[Allergy-like symptom caused by mite-protease].
Explore the source record for details and available documents.
Allergens↗
Biomedical subjects
Y Inada
Publications and source records attributed to Y Inada.
Pharmacological profile of a highly potent and long-acting angiotensin II receptor antagonist, 2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4- yl]methyl]-1H-benzimidazole-7-carboxylic acid (CV-11974), and its prodrug, (+/-)-1-(cyclohexyloxycarbonyloxy)-ethyl 2-ethoxy-1-[[2'-(1H-tetrazol-5- yl)biphenyl-4-yl]methyl]-1H-benzimidazole-7-carboxylate (TCV-116).
The angiotensin II (AII) antagonistic action of 2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl-1H-benzi mid azole-7 - carboxylic acid (CV-11974) was examined in in vitro assay systems, including AII receptor binding assay using membrane fractions of bovine adrenal cortex or rabbit aorta and AII-induced contraction assay using rabbit aortic strips, and CV-11974 and its prodrug, (+/-)1-(cyclohexyloxycarbonyloxy)ethyl 2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]-1H- benzimidazole-7-carboxylate (TCV-116), were examined in an in vivo system of AII-induced pressor response in conscious rats. DuP 753 or EXP3174 (the main active metabolite of DuP 753) was used as the reference compound. CV-11974 inhibited the binding of [125I] AII to the bovine adrenal cortical membrane and rabbit aortic membrane with IC50 values of 1.12 x 10(-7) and 2.86 x 10(-8) M, respectively. Similar results were obtained with EXP3174. CV-11974 interacted with AII in these membrane fractions with subtype 1 receptor in a competitive manner. CV-11974 at 10(-5) M did not affect the binding of [125I]AII to subtype 2 (AT2) receptor in bovine cerebellum. CV-11974 selectively inhibited the AII-induced contraction of rabbit aortic strips in a noncompetitive manner (pD' 2, 9.97); it had no effects on the contraction induced by norepinephrine, KCl, serotonin, prostaglandin F2 alpha or endothelin. EXP3174 showed a pD'2 value of 8.95 for the AII-induced contraction. CV-11974 given intravenously and TCV-116 given orally inhibited the AII-induced pressor response in rats with ID50 values of 0.033 mg/kg and 0.069 mg/kg, respectively. These effects of CV-11974 and TCV-116 were 12 and 48 times more potent than those of EXP3174 and DuP 753, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex↗
Vascularized fibular grafts in the treatment of osteomyelitis and infected nonunion.
From 1976 to 1989, 33 patients with osteomyelitis and infected nonunion of lower extremity bones were treated with vascularized fibular grafts. There were 30 males and three females, and the ages at operation ranged from 17 to 69 years. There were 24 tibial lesions and nine femoral lesions. The fibular graft was performed immediately after lesional debridement in eight patients, but in 25 it was done secondarily after debridement and successful subsidence of inflammation. The mean interval between the last debridement and fibular grafting was ten weeks. Thirty of 33 grafts survived. The mean periods required to obtain radiographic bone union was 6.2 months at the proximal site and 6.3 months at the distal site. Local recurrence of infection occurred in four patients; all but one healed well with saucerization. Vascularized fibular graft is an effective procedure for the treatment of destructive osteomyelitis and infected nonunion.
Adolescent↗
Synthesis and thromboxane A2/prostaglandin H2 receptor antagonistic activity of phenol derivatives.
Consideration of possible structural similarities between thromboxane A2 and the hydroquinone form of (R)-(+)-7-(3,5,6-trimethyl-1,4-benzoquinon-2-yl)-7- phenylheptanoic acid (R-(+)-AA-2414) led to the development of a new series of thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptor antagonists, namely 7-(4-fluorophenyl)-7-(2-hydroxyphenyl)heptanoic acids (I). These compounds were found to be potent TXA2/PGH2 receptor antagonists. Compounds having either a carbonyl or a hydroxymethyl group at the para-position of the phenolic hydroxy group exhibited most potent activities in this series. Compounds 14, 15, 18, and 26 inhibited the specific binding of [3H]U-46619 to guinea pig platelet membranes (IC50 = 4.4, 80, 32, and 13 nM, respectively), and also inhibited U-46619-induced human platelet aggregation (IC50 = 310, 69, 79, and 78 nM, respectively). Comparison of the UV spectra of the compounds with a carbonyl group at the para-position of phenolic hydroxy group revealed that the activity tended to increase in accordance with a decrease in the torsional angle between the carbonyl group and the phenol ring. These results suggested that the spacial location of the carbonyl and hydroxymethyl oxygen are important for significant increase in activity and that the carbonyl and hydroxymethyl oxygen at the para-position of the phenolic hydroxy group might interact with one of the TXA2/PGH2 receptor sites.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Chemical modification of L-asparaginase with a comb-shaped copolymer of polyethylene glycol derivative and maleic anhydride.
L-Asparaginase from Escherichia coli, an anti-tumor enzyme, was chemically modified with two types of maleic anhydride copolymers with a comb-shaped form, the one composed of polyoxyethylene allyl methyl diether with the molecular weight of 13,000 (activated PM13) and the other of polyoxyethylene 2-methyl-2-propenyl methyl diether with 100,000 (activated PM100). The modified asparaginases (PM13- and PM100-asparaginases) exhibited the complete loss of immunoreactivity towards anti-asparaginase serum. The enzymic activity of PM100-asparaginase without immunoreactivity was well retained by 85% of non-modified one, while that of PM13-asparaginase was retained 46%. These results were discussed in relation to the chemical structure of modifying reagents including chain shaped-polyethylene glycol derivatives.
Amino Acids↗
Continuous local intraarterial infusion after prolonged arterial stasis in the fingers and toes.
Seven patients with trauma to eight digits and one toe went untreated for arterial stasis, with subsequent development of posttraumatic changes in skin coloration. In two patients involving two digits, a daily dose of 2,000 ml containing 240,000 U urokinase, 80 micrograms prostaglandin E1, and 10,000 U heparin in lactated Ringer's solution was administered by intravenous infusion for 10 consecutive days; one of the two digits became necrotic. In all subsequent patients, a daily dose of 80 ml containing 240,000 U urokinase, 40 micrograms prostaglandin E1, 10,000 U (maximum) heparin, and low-molecular-weight dextran was administered by continuous local intraarterial infusion for 10 consecutive days. These seven extremities survived, even in the case of two digits and one toe with over 50 hr of arterial stasis. We believe that revascularization of extremities following prolonged periods of arterial stasis may be possible by means of continuous local intraarterial infusion of antithrombotic agents.
Aged↗
Existence of lipid vesicles containing platelet-activating factor in endothelial cell lysate.
Platelet aggregation activity due to platelet-activating factor (PAF) was detected at high molecular weight (HMW) and low molecular weight fractions after gel-filtration chromatography of cell lysate of endothelial cells. [3H]PAF added to the cell lysate was similarly distributed after chromatography. The radioactivity associated with HMW fraction was not reduced by digesting the lysate with trypsin, suggesting that PAF was not making complexes with proteins but was included in lipid vesicles in cell lysate. Further evidence showed that an unknown specific factor(s) was needed to form these PAF-containing lipid vesicles. Radioactivity was not found in HMW fraction when [3H]PAF was mixed with cell lysate of vascular smooth muscle cells. When monomeric PAF was added to endothelial cell lysate, the specific activity of aggregation decreased to the level exerted by endogenous PAF-containing lipid vesicles due to incorporation into lipid vesicles. PAF in the form of lipid vesicles was more stable in plasma than monomeric form.
Animals↗
Fifth digit sesamoid fracture with tenosynovitis.
Explore the source record for details and available documents.
Adult↗
Poly(ADP ribose) polymerase-defective mutant cell clone of mouse L1210 cells.
By a sequential mutation and selection utilizing N-methyl-N'-nitro-N-nitrosoguanidine as a mutagen, we succeeded in separating a poly(ADP ribose) polymerase-defective mutant clone (Cl-3527) from a mouse L1210 cell clone (Cl-3). The enzyme activity per cell in Cl-3527 cells was only 8% of that in wild type L1210 (CCL 219) cells. Immunoblot analysis of the enzyme protein in crude extracts of the mutant and wild type cells revealed that the enzyme defect was manifested as the loss of a 113-kDa wild type enzyme band in Cl-3527. Further analysis of partially purified enzyme from Cl-3527 by immunoblotting revealed that the molecular size of the enzyme in Cl-3527 was 108 kDa and that the amount of the mutant enzyme protein was markedly decreased in Cl-3527. The mutant enzyme was much more heat-labile than the wild type enzyme but the Km for NAD+, requirements for Mg2+ and nicked DNA, and the inhibition by 3-aminobenzamide, a potent inhibitor of the enzyme, however, were not so different from those of wild type enzyme. The mutant cells showed prolonged doubling time, increased temperature-sensitivity, increased percentage of active enzyme on a treatment of cells at high temperature, and increased expression of plasma membrane NADase, compared to wild type cells. Introduction of wild type ADPR pol gene into Cl-3527 cells partially restored the ADPR pol activity and the heat-resistance.
Animals↗
An experimental study of the flow-through venous flap: investigation of the width and area of survival with one flow-through vein preserved.
A quantitative analysis was undertaken to investigate the width and area of survival of flow-through venous flaps in 20 ears of 10 rabbits. The 3.0- x 3.0-cm flap models, which included one flow-through vein, were prepared with additional circulation from the graft bed and surrounding tissue excluded, as far as possible. The flaps were divided as follows: Group A--composite grafts (n = 10), and Group B--flow-through venous flaps (n = 10). All flaps in Group A became necrotic and all those in Group B showed partial survival along the flow-through vein. The average survival width was 1.10 +/- 0.48 cm, and the survival rate was 44 +/- 19.3 percent. Microangiograms revealed patency of the flow-through vein in all flaps of Group B. Histologically, there tended to be progressively more fibrous tissue in the area further away from the flow-through vein. The model is useful to investigate the width and area of survival in flow-through venous flaps.
Angiography↗
Pre-formed vascularized bone grafts using polyethelyne chambers.
Previous work has shown that corticocancellous bone chips placed in a titanium chamber with an arteriovenous vascular pedicle will result in a pre-formed vascularized bone graft. The present study was designed to determine whether these grafts can be transferred as an island or free vascularized bone graft, and to examine the material properties of these grafts. Thirty-two male, New Zealand white rabbits were divided into four groups based on the time of sacrifice following the initial chamber implantation. Injected molded cylindrical polyethelyne chambers, measuring 22 mm long and with an 8-mm inner diameter, were used. Corticocancellous bone chips were placed in the chambers and each chamber was implanted in the mid-thigh, with saphenous vessels running through the chamber. The chambers were implanted into the right and left thigh of each animal. To test the hypothesis of the possibility of transferring this graft as an island or free vascularized graft, ligation of the distal vascular pedicle on one side was achieved at re-exploration at 3, 6, 9, and 12 weeks. The contralateral side served as a control in which the vascular pedicle was not ligated. In the controls, bony bridging between the corticocancellous bone chips was observed after 7 weeks. A solid bone graft was present within the chamber by 10 weeks. However, histomorphometric evaluation indicated significant bone resorption. By 13 weeks, resorption progressed to the point where only small islands of bone remained. Ligation of the distal vessels resulted in thrombosis of the vessels within the chamber. Necrosis of newly-formed bone was observed in the area adjacent to the vascular thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Retinoic acid-specific induction of a protein kinase C isoform during differentiation of HL-60 cells.
Human promyelocytic leukemia cells (HL-60) were treated with several differentiation inducers, then the changes in the activity of cytosolic protein kinase C (PKC) isoforms were examined by hydroxylapatite chromatography and the species of the isoforms were determined immunologically. In three undifferentiated HL-60 cell lines examined, PKC alpha and beta isoforms were present, but PKC gamma isoform was not detected. When the cells were induced by dimethylsulfoxide, dibutyryl cAMP, or nicotinamide to differentiate into granulocytes, these two PKC isoforms each increased to about 2- to 3-fold. When retinoic acid was used as the inducer, in addition to PKC alpha and beta, a third PKC isoform appeared. This isoform was clearly distinct from rat PKC alpha, beta, and gamma, immunologically. This isoform showed a distinctly lower Ca(2+)-requirement (3 microM) than that of PKC alpha or beta (100 microM) and was more dependent on cardiolipin and phosphatidylethanolamine, compared with PKC alpha, beta, and gamma. These results suggest that while the increases in the activities of PKC alpha and beta isoforms are common in the differentiation program initiated by several inducers, including retinoic acid, the emergence of an unclassified PKC isoform is a retinoic acid-specific process.
Animals↗
Proof of plasmatic imbibition in rat musculocutaneous grafts: enzymatic proof using peroxidase.
At present, the concept of plasmatic imbibition is generally accepted. That is, observation of weight change or pigmentation methods of the grafts were established to support it. In the present study, we investigated plasmatic imbibition in rat musculocutaneous grafts histologically using peroxidase, which is one of the reductases. Tissue pigmentation by peroxidase became an insoluble sediment that indicated the sites of peroxidase activity. The entire contact surface of the graft with the recipient bed was stained brown within a few minutes after the operation. At 30 minutes, the panniculus carnosus and dermis were stained dark brown diffusely, extending toward the epidermis. This condition continued until the sixth day at least. As a result, peroxidase that was dissolved with the exudate between the graft and recipient bed was imbibed into the musculocutaneous graft.
Absorption↗
Inhibition of mite protease (Df-protease) with protease inhibitors.
A protease from house dust mite(Dermatophagoides farinae) having high specificity towards a substrate of blood coagulation factor XIIa catalyzes the activation of kallikrein-kinin system in plasma (Takahashi et al., 1990). To prevent the formation of kinin by the mite-protease, inhibition of the protease with its inhibitors was tested in vitro and in vivo. Its kinetic studies revealed that Ki values are 3.9 x 10(-10) M for aprotinin, 3.0 x 10(-9) M for soybean trypsin inhibitor (Kunitz) and 2.5 x 10(-8) M for gabexate mesylate. Enhancement of blood permeability in guinea pigs caused by the protease was markedly suppressed by these inhibitors.
Animals↗
[Hemodynamic effects of infusions of alpha-human atrial natriuretic peptide in anesthetized dogs].
The purpose of this study is to investigate and compare the hemodynamic effects of infusion of alpha-human atrial natriuretic peptide (alpha-hANP) at three different doses. Mongrel dogs were anesthetized with 0.87% halothane in oxygen. alpha-hANP was infused for one hour with a constant rate at either 0.3, 1.0, or 10.0 micrograms.kg-1.min-1, respectively. They were randomly divided into four groups. Group A-1 received 0.3 micrograms.kg-1.min-1 of alpha-hANP; Group A-2 received 1.0 micrograms.kg-1.min-1 of alpha-hANP; Group A-3 received 10.0 micrograms.kg-1.min-1 of alpha-hANP; and Group C received normal saline as the vehicle and served as the control. Control values were obtained before infusion of alpha-hANP or vehicle was started, and hemodynamic variables were measured at 30 minutes intervals for two hours. Mean arterial pressure (MAP) of the group C showed no significant changes from control value. During and after infusion of alpha-hANP, MAP in the group A-2 and A-3 was significantly lower than the control values. The decrease in MAP of the group A-2 was the greatest. Heart rate decreased significantly at 60 minutes after termination of the infusion in all four groups. The reduction of cardiac index (CI) in the group-3 was the greatest. In the group A-3, it decreased for 31% from the control value at 60 minutes during infusion. However, this change was not significant. In contrast, the reduction in CI of the group A-2 was minimal. Mean pulmonary artery pressure (MPAP) of the group C showed no significant change from the control value. The patterns of changes in MPAP were similar to those of the alpha-hANP infused groups. It decreased progressively during the infusion. Systemic vascular resistance (SVR) was essentially unchanged in the group C. In the group A-2, SVR decreased slightly during the infusion period and then tended to increase after the infusion of alpha-hANP. In contrast, in the group A-1 and A-3, SVR increased progressively. The changes in left ventricular maximum dp/dt (LV dp/dt max) of the group C were minimal. The reduction in LV dp/dt max was more pronounced in group A-2 than in group A-3. In conclusion, our data show that hypotensive effects of alpha-hANP are associated with the reduction in cardiac output due to the decrease of cardiac contractility. However, the changes of hemodynamic variable are not dose-dependent.
Animals↗
[Chemical modification of proteins with polyethylene glycol (PEG)].
Explore the source record for details and available documents.
Amino Acid Sequence↗
[Hemodynamic effects of induced hypotension by ketanserin in anesthetized dogs].
Hemodynamic effects of hypotension induced by ketanserin were investigated in 18 mongrel dogs under 0.87% halothane in oxygen (1 MAC). They were randomly allocated to one of two groups. Group C (n = 9) received no vasodilator therapy and served as a control and group K (n = 9) received 0.1% ketanserin solution. Mean arterial pressure decreased and was maintained at 60 mmHg for 60 minutes in group K. No change was noted in hemodynamic variables measured in group C throughout the experiment. During and after induced hypotension in group K, stroke volume index increased significantly compared with the control value. On the other hand, systemic vascular resistance was significantly reduced, reaching 50% of the control value at the end of the hypotensive period. Left ventricular maximum dp/dt showed a significant reduction during hypotension but then increased gradually to the control value. In addition, heart rate decreased significantly during and after induced hypotension, therefore these vasodilator effects were not accompanied by reflex tachycardia. Cardiac index remained unchanged throughout the experiment. Further, no changes in central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance were observed. In conclusion, the data indicate that ketanserin is a potent systemic vasodilator producing stable hemodynamics. It also reduces systemic vascular resistance without reflex tachycardia and this is a favorable effect of ketanserin.
Animals↗
[Endocrine effects of induced hypotension by ketanserin in anesthetized dogs].
Plasma levels of catecholamines, aldosterone and cortisol as well as plasma renin activity during hypotension by ketanserin were studied in 9 mongrel dogs under 0.87% halothane in oxygen (1MAC). Mean arterial pressure was reduced and maintained at 60 mmHg for 60 minutes by the infusion of 0.1% ketanserin solution. Plasma norepinephrine decreased progressively during hypotension to 35% of the control value after induced hypotension. In contrast, plasma epinephrine increased three-four folds compared with the control value during and after induced hypotension, but this change was not statistically significant. Plasma renin activity and plasma aldosterone showed a slight increase during hypotension but returned toward the control value after discontinuing the infusion of ketanserin. Plasma cortisol remained unchanged throughout the experiment. In conclusion, our data show that hypotension by ketanserin is not accompanied by the activation of the renin-angiotensin-sympathetic system or adrenocortical system.
Animals↗