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Biomedical subjects

H Fujisawa

Publications and source records attributed to H Fujisawa.

At least 235 records · Page 13Linked to original sources
PubMed1994

Aortic dissection caused by angiographic procedures.

PURPOSE: To describe findings in, and the clinical course and outcome of, aortic dissection (dissecting aneurysm) caused by angiographic procedures. MATERIALS AND METHODS: The records of approximately 15,500 angiographic procedures performed between 1985 and 1991 were reviewed. In the six cases of iatrogenic aortic dissection identified, computed tomography (CT) was performed for diagnosis, follow-up, or both. RESULTS: The type of aortic dissection was Stanford type A in three patients and Stanford type B in three patients. The sites of injury were the abdominal aorta (n = 2), right brachiocephalic artery (n = 2), middle of the thoracic aorta (n = 1), and right common iliac artery (n = 1). One patient had anterograde dissection from the site of injury; two patients, retrograde dissection; and three patients, extensive dissection that extended in both anterograde and retrograde directions. Retrograde dissections decreased in size or disappeared in 1-3 months due to the absence of reentry, whereas anterograde dissections persisted during follow-up (15-27 months). All patient were treated without surgery. CONCLUSION: Angiographers should be aware of this potentially serious complication. The extent and type of the aortic dissection can be determined with CT.

Aged↗
PubMed1994

Effect of neuroprotective N-methyl-D-aspartate antagonists on increased intracranial pressure: studies in the rat acute subdural hematoma model.

Glutamate antagonists are the most powerful neuroprotective drugs in laboratory studies of focal cerebral ischemia. Because the majority of clinical conditions in which focal brain ischemia occurs are associated with high intracranial pressure (ICP), we have used the rat acute subdural hematoma model to evaluate the effects of three glutamate N-methyl-D-aspartate antagonists, MK-801, CGS 19755 (SELFOTEL), D-CPP-ene, and mannitol, upon ICP and also upon the volume of ischemic brain damage. Only mannitol produced a significant reduction in ICP and improved cerebral perfusion pressure. The three glutamate antagonists did not significantly affect ICP or cerebral perfusion pressure, but they were associated with a significantly smaller zone of focal brain damage, when compared to the mannitol and saline groups. N-methyl-D-aspartate antagonists do not increase ICP or jeopardize cerebral perfusion pressure when administered under anesthesia with a controlled PaCO2 level. Further studies in humans are indicated.

Acute Disease↗
PubMed1994

Anti-inflammatory effects of etodolac: comparison with other non-steroidal anti-inflammatory drugs.

The anti-inflammatory effects of etodolac (Eto) were compared with those of 6 other anti-inflammatory drugs: indomethacin (Ind), diclofenac Na (Dic), piroxicam (Pir), naproxen (Nap), ketoprofen (Ket) and aspirin (Asp). Eto inhibited carrageenin-induced edema in rats, adjuvant-induced arthritis in rats, acetic acid-induced writhing in mice and brewer's yeast-induced hyperalgesia and fever in rats. In the adjuvant arthritis test, the ED30 value (1.88 mg/kg) on day 3 and ED50 values (adjuvant-injected paw: 1.18 mg/kg and non-injected paw: 0.96 mg/kg) on day 18 for Eto were comparable to those for Dic (2.16, 1.72 and 1.28) when given prophylactically and the ED50 values for Eto (adjuvant-injected paw: 1.61 and non-injected paw: 1.20 mg/kg) were comparable to those for Ket (1.24 and 1.22) when used therapeutically. The analgesic activity of Eto (ED50 value: 3.67 mg/kg) in the acetic acid-induced writhing test was greater than that of Nap (9.83) or Asp (31.6) and less than that of Ind (0.71), Dic (1.54), Pir (0.92) or Ket (1.34). In the antipyretic test, the minimum effective dose (MED: 1 mg/kg) for Eto was comparable to that for Ind (1.0), Nap (1.0) or Ket (1.0). Eto was less potent in inhibiting carrageenin-induced edema (ED30 value: 6.99 mg/kg) and inflammatory pain (ED50 value: 9.24 mg/kg) than the other drugs (Ind: 2.32 and 3.47, Dic: 0.69 and 3.80, Pir: 1.31 and 1.94, Nap: 1.83 and 2.78, Ket: 1.12 and 0.63), except for Asp (167 and 51.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1994

[Antigenicity study on lactitol (NS-4)].

Lactitol hydrate (lactitol) was tested for its antigenicity in guinea pigs and mice. The following results were obtained. 1. No active systemic anaphylaxis reactions were found in guinea pigs sensitized subcutaneously with lactitol alone or in combination with Freund's complete adjuvant (FCA). 2. No 24 hr heterologous passive cutaneous anaphylaxis reactions were elicited in rats by sera from mice sensitized intraperitoneally with lactitol alone or in combination with 3% aluminum hydroxide gel. 3. No passive hemagglutination reactions were elicited by sera from mice sensitized subcutaneously with lactitol in combination with FCA. From these results, it is concluded that lactitol has no antigenicity under the present experimental conditions.

Anaphylaxis↗
PubMed1994

Characterization of local hyperfibrinolysis in chronic subdural hematomas by SDS-PAGE and immunoblot.

Fibrinogen, fibrin monomer, and D dimer were analyzed in 41 cases of chronic subdural hematoma (SDH) to characterize local rebleeding, coagulation, and fibrinolysis using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Chronic SDH's were divided into five groups according to their appearance on computerized tomography: high-density, isodensity, low-density, mixed-density, and layering types. The concentration of fibrinogen, which indicates rebleeding, was higher in the mixed-density (15.7 +/- 3.4 mg/dl (mean +/- standard error of the mean)) and layering (15.7 +/- 2.6 mg/dl) types of hematoma, and lower in the low-density hematomas (1.4 +/- 0.6 mg/dl) compared with the isodense hematomas (6.9 +/- 1.1 mg/dl). Fibrin monomer, which indicates coagulative activity, had a distribution similar to that of fibrinogen: 87 +/- 22, 18 +/- 8, 175 +/- 40, and 177 +/- 23 micrograms/ml in isodense, low and mixed-density, and layering types of hematomas, respectively. The D dimer, which indicates fibrinolytic activity, was higher in the layering hematoma type (2032 +/- 384 micrograms/ml), and lower in low-density hematomas (301 +/- 164 micrograms/ml) compared to isodense (1310 +/- 256 micrograms/ml) and mixed-density (1039 +/- 207 micrograms/ml) types of hematomas. These observations suggest the following characterization of each type of chronic SDH. The layering type is active, with a high tendency to rebleed and for hyperfibrinolytic activity. The mixed-density type has a high tendency to rebleed with lower hyperfibrinolytic activity than the layering type. The low-density hematoma is stable with a low tendency to rebleed and to fibrinolytic activity.

Adult↗
PubMed1994

Effect of actarit on type II collagen-induced arthritis in mice.

The effect of actarit (MS-932, CAS 18699-02-0), an antirheumatic drug, on type II collagen (CII)-induced arthritis in DBA/1J mice was studied. Mice were immunized twice with bovine CII, actarit being given orally once a day for 35 days after the 1st immunization. Clinical assessment showed that actarit had no effect on the incidence or day of onset of arthritis but that it lowered the arthritis score dose-dependently. Radiography showed that actarit reduced new bone formation in the limbs, and a histopathologic examination showed that it reduced synovitis, erosion of cartilage and bone destruction. Actarit suppressed the delayed-type mouse ear skin reaction to CII but had no effect on the level of serum anti-CII antibodies. These results suggest that actarit inhibits the development of CII-induced arthritis in mice by suppressing delayed-type hypersensitivity to CII.

Animals↗
PubMed1993

Pharmacological modification of glutamate neurotoxicity in vivo.

The ability of five agents (dizocilpine [MK-801], 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)-quinoxaline [NBQX], enadoline [CI-977], L-nitroarginine methyl ester [L-NAME] and BW 1003c87) with well defined, distinct pharmacological profiles and with established anti-ischemic efficacy, to modify neuronal damage has been examined in a simple in vivo model of glutamate excitotoxicity. Cortical lesions were produced in physiologically-monitored halothane-anesthetised rats by reverse dialysis of glutamate. The volume of the lesion was quantified histologically by image analysis of approximately 20 sections taken at 200 microm intervals throughout the lesion. The AMPA and NMDA receptor antagonists (NBQX and MK-801) and the inhibitor of nitric oxide synthase (L-NAME) significantly reduced the lesion volume by a similar extent (by approximately 30% from vehicle). Two agents (the kappa opioid agonist, CI-977 and the sodium channel blocker, BW 1003c87) which putatively inhibit the release of endogenous glutamate presynaptically, had dissimilar effects on lesion size. CI-977 failed to alter the amount of damage produced by exogenous glutamate, whereas BW 1003c87 reduced the lesion size by approximately 50%. Using this model, the neuroprotective effects of anti-ischemic drugs can be explored in vivo, uncomplicated in contrast to experimental ischemia by reduced oxygen delivery, drug effects on tissue blood flow and compromised energy generation. In consequence, additional mechanistic insight into anti-ischemic drug action in vivo can be obtained.

Amino Acid Oxidoreductases↗
PubMed1993

Structural diversity of neuronal nitric oxide synthase mRNA in the nervous system.

Nitric oxide (NO), generated from L-arginine by an enzymatic reaction of a NO synthase (NOS; EC 1.14.23), is a recently identified biological mediator suggested to be involved in a wide variety of biological processes. In the present work, we isolated and sequenced the entire region of cDNAs encoding mouse neuronal NOS (n-NOS) and demonstrated structural diversity of n-NOS mRNA in the nervous system. Sequence determination revealed a novel mRNA with an inframe deletion in the middle of the n-NOS cDNA. Structural analysis of the corresponding part of the n-NOS gene indicated that the deletion corresponded exactly to two exons. These findings suggest that the variant n-NOS is formed by alternative splicing. Both n-NOSs were found in almost all parts of the nervous system, the expression level of the novel variant being about one twentieth of that of the known n-NOS. Generation of diversity of n-NOS is probably related to diversity of its biological functions.

Amino Acid Oxidoreductases↗
PubMed1993

DNA packaging ATPase of bacteriophage T3.

A defined in vitro DNA packaging system of phage T3, which is composed of purified proheads and two packaging proteins, the products of genes 18 and 19 (gp18 and gp19, respectively), displayed a DNA-dependent ATPase activity. ATP was hydrolyzed to ADP and Pi. The ATPase activity was stimulated by nonpackageable DNA, such as single-stranded or circular DNA, or RNA (nonpac-ATPase). Among the inhibitors of DNA packaging, actinomycin D specifically inhibited the ATPase activity that was tightly coupled to DNA packaging (pac-ATPase), but did not inhibit the nonpac-ATPase activity. Both activities depended upon a functional packaging complex, but the nonpac-ATPase, once activated, did not require DNA. Unpackageable pUC18 DNA inhibited the pac-ATPase and the phage yield in parallel. Approximately one molecule of ATP was hydrolyzed during the translocation of 1.8 bp of T3 DNA.

Adenosine Triphosphatases↗
PubMed1993

Effect of etodolac on type-II collagen-induced arthritis in mice.

We tested the effect of etodolac on the development of type-II collagen-induced arthritis in DBA/1J mice. It was administered orally once daily for 35 days after the primary immunization with type-II collagen. Etodolac (10 mg/kg) significantly inhibited the development of signs of arthritis on day 28 to day 35. Indomethacin (1 mg/kg) also significantly inhibited it on day 29 to day 34. Radiographic examination showed that etodolac (10 mg/kg) significantly prevented the development of osteopenia, bone erosion and new bone formation of the joints on day 35, while indomethacin (1 mg/kg) significantly prevented only the development of bone erosion. Histopathological examination showed that both etodolac (10 mg/kg) and indomethacin (1 mg/kg) significantly prevented the development of synovitis, erosion of cartilage of the joints and bone destruction of the limbs on day 35. Etodolac and indomethacin did not affect the serum level of anti-type-II collagen antibodies. These results suggest that etodolac and indomethacin suppress type-II collagen-induced arthritis without affecting humoral immune responses.

Animals↗
PubMed1993

The membrane protein A5, a putative neuronal recognition molecule, promotes neurite outgrowth.

The A5 is an unique membrane protein that is expressed in the neurons of the visual system and general somatic sensory system of Xenopus laevis. We cultured retinal explants or trigeminal ganglion neurons on the monolayers of A5-expressing line cells obtained by transfection with the cDNA, and found that the A5-expressing transfectants promote neurite outgrowth for these A5-expressing neurons. The neurite outgrowth-promoting effect was inhibited by anti-A5 antibodies. While, the neurite outgrowth-promotion by the A5 transfectants was not observed for the vestibulocochlear ganglion neurons which lack the A5. These results indicate that the membrane protein A5 is a potent substrate for neurite extension of the A5-expressing neurons but not for the A5-negative ones, suggesting its involvement in specific neuronal interaction.

Animals↗
PubMed1993

Autophosphorylation of calmodulin-dependent protein kinase IV from rat cerebral cortex.

Calmodulin-dependent protein kinase IV from rat cerebral cortex undergoes autophosphorylation in response to Ca2+ and calmodulin, resulting in its marked enzymatic activation. Autophosphorylation occurred at several sites on CaM-kinase IV, depending upon the enzyme concentration. Among them, Ser437 was almost exclusively phosphorylated at enzyme concentrations lower than 10 micrograms/ml, and autophosphorylation at Ser437 was responsible for marked activation of the enzyme through decreases in the Km values for its substrates and an increase in the Vmax value. The Ca2+/calmodulin-independent activity of CaM-kinase IV was also markedly stimulated by autophosphorylation, but even after autophosphorylation it amounted only about 17% of the total enzyme activity detected in the presence of Ca2+/calmodulin.

Amino Acid Sequence↗
PubMed1993

Requirement of brain extract for the activity of brain calmodulin-dependent protein kinase IV expressed in Escherichia coli.

Calmodulin-dependent protein kinase IV (CaM-kinase IV) is a Ca(2+)-responsive multifunctional protein kinase which occurs abundantly in the brain. When cDNA for rat brain CaM-kinase IV was expressed in Escherichia coli, the enzyme was produced in a good yield, but it did not show significant activity. The inactive recombinant CaM-kinase IV was phosphorylated and became highly active on incubation with a rat brain extract in the presence of both Ca2+/calmodulin and ATP/Mg2+. The recombinant CaM-kinase IV-activating activity in brain was one to two orders of magnitude higher than that in the other tissues examined. These observations suggest that CaM-kinase IV may undergo a posttranslational modification, probably Ca2+/calmodulin-dependent phosphorylation by CaM-kinase IV kinase, before exhibiting activity in the central nervous system.

Animals↗