Search PubMed⌕ Search

Biomedical subjects

H Fujiwara

Publications and source records attributed to H Fujiwara.

At least 109 records · Page 6Linked to original sources

[Anesthetic management of a hyper-obese patient by target-controlled infusion (TCI) of propofol and fentanyl].

We gave total intravenous anesthesia to an over-100% hyper-obese patient using target-controlled infusion (TCI) of propofol and fentanyl. To keep him asleep, we maintained his BIS in a range of 40 to 60 by adjusting the target concentration of propofol. For the target concentration of fentanyl, we chose 2 ng.ml-1 at incision and 1.6 ng.ml-1 during the operation. At the patient's emergence from anesthesia, his estimated blood concentration of propofol was 1.51 micrograms.ml-1 and his BIS was 80. The relationship between BIS value and effect-site concentration of propofol was almost the same as that assessed in ordinary adults of a normal weight. We conclude that the estimated concentration of propofol is a good indicator of the effect of propofol and that TCI is a useful technique in obese patients as well as in ordinary adults.

Adult↗

[Angiographic findings of hemodialysis access insufficiency].

One hundred forty-six angiographic findings of malfunctioning internal arteriovenous fistulas without any history of interventional procedures were reviewed. Angiographies demonstrated 110 cases of stenosis, 72 of occlusion, 5 of venous varicosity, and 13 of venous aneurysm. Of 182 stenotic lesions, 118 (65%) lesions (74 venous stenoses: 67%; 44 venous occlusions: 61%) were revealed within five centimeters of anastomoses. In 4 of 5 cases of varicosity, proximal venous occlusions were demonstrated. On the other hand, interventional procedures were performed in 81 cases of stenoses and 14 of occlusions in the manner of PTA and fibrinolysis. The initial success rate was 90% in stenotic lesions and 71% in occlusive lesions, not a statistically significant difference. Furthermore, there was no statistically significant difference in initial success rates according to anatomical location and lesion length. Although there was no statistically significant difference according to the angiographic findings of lesions, we would like to emphasize the importance of correct understanding of anatomical changes in the dialysis shunt and of early intervention to improve the initial success rate of PTA.

Adolescent↗

[Anesthetic management for gastrojejunostomy in a patient with hemiplegia and recurrent laryngeal nerve palsy].

A 70-year-old man who had undergone a low anterior resection for primary rectal cancer 9 years before complained of anorexia, hemiplegia, and recurrent laryngeal nerve palsy. The anorexia was caused by duodenal stenosis due to swollen lymph nodes, the hemiplegia was caused by a metastatic brain tumor, and the recurrent laryngeal nerve palsy was caused by metastases of the cancer to the mediastinal space. Metastases were also found in the bilateral lungs, liver, ureter, and cervical vertebra. In choosing the anesthesia for the gastrojejunostomy to improve the malnutrition of this patient, we decided, on the basis of the patient's full stomach, malnutrition, hypovolemia, hemiplegia, cerebral compression, recurrent laryngeal nerve palsy, renal dysfunction, and respiratory dysfunction, to use thoracic epidural anesthesia rather than spinal anesthesia or general anesthesia. Thoracic epidural anesthesia could provide sufficient analgesia, and the operation was uneventful. In anesthetic management of an end-stage patient undergoing a palliative operation like this, we should consider the purpose of the operation, its complications, and further complications which may be induced by anesthesia in order to plan out an anesthetic regimen unlikely to lead to harmful events in perioperative period.

Aged↗

IL-12 plays a pivotal role in LFA-1-mediated T cell adhesiveness by up-regulation of CCR5 expression.

The chemokine receptor CCR5 has been implicated in the recruitment of T cells to inflammatory sites. However, the regulation of CCR5 induction on T cells and its contribution to T cell adhesiveness are poorly understood. Using a Th1 clone, 2D6, that can be maintained with interleukin (IL)-12 or IL-2 alone (designated 2D6(IL-12) or 2D6(IL-2), respectively), we investigated how CCR5 is induced on T cells and whether CCR5 is responsible for up-regulating the function of adhesion molecules. 2D6(IL-12) grew, forming cell aggregates, in culture containing IL-12. This was due to lymphocyte function-associated antigen (LFA)-1-intercellular adhesion molecule (ICAM)-1 interaction, because 2D6(IL-12) expressed both LFA-1 and ICAM-1 and cell aggregation was inhibited by anti-ICAM-1 monoclonal antibody. Despite comparable levels of LFA-1 and ICAM-1 expression, 2D6(IL-2) cells did not aggregate in culture with IL-2. It is important that there was a critical difference in CCR5 expression between 2D6(IL-12) and 2D6(IL-2); the former expressed high levels of CCR5, and the latter expressed only marginal levels. Both types of cells expressed detectable albeit low levels of RANTES (regulated on activation, normal T expressed and secreted) mRNA. Unlike IL-12 or IL-2, IL-18 induced high levels of RANTES mRNA expression without modulating CCR5 expression. Therefore, combined stimulation with IL-12 and IL-18 strikingly up-regulated 2D6 cell aggregation. Notably, LFA-1-mediated aggregation of 2D6(IL-12) cells was suppressed by anti-CCR5 antibody. These results indicate that IL-12 plays a critical role in CCR5 expression on Th1 cells and consequently contributes to CCR5-mediated activation of LFA-1 molecules.

Animals↗

Preferential and persistent activation of the STAT1 pathway in rheumatoid synovial fluid cells.

OBJECTIVE: Inflammatory cytokines such as interleukin 1 (IL-1), IL-6, and tumor necrosis factor-alpha are produced in great quantities in inflamed rheumatoid joints. However, little is known about the pathogenic significance of each cytokine in the proliferative synovitis and destruction of bone and joint. We investigated the role of cytokine receptor signals transduced into cells at the foci of rheumatoid inflammation. METHODS: Synovial fluid (SF) cells from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) were examined for the activation of a group of cytokine receptor signaling molecules, signal transducers and activators of transcription (STAT). RESULTS: DNA binding of STAT1 in SF cells was observed in 8 out of 14 patients with RA, but in none of the 10 patients with OA studied, and this was prevented by preincubation of these cells with neutralizing anti-IL-6 antibody. IL-6 activated both STAT1 and STAT3 in normal peripheral blood (PB) leukocytes, and preferentially STAT1 in rheumatoid SF cells. Moreover, STAT1 activation in rheumatoid SF cells appeared to be continuous, in contrast to the transient activation in normal PB leukocytes. CONCLUSION: STAT1 and STAT3 are differentially regulated in response to IL-6 in different cell types. The continuous STAT1 activation may be of pathogenic significance in the progression and persistence of RA.

Adult↗

[The effects of the fat component of propofol solution of ketogenesis during propofol anesthesia].

To examine the effects of the fat component in propofol solution on the fat metabolism during propofol anesthesia, we measured the urine ketone body (UKB) and blood concentrations of 3-hydroxybutyrate (3-OHBA) and glucose. The anesthesia was maintained with propofol, fentanyl, and vecuronium. Infusion fluid without glucose was used while we measured the concentration of 3-OHBA. UKB was detected only when the concentration of 3-OHBA was more than 400 mumol.ml-1. The blood concentration of 3-OHBA increased in proportion to the total amount of propofol solution, while UKB did not show any such relationship. Furthermore, the rate of increase of 3-OHBA was larger in the group whose concentration of 3-OHBA was higher than the normal range. The blood concentration of glucose ranged within the normal fasting level. There were no cases who needed special treatment for hyperketonemia in this study. We concluded that 3-OHBA was a more sensitive indicator of ketogenesis than UKB, and that ketogenesis was accelerated both by propofol anesthesia with the lipidemic solution of propofol and by fasting before surgery. The acceleration of ketogenesis was especially marked in the patients with hyperketonemia.

3-Hydroxybutyric Acid↗

Metabolic changes in human CD36 deficiency displayed by glucose loading.

Previous in vitro studies have shown that CD36 participates in cellular fatty acid (FA) uptake. In vivo evidence for a physiologic role of CD36 in this process is poor and mostly obtained in animals. To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16). After 30 min, FA levels had fallen by 60.1% in normals but by only 31.7% in Type II deficiency (P <0.01 vs. normals) and 16.5% in Type I deficiency which remained significantly higher than the other two groups out to 2 h. Further, changes in triglyceride and glucose metabolism were observed in the both types of CD36 deficiency. Impaired fast FA clearance by muscle and consequently increased hepatic FA uptake seem to underlie these changes. We conclude that human CD36 deficiency causes systemic metabolic changes.

Adult↗

[Anesthetic management using propofol and fentanyl for transrectal ultrasound-guided prostatic biopsy].

We prospectively evaluated the efficiency of the anesthetic management using propofol and fentanyl for the transrectal, ultrasound-guided, prostatic biopsy. In the anesthetic management for the transrectal, ultrasound-guided, prostatic biopsy, it is required to obtain enough muscle relaxation of the anal sphincter for placing the transrectal ultrasound probe and to secure immobilization of the patient during the prostatic biopsy. Eight patients undergoing the transrectal, ultrasound-guided, prostatic biopsy participated in this study. Without premedication, anesthesia was induced using fentanyl (100 micrograms) and target-controlled infusion of propofol with an estimated blood concentration of 3 micrograms.ml-1. We obtained both sufficient muscle relaxation of the anal sphincter and complete immobilization of the patient during the prostatic biopsy in all patients. Moreover, this anesthetic management assured short awakening time from anesthesia and low incidence of adverse effects. From these results, we conclude that the anesthetic management using propofol and fentanyl for the transrectal, ultrasound-guided, prostatic biopsy is efficient and practical.

Aged↗

Two steroidal saponins from Camassia cusickii induce L1210 cell death through the apoptotic mechanism.

Two steroidal saponins, tigogenin hexasaccharide-1 (TGHS-1, (25R)-5alpha-spirostan-3beta-yl 4-O-[2-0-[3-O-(alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl]-3-0-[4-0- (alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl]-beta-D-glucopyranosyl]-3-D- galactopyranoside) and tigogenin hexasaccharide-2 (TGHS-2, (25R)-5alpha-spirostan-3beta-yl 4-O-[2-0-[3-0-(beta-D-glucopyranosyl)-beta-D-glucopyranosyl]-3-0-[4-0- (alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl]-beta-D-glucopyranosyl]beta-D-galactopyranoside), were isolated from the fresh bulbs of Camassia cusickii. In murine leukemic L1210 cells, both compounds showed cytotoxicity with an EC50 value of 0.06 microM. The morphological observation revealed that TGHS-1 and TGHS-2 induced shrinkage in cell soma and chromatin condensation, suggesting apoptotic cell death. The cell death was confirmed to be apoptosis by Annexin V binding to phosphatidylserine in the cell membrane and excluding propidium iodide. A typical apoptotic DNA ladder and the cleavage of caspase-3 were observed after treatment with TGHS-1 and TGHS-2. In the presence of both the compounds, cells with sub-G1 DNA content were detected by flow cytometric analysis, indicating that TGHS-1 and TGHS-2 (each EC50 value of 0.1 microM) are the most powerful apoptotic saponins known. These results suggest that TGHS-1 and TGHS-2 induce apoptotic cell death through caspase-3 activation.

Animals↗

Comparison of chromatographic methods for hydrogen isotope separation by Pd beds.

Comparison among three chromatographic separation methods, i.e. hydrogen-displacement chromatography, self-displacement chromatography and frontal chromatography, is made in an experimental way using several gas mixtures of hydrogen and deuterium. There is small difference in the height equivalent to a theoretical plate (HETP) based on the plate theory among the three chromatographic techniques. The HETP value for the self-displacement chromatography is 3.9 cm, and that for the frontal or H2-displacement chromatography is 3.0 cm at the same flow-rate. The self-displacement chromatography is more useful for the separation of a small amount of deuterium or tritium from other hydrogen isotopes under a moderate recovery ratio. Since the frontal chromatography uses no other gas than the sample, it is more convenient for the separation of deuterium from natural hydrogen even though a lower recovery ratio.

Chromatography↗

Considerable time from the onset of plaque rupture and/or thrombi until the onset of acute myocardial infarction in humans: coronary angiographic findings within 1 week before the onset of infarction.

BACKGROUND: It has been thought that the thrombi and bleeding in plaques that occur after plaque rupture or endothelial damage from vessels with mild stenosis suddenly occlude the lumen and cause acute myocardial infarction (AMI). However, our hypothesis is that thrombi and bleeding may not suddenly occlude the lumen. METHODS AND RESULTS: The study group consisted of 20 patients who had coronary angiograms performed within 1 week (3+/-3 days) before AMI and 20 control patients who had coronary angiograms performed 6 to 18 months (282+/-49 days) before AMI. The features of infarct-related coronary segments (IRCS) at 3 days before AMI were the presence of a significant stenosis of >50% (95% in incidence and 71+/-12% diameter stenosis) and Ambrose's type II eccentric lesions (plus multiple irregularities), an indicator of plaque rupture and/or thrombi (60% [70%]), and the features at 1 year before AMI were mild stenosis of <50% (95% incidence and 30+/-18% diameter stenosis) with rare Ambrose's type II eccentric lesions (plus multiple irregularities) (10% [10%]). The same relation was observed in each of the 4 subgroups with Q-wave infarction, non-Q-wave infarction, preceding effort angina within 1 month before AMI, and no preceding effort angina. CONCLUSIONS: The appearance of marked progression and Ambrose's type II eccentric lesion on coronary angiograms 3 days before AMI suggests the presence of a considerable time from the onset of plaque rupture and/or thrombi until the onset of AMI. These features may be predictors of AMI. The concept provides new insight into the mechanism and prevention of human AMIs.

Acute Disease↗

Intramolecular carbostannation reaction of active methine compounds with an unactivated C-C pi-bond mediated by SnCl(4)-Et(3)N

In the presence of SnCl(4) and Et(3)N, intramolecular carbostannation reaction of various active methine compounds having an unactivated alkenyl, alkynyl, or allenyl group proceeds in good yields with complete regioselectivity. The subsequent reaction of the resulting Sn intermediates with some electrophiles provides functionalized cyclopentane and cyclohexane derivatives.

Journal Article↗

Metabolism of an ionic contrast medium and the related agents.

Liquid chromatography-atmospheric pressure chemical ionization mass spectrometry was applied to analyze the iodinated compounds and their glycine conjugates. The negative-ion mass spectra of the iodinated compounds gave [M-H]-, [M-COOH]- and [I]- ions. The positive- and negative-ion mass spectra of the glycine conjugates showed abundant [M+H]+ and [M-H]- ions. Fragmentations of the glycine conjugates obtained in the positive-ion mode were different from those in the negative-ion mode, the former providing more useful structural information for the presence of glycine. Mouse kidney mitochondria were more active in glycine conjugation than liver mitochondria. Mono-substituted benzoic acids were conjugated with glycine in liver and kidney, whereas the acids having three functional groups or more did not undergo glycine conjugation in liver and kidney.

Animals↗

Inhibition by parthenolide of phorbol ester-induced transcriptional activation of inducible nitric oxide synthase gene in a human monocyte cell line THP-1.

Excessive nitric oxide production by inducible nitric oxide synthase (iNOS) in stimulated inflammatory cells is thought to be a causative factor of cellular injury in inflammatory disease states. Compounds inhibiting iNOS transcriptional activity in inflammatory cells are potentially anti-inflammatory. An assay method for estimating iNOS transcriptional activity in the human monocyte cell line THP-1 was established using a luciferase reporter gene system. In this study, we demonstrate that parthenolide, the predominant sesquiterpene lactone in European feverfew (Tanacetum parthenium), exerts potent inhibitory effects on the promoter activity of the iNOS gene in THP-1 cells. Parthenolide effectively suppressed iNOS promoter activity in a dose-dependent manner at concentrations higher than 2. 5 microM, with an IC(50) of about 10 microM. A tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), significantly increased the iNOS promoter-dependent reporter gene activity, and the TPA-induced increase in iNOS promoter activity was effectively suppressed by parthenolide, with an IC(50) of approximately 2 microM. The present findings may further explain the anti-inflammatory property of parthenolide.

Anti-Inflammatory Agents, Non-Steroidal↗

Human CD36 deficiency is associated with elevation in low-density lipoprotein-cholesterol.

To find out whether CD36 plays a role in the human lipoprotein metabolism, we studied lipoprotein profiles in subjects with CD36 deficiency. Apparently healthy Japanese volunteers (n = 790) were classified by flow cytometry into three groups of normal (platelet and monocyte CD36+, n = 741, 93.8%), type-II deficiency (platelet CD36- and monocyte CD36+, n = 45, 5.7%), and type-I deficiency (platelet and monocyte CD36-, n = 4, 0.5%). At least one of reported mutations in the CD36 gene was found in all four subjects with type-I deficiency and in 23 of the 45 subjects with type II. Among 779 subjects (731 normals, 44 type II, and four type I) with serum triglyceride levels of <400 mg/dL, serum total cholesterol and low-density lipoprotein (LDL) cholesterol were significantly elevated in type-II deficiency (P = 0.0095 and 0.0382 versus normal, respectively, Scheffe's F-test), while differences were not significant in triglyceride and high-density lipoprotein-cholesterol. Similar tendency was observed in type-I deficiency, although the differences were not statistically significant because of small sample size. We conclude that CD36 deficiency elevates LDL cholesterol, indicating a contribution of CD36 to LDL metabolism.

CD36 Antigens↗

Induction of tryptophan 2,3-dioxygenase in the mouse endometrium during implantation.

Indoleamine 2,3-dioxygenase (IDO) is expressed in trophoblasts and defends the conceptus against rejection by reducing the tryptophan level and suppressing the T cell activity. We isolated a cDNA for tryptophan 2,3-dioxygenase (TDO), another key catabolizing enzyme of tryptophan, from a mouse uterus cDNA library enriched with pregnancy-induced genes. Northern blot and in situ hybridization analyses demonstrated that the TDO mRNA was induced in the decidualized stromal cells around the implanted embryo at the time of implantation. The expression was then upregulated and primarily localized at the mesometrial decidua. TDO mRNA was induced by deciduoma formation as well as embryo transfer but not by ovarian steroid hormones. These findings demonstrated that TDO is induced in the endometrial stromal cells concomitant with decidualization and suggested its involvement in the implantation process by regulating the tryptophan level at the implantation site.

Animals↗

Granulocyte/macrophage colony-stimulating factor inhibits IL-12 production of mouse Langerhans cells.

We investigated the capacity of mouse Langerhans cells (LC) to produce IL-12, a central cytokine in a Th1 type of immune responses. We prepared purified LC (>95%) from BALB/c mouse skin by the panning method using anti-I-Ad mAb. An ELISA showed that purified LC spontaneously produced IL-12 p40, and that its production was up-regulated following simultaneous stimulation with anti-CD40 mAb and IFN-gamma. Surprisingly, GM-CSF strikingly inhibited IL-12 p40 production by anti-CD40/IFN-gamma-stimulated LC (% inhibition = 97.0 +/- 0.9% at 1 ng/ml GM-CSF). Supernatants of 48-h cultured keratinocytes (KC) also caused the inhibition of LC IL-12 p40 secretion, and this effect was neutralized by anti-GM-CSF mAb. IL-1alpha (1 ng/ml)-stimulated KC produced much more GM-CSF than unstimulated KC (60.9 +/- 0.2 pg/ml vs 20.9 +/- 1.7 pg/ml), and IL-1alpha-stimulated KC supernatants strongly inhibited IL-12 p40 production by anti-CD40/IFN-gamma-stimulated LC (% inhibition = 89.4 +/- 1.4%). A bioassay using an IL-12-dependent T cell line demonstrated the correlation of the level of IL-12 p40 with the bioactivity of IL-12. These results provide important implications for the pathogenesis of atopic dermatitis, which involves the participation of LC and KC with the capacity to produce IL-12 and GM-CSF, respectively.

Animals↗