[Angiographic method of subclavian artery by trans-brachial artery approach for selective cerebral angiography].
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Brachial Artery↗
Biomedical subjects
K Fujii
Publications and source records attributed to K Fujii.
[Countermeasures for hypofunction of gut associated lymphoid tissue during TPN in rats].
Total parenteral nutrition (TPN) causes atrophy of the intestinal mucosa, resulting in the degeneration and atrophy of gut associated lymphoid tissues (GALT). This suppressive effect of TPN on GALT was examined using rats. In rats receiving TPN for 2 weeks, a decrease and atrophy of Peyer's patches and a decrease in thoracic duct lymphocytes (TDL) were observed. Daily oral administration of 1000 mg/kg PSK to the rat in the TPN group corrected the number and size of Peyer's patches, and the number of TDL and its subsets were also improved compared with the TPN group. Diminution of the S-IgA of bile and portal venous blood was noticed during TPN in rats. But the groups PSK administrated were increased the amount of S-IgA in bile and portal venous blood. The immune plasma cells in the Peyer's patches were observed, the number of the MHC-class II, T helper, and IL-2 (T CGF) positive cells were decreased in the TPN group compared with control group (PSK group). It has been concluded, therefore, that PSK is effective for improving GALT inhibition caused by TPN.
Animals↗
[Recurrent aseptic meningitis caused by rupture of a pineal cyst].
A 40-year-old woman experienced three attacks of aseptic meningitis in 19 months. Each attack was characterized by sudden onset of meningeal irritation followed by spontaneous remission in several days. The patient was free of neurological symptoms between the attacks. In the acute phase of each attack, her cerebrospinal fluid (CSF) showed mononuclear pleocytosis and increased protein concentration. Epithelial cell clusters in the CSF were evident during the third episode. No pathogenic microorganisms were identified in CSF or blood cultures. Brain imaging revealed a pineal cyst, 1 cm in diameter, and we suspected that the epithelial cell clusters represented the ruptured cystic wall and that the recurrent aseptic meningitis was triggered by spontaneous rupture of the cyst. Recently several new etiologies for the benign recurrent aseptic meningitis (Mollaret's meningitis) have been reported, but its existence as a clinical entity is still in dispute. Our case appears to support "spontaneous rupture of central nervous system epidermoid cysts" as one of the etiologies of recurrent aseptic meningitis.
Adult↗
Isoflurane acts as an inhibitor of oxidative dehalogenation while acting as an accelerator of reductive dehalogenation of halothane in guinea pig liver microsomes.
The effects of isoflurane, 1-chloro-2,2,2-trifluoroethyl difluoromethyl ether, on the oxidative metabolism of halothane to produce trifluoroacetic acid (TFA) and on the reductive metabolism of halothane to produce chlorodifluoroethylene (CDE) and chlorotrifluoroethane (CTE) in liver microsomes of guinea pig were examined. Isoflurane enhanced the production of CDE and CTE and inhibited the production of TFA. Isoflurane enhanced cytochrome P450 reduction and formation of an intermediate complex with cytochrome P450 without enhancement of NADPH-cytochrome P450 reductase (EC 1.6.2.4) activity. We conclude that isoflurane interacts with cytochrome P450 to prevent the formation of the halothane-cytochrome P450 complex, causing inhibition of the oxidative dehalogenation. This interaction of isoflurane enhances the reduction of cytochrome P450 and the formation of a reductive intermediate-cytochrome P450 complex under anaerobic conditions causing reductive dehalogenation of halothane.
Anesthetics, Inhalation↗
L-arginine ameliorates cerebral blood flow and metabolism and decreases infarct volume in rats with cerebral ischemia.
Effects of L-arginine, 300 mg/kg, i.p., on the regional cerebral blood flow (rCBF), brain metabolism, and infarct volume were examined in spontaneously hypertensive rats subjected to occlusion of both left middle cerebral artery and left common carotid artery. Rats treated with L-arginine had higher rCBF, determined by hydrogen clearance method, in the ischemic core (7 +/- 1 ml/100 g/min, mean +/- S.E.M.) and penumbral regions (16 +/- 2) than did rats treated with saline (5 +/- 0 and 7 +/- 1, respectively). Simultaneously, L-arginine attenuated metabolic derangement in the ischemic tissue at 60 min, i.e. well maintained adenosine triphosphate (ATP) in ischemic region (1.29 +/- 0.07 mmol/kg in L-arginine group vs. 1.05 +/- 0.06 in saline group), and also close to normal levels in ATP (2.61 +/- 0.02 mmol/kg vs. 2.45 +/- 0.05), glucose (2.29 +/- 0.12 mmol/kg vs. 1.80 +/- 0.17) and lactate (1.63 +/- 0.10 mmol/kg vs. 2.24 +/- 0.21) in periischemic region. In another experiment, the effects of L-arginine on rCBF in the subcortical regions and on infarct volume were evaluated. L-arginine, compared with saline, increased rCBF by 8 ml/100 g/min in the ischemic side and reduced infarct volume by 29% at 24 h of ischemia. These findings support that L-arginine may be potentially useful for the treatment of acute cerebral ischemia.
Animals↗
Inhibitory effect of cold stress against acetaminophen-induced hepatic injury in B6C3F1 and ICR mice.
The effect of cold stress (at 0 +/- 1 degree C for 3 h) on acetaminophen-induced hepatic injury was investigated in B6C3F1 and ICR mice. When acetaminophen (250 mg/kg) was injected intraperitoneally in B6C3F1 mice, the plasma GPT activity was significantly increased by 93 or 107-fold at 6 h or 24 h after the drug injection. However, when B6C3F1 mice were exposed to cold stress, the increase in plasma GPT activity induced by acetaminophen was significantly inhibited by 53% and 44%, respectively. On the other hand, when acetaminophen at the same dose was injected in ICR mice, the activity of plasma GPT was increased by 9-fold at 6 h, or 16-fold at 24 h after the drug injection. The increased plasma GPT activity elicited a significant inhibition of 35% and 36%, respectively, by the exposure to cold stress. These results suggest that acetaminophen-induced hepatic injury may be blocked by physical stress in mice.
Acetaminophen↗
Treatment of warfarin-induced hair loss with ubidecarenone.
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Alopecia↗
Orally active and long-term acting insulin-mimetic vanadyl complex:bis(picolinato)oxovanadium (IV).
The blood glucose level of rats with streptozotocin (STZ)-induced diabetes has been found to be normalized by administration of vanadyl or vanadate complexes. During our investigations on the development of anti-diabetic vanadyl complexes with various types of coordination mode such as V-O, V-N and V-S, we found that a new bis(picolinato)oxovanadium (IV) complex (VPA) has a strong insulin-mimetic effects as evaluated by an in vitro experiments, in which the inhibition of free fatty acid release in isolated rat adipocytes treated with epinephrine was observed to be similar to that of insulin. VPA was also effective for normalizing the blood glucose level of STZ-induced diabetic rats when given intraperitoneally or orally. The serum glucose level was maintained in the normal range for about 30 days with body weight gain after the end of oral administration of VPA for 14 days. VPA was confirmed to be an orally active and long-term acting insulin-mimetic vanadyl complex to treat insulin-dependent diabetes mellitus (IDDM) in rats.
Adipocytes↗
Precision study of supersymmetry at future linear e+e- colliders.
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Journal Article↗
Inhibitory effect of sevoflurane on nitric oxide release from cultured endothelial cells.
We investigated the effect of sevoflurane (fluoromethyl-2,2,2-trifluoro-1-(trifluoromethyl) ethylether) on intracellular calcium concentration ([Ca2+]i) and nitric oxide (NO) release from cultured porcine aortic endothelial cells using fura-2 fluorometry, and direct (ESR spectrometry with NO-trapping by 2-(4-carboxyphenyl)-4,4,5,5-tetramiethylimidazoline-1-oxyl 3-oxide) or indirect (nitrite accumulation measured by Greiss reaction) NO measurement. Sevoflurane alone did not change resting [Ca2+]i, but diminished bradykinin-induced transient increase in [Ca2+]i in a concentration-dependent manner. The inhibitory effect of sevoflurane on bradykinin-induced transient rise in [Ca2+]i was larger than that of a non-selective Ca2+ channel blocker (CO2+). Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it. Sevoflurane impaired nitrite accumulation stimulated by bradykinin, and reduced the amount of NO released from endothelial cells. Our results indicate that the negative effect of sevoflurane appears to be due to the inhibition of bradykinin-induced Ca2+ efflux from endoplasmic stores and Ca2+ influx through membrane Ca2+ channels.
Analysis of Variance↗
Temporal changes in myocardial perfusion patterns in patients with reperfused anterior wall myocardial infarction. Their relation to myocardial viability.
BACKGROUND: Several studies demonstrated ischemic microvascular damage in patients with acute myocardial infarction (AMI). In this study, myocardial contrast echocardiography (MCE) was used to assess the temporal changes in myocardial perfusion after reflow and to investigate the relation between MCE findings and myocardial viability. METHODS AND RESULTS: MCE was performed with the intracoronary injection of sonicated microbubbles before and shortly after coronary reflow and 1 month later in 45 patients with anterior wall AMI. MCE before reflow was analyzed to determine the risk area as an area of contrast defect in the apical long-axis view. MCE images after reperfusion were analyzed to determine peak contrast intensity, which should be in proportion to the concentration of microbubbles within the microvasculature and in the infarcted and normal myocardium, and the ratio of these (PI ratio) was used to assess microvascular integrity. Areas of residual contrast defect were expressed as a ratio to those of left ventricular myocardial (RCD ratio) to assess the spatial extent of the MCE "no reflow." Regional wall motion (RWM, SD per chord) in the territory of the left anterior descending coronary artery was determined by the centerline method in both the acute and late stages. Although the PI ratio was extremely low shortly after coronary reflow, it increased in the late stage of AMI with the improvement in regional contractile function (RWM, -3.2 +/- 0.5 versus -2.6 +/- 1.0, P < .01; PI ratio, 0.44 +/- 0.25 versus 0.60 +/- 0.29, P < .01). Reduction in the RCD ratio was observed even in 15 patients with MCE no reflow in the acute stage (0.33 +/- 0.09 versus 0.16 +/- 0.11, P < .01). Then we investigated the relation between residual contractile function and microvascular integrity in the late stage. A significant correlation was found between the PI ratio and RWM (r = .73, P < .001) in the late stage of the AMI. CONCLUSIONS: (1) Recovery from ischemic microvascular damage is generally observed in the late stage of AMI in association with improvement in myocardial contractile function. The degree of improvement in contractile function and microvascular integrity, however, varies among patients. (2) Contrast peak intensity in the late stage of infarction may provide a useful estimate of myocardial viability.
Adult↗
Binding affinities of highly repetitive DNA components for a nuclear scaffold protein from rat-ascites hepatoma cells.
Separate samples of a self-ligated tandem dimer of a highly repetitive DNA component (369-bp HindIII fragment) from rat-ascites hepatoma nuclei were digested with different restriction enzymes that cleave only once in the monomer. The resulting 369-bp sequence-permuted monomers showed anomalously slow gel electrophoretic mobility. Of them, the XmnI fragment had the slowest mobility. This suggests that bending of the helix axis is the strongest in this fragment. Our previous work has shown that such a repetitive bent DNA has selective affinities for two nuclear scaffold proteins from rat liver that have molecular weights of 123,000 and 130,000 Hibino et al. (1992) Biochem. Biophys. Res. Commun., 184, 853-858; Hibino et al. (1993) Biochim. Biophys. Acta, 1174, 162-170). In the present experiment, it has been found that the nuclear scaffold fraction from rat-ascites hepatoma cells does not contain these proteins, but does have a repetitive bent DNA-binding protein that has a molecular weight of about 230,000. These results imply that there is some difference in the structure of nuclear DNA attachment region between rat liver and the hepatoma.
Animals↗
Use of a guanidine extract of demineralized bone in the treatment of osteochondral defects of articular cartilage.
In order to evaluate the ability of a guanidine extract of demineralized bone to repair osteochondral defects in articular cartilage, plugs made of this extract were implanted into defects in rabbit knees. The repair tissue was examined macroscopically, histologically, and immunohistochemically at 4, 8, 12, and 30 weeks. Controls (defects that were left empty) showed no cartilage formation. Four weeks after implantation of a guanidine extract plug, histological examination showed a nonhomogeneous metachromatically stained region extending from the surface of the repair tissue down to cancellous bone. This region also was labeled by an anti-type-II collagen antibody, indicating that cartilage-like tissue had been induced. At 8 weeks, the newly formed cartilage in the subchondral and cancellous bone had been partially replaced by bone. At 12 weeks, the thickness of the newly formed cartilage layer had decreased, and most of the newly formed cartilage in the subchondral and cancellous bone had been replaced by bone. In addition, a tidemark was observed. At 30 weeks, the repair tissue was a mixture of cartilage and fibrocartilage, and there was severe degeneration of the cartilage surrounding the repaired defects. These findings indicate that osteochondral defects of articular cartilage can be partially repaired by the implantation of a guanidine extract and that the newly formed cartilage-like tissue is not permanent.
Animals↗
Epidermal growth factor enhancement of HSC-1 human cutaneous squamous carcinoma cell adhesion and migration on type I collagen involves selective up-regulation of alpha 2 beta 1 integrin expression.
Some human neoplasms show aberrant expression or overexpression of epidermal growth factor (EGF) receptor, and the degree of the receptor expression is correlated with the malignant phenotype in certain epithelial tumors including squamous carcinoma cells. Since phenotypic transformation of cells could involve quantitative and qualitative alteration of integrin function, the effects of EGF on cell-matrix interactions were studied using HSC-1 cells, a human squamous carcinoma cell line showing EGF receptor overexpression. The EGF-treated HSC-1 cells interacted with matrix proteins differently from the untreated cells, as shown by cell adhesion and phagokinetic track assays. Among fibronectin, laminin, fibrinogen, and type I collagen, fibronectin was the most efficient substratum to promote untreated HSC-1 cell adhesion and migration. Pretreatment of the cells with 50 ng/ml EGF for 18 h selectively increased the number of spread cells and the size of the individual cell migration area on type I collagen by 250 and 400%, respectively. The same pretreatment diminished cell adhesion and migration on other substrata so that the EGF treatment converted type I collagen as the most efficient substratum for cell adhesion and migration of the HSC-1 cells. ELISA and immunoprecipitation studies showed that EGF up-regulated the expression of alpha 2 beta 1 integrin collagen receptor in a time- and dose-dependent manner by stimulating biosynthesis of alpha 2 subunit, but did not up-regulate those of the alpha 3 beta 1, alpha 5 beta 1, or alpha v beta 3 integrins. These results suggest that EGF preferentially enhances HSC-1 cell interaction with type I collagen, leading to the enhanced cellular migratory activity on the substratum, as a result of selective up-regulation of alpha 2 beta 1 integrin expression.
Antigens, CD↗
Cell surface proteolysis by serine proteinases enhances RGD-sensitive melanoma cell adhesion on fibrinogen and vitronectin.
Tumor cells avidly secrete various proteinases, and cascades of proteolytic activation occur around the cells. Therefore, cell surface receptors of tumor cells are under the constant influence of proteinases. In this study, the effects of serine proteinases on integrin-medicated cell-matrix interactions were studied in C32TG and Mewo human melanoma cells. These melanoma cells were pretreated with proteinases and their adhesive properties on various substrata were evaluated by cell adhesion assays. Paradoxically, appropriate cell surface proteolysis enhanced the RGD-sensitive cell adhesion on fibrinogen and vitronectin, but not the RGD-insensitive adhesion on type I collagen or laminin. Pretreatment of these cells with 0.1 to 1 microM of trypsin, chymotrypsin, or plasmin for 30 min at 37 degrees C increased the number of spread cells on fibrinogen and vitronectin by 200-300%. The enhancement of cell spreading was not accompanied by up-regulation of the relevant RGD-sensitive integrin expression. Analysis of the cell surface receptor by GRGDSPK-Sepharose affinity chromatography showed that trypsin treatment did not up-regulate alpha v beta 3 integrin, an RGD-sensitive receptor for fibrinogen and vitronectin in the melanoma cells, nor the induced appearance of novel receptors. Treatment of cells with 100 nM proteinases increased cell binding of both monoclonal and polyclonal antibodies against alpha v beta 3 integrin subunits by 70%, but not that of monoclonal antibody against alpha 2, alpha 3, or alpha 6 subunit, indicating that cell surface proteolysis exposed more alpha v beta 3 integrin on the cell surface. These results suggest that exposure of alpha v beta 3 integrin is a part of the mechanisms underlying the serine proteinase-induced enhancement of melanoma cell adhesion on fibrinogen and vitronectin.
Amino Acid Sequence↗
Immunohistochemical analysis of nm23 gene product in human gallbladder carcinomas.
The expression of nm23, the product of a candidate suppressor gene for tumour metastasis, was examined immunohistochemically in human gallbladder carcinomas and compared with clinicopathological features. Seventy-eight (72%) of 107 carcinomas expressed nm23 protein regardless of histological type, while non-neoplastic mucosa occasionally showed very weak immunoreactivity to nm23. No obvious correlation was observed between nm23 protein expression and depth of tumour invasion or tumour stage. The expression of nm23 protein was detected in 60% and 74% of the cases with and without lymph node metastasis, respectively, indicating no relationship to metastatic ability. Fifty-eight percent of the cases showed reduction of nm23 immunoreactivity in tumour cells invading the stroma at the border of tumour cell nests compared with cells at the centre of the tumour. Only 7% of the cases showed increased nm23 expression in tumour cells at the border. These results suggest that in gallbladder carcinoma decreased expression of nm23 may not have implications for metastasis but may play a part in local invasion.
Carcinoma↗
Functional mapping of the sensorimotor cortex: combined use of magnetoencephalography, functional MRI, and motor evoked potentials.
Combined use of magnetoencephalography (MEG), functional magnetic resonance imaging (f-MRI), and motor evoked potentials (MEPs) was carried out on one patient in an attempt to localise precisely a structural lesion to the central sulcus. A small cyst in the right frontoparietal region was thought to be the cause of generalised seizures in an otherwise asymptomatic woman. First the primary sensory cortex was identified with magnetic source imaging (MSI) of somatosensory evoked magnetic fields using MEG and MRI. Second, the motor area of the hand was identified using f-MRI during hand-squeezing. Then transcranial magnetic stimulation localised the hand motor area on the scalp, which was mapped onto the MRI. There was a good agreement between MSI, f-MRI and MEP as to the location of the sensorimotor cortex and its relationship to the lesion. Multimodality mapping techniques may thus prove useful in the precise localisation of cortical lesions, and in the preoperative determination of the best treatment for peri-rolandic lesions.
Adult↗
Cholesterol granuloma in the middle cranial fossa: report of two cases.
We report two cases of cholesterol granuloma in the middle cranial fossa. On CT the lesions appeared as a nonspecific, nonenhancing soft-tissue mass with bone erosion. On MRI they were seen as areas of high signal intensity surrounded by a low-intensity peripheral zone on both T1- and T2-weighted images. Cholesterol granuloma is thought to occur when pneumatised cells in the temporal bone become obstructed. Although this lesion usually occurs in the petrous bone, it can extend to the middle cranial fossa. The diagnosis and surgical management are discussed.
Adult↗