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  • 1
    Online Resource
    Online Resource
    Divergent Selection for Pentobarbital-Induced Sedation Times in Mice
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 2 ( 1998), p. 92-100
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 2 ( 1998), p. 92-100
    Abstract: Divergent selection for pentobarbital sedation-time response was practiced in mice for 9 generations. At the end of 9 generations of selection, the long-sedation-time line (LST) slept an average of 433 min; the short sedation time line (SST) slept an average of 29 min. The control line (C) slept an average of 71 min. These differences represent an almost 15-fold increase in sedation time for the LST compared to the SST line and a 6-fold increase compared to the C line. The SST line slept about 40% less than the C line after 9 generations of selection (measured in tenth generation progeny). Analysis of selection differentials and realized heritabilities indicated that selection response did not diminish after 9 generations of selection. Realized heritabilities for sedation time ranged from 0.43 to 0.83 for the LST line and from 0.55 to 0.81 for the SST line. Realized heritabilities did not decrease in magnitude due to selection progress, indicating that more progress can still be achieved. Comparing corrected (for environmental factors) to uncorrected heritabilities showed the importance of including a control line in selection experiments. Crossing of lines to study gene action responsible for this trait revealed that this trait was controlled by a number of genes with additive gene action without dominance, overdominance, epistasis, or maternal effects.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028186
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Sn-mesoporphyrin Suppression of Hyperbilirubinemia in EHBR/Eis Rats, an Animal Model of Dubin-Johnson Syndrome
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 3 ( 1998), p. 158-164
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 3 ( 1998), p. 158-164
    Abstract: Sn-mesoporphyrin (SnMP), a potent inhibitor of heme oxygenase (HO), controlled hyperbilirubinemia in rats of the mutant strain EHBR/Eis. This mutant strain displays pronounced conjugated hyperbilirubinuria and dark pigmentation of hepatocytes, characteristics of the Dubin-Johnson syndrome. SnMP administered at a dose of 10 µmol/kg body weight produced an immediate decrease in plasma bilirubin concentrations which could be maintained by weekly injections of this synthetic heme analogue. Marked inhibition of HO activity was demonstrated in liver, kidney and spleen but not in brain. These results demonstrate that SnMP can lower plasma bilirubin concentrations for extended periods in a new mutant rat model of Dubin-Johnson syndrome.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028194
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Differentiation of the Inhibitory Effects of Calcium Antagonists on Abnormal Behaviors Induced by Methamphetamine or Phencyclidine
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 4 ( 1998), p. 165-174
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 4 ( 1998), p. 165-174
    Abstract: The abnormal behaviors induced by methamphetamine (MAP: 1 mg/kg) or phencyclidine (PCP: 10 mg/kg) were measured using behavioral analysis following the microinjection of one of three calcium (Ca) antagonists (nifedipine: Nif, nicardipine: Nic and flunarizine: Flu) into the rat caudate putamen or amygdala. The intraperitoneal administration of MAP or PCP induced abnormal behaviors in a time-dependent manner; the maximum locomotor activity was measured 30–45 min after the administration of MAP or PCP. This hyperactivity was sustained for more than 2 h. Following microinjection of these Ca antagonists into the caudate putamen, each showed a different pattern of inhibition on MAP- or PCP-induced abnormal behaviors. Nic and Flu were effective at reducing these abnormal behaviors, in contrast, Nif was ineffective. In particular, the inhibitory effect of Nic was stronger than that of Flu. Microinjection of these Ca antagonists into the amygdala did not show any reductive effect on the hyperactivity induced by MAP or PCP. These results demonstrate that these Ca antagonists have different pharmacological properties and that both L- and T-type Ca 〈 sup 〉 2+ 〈 /sup 〉 channels modulate the dopamine release in the rat caudate putamen. These results further lead us to suggest the presence of a subtype of L-type Ca 〈 sup 〉 2+ 〈 /sup 〉 channels in the caudate putamen.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028195
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Roles of zinc-fingers and homeoboxes 1 during the proliferation, migration, and invasion of glioblastoma cells
    IOS Press ; 2017
    In:  Tumor Biology Vol. 39, No. 3 ( 2017-03), p. 101042831769457-
    Details
    In: Tumor Biology, IOS Press, Vol. 39, No. 3 ( 2017-03), p. 101042831769457-
    Abstract: Zinc-fingers and homeoboxes 1 (ZHX1) is a nuclear transcription repressor and known to be involved in cell differentiation and tumorigenesis. However, the pathophysiological roles of ZHX1 have not been characterized in glioblastoma. We examined ZHX1 expression in glioblastoma patients’ tissues and analyzed overall survival of the patients based on expression level of ZHX1. We also examined the effects of ZHX1 on proliferation and motility of glioblastoma cells. In silico analysis and immunohistochemical studies showed that the messenger RNA and protein expressions of ZHX1 were higher in the tissues of glioblastoma patients than in normal brain tissues, and that its overexpression was associated with reduced survival. In vitro, the downregulation of ZHX1 decreased the proliferation, migration, and invasion of glioblastoma cells, whereas its upregulation had the opposite effects. In addition, we showed ZHX1 could contribute to glioblastoma progression via the regulations of TWIST1 and SNAI2. Taken together, this study demonstrates that ZHX1 plays crucial roles in the progression of glioblastoma, and its findings suggest that ZHX1 be viewed as a potential prognostic maker and therapeutic target of glioblastoma.
    Type of Medium: Online Resource
    ISSN: 1010-4283 , 1423-0380
    URL: Article
    DOI: 10.1177/1010428317694575
    Language: English
    Publisher: IOS Press
    Publication Date: 2017
    detail.hit.zdb_id: 605825-5
    detail.hit.zdb_id: 1483579-4
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Esculentoside A Inhibits Tumor Necrosis Factor, Interleukin-1, and Interleukin-6 Production Induced by Lipopolysaccharide in Mice
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 4 ( 1998), p. 187-195
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 4 ( 1998), p. 187-195
    Abstract: Esculentoside A, a kind of saponin isolated from the root of the Chinese herb 〈 i 〉 Phytolaca esculenta 〈 /i 〉 , is reported to possess potent anti-inflammatory effects in acute and chronic experimental models. In the present study, we investigated the effects of esculentoside A on the production of tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) induced by lipopolysaccharide (LPS) in mice. In vitro experiments demonstrated that esculentoside A (0.1–10 µmol/l) significantly reduced the release of TNF from the peritoneal macrophages derived from mice pretreated with thioglycolate. IL-1 and IL-6 secretion was also obviously inhibited in a concentration-dependent manner by esculentoside A from 0.01 to 10 µmol/l. In vivo experiments demonstrated that detectable TNF was observed 0.25 h after injection, was maximal at 0.5 h, and returned to baseline at 4 h. Maximal production of IL-1 and IL-6 were observed to be 1 and 2 h, respectively, after injection of LPS. Pretreatment of mice with 5, 10, or 20 mg/kg esculentoside A once a day for 7 consecutive days dose-dependently decreased the TNF, IL-1 and IL-6 levels in the sera of mice following LPS challenge. TNF, IL-1, and IL-6 are important cytokines involved in the pathogenesis of inflammatory lesions. Inhibition of inflammatory cytokine production may contribute to the anti-inflammatory effects of esculentoside A.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028197
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 6
    Online Resource
    Online Resource
    Impaired Contraction and Relaxation in the Aorta of Streptozotocin-Diabetic Rats
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 4 ( 1998), p. 207-215
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 4 ( 1998), p. 207-215
    Abstract: It is known that diabetes mellitus alters the vascular responsiveness to several vasoconstrictors and vasodilators. Endothelium-derived nitric oxide is a potent endogenous nitrovasodilator, and endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor substance. They play a major role in the modulation of vascular tone. Selective impairment of endothelium-dependent relaxation and impaired vasoconstriction in response to ET-1 could result in vascular disorders. The purpose of our study was to determine whether vascular responses to ET-1 and endothelium-dependent relaxing substances are impaired in rats with streptozotocin-induced diabetes of 2 weeks duration. Endothelium-dependent relaxations produced by carbachol and ATP in aortic rings precontracted with phenylephrine were significantly attenuated in rings from diabetic rats, but the endothelium-independent relaxations produced by sodium nitroprusside and adenosine in diabetic preparations were not changed when compared to the corresponding controls. The ET-1-induced contractions were significantly attenuated with no change in agonist potency (pD 〈 sub 〉 2 〈 /sub 〉 value) in aortae with and without endothelium obtained from diabetic rats when compared to those from controls. Mechanical removal of the endothelium did not significantly change ET-1 responses of aortae from either diabetic or control rats compared with responses of aortae with intact endothelium. These results suggest that, in this diabetic model, the contractile responsiveness of thoracic aortic muscles and the endothelial functions are significantly altered during 2 weeks of diabetes.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028199
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Expression of lactate dehydrogenase C correlates with poor prognosis in renal cell carcinoma
    IOS Press ; 2017
    In:  Tumor Biology Vol. 39, No. 3 ( 2017-03), p. 101042831769596-
    Details
    In: Tumor Biology, IOS Press, Vol. 39, No. 3 ( 2017-03), p. 101042831769596-
    Abstract: Lactate dehydrogenase C is an isoenzyme of lactate dehydrogenase and a member of the cancer–testis antigens family. In this study, we aimed to investigate the expression and functional role of lactate dehydrogenase C and its basic mechanisms in renal cell carcinoma. First, a total of 133 cases of renal cell carcinoma samples were analysed in a tissue microarray, and Kaplan–Meier survival curve analyses were performed to investigate the correlation between lactate dehydrogenase C expression and renal cell carcinoma progression. Lactate dehydrogenase C protein levels and messenger RNA levels were significantly upregulated in renal cell carcinoma tissues, and the patients with positive lactate dehydrogenase C expression had a shorter progression-free survival, indicating the oncogenic role of lactate dehydrogenase C in renal cell carcinoma. In addition, further cytological experiments demonstrated that lactate dehydrogenase C could prompt renal cell carcinoma cells to produce lactate, and increase metastatic and invasive potential of renal cell carcinoma cells. Furthermore, lactate dehydrogenase C could induce the epithelial–mesenchymal transition process and matrix metalloproteinase-9 expression. In summary, these findings showed lactate dehydrogenase C was associated with poor prognosis in renal cell carcinoma and played a pivotal role in the migration and invasion of renal cell carcinoma cells. Lactate dehydrogenase C may act as a novel biomarker for renal cell carcinoma progression and a potential therapeutic target for the treatment of renal cell carcinoma.
    Type of Medium: Online Resource
    ISSN: 1010-4283 , 1423-0380
    URL: Article
    DOI: 10.1177/1010428317695968
    Language: English
    Publisher: IOS Press
    Publication Date: 2017
    detail.hit.zdb_id: 605825-5
    detail.hit.zdb_id: 1483579-4
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Pedigree Analysis of a Subject with Abnormally Slow Renal Elimination of 6-Hydroxychlorzoxazone
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 5 ( 1998), p. 262-266
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 5 ( 1998), p. 262-266
    Abstract: The family of an unusual subject was studied. When tested with chlorzoxazone (CX; 250 mg p.o.) on four separate occasions 5 years ago, this subject showed abnormally slow renal elimination of 6-hydroxychlorzoxazone (HCX), the primary CX metabolite. Since rates of CX biotransformation to HCX have served as a probe of the important cytochrome P450 isozyme, CYP 2E1, it was of interest that this unusual subject had normal conversion of CX to HCX. The present study revealed that over the past 5 years this subject accelerated his renal rate of HCX elimination which now lies at the slow end of the curve for normal subjects. His wife and 5 children all had more rapid rates than he for renal HCX elimination.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028207
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    Coptisine-induced cell cycle arrest at G2/M phase and reactive oxygen species–dependent mitochondria-mediated apoptosis in non-small-cell lung cancer A549 cells
    IOS Press ; 2017
    In:  Tumor Biology Vol. 39, No. 3 ( 2017-03), p. 101042831769456-
    Details
    In: Tumor Biology, IOS Press, Vol. 39, No. 3 ( 2017-03), p. 101042831769456-
    Abstract: This study aimed to explore the effect of coptisine on non-small-cell lung cancer and its mechanism through various in vitro cellular models (A549). Results claimed significant inhibition of proliferation by coptisine against A549, H460, and H2170 cells with IC 50 values of 18.09, 29.50, and 21.60 µM, respectively. Also, coptisine exhibited upregulation of pH2AX, cell cycle arrest at G2/M phase, and downregulation of the expression of cyclin B1, cdc2, and cdc25C and upregulation of p21 dose dependently. Furthermore, induction of apoptosis in A549 cells by coptisine was characterized by the activation of caspase 9, caspase 8, and caspase 3, and cleavage of poly adenosine diphosphate ribose polymerase. In addition, coptisine was found to increase reactive oxygen species generation, upregulate Bax/Bcl-2 ratio, disrupt mitochondrial membrane potential, and cause cytochrome c release into the cytosol. Besides, treatment with a reactive oxygen species inhibitor (N-acetyl cysteine) abrogated coptisine-induced growth inhibition, apoptosis, reactive oxygen species generation, and mitochondrial dysfunction. Thus, the mediation of reactive oxygen species in the apoptosis-induced effect of coptisine in A549 cells was corroborated. These findings have offered new insights into the effect and mechanisms of action of coptisine against non-small-cell lung cancer.
    Type of Medium: Online Resource
    ISSN: 1010-4283 , 1423-0380
    URL: Article
    DOI: 10.1177/1010428317694565
    Language: English
    Publisher: IOS Press
    Publication Date: 2017
    detail.hit.zdb_id: 605825-5
    detail.hit.zdb_id: 1483579-4
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    The Contractile Effect of Fedotozine on Guinea Pig Isolated Intestinal Cells Is Not Mediated by Kappa Opioid Receptors
    S. Karger AG ; 1998
    In:  Pharmacology Vol. 56, No. 6 ( 1998), p. 281-284
    Details
    In: Pharmacology, S. Karger AG, Vol. 56, No. 6 ( 1998), p. 281-284
    Abstract: The compound fedotozine, recently described as a peripheral kappa opioid receptor agonist, was tested on smooth muscle cells isolated from the longitudinal muscle layer of the guinea pig ileum, in comparison with the selective kappa receptor agonist, compound U-50488. Fedotozine (1 nmol/l–1 µmol/l) caused a concentration-dependent contraction of intestinal cells, with a maximum decrease in cell length not significantly different from that caused by acetylcholine. The kappa agonist U-50488 (0.1 pmol/l–100 nmol/l) was without effect. The contractile effect of fedotozine was not significantly modified by naloxone (0.1–1 µmol/l). These results indicate that fedotozine can have direct excitatory effects on intestinal smooth muscle cells from the guinea pig ileum not mediated by activation of kappa opioid receptors.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000028210
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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