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T Miyatake

Publications and source records attributed to T Miyatake.

At least 37 records · Page 2Linked to original sources
PubMed2001

A case of intraoperative acute aortic dissection caused by cannulation into an axillary artery.

Severe atherosclerotic disease of the ascending aorta is one of the risk factors of dissection of the ascending aorta and cerebral embolism during cardiac operations with cardiopulmonary bypass. Aortic dissection is rare, but once it happens, the mortality rate is high. For the patient with severely atherosclerotic or strongly calcified aorta, we should avoid cannulation into the aorta or clamping of it. In this case, we experienced aortic dissection although we chose the arterial cannulations into the axillary arteries because of the strong calcification of the ascending aorta and the abdominal aorta. The dissection was caused by the cannulation into the axillary artery. Transesophageal echocardiography (TEE) showed the dissection during the operation and the ascending aorta was replaced soon. Early diagnosis and treatment saved the patient. This case showed the following points: 1) cannulation into an axillary artery is not always safe; 2) TEE is very useful to detect the complicated dissection during operation; 3) replacement of the ascending aorta alone can be one of the choices for the treatment of aortic dissection caused by cannulation into an axillary artery.

Aged↗
PubMed1999

Suppression of delayed xenograft rejection by specific depletion of elicited antibodies of the IgM isotype.

BACKGROUND: Hamster hearts transplanted into untreated rats undergo delayed xenograft rejection (DXR). This acute inflammatory response is associated with the deposition of anti-graft antibodies of the immunoglobulin (Ig)M isotype in the vasculature. We have previously shown that these antibodies are generated in a T cell-independent manner. In this study, we tested whether the generation of anti-graft IgM antibodies is involved in the pathogenesis of DXR. In addition, we tested whether the suppression of this antibody response would overcome DXR. METHODS: Hamster hearts were transplanted into rats treated with an anti-mu monoclonal antibodies (mAb) to deplete circulating IgM or with an isotype-matched control mAb recognizing the dinitrophenyl epitope. T cell immunosuppression was achieved with cyclosporin A (CsA). RESULTS: Depletion of circulating IgM by anti-mu mAb inhibited DXR, whereas the control mAb had no effect on DXR. In anti-mu-treated rats, xenografts were rejected 5-7 days after transplantation through a T cell-dependent mechanism associated with the generation of antibodies of the IgG isotype. Combination of anti-mu with CsA suppressed the anti-graft IgM and IgG response and resulted in long-term xenograft survival (> 50 days). Xenograft long term survival occurred despite the return of anti-graft IgM antibodies to the circulation, a phenomenon referred to as accommodation. CONCLUSION: This study demonstrates that the pathogenesis of DXR can be initiated by anti-graft antibodies of the IgM isotype, which are generated in a T-cell independent manner. In addition, we show that under T cell immunosuppression, specific depletion of this IgM response by anti-mu mAb administration results in xenograft long-term survival and accommodation.

Animals↗
PubMed1999

Localization of verotoxin receptors in nervous system.

We use immunohistochemistry to show the existence of verotoxin receptor in small sensory neurons in DRG of human, rabbit, rat and mouse. In capillary in nervous system, the verotoxin receptor exists in human and rabbit, but the receptor could not be demonstrated in rat and mouse, by this method. The receptors in sensory neuron of rat and in capillary in rabbit brain are determined as galactosylglobotriaosylceramide (GalGb3) and globotriaosylceramide (Gb3,), respectively. Although verotoxin was reported to bind to glycolipid receptors that possess the terminal disaccharide Galalpha1-4Galbeta (galactobiose), the binding to toxin to galabiosylceramide was half of that of GalGb3 which has galactobiose internally.

Animals↗
PubMed1999

Partial median sternotomy as a minimal access for the closure of subarterial ventricular septal defect. Feasibility of transpulmonary approach.

BACKGROUND: Minimally invasive techniques in congenital heart surgery have evolved steadily over the past few years, but documentation in the literature is rare. The majority of reported techniques involve thoracoscopic approach and partial sternotomy. We have employed a lower partial sternotomy as a minimal-access procedure for the closure of subarterial ventricular septal defect, for situation where this approach would be unsuitable for adequate exposure of the pulmonary artery. The purpose of this study is to demonstrate the feasibility and safety of this technique and report its superior cosmetic result. SUBJECTS AND METHODS: Beginning in 1997, we began approaching the closure of subarterial ventricular septal defect through a lower sternal split incision using a 6 to 10 cm skin opening, associated with a reversed L incision at the left second intercostal space. A total of consecutive 12 patients (6 male and 6 female) have been operated on using this approach. The patients ranged in age from 6 to 21 years (mean, 12.8 +/- 5.0 years). The straight cannula with stylet was used for aortic cannulation. RESULTS: There was no mortality or morbidity, except for late pericardial effusion in 4 cases. The durations of cardiopulmonary bypass and aortic cross-clamping ranged from 94 to 206 (mean, 131 +/- 33) minutes and from 40 to 122 (mean, 70 +/- 26) minutes, respectively. Ten of 12 patients were extubated in the operating room, and no patient required blood transfusion. The postoperative hospital stay ranged from 8 to 21 (mean, 13.4 +/- 4.2) days. No patient developed deterioration of aortic regurgitation or residual ventricular septal defect. CONCLUSIONS: Our experience demonstrates that the lower partial sternotomy for the closure of subarterial ventricular septal defect is technically feasible and can be used with excellent cosmetic results and safety. Although experience is limited and follow-up is relatively short, this less invasive surgical technique may become a beneficial option for the management of subarterial ventricular septal defect.

Adolescent↗
PubMed1999

Mating-induced inhibition of remating in female Mediterranean fruit flies Ceratitis capitata.

Mechanisms producing inhibition of remating in mated female Mediterranean fruit flies Ceratitis capitata, were investigated by matings with surgically altered males. Comparison of remating by females mated with either intact control males or males with a shortened penis, showed that ejaculate or a physical stimulus of penis insertion caused remating inhibition for at least 10 days after first mating. Remating frequency at two days after mating was significantly higher in females mated to castrated (spermless) males than in females mated to sham-operated control males. This difference disappeared by day four after mating, indicating that sperm cause a shorter-term inhibition of remating than does a normal first mating. Other factors in addition to sperm must therefore play a role in inhibition of remating.

Journal Article↗
PubMed1999

GM2 promotes ciliary neurotrophic factor-dependent rescue of immortalized motor neuron-like cell (NSC-34).

We have examined whether ciliary neurotrophic factor (CNTF) can alter serum-free cell survival of immortalized motor neuron-like cells, which were established by fusing mouse neuroblastoma N18TG2 with mouse motor neurons. One of the cell lines, NSC-34 exhibited cell survival in the presence of CNTF. NSC-34 preserves the most characteristics of motor neurons, such as the formation of neuromuscular junctions on co-cultured myotube. GM2 ganglioside is characteristic of motor neurons, and expressed highly in NSC-34. When NSC-34 was cultured with exogenous GM2 ganglioside and CNTF, GM2 facilitated the cell survival effect of CNTF. In the addition, beta 1,4 N-acetylgalactosaminyltransferase (GM2 synthase) activity was enhanced up to 3.9-fold by culture in the presence of CNTF. GM2 might be a functional modulator of CNTF in motor neurons. It might be presented to cell surface by its enzyme activation, and become a signal of early stage, when CNTF rescues motor neurons.

Animals↗
PubMed1999

[The clinical usefulness of high-dose intravenous immunoglobulin therapy for chronic inflammatory demyelinating polyneuropathy and multifocal motor neuropathy].

To explore the optimum dose of intravenous immunoglobulin (i.v.Ig) for treating patients with chronic inflammatory demyelinating polyrneuropathy and multifocal motor neuropathy, we compared the usefulness of i.v.Ig among 3 treatment doses. Fifty-nine patients were randomly divided into three treatment dosage groups: 20 patients for Group I using 50 mg/kg/day x 5 days, 19 patients Group II using 200 mg/kg/day x 5 days, and 20 patients Group III using 400 mg/kg/day x 5 days. We assessed clinically and electrophysiologically the effectiveness of the treatment at 5 weeks after the initial infusion. For patients in Group I and II who had not improved (or worsened) with the first treatment, we gave a one-step larger dose in the second treatment (i.e. 200 mg/kg/day x 5 days for those who had been given 50 mg/kg/day x 5 days, 400 mg/kg/day x 5 days for those who had been given 200 mg/kg/day x 5 days) after more than 9 weeks. We found that 15% of the patients in Group I, 21% in Group II and 60% in Group III improved dose-dependently with the first intravenous immunoglobulin treatment. Seven (47%) of 16 patients in Group I and 4 (40%) of 11 patients in Group II improved after the second treatment with larger doses. Adverse reactions including chill sensation, fever, skin eruption and increase in blood GOT and GPT levels were transient and mild. One patient in Group III developed left hemiparesis showing the small infarction in the right thalamus during the course of the treatment, but the symptom was mild. In conclusion, the high-dose intravenous immunoglobulin therapy (400 mg/kg/day x 5 days) is useful for treating patients with CIDP and MMN, although care must be taken of the risk of causing cerebral infarctions.

Adolescent↗
PubMed1999

[Long-term results of mitral valve regurgitation after surgical repair of incomplete atrioventricular septal defect].

Although the postoperative outcome in patients with incomplete atrioventricular septal defect (iAVSD) is excellent, deterioration of mitral valve regurgitation (MR) is still remained to be resolved. Therefore, this study was undertaken to compare surgical procedures for mitral cleft repair with their long-term results of MR. From 1991 to 1996, 52 patients underwent surgical repair of iAVSD. Age at operation ranged from 2 months to 62 years old with mean age of 14.2 years. Mean follow-up period was 8.6 +/- 4.4 years. All patients underwent patch closure of ostium primum defect. Two patients did not have cleft (Group A). Seven patients did not close the cleft at all (Group B), while 40 patients had the repair of valve by closing cleft near septal attachment only (Group C). The latest 3 patients had the complete closure of cleft from annulus to margin of leaflet where chorda is attached. MR was evaluated by echocardiography grading 0 to IV and regurgitation more than grade II was considered to be significant. In Group A, MR remained grade I. In Group B, MR was deteriorated in 5 patients (71%). Consequently, 6 patients (86%) had grade II or more regurgitation and 4 patients (57%) revealed grade III/IV regurgitation including one (14%) reoperation. In Group C, MR was deteriorated in 10 patients (55%). Consequently, 22 patients (86%) had grade II or more regurgitation and 5 patients (13%) had grade III/IV regurgitation including 3 (7.5%) reoperations. In Group D, no deterioration of MR was noted and all had grade I or less regurgitation. These results suggest that the closure of cleft near septal attachment is not sufficient to prevent MR in late phase and the complete closure of cleft from annulus to margin of leaflet, where chorda is attached, would be useful to prevent the deterioration of MR in late phase.

Adolescent↗
PubMed1999

The effects of morphine-induced increases in extracellular acetylcholine levels in the rostral ventrolateral medulla of rat.

The present study examined the role of the rostral ventrolateral medulla (RVLM) in the modulation of acetylcholine (ACh) release by morphine. We examined the effect of morphine on the release of ACh in the RVLM of freely moving rats using the in vivo microdialysis method. The basal level of ACh was 303.0 +/- 28.2 fmol/20 microliter/15 min in the presence of neostigmine (10 microM). Morphine at a low dose of 5 mg/kg (i.p.) increased ACh release by the RVLM by 42.4%. A higher morphine dose (10 mg/kg i.p.) significantly increased the release of ACh by 75.4%, with a maximal effect (86.4%) at 75 min. This enhancement following i.p. administration of morphine was reversed by naloxone (1 mg/kg i.p.). Addition of morphine (10(-4) M) to the perfusion medium increased the ACh release by 85.8% of the predrug values. The increased ACh release induced by local application of morphine was reversed by pretreatment with naloxone (1 mg/kg i.p.). The antinociceptive effect of locally applied morphine into the RVLM was assessed using the hot-plate test and tail immersion test in unanesthetized rats. Local application of morphine (10(-4) M) via a microdialysis probe induced an increase in both tail withdrawal and hot-plate response. These findings suggest that morphine seems to exert a direct stimulatory effect on ACh release by the RVLM and that morphine-induced nociception is, in part, activated by the release of ACh in freely moving rats.

Acetylcholine↗
PubMed1998

The effect of methamphetamine on the release of acetylcholine in the rat striatum.

We examined the effect of methamphetamine on the release of acetylcholine in the striatum of freely moving rats, using an in vivo microdialysis method. The basal level of acetylcholine was 3.67+/-0.47 pmol/30 microl per 15 min in the presence of neostigmine (10 microM). Tetrodotoxin (1 microM), a selective blocker of voltage-dependent Na+ channels, markedly inhibited the release of acetylcholine in the striatal perfusates. Apomorphine (1.0 mg/kg, i.p.), a dopamine receptor agonist, also significantly attenuated acetylcholine release. Methamphetamine (0.1 and 0.5 mg/kg, i.p.) did not immediately affect acetylcholine release in the striatum, but a dose of 1.0 mg/kg (i.p.) induced an increase of acetylcholine release in the striatum at 15-60 min. Striatal infusion of methamphetamine (5 and 10 microM) did not influence acetylcholine release. The increase following intraperitoneal administration of methamphetamine was slightly diminished by haloperidol (0.5 mg/kg). After microinjection of the neurotoxin, 6-hydroxydopamine (6 microg/3 microl), in the substantia nigra 7 days before, the increase of acetylcholine induced by the administration of methamphetamine (1.0 mg/kg) was slightly attenuated, whereas the administration of reserpine (2 mg/kg, i.p.) 24 h before, combined with alpha-methyl-p-tyrosine (300 mg/kg, i.p.) 2.5 h before, completely blocked the increase in release of acetylcholine. These findings suggest that methamphetamine exerts an excitatory influence on striatal acetylcholine release in freely moving rats, and that this excitatory effect involves the dopaminergic system and the catecholaminergic system.

Acetylcholine↗
PubMed1998

Interactions of mating, egg production and death rates in females of the Mediterranean fruit fly, Ceratitis capitata.

Costs of reproduction include costs of producing eggs and of mating itself. In the present study, we made an experimental investigation of costs of reproduction in the Mediterranean fruit fly (medfly, Ceratitis capitata). We demonstrated that virgins live longer than non-virgin females. However, in strong contrast to most findings within the Diptera, non-virginity had no detectable effect on egg production. Therefore the increased longevity of the virgin females cannot be attributed to an increase in egg production in non-virgin females, and instead indicates a cost of mating. A comparison of the life spans of normal females and those sterilized by low doses of X-irradiation, revealed an additional cost of egg production. There were no significant differences in remating levels between females that did and did not lay eggs, showing that the cost of producing eggs is independent of mating frequency. Medfly females therefore suffer a decrease in survival as a result of egg production and of mating, and these costs are independent of one another. To put our results into context, we reviewed the existing literature on the effects of mating on longevity, egg production and sexual receptivity for 64 species of Diptera, and examined the pattern of mating effects that emerged.

Animals↗
PubMed1998

Survival of accommodated cardiac xenografts upon retransplantation into cyclosporine-treated recipients.

BACKGROUND: Accommodation designates the survival of vascularized grafts in the presence of circulating antigraft antibodies and complement. In the hamster-to-rat model, accommodation is associated with an ongoing T helper (Th)2 cytokine response and the expression of "protective genes" by the graft endothelial cells and smooth muscle cells. In this report, we tested whether accommodated xenografts would be protected from rejection upon retransplantation into second recipients treated with cyclosporine (CsA), a treatment that does not prolong survival of a fresh hamster heart. METHODS: Long-term survival of hamster-to-rat cardiac xenografts was achieved using either CsA plus cobra venom factor (CVF) or CsA plus rapamycin. Xenografts that survived long term in their first recipients were retransplanted into second recipients treated with CsA. RESULTS: Long-term xenograft survival in CsA/CVF-treated recipients was associated with an ongoing Th2 response, expression of protective genes, and deposition of elicited xenoreactive antibodies and complement on the graft endothelium. In CsA/rapamycin-treated recipients, long-term xenograft survival occurred in the presence of basal levels of antigraft antibodies and was not associated with a Th2 cytokine response or the expression of protective genes. Xenografts from CsA/CVF-treated rats survived significantly longer upon retransplantation into second recipients treated with CsA (77.3% >10 days) as compared with xenografts from CsA/rapamycin-treated rats (4-11 days) or naive hearts (3-4 days). Moreover, 30-35% of xenografts from CsA/CVF rats survived long term and accommodated in the second recipient. CONCLUSIONS: Accommodated xenografts can have significantly prolonged acceptance when retransplanted into second recipients treated with CsA alone; in contrast, naive hearts or hearts that survived long term in first recipients, but did not accommodate, did not survive long term in the second recipients. We suggest that prolonged survival of accommodated xenografts is due to the expression of the protective genes A20, bcl-2 bcl-xL, and heme oxygenase-1 in the xenograft endothelium and possibly smooth muscle cells.

Animals↗
PubMed1998

Guillain-Barré syndrome and Fisher's syndrome following Campylobacter jejuni infection.

The patients with Guillain-Barré Syndrome (GBS) subsequent to Campylobacter jejuni enteritis showed axonal degeneration and had IgG anti-GM1 antibody. The most frequently isolated C. jejuni from the patients was specific serotype of Penner's 19 in Japan. In the lipopolysaccharide (LPS) in C. jejuni of this serotype, the same oligosaccharide structure as GM1 ganglioside existed, suggesting the molecular mimicry between GM1 in nervous tissue and C. jejuni LPS. IgG anti-GM1 antibody may bind the nodes of Ranvier and axon terminals and causes degeneration of the motor axon. Some patients develop Fisher's syndrome following C. jejuni infection. C. jejuni strains from the patients who had IgG anti-GQ1b antibody in the acute phase had GQ1b epitope in their LPS, and the molecular mimicry between GQ1b in nervous tissue and an antecedent infectious agent was clarified.

Adult↗
PubMed1998

Transient complement inhibition plus T-cell immunosuppression induces long-term survival of mouse-to-rat cardiac xenografts.

BACKGROUND: The use of anti-B-cell and T-cell immunosuppressive agents leads to only a few weeks' survival of mouse-to-rat cardiac xenografts. METHODS: BALB/c cardiac xenografts were transplanted to Lewis rats treated with cyclosporine (CsA) and/or cobra venom factor (CVF). RESULTS: CsA alone did not prolong xenograft survival (2.2+/-0.4 days), whereas CVF alone led to minimal prolongation of survival (5.6+/-0.8 days) as compared with nontreated recipients (2.4+/-0.5 days). The combination of CsA plus CVF, the latter given for either 2 days or 11 days, resulted in long-term survival of 14/16 hearts (> 100 days). Production of IgM elicited xenoreactive antibodies (EXA) peaked on day 4 after transplantation and decreased thereafter. Production of IgG EXA occurred only in the control group, whereas, in the CsA/CVF-treated group, IgG EXA were totally suppressed. Long-term surviving grafts showed (i) excellent preservation of morphology and minimal leukocyte infiltration, (ii) deposition of IgM, IgG and weak C3 deposition on the graft endothelium, (iii) low level infiltration by rat macrophages, (iv) replacement of mouse dendritic cells by class II+ rat macrophages, and (v) expression within endothelial and smooth muscle cells, macrophages, and myocytes of HO-1, a "protective gene" not seen in the rejected hearts. CONCLUSIONS: Our present findings suggest that long-term mouse-to-rat cardiac xenograft survival is induced by temporary suppression of C activation and sustained T-cell suppression leading to inhibition of IgG EXA production. Florid expression of a protective gene (HO-1) may contribute to survival.

Animals↗
PubMed1998

Complement-fixing elicited antibodies are a major component in the pathogenesis of xenograft rejection.

Hamster to rat cardiac xenografts undergo delayed rejection as compared with the hyperacute rejection of discordant xenografts. Elicited xenoreactive Abs (EXA) are thought to initiate hamster to rat cardiac xenograft rejection. In this study, we demonstrate that following transplantation of a hamster heart, rats generated high levels of EXA. Adoptive transfer into naive recipients of purified IgM, IgG2b, or IgG2c, but not IgG1 or IgG2a EXA, induced xenograft rejection in a complement-dependent manner. Ability of EXA to cause rejection correlated with complement activation, platelet aggregation, and P-selectin expression in the xenograft endothelium. Cyclosporin A (CyA) administration, after transplantation, totally suppressed IgG1, IgG2a, IgG2b, and IgG2c EXA, and inhibited IgM EXA production, but failed to overcome rejection. Administration of cobra venom factor (CVF), 1 day before and at the time of transplantation, resulted in complement inhibition during 3 days after transplantation, which failed to overcome rejection. Combination of CyA and CVF, which we have previously shown to overcome rejection, resulted in suppression of IgG EXA production and in the return of IgM XNA to preimmunization serum levels, 3 to 7 days after xenotransplantation, while complement remained inhibited. Thus, under CyA/CVF treatment, complement activation by hamster cells was suppressed following xenotransplantation, and presumably for this reason xenograft rejection did not occur. In conclusion, our data demonstrate that EXA play a pivotal role in the pathogenesis of xenograft rejection and that CyA and CVF suppress xenograft rejection by preventing exposure of xenograft endothelial cells to complement activation by EXA.

Adoptive Transfer↗