Malignant hemangioendothelioma in discoid lupus erythematosus.
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Biomedical subjects
Publications and source records attributed to M Maeda.
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Intrarectal administration of sodium deoxycholate (SDC) enhances experimental colorectal carcinogenesis, an effect that is partly vitiated by oral metronidazole. The effect of topical SDC with or without concurrent metronidazole on colorectal cell proliferation was explored in male Sprague-Dawley rats (n = 30) allocated to five groups. Two groups received thrice weekly intrarectal instillations of 1 ml N saline or 1 ml 0.12 M SDC. A third group received SDC plus metronidazole 22.5 mg/kg/day in the drinking water. Controls had no instillations or metronidazole alone. At time of killing (10 weeks), crypt cell production rate (CCPR) was determined by the stathmokinetic technique for four large-bowel segments. Saline had no significant effect on colorectal CCPR but SDC produced increases throughout, varying from 53% in the proximal colon to 222% in the rectum (P less than 0.01). Metronidazole did not reduce this effect, although given alone it reduced colonic CCPR by 40 to 50%. The direct tropic effect of bile acids could largely explain their cocarcinogenic properties. Since metronidazole does not prevent this increase in cell proliferation, its mildly protective role against cancer may reflect the presence of fewer anaerobes capable of degrading bile acids to carcinogenic metabolites.
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High-resolution computed tomographic scans of 19 patients with pulmonary asbestosis revealed a subpleural curvilinear shadow (SCLS) parallel to the inner chest wall in the lungs of 15 (78.9%) patients. Most (46.7%) SCLS measured greater than 5 cm but less than 10 cm in length and occurred less than 1 cm from the inner chest wall in all cases. SCLS was distributed mainly in the lower lobe in patients with mild pulmonary fibrosis and in segments where fibrosis was mild in patients with honeycomb shadows. This may reflect initiation of pulmonary fibrosis leading to the formation of a honeycomb shadow. Radiologic-pathologic correlation, achieved in one postmortem specimen, seemed to indicate that SCLS was associated with the initial change of fibrosing bronchioloalveolitis, which is characteristic of pulmonary asbestosis.
Specific-pathogen-free 10-week-old chickens were inoculated via the air sac with Escherichia coli and showed lymphocytic depletion of bursa of Fabricius and thymus. In experiment I, chickens were necropsied at 12 and 24 hours, 2, 3, and 5 days after inoculation. At 12 hours after inoculation there was lymphocytic depletion in the medulla of lymphoid follicles of the bursa. At 24 hours after inoculation there was lymphocytic depletion also in the cortex of follicles and edema in interfollicular interstitium and follicular medulla. At 2 and 3 days after inoculation there were more marked lymphocytic depletion in medulla and cortex, and fibrosis in interfollicular interstitium. Partial repopulation of follicles with lymphocytes was seen at 5 days after inoculation. In the thymus, lymphocytic depletion occurred in the cortex. At 12 hours after inoculation, lymphocytic necrosis increased in number more than that of control chickens. The width of the cortex and medulla decreased. At 24 hours after inoculation, lymphocytic necrosis increased further. At 2 to 5 days after inoculation, the boundary between the cortex and medulla of lobules was obscure and cellular elements of the cortex and medulla were mingled. In experiment II, chickens were necropsied as in experiment I and also at 8 and 14 days after inoculation. The relative weights of the bursa and thymus reduced rapidly to minimal relative weights at 8 days after inoculation. At 14 days after inoculation, both bursa and thymus had normal relative weights and histological structures. These findings indicate that E. coli infection may induce transient lymphocytic depletion of lymphoid tissues in the chicken.
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To elucidate the features of thyroid hormone secretion under conditions of impaired circulation, blood samples were withdrawn at operation from thyroid and peripheral veins of 23 patients with thyroidal and non-thyroidal diseases. They were taken from the respective veins simultaneously, when the arterial supply to the thyroid tissue was partially occluded by surgical manipulation. It was found that triiodothyronine was preferentially, as compared with thyroxine, secreted from the thyroid, irrespective of the disease. Serum levels of thyroglobulin were also markedly elevated in the thyroid vein. These results suggest that episodic degenerative discharge of thyroid hormone from nodular goiters may be a cause of impaired or blunted TSH response to TRH, frequently observed in patients with common nontoxic nodular goiters.
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The brainstem of anesthetized cats was electrically stimulated to examine the changes in the intracranial pressure (ICP). There were pressor and depressor sites, which preferentially produced an immediate increase and decrease in ICP in association with the arterial pressor and depressor responses, respectively. A preferential increase in ICP was also observed by stimulation of some depressor sites. The stimulus-induced ICP responses were usually different from the secondary ICP changes due to nonneurogenic alteration of arterial blood pressure (BP) as evoked by arterial bleeding and infusion of saline solution; the stimulus-induced increase in ICP was greatly enhanced when the stimulation to the pressor sites was applied at lowered BP levels and at moderately elevated ICP levels. In addition, when a gradual elevation in ICP was spontaneously observed with the lowering of the BP level, the pressor site-induced increase in ICP exceeded 70-100 mmHg at the peak plateau-like waves, regardless of the magnitude of accompanying arterial pressor response. We propose that the stimulus-induced ICP responses cannot be explained merely by the metabolic changes, the decreased intracranial compliance, and the secondary transmural action on the intracranial space of the arterial pressor and depressor responses. A neurogenic mechanism that directly affects intracranial blood diameter may be involved in the ICP responses, especially those observed at a lower BP level, in addition to extracranic action of sympathetic and parasympathetic nerve activities.
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The observations of immune complex (IC) deposition in the surface of rheumatoid arthritis (RA) cartilage, in conjunction with degradative changes in superficial and midzone chondrocytes, raised the question of causal relationships. In antigen-induced arthritis in rabbits, cartilage degradation occurred in association with IC deposition and is accompanied by chondrocyte damage. Superficial and midzone chondrocytes in rabbit tibial cartilage of arthritic joints, induced by bovine serum albumin (BSA) or ferritin (Fn), were examined by electron microscopy during the evolution of the arthus response. The first cell changes were noted at six hours, by which time superficially formed IC had begun to extend into the matrix. Elongated cytoplasmic footlets, numerous lysosomes, and lipid droplets occurred initially. By 24 hours, concomitant with the deeper extension of surface IC, prominent changes in chondrocytes of both superficial, and midzones progressed to ultrastructural evidence of cell death. The pinocytosis of electron-dense amorphous materials, which included IC, preceded degradation. These data suggest that the observed cytopathology is a manifestation of locally deposited IC.
The relationship between the saccharide chain on the endothelial cell surface and the permeability of intracerebral blood vessels has been studied. In the present study, wheat germ agglutinin (WGA) was perfused into capillaries in the area postrema of the normal Mongolian gerbil, where the blood brain barrier (BBB) is known to lack, and into intracerebral blood vessels, the BBB of which had been destroyed by experimentally induced brain ischemia. The light microscopic features of the sections from WGA-perfused brain tissues of the normal gerbil revealed that most of the blood vessels, including capillaries in the brain parenchyma, showed positive findings (the reaction induced a very distinct staining of the vascular wall) from which the course and structure of the fine vessels could be determined. The reaction to WGA on the diaphragma fenestra (DF) in capillaries in the area postrema was relatively weak, and DF without the reaction were occasionally revealed by electron microscopy. The gerbil, in which cerebral ischemia had been induced, also showed partial defect of the reaction with WGA on the luminal side of the endothelial cells. The results of the present experiment suggest some degree of correlation between the saccharide chains, including the specific monosaccharide of WGA, on the endothelial cell surface and permeability. It was considered that lectin can be used as an index for morphological observations, suggesting an alteration in function of the endothelial cell membrane. In addition, the perfusion method in this experiment suggested the possibility of distinguishing pinocytotic vesicles from pits of cell membranes.
The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-1) and the permeability of the vascular wall in human autopsied cases of cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface membrane of endothelial cells. Albumin in the neuropil of sections was demonstrated for the estimation of increased vascular permeability. The results showed that endothelial reactivity to UEA-1 was reduced in cases where death had occurred 3 to 5 days after onset of cerebral infarction. Reactivity was also diminished in cases where death had occurred after 13 and 25 days; these cases showed fresh ischemic lesions caused by re-attacks of infarction. Albumin extravasation into the neuropil was demonstrated in these intermediate cases. Chronic cases, dying after more than 52 days, showed no reduction of endothelial reactivity to UEA-1 and no albumin extravasation was proved. It was concluded that UEA-1 can be employed as a useful morphological marker for evaluation of endothelial function and vascular permeability.
Sera obtained from patients with systemic lupus erythematosus (SLE) were tested for their reactivity to cell lines derived from cutaneous T-cell lymphoma (CTCL), or adult T cell leukaemia (ATL), and with other cell lines, by indirect immunofluorescence method. Approximately one half of SLE sera reacted with the surface antigens of HUT-102 cells, a cell line from CTCL, which constitutively expresses Tac antigen. The titre tended to be higher in the active than in the inactive stage. These positive sera also reacted with other neoplastic or normal T cell lines having Tac antigen. SLE sera reacting with HUT-102 surface antigens were further examined for their reactivities to Tac antigen, the putative IL-2 receptor, using HUT-102 or ATL-2. Pretreatment with anti-Tac monoclonal antibody partially blocked the reactivities to HUT-102 surface antigens in nine of 15 SLE sera tested. The binding of 125I-labelled anti-Tac monoclonal antibody was displaced by the addition of sera from six of 15 SLE patients. In addition, nine of the 15 SLE sera could inhibit the binding of 125I-labelled IL-2 to ATL-2 cells. These results suggested that some of SLE sera contained antibodies against the IL-2 receptor.
Seventeen liposoluble bis(carboxylato)-cyclohexane-1,2-diammineplatinum(II) and bis(carboxylato)-cis-diammineplatinum(II) complexes were synthesized and tested for antitumor activity against leukemia L1210 cells in mice. The former complexes had excellent antitumor activity without any toxicity to the host at the therapeutic dose when used with lipiodol as a carrier solvent. The latter complexes had neither antitumor activity nor toxicity in vivo. The former complexes were gradually released from lipiodol to saline in vitro; the latter were not. The activity depended on the chain length of the carboxylato residue and also on the molecular shape of the ligand part of the complexes.
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