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Biomedical subjects

Y Iida

Publications and source records attributed to Y Iida.

At least 37 records · Page 2Linked to original sources

Penetrating knife injury to the heart.

A 39-year-old man attempted to kill himself using a small knife to penetrate the left anterior chest wall because of trouble at work and with his girlfriend. On arrival at the emergency room, his consciousness was not clear and vital signs were unstable. The knife remained vertically located in the left anterior chest wall. A large left hemothorax was identified by chest X-ray, and moderate cardiac tamponade was detected by echocardiography. Left-sided chest drainage was performed by inserting a chest drainage tube, and about 2500 ml of hemorrhagic effusion was drained. An emergency operation was performed to relieve the cardiac tamponade and repair the penetrating cardiac injury. About an hour after arrival at the emergency room, a median sternotomy was performed in the operating room. The knife had injured the surface of the right ventricular outflow tract, the left lung, and the 3rd intercostal artery and vein. Cardiopulmonary bypass was immediately prepared for the repair of the cardiac injury. The wounds were successfully repaired with pledgeted sutures under cardiac beating. The postoperative course was uneventful with no sign of infection. The patient was discharged at 9 days after the operation. Here we have reported a case of successful surgical repair of a penetrating knife injury to the heart, which was managed by immediate resuscitation and emergency surgery.

Adult↗

Surgical repair of postinfarction ventricular septal rupture.

OBJECTIVES: Postinfarction ventricular septal rupture is fatal without surgical repair because of heart failure and secondary multiple organ failure. We investigated surgical results of postinfarction ventricular septal rupture and discussed the surgical strategy of postinfarction ventricular septal rupture. METHODS: Twelve patients (mean age 71.3 +/- 7.4 years, with range from 61 to 81 years) underwent surgical repair of postinfarction ventricular septal rupture, from 1990 to 1998 in our Institute. There were 6 women and 6 men. The ventricular septal rupture was anterior in 10 patients and inferior in 2. The operative technique for anterior ventricular septal rupture was reconstruction of the septum with a Dacron patch after infarctectomy, according to the method of Daggett et al. For posterior ventricular septal rupture, reconstruction of the septum with a Dacron patch after infarctectomy was performed and the ventricular incision was closed with a two-layer patch. Coronary artery bypass grafting was performed in 5 patients for severe proximal coronary artery stenosis using saphenous vein grafts. RESULTS: Overall hospital mortality was 0%. A postoperative residual shunt was recognized in 3 patients, but all were well-controlled conservatively and re-operation was not needed. The patients have been followed up for a mean of 59.5 months. There have been two late deaths due to non-cardiac problems. Acturial survival rate for the 12 patients was 90% at 1 year and 75% at 5 years. CONCLUSIONS: The Daggett method is simple and fast, and is an effective and reliable technique for the repair of ventricular septal rupture.

Aged↗

Aneurysms in the ascending aorta adherent to the sternum after cardiac surgery.

Sternotomy in a patient with an aneurysm in the ascending aorta adherent to the sternum after cardiac surgery can result in fatal hemorrhage or brain damage unless the distal ascending aorta can be identified and secured immediately. A left anterolateral thoracotomy was used in three patients with adherent aneurysms. The distal ascending aorta was isolated, and dissection was performed between the aneurysm and the sternum. There was no complication. This method was safe, and blood loss was minimized.

Adult↗

Effect of chronic (-)-nicotine treatment on rat cerebral benzodiazepine receptors.

The purpose of this study was to clarify the effect of (-)-nicotine on cerebral benzodiazepine receptors (BzR) with radiotracer methods. The effect of (-)-nicotine on BzR was examined in in vitro studies using chronic (-)-nicotine-treated rats using 3H-diazepam. The in vitro radioreceptor assay showed a 14% increase in the maximum number of binding sites of BzR in chronic (-)-nicotine-treated rats in comparison with the control rats. Moreover, a convenient in vivo uptake index of 125I-iomazenil was calculated and a higher uptake of the radioactivity was observed in the chronic (-)-nicotine-treated group than in the control group. Although further studies of the mechanism of (-)-nicotine on such BzR changes are required, an increase in the amount of BzR in the cerebral cortex was found in rats that underwent chronic (-)-nicotine treatment, and this result contributed to the understanding of the effects of (-)-nicotine and smoking on neural functions.

Animals↗

In vitro synergism between nyasol, an active compound isolated from Anemarrhena asphodeloides, and azole agents against Candida albicans.

The antifungal activity of nyasol (NYS) alone or with various antifungal agents was measured in vitro against Candida albicans, Aspergillus fumigatus, and Trichophyton mentagrophytes. NYS is a compound recently purified from a medicinal plant, Anemarrhena asphodeloides. Among 12 agents, miconazole (MCZ), ketoconazole (KCZ), clotrimazole (CTZ), and cerulenin showed marked synergistic effects against C. albicans. The fractional inhibition concentration (FIC) indices against 4 strains of C. albicans were 0.067-0.31 for MCZ plus NYS, 0.078-0.31 for KCZ plus NYS, and 0.098-0.13 for CTZ plus NYS. These values indicate the possibility of using NYS as an adjuvant to azole agents in the chemotherapy of candidiasis.

Antifungal Agents↗

Quantification analysis of translation initiation signal in vertebrate mRNAs: effect of nucleotides at positions +4(-)+6 upon efficiency of translation initiation.

Concerning the translation initiation signal in vertebrate mRNAs, a consensus, sequence, (GCC)GCC(A or G) CCATGG, has been proposed, but actual initiation sequences differ from it in a greater or lesser degree. Kozak monitored selection by ribosomes of the first versus second ATG codons as a function of mutations introduced at positions +4, and +6 of the first ATG codon. Codons possessing G at +4 strongly enhanced selection of the first ATG codon. However, ATG codon recognition was unaffected by most mutations in positions and +6. These data were well understood by our quantification analysis.

Animals↗

Rapid turnover of tryptophan hydroxylase is driven by proteasomes in RBL2H3 cells, a serotonin producing mast cell line.

Previously we demonstrated that tryptophan hydroxylase (TPH) undergoes very fast turnover driven by ATP-dependent proteolysis in serotonin producing mast cells [Hasegawa et al. (1995) FEBS Lett. 368, 151-154]. We searched for the major proteases involved in the rapid degradation of TPH in RBL2H3 cells. Among various protease inhibitors tested, proteasome inhibitors MG115, MG101, MG132, and lactacystin effectively inhibited the intracellular degradation of TPH. Administration of the proteasome inhibitors to cultured cells caused more than a 5-fold accumulation of TPH. Administration of the inhibitors together with cycloheximide stabilized the amount of TPH with no appreciable increase or decrease. Although MG-series proteasome inhibitors could inhibit calpain, the involvement of calpain was excluded since the cysteine protease inhibitor E-64-d, which acts on calpain, had no effect. Extracts of RBL2H3 cells were shown to contain a protease that digests TPH in an ATP-dependent manner and is sensitive to proteasome inhibitors. The ubiquitination of TPH could be visualized by Western blot analysis using both anti-TPH and anti-ubiquitin antibodies. Based on these results, we conclude that 26S proteasomes are mainly involved in the degradation of TPH. In the reported amino acid sequences of TPH from various sources including human, rabbit, rat, and mouse, a PEST sequence that is widely shared among short-lived proteins has been recognized. It was noted that the PEST sequence lies within the most conserved portion of the enzyme, the pteridine binding site.

Amino Acid Motifs↗

Avidin chase can reduce myelotoxicity associated with radioimmunotherapy of experimental liver micrometastases in mice.

Myelotoxicity is the main factor which decides the maximum tolerated dose (MTD) in radioimmunotherapy (RIT). Since bone marrow is mostly irradiated from blood radioactivity, enhancing the clearance of unbound circulating radiolabeled antibody is important to reduce myelotoxicity and to increase the MTD. We applied the avidin chase method, which was devised to obtain high tumor-to-background ratios in tumor-targeting, to RIT of experimental liver micrometastases and evaluated its influence on the side effects and therapeutic outcome. Seven days after intrasplenic injection of human colon cancer LS174T cells, nude mice were intravenously injected with biotinylated (131)I-labeled anti-CEA monoclonal antibody (MAb) (24 - 38 microg, 11.1 MBq). Mice of the chase group then received an intravenous injection of avidin twice (24 and 30 h, 72 - 115 microg each). Biodistribution, side effects (white blood cell counts and body weight change), and short- and long-term therapeutic effects were determined. Avidin chase markedly accelerated the clearance of radiolabeled MAb from the blood (P < 0.0001) and normal tissues, resulting in milder leukocytopenia and body weight loss, both of which recovered earlier than in the non-chase group (P < 0.01). The tumor uptake of radiolabeled MAb was also decreased by avidin chase, but the metastases-to-background ratios were increased. Avidin chase gave the therapeutic gain ratio of 1.89. Treated groups with and without avidin chase showed significant therapeutic effects compared to the non-treated group. There was no significant difference in the therapeutic effects between the two treated groups. Avidin chase effectively reduced the side effects of RIT and should increase the MTD.

Animals↗

B(1) and B(2) bradykinin receptors on adventitial fibroblasts of cerebral arteries are coupled to recombinant eNOS.

Our previous ex vivo and in vivo studies reported that expression of the recombinant endothelial nitric oxide (NO) synthase (eNOS) gene in adventitial fibroblasts recovers NO production in arteries without endothelium in response to bradykinin. The present study was designed to characterize subtypes of bradykinin receptors on adventitial fibroblasts coupled to the activation of recombinant eNOS. Endothelium-denuded segments of canine basilar arteries were transduced with beta-galactosidase (beta-Gal) gene or eNOS gene ex vivo, using a replication-defective adenoviral vector (10(10) plaque-forming units/ml) for 30 min at 37 degrees C. Twenty-four hours later, isometric force recording or cGMP measurement was carried out. B(1) bradykinin receptor agonist (des-Arg(9)-bradykinin, 10(-10)-10(-8) mol/l) did not significantly affect vascular tone in control or beta-Gal gene-transduced canine basilar arteries without endothelium. In contrast, this agonist caused concentration-dependent relaxations in recombinant eNOS gene-transduced arteries without endothelium. Relaxations to B(1) receptor agonist in the eNOS arteries were abolished by B(1) receptor antagonist (des-Arg(9)-[Leu(8)]bradykinin, 6 x 10(-9) mol/l) but not by B(2) receptor antagonist (Hoe-140, 5 x 10(-8) mol/l). Bradykinin did not significantly alter vascular tone in control or beta-gal arteries without endothelium, whereas this peptide (10(-11)-10(-8) mol/l) induced concentration-dependent relaxations, as well as an increase in cGMP formation in endothelium-denuded eNOS-transduced arteries. Stimulatory effects of bradykinin were prevented in the presence of a B(2) receptor antagonist but not in the presence of a B(1) receptor antagonist. B(1) and B(2) receptor antagonists had no effect on relaxations to substance P, confirming the selectivity of the compounds. Our results suggest that B(1) and B(2) bradykinin receptors are coupled to activation of recombinant eNOS expressed in adventitial fibroblasts.

Animals↗

Effects of recombinant eNOS gene expression on reactivity of small cerebral arteries.

Resistance arteries are an important target for vascular gene therapy because they play a key role in the regulation of tissue blood flow. The present study was designed to determine the effects of recombinant endothelial (e) nitric oxide synthase (NOS) gene expression on vasomotor reactivity of small brain stem arteries (internal diameter, 253 +/- 2.5 microm). Arterial rings were exposed ex vivo to an adenoviral vector (10(9) and 10(10) plaque-forming units/ml) encoding eNOS gene or beta-galactosidase gene. Twenty-four hours after transduction, vascular function was examined by isometric force studies. Transgene expression was evident mainly in adventitia. In arteries with endothelium transduced with eNOS gene but not with control beta-galactosidase gene, relaxations to bradykinin and substance P were significantly augmented. Removal of endothelium abolished relaxations to bradykinin and substance P in control and beta-galactosidase arteries. However, in endothelium-denuded arteries transduced with recombinant eNOS, bradykinin and substance P caused relaxations that were abolished in the presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester. In control arteries, endothelium removal augmented relaxations to the nitric oxide donors sodium nitroprusside and diethylamine NONOate. This augmentation was absent in eNOS gene-transduced arteries without endothelium. Our results suggest that, in small brain stem arteries, expression of recombinant eNOS increases biosynthesis of nitric oxide. Adventitia of small arteries is a good target for expression of recombinant eNOS. Genetically engineered adventitial cells may serve as a substitute source of nitric oxide in cerebral arteries with dysfunctional endothelium.

Animals↗

Mechanisms of cerebral arterial relaxations to hydrogen peroxide.

BACKGROUND AND PURPOSE: The role of hydrogen peroxide in the regulation of cerebral arterial tone is not completely understood. Previous studies have demonstrated that hydrogen peroxide causes vasodilation of small cerebral arteries. The present study was designed to determine the mechanisms responsible for relaxations of large cerebral arteries to hydrogen peroxide. METHODS: Rings of canine middle cerebral arteries without endothelium were suspended for isometric force recording in modified Krebs-Ringer bicarbonate solution bubbled with 94% O(2)/6% CO(2) (37 degrees C, pH 7.4). Radioimmunoassay technique was used to determine the levels of cAMP and cGMP. RESULTS: During contraction to UTP (3 x 10(-6) or 10(-5) mol/L), hydrogen peroxide (10(-6) to 10(-4) mol/L) caused concentration-dependent relaxations. Catalase (1200 U/mL) abolished the relaxations to hydrogen peroxide. Inhibition of cyclooxygenase by indomethacin (10(-5) mol/L) significantly reduced relaxations to hydrogen peroxide. In arteries contracted by KCl (20 mmol/L), the relaxations to hydrogen peroxide were significantly reduced. In the presence of a nonselective potassium channel inhibitor, BaCl(2) (10(-4) mol/L), a delayed rectifier potassium channel inhibitor, 4-aminopyridine (10(-3) mol/L), or a calcium-activated potassium channel inhibitor, charybdotoxin (3 x 10(-8) mol/L), the relaxations to hydrogen peroxide were also significantly reduced. An ATP-sensitive potassium channel inhibitor, glyburide (5 x 10(-6) mol/L), did not affect the relaxations to hydrogen peroxide. Hydrogen peroxide produced concentration-dependent increase in levels of cAMP. Indomethacin (10(-5) mol/L) inhibited the stimulatory effect of hydrogen peroxide on cAMP production. In contrast, hydrogen peroxide did not affect the levels of cGMP. CONCLUSIONS: These results suggest that hydrogen peroxide may cause relaxations of large cerebral arteries in part by activation of arachidonic acid metabolism via cyclooxygenase pathway with subsequent increase in cAMP levels and activation of potassium channels.

Animals↗

Mechanisms of [2,3-butanedione bis(N4-dimethylthiosemicarbazone)]zinc (Zn-ATSM2)-induced protection of cultured hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.

Hyperexcitation of glutamatergic neurons may play a key role in ischemia-related neurodegeneration. Recent studies have suggested that the zinc ion (Zn2+), which is present in the central nervous system, has a modulatory role in glutamatergic neuron activity. Zinc ions block glutamate-induced depolarizing currents and neuronal damage by binding with zinc sites on the NMDA subtypes. Therefore, we examined the usefulness of zinc as a therapeutic agent for the prevention of ischemic neuronal damage in the brain. In our previous study, 2,3-butanedione bis(N4-dimethylthiosemicarbazonato) zinc complex (Zn-ATSM2), with high brain uptake, showed significant neuroprotective effects against cerebral ischemia in rats when administered systemically. In this study, to elucidate the mechanism of the neuroprotective effect of Zn-ATSM2, we first examined its in vitro protective effects against glutamate-, NMDA- and kainite-induced neurotoxicity in primary cultures of hippocampal neurons. Zn-ATSM2 elicited protective effects against this glutamate- and NMDA-induced neurotoxicity, but did not affect kainite-induced cytotoxicity. In addition, we studied the effects of Zn-ATSM2 on influx of Ca2+, which undergoes modification subsequent to NMDA activation. Zn-ATSM2 significantly decreased glutamate-induced 45Ca2+ uptake. Thus, Zn-ATSM2 protected against glutamate-induced neurotoxicity and its protective effect was, at least in part, due to the blockage of NMDA receptor-mediated Ca2+ influx.

Animals↗

Hyperthyroid Graves' disease after hemithyroidectomy for papillary carcinoma: report of three cases.

Here we report three cases of hyperthyroid Graves' disease that occurred after partial thyroidectomy for papillary carcinoma. In Case 1, the patient first developed hyperthyroidism 2 years after resection of left thyroid lobe, was treated for 2 years with antithyroid drug which was then discontinued, and relapsed with periodic paralysis after 8 years of remission. In Case 2, a hyperfunctioning remnant thyroid was noted 22 years after right hemithyroidectomy. In Case 3, where thyrotoxic symptoms became evident 7 weeks after right hemithyroidectomy, autoantibodies to thyroglobulin and thyroid microsome were positive in preoperative serum, in line with a report by others detecting these antibodies in 2 out of 3 such cases examined. Later bioassay revealed activity of thyroid stimulating antibodies in that serum, with further increase in titer in the sample taken at the clinical manifestation. Hence in Case 3, surgical stress may have altered immunological homeostasis, promoting a preclinical Graves' disease to full-blown hyperthyroidism.

Adult↗

Malignant colonic obstruction due to extrinsic tumor: palliative treatment with a self-expanding nitinol stent.

OBJECTIVE: The purpose of this study was to evaluate the usefulness of self-expanding nitinol stents for palliative treatment of malignant colorectal obstruction caused by unresectable extrinsic tumor, colorectal metastasis, or peritoneal seeding. SUBJECTS AND METHODS: One covered stent and 10 uncovered stents were deployed in eight patients with colorectal obstruction due to extrinsic tumor under fluoroscopic guidance. The sites of obstruction were located in the rectum (n = 5), in the rectosigmoid colon (n = 2), and from the transverse colon to the descending colon (n = 1). Clinical usefulness and complications were analyzed. RESULTS: Stents were placed successfully in all patients. Minor modifications of the delivery system were required in the tortuous rectosigmoid and lower rectum strictures. Symptoms of obstruction were initially resolved in all but one patient. In that patient, the presence of other points of obstruction was suspected. Bowel obstruction recurred in two patients: one obstruction was due to migration of a covered stent 4 days after the procedure, and the other obstruction was due to peritoneal seeding 33 days after the procedure. Both required colostomy or ileostomy. All patients died 12-111 days after stent placement (mean, 56 days). In five patients (63%), colonic obstruction was palliated by placing a stent until the patients' death between 39 and 111 days after stent placement (mean, 62 days). Six complications occurred in four patients and included stent migration (n = 1), anal bleeding (n = 2), anal pain that required analgesia (n = 1), and fever (n = 2). CONCLUSION; This self-expandable nitinol stent adequately palliated 63% of patients with colonic obstruction due to extrinsic tumor in this small series. Patient selection is very important to the success of this treatment.

Alloys↗

[Effect of paclitaxel on cisplatin resistant head and neck squamous multicellular tumor spheroids].

Paclitaxel has been reported to be effective for the treatment of CDDP resistant tumors. Thus, the efficacy of paclitaxel on CDDP resistant HEp-2 and KB head and neck squamous carcinoma cell lines was evaluated in monolayer and multicellular tumor spheroids (MTS). Cell lines with a tenfold resistance to CDDP were used in this study (Tanaka, K. et al, Keio J Med, 70. 1993). MTS were developed using the liquid overlay culture technique. After exposure to graded concentrations of drugs and different exposure time, the cells were subjected to a clonogenic assay. The effect of paclitaxel on both monolayer and MTS was dependent on the drug concentration and related to the exposure time. For HEp-2 MTS, 10(-7) M/L of paclitaxel resulted in a cell death rate of approximately 90% in both parent and resistant cells. For KB MTS, the cells were more resistant to paclitaxel than the HEp-2 cells, and a 72 hour exposure time was needed to achieve a cell death rate of approximately 90%. These data suggest that paclitaxel may be effective for treating CDDP resistant head and neck cancer.

Antineoplastic Agents, Phytogenic↗

[Coronary revascularization in a patient with bilateral internal carotid artery stenosis and aneurysm of brachiocephalic artery: a case report].

A 67-year-old man with a twenty-year history of effort angina was referred to our hospital. He underwent successful PTCA for the right coronary artery and diagonal branch. However, his angina recurred three months after PTCA due to restenosis and he was recommended to undergo CABG. Because he had concomitant bilateral internal carotid artery stenosis and aneurysm of the brachiocephalic artery, we chose two-staged operation strategy to avoid cerebrovascular complication during CABG. First, he underwent bilateral carotid endarterectomy (CEA), and then he underwent concomitant CABG and grafting of brachiocephalic artery 12 days after CEA. After these operations he recovered uneventfully without neurological complication.

Aged↗