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  • 1
    Keywords: Life sciences ; Plant breeding ; Plant physiology ; Life sciences ; Plant Breeding/Biotechnology ; Plant Genetics & Genomics ; Plant physiology ; Springer eBooks
    Description / Table of Contents: Expression analysis and genome annotations with RNA sequencing -- The application of Next Generation Sequencing techniques to Plant Epigenomics -- Whole genome sequencing to identify genes and QTL in rice -- Variant calling using NGS data in European aspen (Populus tremula) -- Leafy Spurge Genomics: A Model Perennial Weed To Investigate Development, Stress Responses, And Invasiveness -- Utilization of NGS and proteomic-based approaches to gain insights on cellular responses to singlet oxygen and improve energy yields for bacterial stress adaptation -- Experimental evolution and next generation sequencing illuminate the evolutionary trajectories of microbes -- Plant carbohydrate active enzyme (CAZyme) repertoires: a comparative Study -- Metagenomics of Plant- Microbe Interactions -- Genes and trans-factors underlying embryogenic transition in plant soma-cells -- Bioinformatics tools to analyze the proteome and genome data -- High through-put transcriptome analysis of plant stress responses -- CNV and structural variation in plants: prospects of NGS Approaches
    Abstract: This work is a compiled catalogue of such findings, where several NGS technologies ranging from the genomics, transcriptomics, metagenomics, single cell genomics, QTL, patho-genomics and patho-transcriptomics have been applied to delineate the mystery of the associated mutations, biological pathway transitions, transcriptional fluxes and patterns of host associated or adaptations to certain climatic conditions. The aims and scope of this book focuses more on the biological underpinning to initiate the cross-talks across the traits acquired or lost during the course of evolution. The structured framework of the present volume provides the applicative point of view of the NGS technologies and demonstrates the conceptual way of linking the experimentation to the NGS technologies, to aid in researchers to place their biological hypothesis in a larger context
    Pages: XII, 241 p. 40 illus., 31 illus. in color. : online resource.
    ISBN: 9783319171579
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  • 2
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro effects of methotrexate (MTX) on interleukin-2(IL-2)-mediated cytotoxicity of peripheral blood mononuclear cells (PBMC) were studied. PBMC were incubated with human recombinant IL-2 (25 U/ml) for 72 h; during the last 24 h, various concentrations (10 pM–1 µM) of MTX were added to the culture. Cytotoxicity against k562 cells was measured by a 4-h51Cr-release assay. The IL-2-mediated cytotoxicity was paradoxically increased at around a concentration (10 nM) MTX. Such a low concentration of MTX showed no anti-proliferative effect on cell growth. This enhancement with 10 nM MTX was shown only in an E-rosette+ (E+) population, but not in E-rosette− (E−). In addition, when E+ cells were treated with an anti-CD16 monoclonal antibody plus complement after incubation with IL-2 and MTX, MTX-induced enhancement was lost, suggesting that an E+CD16+ cell population was mainly involved in this augmentation. Positively sorted E+CD16+ cells showed similar enhancement of cytotoxicity after treatment with IL-2 plus MTX. On the other hand, MTX treatment did not show the phenotypical changes including of the E+CD16+ cells, indicating that this treatment did not affect the differentiation and proliferation of the specific cell subset. Our results indicate that a low dose of MTX could have a role in the regulation of immunological anti-cancer surveillance systems through the natural killer and lymphokine-activated cytotoxic cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Résumé La lutéoskyrine, pigment cartinogène synthétisé par lePenicillium islandicum Sopp, inhibe la synthèse du RNA nucléaire dans la cellule de la tumeur Ehrlich.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Zusammenfassung Fusarenon-X, ein toxisches Produkt aus dem Kulturfiltrat vonFusarium nivale wurde isoliert, näher charakterisiert und dessen Struktur ermittelt.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: arteriovenous malformation ; pancreas ; duodenal ulcer ; color Doppler ultrasonography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the color Doppler ultrasonography features of arteriovenous malformation (AVM) of the pancreas, a very rare disease. The patient was a 52-year-old man with congenital AVM of the pancreas and a duodenal ulcer that had been resistant to medication. Endoscopic color Doppler ultrasonography (color Doppler EUS) revealed many abnormal color signals showing pulsatile wave form at the portion of the duodenal wall involving the duodenal ulcer. Extracorporeal color Doppler ultrasonography revealed a mosaic-like color signal, caused by turbulent flow, in the portal trunk. Angiography demonstrated a vascular network with extensive proliferation at the pancreatic head and early portal filling. It is possible that the pancreatic AVM had caused the duodenal ulcer. Color Doppler EUS can be a useful modality for detection of vessel abnormalities of the gastrointestinal tract.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1041
    Keywords: alpha-adrenergic blocker ; hypertension ; blood pressure ; pulse rate ; noradrenaline ; plasma renin activity ; plasma aldosterone ; dopamine-beta-hydroxylase ; E-643
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To determine whether E-643, a new α-blocking agent, would reduce the blood pressure, regardless of the posture, a 1 mg dose was given 3 times daily for 7 consecutive days, to 8 male and 7 female inpatients, aged 37–73 years, with essential hypertension. Blood pressure and pulse rate were measured daily in the supine, sitting and standing positions. Before and after the treatment with E-643, plasma levels of noradrenaline, adrenaline, dopamine-β-hydroxylase, renin and aldosterone were determined, samples being obtained with the subjects recumbent and after standing upright for 60 min. A significant reduction in the systolic and diastolic blood pressures was evident in the supine (172±31/100±12 → 151±28/89±14 mmHg), sitting (158±22/101±11 → 138±28/89±15 mmHg) and standing (153±32/103±21 → 129±31/89±20 mmHg) positions. The reduction in blood pressure remained unchanged throughout the period of administration of E-643. Pulse rate was not affected when the subjects were supine (67±10 → 69±10 beats/min), but was increased in the sitting (68±10 → 73±9 beats/min) and standing (73±10 → 81±11 beats/min) positions. The increased pulse rate tended to decline during continued administration of E-643. Treatment with E-643 produced no significant change in plasma levels of adrenaline, noradrenaline, dopamine-β-hydroxylase, renin and aldosterone. The antihypertensive effect of treatment was more prominent in the patients with higher levels of plasma catecholamines and dopamine-β-hydroxylase, and was less prominent in those with higher plasma renin and aldosterone. Two patients had temporary bouts of dizziness and visual disturbances, but there were no subjective complaints during treatment.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0738
    Keywords: Key words Butyltin compound ; Hepatotoxicity ; Lipid peroxidation ; Glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The in vivo induction of hepatotoxicity, as evaluated by the activity of ornithine carbamyl transferase in serum, was investigated in mice administered orally with the following three butyltin compounds: tributyltin chloride (TBTC), dibutyltin dichloride (DBTC) and monobutyltin trichloride (MBTC). The minimal concentrations of TBTC and DBTC that caused hepatotoxicity at 24 h after oral administration were 180 μmol and 60 μmol/kg, respectively, while MBTC did not induce liver injury even at 7000 μmol/kg. Additionally, when the administered doses were equivalent (180 μmol/kg), a time course (3–96 h) study revealed that the hepatotoxicity of TBTC and DBTC appeared at 24 and 12 h, respectively, but that MBTC showed no hepatotoxicity even at 96 h. The amounts of Sn excreted into urine for 4 days were 1.5 fold greater with TBTC than with DBTC treatment and were lowest in MBTC group. Similarly, the total liver Sn content was 2- to 5-fold greater in the TBTC group than in the DBTC group whereas the liver Sn content in the MBTC treatment showed the lowest value throughout the 3- to 96-h period. Thus, the non-hepatotoxicity of MBTC may be due either to low absorption through the digestive tract of mice or to the low levels of Sn in liver; however, the level of Sn in liver was not associated with the induction of hepatotoxicity by TBTC and DBTC. The analysis of metabolites of TBTC (180 μmol/kg) and DBTC (60 μmol/kg) at equivalent hepatotoxicity showed that the main tin compounds in the liver after the administration of TBTC were dibutyltin and monobutyltin as well as inorganic tin compounds, while most (〉78%) of the total tin compounds in the liver of mice treated with DBTC was in the form of dibutyltin. In addition, the levels of monobutyltin and inorganic tin compounds in the livers of mice treated with TBTC were greater than those with DBTC, but the levels of dibutyltin did not differ significantly between TBTC and DBTC. The levels of lipid peroxidation (LPO) and hepatic glutathione (GSH) content in the liver showed a transitory increase after the administration of MBTC and TBTC, respectively. These results suggest that DBTC is more hepatotoxic than TBTC, and that dibutyltin inside the cells may be the main form of tin which is responsible for induction of hepatotoxicity following in vivo administration of TBTC and DBTC. The generation of free radical species, as evaluated by LPO and GSH levels, may not be associated with the hepatotoxicity caused by butyltin compounds.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0738
    Keywords: Key words Butyltin compounds ; Cytochrome P450 ; Hepatotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The role of cytochrome P450 in the induction of hepatotoxicity by butyltin compounds such as tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was investigated in vivo. The pretreatment of mice with SKF-525A, which decreased hepatic levels of cytochrome P450, suppressed TBTC-induced hepatotoxicity, as estimated by serum ornithine carbamyl transferase activity, whereas pretreatment with phenobarbital (PB), which increased the levels of cytochrome P450, enhanced the hepatotoxicity of TBTC. In the case of DBTC, PB pretreatment enhanced hepatotoxicity, while SKF-525A had no effect. Under these experimental conditions only PB pretreatment was found to increase hepatic levels of tin in mice treated with TBTC. These results suggest that hepatic metabolism of butyltin compounds by cytochrome P450 is more closely related to the induction of hepatotoxicity by TBTC than by DBTC. The active tin compounds formed during hepatic metabolism, which are responsible for induction of hepatotoxicity, will be discussed
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0738
    Keywords: Key words Chromium (VI)  ;  Vitamin E  ;  Cytotoxicity  ; Lipid peroxidation  ;  Hepatocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pretreatment of primary cultures of rat hepatocytes with α-tocopherol succinate (vitamin E) for 20 h prior to exposure to K2Cr2O7 resulted in a marked decrease of chromium (VI)-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, without affecting cellular uptake and subcellular distribution of chromium. The levels of chromium (VI)-induced lipid peroxidation, as monitored by malondialdehyde formation, were also inhibited by pretreatment with the vitamin. Pretreatment with vitamin E normalized the levels of nonenzymatic antioxidants such as glutathione and vitamin C suppressed by dichromate, and caused a distinct accumulation of vitamin E in hepatocytes. However, vitamin E pretreatment did not affect the activities of enzymatic antioxidants including glutathione reductase, superoxide dismutase, and catalase suppressed by dichromate. These results indicate that the protective effect of vitamin E against chromium (VI)-induced cytotoxicity as well as lipid peroxidation, may be associated more with the level of nonenzymatic antioxidants than the activity of enzymatic antioxidants.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0738
    Keywords: Key words Butyltin compounds ; Hepatotoxicity ; Cytochrome P450
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of pretreatment with SKF-525A, which inhibits hepatic cytochrome P450 enzymes, on metabolism and hepatotoxicity was examined in mice orally administered tributyltin chloride (TBTC) or dibutyltin dichloride (DBTC) at a dose of 180 μmol/kg. Analysis of butyltin compounds showed that the main metabolites in liver of mice treated with TBTC alone were DBTC (40%) and dibutyl(3-carboxylpropyl)tin chloride (TCOOH; 12–26%), with the levels of other butyltin compounds including TBTC comprising 〈12% of total butyltin compounds at 3–24 h following treatment. The pretreatment with SKF-525A resulted in four- to tenfold increased TBTC levels and a significant decrease of debutylated metabolites, particularly DBTC (60 and 37% decrease) at both 3 and 6 h in liver of mice treated with TBTC, leading to complete inhibition of hepatotoxicity at 24 h. At 24 h after TBTC treatment, hepatic levels of TBTC and most of the debutylated metabolites in mice pretreated with SKF-525A did not differ significantly when compared to those in unpretreated mice, resulting in the induction of hepatotoxicity at 48 h, although levels of TCOOH decreased even at 24 h. In the case of DBTC treatment, 〉95% of the butyltin compounds were detected as DBTC in liver, and the levels of DBTC inside cells as well as the induction of DBTC hepatotoxicity were unaffected by pretreatment with SKF-525A. These results suggest that debutylated metabolites, in particular DBTC, are the main metabolites of butyltin compounds responsible for the induction of hepatotoxicity following in vivo administration of TBTC. The results also indicate that cytochrome P450 enzymes may play a greater role in the metabolism of TBTC to form DBTC or butyltin trichloride (MBTC) than that of DBTC to form MBTC in liver of mice.
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