Axial ligation of nitrogenous bases to five-coordinate chloro-meso-tetraphenylporphyrinatochromium(III)

The axial ligations of nitrogenous bases to the five-coordinate chloro-meso-tetraphenylporphyrinatochromium(III) [Cr(III)(TPP)(Cl)] were studied in a non-coordinating solvent, dichloromethane (CH₂Cl₂), by spectrophotometric methods. A correlation exists between log K for the axial ligation:

and pK_a for the N-donor ligand. This correlation suggests that ligand to metal σ bonding contributes to the complex formation, rather than does metal to ligand π back-donation.     

Forest succession in the subalpine region of Mt. Fuji,Japan

Subalpine forest succession was studied on Mt. Fuji, Japan, where various types of forests in different successional phases occur owing to volcanic action. Ninety stands were subjected to ordination using an index (SI) defined by the relative basal area and the life span of component woody species, and the cover of canopy layer of the sample stands. Two different sequences of sample stands were found. One was from deciduous scrubs, through Larix kaempferi forests and Abies forests, to Tsuga diversifolia forests, and the other from Abies-Tsuga thickets to Abies forests. Through analyses of the forest structure and composition, soil survey and identification of fallen logs, the former sequence was recognized as the primary sere and the latter as a regeneration sere following gap formation. During forest succession, basal area reached a maximum in the seral phase with a multi-layered structure. The Tsuga forests, whose understory is restricted to a moss layer, were regarded as the climax. The death or fall of Tsuga stems resulted in gaps, which were subsequently occupied by Abies-Tsuga thickets. The second Abies forests were distinguished from the ones in the primary sere by the occurrence of Dryopteris and Cacalia and the lack of Rhododendron in the understorey. Both Abies forest types included Tsuga saplings. Thus, a cyclic relation is supposed between Abies and Tsuga.Nomenclature follows Ohwi (1975) and Nakaike (1982) for vascular plants, Iwatsuki & Noguchi (1973) for mosses, Inoue (1981) for hepaticae, Kashiwadani (1981) for lichens, respectively. Abies veitchii, A. mariesii were lumped as Abies spp.I wish to express my sincere gratitude to Prof. Toshio Hamaya, Tokyo, for the cordial guidance and encouragement. I also thank Prof. M. Numata and Dr. M. Ohsawa, Chiba, Prof. K. Okutomi, Tokyo, Dr. K. Suzuki, Tokyo, Dr. M. Suzuki, Kanazawa, and Mr. H. Taoda, Kumamoto, for their valuable advice and discussions.     

Epitope expression on primate lymphocyte surface antigens

The cross-reactivity of peripheral blood mononuclear cells from 28 nonhuman primates was investigated with ten kinds of Leu series of monoclonal antibodies specific to human T-, natural killer/killer-, and B-cells. The chimpanzees possessed all ten epitopes examined but the orangutan lacked Leu4 and Leu7 epitopes and the gibbons lacked Leu4, Leu7, and Leu12 epitopes. In addition to the above epitopes, the Old World monkeys lacked Leu1 and Leu10 epitopes. The Leu3a/Leu2a cell ratios varied from 0 to 1.56 among the 12 macaque species and this enabled classification of these species into three groups. In the New World monkeys, Leu2a epitope was absent, whereas Leu11a epitope was detected in several species and Leu3a epitope was found only in the owl monkeys. The prosimians expressed only HLA-DR epitope.     

Characterization of newly isolated monoclonal antibodies against MHC of a Japanese wild mouse

We have already developed nine B10.MOL congenic strains carrying H-2 haplotypes derived from Japanese wild mice, Mus musculus molossinus, with the C57BL/10 genetic background. To obtain monoclonal antibodies against the H-2 antigen of the Japanese wild mouse, we carried out cell fusion using spleen cells from the animal immunized with one of the B10.MOL strains, B10.MOL-SGR (H-2 ^wm7). As a result, 19 hybridomas producing monoclonal antibodies were produced. Analysis with the intro-H-2 recombinants derived from B10.MOL-SGR indicated that 8 of them reacted with the class I and II with the class II molecule. The class I antibodies were tested for their cross -reactivities on wild mice and on the panels of standard inbred and B10.MOL strains. Most of the antibodies reacted with both the Japanese wild mice and the other subspecies, including standard inbred, while two antibodies highly specific for the donor H-2K region reacted with only three wild-derived mice, two M. m. molossinus from Anj o and Shizuoka, Japan, and one M. m. domesticus from Pigeon, Canada. In addition, all of the other four antibodies reactive with the K antigen of B10.MOL-SGR also reacted with the same three wild mice. The wild mice belonging to different subspecies might share very similar H-2K antigenic determinants in spite of their genetic and geographical remoteness.     

Mode of antitumor action of recombinant human tumor necrosis factor on the sarcoma Meth A transplanted in the mouse

The mode of antitumor action of rHu-TNF was elucidated in BALB/c mice bearing Meth A fibrosarcoma 7 days after transplantation with respect to time course, dose-response relationships and selectivity of the effects. The maximal cytotoxic effect on tumor cells revealed by inhibition of DNA synthesis and maximal lesional effect on tumor vasculature revealed by change in blood pool-size in the tissue were detected at 30 min and I h after administration of rHu-TNF, respectively. The dose-response relationship between cytotoxic and tumoricidal effects of rHu-TNF was irrespective of administration route. ED₅₀s of these antitumor effects afteri.v. administration of rHu-TNF were about 50 times as high as ED₅₀s afteri.t. administration. ED₅₀ ofi.t. given rHu-TNF for vascular effect was about 20 times as high as that for cytotoxicity while ED₅₀ ofi.v. rHu-TNF for vascular effect was only 2–3 times as high as that for cytotoxicity. The whole body autoradiographies with [¹²⁵I] HSA giveni.v. to see the blood influx into tumor tissue and [¹⁴C]thymidine given i.v. to see DNA synthesis in the whole body after administration of rHu-TNF revealed that the distribution of radioactivity was markedly changed in the tumor alone without any detectable change in other whole body tissues.In conclusion, thein vivo antitumor effect of rHu-TNF giveni.t. ori.v., appears to be exerted through the direct action on Meth A sarcoma rather than indirectly on tumor vasculature. Under present conditions, the effect of rHu-TNF in the whole body tissues seems rather selective on cells and vasculature of the tumor.     

Intravesical treatment of bladder cancer with recombinant human interferon-β

Summary In order to examine its clinical efficacy, recombinant human interferon- (rIFN-) was instilled intravesically into 51 patients with superficial bladder cancer. Ten patients, who received intermittent intravesical instillation at a dose of (3–36) × 10⁶ U rIFN- on days 1–3 every week, showed no response. Thirty-two patients received intravesical instillation at a dose of (3–36) × 10⁶ U every day for 10–20 days. Eight patients showed partial response, indicating an efficacy rate of 25%. Nine patients received divided doses of 18 × 10⁶ U twice a day every day for 10–20 days. Six patients showed partial response, indicating an efficacy rate of 67%. This value was significantly higher than that obtained by administering divided doses. The response to intravesical instillation therapy with rIFN- varies with treatment protocol. Frequent and longer exposure to rIFN- may induce better regression of superficial bladder cancer. Six incidences of side-effects were found in five cases (9.8%): pollakiuria in one, pain on micturition in two, fever in two, and eruption in one case. All of these side-effects were slight and reversible after drug withdrawal. Laboratory tests showed only a few changes with low severity. Thus, rIFN- is potentially a new drug for instillation therapy of superficial bladder cancer, in view of the absence of adverse effects.     

Role of growth hormone in modulating the constitutive and phenobarbital-induced levels of two P-450(6)beta (testosterone 6 beta-hydroxylase) mRNAs in rat livers

The role of growth hormone in the expression of two forms of hepatic cytochrome P-450(P-450), P-450(6)beta-1(6 beta-3), and P-450(6)beta-4, was investigated using RNA blots. The level of P-450(6)beta-1(6 beta-3) mRNA was twenty times higher than that of P-450(6) beta-4 mRNAs in untreated male rat livers. The levels of P-450(6)beta-1(6 beta-3) and P-450(6)beta-4 mRNAs were increased two fold and three fold, respectively, by hypophysectomy of adult male rats. By intermittent injection of human growth hormone (hGH) into hypophysectomized male rats, both mRNAs were decreased to the level of normal rats, and almost disappeared after continuous infusion of hGH. In female rats, these two mRNAs were not detected, but were increased remarkably by hypophysectomy. The increases in these mRNAs were almost abolished after continuous infusion of hGH in hypophysectomized female rats. The effect of hGH on PB-mediated induction of P-450(6)beta-1(6 beta-3) and P-450(6)beta-4 mRNAs was also examined. The PB-mediated increases in P-450(6)beta-1(6 beta-3) and P-450(6)beta-4 mRNAs were higher in hypophysectomized male rats (2.5-fold and 10.9-fold, respectively) than in normal male rats (1.5-fold and 5.2-fold, respectively). Thus, the levels of P-450(6)beta-1(6-beta-3) and P-450(6)beta-4 mRNAs were 4.1-fold and 7.3-fold, respectively, higher in PB-induced hypophysectomized rats than in normal male rats. Concerning the postnatal developmental profiles, P-450(6)beta-1(6 beta-3) mRNA was detectable at neonate and reached a maximal level at around 17 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enhancement of adenosine A2 and prostaglandin E1 receptor-mediated cAMP generation by prior exposure of Swiss 3T3 fibroblasts to Ca2+-mobilizing receptor agonists or phorbol ester. Activation of protein kinase C triggers increases in the receptor density in cell membranes

Production of cAMP in response to adenosine A2 or prostaglandin E1 receptor stimulation was, but the production induced by a beta-adrenergic agonist or forskolin was not, enhanced by prior exposure of Swiss 3T3 fibroblasts to agonists of Ca2+-mobilizing receptors or phorbol ester for 3 h. The enhancement reflected potentiation of the receptor-coupled activation of adenylate cyclase and the 2-fold increase in the adenosine A2 receptor number in membranes under these conditions. No enhancement was observed, however, when the medium used for the prior exposure was further supplemented with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) or staurosporin, inhibitors of protein kinase C, neither of which affected the cAMP responses of the nonexposed cells. It is very likely, therefore, that activation of protein kinase C triggers the increase in certain receptor density in membranes, thereby enhancing the receptor-coupled cAMP-generating responses. The physiological significance of such cross-talk between cellular signaling systems is discussed in comparison with similar previous observations.