Aortic root replacement in type A dissection.
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Biomedical subjects
Publications and source records attributed to Y Moriyama.
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To assess the consequence of second BMT (BMT2) for leukemia relapse after allogeneic BMT, we analyzed the clinical course of 66 recipients who were treated by BMT2 in Japan. Diagnoses included 29 ANLL, 27 ALL, six CML and four MDS. Durations between the first BMT (BMT1) to relapse and BMT1 to BMT2 were 13.5 +/- 13.7 months and 17.4 +/- 13.9 months, respectively. Donors for BMT2 were replaced in 11 cases. Thirty-one patients were in CR (or CP) at BMT2. Earlier deaths were observed in those who received BMT2 within 12 months after BMT1, mostly caused by regimen-related toxicity and infections. Overall leukemia-free survival rate was 28% at 2 years and 16% at 4 years. Factors influencing the poor prognosis after BMT2 were early (<6 months) relapse, early (<12 months) BMT2, not in remission at BMT2, and ALL. Intensified conditioning did not affect either remission duration or LFS. Among the 39 cases observed for more than 100 days, 18 developed chronic GVHD (cGVHD) and showed longer remission duration than those without cGVHD. Our analysis indicates that BMT2 as treatment for leukemia relapse is effective in selected cases, and exploration of pre-BMT treatment and post-BMT immunotherapy is warranted.
Rat pinealocytes accumulate glutamate in microvesicles and secrete it through exocytosis so as to transmit signals intercellularly. Glutamate is involved in the negative regulation of norepinephrine-stimulated melatonin production. In this study, we found that aspartate is also released from cultured rat pinealocytes during the exocytosis of glutamate. The release of aspartate was triggered by addition of KCI or A23187 (a Ca2+ ionophore) in the presence of Ca2+ and was proportional to the amount of L-glutamate released. Furthermore, the release of aspartate was inhibited by both botulinum neurotoxin type E and L- or N-type voltage-gated Ca2+ channel blockers. Bay K 8644, an agonist for the L-type Ca2+ channel, stimulated the release of aspartate 2.1-fold. Immunohistochemical analyses with antibodies against aspartate and synaptophysin revealed that aspartate is colocalized with synaptophysin in a cultured pinealocyte. HPLC with fluorometric detection indicated that the released aspartate is of the L form, although pinealocytes also contain the D form in their cytoplasm, corresponding to approximately 30% of the total free aspartate. Radiolabeled L-aspartate was taken up by the microsomal fraction from bovine pineal glands in a Na+-dependent manner. The Na+-dependent uptake of L-aspartate was strongly inhibited by L-cysteine sulfinate, beta-hydroxyaspartate, and L-serine-O-sulfate, inhibitors for the Na+-dependent glutamate/aspartate transporter on the plasma membrane. Na+-dependent sequestration of L-aspartate was also observed in cultured rat pinealocytes, which was inhibited similarly by these transporter inhibitors. These results strongly suggest that L-aspartate is released through microvesicle-mediated exocytosis from pinealocytes and is taken up again through the Na+-dependent transporter at the plasma membrane. The possible role of L-aspartate as an intercellular chemical transmitter in the pineal gland is discussed.
Pinealocytes, the neuroendocrine cells that produce melatonin, accumulate glutamate in microvesicles through a specific vesicular transporter energetically coupled with vacuolar-type proton ATPase. The glutamate is secreted into the extracellular space through microvesicle-mediated exocytosis and then stimulates neighboring pinealocytes, resulting in inhibition of norepinephrine-dependent melatonin synthesis. In this study, we identified and characterized the plasma membrane-type glutamate transporter in rat pinealocytes. The [3H]glutamate uptake by cultured pinealocytes was driven by extracellular Na+, saturated with the [3H]glutamate concentration used, and significantly inhibited by L-glutamate, L-aspartate, beta-threo-hydroxyaspartate, pyrrolidine dicarboxylate, and L-cysteine sulfinate, substrates or inhibitors of the plasma membrane glutamate transporter. Consistently, the clearance of extracellular glutamate, as measured by HPLC, was also dependent on Na+ and inhibited by beta-threo-hydroxyaspartate and L-cysteine sulfinate. Immunological studies with site-specific antibodies against three isoforms of the Na+-dependent glutamate transporter (GLT-1, GLAST, and EAAC1) revealed the expression of only the GLT-1 type transporter in pineal glands. Expression of the GLT-1 type transporter in pineal glands was further demonstrated by means of reverse transcription-polymerase chain reaction with specific DNA probes. Immunohistochemical analysis indicated that the immunological counterpart(s) of the GLT-1 is localized in pinealocytes. These results suggested that the GLT-1-type Na+-dependent transporter is expressed and functions as a reuptake system for glutamate in rat pinealocytes. The physiological role of the transporter in the termination of the glutamate signal in the pineal gland is discussed.
This study showed that nitric oxide (NO)-generating S-nitrosothiols, S-nitroso-N-acetylpenicillamine (SNAP) and S-nitrosoglutathione (GSNO), increased proliferation of BALB/c 3T3 (clone A31-1-1) fibroblasts in vitro. Treatment with SNAP at a relatively low concentration (0.005-0.02 mM) induced an increase in cell number compared to control. SNAP (0.005-0.02 mM) and GSNO (0.025-0.05 mM) both showed an increase of [3H]thymidine incorporation in exponentially growing cells in a dose-dependent manner. The maximal effect was observed at about 40 and 90% above control at 0.02 mM and 0.05 mM, respectively. The increase induced by 0.02 mM SNAP was abolished by the addition of 0.01 mM oxyhemoglobin, a scavenger of NO. [3H]Thymidine incorporation in stationary cells was also increased by SNAP. In addition, 0.02 mM SNAP produced a 1.8-3.2-fold increase of thymidine kinase activity in exponentially growing cells.
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A seventy-three-year-old woman had symptoms of aortic dissection. Initial computed tomographic (CT) scan and angiography showed an extensive intramural hematoma (IMH) of the aortic segment from the ascending aorta to the bulk of the descending aorta without intimal tear or false lumen. Two weeks later the patient's symptoms recurred. A repeat CT demonstrated a classic type A aortic dissection with a false lumen and an intimal defect. The patient underwent a successful hemiarch repair with use of selective cerebral perfusion under profound hypothermic circulatory arrest. This case suggests extensive IMH as an important underlying pathology of the aortic dissection.
1. We evaluated in vitro inhibitory effects of six types of antibiotic, aztreonam (AZT), cefamandole (CMD), cefmetazole (CMZ), cefotiam (CTM), flomoxef (FMOX) and latamoxef (LMOX), on platelet aggregation, using healthy volunteers' blood. Four types--FMOX, LMOX, CTM and CMD--inhibited, in concentration of 2500 micrograms/ml, the secondary aggregation induced by 3.0 microM adenosine diphosphate (ADP), and also inhibited the aggregation induced by 0.5 micrograms/mi collagen. AZT in the same concentration, did not inhibit the aggregation induced by collagen, and it inhibited only ADP-induced aggregation. CMZ, in the same concentration, inhibited neither of the two aggregations. 2. The inhibitory effects of the antibiotics on collagen-induced aggregation were dependent on the concentration of respective antibiotics. When classified by the strength of inhibitory action, LMOX and FMOX were strong, followed by CTM and CMD. The action of AZT and CMZ was weak. In particular, LMOX showed a 32% inhibitory effect at concentration of 50 micrograms/ml, a level near the blood concentration obtained with clinical usual dose. 3. No relationship was observed between inhibitory effects of antibiotics on ADP- or collagen-induced aggregation and the presence or absence of carboxyl group and/or N-methyltetrazolethiol group in the chemical structure.
The absorption characteristics of azasetron, a serotonin type 3 (5-HT3) receptor antagonist which is used for the treatment of chemotherapy-induced emesis and nausea, were investigated in rabbits. The serum concentrations of azasetron following rectal administration as a suppository increased rapidly and showed the mean tmax value of 0.18 h. The concentrations were greater after rectal administration than those after oral administration. The absolute bioavailability was significantly different between the rectal, 52.9% and oral doses, 21.6%. The mean Cmax and tmax values after the rectal dose were 904.8 ng/ml and 0.18 h, respectively, whereas those after the oral dose averaged 124.7 ng/ml and 0.85 h, respectively. These results indicate that azasetron is absorbed to a greater extent and more rapidly into the systemic circulation via the rectum than via the intestine in rabbits. Consequently, the suppository form of azasetron hydrochloride may be feasible for the treatment of chemotherapy-induced acute emesis and nausea.
Recent clinical trials have demonstrated that the administration of angiotensin-converting enzyme (ACE) inhibitors to patients with myocardial infarction reduces the incidence of recurrent myocardial infarction. It has also been reported that an elevated level of plasminogen activator inhibitor (PAI) appears to constitute a marker of the risk of recurrent coronary thrombosis. To determine whether the ACE inhibitor captopril reduces plasma PAI inhibitor activity, we measured changes in plasma PAI activity (IU/ml), tissue plasminogen activator (t-PA) antigen (ng/ml), and serum ACE activity (IU/L) in 14 survivors of myocardial infarction receiving captopril therapy (37.5 mg daily) and compared them with the values in 15 placebo-treated patients chosen at random. Blood sampling was performed at 07.00 h. In the captopril-treated group, serum ACE activity decreased significantly, from 14.0 +/- 0.8 to 11.5 +/- 1.2 IU/L 24 h after captopril therapy (p < 0.01), and those of PAI activity and t-PA antigen also decreased significantly-from 11.9 +/- 2.8 to 5.5 +/- 2.2 IU/ml (p < 0.02) and from 9.9 +/- 1.0 to 7.5 +/- 0.9 ng/ml (p < 0.05), respectively 48 h after captopril therapy. However, the levels of ACE activity, PAI activity, and t-PA antigen remained unchanged during the study period in the placebo group. Thus, our data indicate that the administration of captopril to patients with acute myocardial infarction may result in a reduced frequency of recurrent coronary thrombosis by increasing fibrinolytic capacity.
Ascidians are known to accumulate vanadium in their blood cells (vanadocytes) at extremely high levels which correspond to about 10(6) to 10(7) times the levels of vanadium ions in seawater. The route for the accumulation of vanadium ions from the outside environment into the blood system in ascidians has not yet been discovered. In the present experiments, using a combined technique of anion exchange column and atomic absorption spectrometry, we first extracted a vanadium-associated protein (VAP) from the blood cells of the ascidian Ascidia sydneiensis samea. VAP was estimated to associate with vanadium at an approximate ratio of 1 mol:16 mole. SDS-PAGE and a polyclonal antibody against VAP (anti-VAP) revealed that VAP is composed of at least two types of peptides estimated to be 12.5 kDa and 15 kDa with a minor peptide of 18 kDa and that VAP is localized in the cytoplasm of the vanadocytes.
The polychaete Pseudopotamilla occelata is the first animal revealed to contain high levels of vanadium besides ascidians. The present experiment disclosed that P. occelata has the same antigens with those in the ascidian Ascidia syndneiensis samea, which were recognized by two types of antibodies, a polyclonal antibody against vanadium-associated proteins extracted from blood cells and a monoclonal antibody against vanadocytes in the vanadium-rich ascidian A. sydneiensis samea. There is, therefore, a possibility that similar mechanism works on the accumulation of vanadium between the Polychaeta and the Ascididae.
A 38-year-old woman, who had been suffering from systemic lupus erythematosus (SLE) and receiving steroid therapy for the past 25 years, underwent a successful emergency coronary artery bypass grafting for unstable angina. She had also been treated with a 10-year period of hemodialysis therapy for chronic renal failure. Her coronary angiography revealed the heavily calcified ectatic right coronary artery with a thrombus formation in its proximal portion associated with severe stenosis in the proximal left coronary artery. The left internal thoracic artery was anastomosed to #7 and the saphenous vein to #3, respectively. Postoperative coronary angiography performed one month later revealed both grafts to be patent with no stenosis. Ischemic heart disease (IHD) is one of the major complication limiting the prognosis of the patient with SLE. We discuss the point related to cause of IHD and the surgical management.
A combination of annuloaortic ectasia (AAE) and abdominal aortic aneurysm (AAA) appeared in siblings with Marfan syndrome is presented. The patients were a 53-year-old female and her younger brother. The brother died of arrhythmia twenty years before while waiting for surgical repair of AAE. His AAA and Marfan syndrome were ascertained at autopsy. The female patient received surgical repair for AAA and AAE subsequently. Pathologic study of the resected aneurysm revealed cystic medial necrosis. A combination of AAE and AAA developed in two members of a family with Marfan syndrome is extremely rare.
From May 1995 through June 1996, the gelatin-resorcine-formol (GRF) biological glue was used for tissue reinforcement in 20 patients operated on for acute type A aortic dissections at our institution. The results in these patients (Group I) were compared to those in 37 patients operated on between 1992 and 1994 with conventional techniques (Group II). There were no significant differences between the two groups concerning demographic data. Operative procedures in Group I consist of replacement of the ascending aorta with or without proximal arch (n = 10), total arch replacement (n = 7), and aortic root reconstruction (n = 2), whereas those in Group II were 22, 12, and 3, respectively. Cardiopulmonary bypass time was significantly shorter in Group I than Group II (164 +/- 39 vs 265 +/- 122, p < 0.05). Average blood loss in first 24 hours after operation was 688 +/- 601 ml in Group I and 1481 +/- 1505 ml in Group II (p < 0.05). Consequently operative mortality was significantly (p < 0.05) reduced from 40.5% (Group II) to 15.0% (Group I). In conclusion, the use of GRF glue reduces perioperative bleeding and improves results of operation for acute aortic dissections.
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A 46-year-old woman was hospitalized for aortic valve stenosis (AS) associated with systemic lupus erythematosus (SLE) on April 12, 1996. She had a syncopal episode six months before admission. She was found to have thrombocytopenia, and was diagnosed with SLE by further examination. Irregular genital bleeding was also seen on admission while her SLE was being controlled with steroid therapy. Aortic valve replacement was performed after the steroids had been reduced to avoid excessive bleeding. The aortic valve was the bicuspid with raphe. There was much calcification on the cusps and the annulus, but there were no degenerative changes. The postoperative course was uneventful, and her SLE has been in remission two years after the operation. The management of steroid therapy for SLE patients complicated with cardiovascular disease is discussed.
A 70-year-old female was referred due to chest pain and cardiogenic shock. Echocardiogram showed ventricular septal perforation (VSP) with large left to right shunt. ECG indicated ischemia on the left anterior descending region. Instantaneous coronary angiogram was done under the support of IABP. Neither obstructive nor stenotic lesions were found in the coronary arteries. Coronary artery spasm was a likely cause of VSP. The patient underwent emergency surgery within 12 hours from the onset. The VSP, 2 cm in diameter, was located on the postero-apical portion of the ventricular septum. The defect was closed by endocardial patch method using an equine pericardium. Postoperative course was uneventful, and the patient was transferred 3 weeks after the operation.