Biomedical subjects
Publications and source records attributed to S Furuta.
We report a case of a 31-year-old woman with ageusia. Her ageusia was related to a variety of causes including an unbalanced diet, administration of the anti-epileptic drug, carbamazepine and psychological factors. Her taste function recovered after stopping the carbamazepine and treatment with liver extracts and zinc sulphate.
The free forearm flap is a reliable and versatile tool in head and neck reconstruction. However, the patency of the microvascular anastomosis is difficult to monitor when the flap is buried in the reconstruction of the esophagus or orbital floor. We used a portion of forearm muscle on a branch of the radial artery and vein as a monitor flap. After the free forearm flap transfer, the monitor muscle flap was placed externally through a small skin incision. Flap viability was assessed by observing the color of the bleeding elicited from the muscle flap. Monitor muscle flaps are raised easily during elevation of the forearm flap. This technique was used successfully in 5 patients. This monitoring method provides a simple and reliable assessment of viability when direct monitoring of the forearm flap is not possible.
Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracellular Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca(2+)-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca(2+)-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca(2+)-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequenstration and plasma membrane Ca(2+)-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.
We evaluated the apnea index (AI), the oxygen saturation above 95% (SA95), the lowest oxygen saturation (LSAT), and snoring before and after laser-assisted uvulopalatoplasty (LAUP) in 106 patients with obstructive sleep apnea syndrome (n=59) or snoring (n=47). Type 1 LAUP was performed in 42 patients and type 2 LAUP in 64 patients. A 50% or greater reduction in AI was observed in 15 patients (35.7%) who underwent type 1 LAUP and 37 patients (57.8%) who underwent type 2 LAUP. Snoring was diminished in 18 (51.4%) of 35 patients who underwent type 1 LAUP and 30 (55.6%) of 54 patients who underwent type 2 LAUP. SA95 and LSAT showed no difference. No serious complications such as significant bleeding, postoperative episodes of asphyxia, nasopharyngeal stenosis, or nasal regurgitation were observed. LAUP was an effective outpatient treatment.
The outcome of aortic balloon valvuloplasty (ABV) was compared with that of aortic valve replacement (AVR) in aortic stenosis (AS) patients more than 60 years old. The indications for ABV included low respiratory and renal function, cancer, the patient's refusal of surgery, and low daily activity. Twenty six patients underwent AVR and 13 underwent ABV. Initially, the AVR group was younger and more symptomatic than the ABV group. Two perioperative deaths occurred in the AVR group, while there were none in the ABV group. Twenty-four AVR patients and 12 ABV patients had a successful outcome, with remarkable pressure gradient reduction in both groups. In the follow-up, only 1 death and no cardiac events were detected in the AVR group (mean follow-up of 27 months), whereas 3 deaths, 6 heart failures, 2 repeated ABV, and 4 AVR were seen in the ABV group (mean follow-up of 10 months). The data showed that ABV was safer than AVR, but a higher rate of restenosis limited its efficacy. In the ABV group, a higher ratio of balloon size to aortic diameter correlated with longer event-free survival. We concluded that for elderly AS patients, ABV should be used only in those with high surgical risk as a palliative therapy or a bridge therapy to AVR, and AVR should be primarily recommended under rigid evaluation of the patient's physical status.
In cardiac surgery significant residual lesions increase postoperative morbidity and mortality. To evaluate the usefulness of transesophageal echocardiography (TEE) as a early postoperative monitor in patients immediately after cardiovascular surgery, 500 consecutive patients were studied from April 1990 to December 1994. TEE was performed at the bedside in the intensive-care unit in all of these patients. TEE detected findings unsuspected by other perioperative tests or clinical examination in 103 (20.6%) of 500 patients. Imaging revealed unsatisfactory operative results that necessitated further surgery in 18 (3.6%) of the 500 patients. These data indicate that early postoperative TEE is useful in assessing immediate operative results and identifying patients with unsatisfactory results who are at increased risk for postoperative complications.
A 71-year-old woman with active aortic prosthetic endocarditis due to Methicillin-resistant Staphylococcus epidermidis (MRSE) and subannular mycotic aneurysm and paravalvular leakage and acute mitral regurgitation underwent emergent surgical treatment. The mycotic aneurysm was closed using a prosthetic patch after surgical debridement. Re-aortic valve replacement with a 21-mm Hancock II prosthesis was performed at the paraannular position by utilizing the patch. Mitral valve was also replaced with a 27-mm Hancock II prosthesis. Antibiotic therapy was provided by vancomycin combined with rifampicin and gentamicin. The following regimen was given, vancomycin 1 g i.v. q12h for 6 weeks plus gentamicin 80 mg/day i.v. for 4 weeks plus rifampicin 450 mg/day orally for 6 weeks. Vancomycin and gentamicin doses were modified appropriately according to the monitored serum levels in the patient with renal failure. Postoperative course was uneventful. The patient is doing well 11 months after surgery and no recurrence of infection has been seen. We conclude that prompt surgical removal of the infected sources and appropriate antibiotic therapy based on the bacteriology may be the only curative treatment for uncontrolled infection at the active phase of MRSE prosthetic endocarditis.
The pathogenesis of nonrheumatic calcification of the mitral valve was investigated by analyzing the clinical and echocardiographic characteristics of patients with mitral valvular calcification without any findings suggestive of rheumatic heart disease or infective endocarditis. Calcification of the mitral valve was observed in nine patients, who all had calcified stenotic (aortic valve area < 1 cm2) bicuspid aortic valve. Calcification of the mitral valve was localized to the basal portion of ventricular aspect of the anterior mitral leaflet and contiguous to that of the aortic valve. Mobility and thickness of the mitral leaflet was normal except for the calcified portion. Calcification of the mitral valve was not contiguous to posterior mitral annular calcification nor was related to direction of aortic regurgitant flow. In patients with calcified stenotic bicuspid aortic valve, calcification of the mitral valve was not associated with location of the two aortic cusps, aortic valve area, aortic valvular peak pressure gradient, direction of the left ventricular outflow, end-diastolic left ventricular outflow tract dimension, end-diastolic dimension of the aortic annulus, incidence of aortic regurgitation, calcification of the aortic arch, or risk factors of atherosclerosis. Six patients with mitral valvular calcification had aortic valve replacement. Preoperative coronary angiogram of these patients was normal. Calcification of the aortic valve was on the ventricular and aortic aspects. The calcification of the aortic valve, anterior mitral ring, or anterior mitral leaflet was not rheumatic in these six patients. Rheumatic disease, risk factors of atherosclerosis, mechanical stress by left ventricular outflow or aortic regurgitant flow, or mitral annular calcification did not appear to be related to mitral valvular calcification. The distribution of aortic and mitral valvular calcification suggested that the calcification of the mitral valve was due to progression of calcification of the bicuspid aortic valve.
Third mitral valve replacement (3rd MVR) have become more frequent as use of replacement procedures has become more widespread. However, little information exists to clearly document the determinants of 3rd MVR. To evaluate backgrounds and risks and complications of 3rd MVR, we reviewed data on 10 patients (6 male and 4 female, age averaged 58 +/- 8 years) who underwent 3rd MVR because of prosthetic valve malfunction during December 1986-May 1995. This represented 7.1% of total number of reoperations for valve surgery (10/140) during that period. The incremental effect of the 3rd MVR on hospital mortality and mobidity was studied by comparing first mitral valve replacement (1st MVR) and second mitral valve replacement (2nd MVR) and 3rd MVR. After an interval of 134 +/- 23 months, 3rd MVR was undertaken for congestive heart failure due to primary tissue failure in 65%, paravalvular leakage in 20%, prosthetic valve endocarditis in 15%. One patient died at 11 days postoperatively, for a mortality rate of 10%. Cause of death was related to multiple organ failure due to low cardiac output syndrome. The surgical risk of 2nd MVR and 3rd MVR is higher than that of 1st MVR, but there is no conclusive evidence that the difference between 2nd MVR and 3rd MVR is statistically significant. With improvement intraoperative strategies, the operative risk in patients undergoing 3rd MVR has been markedly reduced.
A 41-year-old Japanese woman complained of a gradually enlarging swelling of her left cheek for seven months. She was diagnosed with osteopetrosis by standard skeletal radiographs, and her cheek swelling was diagnosed as maxillary osteomyelitis secondary to osteopetrosis. She underwent a left partial maxillectomy, and her post-operative course was stable with no complications. A literature review is also presented.
We performed experiments to investigate the participation of nitric oxide (NO) in the delayed neuronal death (DND) of gerbil hippocampal CA1 neurons, following 5-min forebrain ischemia with pretreatment of stereotaxic intraventricular administration of several types of NO synthase inhibitors and biologically inactive control drugs. The number of surviving neurons in the control drug groups administered NG-monomethyl-D-arginine or NG-nitro-D-arginine methyl ester was comparable to that in the group administered artificial cerebro-spinal fluid, while the groups administered NOS inhibitors, such as NG-monomethyl-L-arginine or NG-nitro-L-arginine methyl ester, showed significant preservation of the neuronal densities compared with the control drug groups, to over 60% of the sham operation group value. Furthermore, intraventricular administration of N omega-nitro-L-arginine at various concentrations disclosed a dose-dependent protection against the DND. These results suggest that the generation of NO may act to promote the establishment of DND.
Platelet membrane glycoprotein Ib alpha (GPIb alpha) bears the human platelet alloantigen (HPA)-2 and molecular weight (MW) polymorphisms on sodium dodecyl sulfate-polyacrylamide gels. HPA-2 arises from a threonine/methionine dimorphism at residue 145 of the GPIb alpha sequence, whereas different numbers of tandem repeats of a 39-bp sequence encoding 13-amino acids corresponding to a region between serine399 and threonine411 of the GPIb alpha account for the latter. To identify the genetic basis of the MW polymorphism among Japanese, we counted the tandem repeats in 103 individuals. In addition to the reported three variants with one, two, or three tandem repeats, we identified a new variant with four perfect tandem repeats of the 39-bp sequence that corresponded to the largest phenotype. Phenotypic analysis of the MW polymorphism on 12 individuals including all four phenotypes completely accorded in the genotype. We also determined the genotype of HPA-2 and found that methionine145 was in complete linkage disequilibrium, with the larger variants containing three or four tandem repeats. These results imply a model of evolutionary steps in the gene encoding GPIb alpha.
A 65-year-old woman who had shown no delta waves or atrioventricular block when seen in February 1989, suddenly developed advanced atrioventricular block in April 1990. The first electrophysiologic study revealed that atrioventricular block was caused by His ventricular block, and only weak retrograde conduction was documented. A DDD-type permanent pacemaker was implanted. One month after implantation, delta waves developed. The second electrophysiologic study, performed in February 1993, disclosed that a Kent bundle with bidirectional conduction capacity was located at the posterior septum and that the normal conduction system remained blocked at the His ventricular site. The etiology of the newly developed delta waves seems to be the disappearance of impedance mismatch at the ventricular insertion site of the Kent bundle.
There are few reports about direct effects of specific oxygen products on ciliary function because of their instability and reactivity. We investigated the direct effects of superoxide anion (O2-) and of hydrogen peroxide (H2O2) on the ciliary function of human respiratory epithelial cells, using monolayer cell cultures, high speed video analysis of frequency (CBF), amplitude (CBA), and coordination of ciliary beats and evaluating the surface structural changes of ciliated cells at the same time. 10(-2) M H2O2 decreased ciliary beat activity. The CBF was 36.5 +/- 4.4% and the CBA was 51.0 +/- 3.8% of the baseline (time = 0) after 5 min (all p < 0.001). Catalase (2 micrograms/ml) abolished the ciliotoxic effect of H2O2. The O2- produced by reaction of xanthine (0.06 mM)-xanthine oxidase (0.04 U/ml) caused a temporary rapid increase of 26.8 +/- 1.7% in CBF and an increase of 42.5 +/- 4.1% in CBA after 15 sec (all p < 0.001). Superoxide dismutase significantly reduced these increases. Results indicated that O2- activated ciliary function with a temporary increase in O2(-)-production. This suggests that the removal of H2O2 from the O2- reaction is important in improving mucociliary clearance in excessive oxygen metabolites.
Mitochondria isolated from rat liver were freeze-thawed and washed with 0.1 M potassium phosphate, pH 7.4. Most of the 3-hydroxyacyl coenzyme A (CoA) dehydrogenase activities were removed and this mitochondrial membrane fraction could bind exogenous 3-hydroxyacyl-CoA dehydrogenase. 3-Hydroxyacyl-CoA dehydrogenase-binding protein was extracted from the washed membrane fraction with a buffer containing 2% Triton X-100 and 2% sodium taurodeoxycholate. The binding protein was purified by Ultrogel AcA 34 gel chromatography, calcium phosphate gel-cellulose chromatography and 3-hydroxyacyl-CoA dehydrogenase affinity chromatography. The molecular mass of the purified binding protein was estimated to be 140 kDa by gel filtration and its subunit molecular mass was determined as 60 kDa by SDS-PAGE suggesting that the protein is a homodimer. The binding protein and 3-hydroxyacyl-CoA dehydrogenase formed a complex at low ionic strength and the stoichiometry revealed that 1 mol of the binding protein bound 2 mol of 3-hydroxyacyl-CoA dehydrogenase. Purified 3-hydroxyacyl-CoA dehydrogenase-binding protein interacted with 3-hydroxyacyl-CoA dehydrogenase and 3-ketoacyl-CoA thiolase but did not bind other mitochondrial beta-oxidation enzymes. The pH optimum of the binding activity was from pH 6 to 7 and the binding activity was diminished by increasing the concentration of salt in the medium.
The disposition of polaprezinc in the rat gastrointestinal tract was studied by a double tracer method using [14C]- and [65Zn]polaprezinc. At 0.5 h after oral administration of [14C]-,[65Zn]polaprezinc to rats, the 14C-radioactivity in the gastric contents was comparable with the 65Zn-radioactivity. However, a significant difference was observed in the time course of changes in gastric contents between 14C- and 65Zn-radioactivity over 1 h after administration, indicating that polaprezinc existed in complex form at 0.5 h after administration and was dissociated to L-carnosine and zinc in the gastrointestinal tract as a function of time. The adhesion of zinc to stomach mucosa after oral administration of polaprezinc to rats was significantly increased by treatment with cimetidine. These results suggest that the adhesion of zinc to gastric tissues is increased by inhibiting the dissociation of polaprezinc, and that H2-receptor antagonists, such as cimetidine, may increase anti-ulcer effects of polaprezinc.
Polaprezinc, an insoluble zinc complex of L-carnosine, exhibits anti-ulcer effects by acting directly on mucosal lesions. The disposition of polaprezinc in the stomach was studied to clarify the usefulness of its structure as an insoluble complex. The time courses of 14C-radioactivity in the gastric contents and gastric tissues were parallel to those of 65Zn after oral administration of a mixture of 14C-polaprezinc and 65Zn-polaprezinc (14C-, 65Zn-polaprezinc) to rats. The gastric contents of 14C-polaprezinc and 65Zn-polaprezinc were greater than those of 14C-L-carnosine and 65ZnSO4. Mean residence times (MRT) of 14C-polaprezinc and 65Zn-polaprezinc in the stomach were almost the same (ca. 2 hr), and they were double those of 14C-L-carnosine and 65ZnSO4. In gastric tissues, the area under the concentration curves (AUC0-8 hr) of 14C-polaprezinc and 65Zn-polaprezinc were 1.7 times greater than those of 14C-L-carnosine and 65ZnSO4, respectively. After administration of 14C-, 65Zn-polaprezinc to rats with acetic acid-induced ulcers, 14C and 65Zn-radioactivities in the ulcerous sites were very similar and greater than those of 14C-, 65Zn-polaprezinc dissolved in acid. In conclusion, polaprezinc is retained in the stomach longer and adheres to the ulcerous sites more than zinc or L-carnosine. The characteristics of this compound may arise from its insolubility and contribute to its strong pharmacological action.
Reevaluation of repeated balloon angioplasty as a model of ischemic preconditioning and of the role of collateral circulation and high-frequency electrocardiograms in repeated inflations was carried out. There have been few studies using angioplasty as a model of ischemic preconditioning of the collateral circulation during repeated inflations or of the use of high-frequency electrocardiograms during angioplasty. Twenty patients underwent 3 repeated balloon inflations, each with a duration of more than 138 seconds. During inflation, ipsilateral and contralateral coronary angiography and signal-averaged electrocardiography were performed. At the 1st inflation, the ST segment gradually increased as the inflation time elapsed. During the 2nd and 3rd inflations, in which ST elevation was nearly equal, the ST segment gradually increased, but it was not as prominent as that at the 1st inflation; thus, the concept that ischemia is gradually ameliorated (adaptation to ischemia) was not documented. Comparison of the maximal ST elevation and ipsilateral and contralateral circulation at each inflation revealed that the ST segment became elevated and the contralateral collateral circulation increased significantly at the 1st inflation compared with those in the control. ST elevation, however decreased significantly and collateral circulation remained unchanged at the 2nd inflation; thus, collateral circulation did not cause the ST elevation decrease. The total root mean square voltage detected by signal averaging decreased significantly only at the 1st inflation. Balloon angioplasty is not always suitable as a model of ischemic preconditioning and collateral circulation is not the cause of ischemic preconditioning.