Biomedical subjects
Publications and source records attributed to Y Yajima.
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A seventeen-year-old youth was presented with muscle cramps and convulsions. A brain CT scan showed calcification in the region of the ganglia, and a diagnosis of brain tumor was thus made and an anticonvulsant given for two years. At age nineteen, the patient developed pseudohypoparathyroidism owing to low serum calcium and high serum PTH levels. However, serum alkaline phosphatase and serum osteocalcin levels were high, lesion was detected in the femur neck. These data indicated that the bone remodeling response to PTH had remained intact in this patient. Serum osteocalcin is known to increase in primary hyperparathyroidism. However, unlike patients with hyperparathyroidism, those with pseudohypoparathyroidism show no increase in serum 1,25(OH)2D. The present case was thus useful for examining the direct effect of PTH on serum osteocalcin. The patient was administered 1 alpha (OH)D, and his condition monitored for two years. During this period, osteocalcin and PTH levels decreased while that of 1,25(OH)2D increased. Osteocalcin and PTH levels were found to be closely correlated (r = 0.68, p less than 0.01). The present results indicate the possibility that PTH may increase serum osteocalcin independent of Vitamin D.
In attempt to prove the hypothesis that corneocyte surface area in diabetics is larger than that in age-matched non-diabetics, we collected corneocytes from 50 diabetics and 43 non-diabetics in different decades of life. We measured surface areas of 27 +/- 3 corneocytes in each subject, utilizing an image analyser (Kontron MOP-10), then we counted mean number of corneocytes collected in 7 diabetics and 7 non-diabetics. There was a significant correlation between corneocyte surface area and chronological age in non-diabetics, whereas there was no significant correlation in diabetics. Corneocyte surface area of diabetics was larger than that of non-diabetics in every decades of life. The differences were statistically significant in 4th, 7th and 8th decades of life. Mean number of corneocytes collected in non-diabetics was 2.21 +/- 0.47 (X 10(5)), whereas that in diabetics was 2.49 +/- 0.55 (X 10(5)). The present study suggested that turnover time of corneal layer of the skin might be delayed in diabetics.
Thyrotropin-releasing hormone (TRH) stimulates biphasic prolactin (PRL) secretion from rat pituitary GH3 cells. The pretreatment of cells with EGTA (100 microM) plus arachidonic acid (15 microM), a condition which decreased TRH-responsive intracellular Ca2+ pools, eliminated the activity of TRH on burst PRL secretion (2 min) but did not alter that on sustained PRL secretion (30 min). However, the treatment of cells with EGTA, arachidonic acid and H-7 (300 microM), a potent inhibitor of protein kinase C (PKC), almost completely suppressed the activity of TRH for sustained PRL secretion. In cells down-modulated for PKC, TRH abolished this Ca2(+)-independent sustained PRL secretion. These results suggest that TRH acts through a separate, Ca2(+)-independent secretory mechanism, besides by modulating the Ca2(+)-dependent mechanism and that PKC is involved in this Ca2(+)-independent secretory pathway.
Protein kinase C (PKC) molecular species of GH4C1 cells were analyzed after separation by hydroxyapatite column chromatography. A novel Ca2(+)-independent PKC, nPKC epsilon, was identified together with two conventional Ca2(+)-dependent PKCs, PKC alpha and beta II by analysis of kinase and phorbol ester-binding activities, immunoblotting using isozyme-specific antibodies, and Northern blotting. These PKCs are down-regulated differently when cells are stimulated by outer stimuli; phorbol esters deplete PKC beta II and nPKC epsilon from the cells more rapidly than PKC alpha, whereas thyrotropin-releasing hormone (TRH) at 200 nM depletes nPKC epsilon exclusively with a time course similar to that induced by phorbol esters. However, translocation of PKC alpha and beta II to the membranes is elicited by both TRH and phorbol esters. These results suggest that TRH and phorbol ester activate PKC alpha and beta II differently but that nPKC epsilon is stimulated similarly by both stimuli. Thus, in GH4C1 cells, Ca2(+)-independent nPKC epsilon may play a crucial role distinct from that mediated by Ca2(+)-dependent PKC alpha and beta II in a cellular response elicited by both TRH and phorbol esters.
It is well known that the superficial layers of the dorsal cochlear nucleus (DCN) are rich in GABAergic neurons. We investigated the effects of topical application of GABA receptor agonists and/or antagonists upon the auditory response properties of DCN neurons in rats anesthetized with alpha chloralose-urethane. Auditory stimuli consisted of 20 ms tone bursts presented in a free field. Response properties of DCN neurons were studied before and during iontophoretic application of GABA, bicuculline methiodide (BIC) and muscimol (MUS) alone and GABA with MUS or BIC through triple barrel electrodes glued to the recording microelectrode. Of 68 DCN neurons studied, 27 were sensitive to topical application of the GABA agonists or antagonist. In these neurons, BIC enhanced spontaneous activity as well as auditory responses and decreased the Q-30 quality factor values. MUS reduced auditory responses. BIC often increased the width of the turning curve but GABA and/or MUS reduced it. Without drug application, GABA sensitive neurons tended to have longer response latencies and larger tuning widths at 30 dB above threshold as well as larger Q-30 values as compared with neurons that were insensitive to GABA. These findings suggest that: 1) GABAergic neurons determine the width of the tuning curve in neurons with GABA receptors by curtailing the excitatory response area, and 2) such neurons receive tonic inhibition from intrinsic GABAergic neurons.
We compared heart rates at the anaerobic threshold (AT) with age-adjusted heart rates in two groups of diabetics (DMY, mean age 31; and DMO, mean age 48) to ascertain whether the AT is useful for evaluating the intensity of exercise therapy for diabetics. In both the DMY and DMO groups the AT was reached at lower heart rates than in control groups of healthy subjects, indicating that the metabolism of diabetics may become anaerobic if their age-adjusted heart rate is higher than their heart rate at the AT. In this study, 86% of the DMY and 50% of the DMO group had age-adjusted heart rates, at 70% of maximum, that were higher than the heart rates at the AT. Thus, exercise intensity with an age-adjusted heart rate at 70% of maximum may induce anaerobic metabolism in some diabetics. We also studied the relationship between exercise intensity and the glycosylated hemoglobin (HbA1c) level at the AT in order to understand why the heart rate at the AT in diabetics was less than in healthy subjects. Exercise intensity at the AT in both diabetic groups was less than in healthy groups, and so did not increase the heart rates. Both exercise intensity and the heart rate at the AT were inversely related to the HbA1c level, suggesting that HbA1c may be important for keeping low the exercise intensity and the heart rate at the AT. As far as possible, we excluded cardiovascular autonomic neuropathy, so that it could not explain the mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
In patients with acute liver failure and hepatic coma, an increase in the abnormal "middle molecules" seen on the chromatograms of the sera is suspected of playing an etiologic role in the coma. A pilot study of continuous hemofiltration using a high-performance membrane was conducted in 16 such patients in an attempt to decrease the serum levels of the middle molecules. The procedure was used alternately with plasma exchange. High-performance liquid chromatography showed a notable removal of the substances in the filtrates and a sequential removal from the serum by hemofiltration. Eight (50%) of the 16 patients had amelioration in level of consciousness and were weaned successfully from hemofiltration. Although only three of the 16 patients survived the acute illness, 13 others lived an average of 15 days and five patients survived greater than 3 wk. While the continuous removal of middle molecules from the serum may not reverse liver failure, this procedure used in conjunction with plasma exchange may provide a means of life support, e.g., for patients awaiting a liver transplant.
Development of DNA diagnosis on the monocular level for patients with cleft lip and/or palate may be expected in the near future. The necessary condition for this is to confirm the heredity, elucidate the mode of inheritance and decide on the regional mapping etc. The authors tried a chromosome analysis on a pair of monozygotic twins with cleft lip and palate by using high-resolution banding techniques (about 700 bands). However, chromosome aberration was not confirmed. Therefore, the relation between this congenital anomaly and the chromosome aberration could not be confirmed. In this paper the authors discussed about this problem.
We examined the utility of the anaerobic threshold (AT) for quantifying the intensity of exercise that a diabetic patient is capable of handling. Thirteen diabetic patients treated with buformin exercised on a bicycle ergometer, and comparison was made with 20 healthy subjects matched for age and sex. The AT was determined from VO2 and VE with a personal computer. The intensity of exercise at the AT was 93 +/- 6 W in diabetic men and 80 +/- 10 W in diabetic women, values that were less than those of healthy subjects (P less than 0.05). There was a negative correlation between the intensity of exercise at the AT and the plasma concentration of buformin (P less than 0.01). There were no significant differences in either plasma lactic acid or pyruvic acid concentration at the AT between healthy subjects and diabetics. The plasma glucose at the AT or after exercise was lower than the baseline values in all subjects (P less than 0.01). The plasma insulin at the AT was lower than the baseline values in healthy subjects (P less than 0.01), but not in diabetics. There were no changes in plasma glucagon in any group. We concluded that determination of the AT is a simple, non-invasive procedure useful for ascertaining the optimal intensity of exercise for diabetics.
Laryngeal motoneurons in the nucleus ambiguous (NA) were identified antidromically by stimulation of the ipsilateral superior laryngeal nerve (S) and/or the recurrent laryngeal nerve (R). In some NA motoneurons, antidromic spikes elicited by both S and R stimulation collided with the spontaneously occurring discharges. In the same neuron, spikes evoked antidromically by stimulation of one laryngeal nerve always collided with antidromic spikes elicited by stimulation of the other laryngeal nerve. Of 105 NA neurons activated by S and R stimulation, 36 neurons satisfied the criteria, and were classified as NA neurons with branching axons (branching NA (B-NA) neurons). Those neurons activated by either S or R stimulation but not both were classified as NA neurons without branching axons (unbranched NA (UB-NA) neurons). Mean antidromic latencies of B-NA neurons were 0.79 +/- 0.20 ms to S stimulation and 1.91 +/- 0.45 ms to R stimulation and those values for UB-NA neurons were 0.84 +/- 0.17 ms to S stimulation and 2.10 +/- 0.53 ms to R stimulation respectively. None of these mean values were significantly different from one another. Conduction time in the unbranched portion of the branching axon was estimated according to the equation reported by Anderson and Yoshida. The mean conduction time for 20 B-NA neurons was 0.45 +/- 0.35 ms. The branching point in B-NA neurons was estimated on the basis of the conduction time in the unbranched stem portion and those times in two branches of a branching axon measured electrophysiologically. The results suggest that the majority of B-NA neurons bifurcate within a half axonal length.(ABSTRACT TRUNCATED AT 250 WORDS)
Pure tone burst stimulation was used to study discharge properties and tonotopic organization in the dorsal cochlear nucleus (DCN) of rats anesthetized with alpha-chloralose urethane. An animal's head was fixed with a fine nail embedded in the skull in order to prevent the head from moving. Unit discharges of DCN neurons were recorded with micropipettes filled with fast green dye. Free field pure tone bursts were presented using a ribbon tweeter; it delivered stimuli at a maximum SPL of 96 dB. Electrode tracks were reconstructed through subsequent histological examinations. A total of 429 units were sampled in 51 animals. Of these, 230 units (54%) responded to tone bursts higher than 20 kHz with a mean latency of 6.3 ms. Tonotopical organization was clearly evident throughout the mediolateral axis of the DCN; high frequencies were represented medially and low frequencies laterally. Nearly constant frequencies were represented along the dorso-ventral axis and no systematic organization was observed along the rostrocaudal extension of the DCN. When tuning curves were measured in DCN neurons with excitatory and inhibitory responses, we found that inhibitory sidebands were usually located in a frequency range higher or lower than the excitatory response area and sometimes partially overlapped with it.
We have found that endotoxemia detected by conventional LCT (limulus colorimetric test) in patients with liver diseases could not be detected by endotoxin-specific LCT at all, and proposed that this beta-glucan like activity (BGLA) should be termed as non-septic endotoxemia, distinguishing it from septic endotoxemia seen in gram-negative sepsis. In this study, we investigated non-septic endotoxemia through the clinical course of 8 cirrhotic patients. Non-septic endotoxemia appeared at the onset of DIC but tended to decline in level in the late terminal stage. This phenomenon cannot be consistent with the "spillover" theory which explains the mechanism of endotoxemia without sepsis in liver disease. We think it is an urgent problem to elucidate the nature of BGLA in liver disease, without recourse to the "spillover" theory.
We studied the characteristics of epidermal growth factor (EGF) receptors in plasma membrane fractions derived from normal and diseased human thyroid tissues. The mean maximal specific binding of EGF to membrane fractions of normal thyroid tissue (n = 25) was 1.46 +/- 0.47 (+/- SD) fmol/mg protein. The maximal specific binding was higher than the upper limit of the normal range (2.40) in 12 of the 39 (31%) differentiated carcinomas, 2 of the 3 (67%) undifferentiated carcinomas, and 1 squamous cell thyroid carcinoma. In contrast, the maximal specific binding in samples derived from adenomas (1.13 +/- 0.91), adenomatous goiters (0.92 +/- 0.56), and hyperplastic (Graves') thyroids (1.57 +/- 0.61) was not different from that in normal thyroid tissue. Scatchard plot analysis revealed that all thyroid membrane fractions had two classes of specific receptors for EGF. The mean association constant for the high affinity EGF receptors in normal thyroid tissue was 7.9 +/- 2.9 (+/- SD) X 10(9) mol/L-1, and the capacity was 22.9 +/- 7.0 fmol/mg protein. The capacity of the high affinity receptors was higher (P less than 0.05) in differentiated carcinoma (37.2 +/- 25.5) and undifferentiated carcinoma (32.7 +/- 11.6) than in normal thyroid tissue. In one squamous cell carcinoma, the capacities for the two classes of binding sites were about 15-fold greater than in normal thyroid tissue. In contrast, the association constants of the high affinity receptors from carcinomas (differentiated, 6.9 +/- 2.8; undifferentiated, 11.8 +/- 4.1; squamous cell, 8.2) were similar to that of normal thyroid tissue. In the thyroid tissues from eight patients with Graves' disease the capacity of the high affinity binding sites (37.5 +/- 12.3 fmol/mg protein) was higher than that in normal tissue, but the affinity (4.4 +/- 1.6 X 10(9) mol/L-1) was less, and the maximal specific binding was similar in the two types of tissue. These results suggest that a significant increase in the number of high affinity EGF receptors may play a role in the pathogenesis of human thyroid carcinoma.
A conventional limulus test detects not only endotoxin but also beta (1----3) glucan. Therefore, using a quantitative limulus test (the limulus colorimetric test) we studied the pharmacokinetics of lentinan, an antitumor beta (1----3) glucan, in the blood of 10 health volunteers and three patients with advanced gastric cancer. The calibration curve of lentinan in the human plasma was linear in the range of 0 to 100 ng/ml. When incubated with human plasma at 37 degrees C in vitro, lentinan had the recovery of almost 100% as compared to the initial concentration even after 60-min incubation, indicating the stability of lentinan in human plasma. When 1 mg of lentinan was intravenously administered over a 2 hr period, lentinan concentration reached the maximum levels (50-80 ng/ml) at the end of the drip infusion and decreased gradually thereafter. In the near future, the more appropriate modes of lentinan administration will be determined by further investigation of its kinetics in the human body.
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The possible role of liver parenchymal cells in the uptake and degradation of bacterial lipopolysaccharide (LPS) was investigated in vitro by employing radiolabelled LPS as substrate. Hepatocytes obtained from Wistar rats by collagenase treatment were found to take up LPS only when it was not linked to the polysaccharide of O-antigen. The amount of LPS taken up increased with time and after 48 h incubation it increased in a dose-dependent manner up to at least 30 micrograms. When incubated with LPS radiolabelled exclusively in the fatty-acid moiety, cultured hepatocytes released lipophilic materials into the culture medium. These were identified as beta-hydroxytetradecanoic acid and triglyceride, in the ratio of 7:I. These results indicate that the R-form of LPS which lacks the O-antigen polysaccharide is taken up and deacylated in hepatocytes, and the derived fatty acids are released into the culture medium either in the free form or after conversion to triglyceride.
Graft-versus-host disease (GVDH)-like syndrome occurred in a 45 year-old man with duodenal ulcer who had received a transfusion of 8 units of packed red blood cells. Clinical features included high fever, macropapular rash, hepatic dysfunction, pancytopenia and, finally, fatal septicemia. A skin biopsy obtained from the chest revealed satellite cell necrosis of epidermal cells, mononuclear cell infiltrate of the upper dermis and epidermis, and vacuolar degeneration of basal cells. Autopsy bone marrow was aplastic. The occurrence of GVHD in immunologically normal individuals following blood transfusion is extremely rare.