[Nightingale's ideal in my philosophy].
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Biomedical subjects
Publications and source records attributed to S Takeda.
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Endocrine effects of hypotension induced by nitroprusside, trimetaphan and a nitroprusside-trimetaphan mixture were studied in 34 male rabbits under halothane anesthesia. They were randomly divided into four groups; nitroprusside (group N; n = 8), trimetaphan (group T; n = 10), a nitroprusside-trimetaphan mixture (group M; n = 8) and controls (group C; n = 8). No change was noted in plasma catecholamines measured in group C throughout the experiment, but plasma renin activity decreased progressively. During induced hypotension, plasma catecholamines and plasma renin activity of group N were significantly higher than the control value. In contrast, in group T plasma epinephrine decreased significantly. On the other hand, in group M, plasma renin activity showed a slight but not significant increase, while plasma catecholamines remained unchanged. This may have occurred since a mixture of nitroprusside and trimetaphan produced the dissociation of renin-angiotensin-sympathoadrenal loop. In conclusion, these results suggest that a nitroprusside-trimetaphan mixture is a useful method for hypotensive anesthesia by inhibiting the excessive activation of renin-angiotensin-sympathetic system.
Hepatic calcification in uremia is rare and, to our knowledge, only two cases have been reported in the English literature. In both previous reports, calcification was found in the damaged hepatocytes in the centrilobular to midzonal area of the hepatic lobules. The patient, a 61-year-old man, was uremic due to diabetic nephropathy. He had suffered posttransfusion hepatitis just before his death. Antemortem radiographic examination of the abdomen failed to visualize the calcification in the liver. At autopsy, microscopic examination of the liver revealed bile ductular proliferation and calcification mainly in the ductular epithelial cells. We suggest that calcification could occur preferentially in abnormally proliferated ductules when the serum calcium and serum phosphorus products are elevated.
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In an attempt to clarify the influence of pregnancy on the natural course of IgA nephropathy, the courses of 79 pregnancies occurring in 47 patients with the disease were studied. These resulted in 3 artificial and 10 spontaneous abortions, and two pre-term and 64 full-term deliveries. Fifty four maternity passbooks were analyzed. In 22 pregnancies (40.7%) proteinuria was increased during the third trimester, and in 13 (76.5%) of 17 pregnancies receiving postpartum urinalysis, urinary protein was decreased to the level of the first trimester within one month after delivery. In two of the remaining four patients with a persistent increase in proteinuria, renal biopsy was carried out two months after delivery, revealing focal glomerular sclerotic lesions, in addition to mild mesangial proliferation compatible with IgA nephropathy. These findings indicated that increased urinary protein observed in the two pregnancies might be attributed to a complication of pre-eclamptic focal glomerular sclerosis rather than exacerbation of underlying IgA nephropathy. The glomerular filtration rate (GFR), examined in 27 patients both before and after pregnancy, was decreased in only two patients (7.4%), but these reductions appeared to go with the individual natural course. In 6 (15.0%) of 40 pregnancies, proteinuria was increased within one month after delivery, and one of them was diagnosed both clinically and pathologically as the acute exacerbation of IgA nephropathy. These data suggest that patients with IgA nephropathy might show transient acute exacerbation just after delivery rather than during pregnancy, and that even if such exacerbations occurred, pregnancy might have little influence on the natural course of the disease.
In twenty-nine patients with thalamic hemorrhage, single photon emission CT (SPECT) and CT were performed in the acute stage. Measurement of cerebral blood flow (CBF) was performed by the 133-Xe inhalation method using SPECT (Tomomatic 64). CT findings such as hematoma volume, involvement of internal capsule, ventricular hematoma and topographical localization of hematoma were investigated. We studied etiological analysis of decreased CBF in the acute stage. CBF values in the group of large-volume hematoma (greater than or equal to 10 ml) decreased moderately on the hematoma side and mildly on the nonhematoma side. CBF values in the group of small-volume hematoma (less than 10 ml) decreased mildly on the hematoma side but didn't decrease on the nonhematoma side. CBF values of the former on the hematoma side decreased significantly compared with the latter. Linear correlation between hematoma volume and CBF was significant. As to topographical localization, CBF values of the group which involved medial thalamus decreased significantly compared with the other group. Factors of involvement of internal capsule and ventricular hematoma didn't affect CBF values. In conclusion, major factors which affected decreased CBF in the acute stage were hematoma volume and tomographical localization.
A highly sensitive radioimmunoassay to measure atrial natriuretic peptide (ANP) concentration in urine has been established, and its clinical usefulness is presented. ANP in urine was stable at 4 degrees C for several days and was easily measured by our radioimmunoassay. The average ANP excretion in 65 healthy persons was 25.0 +/- 1.4 ng/day (mean +/- SEM) and the fractional excretion of ANP was 0.7 +/- 0.05%. In 14 patients with congestive heart failure, the average ANP excretion was 119.2 +/- 29.4 ng/day, which decreased to 53.3 +/- 11.0 after successful treatment.
In the present study, an attempt was made to clarify whether ANP molecular forms in the plasma of severe congestive heart failure patients differ from those in healthy persons and whether ANP molecular forms in the plasma of the patients were changed by successful treatment of cardiac disease. Twenty patients with congestive heart failure were treated at Kitasato University Hospital. They were classified as class III or IV by New York Heart Association criteria at the time of admission. Plasma ANP concentrations decreased after treatment from 356 +/- 58.2 to 72.3 +/- 14.8 pg/ml. The gel permeation chromatograms from the plasma of healthy persons showed low, or low and high molecular weight ANP peaks which correspond to the elution positions of authentic alpha-ANP or ribonuclease A (mol. wt., 13.7 kdalton). In patients with severe congestive heart failure at a severe stage, middle molecular weight ANP consisted with the elution position of authentic beta-ANP was particularly noted in addition of low and high molecular weight ANP peaks. This middle molecular weight peak disappears in most of cases by successful treatment. Molecular forms in the plasma obtained from the coronary sinus and the inferior or superior vena cava were essentially the same. These results indicate that the middle molecular weight ANP supposed as beta-ANP may particularly be secreted in severe congestive heart failure patients.
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In spite of the apparent depletion of mast cells in tissues of mutant mice of W/Wv genotype, cells with many features of mast cells do develop when bone marrow cells of W/Wv mice are cultured in the presence of pokeweed mitogen-stimulated spleen cell-conditioned medium (PWM-SCM). In order to resolve this discrepancy and facilitate the analysis of the W mutation, we attempted to establish an in vitro system in which the in vivo defect of W/Wv mice can be reproduced. Cultured mast cells (CMC) were developed from bone marrow cells of either W/Wv or congenic +/+ mice, and then co-cultured with NIH/3T3 mouse fibroblasts in media supplemented only with fetal calf serum (i.e., in the absence of PWM-SCM). Under this condition, CMC from +/+ mice continued to divide and were maintained for more than 4 weeks. The supportive effect of NIH/3T3 cells required close-range interactions with CMC and was not due to synthesis of the known mast cell growth factors, interleukins 3 and 4. By contrast, CMC from W/Wv mice were not maintained, and the number of mast cells remaining after 4 weeks of co-culture was only 1% of the normal +/+ counterparts. Thus, the humoral factor-independent and cell contact-dependent system presented here revealed the intrinsic defects in growth and differentiation of CMC derived from W/Wv mice and might be useful for biochemical and molecular analysis of the gene product(s) encoded at the W locus.
The post-mortem findings are reported of two patients with myoclonus epilepsy associated with ragged-red fibers (MERRF, Fukuhara's disease), whose clinical findings have been described in detail previously. In addition to the mitochondrial myopathy, both patients had consistent lesions in the central and peripheral nervous systems: (1) degeneration of the dentatorubral and pallidoluysian systems, (2) spinal cord lesions resembling Friedreich's ataxia, and (3) degeneration of the substantia nigra, cerebellar cortex, inferior olivary nucleus, locus ceruleus, gracile and cuneate nuclei, and the pontine tegmentum. The nature and distribution of the lesions are different not only from the other mitochondrial encephalomyopathies but also from other known diseases. It is concluded that MERRF is a disease entity.
We described a new type of cytoplasmic inclusion in the choroidal epithelial cells of humans. The inclusions usually appeared as brown, round or elongated bodies with or without an inner core, ranging in size from 1.3 to 7.0 micron. Histochemically, they contained polysaccharides, proteins and compound lipids. Ultrastructurally, they were composed of finely granular and filamentous materials, which are densely packed in the inner core and less dense in the outer zone. The frequency study of the inclusions in 197 autopsied patients revealed that their occurrence had no correlation with the age or the disease category. It is concluded that the inclusions are a nonspecific, but peculiar, change of the choroidal epithelial cells, probably representing the morphological expression of a physiological or pathological alteration of the cellular metabolism at the single-cell level.
We systematically studied the enteric nervous system of the alimentary tract in seven patients with Parkinson's disease. In all patients, characteristic inclusions histologically and ultrastructurally identical to Lewy bodies were found in Auerbach's and Meissner's plexuses. They were most frequent in the Auerbach's plexus of the lower esophagus. Lewy bodies were found in 8 out of 24 age-matched nonparkinsonian patients. However, they were obviously small in number. These findings clearly indicate that the plexuses are also involved in Parkinson's disease.
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In an attempt to clarify a participation of hepatitis B virus (HBV) in the development of hepatic glomerulopathy in adults, kidney specimens obtained from 151 patients with liver diseases were studied. Although mesangial proliferation was more severe in patients with chronic hepatitis or liver cirrhosis than in those with acute hepatitis, no significant difference was observed between 82 serum hepatitis B surface antigen (HBsAg)-positive (HBV-related group) and 69 negative patients (HBV-nonrelated group). However, double contours of the glomerular capillary walls were observed more often in the former group (18/82, P less than .01), especially in the HBeAg-positive subgroup (8/24, P less than .001), than in the latter (3/69). In addition, glomerular capillary spike formation or a bubblelike appearance was observed in seven patients of the former group. Of these, all five patients examined were HBeAg-positive in their serum. By electron microscopic studies, subendothelial dense deposits and mesangial interpositions were observed more frequently in the HBV-related group, and subepithelial deposits were found only in the HBeAg-positive subgroup. The immunofluorescence study revealed IgA-dominant mesangial deposition in both HBV-related and nonrelated groups. As for the capillary wall deposits, however, IgG was dominant in 13 of the HBV-related group, but only one of the nonrelated group (P less than .01). Furthermore, one patient in the HBV-related group showed capillary wall-dominant HBeAg combined with IgG deposition.(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between free radical reactions and the defense mechanisms against them was investigated in the pathogenesis of prolonged vasospasm following experimental subarachnoid hemorrhage (SAH) in dogs. The concentration of lipid peroxides in the cerebro spinal fluid (CSF) increased markedly up to the eighth day following SAH; the concentrations also rose in the arterial wall (p less than 0.01) and the gray matter of the temporal lobe where the subarachnoid blood clots were (p less than 0.01). On the other hand, the activity of superoxide dismutase (SOD) decreased significantly up to the eighth day after SAH (p less than 0.01), and there was a gradual increase of glutathione peroxidase (GSH-px) in the CSF. In the arterial wall, there was a slight decrease in the activity of SOD, a significant decrease in the activity of GSH-px (p less than 0.01), and also a significant decrease in the concentration of glutathione (p less than 0.01) up to the eighth day following SAH. In conclusion, lipid peroxidation with insufficient biological defense mechanisms against it in the arterial wall, concomitant with that in the CSF, might take part in the genesis of prolonged vasospasm following SAH.
In order to elucidate a participation of the mesangiolysis in the formation of diabetic nodular lesions, 355 kidney specimens obtained from 327 patients with primary diabetes mellitus were studied. Mesangiolyses begun by focal and segmental disintegration of the pivotal structure of the mesangium ("torn off phase"), resulting in cystic or aneurysmal dilatation of the involved tuft, were found in 56 specimens (16%). The dilated tufts were filled with lysed mesangial matrix, which showed a reticular or fibrillar arrangement ("structureless phase"), being followed by a concentrical re-arrangement ("reconstructive phase") and by the ultimate formation of diabetic nodules. The mesangiolysis of various phases was frequently found concomitant with severe diabetic arteriolosclerosis and, in the reconstructive phase, the lysed mesangial matrix near the recanalized capillary along the inner aspect of glomerular basement membrane was observed to be rearranged in a layered structure. These results suggest the hypothesis that: 1) the mesangiolysis is the initial lesion occurring in glomeruli in the process of diabetic nodule formation, and disturbed blood flow into glomeruli, caused by diabetic arteriolosclerosis, may be implicated in the development of the mesangiolysis; and 2) concentric compression of the lysed mesangial matrix by recanalized capillaries forms layered structures and ultimate completed diabetic nodules.
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