The incidence, type and degree of acid-base disturbance were studied in patients with compensated liver cirrhosis and chronic hepatitis. Metabolic acidosis was found in 12 out of 25 patients with liver cirrhosis and 13 out of 25 patients with chronic hepatitis. Respiratory alkalosis was found in 3 out of 25 patients with liver cirrhosis. PaCO₂ was decreased in 6 out of 12 patients with liver cirrhosis and 4 out of 13 patients with chronic hepatitis who manifested as metabolic acidosis. Blood lactate levels were not so high as to explain metabolic acidosis in patients with compensated liver cirrhosis and chronic hepatitis. Metabolic acidosis in liver cirrhosis was hyperchloremic, while metabolic acidosis associated with chronic hepatitis was not hyperchloremic but high anion gap. In addition, incomplete renal tubular acidosis was found in 5 out of 9 patients with liver cirrhosis and 3 out of 10 patients with chronic hepatitis.
The results suggest that metabolic acidosis observed in patients with compensated liver cirrhosis appeared to be resulted from abnormalities in the regulation of hydrogen ions and electrolytes in renal tubules. In contrast, majority of metabolic acidosis associated with chronic hepatitis is due to an accumulation of unknown anions other than lactate.

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No electron microscopic research in the neural arch of the pedicle side, (i.e. the remnant laminae of the pedicle side), in patients with spondylolysis has previously been reported.
The purpose of this investigation is to elucidate the electron microscopic findings in parts of the defected neural arch compared with the findings of pseudoarthrosis of the tubular bone.
Results:
1) Macroscopically, the pedicle in the patient with spondylolysis was smaller than that of a normal subject, which was statistically significant (P. 0.005). The isthmus showed a tendency to taper in both the remnant and the mobile laminae.
2) In the conventional light microscopic specimens of spondylolysis obtained from both sides of the neural defected parts, three layers were identified; the fibrous connective tissue (Defective zone: D zone), the fibrocartilagenous tissue (Junctional zone: J zone), and the osseus tissue (Bony zone: B zone). No bone formation was shown in the D zone and fibrocartilagenous tissues were present in the J zone. Atrophied bone trabecula, an enlarged bone marrow canal, sclerotic change of the epiphysis, fibrous tissue and decreased fat tissue in the bone marrow were shown in the B zone.
3) Under electron microscopic examination, the D zone of the mobile laminae showed sparsely distributed fibrous cells and a threedimensional crossing of fibrous bundle, formed by normal collagenous fibrils having 640Å periodicity.
4) In the J zone of the mobile laminae, the scattered cartilagelike cells were shown in the dense collagenous tissue. The cell was a different shape from the normal cartilage cell. These cells with many cytoplasmic processes possessed the PAM positive immature collagenous fibrils in lacunar space and released matrix vesicle-like bodies around the cell.
5) Osteocytic cells and fascicular dense collagenous tissue, corresponding to the laminar structure, were found in the B zone of the mobile laminae.
6) Electron microscopic findings of D, J and B zones of the remnant laminae reveal identical pattern in the mobile laminae.
7) Pseudoarthrosis, macroscopically resembling the spondylolytic isthmus, consisted of D, J and B zones under a light microscope. Although the J zone was irregular in arrangement, osteosclerosis and bone marrow alterations were relatively slight.
8) Under electron microscopic observation of pseudoarthrosis, no outspoken findings were revealed in D and B zones. In the J zone, the following differences were seen in comparison with that of spondylolytic isthmus; (1) relatively narrowed lacunar space, (2) lack of immature collagenous fibrils, seen in lacunar space of spondylolysis, (3) presence of abundant micro filaments within the cytoplasm, (4) marked developed r-ER, (5) relatively increased cytoplasmic processes, (6) absence of a matrix vesicle-like body in the collagenous tissue, markedthickened collagenous fibrils, measuring up to 2, 000 to 2, 300 A in diameter in the collagenous tissue.
9) Based on the above observations, no significant differences between the mobile laminae and the remnant laminae of the pedicle side were obtained either microscopically or under light and electron microscopes. The morphology of matrix and cellular components showed distinct difference between the spondylolytic isthmus and pseudoarthrosis. In conclusion, it was assumed that spondylolysis is an interruption of the continuity of the isthmus in the neural arch with osseus dysplasia, and this might be exerted by a dynamic force during the development of the spinal curvature.

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Adenosine 3′, 5′-monophosphate (cyclic-AMP) level in Vero-S cell line, which was derived from Vero cell line by 20 passages of colonies developed in soft agar, did not definitely change (5.3.7.2pM/mg protein) even after the monolayer became confluency. In contrast, cyclic-AMP level in Vero cell line doubled after the monolayer became confluency. After infection of measles virus, cyclic-AMP in Vero-S cells slightly increased (10.2-13.5 pM/mg protein) until the maximum virus replication and development of the CPE (cytopathic effect), but decreased (7.4.9.7pM/mg protein) thereafter. Multiplication of Vero cells was partially inhibited with 1.10mM and completely with 100mM exogeneous cyclic AMP. But 100mM exogeneous cyclic-AMP did not morphologically affect after monolayer of Vero cells became confluency. Five to 10mM exogeneous cyclic-AMP added at the time of infection decreased the 48 hr-virus yield of measles virus in infected Vero-S cells. In a persistently infected Vero cell line with measles virus, 448-PI-Vero, cells multiplied until 8 days after passage, and infective virus increased sharply until 4 days but slightly thereafter. Cyclic AMP levels in the 448-PI-Vero continued without definite change (8.3.9.5pM/mg protein) through 16 days after passage, but did not decrease as the infected Vero-S cells. Virus yield from 448-PI-Vero decreased with 10mM exogeneous cyclic AMP after 72hr of adding the drug.
From these results, it is apparent that intracellular cyclic-AMP level does not decrease with the production of virus in the persistently infected cells, and inhibition of virus growth with exogeneous cyclic-AMP takes a time lag for the expression; the mechanism which maintains the persistent infection of 448-PI-Vero was related with cyclic-AMP.

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Brazelton's neonatal behavioral assessment scales are useful in evaluating the development of various types of behavior which can not be assessed by ordinary neurologic examinations. However, the scales, 27 in all, are too complicated to be used in daily clinical practices. Furthermore, some of the scales are not applicable to the neonates within 7 days after birth. In the present investigation, the clinical usefulness of each scale was examined by applying it to 80 full-term appropriate-for-dates infants (AFD), 11 heavy-for-dates infants (HFD) and 21 light-for-dates infants (LFD) within 7 days after birth. The following results were obtained:
1) As far as the neonates within 7 days after birth were concerned, the following scales and scores were sufficient to evaluate the development of their behavior.
Scale 4 (response decrement to pinprick), scores 2-4
Scale 5 (orientation, inanimate, visual), scores 1-6
Scale 6 (orientation, inanimate, auditory), scores 1-6
Scale 7 (orientation, animate, visual), scores 1-5
Scale 8 (orientation, animate, auditory), scores 1-6
Scale 9 (orientation, animate, visual & auditory), scores 1-6
Scale 11 (general tonus), scores 2-6
Scale 13 (pull to sit), scores 1-6
Scale 14 (cuddliness), scores 2-7
Scale 15 (diffuse movements), scores 3-8
Scale 16 (consolability with intervention), scores 3-8
Scale 20 (activity), scores 2-7
Scale 22 (amount of startle), scores 2-6
Scale 24 (lability of states), scores 1-6
2) Scales 16-20, 23-25 (characteristics of the neonate) were related neither to the gestational ages, nor to the neonatal weights (i. e., AFD, HFD, LFD). Consequently, these scales were of little clinical value.
3) Compared with AFD and HFD, LFD showed poor scores in scales 1, 11 and 15.

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Although there have been numerous articles concerning the anatomy of the atrioventricular valve in man, only a few publications have recorded the relationship between the chordae tendineae and the papillary muscles. The purpose of this paper is to study the relationship among the shape and size of the atrioventricular valve, the chordae tendineae and the papillary muscles. 50 subjects, as listed in Table 1, were analyzed by the Taniya-Hashimoto Method.
The results obtained were as follows:
1) The right atrioventricular valve was classified into two types: 33 cases (66%) of three irregularly shaped cusps, i. e. type I, and 17 cases (34%) of four or five cusps, i. e. type II.
2) The average circumference of the right atrioventricular orifice (ostium atrioventriculare dextrum) was 11.96cm (9.63.15.06cm) in type I and 12.19cm (9.52.15.22cm) in type H. There existed no significant difference in the circumference of the atrioventricular orifice between type I and II.
3) The average length of the cusp-fundus (the length of the fixed margin of the cusp) was as follows:
type I: anterior cusp…………4.13cm (2.03-6.96cm)
posterior cusp…………3.62cm (1.21-5.44cm)
septalcusp……………4.21cm (3.11-6.08cm)
type II: anterior cusp…………4.10cm (2.68-5.42cm)
posterior cusp…………3.67cm (0.94-5.70cm)
septal cusp……………4.43cm (2.96-6.53cm)
4) The average width of the cusp (the maximum distance between the apex and the fundus of the cusp) was as follows:
type I: anterior cusp…………1.86cm (1.26-2.29cm)
posterior cusp…………1.62cm (0.62-2.94cm)
septal cusp……………1.76cm (1.15-2.72 cm)
type II: anterior cusp…………1.92cm (1.40-2.34cm)
posterior cusp…………1.72cm (0.94-2.42cm)
septal cusp……………1.84cm (1.14-2.53cm)
The length or width of the cusp in type I was similar to that in type II.
5) The papillary muscles consisted of five groups, which were named the anterior, postlateral, postmedial, postseptal and septal muscles. The average number of the papillary muscles per right ventricle was 5.7 (2.0.9.0). The chordae tendineae from the anterior papillarymuscles were attached to the anterior and posterior cusps and those from the postlateral and postmedial muscles were attached to the posterior and septal cusps. The chordae tendineae from the postseptal muscles were linked only to the septal cusp and those from the septal muscles were connected to the septal and anterior cusps.
6) The average number of the stems of the chordae tendineae from the papillary muscles were as follows:
From the anterior papillary muscles………7.2 (2.0-14.0)
the postlateral papillary muscles……3.5 (1.0-8.0)
the postmedial papillary muscles……4.0 (1.0-8.0) the postseptal papillary muscles……4.5 (1.0-13.0) the septal papillary muscles………5.7 (2.0-12.0)
The average n umber of the stems of the chordae tendineae per right ventricle was 24.4 (16.0-35.0).
7) The tip of the chordae tendineae are attached to the fixed margin of the valve cusp, i. e. type A, to the ventricular surface, i. e. type B and to the free margin, i. e. type C. The average number of them were 23.4 (14.0-32.0) in type A, 19.2 (4.0-37.0) in type B and 68.1 (31.0-105.0) in type C. The average number of the apexes of the chordae tendineae per right ventricle was 110.7 (53.0-166.0).
8) The average number of the chordae tendineae for the anterior cusp was 34.9 (12.0-64.0), for the posterior cusp 30.5 (5.0-65.0) and for the septal cusp 45.3 (23.0-68.0).

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caused by small fetus resulting from small maternal body of reasons unknown mostly have satisfactory courses after birth. On the other hand, fetal malnutrition often causes fetal distress and the post-natal prognosis is sometimes unfavorable.
Therefore, in the case of IUGR, it is necessary to judge correctly whether the fetus is in a state of well being or latent fetal distress.
In this study, fetal reserve is examined by means of fetal function testing constituted of fetal response to tone stimulation and by fetal placental function tests including the quantitative determination of urinary estriol, serum Cystine aminopeptidase (CAP), Leucine aminopeptidase (LAP), Heat-stable alkaline phosphatase (HSAP) activities in subjects whose newborns are light for dates after birth.
1) Two hundred and seventy subjects light for dates after birth could be classified as follows: Fetal malnutrition, 181cases (67.04%); fetal hypoplasia, 15 cases (5.56%); uncertain, 68 cases (25.19%); maternal predisposition, 6 cases (2.22%).
2) Fetal response to tone stimulation, maternal urinary estriol, maternal serum CAP, LAP, and HSAP levels were all lower in the subjects than in controls where the course of pregnancy was normal.
3) In the IUGR group, many subjects with fetal malnutrition showed lower values in fetal response to tone stimulation, maternal urinary estriol maternal serum CAP, LAP, and HSAP activities in comparison with others.
4) Fetal response to tone stimulation may not adequately indicate fetal reserve, since the result is sometimes negative even in a normal course of pregnancy during pre-term (less than 37 weeks). However, when the result is positive, this test is very reliable for demonstrating satisfactory fetal reserve.
5) The results of the examinations including fetal response to tone stimulation, maternal urinary estriol, and maternal serum CAP, LAP, and HSAP activities showed lower valves in subjects with toxemia of pregnancy, especially in severe cases, and this tendency was more remarkable in the subjects whose newborns were light for dates after birth.
If IUGR of high-risk pregnancy is clinically suspected, the appropriate consideration of the high frequency of unfavourable prognosis or clinical course, the fetal respons to tone stimulation, maternal urinary estriol, maternal serum CAP, LAP, and HSAP activities test are necessary in view point of evaluating the fetal reserve capacity.

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Although children with congenital heart diseases have been found to have impaired carbohydrate metabolism. Insulin release response of children with congenital heart diseases has not been considered in relation to such factors as age, hypoxemia, and the states of the patients before and after cardiac surgery.
In order to clarify these points, the determination of plasma glucose (BS), immunoreactive insulin (IRI), JIRI/MBS (30 minutes value) after oral glucose tolerance tests were carried out in 83 patients with congenital heart diseases (3 years<; 55 patients, 4 years>; 28 patients) including 13 patients who had received cardiac surgery.
Suppression of insulin release was revealed in children of less than 3 years of age with and without cyanosis, especially in those with congestive heart failure or increased pulmonary flow. In the cyanotic group, the lower the oxygen saturation level the more depressed was the insulin release. Insulin release after cardiac surgery increased to the normal levels. However, patients with severe congenital heart diseases, and/or incomplete cardiac repair exhibited a lesser improvement in insulin release response.
These finding led us to the following conclusions:
Small age, increased pulmonaly flow, congestive heart failure, and cyanosis may be important factors contributing to the suppression of insulin release.
Hypoxemia may suppress the function of B-cell in the pancreas. There may be the clearance of insulin by the lung. The children with severe congenital heart diseases and/or incomplete repair after cardiac surgery may continue to have poorly functioning B-cell in the pancreas.

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The effect of uremic toxin on activities of pyruvate kinase, transaldolase and glucose-6-phosphate dehydrogenase (G-6-PDH) in the nerve strain cells was studied. Blood samples were collected from 8 patients with uremic neuropathy. They were collected prior to and 3 months after hemodialysis, that had been performed 3 times a week. Control specimens were obtained from healthy subjects serum samples. Serum was separated and dialysed against water individually. Subsequently, 5 ml of dialysate was subjected to gel filtrations using sephadex G-15 column (size : 0.5x 95 cm). Effluents were divided into 3 fractions according to daltons: small below 500, middle 1, 000, -4, 500 and large 2, 000-. 5, 000. Each fraction was lyophylyzed and kept under refrigeration until it was used. Monolayer culture of nerve strain cells obtained from human neurinoma was incubated in medium TC 199 under the presence of various serum fractions. Neurotoxic activities of serum fractions were tested in vitro by measuring activities of pyruvate kinase, transaldolase and G-6-PDH in nerve strain cells. Pyruvate kinase, transaldolase and G-6-PDH in cell homogenates were measured by using Shimazu UV-210 self-registering spectrophotometer. Small and large molecular fractions obtained from uremic subjects did not alter enzyme activities as compared to controls. However, middle molecular fractions collected from uremic subjects inhibited significantly enzyme activities as compared to controls.
In additional study, experimental renal failure was produced in 10 wistar rats by ligating bilateral ureter. The sham operated rats were served as control. Forty eight hours after, they were sacrificed by decapitation and the activities of pyruvate kinase, transaldolase, G-6-PDH and LDH in brain tissue excluding cerebellum were measured. However, there observed no differences in brain enzyme activities between control and experimental rats.
Results suggest the following : (1) there exist substances in uremic serum that inhibit activities of enzymes within nerve strain cells obtained from human neurinoma. These enzymes are considered to play important roles to maintain integrity of activities of neuronal cells. (2) Gel filtration study showed that such substances were eluted corresponding to 1, 000.1, 500 dalton.
In conclusion, monolayer culture of nerve strain cells obtained from human neurinoma could offer a useful to elucidate chemical identities of uremic toxins that act neurotoxic.

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Many histopathological studies on the pathogenesis of the cerebrovascular lesions have been made from the aspects of the angiopathy in intracerebral vessels, particularly at basal ganglia, but no systemic histopathological researches in pial vessels located in the peripheral area of the cerebrovascular trees have been documented.
In this communication, the author has made an observation of the angiosclerotic changes of pial vessels induced in cerebrovascular diseases and made the investigation of thevarious degrees of the cerebrovascular disorder which might proceed to the cerebral apoplectic attacks.
In the first part of the present study, the angiosclerotic changes of small and middle sized pial arteries (50.300 micron in diameter), arterioles (under 50 micron in diameter) and veins and also vessels at basal ganglia were observed light microscopically in 37 cerebral hemorrhage and 14 cerebral infarction autopsy cases. Moreover, 10 autopsy cases with hypertension and 14 cases without hypertension, in which no evident macroscopical cerebral lesions had been noticed (except 5 year-old girl case with traumatic epidural hematoma in non-hypertension group), were observed in the same manner as the control groups.
The results obtained from the light microscopical investigations of those autopsy cases were as follows: In the almost cases of cerebral hemorrhages and cerebral infarctions, remarkable perivascular fibrosis of pial arteries by the increase of collagen fibers was found which was not related to the medial and endothelial sclerotic changes. The same perivascular fibrosis was found also in hypertension group as well as in the cases with the possible occurrence of cerebral circulatory derangement without hypertension.
In the second part, the author paid special attention to the perivascular fibrosis of pial arteries and made the experimental pathological investigations using spontaneously hypertensive rats (SHR) for the purpose of clarifying the pathogenesis and the significance of the perivascular fibrosis. Fifteen SHR rats with confirmation of the persisting systolic hypertension over 180 mmHg and ten normotensive Wistar-Kyoto rats as the controls were used. Some of those SHR were fedvascular wall of SHR was substantiated by the visualization of the electron tracing peroxidase and the perivascular fibrosis of pial arteries in SHR was observed accompanied by the perivascular edema. Conclusively, the author is inclined to believe that in the cerebrovascular diseases extensive recurrent cerebrovascular disorder may proceed to the cerebral apoplectic attacks. This may be correlated with the perivascular fibrosis of pial arteries and the pathologic importance of this finding was fully augmented in this communication with 1% saline solution for six to eight weeks. The changes of their intracerebral and pial vessels were observed mainly electron microscopically. Moreover, vascular permeability clearance study was performed using horseradish peroxidase as the electron microscopic tracer.
The results obtained from the electron microscopical investigations of SHR and Wistar-Kyoto rats were as follows: In comparison with the control group, the increased permeability in the vascular wall of SHR was substantiated by the visualization of the electron tracing peroxidase and the perivascular fibrosis of pial arteries in SHR was observed accompanied by the perivascular edema.
Conclusively, the author is inclined to believe that in the cerebrovascular diseases extensive recurrent cerebrovascular disorder may proceed to the cerebral apoplectic attacks. This may be correlated with the perivascular fibrosis of pial arteries and the pathologic importance of this finding was fully augmented in this communication.

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