To examine the frequency and location of the parietal foramen, a total of 117 calvariae of 63 male, 13 female and 41 sex-unknown Japanese cadavers were studied. The results obtained were as follows.
1) Frequency of the parietal foramen
By a total number of the parietal foraminaon both sides, the calvariae were classified into five categories: type A (with a single foramen), type B (with a double foramen), type C (with three foramina), type D (with four foramina) and type E (without any foramen). Furthermore, the calvariae of types A and C were, by a number of the foramina on either side, divided into two subtypes, and those of type D into three.
The percentages of occurrence of the calvariae of types A, B, C, D and E were 26, 48, 16, 1 and 9, respectively. The calvariae of types A-2 and B-3 in which there was no foramen on the left side only was found in 17% of the whole, while those of types A-1 and B-1 where no foramen was present on the right side only occurred in 14%. The highest frequency of occurrence of the foramen in males was 48% in the case of type B-1 (a single foramen on each side), whereas that in females was 39% in the case of type A-2 (a single foramen on the right side only). The lowest frequency of occurrence of the foramen in males was, on the other hand, 7% in the cases of types B-3 (a double foramen on the right side only) and D (a double foramen on each side), while that in females was 5% in the cases of type B-3, C-1 (a single foramen on the left and a double on the right), D and E.
2) Location of the parietal foramen
For measuring, a perpendicular line to the midsagittal plane was drawn from the parietal foramen on the external surface of the calvaria, and the foot of the perpendicular was designated as a point "P". Either antero-posterior or transverse location of the parietal foramen was expressible as a percentage of the lambda-P length to the lambda-bregmatic distance or a percentage of the length of the perpendicular line to the same distance.
The parietal foramen was located antero-posteriorly at about 30%'s distance from the lambda in the case of types A-1, A-2 and B-1 in both sexes. The foramen was transversely at 5% away from the mid-sagittal plane in males, while it was 3% away from this plane in females without distinction of calvarian type.

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The effect of intracisternal (ic) injection of ovine corticotropin-releasing factor (CRF) on the development of gastric mucosal lesions induced by cold-plus-restraint stress was studied in rats. Adult male Wistar rats were fasted for 24h. Following is injection of CRF or saline, they were restrained in wire mesh and placed supine in a cold room at 4°C for 3h. After the 3-h stress, rats were killed by decapitation. Gastric mucosa was exposed and mucosal lesions were assessed. This regimen consistently produced mucosal lesions in control rats. Ic injection of 15 μg CRF significantly inhibited the development of gastric mucosal lesions, while the effect was not reproduced by intraperitoneal injection of 45μg CRF. Ic injection of 5μg somatostatin-28 (SS-28) alone did not influence the development of gastric mucosal lesions in this model. When SS-28 was coadministered with CRF centrally, the cytoprotective effect of CRF in this model was completely abolished. The development of gastric mucosal lesions following the stress was prevented by the prior administration of chlorisondamine, a ganglion blocker or atropine, an antagonist of muscarinic cholinergic receptor, but it was not affected by the injection of phenoxybenzamine, an α-adrenergic blocker. When cold-plus-restraint rats were pretreated with indomethacin, an inhibitor of prostaglandin synthesis, the cytoprotective effect of centrally administered CRF was abolished.
The results show that centrally administered CRF exerted a cytoprotective effect on stress-induced gastric mucosal lesions and the effect was counteracted by somatostatin-28. The action of CRF appears to be mediated centrally by inhibiting the activity of muscarinic cholinergic fibers, while locally, it requires intact prostaglandin synthesis.

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Arachidonic acid (AA) is a potent stimulator of platelet aggregation and is known to induce endothelial cell damage and edema in the brain. An ischemic cerebral infarction model can be produced in rats by an internal carotid injection of AA. In this study, water content, ATP and lactate in the brain and plasma prostaglandins (thromboxane B₂; TXB₂ and 6-keto-prostaglandin F₁α; 6-keto-PGF₁α) were measured and histological observations were made after an internal carotid injection of AA in two strains of rats: stroke-resistant spontaneously hypertensive rat (SHRSR) and normotensive Wistar-Kyoto (WKY) rats. It is known that the blood pressure of the SHRSR begins to rise at about 8 weeks old.
Throughout the study, AA was administered into the internal carotid artery under 2% fluothane anesthesia. In the first study, AA (1.7 mg/kg BW) was administered to 8-and 16-week-old rats and the length of survival was observed. In the second study, water content, ATP and lactate in the brain and plasma TXB₂ and 6-keto-PGF₁α were measured 3 hours after AA (0.85 mg/kg BW) administration. In the third study, rats were perfusion-fixed 3 hours after the AA (1.7 mg/kg BW) injection and cerebral arteries were observed by scanning (SEM) and transmission electron microscope (TEM).
During the 6 hour observation period, there was no difference between the two groups in the number of 8-week-old rats which survived. However, the figure became significantly lower in the SHRSR at 16 weeks old. The water content in the bilateral cerebral hemispheres was significantly larger in the SHRSR than in the WKY rats. The ATP content of the region was significantly less in the SHRSR than in the WKY rats. The lactate content in the frontal region was significantly larger in the SHRSR than in the WKY rats, but there were no differences between the two strains in the occipital region. Prior to AA administration, there were no differences in plasma TXB₂ and 6-keto-PGF₁α levels of the two strains. After the AA injection, the magnitude of plasma prostaglandin elevations was significantly larger in the SHRSR than in the WKY rats. Upon SEM examination, the luminal surfaces of the middle cerebral arteries and intracerebral arterioles revealed endothelial damage and thrombi formations were more prevalent in the SHRSR than in the WKY rats. TEM observations of the cerebral cortex revealed that the extent of perivascular edema and diffusely destroyed luminal unit membrane of the capillary endothelium were more severe in the SHRSR than in the WKY rats.
These results show that the AA metabolism and the responses to injected AA in platelets and cerebrovascular endothelial cells differ between SHRSR and WKY rats. These differences may contribute to severity of cerebral ischemia in SHRSR. The development of hypertension in SHRSR may be related to the differences in the AA metabolism of the two strains.

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The present study was undertaken to compare hemodynamic status during ventricular pacing at different sites. Ten mongrel dogs were used. By epicardial mapping the point of an early breakthrough was determined on each of the body surface areas corresponding to the left and right ventricles place with bipolar pacing electrodes. Then measurements of hemodynamic parameters and epicardial mapping were done during left ventricular pacing, during right ventricular pacing and during biventricular pacing. The pattern of epicardial mapping varied with different pacing sites and was invariably different from that of the sinus rhythm. The time required for spread of epicardial excitation was remarkably longer during ventricular pacing than during the sinus rhythm and did not become noticeably shorter during the biventricular pacing than during the left ventricular pacing. As for hemodynamic parameters, a significantly higher max dp/dt value for the left ventricule was obtained during the left ventricular pacing than during the right ventricular pacing, with differences between the pacing sites being noticeably significantt in this respect. In terms of hemodynamics, the left ventricular pacing was found to be better than the right ventricular pacing and virtually equivalent to biventricular pacing.

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In order to elucidate the structure and function of the mitochondrial genome from comparative aspects, the author cloned the entire sequence (17.6 Kb) of the mitochondrial genome of Rana catesbeiana and determined the nucleotide sequences of the URF2 gene and of its flanking genes. The results obtained in the present study are as follows:
1) The Rana catesbeiana URF2 gene contains 1, 033 bases, and, as deduced from its nucleotide sequence, the URF2 protein consists of 344 amino acids with a molecular weight of 37, 561.
2) The URF2 gene is flanked on the 5' side by the tRNA genes for isoleucine, glutamine and methionine and on the 3' side by those for tryptophan and alanine. These genes are identical in their organization to those in the mammalian and Xenopus laevis mitochondrial genomes.
3) A comparison of the putative amino acid sequences of the URF2 proteins of different animal species reveals that six regions in the sequence are well conserved during evolution, suggesting that some of these conserved sequences are crucial for biological activity of the URF2 protein.
4) The nucleotide sequences of the five tRNA genes, tRNA^Ile, tRNAG^Gln, tRNA^Met, tRNAT^Trp and tRNA^Ala exhibit homologies between 55-85% with the mammalian and Xenopus laevis counterparts.

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The rat brain in acute hepatic failure induced by D-galactosamine hydrochloride was examined by a enzyme histochemical techniques. The Na-K-ATPase was assayed by a biochemical method. From an electron microscopic observation of hepatic encephalopathy, the brains showed an intracellular edema in the blood-brain barrier associated with a hydropic swelling of astrocytic foot process and increased pinocytotic vesicles in the capillary endothelium. The impairment of Na-K-ATPase and Mg-ATPase were histochemically demonstrated in the cytoplasmic membrane of capillary endothelium and astrocyte. The total ATPase and Na-K-ATPase ratio decreased in brain assay. A change in vascular permeability was revealed in the increasing number of HRP containing pinocytotic vesicles in the capillary endothelium.
These results suggest that in hepatic encephalopathy various toxic substances accumulate in the brain tissue with the functional disturbance of a membrane enzyme as Na-K-ATPase, contributing to the enhancement of cytotoxic edema.

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The spinocerebellar tract neurons and their fibers were observed throughout the spinal cord and lower medulla in the Wistar rat following injections of horseradish peroxidase (HRP) into the cerebellum.
The fiber course before reaching into the periphery of the lateral funiculus was classified into three types. Type I fibers crossed contralaterally through the anterior white commissure, and then ascended obliquely in the periphery of the anterior funiculus to reach into the periphery of the lateral funiculus. These fibers mainly originated from Co-L6 (neurons in laminae V, VII, ventrolateral part of the ventral horn), L3-Tll (lamina VII neurons, spinal border cells) and C3-C1 (central cervical nucleus neurons). The fibers in Co-L6 and L3-Tll ascended obliquely for 2-4 segments to reach into the periphery of the lateral funiculus, while the fibers in C3-C1 ascended obliquely for 1-2 segments. Type II fibers entered the ipsilateral lateral funiculus through the dorsal part of the intermediate substance, and ascended obliquely for 2-9 segments in the medial part of the lateral funiculus to reach into the periphery of the lateral funiculus. The fibers of this type arose mainly from L2-T1 (neurons in lamina V, Clarke's column). Thpe III fibers entered the ipsilateral lateral funiculus from the lateral corner of the anterior horn, and ascended obliquely for 2-4 segments to reach into the periphery of the lateral funiculus. The fibers of this type mainly occurred in T3-C5 (lamina VII neurons).
After reaching into the periphery of the lateral funiculus, the majority of type I fibers ascended in the ventral half of the periphery of the lateral funiculus, but the minority migrated dorsalward and ascended in the dorsal half. In the periphery of the lateral funiculus, most of type II fibers ascended in the dorsal half, but some of them ascended in the posterior part of the ventral half. Type III fibers ascended in the ventral half of the periphery of the lateral funiculus.
There is a classical conception that the ventral spinocerebellar tract and dorsal spinocerebellar tract ascend through the ventral half of the lateral funiculus and through the dorsal half of it, respectively. The present results indicate that this should be modified.

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Twenty one cases with chronic bronchitis by the habitual smoking were forced to quit the habitus. The clinical effects of the cessation were estimated by bronchoscopic, pathologic and symptomatic analyses. Results obtained were as follows,
1) After abstaning from smoking, subjective symptoms were improved in 76% of the cases. The bronchoscopic findings showed decrease in both the redness and the swelling with redness, and the normal appearances increased remarkably. Also 19% of the cases showed an improvement of pathological changes of bronchial mucosa.Therefore, the abstinence from smoking in the patients with chronic bronchitis was an effective remedy for the improvement of clinical symptoms and bronchial mucosal pathology.
2) Eleven to 30 weeks after the abstienence of smoking, about 80% of the cases were found to be improved in clinical symptoms and bronchoscopic findings. However, from the stand point of pathological views, a longer period of time would be needed for the improvement of the bronchial mucosa.
3) On the patients with chronic bronchitis under 40 years old or under 400 Brinkman index the effects of smoking cessation was relatively poor. This fact showed that in this group the other factors would played a part in an outbreak of chronic bronchitis.
4) It was not obvious in the present study that the effect of smoking cessation had any correlation with the grade of Brinkman index. This was presumably due to the fact that in the patients on whom habitual smoking caused chronic bronchitis, the changes of bronchial mucosa would be reversible in many cases even with a high Brinkman index.
5) By means of the fractional analysis of broncho-alveolar lavage on chronic bronchitis, a remarkable increase of bronchial epitherial cells could be observed in the First FBAL (FBAL-I) fluid, as well as neutrophilic cells in the Third FBAL (FBAL-III) fluid. These cells decreased after the smoking cessation.

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A new endoscopic spraying technique has been developed to control hemorrhage from the upper gastrointestinal tract by evaluating the efficacy of various blood clotting factors and by improving the spraying device. The results are follows:
1) Aprotinin, a proteolytic enzyme, inhibited fibrinolytic action of fresh gastric juice on fibrin clot in vitro. In a dog model of acute gastric bleeding, a significant reduction in bleeding time was accomplished by spraying thrombin together with fibrinogen or cryoprecipitate as compared to thrombin alone.
2) Fibrinogen dissolved in saline and thrombin dissolved in saline containing Aprotinin solution, were simultaneously sprayed under direct vision through the lumens of the 4-lumen tube placed in the biopsy channel of a fiberoptic endoscope. Hemostasis was successful in 38 of 43 patients, or 88%, showing upper gastrointestinal bleeding. The spraying technique following local injection of ethanol resulted in hemostasis in all or 8 patients with severe arterial bleeding from gastric ulcer.

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The effects of disopyramide on insulin secretion were studied by perfusing the isolated rat pancreas in situ. In experiments carried out using Krebs-Ringer bicarbonate buffer containing 0.1% glucose (0.1% glucose buffer), the immunoreactive insulin (IRI) levels in the perfusate did not change after the administration of disopyramide (300μg/0.1 ml, i.c.a.). When Krebs-Ringer bicarbonate buffer containing 0.3% glucose (0.3% glucose buffer) was substituted, IRI levels increased significantly after the disopyramide administration. The disopyramide-induced IRI rise was not affected by pretreatment with propranolol, phentolamine or atropine. The increase of insulin secretion induced by increasing glucose concentration from 0.1% to 0.3% in the perfusion fluid was suppressed by disopyramide. The suppressing action of disopyramide on glucosestimulated insulin secretion was partially recovered after pretreatment with propranolol or phentolamine. Results show that disopyramide acts both as a stimulator and an inhibitor of insulin secretion.

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