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The activation energy of recovery in 99.999% aluminium deformed at 4.2 K is investigated at temperatures between 50 to 180 K by means of the change of slope method. The activation energy varies from 0.15 to 0.60 eV with raising temperature. This behaviour is simulated by considering an overlapping of several first order processes within stage II. It is supposed that the variation of activation energy in stage II is due to recovery of vacancies and their small clusters by pipe diffusion mechanism.Die Aktivierungsenergie der Erholung in 99,999% bei 4,2 K deformiertem Aluminium wird bei Temperaturen zwischen 50 bis 180 K mittels Anstiegswechselmethode untersucht. Die Aktivierungsenergie variiert von 0,15 bis 0,60 eV bei steigender Temperatur. Dieses Verhalten wird unter Berücksichtigung einer Überlappung verschiedener Prozesse erster Ordnung in der Stufe II simuliert. Es wird angenommen, daß die Variation der Aktivierungsenergie in Stufe II durch Ausheilung von Leerstellen und ihrer kleinen Cluster über einen Pipe‐Diffusionsmechanismus verursacht wird.

Activation signal requirements for the induction of the IL-2 responsiveness in purified subsets of human resting T cells, T4+ or T8+, have been investigated under the monocyte-depleted conditions. Substantial levels of IL-2 responsiveness were induced in T8+ cells by lectin, Con A, mAb directed against the CD3 Ag, OKT3, Ca2+ ionophore, ionomycin or phorbol ester, PMA. In contrast, none of these stimuli was by itself sufficient for the induction of IL-2 responsiveness in the T4+ subset. The latter cells could, however, be induced to respond to IL-2 by combinations of PMA plus either of Con A, OKT3, or ionomycin (but not any combination of Con A, ionomycin, and OKT3). These data indicate that induction of IL-2 responsiveness in the resting T4+ subset is more complex, possibly requiring two intracellular activation signals, increase in the concentration of intracellular Ca2+ and activation of protein kinase C, whereas either signal may directly trigger IL-2 responsiveness in the resting T8+ cells. The data further suggest that under optimal conditions, growth of both resting T4+ and T8+ subsets may be independent of monocytes.

In this study, we determined whether Langerhans cells (LC) can function as both stimulatory and accessory cells (ACC) in alloreactive and syngeneic modified CTL induction in vitro. LC exhibited potent Ia+ stimulatory function, comparable to spleen cells, in both allo-CTL induction and in TNP-modified CTL induction assays. In contrast to spleen cells, however, when LC were syngeneic to the responders in an Ia+-adherent cell-depleted CTL culture, they could not restore the CTL responses. This was due, in part, to the suppression of CTL induction, presumably via secretion of prostaglandin E by epidermal cells (EC), because addition of indomethacin reversed the suppression. Even in the presence of indomethacin, however, LC were unable to exhibit ACC function. Finally, we tested the possibility that both Ia+ and Ia- cells were required to fulfill ACC functions. However, when spleen cells treated with anti-Ia antibody and complement and EC and indomethacin were added to an Ia+-adherent cell-depleted CTL culture, there was no significant restoration of the CTL response. Thus, LC can clearly act as Ia+ stimulatory cells in CTL induction but cannot serve as ACC in CTL induction, whereas Ia+ spleen cells may subserve both functions. These data suggest a functional heterogeneity of Ia+ antigen-presenting cells in spleen and in epidermis.

The immunologic nature of tumor-associated transplantation antigens (TATA) of MM102 mammary tumor that originated spontaneously in C3H/He (H-2k) mice was analyzed. The TATA of MM102 tumor have been demonstrated in our laboratory to induce preferential generation of helper T cell activity without any significant killer T cell generation. The helper T cells that were generated by the immunization of syngeneic C3H/He mice with MM102 tumor and specifically reactive to the TATA of MM102 tumor were also reactive with the cellsurface antigens present on the normal or malignant lymphoid cells of allogeneic C57BL/6 (B6) and C57BL/10 (B10) mice. The reactivities of such TATA-reactive helper T cells were eventually the same irrespective of whether those lymphoid cells are derived from B10 (H-2b) mice or B10.BR (H-2k), the congenic strain of the same B10 background. Furthermore, in addition to the fact that the immunization of C3H/He mice with those lymphoid cells could induce the resistance against the challenge with viable MM102 cells, C3H/He mice that had been neonatally rendered tolerant to B10.BR could not develop the immune resistance against MM102 tumor. These results clearly indicate that TATA of MM102 tumor are closely similar or identical to the non-H-2 antigens of allogeneic B10 mice on the level of helper T cell recognition, and that those non-H-2 alloantigens are capable of acting as the adequate transplantation antigens required for the effective induction of immune resistance against MM102 tumor.

An enzyme electrode system for the determination of creatinine and creatine was developed by utilizing three enzymes: creatinine amidohydrolase (CA), creatine amidinohydrolase (Cl), and sarcosine oxidase (SO). These enzymes were co-immobilized onto the porous side of a cellulose acetate membrane with asymmetric structure, which has selective permeability to hydrogen peroxide. Two kinds of multi-enzyme electrodes were constructed by combining a polarographic electrode for sensing hydrogen peroxide and an immobilized CA/Cl/SO membrane or Cl/SO membrane for creatinine plus creatine or creatine, respectively. The multi-enzyme electrodes responded linearly up to 100 mg of creatinine and creatine per liter in human serum. Response time was 20 s in the rate method and the detection limit was 1 mg/L. Only 25 microL of serum sample is required. Analytical recoveries, precisions, and correlations with the Jaffé method were excellent, and the multi-enzyme electrodes were sufficiently stable to perform more than 500 assays. No loss of activity of immobilized enzymes was observed after nine months of storage at 4 degrees C in air.

Spleen cells from C3H/He or BALB.K mice immunized to the newly synthesized amino-reactive hapten 5-sulfo-1-naphthoxy acetic acid N-hydroxysuccinimide ester (AED-NH2) were stimulated in vitro with AED-NH2-modified syngeneic cells. After 5 days of culture, effector cells were assayed for their cytotoxic activity against AED-NH2-modified target blast cells. C3H/He and BALB.K mice exhibited the respective high and low anti-AED-NH2 cytotoxic T lymphocyte (CTL) responses. This contrasted with the observation that both of these H-2k strains generated potent CTL responses against aminoreactive haptens, e.g., trinitrophenyl (TNP). Because C3H.SW and BALB.B strains, which are the H-2b counterpart of the above two strains, also represented the respective high and low responders to AED-NH2 hapten, this hapten model enabled us to investigate cellular mechanisms underlying the above non-H-2-associated genetic regulation of CTL responses (C3H vs BALB non-H-2 backgrounds). The results demonstrated that there was no detectable difference between C3H/He and BALB.K strains in the lysability of target cells and the ability of stimulating cells to activate primed spleen cells. Anti-AED-NH2 CTL responses were only marginal when antigen-presenting cells (APC) were eliminated from the primed spleen cells of high responder C3H/He or (C3H/He X BALB.K)F1 mice. The addition of APC to cultures free of APC regained an appreciable CTL response in C3H/He or (C3H/He X BALB.K)F1 mice, irrespective of whether APC were derived from high (C3H/He) or low (BALB.K) responders. We have also demonstrated that allogeneic radiation bone marrow chimera (BALB.K----C3H/He) exhibited a CTL response comparable to that induced by C3H/He mice, whereas the reverse direction of allogeneic chimera (C3H/He----BALB.K) induced a marginal CTL response. These results indicate that this non-H-2-associated Ir gene defect is expressed on T cells (CTL precursors and/or helper T cells) rather than APC, and that this T cell defect is not predetermined at the level of bone marrow cells. The results are discussed in the light of the genetic and cellular mechanisms underlying non-H-2-linked Ir gene control.

In the present study we investigated some of the cellular mechanisms for the generation of macrophage-activating factor(s) (MAF) in immune responses to tumor antigens. C3H/HeN mice were immunized to syngeneic MH134 hepatoma or MCH-1-A1 fibrosarcoma by intradermal inoculation of viable tumor cells, followed by the surgical resection of the tumor. Spleen and lymph node cells from these tumor-immune mice were stimulated in vitro with the corresponding tumor cells, and supernatant from such a culture was tested for an ability to activate macrophages to exert their cytostatic and cytolytic activities as detected on tumor cells unrelated to immunizing tumors. Peritoneal adherent cells as a macrophage source, which were preincubated with supernatant from co-culture of tumor-unimmunized normal spleen and lymph node cells plus tumor cells, failed to exhibit any significant antitumor effect on unrelated X5563 tumor cells, whereas the addition of supernatant from cultures containing immune lymphocytes to adherent cells resulted in appreciably potent cytostatic and cytolytic effects on X5563 tumor cells, indicating the generation of MAF in culture supernatant. The activation of tumor-immune spleen and lymph node cells for MAF generation was tumor-specific, because anti-MH134- and anti-MCH-1-A1-immune lymphocytes produced MAF by the stimulation with the respective but not with the other alternative tumor cells. Such MAF production was abolished by treatment of tumor-immune spleen and lymph node cells with anti-Thy-1.2 or anti-Lyt-1.1 but not with anti-Lyt-2.1 antibody plus complement before culturing. These results indicate that the tumor-specific Lyt-1+2- T cell subset has a crucial role in generating MAF by which an adherent cell population as a source of macrophages acquires the potential for inducing a cytolytic as well as a cytostatic effect on tumor cells.

The rate of ZnAl2O4 formation was measured for η-, γ-; and α- Al2O3 in order to distinguish the reactivity of them. The reactivity decreased as follows: η- > γ- > α-Al2O3. The reaction rate fitted to Jander's equation and the activation energies calculated were 33, 47 and 113 Kcal/mol for η-, γ- and α-Al2O3 systems, respectively. These differences are explained by an assumption that η- and γ-Al2O3 resulted in a ZnAl2O4 with imperfect spinel structure, but α-Al2O3 gave the perfect spinel structure. This assumption is based on the theoretical consideration of the activation energy needed for the diffusion-controlled reaction and date of lattice constant of each ZnAl2O4 obtained from three aluminas. The fact that η-Al2O3 shows very high reactivity compared with that of γ-Al2O3 was found to be explained on the basis of Jander's equation, a comparison of specific surface area and the defect structures of the aluminas. Reaktionsfahigkeit des η-, γ- und α-Al2O3 bei der ZnAl2O4-Bildung Die Geschwindigkeit der ZnAl2O4-Bildung wurde fur η-, γ- and α-Al2O3 gemessen, um ihre Reaktivitut zu bestimmen. Die Reaktivitut fullt in der Reihe η- > γ- > α-Al2O3. Die Reaktionsgeschwindligkeit gehorcht der JANDERschen Gleichung, und die berechneten Aktivierungsenergien betragen 33, 47 und 113 kcal/Mol fur η-, γ- und α-Al2O3. Diese Unterschiede werden durch die Annahme erklurt, das η- und γ-Al2O4 unvollstundiger Spinelstruktur ergeben, wuhrend α-Al2O4 eine vollstundige Spinelstruktur ergibt. Diese Annahme basiert auf den fur die diffusionskontrollierte Reaktion benutigten Aktivierungsenergien und auf den Daten fur de Gitterkonstanten der aus den drei Aluminaten erhaltenen Zinkspinelle. Die Tatsache, Das η-Al2O4 eine sehr hohe Reaktivitut zeigt verglichen zu der des γ-Al2O4, kann auf Grund der JANDERschen Gleichung, durch Vergleich der spezifischen Oberfluchengruszlig;en und der Defektstrukturen der Aluminiumoxide erklart werden.

The present study was designed to investigate the generation of trinitrophenyl (TNP)-reactive helper T cell activity potent enough to induce the regression of a syngeneic tumor; this occurs by augmenting antitumor-specific immunity through T-T cell interaction. Mice whose skin was painted with trinitrochlorobenzene (TNCB) exhibited a variety of anti-TNP T cell responses, including delayed-type hypersensitivity (DTH) and cytotoxic T cell responses, as well as helper T cell activity. Pretreatment of C3H/He mice with TNP-conjugated copolymer of D-glutamic acid and lysine (TNP-D-GL) or cyclophosphamide, which have been shown, respectively, to inactivate TNP-specific suppressor T cells or suppressor T cells in general, exhibited a slight or marginal augmentation of DTH and cytotoxic potentials when tested 5 wk after TNCB painting. In contrast, the same pretreatment regimens induced an appreciably amplified generation of anti-TNP helper T cell activity. This amplified TNP-helper T cell activity was demonstrated to enhance cytotoxic responses to antigens other than TNP in an antigen-nonspecific way. In fact, such helper T cells enhanced antitumor CTL responses when co-cultured with spleen cells from syngeneic X5563 plasmacytoma-bearing mice in the presence of TNBS-modified X5563 tumor cells. This amplified TNP-helper cell system was utilized for its immunotherapeutic potential. When TNCB was injected into X5563 tumor mass of syngeneic C3H/He mice in which the amplified TNP-helper T cell activity had been generated, an appreciable number of growing tumors was observed to regress. This contrasted with the low incidence of tumor regression observed in mice in which TNP-helper activity had been induced by TNCB painting without inactivation of suppressors. Thus, the present model provides an effective immunotherapeutic manipulation for eliciting enhanced in vivo tumor regression, and emphasizes a role of helper T cells in augmentation of syngeneic tumor immunity.

Bericht uber einen Fall mit rezidivierendem Aneurysma der A. carotis interna — communicans posterior nach erfolgreicher Verclippung mit einem Heifetz-Clip. Ursache des Rezidivs war das Abbrechen eines Clipblattes an seinem proximalen Ende langere Zeit nach der Operation. Ursache scheinen strukturelle Fehler des Aneurysmaclipmetalles gewesen zu sein.

Pure aluminum and its dilute alloys are deformed by about 10% at 4.2 K with a tensile testing machine. A recovery of the electrical resistivity due to isochronal and isothermal annealings is measured at temperatures ranging from 30 to 170 K. The main recovery peak observed up to 170 K appears around 85 K with associated activation energies of (0.21 ± 0.02) eV for pure aluminum and (0.24 ± 0.01) eV for AlGe alloy. The suppressive effect of impurities on the recovery is ordered as Ge > Si > Cu > Ag > Mg. An interpretation of stage II recovery is proposed on the basis of these results. Reines Aluminium und seine verdunnten Legierungen werden um etwa 10% bei 4,2 K mit einer Dehnungstestmaschine deformiert. Eine Erholung der elektrischen Leitfahigkeit nach isochroner und isothermer Temperung wird im Temperaturbereich von 30 bis 170 K gemessen. Das Hauptmaximum der Erholung, das bis 170 K beobachtet wird, erscheint bei etwa 85 K, mit einer dazugehorigen Aktivierungsenergie von (0,21 ± 0,02) eV fur reines Aluminium und (0,24 ± 0,01) eV fur die AlGe-Legierung. Der Unterdruckungseinflus von Storstellen auf die Erholung erfolgt in der Reihenfolge Ge > Si > Cu > Ag > Mg. Eine Interpretation der Erholungsstufe II wird auf der Grundlage dieser Ergebnisse vorgeschlagen.

Four kinds of prostaglandins (PGs), 6-keto-PGF1 alpha, PGF2 alpha, PGE2 and PGD2, in rat gastric mucosa were decreased at 1 or 6 h after oral administration of indomethacin (2 or 12 mg/kg). With 2 mg/kg of indomethacin, the PG levels had slightly recovered 6 h later. Gastric lesions were observed 6 h after administration of indomethacin (12 mg/kg), but not with 2 mg/kg. Omeprazole (20 mg/kg, i.p.) prevented ulcer formation caused by indomethacin, without improvement of the reduced gastric mucosal PG levels. PGD2 (0.5 mg/kg, p.o.) reduced indomethacin-induced gastric lesions and considerable amounts of PGD2 existed in the gastric mucosa. We conclude that H+ is a determining factor in the genesis of indomethacin-induced gastric lesions and persistent decreases in tissue PG levels also participate in ulcer formation.

Concanavalin A (Con A)-activated T lymphocytes from patients with active, but not inactive, systemic lupus erythematosus (SLE) failed to express normal suppressor activity, regardless of the phenotype of CD4+ or CD8+. Con A-activated CD4+ or CD8+ T lymphocytes from the SLE patients and from normal controls were further separated into two populations, using the autologous erythrocyte rosette technique. One population very rich in cells capable of forming rosettes with autologous erythrocytes from the active patients showed the same degree of suppressor activity, as did that from normal controls; the CD4+ or CD8+ population poor in autorosetting cells derived from Con A-activated T lymphocytes from both the controls and patients did not express suppressor activity. Moreover, when autorosetting T cells from the active patients and nonrosetting cells from the same patients were mixed at a normal ratio (4:6), normal suppressor activity could be restored. It was notable that the frequency of autorosette-forming cells was markedly reduced in the Con A-activated T lymphocytes from the active, but not inactive, SLE patients, regardless of the phenotype of CD4+ or CD8+. These findings indicate the presence of a normally functioning suppressor T cell population in patients with active SLE. It seems that the lack of suppressor T cell function in patients with active SLE is due to the dilution of a few normal suppressor T cells by large numbers of nonsuppressor T lymphocytes.

Chronic toxicity of hydrocortisone 17-butyrate 21-propionate (HBP), a new synthetic corticosteroid, was studied in rats. HBP was subcutaneously injected to rats as the daily doses of 0.001, 0.01, 0.01, 1.0 and 3.0 mg/kg for 6 months, and the following recovery test was carried out for 4 weeks. Hydrocortisone 17-butyrate (HB) and betamethasone 17-valerate (BV) were used as the reference drugs at the doses of 0.1, 1.0 and 3.0 mg/kg. The suppression of body weight gain by the administration of HBP was observed at the doses more than 1.0 mg/kg in male and more than 0.1 mg/kg in female, and the dead animals were sent at the highest dose of HB and BV. Mainly at the doses more than 0.1 mg/kg HBP induced the dose-dependent symptoms such as decrease in the number of white blood cells and total protein level in serum, and increase in total cholesterol, GOT and GPT level in serum, and atrophic changes of adrenals, lymphatic tissues, skin and subsexual organs. No usual abnormality was recognized at the doses less than 0.01 mg/kg of HBP. These symptoms were more toxic in male, and the strength of toxicity was in the order of BV greater than HB greater than HBP. Many of these findings have known as common effects of corticosteroids. The changes observed in this study were almost recovered after withdrawal of HBP at the doses less than 0.1 mg/kg. As the result, it was suggested that the maximum non-toxic dose of HBP was 0.001 mg/kg.

患者は22歳(初診時)男性で18歳時に他院で潰瘍性大腸炎として治療され緩解し,4年後に下痢体重減少にて当院受診した。大腸X線・内視鏡検査でS状結腸から横行結腸半ばまで潰瘍がびまん性にみられ潰瘍性大腸炎と診断した。disodium cromogrycate(DSCG)経口投与単独で2カ月後に症状緩解し,内視鏡検査で潰瘍は消失,粘膜橋,炎症性ポリープの形成がみられ,血沈やCRPも正常化した。その後治療を中断,1年2カ月後に発熱,粘血便性下痢にて再燃,入院した。X線・内視鏡所見は初診時と同様で,DSCG経口投与で症状はやや軽快したが微熱は続き,排便回数も多かったので注腸投与にかえ,2カ月後に症状の緩解をみた。その後経口投与にしたが症状の悪化はなく,内視鏡検査でも潰瘍は消失し退院した。近年本邦でも潰瘍性大腸炎の治療に抗アレルギー剤が用いられるようになったが,DSCGが有効であったという報告はなく,今後多くの施設での検討が期待される。

We have treated three cases of shotgun injury of the extremities. They were 43, 50 and 67 years old males.Generally, the shotgun injury of the extremities somewhat differs from that of the other parts according to the condition of the wounds and the method of treatment.These wounds are usually associated with massive tissue destruction.From our experience, we would recommend extensive debridement, internal fixation of fractures and primary would closure with split-thickness skingraft.

The magnetic behavior of CeP, CeAs, CeSb, PrP, PrAs, and PrSb has been investigated over the temperature range extending from 4° to 300°K. Curie—Weiss behavior is observed for all compounds in the upper portion of the temperature range studied with effective moments in fair agreement with those expected for the free tripositive ions. The cerium compounds have Neel points at temperatures ranging from 8° to 25°K. The praseodymium compounds give no evidence of magnetic ordering. At low temperatures they exhibit the Van Vleck temperature‐independent paramagnetism. This is attributed to the influence of the crystal field in splitting the ninefold degenerate ground state of the free Pr3+ ion. The susceptibility—temperature behavior of PrSb can be accounted for in terms of a single parameter from which an over‐all crystal field splitting of 157 cm−1 is deduced. Similar attempts for PrP and PrAs were unsuccessful, presumably because of the increased importance of nonlinear shielding effects in these materials. Th...

Magnetization-temperature data have been obtained for TiFe2, ZrFe2, YFe2, YMn2 and a series of alloys represented by the formula YMn2−xAlx. Curie-Weiss behavior is observed for all the systems studied except for YMn2 and the ternary alloys with x 1.5 is in a 3d3 configuration, corresponding to Mn+4. The difference in phase relations observed in ternaries involving the lanthanides and aluminum combined with Mn on the one hand and Fe or Co on the other is attributed to the shift of Mn d electrons from a localised to a delocalised condition and the involvement of the d electrons in the latter case in the establishment of the Fermi Surface. In this group of compounds Fe and Mn (in dilute solution) contribute 0.2 and 4 electrons, respectively, to the electron concentration. This is in close accord with valence of zero for Fe advanced many years ago by Hume-Rothery .

The magnetic behavior of the series of lanthanide—bismuth compounds having the formula LnBi was investigated over a range of temperature extending from 4° to 300°K and at field strengths ranging from 5 to 21 kOe. Ln represents Ce, Pr, Nd, Sm, Gd, Tb, Dy, and Er. Curie—Weiss behavior was observed in the upper portion of the temperature range covered for all except SmBi. Effective moments were obtained which were in close agreement with that expected from theory for the free tripositive ions. The behavior for SmBi resembles that of elemental Sm and other Sm intermetallics and is attributed to contribution of the first excited multiplet (J=7/2). Antiferromagnetic ordering was observed for all compounds except the Pr and Sm. A Neel point for the latter probably exists but below 4°K. PrBi exhibits only Van Vleck paramagnetism to the lowest temperatures studied. This is ascribed to crystal field splitting which produces a singlet (nonmagnetic) ground state. From the limiting susceptibility an over‐all splitting by the crystal field of 140 cm−1 is estimated. CeBi exhibits metamagnetism with a critical field of about 10 kOe. Its behavior as a metamagnet is atypical and is generally complex in the region where magnetic ordering occurs.

The magnetic behavior of CeIn3, CePb3, and the series of compounds represented by the formula LnSn3 with Ln=Ce, Pr, Nd, Sm, and Gd has been investigated over the temperature range 2° to 300°K. Curie—Weiss behavior was observed in the upper portion of the temperature range for all compounds except SmSn3, and effective moments were in close agreement with those expected for the free tripositive ions. The behavior for SmSn3 is attributed to contribution of the first excited multiplet (J=7/2). Neel points were observed for CeIn3, PrSn3, NdSn3, and SmSn3. Deviations from Curie—Weiss behavior at low temperatures were observed in all cases and were ascribed to antiferromagnetic ordering, crystal‐field effects, and ionization of Ce in the Ce compounds into the quadripositive state. GdSn3 is complex in that it shows deviation from Curie—Weiss below 40°K but it has no susceptibility peak.

Experience with Radio Isotope Myelography is reported here. 169Yb-DTPA as a tracer was intrathecally injected at lumbar region in twenty three patients with various spinal cord lesions. The first scanning is perfomed after comfirming by gamma-camera that the tracer reaches to the lesion, the second and the third scannings are done according to the ascending rate of the tracer. (I) Normal scintimyelogram (A) In normal case, the shape of the Radio Isotope Myelogram well corresponds the shape of anatomical subarachnoid space. (B) In normal adult cases, the tracer comes up to the cisterna magna in 20-25 minutes after the lumbar injection. Therefore, the scintimyelographic diagnosis should be made not only by the shape but also by the ascending rapidity of the tracer. (II) Abnormal scintimyelogram Abnormal scintimyelograms could be summarized as following three categories. (A) "Delay": It means delay of the ascending of the tracer. Besides, "Transient delay" found in a case of Arnord-Chiari's malformation was proposed. (B) "Partial block": It meas a defect at the level of the lesion. This "Partial block" were observed in cases of spinal cord angioma, cervical spondylosis and spinal cord tumor etc. (C) "Complete block": It means the stagnation of the tracer below the lesion. To sum up, Rario Isotope Myelography, especially in partial block, can more easily and more sensitively represent the maximum extent of the spinal cord lesion than other myelographic study or angiographic one. On the other hand, we can not qualitatively diagnose about the lesions by its indistinct border.

This study was undertaken to examine and quantitate the chemical injury and repair of the dog nucleus pulposus in collagenase-induced chemonucleolysis. Thirty three adult mongrel dogs were used into which the purified collagenase was injected at a rate of 200 units. The dogs were sacrificed after roentgenography. Disc specimens were stained primarily with safranin-O for microscopic study, and fresh tissues were used for electron microscopic study. For immunohistochemical analysis, paraffin sections were reacted with anti-bovine types I, II and III collagen antibodies. Two weeks after the injection, the height of the injected disc was reduced by about 50% and there was no sign of recovery for 52 weeks. There was a profound loss of safranin-O stainability in the nucleus pulposus, annulus fibrosus and cartilagenous endplate. By 8 weeks, regeneration of the nucleus pulposus began and chondrocytes appeared from the junctional area. The regenerated nucleus pulposus was stained well with safranin-O and consisting largely of type II collagen immunohistochemically. In the regenerated nucleus pulposus, collagen fibers and proteoglycans were reconstructed in a net-work with hyaluronic acids.

The present study deals with the influence of presensitization with tumor antigens via the intragastric route on the development of syngeneic tumor-specific immunity. Tumor-specific T cell-mediated immunity could be induced in C3H/He mice by intradermal inoculation of syngeneic X5563 tumor cells, followed by the surgical resection of the tumor 7 days later (immunization procedure). However, when the mice were presensitized intragastrically (ig) with 10(8) X-irradiated (10,000 R) tumor cells for four consecutive days, these mice failed to show in vivo protective immunity even after the above immunization procedure. Winn assays performed with spleen cells from mice presensitized ig with X5563 tumor cells revealed that ig-induced suppression was specific for the tumor antigen used for the presensitization, and that suppressor cell activity was not detected in the induction or implementation of in vivo tumor-specific effector cell activity. It was also demonstrated that such unresponsiveness was accompanied by failure to develop delayed-type hypersensitivity and cytotoxic T cell responses to X5563 tumor antigens. These results are discussed in the light of the effect of presensitization with tumor antigens via inappropriate routes on the subsequent induction of in vivo tumor-specific immunity and in relation to the tumor escape mechanism which could occur in gastrointestinal cancers.

Chronic toxicity of a new synthetic corticosteroid, hydrocortisone 17-butyrate 21-propionate (HBP), was investigated in rats of both sexes. HBP was percutaneously given to rats with 0.1%, 0.5% cream and ointment at the daily dose level of 150 mg per 100 g body weight for 6 months. For the comparison, the percutaneous toxicity with 0.12% betamethasone 17-valerate (BV) cream and ointment, and 0.1% hydrocortisone 17-butyrate (HB) cream and ointment at the daily dose level of 150 mg per 100 g body weight were studied. Rats receiving HBP showed the dose-dependent changes such as the suppression of body weight gain and food intake, emaciation, decrease in the number of white blood cells and lymphocytes, total protein, increase in the number of red cells, hematocrit, hemoglobin, blood sugar and total cholesterol, regressive changes in adrenal cortex, lymphatic and hematopoietic tissues and skin, and gastric erosion, which have been well known as toxic effects of synthetic corticosteroids. These findings were comparatively high toxic in male, and almost disappeared in rats elapsed recovery time of month after withdrawal of HBP. The toxicities of HBP, BV and HB were qualitatively same. However, the grade of effects of HBP toxicity was similar to that of HB, weaker than of BV.

We report on 4 cases of brain tumors associated with tuberous sclerosis. In each case the tumor was in the region of Monro's foramen and was associated with ventricular dilatation. Computer tomography scans, which were performed in 3 cases, revealed well-circumscribed high-density masses which were markedly enhanced by contrast medium. 3 patients underwent craniotomy. Total extirpation was performed in 2 patients. Both of them are doing well postoperatively. However, 1 patients whose tumor had been partially resected died of recurrence 6 years after surgery. The pathology of three tumors was different in each case: plump cell astrocytoma, hemangioma and astroblastoma.

The present study was carried out to investigate the preventive effect of Propionibacterium acnes (P. acnes) on metastasis formation of C3H/He mice which has been rendered tolerant to tumor-associated transplantation antigen (TATA) of syngeneic X5563 plasmacytoma. C3H/He mice inoculated intravenously (iv) with 10(6) 7000 R X-irradiated X5563 tumor cells 3 times at 4-day intervals. These pretreated mice could not develop immune resistance against X5563 tumor even after the appropriate immunization procedure. In these TATA-tolerant mice, enhanced metastasis associated with the development of visually apparent metastatic nodules in the spleens was observed after intradermal (id) implantation with viable tumor cells, even if the tumor was resected surgically 7 days thereafter. Administration of P. acnes to these TATA-tolerant mice appreciably reduced the metastasis formation. Although the growth of the id primary tumor was not affected by injection with P. acnes, the combined treatment of surgical resection of the primary tumor and P. acnes administration resulted in complete protection against metastasis in TATA-tolerant mice. These results unequivocally demonstrated that the administration of P. acnes is effective for preventing the outbreak of metastasized tumors, which are readily inducible in the TATA-tolerant state.

A case of deep sylvian meningioma is reported which is unusual in the aspect that the initial symptoms were headache and vomiting due to intracerebral hemorrhage from meningioma. After evacuation of hematoma in the right temporal lobe and biopsy of the tumor, it was found to be meningothelial meningioma with psammoma bodies. Cerebral angiography showed characteristic findings of intrasylvian vascular tumor. Complete removal of this tumor was performed under microscopy, dissecting dense adhesion between the tumor and main branches of the middle cerebral artery. Consequently, the patient showed only slight impairment of fine movement of his left fingers. Deep sylvian meningioma designated by Cushing and Eisenhart is very rare. This case is the only one of deep sylvian meningioma in our whole series of 181 intracranial meningiomas and probably the twentieth case reported so far in the literature.