The epidural space lies between the dural tube and the inside wall of the spinal canal. It contains fibrous tissues which adhere snugly to both walls filling the dead space between them. In the space, there are a large number of venous vessels anteriorly, a little fat tissue posterioly and nerve roots laterally.
The space can be examined clinically by a peridurographic technique in which the epidural space is filled with an iodine contrast medium. In patients with lumbar intervertebral disc herniation (IDH), this examination is useful to determine the location of the prolapsed nucleus pulposus and the pathological adherent condition by the filling defect of contrast medium. For the purpose of determining the pathology of the prolapsed nucleus pulposus, peridurographic examinations were performed on 40 patients with IDH and the following results were obtained:
1) The existence and location of the IDH were shown by the peridurograms.
2) Adhesion around the involved and uninvolved nerve roots was shown in proportion to clinical symptoms.

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Among 78 carefully diagnosed dementia of Alzheimer type (DAT) patients, periodic synchronous discharges (PSD) on electroencephalograms (EEGs) were obserbed in 12 advanced cases. Although several case studies have been made since 1970, it is not widely recognized that PSD can be observed in advanced DAT patients. In this study the clinical picture, the nature of PSD, background activity of EEGs and 2 autopsied cases have been clinicopathologically investigated.
The mean duration of the disease in the 12 cases was 6.7 years. The mean age of onset of the disease was 67 years of age. Among the 12 cases, 9 patients presented akinetic mutism or symptoms closely resembling akinetic mutism, who were completely bed-ridden with their extremities fixed in flexion. The other 3 patients were severely demented. They presented various degrees of Parkinsonian syndromes or paratonic rigidity accompanied by some infection and general fatigue. In one of these 3 patients, PSD were observed during the transient apallic state and the PSD themselves were also transient.
The basic rhythm in EEGs were 4-6 c/s: middle amplitude theta waves dominant with delta waves on frontal leads. Triphasic delta, theta and sharp waves of PSD were dominant on centro-parieto-occipital leads. Background activity was not suppressed differing from that of Creutzfeld Jacob disease (CJD). According to the interval histograms of PSD, the majority presented an interval of 1-2 s (1.5 s mean) with some lability which was relatively slower than that of CJD. Fronto-parieto-occipital delay was not observed. By 1 c/s photic stimulation, PSD was not driven. From the stand point of the ordinary course of EEG change, which can be seen as the clinical stage of DAT advances, the EEGs of these 12 cases were situated on the so called subcortical slow wave stage or on the transitional stage between the cortical slow wave stage and the subcortical slow wave stage.
Form the above results, it was assumed that the etiology of PSD does not depend on the rapidity of clinical progress itself but on spread of lesion to the subcortical area in addition to the primary cortical lesion.
The clinicopathological evaluation of the 2 autopsied cases, sponginess and gliosis of cortical gray matter, and severe gliosis of subcortical white and gray matter were marked changes as the most case studies point out. In one of the cases, diffuse cortical Lewy bodies were observed. According to this case and the case which presented transient PSD, it seems that some functional change contribute to the etiology of PSD. With more careful and detailed examination of EEGs of advanced DAT, cases that present PSD are likely to be found.

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Thirty-four primary lung cancers were analyzed for abnormalities in the myc family geners (c-myc, N-myc, L-myc), using the Southern blot hybridization method. They were subcutaneously transplanted into nude mice. The Southern blot analysis showed that c-myc and L-myc genes were amplified in 4 non-small cell carcinomas and 3 small cell carcinomas respectively. Allelic deletion of the L-myc gene was observed in 7 cancers, including 2 carcinomas which also had an additional band of the c-myc gene or amplification of the L-myc gene. No abnormalities in the N-myc gene were observed in this study. Of 13 cancers with abnormalities in the myc family genes, 11 including all tumors with myc gene amplification were transplantable to nude mice. Of 21 tumors without any abnormalities in the myc family genes, however, only 6 were transplantable to nude mice (p<0.005). These results indicate that abnormalities in the myc family genes, especially gene amplification might promote tumor-forming capacity in xenotransplantation of lung cancers and this phenomenon might be closely related to the function of the myc gene.

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The author has performed study on the histogenesis of the nevus cells in the nevocellular nevi. In the study, specimens of the intradermal nevi in 124 cases were evaluated histologically and immunohistochemically and the following results were obtained:
1) Findings of hematoxylin eosin staining
It was observed that three types of cells, including type A cells (epidermoid type cells), type B cells lymphoid type cells), type C cells (neuroid type cells) were found to run through an intermediate stage f r (om the upper part to the lower part of the nevocellular structure, although they disclosed different histological structures. In 39 (31.5%) of the 124 cases, Meissner's corpuscle-like cells were confirmed.
2) Findings of immunohistochemical staining
i. Of the type A, type B and type C cells, the S-100 α protein stain was essentially negative. Meissner's corpuscle-like cells were selectively positive by this stain.
ii. Although no particular difference was noted in the staining of S-100 protein between the type A and type B cells, a somewhat greater proportion of positive cells was noted in type C cells. In the Meissner's corpuscle-like cells, a notably higher positive conversion of cells was observed as compared to those of the three other types of cells.
iii. Type A, type B and type C cells compared more or less similarly for the positive ratio of neuronspecific enolase but the ratio was unusually high in the Meissner's corpuscle-like cells.
3) Findings from routine electron microscopic staining
i. Similar to the light microscopic findings, the nevus cells were found to change in shape uninterruptedly from the upper layer to the lower layer of the dermis. Unusually marked changes were noted both in the number and shape of the melanosome and premelanosome in the cytoplasm.
ii. In the Meissner's corpuscle-like cells both melanosomes and premelanosomes were missing but a finding suggestive of a neuroid structure was affirmed.
As noted above, the results of the histological, immunohistological and electron microscopic studies were in support of the general findings suggestive of a gradual shift of the nevus cells from the upper layer to the lower layer in the dermis, which prompted the author to support the so-called “neural crest origin hypothesis”.

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The responses of eicosanoids to acute myocardial ischemia induced by either exercise stress testing (EX)or percutaneous transluminal coronary angioplasty (PTCA) were investigated in 23 patients with effort angina pectoris (EAP). EX was useful procedure to determine the therapeutic plan in each cases, and PTCA is the novel therapeutic operation for EAP. The relations between these metabolites and either hemodynamics or coronary circulation were then evaluated. The effect of the calcium entry blocker nisoldipine (oral administration of 5 mg) was also studied in 10 patients with EAP. The plasma levels of thromboxane B₂ (TXB₂), 6-keto-prostaglandin F_1α. (6KPGF_1α) and leukotriene C₄ (LTC₄) were determined by radioimmunoassay in arterial and coronary sinus blood samples before and immediately after acute myocardial ischemia. The changes in hemodynamics and coronary circulation during exercise stress testing were assessed by measuring direct brachial artery pressure, cardiac output by the dye dilution method and coronary sinus flow by the thermodilution method.
The TXB₂/6KPGF_1α ratio in coronary sinus blood significantly increased after ischemia in both EX and PTCA, but there was no significant change in LTC₄ levels of coronary sinus blood immediately after acute ischemia. The 6KPGF_1α levels in both arterial and coronary venous blood were significantly correlated to coronary perfusion pressure and mean brachial artery pressure. Arterial LTC₄ levels tended to correlate to mean brachial artery pressure and coronary sinus flow. Nisoldipine improved the ischemic electrocardiography response to EX. Nisoldipine also significantly increased arterial 6KPGF_1α at peak exercise. It significantly decreased brachial artery pressure, pressure rate product (PRP), mean coronary sinus pressure and coronary vascular resistance both at rest and peak exercise. The response of PRP significantly correlated with the response of arterial 6KPGF_1α.
These results suggest: (1) The imbalance of the TXB₂/6KPGF_1α ratio may be induced more rapidly than LTC₄ (2) PGI₂ and LTC₄ may have some role in the regulation of hemodynamics and coronary circulation during acute myocardial ischemia. (3) Nisoldipine may ameliorate myocardial ischemia through improvement of systemic hemodynamics and prostaglandin metabolism apart from through direct action on the heart.

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Fetal and neonatal hypoxia is suggested as a noticeable risk factor related to the occurrence of subependymal hemorrhages. To investigate the cause of newborn subependymal hemorrhages, a 0 day old newborn rabbit was exposed to either 5 or 10 minutes hypoxia by N₂ box. After exposure, the brain was observed by optical and electric microscope using horseradish peroxidase (HRP) as the protein tracer to study the change in the capillary permeability.
The result obtained were as follows;
1) In the newborn rabbit blood gas analysis, PO₂ (mmHg) decreased more in the 5 and 10 min hypoxia groups than the control group which used the N₂ box. pH and BE changes were similar to PO₂ (mmHg). On the other hand, PCO₂ (mmHg) increased proportionately. These results indicated that this hypoxic method changed blood gas and caused asidosis.
2) In the optical microscopic examination, the 0 day old newborn rabbit brain was found to have a thin subependymal layer. We could not find obvious subependymal hemorrhage using optical microscope.
3) In the electric microscopic examination, HRP was found in the cavity of the brain capillary at the subependymal layer and was slightly incorporated into the pinocytic vesicle of the lumen on the control. Since the tight junction filled the roll out, HRP was not found outside the capillary.
4) The 5 min hypoxia group caused astrocyte foot swelling, edema and slight opening of the tight junction. HRP was passed through the tight junction, but not outside the capillary.
5) The 10 min hypoxia group caused destruction of astrocyte and edema around the capillary. The tight junction was more opened than in the 5 min hypoxia group and HRP leaked out of the capillary through the tight junction.
From the findings mentioned above, it is suggested that our hypoxic model increased permeability of the capillary in subependymal layers and that this change might be the first ultrastructual change before the onset of subependymal hemorrhage.

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Using the islet perifusion preparation and the isolated rat pancreas in situ perfusion preparation, the effects of disopyramide (Diso) on insulin secretion were studied. In an isolated pancreatic islet perifusion experiment, Diso (300 μg/ml) produced a significant increase in the immunoreactive insulin (IRI) level in the perifusate. The Diso-induced IRI rise was not affected by pretreatment with various autonomic blocking agents, such as propranolol, phentolamine or atropine. In an isolated rat pancreas in situ perfusion experiment, the IRI level in the perfusate increased significantly after the administration of Diso (300 μg/0.1ml) under the perfusion of Krebs-Ringer bicarbonate buffer solution containing 0.3% glucose (0.3% glucose buffer), but not under the perfusion of Krebs-Ringer bicarbonate buffer solution containing 0.1% glucose (0.1% glucose buffer). The Diso-induced IRI rise was not affected by pretreatment with the autonomic blocking agents.
Diso suppressed the IRI rise which was induced by additional glucose application (25%, 0.2ml) under the perfusion of 0.1% glucose buffer, but not under the perfusion of 0.3% glucose buffer. Furthermore, Diso also suppressed the hypersecretion of insulin induced by increasing the glucose concentration from 0.1% to 0.3% in the perfusion fluid. The suppressing action of Diso on glucose-stimulated insulin secretion was partially recovered after pretreatment with propranolol or phentolamine.
These findings show that Diso has both stimulatory and inhibitory effects on insulin secretion processes, and that the inhibitory action of Diso is suppressed by high glucose solution.

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