Coronary artery-left atrial fistula caused by feeding artery rupture in cardiac myxoma.
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Aged, 80 and over↗
Biomedical subjects
K Zen
Publications and source records attributed to K Zen.
IL-4-producing CD8(+) T cells may be an immunological hallmark of chronic GVHD.
Chronic graft-versus-host disease (cGVHD) occurs in approximately 60-80% of those who survive over 100 days after allogeneic hematopoietic stem cell transplantation (allo-HSCT). However, the pathophysiology of cGVHD is poorly understood. To gain more insight into the immunological mechanism of cGVHD, we examine cytokine production of peripheral blood T cells from 19 patients in the chronic phase of allo-HSCT. The percentage of IFN-gamma-producing CD8(+) T cells among CD8(+) T cells was significantly higher in patients with or without cGVHD than in normal control subjects (P<0.001). On the other hand, the percentage of IL-4-producing CD8(+) T cells among CD8(+) T cells was significantly higher in patients with cGVHD (mean 3.3%; range 1.3-8.2%) than in patients without cGVHD (mean 1.2%; range 0.8-1.7%) and normal control subjects (mean 1.1%; range 0.1-1.6%) (both P<0.001). By contrast, the percentage of IL-4-producing CD4(+) T cells was not different among patients with and without cGVHD and normal controls. These findings suggest that IL-4-producing CD8(+) T cells may be an immunological marker of cGVHD.
Adolescent↗
Blood dendritic cells are decreased in acute graft-versus-host disease.
The recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT) often develop acute graft-versus-host disease (aGVHD), which is closely related to morbidity and mortality. However, the essential part of the immune responses elicited in aGVHD remains largely unknown. We attempt to determine if peripheral blood dendritic cells (PBDCs) are altered in aGVHD, and find that the number of PBDCs (both myeloid and lymphoid DCs) is significantly decreased. Immunohistochemical staining of the biopsied skin from patients with aGVHD demonstrates that a number of fascin(+) cells with dendritic projections infiltrate the dermis of the skin. Based on these findings, we hypothesize that the PBDCs are recruited to the affected tissues and may thus play important roles in immune responses elicited in aGVHD.
Acute Disease↗
Intra-arterial steroid-injection therapy for steroid-refractory acute graft-versus-host disease with the evaluation of angiography.
We treated three patients with steroid-refractory acute graft-versus-host disease (aGVHD) with intra-arterial steroid-injection therapy (IAST). Two patients with gut aGVHD received IAST into both superior and inferior mesenteric arteries, while one patient with liver aGVHD received IAST into the proper hepatic artery. The volume of stools and the bilirubin level improved soon after IAST. Angiography of the superior and inferior mesenteric arteries was performed in the two patients with steroid-refractory gut aGVHD, and identical abnormal findings were obtained. IAST might be an earlier option for steroid-refractory aGVHD.
Acute Disease↗
[Stent implantation in a case of myocardial bridging with resistant angina pectoris].
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Coronary Angiography↗
A patient with type I CD36 deficiency whose myocardium accumulated 123I-BMIPP after 4 years.
A 73-year-old man with aortic regurgitation was examined by 123I-alpha-methyl-p-iodophenylpentadecanoic acid (BMIPP) myocardial single photon emission computed tomography (SPECT) in 1995. Myocardial accumulation was not evident on either the early or the delayed image obtained 15 minutes and 3 hours, respectively, after injecting 123I-BMIPP. Flow cytometric analysis of CD36 expression in monocytes and platelets identified a type I CD36 deficiency. The patient was hospitalized for severe heart failure in 1999. Upon admission, the cardiothoracic ratio on chest X-rays was 73%, and the left ventricular end-diastolic diameter on echocardiograms was enlarged to 77 mm. On the second day, we performed 123I-BMIPP myocardial SPECT. Myocardial accumulation was evident in the delayed, but not in the early image. We repeated 123I-BMIPP myocardial SPECT on the 10th day after admission. Myocardial accumulation was evident on both early and delayed images. 99mTc-tetrofosmin myocardial SPECT was immediately performed after 123I-BMIPP myocardial SPECT to distinguish myocardial from pooling images in the left ventricle, but, because the images from both 99Tc-tetrofosmin and 123I-BMIPP myocardial SPECT were idential, we considered that the 123I-BMIPP myocardial SPECT images reflected the actual myocardial condition. The CD36 molecule transports long-chain fatty acid (LCFA) on the myocardial membrane, but 123I-BMIPP scintigraphy does not show any myocardial accumulation in patients with type I CD36 deficiency, indicating that myocardial LCFA uptake occurs through CD36 on the human myocardial membrane. Even though our patient had type I CD36 deficiency, BMIPP was uptaken by the myocardium during heart failure, suggesting a variant pathway on the human myocardial membrane for LCFA uptake.
Aged↗
[Unusual changes detected by iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography in the process of acute myocardial infarction: a case report].
Iodine-123 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography(iodine-123 BMIPP myocardial SPECT) is useful for the diagnosis and evaluation of ischemic myocardial disease or cardiomyopathy. Changes in fatty acid metabolism in the post-myocardial ischemic state were evaluated using iodine-123 BMIPP myocardial SPECT. A 77-year-old woman was hospitalized for treatment of acute myocardial infarction. Emergency coronary angiography showed severe stenosis with delayed filling of contrast medium in the middle portion of the left anterior descending artery, so primary percutaneous transluminal coronary angioplasty was performed successfully. On the second day, iodine-123 BMIPP uptake was decreased slightly on the early imaging in the apico-anterior region, and increased slightly on the delayed imaging. On the seventh day, iodine-123 BMIPP uptake was decreased moderately or markedly in the apico-anterior region on the early imaging, and decreased markedly on the delayed imaging. Iodine-123 BMIPP myocardial SPECT subsequently became almost normalized. These unusual dynamic changes In iodine-123 BMIPP myocardial SPECT imaging may reflect metabolic changes of fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool.
Aged↗
Uncommon and dynamic changes detected by 123I-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography in a stunned myocardium induced by coronary microvascular spasm.
A 55-yr-old man underwent surgery. Soon after the procedure was finished, the patient complained of chest pain, and the electrocardiogram showed increase in the ST-segment in some leads. Emergency angiography showed normal coronary arteries, but there was asynergy in the left ventricle, and delayed filling of contrast medium was observed in the LCA. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment increase in the electrocardiogram. Soon after nicorandil was injected into the LCA, the patient's symptoms, electrocardiogram, and delayed filling of contrast medium dramatically improved. On the second day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate increase in tracer uptake in the apico-anteroseptal region and a moderate decrease in tracer uptake in the lateral region, in which the first left ventriculography showed akinesis, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. On the sixth day, initial imaging by 123I-BMIPP myocardial SPECT showed a moderate decrease in tracer uptake in the apical and lateral regions and a mild decrease in tracer uptake in the anteroseptal region, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of 123I-BMIPP in the anteroseptal and lateral regions. By the 30th day, 123I-BMIPP myocardial SPECT had normalized. We consider that these dynamic changes in 123I-BMIPP myocardial SPECT imaging may reflect metabolic changes in fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool.
Coronary Vasospasm↗
[Bone marrow transplantation-associated thrombotic microangiopathy manifested by visual disturbance].
In October 1996, a 26-year-old woman was given a diagnosis of acute myeloblastic leukemia, FAB subtype M1. Treatment with combined chemotherapy achieved a complete remission (CR). In May 1997, the patient received an allogenic bone marrow transplant (BMT) from an HLA-identical sibling donor. Cyclosporine (CsA) and short-term methotrexate were given for graft-versus-host disease (GVHD) prophylaxis. Successful engraftment was obtained and signs of acute or chronic GVHD never developed. Five months after BMT, the patient experienced low-grade fever and blurred vision. Retinal examination demonstrated intraretinal hemorrhages, cotton-wool spots, and retinal detachments, which were presumably attributable to multiple thrombosis of retinal microvessels. The patient also exhibited hemolytic anemia with red cell fragmentation, thrombocytopenia, elevated lactate dehydrogenase, and renal impairment, and was thus given a diagnosis of BMT-associated thrombotic microangiopathy (BMT-TM). Discontinuation of CsA and administration of ticlopidine and prednisolone induced successful recovery from BMT-TM. Three months after the onset of BMT-TM, however, the patient experienced generalized clonic-tonic seizures with consciousness loss. Single-photon-emission computed tomography revealed blood-flow disturbances in the brain, suggesting the recurrence of microthrombosis. Accordingly, multiple transfusions of fresh frozen plasma were administered together with dipyridamole and aspirin. The patient gradually recovered and remained asymptomatic through the following 13 months. Currently, early diagnosis of BMT-TM is considered to be difficult. We suggest that careful examination of the ocular base may be useful for the early detection of BMT-TM.
Adult↗
[Two cases of microvascular vasospastic angina usefulness of 99mTc-tetrofosmin myocardial SPECT in clinical diagnosis].
Case 1 involved a 52-year-old man with angina chest pain at rest and case 2 involved a 63-year-old woman with chest oppression at rest. An electrocardiogram (ECG) showed negative T wave in III and aVF leads in case 1, and complete atrioventricular block and ST segment depression in II, III, aVF, and V5-6 leads in case 2. In both cases, 99mTc-tetrofosmin myocardial SPECT showed reduced uptake in the inferior and posterior wall. Although bath patients' left coronary arteriographies were normal, right coronary arteriographies revealed severely delayed filling of contrast medium without significant narrowing of epicardial coronary arteries, suggesting microembolism or microvascular vasospasm. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment depression on ECG. Soon after intracoronary infusion of diltiazem in case 1 and nicorandil in case 2, coronary arterial flows were normalized, chest symptoms disappeared, and ECG findings were normalized. The next day, both patients' 99mTc-tetrofosmin myocardial SPECT showed normal uptake. These findings suggest that myocardial ischemia in these cases might be explained as having been caused by microvascular spasm.
Calcium Channel Blockers↗
[Impairment of septal uptake and washout on 123I-BMIPP myocardial SPECT after pacemaker implantation: report of two cases].
Case 1 involved a 62-year-old woman with complete atrioventricular block and case 2 involved a 70-year-old woman with sick sinus syndrome. In both cases, echocardiography, 123I-15-(p-iodophenyl)-3-R,S-methyl pentadecanoic acid (BMIPP) and 99mTc-tetrofosmin myocardial single photon emission computed tomographic (SPECT) findings were normal. Coronary arteriography and left ventriculography also revealed normal in both cases. After pacemaker implantation (DDD-type in case 1 and VVI-type in case 2), both patient's electrocardiograms revealed left bundle branch block-type conduction disturbance, and echocardiography showed asynchronous hypokinesia in the septal region. One year later, although both patient's ATP loading tetrofosmin SPECT were normal, BMIPP SPECT showed reduced uptake and increased washout in the septal region. These findings suggest that these changes of BMIPP SPECT might be caused by left bundle branch block-type conduction disturbance after pacemaker implantation.
Aged↗
[Clinical usefulness of delayed exercise images on 99mTc-Tetrofosmin myocardial SPECT in the diagnosis of vasospastic angina pectoris].
This study was designed to evaluate the clinical usefulness of delayed exercise images in 99mTc-tetrofosmin (TF) myocardial SPECT in the diagnosis of vasospastic angina pectoris. We studied 30 patients with vasospastic angina, 10 of 30 patients (group A) had both effort and rest angina, 20 of 30 patients (group B) had rest angina. A 370 MBq of TF was intravenously injected at peak exercise, and initial (EX-I) and delayed exercise (EX-D) images were obtained at 30 min and 180 min after the injection. An additional 740 MBq of TF was intravenously reinjected after EX-D image acquisition, and rest images were obtained 30 min after the reinjection. The left ventricular wall was divided into 9 segments. Regional myocardial uptakes of TF were scored by 4-point defect score (0 = normal, 1 = mildly reduced, 2 = moderately reduced, and 3 = severely reduced). Total defect score (TDS) was calculated from the sum of defect scores in 9 segments. Reverse redistribution (RR) was defined as increase of more than 2 in TDS on EX-D images. In group A, 4 of 10 cases (40%) showed decreased uptake on EX-I images, 6 of 10 cases (60%) revealed RR on EX-D images, and none of the patients showed decreased uptake on rest images. In group B, no one showed decreased uptake on EX-I and rest images, 11 of 20 cases (55%) revealed RR on EX-D images. The mean +/- SD of TDS were 2.9 +/- 3.4, 5.1 +/- 4.5, 0.5 +/- 0.5 on EX-I, EX-D, rest images in group A, and serially 0.4 +/- 0.5, 3.3 +/- 3.6, 0.4 +/- 0.5 in group B. Regional wall motion abnormality was reduced in regions with RR. RR on EX-D images may reflect ischemic damaged but viable myocardium in vasospastic angina. The clinical usefulness of exercise-rest TF imaging in detection of organic coronary artery disease has been well established. Therefore, exercise-rest TF imaging with additional delayed exercise image could evaluate not only organic coronary artery disease but also coronary artery vasospasm.
Aged↗
[Clinical usefulness of 123I-BMIPP myocardial SPECT in collagen disease].
This study was designed to evaluate the clinical usefulness of 123I-BMIPP myocardial SPECT for detecting cardiac involvement in patients with collagen disease. We studied 12 patients with systemic lupus erythematosus (SLE), 8 with progressive systemic sclerosis (PSS), 6 with polymyositis/dermatomyositis (PM/DM) and 3 with allergic granulomatosis and angiitis (AGA). A 111 MBq of 123I-BMIPP was intravenously injected at rest, and SPECT images were obtained at 15 min after the injection. Seven of 12 SLE, 6 of 8 PSS, 3 of 6 PM/DM and all 3 AGA patients showed an abnormal tracer uptake. The left ventricular ejection fraction was inversely correlated with a BMIPP abnormality. The regional wall motion abnormality was reduced in regions with reduced tracer uptake. These findings suggest that 123I-BMIPP imaging could be useful for assessment of cardiac involvement in patients with collagen disease.
Aged↗
NF-kappaB activation is required for human endothelial survival during exposure to tumor necrosis factor-alpha but not to interleukin-1beta or lipopolysaccharide.
In the presence of a protein synthesis inhibitor, cycloheximide, tumor necrosis factor-alpha (TNF-alpha), interleukin 1-beta (IL-1beta), or lipopolysaccharide (LPS) induces human umbilical vein endothelial cells (HUVECs) to undergo apoptosis, suggesting that constitutive or inducible cytoprotective pathways are required for cell survival. We studied the correlation between nuclear factor-kappaB (NF-kappaB) activation and cell death induced by TNF-alpha, IL-1beta, or LPS. Adenovirus-mediated overexpression of a dominant-negative IkappaBalpha (inhibitor of kappaB) mutant blocked NF-kappaB activation by gel shift assay and blocked induction of vascular cell adhesion molecule-1 protein by TNF-alpha, IL-1beta, and LPS, a NF-kappaB-dependent response. In cells overexpressing the IkappaBalpha mutant, TNF-alpha induced cell death, whereas IL-1beta or LPS did not. We conclude that cell survival following TNF-alpha stimulation is NF-kappaB-dependent but that a constitutive or inducible NF-kappaB-independent pathway(s) protects IL-1beta- or LPS-treated HUVECs from cell death.
Adenoviridae↗
Lipopolysaccharide-induced NF-kappaB activation in human endothelial cells involves degradation of IkappaBalpha but not IkappaBbeta.
We studied the signal transduction pathways involved in NF-kappaB activation and the induction of the cytoprotective A20 gene by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC). LPS induced human A20 mRNA expression with a maximum level 2 h after stimulation. The proteasome inhibitor N-acetyl-leucinyl-leucinyl-norleucinal-H (ALLN) and the tyrosine kinase inhibitor herbimycin A (HMA) blocked A20 mRNA expression and partially inhibited NF-kappaB DNA-binding activity induced by LPS treatment. LPS induced IkappaBalpha degradation at 30-60 min after treatment, but did not induce IkappaBbeta degradation up to 120 min. In contrast, TNF-alpha rapidly induced IkappaBalpha degradation within 5 min and IkappaBbeta degradation within 15 min. Cycloheximide did not prevent LPS-induced IkappaBalpha degradation, indicating that newly synthesized proteins induced by LPS were not involved in LPS-stimulated IkappaBalpha degradation. LPS-induced IkappaBalpha degradation was inhibited by ALLN, confirming that ALLN inhibits NF-kappaB activation by preventing IkappaBalpha degradation. Of note, HMA also inhibited LPS-induced IkappaBalpha degradation. However, tyrosine phosphorylation of IkappaBalpha itself was not elicited by LPS stimulation, suggesting that tyrosine phosphorylation of a protein(s) upstream of IkappaBalpha is required for subsequent degradation. We conclude that in HUVEC, LPS induces NF-kappaB-dependent genes through degradation of IkappaBalpha, not IkappaBbeta, and propose that this degradation is induced in part by HMA-sensitive kinase(s) upstream of IkappaBalpha.
Calcium-Calmodulin-Dependent Protein Kinases↗
Generation and characterization of monoclonal antibodies to alveolar type II cell lamellar body membrane.
Monoclonal antibodies against the limiting membrane of alveolar type II cell lamellar bodies were obtained after immunization of mice with a membrane fraction prepared from lamellar bodies isolated from rat lungs. The specificity of the antibodies was investigated with Western blot analysis, indirect immunofluorescence, and electron-microscopic immunogold studies of freshly isolated or cultured alveolar type II cells, alveolar macrophages, and rat lung tissue. One of the monoclonal antibodies identified, MAb 3C9, recognized a 180-kDa lamellar body membrane (lbm180) protein. Immunogold labeling of rat lung tissue with MAb 3C9 demonstrated that lbm180 protein is primarily localized at the lamellar body limiting membrane and is not found in the lamellar body contents. Most multivesicular bodies of type II cells were also labeled, as were some small cytoplasmic vesicles. Golgi complex labeling and plasma membrane labeling were weak. The appearance of lbm180 protein by immunofluorescence in fetal rat lung cryosections correlated with the biogenesis of lamellar bodies. The lbm180 protein decreased with time in type II cells cultured on plastic. The lbm180 protein is an integral membrane protein of lamellar bodies and was also found in the pancreas and the pancreatic betaHC9 cell line but not in the rat brain, liver, kidney, stomach, or intestine. The present study provides evidence that the lbm180 protein is a lung lamellar body and/or multivesicular body membrane protein and that its antibody, MAb 3C9, will be a valuable reagent in further investigations of the biogenesis and trafficking of type II cell organelles.
Animals↗
Monocyte-derived macrophages prime peripheral T cells to undergo apoptosis by cell-cell contact via ICAM-1/LFA-1-dependent mechanism.
We designed the present study to clarify the mechanism of superantigen-induced apoptosis of human mature T cells and to elucidate the pivotal roles of monocyte-derived macrophages in induction of T cell apoptosis. Exposure of unfractionated human peripheral blood mononuclear cells to SEA, SEB or PHA elicited apoptosis in T cells after 5-day culture. In purified T cell preparations, SEB was unable to induce apoptosis, but was inductive when the purified T cells were cocultured with monocyte-derived macrophages adhering to plastic culture dishes. Placing the T cells in the insert wells which physically separated them from the adhering macrophages resulted in a complete loss of SEB-induced apoptosis. The addition of blocking antibodies against LFA-1, ICAM-1 and CD2 to the cocultures significantly inhibited the SEB-induced T cell apoptosis. We concluded therefore that direct contact of macrophages with T cells is critical in SEB-induced T cell apoptosis, and that adhesion molecules such as LFA-1/ICAM-1 and CD2 may be involved in the mechanism of this effect.
Apoptosis↗
Protein tyrosine kinase inhibitors inhibit both proliferation and chemotaxis of vascular smooth muscle cells.
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Animals↗