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Biomedical subjects

R Tanaka

Publications and source records attributed to R Tanaka.

At least 235 records · Page 13Linked to original sources
PubMed1998

The significance of retrograde thrombosis following removal of arteriovenous malformations in elderly patients.

BACKGROUND: Retrograde thrombosis of former feeding arteries should be considered as a distinct postoperative complication following surgery for arteriovenous malformation (AVM). Regardless of the presence of AVMs, the cerebral arteries undergo atherosclerotic changes with advancing age. In the present study, three cases in elderly patients who developed retrograde thrombosis are reported, and the effect of the patient's age on this complication is discussed. CLINICAL MATERIALS AND METHODS: The present study group consisted of 158 patients who underwent AVM resection and postoperative angiographic studies. Five patients were 65 years of age or older (elderly group) at the time of operation, 108 were between 20 and 64 years of age (adult group), and 45 were less than 20 years of age (young group). The incidence of retrograde thrombosis in the elderly group was compared with that of the other two groups. RESULTS: We found that surgery in the elderly group was accompanied by a significantly higher incidence of retrograde thrombosis (60%) than in the adult group (4%), or the young group (0%). CONCLUSIONS: The present study suggests that this complication should be considered as a serious possibility following removal of an AVM, especially in elderly patients.

Adult↗
PubMed1998

The role of microglia and tumor-primed lymphocytes in the interaction between T lymphocytes and brain endothelial cells.

We investigated the role of IFN-gamma activated microglia in the passage of T lymphocytes across a monolayer of brain endothelial cells (EC) in vitro. Microglia isolated from Fisher 344 (F344) newborn rats were stimulated with IFN-gamma (100 U/ml) for 48 h. T lymphocytes primed with glioma cells were 51Cr-labeled, and added to the monolayer of F344 brain EC. In the adhesion assay, when EC were cultured in medium containing the supernatant of reactive microglia before the assay was carried out, the number of T lymphocytes adhering was increased. In addition, this adhesion was blocked by the addition of anti-ICAM-1 mAb to the EC. In the migration assay, performed using the double chamber system, when reactive microglia adhered to the other side of EC, the number of T lymphocytes migrating to the underwell was also increased. When T lymphocytes were primed to tumor cells in vivo, both their adhesion and migration were enhanced. These results suggest that some soluble factors from reactive microglia are capable of enhancing the expression of ICAM-1 on the brain EC. As a consequence, large numbers of tumor-primed T lymphocytes can adhere to EC and migrate across the EC monolayer.

Animals↗
PubMed1998

ACE gene polymorphism in childhood IgA nephropathy: association with clinicopathologic findings.

A deletion polymorphism in the angiotensin-converting enzyme (ACE) gene has been reported to be a risk factor for progression to chronic renal failure in immunoglobulin A nephropathy (IgAN). In this study, we investigated the association between ACE gene polymorphism and clinical findings, early biopsy findings such as the extent of mesangial proliferation, focal lesions (capsular adhesions, glomerulosclerosis, and crescents), and the glomerular area in childhood IgAN. Genomic DNA was obtained from 97 patients and control subjects. Gene polymorphisms, consisting of an insertion (I) or deletion (D) of the 287-base pair Alu sequence, were detected using the polymerase chain reaction. The extent of capsular adhesions and glomerulosclerosis was significantly higher in patients with the ID/DD genotypes than in those with the II genotype (ID/DD v II: 8.0%+/-1.4% v 2.5%+/-0.8% [P = 0.017] and 5.1%+/-1.3% v 1.4%+/-0.6% [P = 0.028], respectively). Whereas there was no difference in the extent of mesangial proliferation and crescents between the ID/DD genotypes and the II genotype. Urinary protein excretion at the time of biopsy was significantly greater in patients with the ID/DD genotypes than in those with the II genotype (1.02+/-0.15 g/d/m2 body surface area v 0.56+/-0.13 g/d/m2 body surface area; P = 0.012). These results indicate that ACE gene polymorphism may not influence the extent of mesangial proliferation and crescents that are acute lesions. However, the ID/DD genotypes are associated with chronic lesions, such as capsular adhesions or glomerulosclerosis and urinary protein excretion in childhood IgAN.

Alleles↗
PubMed1998

Effect of isoleucine on toxin production by Clostridium difficile in a defined medium.

Supplementation of a carbohydrate-free minimal medium with a high level (100 mM) of histidine, methionine, valine, isoleucine, proline and leucine, in particular isoleucine, markedly increased toxin production by Clostridium difficile VPI 10463. The effect of isoleucine was further examined. Increasing the concentration of isoleucine from 20 to 100 mM remarkably increased toxin production, while bacterial growth decreased gradually. Amino acid analysis of the culture revealed that, at 100 mM isoleucine, consumption of isoleucine was remarkably increased. During the incubation period when toxin titers increased markedly but bacterial growth was declining, isoleucine, leucine and cysteine were taken up preferentially and alanine and cystathionine, which were not found at 1 mM isoleucine, were produced in large quantities. These findings suggest that isoleucine may play an important role in toxin production by C. difficile and that alanine and cystathionine production may be co-regulated with the toxin production in the absence of fermentable carbohydrates.

Amino Acids↗
PubMed1998

Abietane diterpenoids from the cones of larix kaempferi

Three new abietane-type diterpenes, 7alpha,15-dihydroxyabieta-8,11, 13-trien-18-al (1); 15,18-dihydroxyabieta-8,11,13-trien-7-one (2); and 18-nor-4,15-dihydroxyabieta-8,11,13-trien-7-one (3), were isolated from the cones of Larix kaempferi, together with three known diterpenes, abieta-8,11,13-trien-18-yl succinate, 16-nor-15-oxoabieta-8,11,13-trien-18-oic acid, and 7beta-hydroxyabieta-8,11,13-trien-18-oic acid. The structures of 1-3 were determined on the basis of chemical and spectral evidence.

Journal Article↗
PubMed1998

Characterization of peripheral blood progenitor cells mobilized by nartograstim (N-terminal replaced granulocyte colony-stimulating factor) in normal volunteers.

We performed an optimal dose-finding study of nartograstim, N-terminal amino acids-replaced rhG-CSF, for mobilization of PBPC in normal volunteers. Nartograstim was injected subcutaneously for 5 days (days 1-5) at a dose of 1 (n = 3), 2 (n = 3), 4 (n = 6) or 8 microg/kg/day (n = 6), and blood samples were obtained by venipuncture on days 1 (pre-treatment), 4, 5 and 6. Nartograstim was well tolerated up to 8 microg/kg/day. Many kinds of PBPC, such as various hematopoietic progenitors in clonal culture, long-term culture-initiating cells (LTC-IC), and CD34+ cells and their primitive subsets (CD33-, HLA-DR-, CD38-) were mobilized in a dose-related manner. At 8 microg/kg/day, the peak number of CD34+ cells and granulocyte-macrophage colony-forming unit (CFU-GM) reached 82.8 x 10(3)/ml and 16.7 x 10(3)/ml, respectively; LTC-ICMiX, which have the capability to produce mixed colony-forming units (CFU-Mix) for over 5 weeks on stromal cells, were detected after the administration of nartograstim. There is a significant relationship between the number of mobilized CD34+ cells and the number of various progenitor cells including LTC-IC. These results indicate that a 5-day administration of nartograstim at 8 microg/kg/day could mobilize PBPC effectively for allografting.

ADP-ribosyl Cyclase↗
PubMed1998

A canine model of intracranial arteriovenous shunt with acute cerebral venous hypertension.

Increased pressure of draining veins in intracranial arteriovenous fistula is considered an important cause of clinical symptoms. To investigate hemodynamic changes in intracranial arteriovenous fistula with cerebral venous hypertension, we developed a new canine model of this condition. A lingual artery-superior sagittal sinus (SSS) shunt was constructed using a section of the femoral artery as an interposed graft; immediately after which, monitoring of SSS pressure (SSSP) and regional cerebral blood flow (rCBF) was started. The baseline SSSP was 4.1 +/- 3.7 mmHg. After shunt opening, it increased slightly but not significantly. When the SSS was occluded with a clip with the shunt closed, SSSP rose to 20.3 +/- 9.0 mmHg (p < 0.01). Finally, on shunt opening, with the SSS caudal (downstream) to it occluded, the SSSP increased to 59.5 +/- 22.9 mmHg (p < 0.01, multiple analysis of variance, contrast). The frontal lobe rCBF decreased as the cerebral perfusion pressure (CPP) (mean blood pressure minus SSSP) fell. However, cerebral vascular resistance decreased significantly and proportionately to the reduced CPP (r = 0.66, p < 0.0001). In conclusion, when an intracranial arteriovenous shunt was present, venous outflow obstruction was shown to be necessary for cerebral venous hypertension to occur. In acute venous hypertension, decreases in rCBF occurred, but the autoregulatory vasodilating response was also active.

Animals↗
PubMed1998

Pial arteriovenous malformation with massive perinidal edema.

It is generally considered that perinidal edema in an arteriovenous malformation (AVM) is caused by a concomitant intracerebral hematoma. We report a rare case of AVM with perinidal massive edema which was possibly not due to hemorrhage, and discuss the pathophysiological mechanisms of such edema development. A 60-year-old woman presented with a sudden onset severe headache. Computed tomography (CT) scans obtained two hours after the onset showed an AVM-like lesion with a small hematoma in the right parieto-occipital lobe, and unexpectedly early development of massive edema adjacent to the hematoma. Angiograms demonstrated a medium-sized AVM, and severe stenosis in the draining vein which suggested the presence of venous hypertension at prestenotic sites. Repeated CT scans and magnetic resonance (MR) images in the chronic period after the hemorrhage demonstrated persistence of the perinidal edema with mass effect. Removal of the lesion was achieved 2 months after the onset. MR images 3 months after the operation showed marked reduction of perinidal edema. The time course of the perinidal edema suggests that its development was unrelated to the hemorrhage. The findings indicate that increased venous pressure secondary to severe stenosis of the draining vein may possibly contribute to the development of perinidal edema.

Arteriovenous Malformations↗
PubMed1998

Aneurysm of a subclavian-vertebral artery saphenous vein bypass graft: case report.

OBJECTIVE AND IMPORTANCE: Although an autogenous saphenous vein is frequently used as a bypass graft, an aneurysm of a venous graft is a rare complication, especially in the case of cerebrovascular revascularization. We report a case of a successfully treated aneurysmal change in a venous graft after short vein bypass grafting. CLINICAL PRESENTATION: A 60-year-old man underwent a left subclavian-to-vertebral artery bypass operation with an interposed saphenous vein graft because of severe stenosis of the vertebral artery bilaterally. Angiograms of the left subclavian artery, obtained 4 months later, showed good patency of the graft without any dilation or stenosis. One year after the bypass surgery, the patient became aware of a pulsating mass in the left supraclavicular region, which was regarded as the grafted vein itself. A giant aneurysm of the vein graft, which developed at the nonanastomotic site, was shown in the angiogram 4 years later. INTERVENTION: The aneurysm was resected, and patch grafting of the orifice of the aneurysmal neck covered with an artificial vessel as a reinforcement was performed. CONCLUSION: The aneurysm seemed to have developed in a curved segment because of hemodynamic stress.

Anastomosis, Surgical↗
PubMed1998

Multivariate analysis of predictors of hematoma enlargement in spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: We conducted this study to determine, through use of multivariate analyses, the independent predictors of hematoma enlargement occurring after hospital admission in patients with spontaneous intracerebral hemorrhage (i.c.h.). METHODS: We reviewed 627 patients with ICH admitted within 24 hours of onset. The first CT was performed at admission and the second within 24 hours of admission, and a blood sample was taken for laboratory examinations. Univariate and multivariate analyses were performed to assess the relationships between hematoma enlargement and time from onset, consciousness level, CT findings, amount of alcohol consumption, systolic blood pressure at and after admission, clinical outcome, and hematologic parameters. RESULTS: Eighty-eight patients (14.0%) showed enlarged hematomas after admission. Multivariate analyses revealed that the following five factors were independently associated with hematoma enlargement: the time from onset (odds ratio [OR], 0.26 for a 1-SD change; 4.9 hours; P < 0.001); the amount of alcohol consumption (OR, 1.50 for 1 SD; 46.3 g/d; P = 0.002); the sharp of hematoma (OR, 1.40 for 1 SD; 0.45 round; P = 0.006); the presence of consciousness disturbance (OR, 1.38 for 1 SD; 0.50 coma; P = 0.026); and the level of fibrinogen (OR, 0.74 for 1 SD; 87.1 mg/dL; P = 0.042). Hematoma enlargement was an independent factor increasing the mortality rate in the ICH patients (OR, 1.57; P < 0.001). CONCLUSIONS: A particularly high likelihood of hematoma enlargement was observed in patients who (in order of importance) were admitted shortly after onset, who were heavy drinkers; who had an irregularly shaped hematoma, whose consciousness was disturbed, and who had a low level of fibrinogen.

Aged↗
PubMed1998

Dural-pial arteriovenous malformation after sinus thrombosis.

BACKGROUND: We report an unusual case of acquired dural-pial arteriovenous malformation (AVM) following sinus thrombosis. CASE DESCRIPTION: Initial angiography performed in a 39-year-old man showed thrombosis of the superior sagittal sinus (SSS) and the right transverse sinus (TS) but no vascular malformations. Follow-up angiography 29 months later revealed recanalization of the SSS and the TS, retrograde cortical venous drainage which suggested that thrombosis of the sinuses probably propagated into the adjacent parietal cortical veins, and development of a dural-pial AVM at or near the site of thrombi in more than one cortical vein. Complete surgical excision of the lesion was accomplished without neurological deterioration. CONCLUSIONS: The present case suggests the possibility that the pial AVM is not only a congenital condition but also may develop as an acquired lesion.

Adult↗
PubMed1998

Quinolone-resistant mutations of DNA gyrase increase sensitivity to acriflavine.

DNA gyrases were constructed to possess the quinolone-resistant (D87N in GyrA or K447E in GyrB) and acrB (S759R-R760C in GyrB) mutations and their sensitivities to acriflavine and oxolinic acid were examined. Both quinolone-resistant mutations in GyrA and GyrB increased acriflavine sensitivities in the supercoiling assay irrespective of the co-presence of the acrB mutation. In the DNA binding assay, however, the hypersensitvity caused by the GyrB (K447E) mutation was observed only in the co-presence of the acrB mutation; the presence of the acrB mutation, which not affecting acriflavine sensitivity, reduces the extent of DNA binding, as reported previously. Thus, the quinolone-resistant mutation site in GyrB is likely to be involved in DNA binding which is not detectable in acrB+ gyrase. Furthermore, oxolinic acid was found to enhance DNA binding of the gyrase having GyrB (acrB-K447E), supporting a recent proposal that quinolone binding to the DNA-gyrase complex does not require DNA breakage.

4-Quinolones↗
PubMed1998

[Functional analysis of G protein-coupled receptor kinase (beta ARK1) by intracellular immunization].

G protein-coupled receptor kinases (GRKs) are believed to involve in desensitization of the G protein-coupled receptors. So far, cDNAs of six GRKs were cloned from several species including human and rat. However, it is unknown whether single GRK phosphorylates various receptors and desensitizes them in the cells. To determine whether GRK2 (also called beta ARK1) involves desensitization of the beta 1-adrenergic receptor-mediated response in heart, we tried to apply monoclonal antibody which could recognize only beta ARK1 and inhibit its phosphorylating activity to the heart cells. Monoclonal antibody was obtained by immunization of carboxyl terminus of beta ARK1 as fusion protein of glutathione-S-transferase (GST). The resulting monoclonal antibody specifically reacted with beta ARK1, and inhibited the binding of purified beta gamma subunit to the carboxyl terminus. Monoclonal antibody completely inhibited phosphorylation of the m2 muscarinic acetylcholine receptor as well as phosphorylation of GST-intracellular third loop fusion protein of the m2 receptor. When monoclonal antibody was applied to myocyte prepared from guinea pig heart, the desensitization of the beta 1-adrenergic receptor was partially inhibited as measured by Ca2+ channel activation. Thus intracellular application of monoclonal antibody is promising approach to analyze function of GRKs.

Animals↗
PubMed1998

Expression and purification of cytokine receptor homology domain of human granulocyte-colony stimulating factor receptor in Escherichia coli.

In an attempt to generate a stable non-glycosylated cytokine receptor homology (CRH) domain (Tyr97-Ala309) of human granulocyte-colony stimulating factor (G-CSF) receptor, two free cysteines in the CRH domain were converted to serine by site-directed mutagenesis. Taking advantage of the tight regulation for the expression of T7 RNA polymerase, the mutated CRH domain was successfully expressed in Escherichia coli (E. coli) with a pelB signal sequence at its NH2-terminus and with a His tag at its COOH-terminus. The processed and secreted CRH domain after solubilization and in vitro refolding retained G-CSF binding activity, and its yield (approximately 40 micrograms/30 ml culture) was more than 100-fold higher than that of the mouse CRH domain expressed by the MalE fusion system in E. coli.

Amino Acid Sequence↗
PubMed1998

Trigeminal neuralgia caused by the vertebral artery associated with primitive trigeminal artery and agenesis of the internal carotid artery.

A 69-year-old female presented with trigeminal neuralgia caused by tortuous vertebrobasilar artery associated with primitive trigeminal artery (PTA) and agenesis of the ipsilateral internal carotid artery (ICA). Left vertebral angiography showed marked elongation of the left vertebral artery and filling of the left ICA via the PTA. Bone window computed tomography suggested agenesis of the left ICA. Intraoperative findings showed that the vertebrobasilar junction had compressed the root entry zone of the trigeminal nerve. The neuralgia improved immediately after microvascular decompression. There has been no recurrence for 20 months. Trigeminal neuralgia may be caused by a tortuous vertebrobasilar system due to hemodynamic stress associated with PTA and agenesis of the ICA.

Aged↗
PubMed1998

[Evaluation of 99mTc-DTPA-HSA abdominal imaging of protein-losing gastroenteropathy].

Abdominal images were obtained after the intravenous injection of 99mTc-HSA-D in 8 patients with protein-losing gastroenteropathy (PLG). Six neck images and 7 abdominal images were obtained in 11 patients with ischemic heart disease as a control study. We evaluated all the images with respect to visualization, initial appearance time, and movement of abnormal radioactivity. In 7 of 8 patients with PLG, abnormal radioactivity in the intestine appeared from 10 min to 4 hours after injection, and moved 6 hours after injection. In 6 of 7 abdominal images of control cases, slight activity was observed in the alimentary tract 6 hours or 24 hours after injection. The thyroid was not visualized in any of the 6 cases. In conclusion, if radioactivity in the alimentary tract was first observed 6 hours or later after injection, the diagnosis of PLG may be difficult by this method alone. It still may be necessary to perform the alpha 1-antitrypsin test for the correct diagnosis of PLG.

Abdomen↗