[A case of autoimmune pancreatitis: follow-up study of imaging].
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Biomedical subjects
Publications and source records attributed to H Shigematsu.
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Midgraft stenosis of the prosthesis after bypass surgery has seldom been reported. A man presented with an ischemic ulcer of the left foot. He had undergone bilateral femoropopliteal bypass surgery as well as left-sided iliofemoral bypass surgery with a knitted Dacron graft. The graft in his left thigh was occluded. A knitted Dacron conduit with 8-mm diameter was interposed between the iliofemoral bypass graft and the left profunda femoris artery, and graft-popliteal jumping bypass surgery was added. The postoperative angiogram showed a short-segmental severe stenosis of the interposed graft neighboring the proximal anastomosis. Repeat surgery showed that the stenotic lesion was located separately from the anastomosis. This midgraft stenosis was considered to consist of dissection of pseudointima associated with the intraoperative procedures. In cases of repeat surgery around the inguinal ligament, procedures should be performed with great care.
In this study, we examine the role of NO located in the rostral ventrolateral medulla (RVLM) in the control of blood pressure and the activity of the sympathetic nervous system. To determine the effect of an increase in NO production in the RVLM on blood pressure in conscious rats, adenovirus vectors encoding either endothelial NO synthase (AdeNOS) or beta-galactosidase (Adbetagal) were transfected into the bilateral RVLM. The local expression of endothelial NO synthase (eNOS) protein in the RVLM was confirmed by immunohistochemical staining for the eNOS protein and by Western blot analysis. Mean arterial blood pressure (MAP) and heart rate, which were monitored using a radio-telemetry system, were significantly decreased in the AdeNOS-treated group from day 5 to day 10 after the gene transfer. Urinary norepinephrine excretion was decreased on day 7 after the gene transfer in the AdeNOS-treated group. Microinjection of either N(G)-monomethyl-L-arginine (L-NMMA) or bicuculine, a gamma-amino butyric acid (GABA) receptor antagonist, into the RVLM at day 7 after the gene transfer increased MAP to significantly greater levels in the AdeNOS-treated group. However, microinjection of kynurenic acid into the RVLM on day 7 after the gene transfer did not alter MAP levels in either group. GABA and glutamate levels in the RVLM, when measured by in vivo microdialysis, were significantly increased in the AdeNOS-treated group. These results suggest that the increase in NO production caused by the overexpression of eNOS in the bilateral RVLM decreases blood pressure, heart rate, and sympathetic nerve activity in conscious rats. Furthermore, these responses may be mediated by an increased release of GABA in the RVLM.
Two spatially resolved oximeters, NIRO-300 and OM-200, were compared with regard to the measurement of oxygen saturation values in two forearm muscle groups at rest and during arterial occlusion in nine healthy volunteers. There was a significant correlation between the muscle oxygen saturation values obtained at rest using the two oximeters (n=33, r(2)=0.43, P<0.0001), whereas these values were significantly different during arterial occlusion. Thus, although there was good agreement between muscle oxygen saturation values measured using the two oximeters, the operating range of the tissue oximeters should be recognized and indicated.
The purpose of this study was to clarify the current etiology of and prognosis for iatrogenic vascular injuries. The study involved patients who underwent surgery for vascular injury. The patient record was retrospectively reviewed to collect information on the patient profile and type of vascular injury. The surgical techniques used were classified as simple or complex. The outcome was measured as morbidity and 30-day hospital mortality due to vascular injuries. The average age of the group with iatrogenic injury was significantly older than the group without. The number of males and females with iatrogenic injuries were almost equal, whereas males predominated in the group with noniatrogenic injuries. During the first half of the study period, more injuries were noniatrogenic; during the second half, most were iatrogenic. Most injuries due to angiographic procedures could be treated by a simple repair. Injuries due to operative procedures and noniatrogenic traumas had to be repaired by complex techniques. The overall morbidity rate was 3.8%, and the 30-day hospital mortality rate was 1.9%. The recently developed minimally invasive surgical techniques tend to increase the risk of vascular injuries whereas catheterization remains the most important cause of iatrogenic vascular injuries. However, as long as such injuries are treated promptly, the prognosis is good.
We describe herein the case of a patient with severe liver failure in whom an abdominal aortic aneurysm (AAA) extending to the right iliac artery was diagnosed. Because the risk of performing a standard open repair was considered too high in this patient, the aneurysm was uneventfully repaired using a technique of transfemoral endovascular stent-grafting with femorofemoral bypass and occlusion of the left common and right internal iliac arteries. Unfortunately, multiorgan failure associated with adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) suddenly developed on postoperative day (POD) 2 and the patient died on POD 9. Thus, although endovascular stent-grafting is generally assumed to be less invasive and therefore feasible for high-risk patients, patients with severe liver dysfunction may not be suitable candidates.
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A female case of developmental arrest, early-onset seizures, retinal pigmentary degeneration, progressive central nervous symptoms and peripheral neuropathy, associated with progressive renal dysfunction, anemia and nephrotic syndrome, was presented. Her epileptic syndrome was possibly an early myoclonic encephalopathy, though neonatal seizures were not evident. Serial cranial MRIs showed progressive brain atrophy and a white matter change. Neuropathological examination revealed a neurodegenerative disease mainly involving the white matter with olivopontocerebellar degeneration. She also had the nephronophthisis-medullary cystic disease complex and an early stage of focal segmental glomerulosclerosis. Her grandaunts had renal diseases, one of whom died of renal failure in adolescence, and her father showed cerebellar symptoms since the middle age. All possible metabolic studies were negative. This case is similar to Senior-Loken syndrome, but distinct in terms of the severe and progressive neurological symptoms, suggestive of a new malignant syndrome with some inherent metabolic derangement affecting both the nervous system and the kidneys.
Homeobox genes have important roles in haematopoiesis and are regulated in an activated state by the trithorax group (trxG) of genes. In a repressed state, they are regulated by the Polycomb group (PcG) of genes. ENX-1, a putative human PcG gene product, interacts with the proto-oncogene product Vav. We report an investigation of the role of ENX-1 in human haematopoiesis. CD34+ cells mobilized to peripheral blood strongly expressed ENX-1. When stimulated to proliferate, both T and B lymphocytes rapidly up-regulated ENX-1. ENX-1 was expressed in all cell lines of the various lineages examined. When HL-60 cells were differentiated to mature granulocytes with all-trans retinoic acid, ENX-1 was down-regulated. Moreover, ENX-1 antisense oligodeoxynucleotide suppressed DNA synthesis in HL-60 cells. Our data indicate that ENX-1 is involved in the proliferation of both normal and malignant haematopoietic cells.
BACKGROUND: The aim of this study was to evaluate near-infrared spectroscopy (NIRS), combined with a treadmill-walking test, as a method of assessment of intermittent claudication (IC) in diabetic patients. METHODS: Some 208 symptomatic legs in 153 consecutive patients who complained of calf IC due to atherosclerotic disease were studied with NIRS and resting ankle : brachial pressure index (ABPI). RESULTS: There was good reproducibility of NIRS measurements. Three distinct types of IC were detected by NIRS. ABPI was significantly different between these three types in non-diabetic patients, but could not grade the severity of IC in diabetic patients. Recovery time (RT) of muscle oxygenation differentiated more accurately between severe and moderate claudication than ABPI in diabetics, although RT and ABPI had similar accuracy in non-diabetics. There was a significant correlation between RT and ABPI in non-diabetic patients and patients who had been diabetic for less than 10 years, while there was no correlation in patients who had had diabetes for over 10 years. CONCLUSION: Measurement of muscle oxygenation during exercise by NIRS graded the severity of IC in diabetic patients more accurately than resting ABPI. An abstract based on this paper was presented to the symposium of the 18th World Congress of the International Union of Angiology in Tokyo, Japan, September 1998
BACKGROUND: aortic aneurysm is a rare but life-threatening cardiovascular complication in patients with systemic lupus erythematosus (SLE). The purpose of this study was to clarify the characteristic clinical features and the pathological mechanism of aneurysmal formation in these patients. METHODS: among 429 patients operated on for abdominal aortic aneurysm (AAA) during the past 10 years, five cases with SLE were treated surgically. Their clinical data were reviewed, and the resected aneurysmal wall of the five patients was also examined histologically. RESULTS: the mean age of the patients with SLE was 55 years, which was statistically younger than that of the other patients (mean 77 years, s.d. 7.9, p <0.05). They had received long-term corticosteroid therapy for the treatment of SLE for a mean of 23 years. Histologically, destruction of the medial elastic lamina was characteristic. Four patients had no complications in the postoperative follow-up period (mean 4 years), while the remaining patient died of rupture of a dissecting aneurysm two years after operation. CONCLUSION: prolonged steroid therapy may play a major role in accelerating atherosclerosis, which can result in aortic aneurysmal enlargement, possibly together with primary aortic wall involvement and/or vasculitic damage in patients with SLE.
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The anti-mitochondrial antibody response in primary biliary cirrhosis (PBC) is primarily directed at E2 components of PDC, OGDC, and BCOADC, and E3BP. Previous work has shown that the immunodominant autoreactive T- cell epitope is the PDC-E2 163-176 peptide, restricted by HLA DR53. To address molecular mimicry and cross-recognition among mitochondrial autoantigens, we analyzed reactivity, including agonism and antagonism assays, to a series of single amino acid-substituted peptides using cloned T-cell lines in PBC and controls. Interestingly, fine specificities were unique for every single T-cell clone, but the clones could be categorized into two distinct groups based on recognition motifs of the T-cell receptor (TCR) ligand: group A (170)ExDK(173) and group B (168)EIExD(172). (170)E is the most critical TCR contact residue for both groups of cloned T-cell lines, whereas (173)K and (168)E are the critical TCR contact residues for group A and group B cloned T-cell lines, respectively. More importantly, some group A-cloned T-cell lines cross-reacted to human E3BP 34-47, human OGDC-E2 100-113, and several peptides derived from various microbial proteins carrying an ExDK motif, whereas group B-cloned T-cell lines reacted only to E3BP 34-47 carrying an EIExD motif. Furthermore, an RGxG motif was exclusively found in the complementarity-determining region (CDR3) of the TCR Vbeta in the group B-cloned T-cell lines, while G, S, and/or R were frequently found in the CDR3 of the TCR Vbeta in the group A-cloned T-cell lines. These data provide a framework for understanding molecular mimicry among mitochondrial antigens.
The human PDC-E2 163-176 peptide (GDLLAEIETDKATI) is an immunodominant autoreactive T-cell epitope in patients with primary biliary cirrhosis (PBC), restricted by HLA DRB4*0101. We have previously reported that the ExDK sequence is essential for recognition of this epitope and identified 1 mimicry peptide, Escherichia coli PDC-E2 peptide (EQSLITVEGDKASM), which can activate human PDC-E2 163-176 peptide-reactive T-cell clones. In the present study, to further investigate mimicry peptides possibly involved in PBC, we generated 13 different T-cell clones reactive to the human PDC-E2 163-176 peptide following repeated in vitro stimulation of peripheral T lymphocytes with the human PDC-E2 163-176 peptide (native peptide) and tested for the reactivity of these T-cell clones to 30 different mimicry peptides derived from various self- and nonself proteins that have an ExDK-sequence. We found 7 mimicry peptides derived from microbial proteins that can activate at least 1 of these T-cell clones; 7 of 7 T-cell clones from patients with PBC and 2 of 6 T-cell clones from healthy subjects were activated by at least 1 to 6 different mimicry peptides. Two of 6 T-cell clones from healthy subjects were activated by specific mimicry peptides more strongly than by the native peptide, and 2 of 6 T-cell clones from healthy subjects were not activated by any mimicry peptides tested. Thus, the pattern and degree of activation by mimicry peptides differed in each T-cell clone, indicating the presence of a diverse spectrum of autoreactive T cells that are reactive to a single minimal epitope of the human PDC-E2 163-176 peptide.
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Sphingosine-1-phosphate (S1P) is a bioactive lysophospholipid that induces a variety of biological responses in diverse cell types. Many, if not all, of these responses are mediated by members of the EDG (endothelial differentiation gene) family G protein-coupled receptors EDG1, EDG3, and EDG5 (AGR16). Among prominent activities of S1P is the regulation of cell motility; S1P stimulates or inhibits cell motility depending on cell types. In the present study, we provide evidence for EDG subtype-specific, contrasting regulation of cell motility and cellular Rac activity. In CHO cells expressing EDG1 or EDG3 (EDG1 cells or EDG3 cells, respectively) S1P as well as insulin-like growth factor I (IGF I) induced chemotaxis and membrane ruffling in phosphoinositide (PI) 3-kinase- and Rac-dependent manners. Both S1P and IGF I induced a biphasic increase in the amount of the GTP-bound active form of Rac. In CHO cells expressing EDG5 (EDG5 cells), IGF I similarly stimulated cell migration; however, in contrast to what was found for EDG1 and EDG3 cells, S1P did not stimulate migration but totally abolished IGF I-directed chemotaxis and membrane ruffling, in a manner dependent on a concentration gradient of S1P. In EDG5 cells, S1P stimulated PI 3-kinase activity as it did in EDG1 cells but inhibited the basal Rac activity and totally abolished IGF I-induced Rac activation, which involved stimulation of Rac-GTPase-activating protein activity rather than inhibition of Rac-guanine nucleotide exchange activity. S1P induced comparable increases in the amounts of GTP-RhoA in EDG3 and EDG5 cells. Neither S1P nor IGF I increased the amount of GTP-bound Cdc42. However, expression of N(17)-Cdc42, but not N(19)-RhoA, suppressed S1P- and IGF I-directed chemotaxis, suggesting a requirement for basal Cdc42 activity for chemotaxis. Taken together, the present results demonstrate that EDG5 is the first example of a hitherto-unrecognized type of receptors that negatively regulate Rac activity, thereby inhibiting cell migration and membrane ruffling.