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  • 1
    Keywords: Bioinformatics ; Microbiology ; Biomedical Engineering ; Bioinformatics ; Microbiology ; Biomedical Engineering/Biotechnology ; Springer eBooks
    Description / Table of Contents: Chapter 1: Introduction -- Chapter 2: DNA sequence assembly and annotation of genes -- Chapter 3: Databases and protein structures -- Chapter 4: Pair-wise alignment, multiple alignment and BLAST -- Chapter 5: Primer design -- Chapter 6: Short introduction to phylogenetic analysis of molecular sequence data -- Chapter 7: Sequence based classification and identification of prokaryotes -- Chapter 8: 16S rRNAampliconsequencing for metagenomics -- Chapter 9: Full DNA metagenomics -- Chapter 10: Transcriptomics -- Chapter 11: Molecular typing of prokaryotes
    Abstract: This textbook introduces to the basic concepts of bioinformatics and enhances students’ skills in using software and tools relevant for investigations in microbiology. The most relevant methods to analyze data are shown and readers are introduced on how to draw valid conclusions based on the results obtained. Software and servers which are free to use on the internet are presented and more advanced stand-alone programs are suggested as a second option. Exercises and training quizzes are provided at the end of each chapter to facilitate learning. The book targets Ph. D. students and advanced undergraduates in microbiology, biotechnology, and (veterinary) medicine with little to basic knowledge in bioinformatics
    Pages: X, 213 p. 105 illus. in color. : online resource.
    ISBN: 9783319992808
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  • 2
    ISSN: 1439-6327
    Keywords: Erythropoietin ; Carbon dioxide ; Haemoglobin oxygen affinity ; Human ; Hypoxia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVAP = 0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U · 1−1, post-hypoxia 10.24 (SEM 0.95) U · 1−1, P = 0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVAP 〉 0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r = −0.81,P = 0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1439-6327
    Keywords: Key words Erythropoietin ; Carbon dioxide ; Haemoglobin oxygen affinity ; Human ; Hypoxia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVA P=0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U⋅1-1, post-hypoxia 10.24 (SEM 0.95) U⋅1-1, P=0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVA P〉0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r=−0.81, P=0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
    Type of Medium: Electronic Resource
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