Mapping of a New Deformation Region around

We performed the first direct mass measurements of neutron-rich scandium, titanium, and vanadium isotopes around the neutron number 40 at the RIKEN RI Beam Factory using the time-of-flight magnetic-rigidity technique. The atomic mass excesses of ^{58-60}Sc, ^{60-62}Ti, and ^{62-64}V were measured for the first time. The experimental results show that the two-neutron separation energies in the vicinity of ^{62}Ti increase compared to neighboring nuclei. This shows that the masses of Ti isotopes near N=40 are affected by the Jahn-Teller effect. Therefore, a development of Jahn-Teller stabilization appears below the Cr isotopes, and the systematics in Sc, Ti, and V isotopes suggest that ^{62}Ti is located close to the peak of the Jahn-Teller effect.

How Different is the Core of

The structure of a neutron-rich ^{25}F nucleus is investigated by a quasifree (p,2p) knockout reaction at 270A MeV in inverse kinematics. The sum of spectroscopic factors of π0d_{5/2} orbital is found to be 1.0±0.3. However, the spectroscopic factor with residual ^{24}O nucleus being in the ground state is found to be only 0.36±0.13, while those in the excited state is 0.65±0.25. The result shows that the ^{24}O core of ^{25}F nucleus significantly differs from a free ^{24}O nucleus, and the core consists of ∼35% ^{24}O_{g.s.}. and ∼65% excited ^{24}O. The result may infer that the addition of the 0d_{5/2} proton considerably changes neutron structure in ^{25}F from that in ^{24}O, which could be a possible mechanism responsible for the oxygen dripline anomaly.

Excitation of the Isovector Spin Monopole Resonance via the Exothermic

The (^{12}N, ^{12}C) charge-exchange reaction at 175 MeV/u was developed as a novel probe for studying the isovector spin giant monopole resonance (IVSMR), whose properties are important for better understanding the bulk properties of nuclei and asymmetric nuclear matter. This probe, now available through the production of ^{12}N as a secondary rare-isotope beam, is exothermic, is strongly absorbed at the surface of the target nucleus, and provides selectivity for spin-transfer excitations. All three properties enhance the excitation of the IVSMR compared to other, primarily light-ion, probes, which have been used to study the IVSMR thus far. The ^{90}Zr(^{12}N,^{12}C) reaction was measured and the excitation energy spectra up to about 70 MeV for both the spin-transfer and non-spin-transfer channels were deduced separately by tagging the decay by γ emission from the ^{12}C ejectile. Besides the well-known Gamow-Teller and isobaric analog transitions, a clear signature of the IVSMR was identified. By comparing with the results from light-ion reactions on the same target nucleus and theoretical predictions, the suitability of this new probe for studying the IVSMR was confirmed.

Extraction of the Landau-Migdal Parameter from the Gamow-Teller Giant Resonance in

The key parameter to discuss the possibility of the pion condensation in nuclear matter, i.e., the so-called Landau-Migdal parameter g^{'}, was extracted by measuring the double-differential cross sections for the (p,n) reaction at 216 MeV/u on a neutron-rich doubly magic unstable nucleus, ^{132}Sn with the quality comparable to data taken with stable nuclei. The extracted strengths for Gamow-Teller (GT) transitions from ^{132}Sn leading to ^{132}Sb exhibit the GT giant resonance (GTR) at the excitation energy of 16.3±0.4(stat)±0.4(syst) MeV with the width of Γ=4.7±0.8 MeV. The integrated GT strength up to E_{x}=25 MeV is S_{GT}^{-}=53±5(stat)_{-10}^{+11}(syst), corresponding to 56% of Ikeda's sum rule of 3(N-Z)=96. The present result accurately constrains the Landau-Migdal parameter as g^{'}=0.68±0.07, thanks to the high sensitivity of the GTR energy to g^{'}. In combination with previous studies on the GTR for ^{90}Zr and ^{208}Pb, the result of this work shows the constancy of this parameter in the nuclear chart region with (N-Z)/A=0.11 to 0.24 and A=90 to 208.

Magic Nature of Neutrons in

We perform the first direct mass measurements of neutron-rich calcium isotopes beyond neutron number 34 at the RIKEN Radioactive Isotope Beam Factory by using the time-of-flight magnetic-rigidity technique. The atomic mass excesses of ^{55-57}Ca are determined for the first time to be -18650(160), -13510(250), and -7370(990) keV, respectively. We examine the emergence of neutron magicity at N=34 based on the new atomic masses. The new masses provide experimental evidence for the appearance of a sizable energy gap between the neutron 2p_{1/2} and 1f_{5/2} orbitals in ^{54}Ca, comparable to the gap between the neutron 2p_{3/2} and 2p_{1/2} orbitals in ^{52}Ca. For the ^{56}Ca nucleus, an open-shell property in neutrons is suggested.

Candidate Resonant Tetraneutron State Populated by the

A candidate resonant tetraneutron state is found in the missing-mass spectrum obtained in the double-charge-exchange reaction ^{4}He(^{8}He,^{8}Be) at 186 MeV/u. The energy of the state is 0.83±0.65(stat)±1.25(syst) MeV above the threshold of four-neutron decay with a significance level of 4.9σ. Utilizing the large positive Q value of the (^{8}He,^{8}Be) reaction, an almost recoilless condition of the four-neutron system was achieved so as to obtain a weakly interacting four-neutron system efficiently.

Surfactant protein C G100S mutation causes familial pulmonary fibrosis in Japanese kindred.

Several mutations in the surfactant protein C (SP-C) gene (SFTPC) have been reported as causing familial pulmonary fibrosis (FPF). However, the genetic background and clinical features of FPF are still not fully understood. We identified one Japanese kindred, in which at least six individuals over three generations were diagnosed with pulmonary fibrosis. We examined the patients radiologically and histopathologically and sequenced their SFTPC and ABCA3 genes. We also established a cell line stably expressing the mutant gene. All the patients had similar radiological and histopathological characteristics. Their histopathological pattern was that of usual interstitial pneumonia, showing numerous fibroblastic foci even in areas without abnormal radiological findings on chest high-resolution computed tomography. No child had respiratory symptoms in the kindred. Sequencing of SFTPC showed a novel heterozygous mutation, c.298G>A (G100S), in the BRICHOS domain of proSP-C, which co-segregated with the disease. However, in the ABCA3 gene, no mutation was found. In vitro expression of the mutant gene revealed that several endoplasmic reticulum stress-related proteins were strongly expressed. The mutation increases endoplasmic reticulum stress and induces apoptotic cell death compared with wild-type SP-C in alveolar type II cells, supporting the significance of this mutation in the pathogenesis of pulmonary fibrosis.

Germination constraints of dicarpic cypselae of Bidens pilosa L.

Bidens pilosa L. is a heterocarpic weed species with two cypselae types that present morpho-physiological differences, being the peripheral type smaller and slower to germinate than the central one. We aimed to verify how the germination mechanism varied between types. We focused on two mechanisms: (1) pericarp constraints (physical and chemical) and (2) hormonal stimulation (Abcisic acid [ABA] and Gibberellin [GA]). Both cypselae types are physically constrained by the pericarp, for when it is excised both seed types increase their germination, but behavioral differences still remain. The pericarp of the peripheral type also has chemical inhibitors that effectively inhibited germination of the intact central cypsela. To test the hormonal effects, we focused on the ABA:GA control. Both cypselae responded to an exogenous ABA concentration gradient, however there is no variation between types on the sensitivity to it. Also, both cypselae types were indifferent to Fluridone (ABA inhibitor), which indicates that the dormancy is not maintained by de novo ABA synthesis. Cypselae types had different sensitivity to an exogenous GA3 gradient, the central type being more sensitive to the treatment than the peripheral one. But when the endogenous GA synthesis was blocked by Paclobutrazol, both types responded equally to same GA3 concentrations. This indicates that endogenous GA synthesis may be related to differences observed on germination of cypselae types. To conclude, seed types differ on their growth potential to overcome the pericarp resistance: while the inhibitor in the peripheral pericarp reduces growth potential, GA increases it.

Energetics of the negative and positive inotropism of pentobarbitone sodium in the canine left ventricle.

OBJECTIVE: Pentobarbitone (sodium) is an anaesthetic widely used in animal experiments. It is known to be a cardiovascular depressant and a coronary dilator, but its effects on myocardial energetics in relation to its negative and positive (due to Gregg's phenomenon) inotropism have not been studied. The aim of this study was therefore to determine whether and how pentobarbitone affects cardiac mechanoenergetics compared with other negative inotropic agents for which data are already available. METHODS: The effects of graded doses of intracoronary pentobarbitone on mechanoenergetics were studied in the excised cross circulated left ventricles of 12 dogs. The framework of the Emax (a contractility index)--VO2 (myocardial oxygen consumption)--PVA (systolic pressure-volume area, a measure of total mechanical energy) relationships was fully utilised. RESULTS: Pentobarbitone increased Emax at low doses in five of the 12 hearts. In two of these five hearts, a marked coronary dilatation was found. Pentobarbitone decreased Emax dose dependently at high doses in all the hearts and lowered the VO2 intercept but not the slope (oxygen cost of PVA) of the VO2-PVA relation. There was no difference in oxygen cost of Emax between pentobarbitone and CaCl2, although they have opposite inotropism. These findings suggest that pentobarbitone depresses myocardial mechanoenergetics via suppression of total calcium handling in the excitation-contraction-relaxation coupling. CONCLUSIONS: Pentobarbitone at low doses partly acts as a positive inotropic agent, but at high doses it acts as a negative inotropic agent like beta blockers and calcium antagonists on cardiac mechanoenergetics in canine blood perfused hearts.

Heterogeneity of ganglia of the guinea pig myenteric plexus: an in vitro study of the origin of terminals within single ganglia using a covalently bound fluorescent retrograde tracer.

Experiments were done to test the hypothesis that individual ganglia of the myenteric plexus of the guinea pig small intestine are heterogeneous with respect to the location of the neurons that provide terminals to them. The myenteric plexus, attached to the longitudinal layer of smooth muscle, was maintained in vitro. Individual ganglia were injected with a variety of potential retrograde tracers by pressure microejection from the tip (20-micron diameter) of a glass micropipette. The fluorescent dye 4-acetoamido, 4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) was found to be an effective tracer, labeling neuronal perikarya, evidently by retrograde transport. SITS has previously been shown not to cross plasma membranes, but to be covalently bound to the outer surface of that membrane, and to be taken up by nerve terminals to be retrogradely transported to label neuronal cell bodies. SITS fluorescence was found in about 12% of the neurons within the ganglion into which it was injected and also in approximately ten times more neurons in discretely located distant ganglia. No labeling of neurons was found when SITS was injected into the bath or into the smooth muscle below the myenteric plexus. Damage to neural connectives obstructed the labeling of neurons in ganglia distal to the injection site. Individual SITS-injected myenteric ganglia were found to vary greatly in the ratios of intraganglionic SITS-labeled neurons to the total number of neurons within the injected ganglion. The ratios of the number of intraganglionic SITS-labeled neurons to SITS-labeled neurons in distant ganglia projecting to the injected ganglion from elsewhere in the myenteric plexus also varied greatly. More strikingly, individual ganglia differed over a wide range with respect to whether the neurons in distant ganglia that provided them with terminals were situated in the oral, anal, or circumferential direction. Although the majority of projections were found to be from orally located ganglia, individual ganglia were observed that received predominantly or exclusively anal or oral projections. Others received mixtures of terminals from ganglia that were anal, oral, or circumferential. This anatomical heterogeneity in the location of afferent inputs to individual myenteric ganglia is probably reflected in a functional heterogeneity as well and will have to be taken into account in further studies of the physiology of the myenteric plexus. Individual ganglia of the plexus can no longer be taken as anatomically and functionally equivalent to one another.

Physiological responses of guinea-pig myenteric neurons secondary to the release of endogenous serotonin by tryptamine.

Intracellular recordings showed that administration of pulses of tryptamine mimicked one of the actions of serotonin (a slow depolarization associated with an increased input resistance) on type II/AH neurons of the myenteric plexus. After superfusion at high concentration tryptamine initially acted like serotonin, but then blocked the action of serotonin on these cells. Measurements of the release of preloaded [3H]serotonin or [3H]norepinephrine revealed that tryptamine is a potent releaser of these labeled amines; this release is Ca2+ independent but temperature dependent. Moreover, incubation with tryptamine depleted the myenteric plexus of endogenous serotonin. Since tryptamine has previously been demonstrated not to inhibit the binding of [3H]serotonin to its enteric neural receptor we framed the hypothesis that the serotonin-releasing action of tryptamine is responsible for its ability to mimic serotonin when given in pulses or to desensitize serotonin receptors through the prolonged release of serotonin when it is superfused. This hypothesis was tested by examining the action of tryptamine on the serotonin-mediated slow excitatory postsynaptic potentials evoked in type II/AH neurons by fiber tract stimulation. Tryptamine superfusion antagonized these slow potentials as predicted. Moreover, after a long time when endogenous serotonin was depleted, the response of type II/AH neurons to exogenous serotonin recovered but the slow synaptic potential did not. The action of tryptamine on this neuron was relatively specific. When the slow synaptic potential and serotonin responses were blocked by tryptamine the type II/AH neurons still responded to acetylcholine. Fast excitatory postsynaptic potentials were not affected by tryptamine. Furthermore, other types of neurons (I/S) and other neuronal responses to serotonin (such as a fast depolarization with decreased input resistance or presynaptic inhibition of acetylcholine release) were not blocked by tryptamine. Finally, radioautographic studies revealed a neural uptake of tryptamine in the chemically sympathectomized myenteric plexus; however, the distribution of tryptamine in the plexus was different from that of serotonin and was not blocked by excess non-radioactive serotonin. Therefore tryptamine does not enter myenteric neurons via the specific serotonin uptake mechanism; however, zimelidine, found to be a selective inhibitor of the enteric uptake of serotonin, antagonized the release of serotonin by tryptamine and attenuated the effect of tryptamine on responses to serotonin.(ABSTRACT TRUNCATED AT 400 WORDS)

Prejunctional modulatory action of neuropeptide Y on responses due to antidromic activation of peripheral terminals of capsaicin-sensitive sensory nerves in the isolated guinea-pig ileum.

1. The effect of neuropeptide Y (NPY) on motor responses produced by activation of capsaicin-sensitive primary afferents in the guinea-pig isolated ileum was determined by use of capsaicin itself and electrical mesenteric nerve stimulation as stimuli. 2. NPY inhibited or suppressed the cholinergic contractile response produced by electrical mesenteric nerve stimulation while leaving the contractile response to a threshold concentration of capsaicin. 3. NPY had no effect on motor responses produced by a submaximal concentration of substance P, the putative endogenous mediator of the 'efferent' function of sensory fibres in this preparation. 4. It is concluded that NPY exerted a prejunctional inhibitory action on transmitter release from peripheral endings of capsaicin-sensitive nerves at interneuronal synapses.

Inorganic phosphate-dependent ADP binding on the chloroplast coupling factor and its participation in ATP synthesis.

ADP binding brought about by inorganic phosphate addition (Pi-dependent ADP binding) on membrane-bound chloroplast coupling factor was studied and the following results were obtained. Under energization by illumination or by acid-base transition, Pi brought about the binding of ADP with an apparent Km value of 0.22 mM. This effect of Pi was lost rapidly after turning the light off or after acid to base transition, concomitant with the loss of ATP synthesizing activity. Pi-dependent ADP binding was inhibited by phlorizin to nearly the same extent as was ATP synthesis. The inhibitory effects of phlorizin on both the Pi-dependent ADP binding and ATP synthesis increased with the decrease of Pi concentration. These results suggest that the Pi-dependent ADP binding reaction participates in the ATP synthesis reaction and that phlorizin inhibits the P1 binding process.

Increased expression of synaptophysin and stathmin mRNAs after methamphetamine administration in rat brain.

The rearrangement of neural networks associated with the behavioral sensitization induced by psychostimulants is poorly understood. We have investigated the effect of methamphetamine (METH) administration on the mRNA levels of three different classes of plasticity-related genes in the rat brain. The expression of synaptophysin mRNA increased 20-40% in the nucleus accumbens, prefrontal and temporal cortices, 1-24 h after acute METH administration, and that of stathmin mRNA increased about 20% in the prefrontal cortex 1 h later. They did not change after subchronic administration. The level of alpha-tubulin mRNA was constant. Therefore, synaptophysin and stathmin play an important role in the neural plastic changes involved in the early induction process of METH-induced sensitization, but not in the later maintenance process.

Desulfurization of alkylated forms of both dibenzothiophene and benzothiophene by a single bacterial strain.

Thirty-five bacterial strains capable of converting dibenzothiophene into 2-hydroxybiphenyl were isolated. Among them Rhodococcus erythropolis KA2-5-1 was chosen for further characterization because of its ability to retain high desulfurization activity stably. PCR cloning and DNA sequencing of a KA2-5-1 genomic DNA fragment showed that it was practically identical with dszABC genes from Rhodococcus sp. IGTS8, a representative carbon-sulfur-bond-targeted dibenzothiophene-degrading bacterium. KA2-5-1 desulfurized a variety of alkyl dibenzothiophenes through the specific cleavage of their C-S bonds. In addition, unexpectedly, KA2-5-1 also attacked alkyl benzothiophenes in a C-S-bond-targeted fashion. The purified monooxygenase, encoded by dszC of KA2-5-1, converted benzothiophene and dibenzothiophene into benzothiophene sulfone and dibenzothiophene sulfone, respectively, with the aid of an NADH-dependent oxidoreductase. This result raises the possibility that the same enzymatic step may be involved in desulfurization of alkylated forms of both dibenzothiophene and benzothiophene in KA2-5-1 cells.

Pacemaker activity from submucosal interstitial cells of Cajal drives high-frequency and low-amplitude circular muscle contractions in the mouse proximal colon.

The present study was aimed at elucidating how pacemaker activity (plateau potentials) (mean frequency: 15.9 +/- 2.8 times min(-1)) from submucosal interstitial cells of Cajal (ICC-SM) control spontaneous contractions in the mouse proximal colon. Mechanical activities in the circular muscle direction showed high-frequency (mean frequency: 15.6 +/- 2.7 times min(-1)) and low-amplitude (mean amplitude: 0.01 +/- 0.005 g) (HFLA) rhythmic contractions. Simultaneous recordings of circular muscle mechanical activity and electrical activity from ICC-SM revealed that HFLA contractions were synchronized with plateau potentials (mean frequency: 15.9 +/- 2.8 times min(-1)). Although low-frequency (3.5 +/- 2.1 times min(-1)) and high-amplitude (0.12 +/- 0.03 g) (LFHA) contractions in both longitudinal and circular muscle directions were synchronized with burst of action potentials in both muscle cells, these LFHA contractions were not synchronous with plateau potentials. Intracellular Ca2+ release from the internal stores through IP3 receptors is not a major factor to generate both action potentials differently from plateau potentials. Neither tetrodotoxin nor atropine affected the plateau potentials. The results reveal that the pacemaker activity from ICC-SM drives only the spontaneous HFLA (one-tenth amplitude of the LFHA circular and longitudinal muscle contractions) circular muscle contractions without control by enteric nerves.

Effects of mesenteric nerve stimulation on the electrical activity of myenteric neurons in the guinea pig ileum.

Effects of mesenteric nerve stimulation on the electrical activity of 28 myenteric neurons were investigated in the myenteric flaps innervated with mesenteric nerves. Mesenteric nerve stimulation evoked slow excitatory postsynaptic potentials (EPSPs), whose amplitude and duration were 24.5 +/- 5.5 mV and 374.6 +/- 58.9 s in 7 AH/Type 2 neurons, respectively. Such slow EPSPs mimic the slow depolarizing action induced by exogenous substance P. It is, therefore, likely that slow EPSPs might be in part mediated by the release of substance P.

Ruthenium red antagonism of the effects of capsaicin mediated by extrinsic sensory nerves on myenteric plexus neurons of the isolated guinea-pig ileum.

The effects of Ruthenium red and its antagonism of capsaicin-induced action on the electrophysiological behavior of myenteric neurons were investigated with intracellular recording techniques in the isolated guinea-pig ileum. Ruthenium red antagonized dose-dependently (1-10 microM) a capsaicin-induced marked long-lasting slow depolarizing action associated with increased input resistance, during which the cells spiked repeatedly or displayed anodal break excitation. This action of capsaicin has been found to be mediated via a release of substance P from sensory nerve endings. The slow depolarizing response to exogenous substance P applied by pressure microejection, which mimicked the capsaicin-induced action, was not affected by Ruthenium red. Therefore, present results indicate that Ruthenium red antagonizes the specific effect of capsaicin on myenteric neurons by acting on the presynaptically located peripheral nerve terminals of sensory neurons and inhibiting the release of substance P. Electron-microscopic examination showed that the neurotoxic action of capsaicin towards extrinsic sensory nerve fibers was also dose-dependently (1-10 microM) protected by pretreatment of ruthenium red. Present results suggest that Ruthenium red inhibits a capsaicin-induced activation of cation channels at the cell membrane of sensory nerves.

Possible involvement of calcitonin gene-related peptide (CGRP) in non-cholinergic non-adrenergic relaxation induced by mesenteric nerve stimulation in guinea pig ileum.

Mesenteric nerve (MN) stimulation produced a biphasic response, i.e., a contraction followed by a prolonged relaxation in the isolated guinea pig ileum after complete adrenergic neuron blockade with guanethidine. This biphasic response mimicked the effect of capsaicin by itself. The latter relaxation response to MN stimulation was unaffected by hexamethonium, but was abolished by capsaicin in an irreversible fashion. Calcitonin gene-related peptide desensitization (CGRP-D) reduced the relaxation response to about 20% of the control. After pretreatment with atropine and guanethidine, MN stimulation provoked a pure relaxation, which was significantly reduced to about 20% of the control by CGRP-D. Therefore, it seems likely that the non-adrenergic non-cholinergic relaxation response to MN stimulation is partly mediated via a release of CGRP from sensory nerve endings.

Possible mechanism of ruthenium red antagonism of capsaicin-induced action in the isolated guinea pig ileum.

Ruthenium red (3-5 microM) antagonism of the inhibitory effect of capsaicin (1 microM) on the contractile response to mesenteric nerve stimulation in the presence of hexamethonium (50 microM) and guanethidine (2 microM) was reversed significantly by sialic acid (2 mM) or neuraminidase (0.1 U/ml). These results suggested that ruthenium red at low concentrations inhibits the capsaicin-induced desensitization of activated Ca2+ influx into sensory nerves at least in part by binding to sialic acid residues.