Biomedical subjects
Publications and source records attributed to K Uchida.
A 24-year-old woman with radiation-induced breast cancer is reported. At 9 years of age she had received 4,000 R irradiation to her chest to treat an eosinophilic granuloma of the rib. Fifteen years later, she suffered from breast cancer. We suggest that the irradiation-induced the breast cancer.
Diosgenin and beta-sitosterol (1% in diet) were administered to CRJ:CD-1 male mice for 15 days, in order to examine the changes in bile acid metabolism. There were some differences between diosgenin and beta-sitosterol in their effects on diet intake, liver weight, and plasma cholesterol level. However, both phytosterols caused no statistically significant changes in body weight gain, decreased cholesterol absorption to about one-third that observed in control mice, decreased liver cholesterol level, increased fecal excretion of cholesterol, and decreased fecal excretion of bile acids. Most of the increase in fecal excretion of cholesterol occurred 2 days after the start of feeding of phytosterols and gradually declined thereafter, but the levels on day 15 were nevertheless higher than those in the control mice. The fecal excretion of bile acids decreased progressively after the treatment with phytosterols. The decrease of bile acid derived from chenodeoxycholic acid was more predominant than the decrease of those derived from cholic acid, resulting in an increase of the cholic acid/chenodeoxycholic acid ratio. The biliary cholesterol, phospholipid, and bile acid mole % ratios and the lithogenic index were not changed, but the percentages of cholic acid and its related bile acids (the cholic acid group) to the total bile acids increased and those of the chenodeoxycholic acid group decreased after the treatments. The pool size of bile acids decreased in the mice given diosgenin but not in those given beta-sitosterol. Distribution of bile acids between the gallbladder and intestine was not altered by either phytosterol.(ABSTRACT TRUNCATED AT 250 WORDS)
Several studies reported that ursodeoxycholate (but not its conjugates), when administered intravenously, increased the biliary bicarbonate concentration in the rat (1-3). At the same time, a complete dissociation between bile flow and the bile salt excretion rate was produced in the second hr of infusion (2). In order to examine whether this property was due to the 7 beta-hydroxy group in its molecular structure, the choleretic property of ursocholate (3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid) was investigated in male Wistar rats. Immediately after the start of iv infusion of ursocholate at a rate of 1.2 mumole/min/100 g b. wt., both the bile flow and bile salt excretion rate began to increase. However, unlike with ursodeoxycholate, the bile salt excretion rate continued to be high in the second and third hr of infusion, while the bile flow rate gradually increased. Furthermore, the bicarbonate concentration in the bile fell slightly 10 min after the start of ursocholate infusion. Although the concentration tended to return to the baseline value before the bile salt infusion in the later period of observation, no significant increase in bicarbonate concentration was observed during the whole observation period. These properties were quite similar to those of cholate rather than those of ursodeoxycholate. However, a cholate infusion at the same rate of 1.2 mumole/min/100 g b.wt. caused a cholestasis as early as 20 to 30 min after the start of an infusion. These results suggest that the previously reported properties of ursodeoxycholate (that it causes a complete dissociation between the bile flow and bile salt excretion rate in the second hr and that it increases the biliary bicarbonate concentration) were not due to the 7 beta-hydroxy group in its steroidal structure, and that the choleretic property of ursocholate is similar to its 7 alpha-hydroxy epimer, cholate. However, the much lower cytotoxicity of ursocholate compared to cholate appears to be due to the 7 beta-hydroxy group that ursocholate has.
Partial thyroxine-binding globulin (TBG) deficiency in a family is described. A 43-year-old male was admitted because of the association of low thyroxine level but markedly elevated triiodothyronine resin-uptake despite his complaints of palpitation and excessive sweating. TBG was low (6 micrograms/ml) by radioimmunoassay. His free thyroxine level was normal. 123I uptake at 24 hours was normal and was suppressed following oral administration of triiodothyronine. Serum TSH level was normal and responded normally to TRH stimulation. Similar low level (6 micrograms/ml) in TBG was found in his elder brother who had no complaints. Another brother and 3 sisters had normal TBG levels. According to the classification of the TBG deficiency proposed by Barbosa et al., a family described here is considered to have the type II TBG deficiency which shows a much lower TBG level in male than in female with X-linked inheritance.
So many problems have been left unsolved by x-ray pelvimetry for the prognostic diagnosis of cephalopelvic disproportion that the clinical usefulness of x-ray pelvimetry has been questioned and a more scientific approach to evaluation of cephalopelvic disproportion has been sought. By unifying various factors that impose problems in cephalopelvic relationships into one index via new mathematical models, we attempted to estimate quantitatively the potential dystocia caused by inlet disproportion. The index is calculated from ten measurements of data obtainable on roentgenograms, and the practical calculations can be readily done with a programmable calculator. The validity of the assumptions used in the mathematical models and the reliability of the developed index were retrospectively analyzed in 300 primiparous women with cephalic presentations. This study suggests that the mathematical index could serve as a useful prognostic guide to the proper management of labor in association with disproportion.
Two male patients with 'Hashitoxicosis', who revealed histologic pictures of adenomatous goiter in addition to findings of chronic thyroiditis, are described. Case 1. A 55-year-old man was admitted on May 7, 1981, for evaluation of hyperthyroidism. He had exophthalmos with positive Moebius and von Graefe's signs, and a firm, asymmetrically enlarged non tender thyroid gland with multiple cysts. The BMR was +60%, T4 26.4 micrograms/dl, free T4 7.2 ng/dl, T3 5.62 ng/ml and 24 hr radioiodine uptake 49.5%. TSH was undetectable and did not respond to TRH. 123I scan showed multiple defects in the bilateral upper poles of the thyroid gland. Antithyroglobulin and antimicrosomal antibodies were positive. He then underwent a total thyroidectomy with removal of multinodular goiter. The mutinodular goiter was associated with cystic degeneration which contained the thyroid hormone-rich fluid. Histologic examination revealed multiple adenomatous nodules and lymphocytic infiltration and degeneration in the surrounding tissues of the nodules. Case 2. A 43-year-old man was admitted on May 14, 1975, because of an 8 month history of hand tremor, weight loss (5 kg), facial and upper palpebral edema and an enlarged thyroid. He had mild exophthalmos and a firm, asymmetrically enlarged thyroid gland with multiple nodules. The BMR was +35%, T4 20.0 micrograms/dl, T3(Resomat) 0.78 ng/ml and PBI 20.0 micrograms/dl. TSH was 1.0 muU/ml and responded slightly to TRH. 24 hr radioiodine uptake was 84.4% and did not respond to T3 administration. Antithyroglobulin and antimicrosomal antibodies were positive. 123I scan showed diffusely increased uptake and no defects. Histologic examination of the biopsy specimen of the thyroid gland showed multiple adenomatous nodules in addition to typical findings of chronic thyroiditis in the surrounding tissues of the nodules. From the above observations, it is suggested that multiple adenomatous nodules accompanying chronic thyroiditis show clinical features resembling Basedow's disease rather than Plummer's disease.
Cerebellar projections to the superior colliculus in the rabbit were studied by the anterograde and retrograde HRP methods. Cerebellotectal fibers arise mainly from the anterior and posterior interpositus nuclei and terminate contralaterally in layer VII, layer VI, layer V, and the deep tier of layer IV of the superior colliculus. Cerebellotectal fibers from the posterior interpositus nucleus originate from the lateral part of the nucleus and end chiefly in the caudal part of the superior colliculus. Cerebellotectal fibers from the anterior interpositus nucleus arise from the ventral part of the nucleus and terminate mainly in the rostromedial part of the superior colliculus. Some neurons in the lateral cerebellar nucleus also send fibers contralaterally to the intermediate and deep layers of the superior colliculus, especially to its rostral and lateral parts. Few, if any, cerebellotectal fibers arise from the medial cerebellar nucleus.
The ferric form of L-tryptophan 2,3-dioxygenases from both Pseudomonas acidovorans (ATCC 11299b) and rat liver showed magnetic CD spectra ascribable to a high spin protohemoprotein at neutral pH, whereas the ferric indoleamine 2,3-dioxygenase from rabbit intestine exhibited a spectrum due to a mixture of high and low spin states under comparable conditions. Upon addition of L-tryptophan, the spectra of the former enzymes changed to another type of high spin spectra, while the latter showed a marked increase in the low spin component. From these findings and effects of pH on the spectra, it is suggested that the sixth ligand of ferric L-tryptophan 2,3-dioxygenases is water at a neutral pH and that for the ferric indoleamine 2,3-dioxygenase is a strong field ligand such as an imidazole nitrogen. The mixed spin state observed for the latter enzyme was ascribable to a thermal equilibrium between high and low spin states as judged by low temperature spectroscopy. With the ferrous form, the Soret magnetic CD spectra of these enzymes were all similar, giving those of a typical high spin ferrous protohemoprotein, whereas visible spectra were different from one another, suggesting differences in the electronic structure of the heme and its vicinity. The natural CD spectra of both ferric and ferrous forms of each enzyme showed negative Cotton effects in the Soret region. Their intensities were different from one another, presumably due to some differences in the interaction of the heme with nearby aromatic amino acid residue(s).
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A semiquantitative x-ray microanalytical study was made of dense bodies in rat and human blood platelets prepared by freeze substitution. After the freeze substitution, electron dense bodies containing 5-hydroxytryptamine(5-HT) were well preserved. Electron probe x-ray microanalyses clearly defined species differences in the cations of dense bodies of rat and man. Direct calculation of elemental concentration ratios demonstrated a high level of Mg, with lesser amounts of K and Ca in rat, while there was a negligible level of Mg in man but a high amount of Ca. These results indicate that freeze-substitution is a suitable preparation for the study of diffusible electrolytes which may open the way to quantitative analysis using appropriate standards for analytical electron microscopy of resin sections.
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We report that protein synthesis inhibitors exert an inhibitory effect on the trophic action of the nerve stump. The sciatic nerve innervating the extensor digitorum longus muscles of mice was cut either as close to, or as far from, the muscle as possible. Denervation changes in the muscle were evaluated using the resting membrane potential and dose-response curves obtained by plotting acetylcholine-induced contractures. Actinomycin D (2 micrograms/kg, i.p.), ethidium bromide (10 micrograms/kg, i.p.), cycloheximide (1 or 5 mg/kg, i.p.), or chloramphenicol (100 mg/kg, p.o.) administration was immediately after neurotomy and continued daily until the day preceding muscle removal. Although denervation changes occurred significantly later in muscles with a long rather than a short nerve stump, the administrated antibiotics, excluding cycloheximide, accelerated the manifestation of denervation changes in muscles with long nerve stumps without affecting those in muscles with short nerve stumps.
The effects of aging on serum lipids, lipoproteins and apolipoprotein C subclasses in very low density lipoprotein (VLDL) were investigated in healthy male subjects aged from the 1st to the 9th decade. The serum cholesterol, phospholipid and triglyceride concentrations, the serum beta-lipoprotein concentration determined immunologically, and the beta-lipoprotein percentage determined by electrophoresis showed the lowest levels in the 2nd decade, increased gradually with age, attained the highest level in the 6th to 7th decade and slightly declined in the 9th decade. The VLDL-low density lipoprotein (LDL) cholesterol level changed almost in parallel with the serum total cholesterol level, but the HDL cholesterol level and the apolipoprotein A concentration remained almost constant showing no age-related change. The free cholesterol percentages in every lipoprotein fraction and the apolipoprotein content in LDL were higher in the subjects in the 6th and 7th decade than those in the 2nd to 3rd decade. The apo C II/C III ratio in VLDL increased with age. These data suggest that the ability to active lipoprotein lipase may not be impaired but the lecithin:cholesterol acyltransferase (LCAT) activity declines with age.
Twenty-two out of 31 patients with chronic renal failure and secondary hyperparathyroidism who underwent parathyroidectomy before operation underwent non-invasive image diagnosis of parathyroid glands by computed tomography (CT), scintigraphy with 201TlCl and 99mTcO4+, and/or ultrasonography. CT visualized 39 of 45 parathyroid glands (86.7%), weighing more than 500 mg. Scintigraphy with a subtraction method using a computer performed the diagnosis in 19 of 27 glands (70.4%). Ultrasonography detected 21 of 27 glands (77.8%). Image diagnosis was also useful in the postoperative follow-up study. The non-invasive image diagnosis of parathyroid glands in patients with chronic renal failure is thus valuable for 1) definite diagnosis of secondary hyperparathyroidism, 2) localization, and 3) diagnosis for effectiveness of conservative treatment.
Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on serum and liver cholesterol levels, bile flow, biliary cholesterol, phospholipid and bile acid secretions, and fecal sterol and bile acid excretions were examined with Wistar strain male rats fed ordinary and 2% cholesterol supplemented diets. Dehydrocholate increased the liver cholesterol level, bile flow and biliary lipid secretion, but ursodeoxycholate and hyodeoxycholate did not. The serum cholesterol level was not changed by the treatments. Ursodeoxycholate and hyodeoxycholate increased their own secretion into the bile and decreased cholic acid secretion, while dehydrocholate increased deoxycholic acid and oxo bile acid secretion. Ursodeoxycholate increased but dehydrocholate decreased the fecal sterol excretion, and hyodeoxycholate caused no change. Dehydrocholate decreased the fecal coprostanol level. The total amounts of the fecal bile acids were similar in all the treated groups, but ursodeoxycholate increased lithocholic acid, alpha, beta- and omega-muricholic acids and ursodeoxycholic acid; hyodeoxycholate increased hyodeoxycholic acid, 3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid and oxo bile acids; and dehydrocholate increased deoxycholic acid, cholic acid, omega-muricholic acid and oxo bile acids and decreased hyodeoxycholic acid. These data suggested that ursodeoxycholate was transformed into lithocholic and muricholic acids, and dehydrocholate into cholic and deoxycholic acids during the enterohepatic circulation, but hyodeoxycholate showed almost no change. Ursodeoxycholate and hyodeoxycholate caused neither accumulation of cholesterol in tissues nor increase in bile flow and biliary lipid secretion as well as chenodeoxycholate did. The biological effect of dehydrocholate was similar to that of cholate, and this was partially due to its conversion into cholic acid and deoxycholic acid.
Effects of spinasterol and sitosterol on plasma and liver cholesterol levels and biliary and fecal sterol and bile acid excretions were examined with male mice. Both phytosterols were added to the diet at a 1% concentration and fed to mice for 15 days. Spinasterol increased the fecal cholesterol excretion and decreased the plasma and liver cholesterol levels, the bile acid pool size and the fecal bile acid excretion, especially those derived from chenodeoxycholic acid. Fecal coprostanol excretion remained unchanged. These changes were similar to those produced by sitosterol. These data led to the conclusions 1) that spinasterol, as well as sitosterol, inhibits cholesterol absorption, resulting in decreases of the plasma and liver cholesterol levels and 2) that when cholesterol absorption is inhibited, the synthesis of bile acids, especially that of chenodeoxycholic acid, decreases, suggesting that the dietary cholesterol is preferentially metabolized to chenodeoxycholic acid in mice.
The excised parathyroid glands of twenty-one patients with secondary hyperparathyroidism due to chronic renal failure were submitted to careful histopathologic examinations including electron-microscopy. The previous history of these patients who had been on hemodialysis treatment for a certain period was relatively uniform with no association with primary hyperparathyroidism. Although eleven patients had four evenly enlarged parathyroid glands, eight patients showed four unevenly enlarged parathyroid glands with one or two glands weighing less than 100 mg. Histopathologic patterns of hyperplasia are easily divided into two distinctly different patterns, diffuse and nodular. Thirteen cases showed the same histopathological patterns of hyperplasia, either diffuse or nodular, in all excised glands. However, one or two out of four glands in eight patients evidenced a different histopathological pattern.
Aldosterone responsiveness to angiotensin II (A II) was evaluated in 65 diabetic patients with and without various diabetic complications versus 38 age-matched non-diabetic subjects. Plasma aldosterone (PA), together with plasma renin activity (PRA), was low and responded poorly to furosemide (80 mg, orally) plus upright posture (4 hours) stimulation in diabetic patients. When the PA response to stimulation relative to PRA response was estimated from the ratio of PA increase to PRA increase after stimulation (delta PA/delta PRA), the 38 non-diabetic subjects had ratios more than 3.0. Of the 65 diabetic patients, 48 had normal delta PA/delta PRA ratios (more than 3.0) and 17 had low delta PA/delta PRA ratios (less than 2.9). Graded A II infusions (1, 2, and 4 ng/kg/min each for 30 min) were performed under a low sodium intake (sodium, 120 mEq/day) in 25 of the 65 diabetic patients, whose delta PA/delta PRA ratios were normal in 15 and low in 10, and in 16 non-diabetic subjects. The PA responses to the graded A II infusions in the normal delta PA/delta PRA diabetic patients were similar to those in the non-diabetic subjects. However, the PA responses to the graded A II infusions in the low delta PA/delta PRA diabetic patients were significantly lower. It is concluded that, although the majority of diabetic patients have normal aldosterone responsiveness to A II, some diabetic patients have blunted aldosterone responsiveness to A II probably attributable to the abnormality of the adrenal cortex in addition to the impaired renin secretion.