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Twenty-five patients (30 hips) have had a total hip replacement using the cup supporter developed in our department. This report describes the follow-up findings on these patients. The mean period after hip replacement was 2 years and 8 months (range from 6 months to 6 years). The cup supporter was used in patients with rheumatoid arthritis with acetabular protrusions, central migration of the prosthesis after hemi-arthroplasty, revision operation for a defecting acetabular floor, primary acetabular protrusions (including osteoarthritis with acetabular protrusions) and traumatic fracture-dislocation of the hip. In five cases, autograft of bone was used in addition to the cup supporter for reinforcement of a thin acetabular floor. This combination appeared to provide good clinical results. The cup supporter was of value in revision operations due to loosening of the acetabular cup with severe acetabular protrusions.

Fulminant hepatic failure (FHF) was produced in rats with intraperitoneal injection of D-galactosamine. Control rats received only physiological saline. 15N-leucine (200 mg/kg of body weight) was injected into the rats via the tail vein. Arterial blood was drawn before and 5, 15, 30 and 60 min after the injection of 15N-leucine. 15N-amino acids were determined quantitatively by gas chromatography and mass spectrometry. The plasma 15N-leucine level decreased logarithmically in the same manner in both groups. This result suggests that leucine is mainly metabolized in extrahepatic tissues. The incorporation of 15N into plasma isoleucine and valine was not significantly different between the groups. Plasma alanine and glutamine concentrations increased in controls and decreased in FHF rates after the injection. The incorporation of 15N into plasma alanine in rats with FHF was significantly later than in controls. This result may suggest that undergoing hyperammonemia causes to form more glutamine from glutamate in extrahepatic sites as the same manner as for chronic hepatic failure. Additionally, insulin levels increased temporarily after the injection of leucine in both groups. This increase may play a role in the decrease in plasma isoleucine and valine concentrations after injection of leucine.

Three linear plots by which the liver's maximum removal rate (Rmax) of indocyanine green (ICG) and the Michaelis constant (Km) can be calculated were compared in a microcomputer simulation study. The widely-used Lineweaver-Burk plot (1/V vs. 1/S; V, ICG initial removal rate (mg/kg/min); S, ICG loading dose (mg/kg] presented the greatest bias and variance. There was no remarkable difference in bias between the S/V vs. S plot and the V vs. V/S plot, but the latter possessed a smaller variance. Therefore, the V vs. V/S plot was considered the best for estimating Rmax. The best combination of three ICG loading doses was 0.5, 2, and 5 mg/kg. This combination was selected by comparison of the Rmax estimated from three points with that estimated from six points (0.5, 1, 2, 3, 4 and 5 mg/kg).

A high performance liquid chromatographic (HPLC) method with electrochemical detection (ECD) was developed for the simultaneous measurement of estrone, estradiol, estriol and estetrol in serum. These hormones were extracted with diethylether, chromatographed on an silica-octadecyl silane (ODS) column with an eluent of phosphate buffer solution-acetonitrile-methanol (volume ratio 152:85:40), and detected by ECD at +1.0V vs. Ag/AgCl. In comparisons between the values measured by this method and radioimmunoassay, significant correlations were noted for estrone (r = 0.759, p less than 0.01), estradiol (r = 0.816, p less than 0.001) and estriol (r = 0.830, p less than 0.001). In clinical applications of this method, differences between cases of the normal and the anencephalic pregnancy in the thirty-eighth week of gestation were distinct not only in the individual estrogen, but also in the profile analysis of estrogens. With this method, all 4 serum estrogens above approximately 500 pg/ml could be measured within 2 h, and the method seemed to be clinically applicable.

The effect of a change in cecal volume on gastric motility was studied in 24 h fasted rats anesthetized with urethane (0.8 g/kg, i.p.). A cecal volume increase from 1 to 10 ml (in 1 ml steps) produced a decrease in the basal tone of the stomach. The maximal inhibitory response was produced with an 8 to 10-ml increase in cecal volume. The gastric inhibitory response continued as long as the increased cecal volume was maintained. It was abolished by a combination of a splanchnicotomy and vagotomy, or only a splanchnicotomy in a few cases. The inhibition of gastric motility by increasing the cecal volume also occurred after severance of dorsal roots between T8 and L4 and gastric branches of vagus nerves. It is suggested that an increase in cecal volume induces gastric relaxation mainly via the splanchnico-splanchnic pathway and partly via the vago-vagal and vago-splanchnic pathways. Therefore, retardation in transit of the gastric contents in germ free rats having an enlarged cecum may be attributed to an enhancement of the ceco-gastric inhibitory reflex. The ceco-gastric inhibitory response mediated by the splanchnic pathway was abolished by guanethidine (3-5 mg/kg, i.v.), but the response mediated by the vagal pathway was resistant to guanethidine as well as to atropine (0.2 mg/kg, i.v.). This result indicates that splanchnic postganglionic efferents are adrenergic, while vagal postganglionic efferents are non-adrenergic and non-cholinergic.

We report a family whose members have familial spastic paraplegia (FSP) associated with epilepsy. A man and his sister initially had primary generalized epilepsy with tonic-clonic seizures, but they have had no seizures for years. However, they developed spastic paresis of the lower extremities and presently show features of FSP. Their mother seemed to have suffered from FSP. One son of the female patient has epilepsy. The clinical picture of this family suggests a close relationship between FSP and epilepsy.

Peritoneoscopic findings of 39 patients with alcoholic liver cirrhosis (ALC) were compared with those of 95 patients with non-alcoholic liver cirrhosis (NALC). They were selected from 245 patients with liver cirrhosis subjected to peritoneoscopy in the 7 year period from 1975 to 1981. Out of the 95 NALC patients, 24 had hepatitis B surface antigen. The ALC patients had nodules which varied in size (61%), large depressions (69%), and a markedly rounded edge of the liver (33%) more often than NALC patients (18, 43 and 3%, respectively). Nodularity differed between the right and left lobes in ALC (41%) more often than in NALC (16%). Interstitial reddish markings and patchy nodules were, however, more frequent in NALC (51 and 28%, respectively) than in ALC (8 and 5%, respectively). Lymphatic vesicles were observed both in ALC (85%) and NALC (78%). In conclusion, the peritoneoscopic features which suggested ALC were the coexistence of nodules of various sizes, large depressions and a markedly dull edge of the liver. Interstitial reddish markings and patchy nodules were more indicative of NALC than ALC.

Co-cultivation of human thymus and spleen lymphocytes, which were obtained from 26-week and 27-week fetuses, with a lethally-irradiated human cord T-cell line harboring human T-cell leukemia virus type Ι(HTLV-Ι) resultes in the establishment of T-cell lines positive for adult T-cell leukemia-associated antigens and producing HTLV-Ι. These cell lines had the phenotype of a helper/inducer subset of peripheral T-cells as evidenced by the reactivity with monoclonal antibodies to human T-cells.

The extent of homology between two protein fractions was compared by simple electrophoretic analysis. Nuclear proteins of several rodent cells of different origins were fractionated into acid-soluble and acid-insoluble fractions. The two protein fractions were subjected to polyacrylamide gel electrophoresis in separate gel systems, and protein bands with identical mobilities were sought either in all possible combinational pairs of cell types or in all cell types. The paired and overall homology indices calculated from these data and chi-square testing of the results indicated that acid-soluble nuclear nonhistone proteins are more homologous than acid-insoluble nuclear proteins. Several factors which might have affected the results were discussed.

The anti-tumor effect of immunization with heat-killed Mycobacterium tuberculosis (Tbc) and Tuberculin (PPD)-coupled syngeneic tumor cells was examined in vivo. Three tumor cell lines were employed. Immunization of Tbc-primed BALB/c mice with PPD-coupled syngeneic Meth-A tumor cells displayed a potent anti-tumor effect on viable Meth-A cells inoculated subcutaneously. Neither PPD-coupled LLC (Lewis Lung Carcinoma) cells nor sonicated PPD-coupled Meth-A cells were capable of immunizing these mice. PPD-coupled syngeneic whole tumor cells were indispensable for induction of this tumor-specific resistance. Immunization of Tbc-primed C3H/He mice with PPD-coupled syngeneic MH134 tumor cells did not elicit anti-tumor activity against MH134, but additional pretreatment of mice with cyclophosphamide brought on an anti-tumor effect. Antimetastatic reactivity was investigated in C57BL/6 mice bearing LLC, with a reduction in metastases noted. This antimetastatic effect was observed even when the mice were immunized with PPD-coupled LLC cells three days after removal of the initial tumor. Immunization with Tbc and PPD-coupled Meth-A cells together with intraperitoneal administration of murine or rat interleukin 2 (IL 2) further augmented anti-Meth-A resistance. Murine IL 2 further inhibited tumor growth during the early stage, while rat IL 2 showed an anti-tumor effect throughout the course of tumor growth.

Serum fucose levels and fucosyl transferase activities have been designated as nonspecific markers of malignancy, and play an important role in the diagnosis of different types of malignancies. In the present study, attempts were made to determine the prognostic significance of these markers in patients with cancer of the uterine cervix after therapy. It was found that both serum fucose and fucosyl transferase, which were elevated in untreated patients declined significantly in patients responsive to therapy at different follow-up intervals, but not in patients unresponsive to therapy.

Glial fibrillary acidic protein (GFAP) was purified from human spinal cord and cerebral white matter. GFAP was localized by an immuno-peroxidase method in normal adult and fetal human brains, rat brains, and 152 central nervous system (CNS) tumors. GFAP was found in reactive and normal astrocytes, immature cells of fetal brain at the 18th to 21st gestational weeks, and normal rat astrocytes. This GFAP staining was quite specific for glial tumors, including astrocytomas, glioblastomas, astroblastomas, and ependymomas. GFAP-positive cells were also found in oligodendrogliomas and choroid plexus papillomas, and they were interpreted as being astroglial or ependymal differentiations. Stromal cells in cerebellar hemangioblastomas were negative. However, engulfed astrocytes were found at the periphery of such tumors and often adjacent to the proliferate blood vessels. In meningiomas, neurinomas, metastatic carcinomas, pituitary adenomas and other non-glial tumors, GFAP-positive cells were not identified.

An autopsy case of hypertrophic cardiomyopathy showing clinical features of dilated cardiomyopathy was reported. The patient was a 60-year-old female complaining of chest discomfort from the age of 40. At autopsy, both ventricles were dilated. Microscopically myocardial loss, fibrosis and disarray of hypertrophic myocardial fibers were observed. The areas showing myocardial disarray were distributed close to the scar-like fibrotic areas. Coronary arteries and intramyocardial arterioles showed minimal stenotic changes.

Free amino acid contents in various guinea pig tissues were determined with an amino acid analyzer. The most abundant amino acids in these tissues were: Gly and Glu in the liver and kidney, Gln, Glu and Ala in the heart, Glu and Gln in the brain, Gly in the blood plasma and Lys in erythrocytes. Glutathione was present as the reduced form in these tissues. Cystine was not detected except in the blood plasma, but cysteine was present in these tissues. These results indicate that most thiols are present in the reduced form in these guinea pig tissues. Taurine contents were low compared with those in rat tissues. The results were discussed in relation to the metabolism of sulfur-containing amino acids, and it was suggested that the oxidative metabolism of L-cysteine was lower in guinea pig tissues than in rat tissues.

Age-related alterations in the host defense system have been vigorously investigated because of increased susceptibility to infection and neoplasms in the aged. Although monocyte-macrophages form a major part of the cellular defense against microorganisms, the majority of investigations has been limited to neutrophils and lymphocytes. The present study, designed to determine the influence of age on mononuclear phagocytes, revealed no significant decrease in the absolute number of blood monocytes, but did reveal a tendency for the chemiluminescence of blood monocytes to decrease (p less than 0.10) and a significant decrease in the numbers of macrophage precursors (p less than 0.05) in the aged (over 70 year old), in comparison with controls (under 40 years old). On the basis of these findings, functional alterations of monocyte-macrophages seem to participate in the increased susceptibility to infection in the aged.

Basophil histamine release induced by allergens (house dust and Candida albicans) and anti-IgE was examined in 31 patients with bronchial asthma in relation to patient age, age at onset of the disease and serum IgE levels. Basophils from patients under 40 years of age generally released a significantly large amount of histamine by stimulation with house dust and anti-IgE. On the other hand, histamine release from patients over 41 years of age was generally not marked when the cells were incubated with house dust and anti-IgE, although, in some cases, the release induced by C. albicans was fairly marked. Basophils from patients under 30 years of age at onset were reactive to house dust and anti-IgE, while the cells from patients over 41 years of age at onset tended to be reactive only to C. albicans. Basophils from patients with low serum IgE levels were less reactive than the cells from patients with high levels of IgE to house dust and anti-IgE. C. albicans-induced release of histamine did not correlate with serum IgE levels.

The appearance of epileptiform discharges in electrocorticograms was induced by a unilateral injection of CoCl2 solution into the sensorimotor cortex of rats. Accumulation of cyclic AMP elicited by ouabain or a high concentration of potassium ions was determined in slices from different cortical areas of rats 9 or 10 days after the injection. In the anterior cortex, the depolarization-elicited accumulation of cyclic AMP was significantly higher in the cortical area ipsilateral to the injection site than in the contralateral cortical area. In the posterior cortex, a similar but not significant difference in the accumulation of cyclic AMP was noted.

The effects of caerulein on gastric motility in urethane-anesthetized rats were studied. Caerulein administered into the lateral cerebral ventricle (i.c.v.) and jugular vein (i.v.) caused predominantly an inhibitory effect on gastric motility but sometimes an excitatory or a biphasic effect. The inhibitory response was reduced after vagotomy and/or splanchnicotomy, or after guanethidine. The remaining inhibitory response was abolished by tetrodotoxin, but was resistant to atropine and guanethidine. The excitatory response was abolished by atropine. Discharges of the gastric branch of the vagus nerve were decreased by i.v. injection of caerulein but increased by i.c.v. injection, whereas those of the splanchnic nerve were increased by both i.v. and i.c.v. injection. These results suggest that caerulein causes an inhibition of gastric motility by centrally stimulating vagal non-adrenergic inhibitory nerves and splanchnic adrenergic nerves and inhibiting vagal cholinergic nerves, and by peripherally stimulating non-adrenergic inhibitory neurons of the myenteric plexus. This peptide causes an excitation by stimulating cholinergic neurons of the myenteric plexus.

Vecuronium is hydrolyzed in the body to 3-deacetyl (ORG 7268), 17-deacetyl (ORG NC58), and 3, 17-bis-deacetyl (ORG 7402) derivatives. Interactions of vecuronium and these metabolites were studied in phrenic nerve-hemidiaphragm preparations of rats. As already reported, ORG 7268 had a potent neuromuscular blocking action, and ORG NC58 and ORG 7402 had a weak neuromuscular blocking action. As expected, ORG 7268 increased the degree of neuromuscular block by vecuronium. However, a low concentration (10 microM) of ORG NC58 and ORG 7402 reversed the block by vecuronium. At a high concentration (50 microM), ORG NC58 and ORG 7402 increased the degree of block by vecuronium. Although we do not have enough data to explain these paradoxical reversal of neuromuscular block at this moment, we postulate that these results reflect the interaction between "slow" and "fast" competitive antagonists. Regardless of the mechanism, it should be emphasized that the concentrations of ORG NC58 and ORG 7402 which are necessary to reverse the block are much lower than those which facilitate the block. It is conceivable that this paradoxical reversal of the block occurs in experimental and clinical situations. Therefore, in determining the neuromuscular blocking action of a compound, the "antagonistic" effect of its metabolites should also be considered.

The effects of morphine on the hypothalamic corticotropin-releasing factor (CRF), norepinephrine (NE) and dopamine (DA) concentrations were investigated in non-stressed and stressed rats. Acutely administered morphine stimulated both the synthesis and release of CRF in the hypothalamus, thereby activating the pituitary-adrenocortical system in non-stressed rats, but inhibited the stress-induced CRF synthesis and ACTH-corticosterone secretion. Either a morphine or ether-laparotomy stress reduced NE and DA concentrations in the hypothalamus. A pretreatment with morphine inhibited the stress-induced reduction in the hypothalamic NE and DA concentrations, and induced a significant increase in the DA concentration. These observations suggest that hypothalamic NE and DA are involved in morphine-induced changes in hypothalamo-pituitary-adrenocortical (HPA) activity and that endogenous opiates have a role in regulating CRF secretion by interacting with hypothalamic biogenic amines.