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  • 1
    ISSN: 1467-6494
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Psychology
    Notes: Theoretical assumptions regarding the genetic and environmental structure of personality proposed in Cloninger's seven-factor model of temperament and character were verified in a Japanese sample by using the twin method. The Temperament and Character Inventory (TCI) was administered to 296 twin pairs ranging in age from 14 to 28 years old. Among four temperament dimensions (novelty seeking [NS], harm avoidance [HA], reward dependence [RD], and persistence [PS]), HA and PS showed significant additive genetic contributions and no shared environmental effect, supporting the original theoretical assumption. NS and RD could be explained by either genetic or shared environmental factors with nonshared environment. All three character dimensions (cooperativeness [CO], self-directedness [SD], and self-transcendence [ST]) could be explained exclusively by additive contributions and no shared environmental effect. Multivariate genetic analysis indicated that there were no significant associations between NS, HA, and RD, as the theory predicts, and the genetic components of PS, SD, and CO were derived from those of the temperament dimensions. The fourth genetic component, which had a substantial load specifically on ST and overlapped with PS, was identified. Although most of the nonshared environmental effects were trait-specific, the phenotypic correlation between NS and HA could be explained by nonshared environmental overlap.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The binding of [3H]neurotensin to membranes from human brain at 0°C was specific, saturable, and reversible. In the frontal cortex, the equilibrium dissociation constant (KD) for [3H]neurotensin determined from the ratio of rate constants (k-1/k1), saturation isotherms, and inhibition binding experiments was 0.80, 2.0, and 2.0 nM, respectively, and the maximum number of binding sites (Bmax) from the saturation isotherms and the competitive binding experiments was 2.4 and 2.2 pmol/g of tissue, respectively. Hill coefficients for binding were equal to 1, indicating the presence of single, noncooper-ative binding sites. Inhibition of specific binding of [3H]neurotensin by several analogs of neurotensin showed that [Gln4]neurotensin and neurotensin(8–13) had the highest affinities for these binding sites in human frontal cortex, with each analog being ∼13-fold more potent than neurotensin. In addition, these data showed that the carboxy-terminal portion of neurotensin played an important part in the binding of this neuropeptide in human brain, a result described for other species. Regional distribution of binding sites was different from that reported for animal brains. Of the 33 different regions investigated, the uncus and substantia nigra showed the highest specific binding of [3H]neurotensin, whereas such areas as the pineal body, medulla, and corpus callosum had few binding sites.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The binding of [3H]neurotensin(8–13) to membranes from human frontal cortex at 0°C was time dependent, specific, saturable, and reversible. Saturation isotherms provided an equilibrium dissociation constant (KD) of 0.52 nM, and the maximal number of binding sites (B max) was 3.5 pmol/g original wet weight of tissue. Scat-chard analysis yielded a straight line, and the Hill coefficient was equal to 1, a result indicating that [3H]-neurotensin(8–13) bound to single, noncooperative sites. The KD values of several analogs of neurotensin determined in competition with [3H]neurotensin(8–13) were similar to those previously determined in competition with [3H]-neurotensin. The regional distribution of binding sites for [3H]neurotensin(8–13) was also similar to that for [3H]-neurotensin. These results suggest that [3H]neurotensin(8–13) binds to the same sites as [3H]neurotensin and that [3H]neurotensin(8–13) has a higher affinity than [3H]-neurotensin for these sites in human brain.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: When [3H]inositol-prelabelled N1E-115 cells were stimulated with carbamylcholine (CCh) (100 μM), high K+ (60 mM), and prostaglandin E, (PGE,) (10 μM), a transient increase in [3H]inositol pentakisphosphate (InsP5) accumulation was observed. The accumulation reached its maximum level at 15 s and had declined to the basal level at 2 min. CCh, high K+, and PGE, also caused accumulations of [3H]inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], [3H]inositol 1,3,4,6-tetrakisphosphate [Ins(1,3,4,6)P4], and 13H]inositol hexakisphosphate (InsP6). Muscarine and CCh induced accumulations of [3H]Ins(1,4,5)P3, [3H]-Ins(1,3,4,6)P4, [3H]InsP5, and [3H]InsP6 with a similar potency and exerted these maximal effects at 100 μM, whereas nicotine failed to do so at 1 mM. With a slower time course, CCh, high K+, and PGE1 caused accumulations of [3H]-inositol 1,3,4-trisphosphate [Ins(1,3,4)P3] and [3H]inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. In an N1E-115 cell homogenate, [3H]Ins(1,4,5)P3, [3H]Ins(1,3,4,5)P4, and [3H]Ins(1,3,4)P3 were converted to [3H]InsP5 through [3H]-Ins(1,3,4,6)P4. The above results indicate that Ins(1,3,4,6)P4, InsP5, and InsP6 are rapidly formed by several kinds of stimulants in N1E-115 cells.
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  • 5
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Prostaglandin E1 (PGE1)-mediated transmembrane signal control systems were investigated in intact murine neuroblastoma cells (clone N1E-115). PGE1 increased intra-cellular levels of total inositol phosphates (IP), cyclic GMP, cyclic AMP, and calcium ([Ca2+]i). PGE1 transiently increased inositol 1,4,5-trisphosphate formation, peaking at 20 s. There was more than a 10-fold difference between the ED50 for PGE1 at cyclic AMP formation (70 nM) and its ED50 values at IP accumulation (1 μM), cyclic GMP formation (2 μM), and[Ca2+]i increase (5 μM). PGE1-mediated IP accumulation, cyclic GMP formation, and [Ca2+]i increase depended on both the concentration of PGE1 and extracellular calcium ions. PGE1 had more potent intrinsic activity in cyclic AMP formation, IP accumulation, and cyclic GMP formation than did PGE2, PGF2α, or PGD2. A protein kinase C activator, 4β-phorbol 12β-myristate 13α-acetate, had opposite effects on PGE1-mediated IP release and cyclic GMP formation (inhibitory) and cyclic AMP formation (stimulatory). These data suggest that there may be subtypes of the PGE1 receptor in this clone: a high-affinity receptor mediating cyclic AMP formation, and a low-affinity receptor mediating IP accumulation, cyclic GMP formation, and intracellular calcium mobilization.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] To the editor: It was reported that mice with targeted disruption of the gene that encodes serum amyloid P-component (Sap, encoded by Apcs) with a mixed genetic background (129/Sv × C57BL/6; F2) developed high titers of antibody to nuclear antigens (ANA) and severe glomerulonephritis, a ...
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  • 7
    ISSN: 1432-2072
    Keywords: Lithium ion ; Muscarinic acetylcholine receptor ; Prostaglandin E1 receptor ; Cyclic GMP ; Cyclic AMP ; Guanylate cyclase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Murine neuroblastoma cells (clone N1E-115) possess both high- and low-affinity muscarinic receptors. The low-affinity muscarinic receptor, when stimulated, initiates the formation of cyclic GMP by activating the enzyme guanylate cyclase; whereas stimulation of the high-affinity receptor inhibits prostaglanding E1-mediated cyclic AMP formation by inhibiting the enzyme adenylate cyclase. We have reported that lithium ion (Li+) inhibits cyclic GMP formation mediated by the muscarinic receptor agonist, carbachol. in a concentration-dependent manner and that neither ammonium nor sodium ions have such an effect. We extended this study to show that Li+ was an apparently noncompetitive inhibitor of the low-affinity muscarinic receptor with an IC50 (±SEM)=13.6±0.8 mM. In addition, Li+ with a similar IC50 inhibited the cyclic GMP response in intact cells to sodium azide, which is thought to stimulate guanylate cyclase directly. Moreover, though Li+ was found to have a slight inhibitory effect on prostaglandin E1-stimulated cyclic AMP formation (15% inhibition at 10 mM), it had no effect on the function of the high-affinity muscarinic receptor in intact murine neuroblastoma cells.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-6830
    Keywords: interleukin-1β ; interleukin-1 receptor antagonist ; immobilization stress ; reverse transcription–polymerase chain reaction ; brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. Interleukin-1 receptor antagonist (IL-1Ra), as well as the interleukin-1β (IL-1β) gene response to immobilization stress (IMS), was examined in the rat brain. The reverse transcription–polymerase chain reaction was employed to determine mRNA levels. 2. IL-1β and IL-1Ra mRNA levels peaked at approximately 0.5 and 2–4 hr, respectively. The maximum mRNA levels of IL-1β were 15-fold higher than pre-IMS levels, whereas those of IL-1Ra were 250-fold higher in the hypothalamus. 3. After the biosynthesis of IL-1β has peaked, IL-1Ra may contribute to attenuation of the IL-1 activity which has been enhanced by IMS.
    Type of Medium: Electronic Resource
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