Journal of Nippon Medical School
Online ISSN : 1884-0108
Print ISSN : 0048-0444
ISSN-L : 0048-0444
Volume 55, Issue 1
Displaying 1-12 of 12 articles from this issue
  • Ryo Ogawa
    1988 Volume 55 Issue 1 Pages 4-12
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
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  • An ultrastractural investigation on changes in the subependymal layer of the rat fetus
    Satoru Yamaguchi
    1988 Volume 55 Issue 1 Pages 13-21
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
    To investigate the causes of the onset of newborn intraventricular hemorrhages, perplacental ischemic loads were applied and ultrastructural changes in the subependymal layer, which is assumed to be one of the most predominant site of hemorrhages were observed in rat fetuses at 17, 19 and 21 days of gestation.
    The following results were obtained :
    1) The subependymal layer of the rat fetus was not well devoloped and scanty fibrous component was discernible. Junctional complexes between the cells were incomplete and structural maturation was not well comfirmed.
    2) With respect to intracellular organelles, the cells of the subependymal layers at 17 days of gestation cotained mainly ribosomes and were undifferentiated. However, in the cells of the subependymal layer at 19 and 21 days of gestation, the number of organelles such as Golgi complexes, mitochondria and rough-surfaced endoplasmic reticulum was increased and the increase of filament was observed, suggesting differentiation and maturity had far progressed.
    3) The perplacental ischemic loads caused dilatation of the intercellular space, elongation of the cellular processes and destruction of the cytoplasm in the subependymal layer at 17 days of gestation. In the subependymal layer at 19 and 21 days of gestation, the intercellular space had dilated mainly in the pericapillary space.
    From the above mentioned findings, it was suggested that the increased capillary permeability and subsequent intercellular edema may play an important role as one of the initial pathological causative factors of the newborn intraventricular hemorrhages. It was also suggested that the structural immaturity as well as the poor development of the cell constituents, might participate in the causation of the hemorrhages.
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  • Comparison with insulin-induced hypoglycemic challenge and L-dopa test
    Fumie Takahashi
    1988 Volume 55 Issue 1 Pages 23-28
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
    An intravenous injection of human GH-releasing factor (GRF) was evaluated as a test of GH reserve in 26 healthy male subjects ranging in age between 26 and 53 years old. Results obtained were compared with those after insulin-induced hypoglycemia (ITT) and oral administration of L-dopa. After a dose of 0.5 or 2μg GRF/kg BW, the mean peak GH levels were 15.4±4.5 and 19.4±5.0 (± SE) ng/ml in healthy male subjects, respectively. Eight out of 22 healthy male subjects failed to attain GH levels exceeding 10ng/ml following 2μg GRF/kg BW. The overall plasma GH response to GRF was similar to that after L-dopa (500mg). In contrast, ITT resulted in a consistent stimulation of GH that exceeded long/ml in 22 out of 23 healthy male subjects. The mean peak GH level after ITT was 35.3±5.3 ng/ml, which was significantly higher than that after 2μg GRF/kg BW.
    Eight patients with GH deficiency due to various hypothalamic-pituitary diseases were subjected to ITT and GRF (lug/kg BW) tests. Plasma GH levels after ITT did not rise in any of the patients, while clear-cut plasma GH elevations were observed in 6 out of the 8 patients after GRF.
    GRF test has the potential disadvantages of failing to elicit GH release in healthy male subjects. However, a combination of GRF test with other traditional GH provocation tests such as ITT could add useful information on the pathophysiology of GH deficiency. An additional important finding of the present studies was that a significant divergence existed in plasma GH responses between GRF and ITT in healthy male subjects. This suggests that the stimulation of GH release following ITT is not solely mediated by endogenous GRF.
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  • Toshimitsu Oda
    1988 Volume 55 Issue 1 Pages 29-37
    Published: February 15, 1988
    Released on J-STAGE: December 04, 2009
    JOURNAL FREE ACCESS
    One hundred and thirty-eight cries of 56 infants were examined during first 14 days after birth. Crying in neonates was classified into three types of situational cry: hunger cry, discomfort cry and pain cry, and the temporal patterns of each type of cry were investigated on the basis of the parameters of cry duration and cry interval. The following results were obtained:
    1) In the case of the hunger cry, the cry duration was 0.69±0.31s, the cry interval 0.32±0.25s and the number of cries 9.3 ± 2.9 times/10s. The coefficient of cry duration variance showed the minimum value (=0.44) among the three types of cry, indicating that a constant cry duration was characteristic of the hunger cry. The coefficient of the cry interval variance (=0.79) was almost the same as that for the pain cry, but was lower than that for the discomfort cry. A rhythmical crying pattern was found in 72.7% of the cases of the hunger cry, which suggested a correlation between the hunger cry and a rhythmical crying pattern.
    2) In the discomfort cry, the cry duration was 0.82±0.62s, the cry interval 0.41±0.32s, and the number of cries 6.7±2.6 times/10s. The maximum coefficients of variance were seen for the cry duration and the cry interval, showing that this type of crying was characterized by large variations in the parameters. A rhythmical crying pattern was seen in only 19.0% of the cases of the discomfort cry.
    3) In the pain cry, the cry duration was 1.06±0.75s, the cry interval 0.39±0.92s and the number of cries 5.6±2.1 times/10s. The cry duration showed the longest value. A rhythmical crying pattern was seen in only 12.2%.
    4) The cry duration of the hunger cry gradually decreased during first 8 days after birth. The cry duration of the pain cry did not change during first 5 days after birth, but decreased during 6 to 8 days after birth. The cry duration of the discomfort cry showed no sequential changes in these periods.
    From the results, it was evident that there were characteristics in the cry durations and intervals and also were the crying patterns of neonates in accordance with the situation of them and the number of days after birth, so it was suggested that these can serve as points to distinguish when the mother hears the infant crying.
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  • Tatsuko Tastuoka
    1988 Volume 55 Issue 1 Pages 38-50
    Published: February 15, 1988
    Released on J-STAGE: March 05, 2010
    JOURNAL FREE ACCESS
    The influence of insulin on hepatocellular glycogenesis was investigated by isolating hepatocytes obtained from growing rats at several different stages and the following results were observed.
    1) The isolation of hepatocytes was performed by collagenase perfusion following a slight modification of Seglen's method. Over 80% cell viability was achieved by this method.
    2) The number of insulin molecules bound to an aliquot of hepatocytes was the highest at 15°C within the three incubating temperatures of 4, 15 and 37°C during a period of 120 minutes. Meanwhile the amount of degradation products from insulin, which was detected by the fall in molecular weight of 125I labelled insulin, was markedly increased at 37°C. This phenomenon suggested an acceleration of the interaction between the ligand and the cells dependent on a rise in temperature.
    3) The numbers of insulin receptors were 1.41±0.06, 2.48±0.30, and 3.76±0.16×105 site/cell in hepatocytes obtained from rats at 7, 14 and 21 days after birth by a 4°C measurement. However, there was no difference in receptor numbers between weaning and adult rats.
    4) The patterns of Scatchard analysis were hyperbolic in the three growth stages. There were no significant differences in binding constants of Ke (empty sites) and Kf (filled sites) by De Meyts's negative cooperative method in the three growth stages.
    5) Incorporation of 14C labelled glucose into hepatocyte glycogen was stimulated significantly by insulin in 7-day-old rat and adult rats, in contrast to the controls which were not administered insulin.
    6) The levels of insulin which maximally stimulated glycogenesis in hepatocytes were approximately 10ng/ml in the media at 37°C in every stage. When a comparison was made between the saturation phenomenon of insulin receptors and glycogenesis in the cells, only 20% of the insulin conjugated to the receptors was estimated to be a factor contributing to glycogenesis. This phenomenon suggested the concept of "spare receptors" for insulin working other than as glycogenesis on the cell membrane.
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  • Toshimichi Shibuya
    1988 Volume 55 Issue 1 Pages 51-58
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
    Protein C is a vitamin K-dependent anticoagulant plasma zymogen. In plasma protein C there is an inactive precursor, but it is converted to a serine protease called activated protein C through a catalyzing reaction of the thrombin-thrombomodulin complex.
    Protein C deficiency is known to be associated with a risk factor for thrombosis. In this paper plasma protein C levels were studied in healthy Japanese adults and patients with cerebral infarction with respect to antigenicities and biological activities. Some relationship between the level of plasma protein C and the occurrence of cerebral infarction was found. Protein C antigen was measured with enzyme-linked immuno-sorbent assay and enzymatic activity with a new amidolytic method. This amidolytic measurement was free from the influence of thrombin-a2macroglobulin complex of protein C like fraction and protein C inhibitors.
    In healthy Japanese adults, there was no significant difference in plasma protein C levels between subjects of different ages. The plasma protein C levels in patients with cerebral infarction, however, was found to be significantly lower than those in Japanese adults.
    The protein C level did not correlate with clinical courses or location of the infarction on CT-scan: no significant difference was recognized in the plasma antigen and enzymatic activity of protein C between patients with acute or subacute cerebral infarction or with lesions in the cortical or perforating arteries.
    The protein C level was significantly lower in patients with severe symptoms, at onset than in those with mild symptoms and in patients with bad clinical courses.
    It was suggested that the low level of plasma protein C has some relevance to the occurrence of cerebral infarction and, furthermore, that a low protein C level at the first attack might indicate poor prognosis with likelihood of relapse.
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  • Mineo Hanawa
    1988 Volume 55 Issue 1 Pages 59-72
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
    Progressive systemic sclerosis (P.S.S.) is one of the collagen diseases which involves not only the skins but also various organs e.g. bones, heart, lungs, gastro-intestinal tract and others. The present study was carried out for the further evaluation of the radiological changes on thirty-five patients which clinically diagnosed and histologically verified P.S.S. during the period of May, 1964 to May, 1982 at Nippon Medical School Hospitals and Chichibu Hospital. The frequency of various radiological changes in the hands, thoraces and gastro-intestinal tract were analysed and following results were obtained.
    1) Bone atrophy and narrowing of the finger joints were more frequent, which was seen in 16/33 cases (48.4%) of these patients. The absorption of turfts of the terminal phalanges was noted in 11/33 cases (33.3%). Soft tissue calcifications were seen in 8/33 cases (22.8%).
    2) Measurement of right 2nd fingertips revealed shortening of vertical length of terminal phalanges in 4/17 cases (23.5%).
    3) Bilateral diffuse fibrosis especially in the lower lung fields, with or without small cystic change, was seen in 22/35 cases (62.0%).
    4) Cardiomegaly was seen in 15/35 cases (42.8%), two of whom had pericardial effusion.
    5) An upper gastro-intestinal study demonstrated diminished peristalsis of the esophagus in 21/35 cases (60.0%). Fourteen patients had air shadows in the plain chest films termed as "air esopha-gram".
    6) The barium meal retention and dilatation in the duodenal loops was noted in 22/35 cases (62.8%).
    7) Dilatation and diminished peristalsis of the small intestine were the most frequent and occured in 25/35 cases (71.4%), these findings were more significantly noted in the jejunum than ileum. The widest diameter of the small bowel was measured and the diameter of the jejunum was over 30mm in 18/25 cases (72.0%), while in the ileum it was over 25mm in 14/25 cases (56.0%).
    In conclusion, the present results suggest that awareness of roentgenological fidings in these patients gives us greater opportunity for the correct diagnosis in everyday practice.
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  • Hiroaki Minamisawa
    1988 Volume 55 Issue 1 Pages 73-81
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
    The effects on eicosanoid levels were investigated in the stroke-resistant spontaneously hypertensive rat (SHRSR) brain and the relation of eicosanoid to the progression of cerebral edema was studied. The effects of dexamethasone, indomethacin and AA-861 on the induction of eicosanoids and cerebral edema were also studied in this model. Global cerebral ischemia was induced by occluding the bilateral common carotid arteries (BLCO) with clips. After two hours of BLCO the blood was reperfused by removing the clips. After each period of reperfusion the rat brain was used for the radioimmunoassay of eicosanoids. The time period of cerebral edema was also investigated by measuring the water content of the brain after the reperfusion. The TXB2 (stable metabolite of TXA2) was elevated significantly 5 minutes after reperfusion and the 6-keto PGF1a (stable metabolite of PGI2) was also markedly increased at the same time and returned to control levels at 15 minutes. In contrast, the LTC4, levels showed an increase at the end of BLCO and the beginning of reperfusion and reached a peak at 30 minutes. Furthermore, the high levels persisted until 60 minutes after reperfusion. Indomethacin did not fully suppress the increase of brain water content. However, dexamethasone and AA-861 completely suppressed brain water content and the production of LTC4 This fact may indicate that these compounds have the function of suppressing the ischemic cerebral edema.
    It has been previously reported that in the BLCO model the procedure can produce a sudden elevation of prostaglandins. The results of the present investigation are consistent with the previous observation. TXB2 and 6-keto PGF1a in the ischemic brain were significantly increased only 5 minutes after reperfusion and decreased in 15 minutes to almost the same level as that of 0 time. This time phase did not correspond to the time phase of cerebral edema. The 6-keto PGF1a and TXB2 concentration may correlate with platelet and vascular endothelial cell response in the early stage of reperfusion. By reperfusion of the ischemically injured tissue, LTC4 level elevated significantly and its time phase corresponded to the progression of the cerebral edema showing the induction of brain water contents during BLCO and the significant increase 30 and 60 minutes after the reperfusion. These results indicate a close relationship between LTC4 and ischemic brain edema.
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  • Yuichi Ochiai
    1988 Volume 55 Issue 1 Pages 82-88
    Published: February 15, 1988
    Released on J-STAGE: December 04, 2009
    JOURNAL FREE ACCESS
    Changes in the amount of urinal protein and β2-microglobulin (β2-MG) were observed after middle distance running in 46 primary school boys and 46 junior high school boys, aged from 6 to 14 years old.
    The running distance was varied according to their age, 800m for boys aged from 6 to 7-year-olds, 1, 200m for 8 to 9-year-olds, 1, 700m for 10 to 11-year-olds and 1, 500m for 12 to 14-year-olds.
    Urine was collected from each subject before and 30min after running, and its total urinal protein was analyzed by the Lowry method and β2-MG by the reverse passive hemaggulutination method.
    In the primary school boys at rest, total urinal protein was 16.8mg/dl and β2-MG 5.69μg/dl, while 39.3mg/dl and 133.22μg/dl, respectively, at 30min after running. In the junior high school boys at rest, they were 18.9mg/dl and 4.32μg/dl, respectively, and 78.3mg/dl and 662.98μg/dl, respectively, at 30min after running. Other urinal protein, which did not have its origin in blood plasma, was calculated before and 30min after running utilizing the results of Poortmans' research (1968), and no change was observed in the concentration before and after running. Therefore the increase in urinal protein after exercise would seem to have originated mainly from blood plasma.
    β2-MG increased not only its quantity in the urine (see above) but also its ratio in the urinal protein (7 to 80 times larger after running than before). There results indecate that permiability in the glomerulus and absorption in the proximal tubule changed as regards low molecular protein.
    By multiple regression analysis it was revealed that urinal protein at 30min after running was significantly correlated to weight, running time and concentration of urinal protein at rest of the subject. The contribution rate was from 60.02 to 74.59% in each aged group. It was found that there was a positive correlation between weight and concentration of urine protein at rest, but a negative correlation between running time and the concentration at 30min after running.
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  • Takashi Hasegawa, Shinji Nakajima
    1988 Volume 55 Issue 1 Pages 89-93
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
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  • Kuniyasu Kuki, Nozomu Takahashi, Hiroyuki Takeda, Goro Asano, Tasuku S ...
    1988 Volume 55 Issue 1 Pages 94-96
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
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  • 1988 Volume 55 Issue 1 Pages 97-104
    Published: February 15, 1988
    Released on J-STAGE: July 10, 2009
    JOURNAL FREE ACCESS
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