[A case of mature retroperitoneal teratoma producing CEA].
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Biomedical subjects
Publications and source records attributed to N Masawa.
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The spatial distribution of intimal thickening was determined for each of 42 carotid bifurcations removed at autopsy from patients with no clinical or anatomic evidence of cerebrovascular disease. Both right and left specimens were available for six of the individuals. Each bifurcation was removed intact and included a 1.5-2.9-cm length of the common carotid artery and a 1.5-2.5-cm length of the internal carotid artery. The specimens were restored to in situ length, fixed under conditions of controlled-pressure perfusion at 100 mmHg, filled with a radio-opaque mixture, radiographed and sectioned at 0.5-cm intervals. Computer assisted contour tracing of projected images of histologic sections was used to determine intimal thickness, intimal cross sectional area and lumen area within each of eight equal 45 degrees polar sectors with 0 degree indexed at the flow divider, 90 degrees at the outside wall, 180 degrees opposite the flow divider and 270 degrees at the inner side wall. Intima occupied 0.9-42% of the area encompassed by the internal elastic lamina, i.e. the potential lumen area if no intimal thickening were present, but there was no lumen narrowing on lateral X-ray projections. Intimal thickening was eccentric at each level of section but the circumferential location of maximum intimal thickness (MIT) shifted in a continuous helix from level to level. At the common carotid artery level 1.0 cm proximal to the bifurcation, MIT tended to be at the flow-divider side at 15 +/- 59 degrees. Immediately proximal to the flow divider, MIT was at the lateral side wall. In the mid-sinus region of the internal carotid artery MIT was opposite the flow divider at 179 +/- 64 degrees. At the distal internal carotid just beyond the sinus, MIT was at the inner side wall. The distal internal carotid was minimally involved or free of intimal thickening. Comparison of right and left bifurcations revealed that the helical spatial distribution of MIT was in mirror-image symmetry for the two sides. The findings correspond closely with previous demonstrations of a helical flow pattern in the region of the bifurcation. Although locations of MIT just proximal and just distal to the bifurcation are similar and tend to be at the 'far wall', individual differences in the shifts of MIT with axial location should be taken into account when sites of interrogation by non-invasive clinical methods are selected for detection of intimal thickening.
Arteries enlarge where intimal plaques form, tending to preserve lumen cross sectional area but causing an increase in mural tangential tension due to the increase in radius. To characterize the compensatory enlargement process at the carotid bifurcation and to evaluate the possible contribution of intima thickening to mural tensile support during the enlarging process, we assessed the relationships among intimal thickening, artery size and estimated tensile stress at 9 sequential axial levels in 42 human carotid bifurcations obtained during post-mortem examinations of 36 adults with no clinical or anatomical evidence of cerebrovascular disease. Right and left bifurcations were available for 6 patients. The arteries were fixed under conditions of controlled pressure distention and histologic sections were prepared at 0.5 cm axial intervals. We determined vessel radius (r), intima thickness (IT), media thickness (MT), intima area (IA), lumen area (LuA) and the area encompassed by the internal elastic lamina (IELA), i.e. the lumen area if there were no intimal thickening. Although IT, IA and r were greatest in the proximal sinus region, there was a highly significant linear relationship between IA and IELA at each axial level; correlation coefficients ranged from 0.64 to 0.97 with P < 0.001 at each level. Stenosis (IA/IELA x 100) ranged from 10.8 +/- 8.0% at the common carotid level immediately proximal to the bifurcation angle to 22.3 +/- 17.9% at the level immediately distal to the angle, but LuA remained nearly constant at each level regardless of IA.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND AND PURPOSE: Medial smooth muscle cell necrosis has been reported as a lesion that may precede angionecrosis, which is a major cause of not only hypertensive brain hemorrhage but also lacunar infarct. We morphometrically studied a loss of smooth muscle cells in the media of cerebral arteries in relation to clinical risk factors. METHODS: The lateral striate, ie, perforating arteries and the medullary arteries in the subcortical white matter of the temporal lobe (100 to 400 microns in diameter) were histologically investigated in 121 autopsied brains. Medial area was measured quantitatively, and the number of nuclei of smooth muscle cells in the area was calculated in 1210 cross-sectional arteries of histological sections. The influence on the structural (ie, smooth muscle cell) preservation of the tunica media (ratio of number of smooth muscle cell nuclei to medial area [N-MA ratio]) of age, blood pressure, serum lipids, and presence of absence of extracerebral severe atherosclerosis was investigated. RESULTS: The N-MA ratio decreased slightly with age in both arteries. A reverse correlation between N-MA ratio and age was seen in groups both with and without hypertension. The mean N-MA ratio in the hypertensive group was significantly lower than that of the nonhypertensive group (P < .001) in all decades of life. The mean N-MA ratio of the perforating arteries was slightly lower than that of the medullary arteries in both groups. Severe atherosclerosis of the internal carotid arteries, even with hypertension, mitigated a decrease of the N-MA ratio, which was as slight as that in the nonhypertensive group. Serum cholesterol in this group was higher than in both the conventional hypertensive group (P < .005) and the nonhypertensive group (P < .001). CONCLUSIONS: Although both hypertension and age were significant risk factors for medial smooth muscle cell necrosis, hypertension was relatively more significant. Medial smooth muscle cells of the perforating arteries in the basal ganglia were more vulnerable than those of the medullary arteries. Cerebral small arteries in subjects with severe atherosclerosis of the carotid and major cerebral arteries (hypertension in eight of nine subjects) may have been protected from extensive loss of medial smooth muscles presumably because of both high serum cholesterol and decreased wall tensile stress associated with reduced blood perfusion due to severe atherosclerotic stenosis.
Progestin supplementation has been advocated in estrogen treatment for postmenopausal women to avoid proliferation of the endometrium. In this study we investigated the morphologic and biochemical effects of progestins on the endometrium of estrogen primed, ovariectomized rats. As the progestin derivatives, Allylestenol (AE), Norethisterone (NE), Danazol (DZ), Dydrogesterone (DG), Medroxyprogesterone acetate (MPA) and Cyproterone acetate (CPA), and as a anti-estrogen compound, Tamoxifen (TMX), were applied. To evaluate the effects of these different compounds on the endometrium, histologic studies and measurement of estrogen receptor concentrations were performed. When 19-nortestosterone groups, AE, DZ and NE, were orally administered to the conjugated equine estrogen (CE) treated, ovariectomized rats, the histologic pattern of the endometrium revealed rather a marked inhibition of hyperplasia induced by CE than a progestational response. Two of 3 of 17 alpha-hydroxyprogesterone groups, DG and MPA, provided slightly endometrial protection against the hyperplastic response, but another one, CPA, did not have any inhibitory effect on the estrogenic stimulation of the endometrium. TMX was not capable of suppressing the endometrial hyperplasia caused by CE administration. The average plasma concentrations of estradiol (E2) were 82.0 +/- 27.0 pg/ml (Mean +/- SD) after CE administration and there were no significant differences among these groups. Estrogen receptor concentrations of endometrium of progestins or antiestrogen added groups were not changed, when compared with the CE alone group. There was also no relationship between the estrogen receptor concentrations and the histologic findings in the endometrium. This discrepancy may be chiefly due to the low dose of the progestins as compared with the CE dose.(ABSTRACT TRUNCATED AT 250 WORDS)
This experiment was performed to investigate whether hypertonic saline has a preventive effect on delayed neuronal death in the CA1 subfield of the hippocampus. Twenty gerbils were used, and after being anesthetized by inhalation of 1% halothane, both common carotid arteries were occluded for 2.5 min. The animals were injected intravenously with 2 ml/kg of 10% NaCl immediately after reperfusion, and 2 ml/kg of physiological saline solution was used in the same manner in a control group. Five days later, histopathological changes in the CA1 subfield were observed by staining with hematoxylin-eosin and examining sections of the brain under a light microscope. Degenerative or necrotic pyramidal cells exhibited cell shrinkage, nuclear pyknosis, dark staining of the cytoplasm vacuolation and disappearance of the radial striated zone. The pyramidal cell degeneration rate in a 1 mm length of CA1 subfield was 95.6 +/- 1.6% in the ischemia-reperfusion-saline group and 7.1 +/- 3.0% in ischemia-reperfusion-hypertonic saline group, and the difference was statistically significant. This study verified that hypertonic saline prevented delayed neuronal death in the CA1 subfield of hippocampal area after ischemia-reperfusion.
Cardiac thrombosis due to atrial fibrillation (AF) has been recognized as the most common cause of cerebral embolism. However, sometimes no macroscopic thrombus is found at autopsy in the heart of a victim of this type of cerebral embolism. We investigated morphological changes in the left atrial endocardium of 31 patients (including 21 cases with AF) who had died of cerebral embolism. "Rough endocardium" (RE) seen macroscopically provided evidence for the existence of atrial thrombosis. The RE that appeared in AF cases was due to a granular and wrinkled appearance of the endocardium associated with oedematous and fibrous thickening. Fibrin-thread deposits were also always distinguishable. Mural thrombi and oedema with neutrophil infiltration in the subendocardium could be seen under the microscope. Small areas of endothelial denudation and thrombotic aggregations were commonly observed by scanning electron microscopy (SEM). These SEM lesions were significantly more frequent in cases with AF than in controls (P < 0.001). The diagnostic success rate for atrial thrombosis among cases with AF increased from 33.3% to 81% when thrombi proven by histological investigation of the areas with RE were added. Left atrial RE may be an anatomically relevant finding for the existence of atrial thrombosis with AF, when the thrombosis cannot be detected upon gross observation at autopsy.
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Arteries adjust to alterations in wall shear stress or tensile stress by changes in diameter, wall thickness, structure and composition. The intima participates in these adaptive reactions, particularly when changes in mechanical stresses are imposed after physiologic stress levels have been established during growth. Decreased wall shear stress due to decreased flow, flow separation or complex flow patterns, or increases in tensile stress due to increases in pressure or radius stimulate non-atherosclerotic intimal proliferation. Intimal fibrocellular hypertrophy (IFH), in the form of compact fibrocellular layers resembling the media, stabilizes when the lumen diameter is reduced sufficiently or wall thickness is increased sufficiently to restore baseline wall shear or tensile stress. Reactive-adaptive intimal proliferation is not necessarily self-limiting and may continue in the form of intimal hyperplasia (IH) which is relatively matrix-free and poorly organized. If mural and intimal changes do not result in restoration of baseline wall shear and tensile stress, IH may proceed to further narrowing and stenosis. Identification of the cellular and molecular mechanisms which underly the responses which link flow to diameter, diameter and pressure to mural restructuring, and mural restructuring to intimal thickening should provide new insights into the nature of vessel adaptations in the absence or presence of atherogenesis.
A case of congenital familial goiter with impaired thyroglobulin (Tg) synthesis has been reported. The patient is the fifth in a family of six children, three of whom have a goiter. The parents are cousins. The patient's thyroid function tests showed low T4 (1.0 microgram g/dl) and free T4 (0.2 ng/dl), normal or slightly increased T3 (1.8 ng/ml) and free T3 (7.4 pg/ml), and high TSH (57 micrograms U/ml). Serum Tg was 5.1 ng/ml (normal less than 30). The thyroidal 123I-uptake was 59.8% before and 54.5% after perchlorate test. Gel filtration with Bio-Gel A 5m demonstrated the presence of albumin-like protein probably iodinated as a major protein in the thyroid and very low content of Tg which was smaller than the normal 19S Tg. Histologically microfollicular adenoma and negative Tg immunostaining were the dominant findings. Segregation of Tg alleles in the family was studied by Southern blotting with a probe revealing a diallelic RFLP. The results demonstrated that the affected siblings had received the same alleles from both parents and were homozygous for the RFLP. Northern blotting analysis of the goiter RNA with a Tg probe revealed that, whereas the amount of Tg mRNA was normal, its size seemed slightly reduced. PCR amplification of Tg mRNA as six overlapping cDNA fragments demonstrated that a 200bp fragment was missing from the 5' region of the goiter mRNA. Subcloning and sequencing of the cDNA fragments, and of the patient's genomic DNA amplified from this region, revealed that this aberrant splicing is due to a cytosine to guanine transversion at position minus 3 in the acceptor splice site of intron 3. The presence in exon 4 of a putative donor tyrosine residue (tyr 130) involved in thyroid hormone formation provides a coherent explanation of the hypothyroid status of the patient. To our knowledge, this is the first identified mutation responsible for congenital familial goiter in humans.
A biopsy case of basal cell adenoma of the submandibular gland was reported in a 15-year-old boy. The tumor was pigeon's egg-sized, spherical in shape and encapsulated by fibrous tissue, and its cut-surface was grayish white. Histologic feature of this neoplasm was a trabecular or tubular monomorphic adenoma with well-developed elastic fibers (elastin-basement membrane complex) in the interstitial tissue. Electron microscopy disclosed 4 kinds of tumor cells, that is, secreting cells, squamous cell-like cells with tonofibrils and tonofilaments, clear cells with a few filaments, and myoepithelial cells. The interstitium contained elastin, collagen fibrils and basement membrane-like substance. Possible production of elastic fibers by the myoepithelial cells of this adenoma was discussed.
To clarify the mechanism of ulcer formation of atherosclerotic plaques in human carotid arteries, autopsy investigations were performed on eight patients who had died of cerebral infarction due to recent carotid thrombosis. Eleven control patients who had carotid atherosclerosis without thrombosis were also investigated. Histological changes of the arteries in serial sections were reconstructed three-dimensionally. Each artery with occlusive thrombosis was found to have an intimal ulcer at the head of the thrombus on the proximal slope near the base of the thickened atheromatous plaque at the carotid sinus. Most ulcers formed obliquely or longitudinally, were parallel to the vessel axis, had a fusiform shape, and measured 7 +/- 2 x 3 +/- 1 mm (mean +/- s.d.). The ulcers arose by marginal separation of the innermost layer from the underlying layer of the stratified intima. An underlying atheroma developed along the borders of these intimal layers reaching the subendothelium, with thinning of the intimal cap to less than 150 microns. The process of ulceration may be generated by vessel injury induced by hemodynamic forces, such as tensile forces and shear stress. The ulcer may extend along the fragile region where the wall may exhibit uneven compliance due to differences in the tissue structures of each intimal layer. Furthermore, macrophages may play a key role in ulcer formation.
Lymph node enlargement is common in active systemic lupus erythematosus (SLE), a disease that is characterized by well-defined clinical criteria. Histologically, although lymphadenopathy associated with SLE exhibits marked histological diversity and occasionally shows atypical lymphoproliferative disorders, there has not been any description of the histopathological features of reactive lymph node hyperplasia with giant follicles (RHGF). We here report three such cases. The subjects were a 23-year-old Japanese female, a 44-year-old Japanese female and a 49-year-old Japanese male. All three patients initially presented with systemic lymphadenopathy. They also had systemic symptoms and abnormal laboratory findings indicating active disease, although two patients did not fulfill the diagnostic criteria for SLE at lymph node biopsy. Histologically, three lesions were characterized by numerous enlarged, coalescing lymphoid follicles with distortion rather than effacement of the lymph node architecture. By in situ hybridization, Epstein-Barr virus (EBV) genomes were demonstrated in two cases. The present three cases indicate that lymphadenopathy associated with SLE representing RFGH should be differentiated from the early stage of HIV-related lymphadenopathy as well as follicular lymphoma, particularly the floral variant. The authors would like to stress that the RHGF which is described in the present study should be listed in the pathohistology of SLE lymphadenopathy.
BACKGROUND: Cytologic findings of toxoplasmic lymphadenitis (TL) have been only sporadically reported. Intramammary lymph node is an extremely rare site for TL. CASE: A 47-year-old, healthy, female presented with a breast tumor, which was aspirated. The cytomorphologic features were interpreted as suggestive of TL. Histopathology of the excisional biopsy specimen and subsequent serologic examination confirmed the diagnosis. CONCLUSION: We obtained several characteristic findings in aspiration of TL. Of these, epithelioid cell clusters and monocytoid cells were the most diagnostic.
BACKGROUND: Granulosa cell tumor (GCT) of the ovary is an uncommon but not rare tumor, and the adult type usually affects postmenopausal women. The adult type of GCT has several characteristic clinicopathologic features, including a composition of small, uniform cells with Call-Exner bodies and an ability to metastasize to extrapelvic organs, even several decades after the initial operation. CASE: A 62-year-old female was incidentally found to have multiple shadows in the peripheral portions of both lung fields on roentgenography. She had a past history of oophorectomy for an ovarian carcinoma more than 20 years earlier. A transbronchial lung biopsy series was nondiagnostic. An aspirate obtained by transthoracic fine needle aspiration (FNA) biopsy revealed clusters of rather uniform, small cells with nuclear grooves, suggestive of a metastatic lung tumor. Histologic examination of the lung tissue in comparison with the previous oophorectomy specimen confirmed the impression of GCT metastatic to the lung. CONCLUSION: A preoperative diagnosis of metastatic lung tumor was established by transthoracic FNA cytology. The important cytologic criteria for the differential diagnosis are uniformity of tumor cells, coffee bean-like nuclear grooves and Call-Exner bodies. The possibility of late recurrence of this kind of tumor, even two or three decades after surgical resection, should be kept in mind.
In an attempt to better understand the cytopathologic features of phyllodes tumors (PTs) and to differentiate PTs from fibroadenomas (FAs) of the breast, cytologic smears prepared from 17 and 19 histologically diagnosed cases of PT and FA, respectively, were reviewed. PT cases were histopathologically graded as benign, borderline and malignant. Cytologically, hypercellularity of stromal cells with recognizable cytoplasm was observed in 6 of 7 borderline and malignant PT cases, but none of the benign PT or FA cases revealed such hypercellular stroma. Between all PT and FA cases, no statistically significant differences could be obtained in the nuclear size of stromal cells, folding of epithelial cell sheets or number of foamy macrophages. The study revealed that the abundance of stromal cells with cytoplasm, not naked nuclei, was strongly suggestive of borderline and malignant PT, but the differentiation between benign PT and FA was difficult on the basis of the cytopathologic findings.