During phagocytosis, pulmonary alveolar macrophages(PAM) produce superoxide (O^-₂), which is highly reactive and bactericidal. Therefore, PAM has an important role in the host defense machanisms in the lung. Generally, patient with diabetes mellitus are susceptible to pulmonary infections. It is supposed that a defect in the bactericidal activity of phagocytes is responsible for pulmonary infection. In this experiment superoxide production formed by PAM stimulated with concanavalin A and cytochalasin D was examined in relation to blood glucose concentration and other conditions. Superoxide production by PAM was maximum when the pH was 7.5, the temperature was 37°C, the glucose concentration was 100mg/dl and Ca⁺⁺ concentration was 1mM. A glucose concentration of more than 100mg/dl suppressed the superoxide production, and a high glucose level may be related to the high susceptibility of diabetics of pulmonary infections. The energy of superoxide production by PAM depends on both glycolysis and mitochondrial phosphorylation. On the other hand, polymorphonuclear leucocytes mostly depend on glycolysis. The superoxide dismutase (SOD) activity of PAM is remarkably higher than that of polymorphonuclear leucocytes.

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Patients with diabetes mellitus are susceptible to infections, due to the disturbance of host defense mechanisms, such as chemotaxis, phagocytosis and killing of bacteria. In this experiment superoxide production and lipid peroxide production, by peroxidation of unsaturated fatty acid, were examined. The superoxide production activity of PAM in hyperglycemics was significantly lower (P<0.005) than that in normal controls. The values were 5.68±1.68 nmol/10⁶ cells/min in the former and 8.20±2.60 nmol/10⁶ cells/min in the latter. The lipid peroxide production activity (Δ TBARS) in hyperglycemics (0.06±0.04 nmol/10⁶ cells) was lower (P<0.05) than that of normal controls (0.10±0.07 nmol/10⁶ cells). The lipid peroxide production activity (Δ TBARS) was proportionate to the superoxide production activity (r=0.570, P<0.02). Therefore, the Δ TBARS may depend on superoxide production. There was no significant difference in superoxide dismutase (SOD) activity between hyperglycemics and normal controls. The SOD activity was proportionate to the superoxide production activity in normal controls, and thus, SOD activity seems to depend on superoxide production.

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Fifty-five patients with advanced lung cancer were divided at random into three groups. The first group of 19 patients was treated with OK-432 administered intramuscularly in addition to combination chemotherapy. The second group of 18 patients was treated with PSK in addition to combination chemotherapy. The third group of 18 patients was treated with combination chemotherapy only. There were no significant differences in age, histological type, extent of disease, Performance status or initial chemotherapy between the three treatment groups.
The median survival was longer in the patients who received OK-432 (7.5 months) than that of the patients who received either PSK (7.0 months) or no immunotherapy (5.8 months), but this difference was not statistically significant. The degree of myelosuppression induced by the combination chemotherapy and the frequency of febrile episodes were less in the groups administered OK-432 and PSK.
These results suggest that these immunopotentiators, especially OK-432, may be useful immunotherapeutic agents in combination with chemotherapy in advanced stages of lung cancer.

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The functions of peripheral blood monocytes in 14 untreated patients with lung cancer were examined before and after a 1-week course of OK-432 therapy(1 KE every day).
The absolute monocyte count was calculated from the percent of monocytes in the total leukocyte count. The mean absolute numbers of monocytes before and after administration of OK-432 were 400/cmm and 437/cmm, respectively though the difference was not statistically significant.
The lysosomal enzyme activity of monocytes was histochemically determined by beta-galactosidase staining. The mean percentages of beta-galactoside positive monocytes before and after administration of OK-432 were 31.2 and 47.7 respectively. The increase was significant (P<0.05).
The monocyte chemotactic response was measured in vitro by Boyden's millipore technique using zymosan activated human serum as the chemoattractant. The monocyte chemotactic responses before and after administration of OK-432 were 20.1 and 25.2, respectively and a significant difference was found between the two groups(P<0.01).
The ability of monocytes to phagocytose complemented zymosan was accelerated by OK-432 administration, but the acceleration was not statistically significant.
Cytostatic activities of monocytes on EBC-1 target cells before and after administration of OK-432 were 84.5 and 91.4, respectively the difference was significant (P<0.05).
These results indicate that OK-432 activates the reduced monocyte functions in lung cancer patients in vivo, and that OK-432 may be a useful immunotherapeutic agent in man.

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Cell components in the peripheral lung area were examined in 24 asthmatic subjects by bronchoalveolar lavage (BAL) and transbronchoscopic lung biopsy (TBLB). In cases with increased percentage of lymphocytes in bronchoalveolar lavage fluid (BALF), the infiltration of eosinophils and mononuclear cells in the peripheral lung tissue was observed with a high frequency. The increased percentage of eosinophils in BALF correlated with the infiltration of eosinophils and neutrophils in the bronchiolo-alveolar region. A reverse correlation was observed between the macrophage count in the alveolar region and the percentage of eosinophils and lymphocytes in BALF. No significant correlation was present between the percentage of neutrophils in BALF and the infiltration of any type of cell in the lung tissue.

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The mechanism of rejection of allogeneic organ grafts is not fully understood. The rejection of grafted skin is complicated as skin epidermal cells express skin specific antigens. Thus skin epidermal cells are suitable target cells for analyzing skin graft rejection in in vitro studies.
In this study, ⁵¹Cr labeled skin epidermal cells were prepared from rat tail skin by trypsin digestion. The susceptibility of skin epidermal cells to immune spleen cells in a lymphocyte mediated cytotoxicity assay and LDA in an antibody dependent cytotoxicity assay was examined in allogeneic skin grafts in rats. Skin epidermal cells were specifically killed by immune killer lymphocytes or LDA in combination with normal rat spleen cells. The optimal condition for assays were 10 to 12 hours of incubation and a 100:1 to 200:1 effector to target cell ratio. When the kinetics of LDA activity after allogeneic skin graft was examined, LDA appeared in the recipient serum just after the rejection and maintained activity for more than 40 days after the skin graft.
To analyze the mechanism of graft rejection, it is resonable to use the same target cells as the graft itself in both cellular and humoral immunoassays. In this sense, skin epidermal cells are useful for the study of skin rejection.

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In order to evaluate the sensitivity of the exocrine pancreatic function test employing a new synthetic peptide, N-Benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA), studies were performed on 18 control subjects, 14 patients with suspected chronic pancreatitis and 32 patients with chronic pancreatitis, comparing three oral doses: 0.5g BT-PABA, 1.0g BT-PABA and combined use of 0.5g BT-PABA and 50g of test meal (Sustagen). Patients with chronic pancreatitis showed signigicantly lower PFD values than control subjects regardless of the dose. Administration of 0.5g BT-PABA gave not only the best result in detecting exocrine pancreatic dysfunction, but also the highest correlation with the results of the PS test, followed by the 1.0g BT-PABA administration and then by the combined use of 0.5g BT-PABA and 50g Sustagen. The highest correlation coefficient was noted between the first two methods, whereas only a poor correlation was noted between the combined method and the other two methods. No improvement in sensitivity was attained by administering 1.0g BT-PABA or 0.5g BT-PABA in combination with test meal.

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Although the exocrine pancreatic function test (PFD) using a synthetic peptide is a simple and useful test, it often gives a false positive result in hepatic diseases, renal diseases, and gastrointestinal diseases. Attempts were made to solve this problem. PFD combined with the PABA test, PFD combined with the D-xylose test as well as PFD alone were consecutively performed in 15 healthy controls, 15 patients with chronic pancreatitis, 15 with chronic hepatic diseases, 14 with chronic renal diseases and 16 with gastrointestinal diseases. Results of the tests were interpreted according to the following three criteria indicating exocrine pancreatic dysfunction: (A) an abnormal PFD with normal PABA or normal D-xylose test value, (B) a decreased PFD/PABA ratio or PFD/D-xylose ratio and (C) a large difference between PABA and PFD or a small difference between PFD and D-xylose. Specificity and sensitivity, were evaluated. PFD with the PABA test and PFD with the D-xylose test are very useful for avoiding false results. Criterion (A) with the PFD and PABA tests is the most suitable for the evaluation of exocrine pancreatic function in patients with possible hepatic, renal and gastrointestinal diseases. Criterion (A) with the PFD and D-xylose tests is almost as useful.

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The monocyte-mediated cytostatic acitivity against human tumor cells was measured in healthy donors and patients with bronchogenic carcinoma, malignant lymphoma, sarcoidosis and pulmonary tuberculosis. The target cells employed were HeLa cells and squamous cell-type lung cancer derived EBC-1 cells. Cytostatic activity was measured by inhibition of ³H-thymidine uptake by target cells.
The mean value of monocyte-mediated cytostasis in HeLa cells was 46.4±11.8% in 18 healthy donors, 47.7±19.0% in 31 patients with bronchogenic carcinoma, 39.9±21.7% in 19 patients with malignant lymphoma, 46.2±17.7% in 14 patients with sarcoidosis, and 48.6±15.7% in 9 patients with pulmonary tuberculosis. The mean value of monocyte-mediated cytostasis in EBC-1 cells was 87.4±8.5% in 18 healthy donors, 78.9±16.8% in 39 patients with bronchogenic carcinoma, 82.5±15.1% in 25 patients with malignant lymphoma, 87.0±6.7% in 16 patients with sarcoidosis, and 94.3±8.8% in 8 patients with pulmonary tuberculosis.
No significant difference between healthy donors and patients with the above mentioned disorders was observed in the HeLa cell assay. But there were remarkably low activities, two standard deviations below the mean value of healthy donors, in 30% of the patients with bronchogenic carcinoma and 14% of the patients with malignant lymphoma in the EBC-1 cell assay. In lung cancer patients no significant positive correlation was observed between monocyte-mediated cytostatic acitivity and other monocyte functions. The data suggest that the tumor cell killing activity of peripheral monocytes was decreased in patients with malignant neoplasma.

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The human peripheral monocyte-mediated cytolytic acitivity against tumor cells derived from human squamous cell-type lung cancer was measured in 16 healthy donors, 24 patients with bronchogenic carcinoma, 6 patients with malignant lymphoma and 8 patients with sarcoidosis. The activity was significantly depressed in patients with bronchogenic carcinoma (p<0.05) and in patients with malignant lymphoma (p<0.01). However, there was no significant difference between normal controls and patients with sarcoidosis. There was no significant difference monocyte-mediated cytolytic activities according to clinical stage and histologic type in lung cancer patients. A statistically significant positive correlation between phogocytic acitivity and cytolytic activity of monocytes, between monocyte-mediated cytolytic activity and cytostatic activity was observed in lung cancer patients. The data suggest that monocyte-mediated cytolytic activity in tumor bearing hosts is suppressed, and this lower activity effects the immunological surveillance and host defence mechanism against malignant tumors.

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Electrical stimulation of the posterior limb of the internal capsule was performed in seven patients with central pain due to vascular lesions of the thalamus or due to multiple sclerosis. Three patients suffered from thalamic hemorrhage and three others from thalamic infarction, and one from multiple sclerosis. These patients developed dysesthesia, hyperpathia and spontaneous burning pain several months after the onset of the disorders. The severe pain was not relieved by any anticonvulsant, psychopharmacological drug or analgesic drug, nor even by the intrathecal infusion of morphine.
Stimulating electrodes were implanted stereotaxically in the posterior limb of the internal capsule 25mm lateral to the posterior commissure for one-week stimulation trials. The patients reported pain relief and sensations such as warmth or comfortableness in the appropriate portion of the body during the electrical stimulation with a square pulse of 2-3 v, 0.2 msec, 50 Hz. In the patients whose pain was relieved successfully, a receiving unit manufactured by Medtronic Co. was internalized for transduced transcutaneous stimulation. The patient with multiple sclerosis felt no pain relief during stimulation of either the posterior limb of the internal capsule or the posterior ventral nucleus of the thalamus, so the electrode was removed. Satisfactory relief of pain was obtained by 30minute stimulation twice or three times a day for 10 to 14 days after surgery.
Long-term observations from three months to two years showed that three patients had good results (incomplete pain relief with the stimulator with no medication required), two had fair results (incomplete pain relief with the stimulator with small doses of medication) and another had poor results in which the pain recurred within one month. No remarkable side effects were seen.
These results indicate that internal capsule stimulation is more effective and lasts longer than the various ablative methods to relieve central pain. The mechanism of pain relief by internal capsule stimulation was discussed briefly.

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It is well known that electrical stimulation of the posterior limb of the internal capsule can relieve central pain resulting from neuronal damage in the central somatosensory pathways, though the mechanism of pain control is still unknown. Cats were employed in this study to investigate how internal capsule stimulation influences the unitary discharges of the nociceptive neurons of the thalamus.
Electrical stimulation of the internal capsule was carried out with a bipolar stimulating electrode whose tip was introduced into the internal capsule (A:17.0, L:6.0, H:+5.0). A bipolar stimulating electrode was inserted into the tooth pulp of the left lower incisor, and microelectrodes for recording unitary discharges which were placed into the ventralis posteromedialis (VPM) (A:7.5-10.0, L:3.0-6.5, H:-1.0- +2.0), posterior nuclear group (PO) (A:3.5-7.0, L:4.0-6.5, H:+1.0- +4.0) and centre median (CM) (A:6.5-7.5, L:2.0-3.0, H:0- +1.5) of the right thalamus under local anesthesia. Unitary discharges responsive to the contralateral tooth pulp stimulation were found in the VPM, PO and CM of the thalamus. The unitary discharges in the VPM were suppressed for more than 15 seconds after electrical stimulation (2.0 V, 50 Hz, 0.5 msec., 2 seconds) of the internal capsule which contains sensori-motor fibers. However, stimulation of the internal capsule did not suppress the unitary discharges in the PO and CM of the thalamus.
On the other hand, intraventricular administration of morphine (0.05 mg) suppressed the discharges of both PO and VPM neurons responsive to the pulp stimulation, and the suppression of PO discharges lasted for much longer periods. These results suggest that pain relief obtained by electrical stimulation of the internal capsule is not an analgesic effect related to the opioid system, but due to the activation of the non-opioid central pain-inhibiting system, resulting in the suppression of nociceptive neurons of the sensory thalamus.

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The problem of juvenile delinquency is now managed by welfare or judicial institutions and not by medical practitioners in the field of child psychiatry. Therefore the problem is mainly discussed sociologically and psychologically, and not clinically from the standpoint of child psychiatry. Clinical classification of juvenile delinquents is necessary for their diagnosis and treatment in terms of the analysis of their behavior and criminality. Family research and Rorschach tests were performed, and four types of juvenile delinquents were defined. Those of the first type, which characteristically undergo early socialization and look for an identifying object in their group, have broken families with economic problems. The second type, which is unadaptable and dependent on the group mind, has over-protective parents. The third type, which takes on a counter identity, shows substantial broken family relations and poverty. The fourth type, which is asocial and acts out obsessively with hard conflict, reflects the mother's own problems. The CNV test was also employed. It seems that central nervous dysfunction plays an important part directly or indirectly in juvenile delinquency. From the developmental point of view, the first type of juvenile delinquent is considered to have a passing disorder of the later 2nd individuation process which I have proposed here. Also the second type one of the earlier 2nd individuation process, the third type one of the 1st grouping and individuation process and the fourth type one of the 1st individuation process.
The problem of juvenile delinquency was discussed in relation to other asocial problems in child psychiatry in relation to the classification and developmental process.

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Sera from 298 patients with sicca syndrome and connective tissue diseases were examined for the presence of anti SS-A, SS-B and RNP antibodies using double diffusion techniques, and the clinical implication of these antibodies was studied.
Among the 298 patients, 147 had sujective symptoms of dry eye and/or dry mouth, and abnormal lacrimal and/or salivary glands (clinical Sjogren's syndrome). The other 51 patients lacked subjective symptoms, but had histologically abnormal salivary glands (subclinical Sjogren's syndrome). Anti SS-A antibody was present in high incidence both in the patients with sicca syndrome and in those with Sjogren's syndrome associated with connective tissue diseases. In contrast, when present, anti SS-B antibody was always accompanied with anti SS-A antibody and was specific to sicca syndrome patients, although its incidence was lower than that of anti SS-A antibody.
Patients with sicca syndrome who had anti SS-A antibody alone or both antibodies developed more severe sicca features of the salivary gland, but extraglandular symptoms were less frequent. In contrast, sicca syndrome patients with anti RNP antibody had mild sicca features of Sjogren's syndrome, and showed clinical characteristics suggestive of connective tissue diseases, including Raynaud's phenomenon and hypocomplementemia.
The present study suggests that the detection of anti SS-A, SS-B and RNP antibodies is a useful tool for the diagnosis and the classification of Sjogren's syndrome.

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Anti SS-A antibody was positive in 61 (78%) of 78 patients with systemic lupus erythematosus (SLE), and anti SS-B antibody was positive in 7 (9%) of the patients. Among 50 of the patients there was no significant correlation between the presence of sicca features of Sjogren's syndrome and anti SS-A antibody. In addition, a high incidence of clinical and laboratory data indicating SLE was not found significantly in patients with anti SS-A antibody. In contrast, Raynaud's phenomenon and LE cell phenomenon predominated in 11 patients without anti SS-A antibody. In the majority of the SLE patients, anti SS-A antibody was accompanied with other antibodies against non-histone protein antigens, and this complexity of antibodies might prevent the clarification of the clinical characteristics of anti SS-A antibody in SLE patients.

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In order to clarify the electrophysiological aspects of the hyperkinetic syndrome, the late component of CNV (CNV immediately before S₂ for 200 msec) and reaction time (RT) were measured in 15 patients with hyperkinetic syndrome, 15 patients with emotional disturbance, and 30 normal children, all 7-12 years old. In the normal children the late component of CNV increased in amplitude, while RT was shortened, as the age increased. The late component of CNV was considered to attain a level comparable to that of adults by the age of approximately 9 years. Only in the cases of hyperkinetic syndrome was the late component of CNV significantly low in amplitude. As to RT, however, no significant difference was observed among the three groups. In the hyperkinetic children, significant correlation was observed neither between IQ and the late component of CNV, nor between the normal and abnormal EEG groups and the late component of CNV and RT. Comparing responders with nonresponders to methylphenidate, it was found that the late component of CNV of the responders was significantly lower in amplitude than that of the nonresponders, but no such difference in RT was observed. In the two cases of hyperkinetic syndrome, methylphenidate was effective in increasing the amplitude of the late component of CNV.
Concerning the hyperkinetic syndrome, the present findings were discussed in relation to the functional balance of midbrain reticular formation and the thalamus, and to the possible application of the late component of CNV to the clinical fields.

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To determine whether the analysis of lymphocyte surface markers provides clinically useful information, neoplastic cells from 51 adult patients with NHL were studied for surface markers and phagocytosis. The analysis revealed that NHL could be classified into four types according to the neoplastic cell type; T-cell, B-cell, Null-cell and true histiocyte types. On the basis of this immunofunctional classification, response to chemotherapy and survival of the patients were evaluated. The chemotherapeutic responsiveness rate (CR+PR rate) and complete remission (CR) rate of the T-cell type were shown to be the lowest in stage III and IV patients. Especially in stage IV, the CR rate of the T-cell type was statistically the lowest. Patients in both stages III and IV of the B-cell type survived the longest and those of the T-cell type, the shortest. In stage IV, the survival period of the T-cell type NHL patients was significantly shorter than those of the non-Burkitt B-cell type or Null-cell type. However, the difference between the survival of the B- and Null-cell types was not clear. These results indicate that the immunofunctional classification is some what useful for prediction of chemotherapeutic response and prognosis in NHL.

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Twenty-six patients with non-Hodgkin's lymphoma (NHL) born in Ehime Prefecture were classified immunofunctionally by testing E, EA and EAC rosettes, surface immunoglobulin, Ia antigen and terminal trasferase (TdT) of lymphoma cells. Geographical distribution of the immunofunctional cell type, clinical stage and PPD and PHA skin test values was examined. According to cell type, there were those types of patients: 13 cases of the T-cell type (50%), 10 cases of the B-cell type (38%) and 3 cases of the Null-cell type (12%). There was no true histiocyte type. In the geographic study, the percentage of the T-cell type in the Matsuyama district was less than that in Kyushu island, but more than that in the northeast part of Japan. The number of T-cell type patients was much larger in the southwest part of the prefecture. B-cell type patients in stage I or II and T-cell type patients in stage III or IV were predominant. Rare cases of the T-cell type with EA or EAC rosetting were observed. Cells from Null-cell type patients and a T-cell type patient with diffuse lymphoblastic histology were TdT-positive, but others were negative. PPD and PHA skin tests showed a much weaker reaction in the T-cell type than in the B- and Null-cell types.

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It was examined whether or not steroid and reticuloendothelial system (RES) stimulants had any effect on serum clearance and tissue uptake of aggregated human IgG (AHG), as a model of soluble immune complexes, in mice. Eighty percent of the AHG administered cleared from circulation within 1 hr, predominantly by the liver and partially by the spleen in control mice. The clearance of AHG was delayed (p<0.001) in steroid-treated mice. This was most prominent when mice were treated with 200mg/50kg PSL for one week. After administration of 1000mg/50kg Methyl-PSL for 3 days serum AHG clearance was less than after adminstering 50mg/50kg PSL. Suppression of RES by steroid increased the accumulation of AHG in the kidney (p<0.05), possibly by inhibiting hepatic uptake of AHG. PVP and LPS unexpectedly suppressed RES function. Zymosan had no effect on RES function. It was found that suppresion of RES was the main factor in induction of tissue damage (nephropathy) due to delay in the clearance of soluble immune complexes and increased the deposition of that into the kidney.

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The function of the reticuloendothelial system (RES) is important for deposition of circulating immune complexes (IC) in tissue. However, little is known about how IC located in tissues in patients with systemic lupus erythematosus (SLE). Splenic Fc-Receptor function (SFcF) was studied in 29 patients with SLE using IgG coated ⁵¹Cr labelled autologous erythrocytes, and was compared with immunological abnormalities in sera and kidney. Impairment of SFcF was found in 21 of the patients (72.4%). There was a close inverse correlation between SFcF and CH50 (p<0.05). Patients with impaired SFcF tended to have a high level of circulating IC, but this was not statistically significant (p>0.05). A marked decrease in SFcF was found in patients with mesangial lupus nephritis and those with diffuse proliferative lupus nephritis. Patients with membranous lupus nephritis showed a mild SFcF abnormality. Decreased SFcF was reversible by steroid and/or plasma exchange (PE) therapy. Decreased SFcF could be improved after PE therapy alone. It was suggested that an abnormality in SFcF might force the progress of the diesase in patients with SLE.

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Assessment of the prognosis of fulminant hepatitis was made from clinical findings at the time of the appearance of hepatic encephalopathy using five living and ten fatal cases of fulminant hepatitis. Those patients who died tended to be old, especially in the subacute type of fulminant hepatitis, and frequently had disseminated intravascular coagulation. Prognosis scoring by assessing clinical findings in these patients was calculated during their clinical courses. From differences in scores, the treatment performed following the occurrence of hepatic encephalopathy was judged to be effective in some of the surviving patients. Other patients died, however, because of the difficulty of sufficiently controlling complications. The prognosis scoring at the time of the appearance of encephalopathy was valid for female patients who survived. Clinical evaluation of this scoring method will be further evaluated with more cases in the future.

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The effect of extracorporeal circulation (ECC) on myocardial myosin adenosine triphosphatase (ATPase) activity was studied in 23 dogs with normal heart and 17 dogs with left ventricular hypertrophy. Intermittent aortic cross clamping for 60 minutes was done in some dogs and not in others during ECC. The cardiac functions and myocardial ATPase activity before and 60 minutes after ECC were compared.
Cardiac function was depressed in dogs undergoing aortic cross clamping, especially in those with hypertrophied heart after ECC. It was observed that cardiac myosin ATPase activity was diminished in dogs with hypertrophied left ventricles. In the other dogs, no remarkable changes were observed in the myosin ATPase activity.
It was concluded that myosin ATPase activity was depressed during aortic cross clamping in dogs with hypertrophied left ventricles and that the disturbance of energy utilization in the myocardium was one of the causes of depressed cardiac function after ECC.

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The use of lithium carbonate as a prophylactic therapy to affective disorders has now become widespread. The evaluation of the patients' attitudes toward their lithium therapy and affective disorders is very important in the decision to continue therapy. We issued a questionnarie to 41 outpatients in the Psychiatric Clinic of Okayama University Hospital. All patients have continued lithium therapy for at least 3 months because of two or more manic-depressive episodes over the past two years, and all of them were in remmission and had normal intelligence. The patients wanted more information on following questions: possible risk of relapses, heredity of affective disorders, methods for preventing relapses, how to handle theirselves at further psychotic episodes, duration of their nedication, side effects of long-term lithium therapy, the degree of prophylactic effects of lithium, and the combined use of lithium with other drugs. Forty-nine percent of the patients had read about the affective disorder and 59% of the patients wanted to learn about lithium therapy.
These results suggest that patients on prophylactic lithium therapy may want more active and easily understandable guidance concerning affective disorders and lithium therapy. Prophylactic lithium therapy is a long-term procedure which requires assistance from the patient's physician and family. We should guide and support patients toward a more effective and safe continuation of lithium therapy.

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Epileptogenic activities of certain cephalosporins administered intravenously into rats with stainless steel electrodes implanted into the frontal cortex, occipital cortex, hippocampus and amygdala were investigated. At doses of less than 200 mg/kg, the cephalosporins did not induce any EEG or behavioral signs. At doses greater than 500 mg/kg, seizure effects were noticed in both EGGs and behavior in the decreasing order of ceftezole, cefotiam, cefazolin and cephaloridine. Especially at a dose of 1, 000 mg/kg, seizure signs were noticed. Effects of diazepam, phenobarbital and phenytoin in preventing generalized seizures induced by intraventricular injection of 100 μg cefazolin were investigated. Intravenous administrations of diazepam and phenobarbital inhibited cefazolin-induced seizures markedly. The ID50_s of inhibition of seizure patterns in EEG were 3.4 mg/kg and 30.5 mg/kg, respectively, and the ID50_s of seizure behavior suppression were 4.7 mg/kg and 49 mg/kg respectively. However, phenytoin did not repress cefazolin-induced seizures even at 100 mg/kg (i.v.).

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