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A Okamura

Publications and source records attributed to A Okamura.

At least 91 records · Page 5Linked to original sources
PubMed1997

Upregulation of angiotensin-converting enzyme during the healing process after injury at the site of percutaneous transluminal coronary angioplasty in humans.

BACKGROUND: Balloon injury models in rat have shown enhanced expression of ACE in the developing neointima. However, neointimal lesions in human coronary arteries are complex due to atherosclerosis and different types of wall laceration. This study was designed to investigate whether ACE is present in the neointima of humans, including patients with restenosis after percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: Thirty-seven sites with angioplasty injury, obtained at autopsy, were studied using immunocytochemical techniques. Sites with injury limited to a fibrous plaque and those with injury extending into the media (<2 months after PTCA) showed fibrocellular repair tissue composed mainly of smooth muscle cells that were distinctly positive for ACE. In cellular reactions at the site of injury limited to the atheromatous plaque (<2 months after PTCA), the expression of ACE appeared first in accumulated macrophages; once smooth muscle cells appeared in the repair tissue, they also expressed ACE. At a later stage (3 months after PTCA), the number of cells with ACE expression decreased markedly; from 7 months on, ACE was no longer expressed within the repair tissue. Basically, there were no differences with regard to ACE expression during the healing process after PTCA between segments with and those without angiographic evidence of restenosis. CONCLUSIONS: These results show that PTCA injury in humans results in upregulation of ACE at sites of active repair and, therefore, ACE could play an important role as one of the mediators of the healing process after PTCA.

Aged↗
PubMed1997

Postnatal ontogeny of striatal-enriched protein tyrosine phosphatase (STEP) in rat striatum.

The present study was undertaken to examine developmental change in expression of striatal-enriched protein tyrosine phosphatase (STEP) in the postnatal striatum of rats. For this purpose, immunohistochemical staining and transimmunoblotting analyses were carried out using a cDNA-generated polyclonal antibody to the STEP with a molecular weight of 46 kDa. Immunostaining showed that in neonatal striatum STEP-immunoreactivity was found in discrete patches composed of many immature cells, which corresponded to the tyrosine hydroxylase-immunopositive "dopamine islands." With development there was an increase in staining intensity and in the number of positively reacting cells. By 4 weeks postnatally, STEP-immunoreactivity was almost homogeneously distributed throughout the striatum, as was seen at the adult stage. Immunoblotting analysis showed that STEP protein expression abruptly increased from 2 to 4 weeks postnatally when it reached the adult level. These findings suggest that STEP is involved in development and maturation of the striatal neurons.

Animals↗
PubMed1997

GABA receptor agonist promotes reformation of the striatonigral pathway by transplant derived from fetal striatal primordia in the lesioned striatum.

Striatal lesions are known to cause the anterograde transneuronal degeneration of the substantia nigra pars reticulata (SNr) neurons in consequence to loss of GABAergic inhibitory striatonigral efferents. The present study was undertaken to examine whether long-term intraventricular administration of the GABA agonist muscimol could promote reformation of the striatonigral pathway arising from transplants by rescuing host SNr neurons from transneuronal death in rats with striatal ischemic lesions. Compared to nongrafted rats with striatal lesions, (i) a prominent axonal projection from the transplants to the ipsilateral substantia nigra, (ii) a significant increase in number of survived neurons in the ipsilateral SNr, and (iii) a significant reduction in number of apomorphine-induced turning behaviors were found in grafted animals with muscimol infusion, but not in those without muscimol administration. These findings suggest that preservation of the host target neurons for grafted cells may increase an efficacy of cerebral implants in establishment of the host-graft fiber connections, possibly, leading to functional restoration.

Animals↗
PubMed1997

Distribution of epithelial-specific antigen in uterine cervix with endocervical glandular dysplasia.

The natural history of cervical adenocarcinoma is largely unknown, and whether endocervical glandular dysplasia is a precursor lesion to malignant tumor formation is a controversial issue. The aim of this study was to clarify the relationship of endocervical glandular dysplasia to the uterine endocervical adenocarcinoma. Thirty-one cases of glandular abnormalities of the uterine cervix were identified histologically from January 1984 to April 1992. These included 11 cases of endocervical glandular dysplasia, 5 cases of adenocarcinoma in situ, 4 cases of microinvasive adenocarcinoma, and 11 cases of invasive adenocarcinoma. The immunohistochemical localization of epithelial-specific antigen (ESA) was examined in these cases of endocervical glandular dysplasia and related lesions, and was compared to 10 normal endocervical specimens. ESA immunoreactivities were usually present in the basolateral membrane of endocervical cells in the normal endocervix. However, the expressions of ESA were increasing from the basolateral membrane to the diffuse cytoplasmic membrane, along with the malignant transformation of the endocervical cells, in 6 of 11 cases with glandular dysplasia, in 9 of 9 cases with in situ and microinvasive adenocarcinomas, and in 11 of 11 cases with invasive adenocarcinomas. This finding indicates that ESA is a useful marker for endocervical glandular dysplasia and related lesions with malignant transformation, and suggests that endocervical glandular dysplasia may be a precursor lesion to uterine cervical adenocarcinomas.

Adenocarcinoma↗
PubMed1997

Results of surgery for bronchogenic carcinoma located in the aortic window.

Because of its critical location, lung cancer located in the aortic window can cause complications affecting the pulmonary artery trunk, aortic arch and esophagus. The results of surgical treatment are poor; however, there are few long-term survivors. In an attempt to define the indications for extended surgery, we evaluated eleven patients with non-small cell lung cancer. The tumors were classified according to their clinical extent of invasion as Type A (invading the anterior mediastinum including the central part of the pulmonary artery), Type B (invading upwardly to the mediastinum through the aortic window) or Type C (invading the posterior mediastinum including the thoracic aorta or esophagus). In the five patients with type A invasion, no metastases to the upper mediastinal lymph nodes other than the subaortic lymph nodes were found. The three patients with type B invasion had many metastases to the upper mediastinal lymph nodes. There were no metastases in the upper mediastinum in any of these patients with type C invasion, but metastases were found in a lower mediastinal lymph node #9, and a carinal lymph node. Each group clearly demonstrated a different site of mediastinal lymph nodes metastasis. The long term result was good in Type A invasion, in contrast to Type B or C invasion. Our classification may be useful for planning one's surgical approach to advanced lung cancer of the aortic window.

Adult↗
PubMed1997

Continuous intraventricular drug infusion for the in vivo study of transneuronal degeneration in the striatonigral system of the rat.

Injuries to certain parts of the brain may induce neuronal death in distant areas innervated by the sites of the primary lesion. Such characteristic pathological changes, known as anterograde transneuronal degeneration, may occur at the next and more distant synaptic levels and play a part in the slow progression of some types of system degeneration. Delayed transneuronal degeneration of the substantia nigra pars reticulata (SNr) is one example of this form of cell death, and it occurs as a consequence of a neostriatal lesion caused by focal ischemia, Huntington's disease, or experimental axon-sparing injections of neurotoxin. Ever since the demonstration by Saji and Reis that the administration of GABA receptor agonist effectively prevented delayed transneuronal degeneration of the SNr, the degeneration of nigral reticulata cells has been attributed to the loss of striatal inhibition (Fig. 1A). The latter process severely upset the balance of membrane potential of nigral reticulata cells, producing an effect resembling excitotoxicity. In this report, we describe a continuous intraventricular MK-801 infusion technique that is useful in clarifying the role of glutamatergic action via N-methyl-D-aspartate (NMDA) receptor subclasses involved in exo-focal postischemic death of the SNr.

Animals↗
PubMed1997

Adenoid basal carcinoma of the uterine cervix: immunohistochemical study and literature review.

Adenoid basal carcinoma of the uterine cervix is rare and its cell origin is still obscure. We report a case of adenoid basal carcinoma of the uterine cervix discovered incidentally in a 69-year-old woman who had been hysterectomized due to endometrial adenocarcinoma of the uterine corpus. Histologically, small round-to-oval cancer cell nests with peripheral cell palisading were seen budding from the basal cell layer of the uterine cervix showing carcinoma in situ. Immunohistochemically, the basaloid cells of the adenoid basal carcinoma were positive for keratins 14, 17 and 19 and resembled reserve cells of the cervical epithelium. The results of this study clearly demonstrated that adenoid basal carcinoma shows a phenotype similar to reserve cells of the uterine cervix. A review of the literature indicated that this tumor has a favorable prognosis and should be clearly separated from adenoid cystic carcinoma, which has a much poorer outcome.

Aged↗
PubMed1997

Enhanced expression of angiotensin-converting enzyme is associated with progression of coronary atherosclerosis in humans.

BACKGROUND: The clinical usefulness of angiotensin converting enzyme (ACE) inhibitors in preventing the recurrence of myocardial infarction has been investigated in large randomized trials. Results from many studies using animal models have suggested that ACE inhibitors have vasculoprotective effects, which may contribute to the prevention of coronary atherosclerosis. OBJECTIVE: To examine the association between vascular angiotensin generation and the development of coronary atherosclerosis in humans. METHODS: We used immunocytochemical techniques to examine frozen sections from 44 coronary artery segments from 19 corpses. RESULTS: Three segments were sites of plaque rupture in patients who had died from acute myocardial infarction. Other specimens of coronary artery segments were characterized histologically to be normal artery segments with diffuse intimal thickening (n = 6), hypercellular lesions composed of smooth muscle cells with or without infiltration of macrophages (n = 11), atheromatous plaque (n = 12), and fibrosclerotic plaque (n = 12). In normal arteries with diffuse intimal thickening, ACE was expressed in endothelial cells. In those with hypercellular lesions and atheromatous plaques, however, enhanced ACE expression was found in macrophages and smooth muscle cells. In contrast, arteries with fibrosclerotic plaques exhibited little or no ACE expression within the plaque. All three ruptured plaques expressed ACE strongly in macrophages accumulated around the attenuated fibrous cap. CONCLUSION: The strong association of enhanced ACE expression with the histologic characteristics of plaques suggests that ACE in hypercellular lesions, atheromatous plaques, and ruptured plaques contributes greatly to the further progression of atherosclerosis via an increase in vascular angiotensin II formation and inactivation of bradykinin.

Adult↗
PubMed1997

Extravesical tumor implantation caused by perforation during transurethral resection of a bladder tumor: a case report.

We report a case of invasive bladder cancer in which cancer dissemination occurred through a perforation of the vesical wall during transurethral resection of the tumor. A radical cystectomy was performed 1 month later and several clusters of viable cancer cells were histologically identified in a fibrous foreign body granuloma in the paravesicular adipose tissue of the lymphadenectomy specimen. The patient received adjuvant chemotherapy, but developed right inguinal lymph node metastasis 21 months after cystectomy.

Aged↗
PubMed1997

Recognition of tissue- and subtype-specific modulation of angiotensin II receptors using antibodies against AT1 and AT2 receptors.

Polyclonal antibodies have been prepared against synthetic peptides of human angiotensin II type-1 (AT1) and type-2 (AT2) receptors. Synthetic peptides corresponded to amino acids 15-24 of AT1 receptor and amino acids 241-253 of AT2 receptor. Western blot analysis of membranes from cell homogenates of COS-7 cells transfected with expression plasmids for mouse AT1b receptor, human vascular smooth muscle cells, and rat peripheral tissue demonstrated a major band of MW 44,000 with AT1 receptor antibody. Cell homogenates of COS-7 cells transfected with expression plasmids for human AT2 receptor showed a band of MW 44,000 with AT2 receptor antibody. Tissue homogenate of rat adrenal medulla and human pheochromocytoma presented a major band of MW 52,000 and a minor band of MW 44,000 with AT2 receptor antibody. AT1 receptor expression was in the following order: rat aorta > > lung, kidney, spleen, adrenal cortex > adrenal medulla, heart. Expression of AT2 receptor was in the following order: rat adrenal medulla > cortex, kidney, heart. Three-day treatment with CS866, an AT1 receptor antagonist, and temocapril, an angiotensin-converting enzyme inhibitor, suppressed AT1 receptor expression in the rat adrenal cortex, but not in the heart or adrenal medulla. AT2 expression was not affected by treatment with these drugs. These results suggest that newly developed antibodies for AT1 and AT2 receptors are useful in elucidating the regulation of subtype-specific receptor expression, and that AT1 but not AT2 receptors in adrenal tissue are regulated by angiotensin II.

Adrenal Glands↗
PubMed1997

Polyangiitis overlap syndrome.

A 33-year-old man was admitted to our hospital because of intermittent claudication and finger tip ulceration with a skin rash on the upper and lower extremities. He later developed a massive melena. Angiography revealed arterial occlusion in the hand and foot, skin biopsy showed vasculitis with eosinophilic infiltration, and biopsy of the colon showed mucosal vasculitis with thrombosis. A diagnosis of polyangiitis overlap syndrome was made, and all these symptoms improved after corticosteroid therapy.

Adult↗
PubMed1997

[Bronchogenic carcinoma located in the aortic window].

In the patients with invasion to the aortic window, we performed operation via median sternotomy combined with anteroaxillar thoracotomy. In such patients with T4 invasion, conventional pneumonectomy could not be performed because of the extensive invasion near the main pulmonary artery trunk. In these patients in this study, complete resection of the involved pulmonary artery could be performed using a vascular clamp without CP bypass. Operative technique was as follows: first, the pericardium was opened and taping of the aorta was applied. When the uninvolved part of the intrapericardial pulmonary artery was long enough to cut, we could use a stapling device, but the stapling device could not be used in many cases because the length of the uninvolved segment was too short to cut the left pulmonary artery. In order to carry out complete resection, it was necessary to clamp the central part of the main pulmonary artery diagonally from the left lower side to the right upper side. The pulmonary arterial stump was closed with continuous 4-0 monofilament mattress and over and over suture. We recommend an aggressive surgical approach for the tumor with invasion to the aortic window, because the prognosis is dismal in nonresected locally advanced lung cancer.

Aorta, Thoracic↗
PubMed1997

[Changes in the extent of mitral regurgitation during hemodialysis: color Doppler echocardiographic study].

The changes in the extent of mitral regurgitation (MR) during maintenance hemodialysis patients were studied in six patients with MR by color Doppler echocardiography. M-mode, two-dimensional and color Doppler echocardiography were performed before and every hour during hemodialysis. The severity of MR was evaluated by a semiquantitative grading system and maximal MR area. Hemodialysis removed 2.1 +/- 0.9/body fluid. Blood pressure and heart rate did not change systematically by hemodialysis. Left atrial, left ventricular end-diastolic and end-systolic dimensions were significantly decreased by hemodialysis (p < 0.05). Stroke volume and left ventricular wall stress were also significantly decreased (p < 0.01). MR area was significantly smaller at the end of hemodialysis compared to pre-hemodialysis (49.0 +/- 20.5 vs 171.0 +/- 49.2 mm2, p < 0.05). During hemodialysis, the extent of MR was continuously decreased. In two out of six patients, the MR jet disappeared. The extent of MR may depend on the fluid volume removed by hemodialysis because the MR area diminished more as more fluid was removed. No major disorders of the mitral complex were detected when the MR area was decreased rapidly to less than 60 mm2 in response to the removal of a small amount of fluid. The dry weight should be determined as the body weight when MR is as small as possible by color Doppler echocardiography.

Adult↗