfide bonds in hen egg-white lysozyme, ribonuclease A, and soybean trypsin inhibitor were quantitatively reduced by 2-aminothiophenol in phosphate buffer, pH6, containing 8 M Gdn HCl, 1 mM EDTA, and 20% ethanol, for 60 min at 40 degrees C. On analysis of the RP-HPLC patterns of tryptic peptides, which were derived from reduced and S-alkylated lysozyme and ribonuclease A at pH 6, it was confirmed that no side reaction occurred. Moreover, the reduction under weakly acidic conditions was demonstrated to be applicable for the location of such a labile residue as O-acetylated tyrosine.

Aniline Compounds↗
PubMed1994

Isolation and analysis of cDNA encoding a precursor of Canavalia ensiformis asparaginyl endopeptidase (legumain).

Recently, asparaginyl endopeptidase was purified to homogeneity from jack bean (Canavalia ensiformis) seeds, and its NH2-terminal amino acid sequence was determined for 25 residues [Abe, Y. et al. (1993) J. Biol. Chem. 268, 3525-3529]. On the basis of this sequence information, we searched for seed cDNAs encoding this enzyme. Seven clones were obtained and sequenced. By combining four of them, we obtained a cDNA for a precursor of the enzyme containing the reported NH2-terminal sequence. The other three clones seemed to be for precursors of its isozymes. When the deduced amino acid sequences of these enzyme precursors were compared with those in the GeneBank, EMBL, and NBRF databases, only one protein was found with a homologous sequence. It was a precursor of hemoglobinase from a blood fluke (Schistosoma mansoni). Significant homology was observed only in the range of sequence for the mature form. Although hemoglobinase and asparaginyl endopeptidase behave as cysteine proteinases, their protein natures are distinct from either papain-type proteinases or clostripain. Various plant seeds have been reported to contain asparaginyl endopeptidases. This may be the first report, however, that deals with the primary structure of such a proteinase.

Amino Acid Sequence↗
PubMed1994

Lysozyme requires fluctuation of the active site for the manifestation of activity.

Mutations around His15 which lie far away from the active site, stimulated glycol chitin activity of lysozyme at physiological temperature. Del-Arg14His15 lysozyme, a mutant lysozyme whose Arg14 and His15 were deleted together, and has the highest activity among these mutant lysozymes, had a similar binding ability to a trimer of N-acetyl-glucosamine, a substrate analogue, relative to native lysozyme. This suggests that the increased activity was due to an increased kcat in the catalysis reaction. The H-D exchange rate of the N-1 proton in the Trp63 which is located in the active site cleft, was enhanced in the Del-Arg14His15 lysozyme, while 2-D proton NMR analysis revealed no conformational change around Trp63. We conclude that some sort of fluctuation at the active site might be required for the manifestation of activity. This theory is supported by the finding that the Del-Arg14His15 lysozyme showed a shift in temperature dependency of activity to lower temperatures compared with that of native lysozyme.

Acetylglucosamine↗
PubMed1994

Residual left ventricular pump function following acute myocardial infarction in postmenopausal diabetic women.

BACKGROUND: The Framingham Study indicated that women with diabetes mellitus developed cardiac failure four times more often than those without diabetes mellitus after acute myocardial infarction. However, there is little information on residual left ventricular pump function after myocardial infarction in female diabetic patients. METHODS: To evaluate the difference between postmenopausal women and age-matched men in the impact of diabetes mellitus on left ventricular pump function during the first year after myocardial infarction, radionuclide angiography was performed during the third week after acute myocardial infarction and again 1 year later in 50 patients (21 women, 29 men) with diabetes mellitus and 62 patients (25 women, 37 men) without diabetes mellitus. RESULTS: Although the radionuclide angiographic indices did not change during the first year after myocardial infarction in non-diabetic patients, left ventricular end-diastolic volume increased, and the left ventricular ejection fraction, the regional ejection fraction of the non-infarcted area, and the ratio of arterial systolic blood pressure to left ventricular end-systolic volume (pressure:volume ratio) decreased in the diabetic patients. Furthermore, the degree of change in the left ventricular end-diastolic volume, the left ventricular ejection fraction, the regional ejection fraction of the non-infarcted area, and the pressure:volume ratio in diabetic women was larger than that in diabetic men. CONCLUSION: The increase in the left ventricular end-diastolic volume and the decrease in the regional ejection fraction of the non-infarcted area during the first year after myocardial infarction in postmenopausal women with diabetes mellitus indicate that female sex associated with diabetes mellitus may be important factors in left ventricular remodeling in postmenopausal women.

Aged↗
PubMed1994

Acute febrile neutrophilic dermatosis (Sweet's syndrome) associated with extreme infiltration of eosinophils.

A remarkable infiltration of eosinophils was observed in skin biopsy specimens in two cases of Sweet's syndrome. One patient was a 29-year-old woman, whose clinical and histological features included associated asthma, a prior respiratory tract infection, red plaques, blood eosinophilia, and a dense dermal infiltrate of neutrophils and eosinophils, without evidence of vasculitis. The other patient was a 61-year-old man characterized by a fever, red plaques, erythema nodosum-like lesions, hepatic dysfunction, a dermal infiltrate of neutrophils accompanied by eosinophils, and a subcutaneous prominent infiltrate of eosinophils. Clinical and histological evidence supported the diagnosis of Sweet's syndrome in both of these patients. While the literature describes eosinophil infiltration in this disease, extreme eosinophil infiltration could be misleading in the diagnosis.

Adult↗
PubMed1994

Expression of the multidrug resistance gene (MDR1) in non-small cell lung cancer.

To ezamine the clinical relevance of P-glycoprotein, encoded by the human multidrug resistance gene (MDR1), to multidrug resistance in lung cancer, we examined the expression of MDR1 in 107 non-small cell lung cancer (NSCLC) specimens and 20 corresponding specimens of normal lung tissues. We also evaluated the relationship between MDR1 expression and the histopathology and pathological staging of NSCLC. The tumors consisted of 60 adenocarcinomas, 38 squamous cell carcinomas, 8 large cell carcinomas, and 1 adenosquamous carcinoma. MDR1 expression was semi-quantified by use of the reverse transcriptase-polymerase chain reaction method. We subclassified the NSCLC into 3 grades according to the MDR1 expression level (-, +, ++). Sixty-one of the 107 tumor specimens (57%) and 18 of the normal lung tissue specimens (90%) expressed various levels of the MDR1 gene. Only one tumor specimen showed higher MDR1 expression than the corresponding normal lung tissue. The relationship between pathological stage and MDR1 expression levels was not significant. These results suggest that the level of MDR1 expression in lung cells is decreased as cells progress from the normal to the transformed state.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Role of membrane-associated lymphotoxin (mLT) in the killing activity of lymphokine-activated killer (LAK) cells towards various tumour cell lines.

Human lymphokine-activated killer (LAK) cells developed by an incubation of peripheral mononuclear cells with IL-2 express the membrane-associated lymphotoxin (LT)-related molecule (mLT). By a further cultivation of mLT expressing (mLT-positive) LAK cells for 24 h without IL-2, mLT disappears (mLT-negative LAK cells). Cytotoxicities of various tumour cell lines by either mLT-positive or -negative LAK cells were compared. Eight out of 12 tumour cell lines, less susceptible to mLT-negative LAK cells than mLT-positive LAK cells, were categorized as group A. Two tumour cells (K562 and Molt-4) had the same susceptibility to both kinds of LAK cells. The others (Daudi and Jurkat) had less susceptibilities only when they were assessed at E:T ratios of less than 5. The four tumour cell lines in the latter two cases, containing K562, Molt-4, Daudi and Jurkat cells, were categorized as group B. The cytotoxicities of group A tumour cells, but not group B tumour cells, by LAK cells were significantly suppressed by the presence of anti-LT antibody. Group A tumour cells had higher LT-binding ability (2.82-16.44 fmol/10(6) cells) than group B tumour cells (less than 1.46 fmol/10(6) cells). Both mLT-positive and -negative LAK cells had similar perforin activities and tumour cell-binding capacities. These results suggest that the mLT-mediated killing mechanism is involved in tumour cell killing by LAK cells. Further, various tumour cell lines can be classified into two large groups according to their susceptibilities to the mLT-mediated killing by LAK cells.

Animals↗
PubMed1994

Experimental assessment of right ventricular function in normal pigs with a left ventricular assist device.

Right ventricular (RV) failure during the use of a left ventricular assist device (LVAD) is the leading cause of death in circulatory support patients. Previous work, both experimentally and clinically, has shown the difficulties in predicting the behavior of the right ventricle at the start of LVAD. An experimental study has been designed to evaluate RV functional changes during LVAD and its relation to preload changes. The model used adult mongrel pigs (n = 10). Right ventricular functional parameters were measured with a thermodilution RV ejection fraction catheter. The left ventricle was supported by a Nippon Zeon blood pump. Two groups were studied, the first one was the LVAD-off group (n = 5) and the other was the LVAD-on group (n = 5) which was supported by LVAD at maximum flow. Change of cardiac output, mean pulmonary artery pressure (PAP), RV stroke work, and RV ejection fraction in both groups were not significantly different. However, the relationship between right ventricular end-diastolic pressure (RV-EDP) and right ventricular stroke volume (RVSV) was significantly changed at a high level of RV-EDP. When RV-EDP was over 6.5 mm Hg in the LVAD-off group, RVSV decreased to 52.3 +/- 11.5 ml while in the LVAD-on group, RVSV increased to 97.2 +/- 22.0 ml. The change in PAP in the LVAD-on group was lower than in the LVAD-off group. We conclude that, at the volume overload state, LVAD can reduce the afterload of the right ventricle and maintain Frank-Starling's effect, thus having a beneficial effect on right ventricular performance.

Animals↗
PubMed1994

Role of vasopressin on cardiovascular changes during hemorrhage in conscious rats.

Hypotensive hemorrhage decreases heart rate (HR) and renal sympathetic nerve activity (RSNA). Hemorrhage is a potent stimulus for arginine vasopressin (AVP) release; therefore, AVP may contribute to such inhibitory action of HR and RSNA during hemorrhage. We evaluated the roles of vasopressin on the regulation of blood pressure (BP), HR, and RSNA during hemorrhage using nonpeptide and selective V1- and V2-receptor antagonists (OPC-21268 and OPC-31260) in conscious rats. After hemorrhage (20 ml/kg body wt) BP decreased by 62 +/- 10 mmHg along with bradycardia (-110 +/- 15 beats/min) and renal sympathoinhibition (-50 +/- 8). Pretreatment of V1-receptor antagonist (5 mg/kg iv) did not affect the initial fall of BP but attenuated subsequent BP recovery. Bradycardic and renal sympathoinhibitory responses following hemorrhage were abolished (-14 +/- 24 beats/min and -7 +/- 9) by V1-receptor antagonist. Pretreatment of V2-receptor antagonist (1 mg/kg iv) did not affect the response of BP; however, it did slightly strengthen bradycardia and prolong renal sympathoinhibition. Hemorrhage increased the plasma AVP concentration more than 50-fold. These results indicate that when the plasma concentration of AVP is extremely high during hemorrhage, vasopressin via V1 receptor contributes to BP recovery by the peripheral vasoconstriction and exerts an inhibitory action on RSNA, and vasopressin via V2 receptor exerts opposite stimulatory action on RSNA.

Animals↗
PubMed1994

Glycine response in acutely dissociated ventromedial hypothalamic neuron of the rat: new approach with gramicidin perforated patch-clamp technique.

1. We investigated the glycine-induced response in ventromedial hypothalamic (VMH) neurons freshly dissociated from 8- to 12-day-old rats using the nystatin and gramicidin perforated patch recording modes. The nystatin-formed pores in the plasma membrane are permeable for both monovalent cations and anions, whereas those formed by gramicidin are permeable only to monovalent cations. Therefore, when the patch-pipette contains 150 mM Cl- and gramicidin, the physiological intracellular Cl- concentration ([Cl-]i) is undisturbed in the cell-attached condition of the pipette. 2. At holding potentials of -40 to -60 mV, glycine induced inward currents and outward currents in the nystatin and gramicidin perforated patch recording modes, respectively. The values of the half-maximum effective concentration (EC50) and the Hill coefficient in the concentration-response relationships of the glycine responses were 2.9 x 10(-5) M, 1.1, and 4.2 x 10(-5) M, 1.4, respectively. These values were quite similar in both recording modes. 3. The reversal potentials of the glycine responses (EGly) were -1.5 mV in the nystatin perforated patch recording and -75.0 to -24.8 mV in the gramicidin perforated patch recording. 4. Strychnine (3 x 10(-8) M) inhibited the glycine-induced outward currents in a competitive manner and the half-inhibition concentration (IC50) of strychnine on the 10(-4) M glycine-induced response was 1.9 x 10(-8) M. 5. The physiological [Cl-]i in the VMH neurons calculated from the EGly obtained by the gramicidin perforated patch mode ranged from 6.0 to 43.8 mM (n = 28).

Animals↗