Books: 'Oxidative state of protein'

1

Oxidative folding of peptides and proteins. Cambridge, UK: Royal Society of Chemistry, 2009.

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2

Lantto, R. Protein cross-linking with oxidative enzymes and transglutaminase: Effects in meat protein systems. [Espoo, Finland]: VTT Technical Research Centre of Finland, 2007.

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3

Catala, Angel. Reactive oxygen species, lipid peroxidation, and protein oxidation. New York: Nova Publishers, 2014.

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4

The unfolded protein response und cellular stress. Amsterdam [etc.]: Elsevier, 2011.

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5

Protein absorption: Development and present state of the subject. New York: Wiley-Liss, 1991.

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6

Northey, Julian G. B. Protein folding determinants and transition state analysis of the Fyn SH3 domain. Ottawa: National Library of Canada, 2001.

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7

Local and state political campaign management. Commack, N.Y: Nova Science Publishers, 1996.

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8

Penn State Symposium in Plant Physiology (6th 1991 Pennsylvania State University). Active oxygen/oxidative stress and plant metabolism: Proceedings, 6th annual Penn State Symposium in Plant Physiology, May 23-25, 1991. Rockville, Md: American Society of Plant Physiologists, 1991.

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9

Th, Vanden Driessche, Guisset J. -L, and Petiau-de Vries G. M, eds. The redox state and circadian rhythms. Dordrecht: Kluwer Academic, 2000.

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10

Lavoie, Theresa I. The effects of an aversive noise stimulus on caloric consumption of various nutrient mixtures by wistar rats: Complex carbohydrate, fat, and protein in liquid and solid state. Sudbury, Ont: Laurentian University, 2005.

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11

Oxidative Folding of Proteins: Basic Principles, Cellular Regulation and Engineering. Royal Society of Chemistry, 2018.

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12

Protein Oxidation and Aging Wiley Series in Protein and Peptide Science. John Wiley & Sons, 2012.

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13

Ariga, Hiroyoshi, and Sanae M. M. Iguchi-Ariga. DJ-1/PARK7 Protein: Parkinson’s Disease, Cancer and Oxidative Stress-Induced Diseases. Springer, 2018.

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14

Ariga, Hiroyoshi, and Sanae M. M. Iguchi-Ariga. DJ-1/PARK7 Protein: Parkinson’s Disease, Cancer and Oxidative Stress-Induced Diseases. Springer, 2017.

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15

Ariga, Hiroyoshi, and Sanae M. M. Iguchi-Ariga. DJ-1/PARK7 Protein: Parkinson's Disease, Cancer and Oxidative Stress-Induced Diseases. Springer, 2017.

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16

Sharma, Chandra Kant, and VINAY SHARMA. Protein biomarker, oxidative stress & DNA strand breaks in leukemia: Detection and evaluation in leukemic patients. LAP Lambert Academic Publishing, 2012.

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17

Matthews, David M. Protein Absorption: Development and Present State of the Subject. Wiley-Liss, 1992.

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18

Schaeffer, Cathy Jo. The cost of segregating low protein soft white wheat in Washington State. 1992.

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19

The Redox State and Circadian Rhythms. Springer, 2000.

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20

Huang, Jing. Control of muscle protein degradation and steady-state poly(ADP-ribose) polymerase concentration by calpain. 1998.

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21

Ollerenshaw, Jason Edward. Applications of liquid state NMR spectroscopy for protein structure, dynamics, and folding, and for quantum computation. 2005.

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22

MARROQUÍN-DE JESÚS, Ángel, Juan Manuel OLIVARES-RAMÍREZ, Andrés DECTOR-ESPINOZA, and Luis Eduardo CRUZ-CARPIO. CIERMMI Women in Science Biology, Chemistry and Life Sciences Handbook T-XIV. ECORFAN-Mexico, S.C., 2021. http://dx.doi.org/10.35429/h.2021.14.1.119.

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This volume, Women in Science T-XIV-2021 contains 7 refereed chapters dealing with these issues, chosen from among the contributions, we gathered some researchers and graduate students from the 32 states of our country. We thank the reviewers for their feedback that contributed greatly in improving the book chapters for publication in these proceedings by reviewing the manuscripts that were submitted. As first chapter, Martínez, Bravo, Sánchez and Montoya present Effect of the consumption of Stevia rebaudiana Bertoni as a natural and artificial sweetener on fatigue and oxidative stress of skeletal muscle, as second chapter, Hernández, Ramírez, Chávez and Oliart, will talk about Cashew bagasse (Anacardium occidentale L. ) as a source of fiber-antioxidant and its possible use in lipoinflammation models as the third chapter, Marcos, Ramirez, Oliart, and Guadarrama present The relevance of the source of animal or vegetable proteins on the metabolic syndrome and its comorbidities, as the fourth chapter, Damián, Rivera, Lizárraga and Vázquez. propose Wanderings of a magic element: the biogeochemical cycle of manganese, as the fifth chapter, Sánchez, Paniagua, Temiche and Alexander, perform Methods of physical control of pathogenic microorganisms in hospital areas, as the sixth chapter, Paniagua, Sánchez, Corro and Alexander develop Use of power ultrasound, supercritical fluids and membrane technology to obtain and/or preserve biological products for clinical use, and as the last chapter, Estrada, Figueroa, Sierra and Aguilar, focus on Obtaining and characterization of the ethanolic extract of the leaves of the Tradescantia Spathacea SW.

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23

Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.

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24

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of nutrition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0201.

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Energy is derived from three major categories of macronutrient—carbohydrate, lipid, and protein. While energy requirements to maintain stable weight can be estimated, it is uncertain if meeting these energy requirements improves outcomes in the critically ill. In health, excess energy is stored via non-oxidative metabolism and during periods of inadequate energy delivery catabolism of storage products occurs. Both storing and using the stores cost energy, each may require up to quarter of energy contained in stored nutrient. Excess carbohydrate stored as glycogen is easily available, albeit in a limited amount. Storage of lipid is the largest energy repository, but requires complex metabolism and is limited by low oxidative capacity. Protein catabolism normally contributes less than 5% of energy requirements, but during periods of inadequate energy delivery or increased catabolism there is a marked increase in endogenous protein breakdown.

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25

Hum, Gabriel. Novel approaches towards the synthesis of protein tyrosine phosphatase inhibitors and alternative strategies in the design of transition state analogues for phosphatase abzymes. 2002.

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26

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.

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27

Gray, Doug, Carole Proctor, and Tom Kirkwood. Biological aspects of human ageing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0001.

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At the molecular and cellular levels human ageing is characterized by the accumulation of unrepaired random damage, and an accompanying loss of function. A major source of damage is oxidative stress caused by the generation of reactive oxygen species as a by-product of respiration. DNA and proteins are both susceptible to damage but whereas DNA damage repair systems exist, faulty proteins are generally removed by protein degradation systems. During ageing these systems become less efficient and the subsequent accumulation of damaged protein promotes protein aggregation, a process which is especially problematic in the ageing brain. Other aspects of ageing include genetic and epigenetic changes, mitochondrial dysfunction, telomere shortening, and cellular senescence, all subject to stochasticity. The complexity of the biology of ageing has led to an increase in the use of systems biology approaches whereby the use of mathematical modelling and bioinformatic tools complement the more traditional experimental approaches.

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28

Gapstur, Susan M., and Philip John Brooks. Alcohol and Cancer Risk. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0012.

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In 2010, alcoholic beverage consumption caused an estimated 3.3 million deaths worldwide, and contributed to injuries, violence, liver cirrhosis, social disruption and at least seven different types of cancer. The International Agency for Research on Cancer (IARC) classifies exposure to both ethanol in alcoholic beverages and acetaldehyde, the primary metabolite of ethanol, as carcinogenic to humans (Group 1) based on “sufficient” evidence that alcoholic beverage consumption is causally related to cancers of the oral cavity, pharynx, larynx, esophagus, liver, colorectum and female breast. The biologic mechanisms by which alcohol and its primary metabolite acetaldehyde affect cancer risk appear to vary across anatomic sites. Broadly, these mechanisms involve DNA and protein damage from acetaldehyde and oxidative stress, nutritional malabsorption and metabolic effects, and for breast cancer, increased estrogen levels. The World Health Organization has increased global surveillance of alcohol consumption and encourages national efforts to apply evidence-based policies to reduce consumption.

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29

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.

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30

Maj, Dorota. Modyfikujący wpływ roślinnych dodatków paszowych na użytkowość mięsną i ekspresję wybranych genów u królików w zależności od wieku i płci. Publishing House of the University of Agriculture in Krakow, 2017. http://dx.doi.org/10.15576/978-83-66602-29-8.

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The aim of the study was to determine the effect of feed additives (algae, soybean, and sunflower oil) used in the rabbit feed on: growth indices and slaughter traits, pH, colour, texture, chemical composition, fatty acid profile and oxidative stability (TBARS) of the meat as well as FTO and FABP4 genes expression in the meat’s intramuscular fat (m. longissimus lumborum), depending on the age and sex. The experimental material consisted of Termond White rabbits (n = 160, 80 females and 80 males). Animals were weaned on the 35th day of life, and housed in metal cages arranged in batteries (4 rabbits of the same sex in a cage). From weaning to 12 or 18 weeks of age, the rabbits were fed pellets ad libitum. Animals in the control group (C) received non-supplemented pellets throughout the experiment. In the other groups, the pellet contained 1% algae (A), 3% sunflower oil (OS), and 3% soybean oil(SO).The experimental diets were formulated to have similar protein and energy content. Diets were balanced by lowering the proportion of other feed components. The total share of all components remained at 100%. The results indicate that 3% vegetable oils (soybean or sunflower) supplementation of diets for growing rabbits leads to an increase of body weight and improvement of some of the slaughter traits, while 1% addition of algae to the feed causes deterioration of body weight and slaughter traits. The effect of oil additive depends on the animals’ age. Supplementation of the rabbits’ diet with algae (1%) or sunflower and soybean oils (3%) led to an increase in the dressing percentage of rabbits slaughtered at 18 weeks of age (approx. 3%), but had no effect on the dressing percentage of rabbits slaughtered at 12 weeks of age. Feeding pellets with either 3% vegetable oils or 1% algae additive to the rabbits did not significantly change the chemical composition of the meat. Protein content increased and intramuscular fat content decreased with age, while ash and water content were similar. The feed additives significantly differentiated meat acidity without deteriorating meat quality. Diet modification has not affected negatively meat colour. 24 h after the slaughter, the colour of rabbit meat was similar across the studied feeding groups. Correlation between diet and rabbits’ age was found. Meat texture (hardness, springiness and chewiness) of all rabbit groups slaughtered at 12 weeks of age was similar, and the shear for cewas greater in rabbits fed pellets with algae and soybean oil. At 18 weeks of age, rabbit meat from experimental groups had lower hardness and chewiness, compared to meat of the animals from the control group. Meat shear force was higher in the control group, and from algae-supplemented group. The correlation between diet and age was also found. The use of 3% vegetable oils or 1% algae as feed additives significantly reduced meat oxidative stability. Soybean or sunflower oil (3%) usedas feed additives favourably modified the fatty acid composition of intramuscular fat. Polyunsaturated fatty acids (PUFA) content was increased, including linoleic acid, and PUFA/MUFA ratio was improved. The content of these acids decreased with age. The use of algae (1%) as a feed additive resulted in positive effect on the increase of n-3 fatty acid content (EPA and DHA) in meat intramuscular fat. Algae supplementation improved pro-health properties of meat, with low n-6/n-3 acid ratio (2.5), indicating that diet modification may affect the fatty acid composition of rabbit meat. The influence of diet and age on FTO and FABP4 gene expression in meat intramuscular fat (m. longissimus lumborum) was found. FTO and FABP4 gene expression increased with age and was the highest in the group of rabbits with 1% algae supplementation in the diet. The effect of rabbits’ gender on growth, slaughter traits, meat quality and gene expression in rabbits was not observed. In conclusion, the use of natural feed additives, such as sunflower, soybean oil or algae, can improve the nutritional value of rabbit meat, without changing its chemical or physical properties, and therefore the meat can serve as functional food, with properties beneficial to human health. The results obtained in this study also indicate that the expression of FTO and FABP4 genes in rabbit muscles is regulated by dietary factors and age, which, in addition to cognitive significance, has practical implications for improving technological and dietary quality of rabbit meat.

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31

Schadt, Eric E. Network Methods for Elucidating the Complexity of Common Human Diseases. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0002.

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The life sciences are now a significant contributor to the ever expanding digital universe of data, and stand poised to lead in both the generation of big data and the realization of dramatic benefit from it. We can now score variations in DNA across whole genomes; RNA levels and alternative isoforms, metabolite levels, protein levels, and protein state information across the transcriptome, metabolome and proteome; methylation status across the methylome; and construct extensive protein–protein and protein–DNA interaction maps, all in a comprehensive fashion and at the scale of populations of individuals. This chapter describes a number of analytical approaches aimed at inferring causal relationships among variables in very large-scale datasets by leveraging DNA variation as a systematic perturbation source. The causal inference procedures are also demonstrated to enhance the ability to reconstruct truly predictive, probabilistic causal gene networks that reflect the biological processes underlying complex phenotypes like disease.

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32

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Nephrotic syndrome. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0161.

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Nephrotic syndrome is a clinical syndrome of heavy proteinuria (greater than 3.5 g per 24 hours), oedema, and hypoalbuminaemia, which is associated with hyperlipidaemia and a procoagulant state. Causes of nephrotic syndrome are traditionally classified by their histopathological descriptions. In most cases, the histological picture can have a primary (idiopathic) or secondary cause. Minimal change, membranous nephropathy, and focal segmental glomerulosclerosis account for over 60% of cases. Diabetic nephropathy and renal amyloidosis are common secondary causes of nephrotic syndrome. Nephrotic-range proteinuria will show up as at least 3+ protein on urinalysis. The diagnosis is confirmed by a urinary protein-to-creatinine ratio over 300 mg/mmol, and hypalbuminaemia. In adults, renal biopsy is the diagnostic test. This chapter addresses the causes, diagnosis, and management of nephrotic syndrome in adults.

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33

Soler, Ximena, and Lori A. Aronson. Diabetic Ketoacidosis During Appendicitis with Perforation. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0047.

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Type 1 diabetes mellitus (DM) is a chronic disease of carbohydrate, fat, and protein metabolism caused by a functional lack of insulin. Diabetic ketoacidosis (DKA) involves a combination of hyperglycemia, acidosis and ketosis, and is more often associated with type 1 DM. A child in DKA who presents for emergency surgery may be critically ill and requires expert management of his or her metabolic state to ensure a safe outcome.

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34

Keshav, Satish, and Alexandra Kent. Starvation and malnutrition. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0332.

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Starvation is a state of severe malnutrition due to a reduction in macro- and micronutrient intake. The basis underlying starvation is an imbalance between energy intake and energy expenditure. The commonest cause of starvation is lack of available food, usually due to environmental, social, and economic reasons, although other causes include anorexia nervosa; depression and other psychiatric disorders; coma and disturbance of consciousness; intestinal failure; and mechanical failure of digestion, including poor dentition and intestinal obstruction. Protein energy malnutrition is usually seen in developing countries. This chapter discusses starvation and malnutrition, focusing on their etiology, symptoms, demographics, natural history, complications, diagnosis, treatment, and prognosis.

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35

Vernon, Hilary. Phenylketonuria. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0064.

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Phenylketonuria is an autosomal recessive biochemical disorder most often resulting from a deficiency of phenylalanine hydroxylase, the enzyme which catalyzes the conversion of phenylalanine to tyrosine. The remainder of the cases are caused by abnormalities in the phenylalanine hydroxylase cofactor, tetrahydrobiopterin. Phenylketonuria can be divided into three subgroups based on the elevation of plasma phenylalanine in the untreated state: “classical,” “variant,” and “benign.” Untreated individuals with classical phenylketonuria develop neurocognitive abnormalities including seizures, microcephaly, and severe intellectual disability. Other clinical effects include a musty body odor, eczema, and reduced skin pigmentation. Treatment, which includes dietary restriction of phenylalanine, supplementation with synthetic protein, and, in some cases, administration of a synthetic form of tetrahydrobiopterin, is successful in preventing the long-term consequences of phenylketonuria.

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36

Kirchman, David L. Elements, biochemicals, and structures of microbes. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0002.

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Microbiologists focus on the basic biochemical make-up of microbes, such as relative amounts of protein, RNA, and DNA in cells, while ecologists and biogeochemists use elemental ratios, most notably, the ratio of carbon to nitrogen (C:N), to explore biogeochemical processes and to connect up the carbon cycle with the cycle of other elements. Microbial ecologists make use of both types of data and approaches. This chapter combines both and reviews all things, from elements to macromolecular structures, that make up bacteria and other microbes. The most commonly used elemental ratio was discovered by Alfred Redfield who concluded that microbes have a huge impact on the chemistry of the oceans because of the similarity in nitrogen-to-phosphorus ratios for organisms and nitrate-to-phosphate ratios in the deep oceans. Although statistically different, the C:N ratios in soil microbes are remarkably similar to the ratios of aquatic microbes. The chapter moves on to discussing the macromolecular composition of bacteria and other microbes. This composition gives insights into the growth state of microbes in nature. Geochemists use specific compounds, “biomarkers”, to trace sources of organic material in ecosystems. The last section of the chapter is a review of extracellular polymers, pili, and flagella, which serve a variety of functions, from propelling microbes around to keeping them stuck in one place.

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37

Sherwood, Dennis, and Paul Dalby. Modern Thermodynamics for Chemists and Biochemists. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198782957.001.0001.

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This book will equip a student of any physical or biological science with a sound understanding of thermodynamics, and will build confidence in using thermodynamics in practice. The emphasis is towards chemical thermodynamics, but the principles of the First, Second and Third Laws apply to all sciences. Importantly, the final four chapters show how thermodynamics can be applied to biological systems, discussing the biochemical standard state, bioenergetics, protein folding, and the self-assembly of smaller components to form higher-level structures. The book has not been written to support a particular curriculum; rather, it covers all the fundamental principles, so providing a comprehensive grounding, as well as a strong foundation for further study. It is therefore likely that there will be more material in this book than is required for any one particular curriculum, but we trust there is sufficient material for almost every curriculum. A key feature of the book is the style. It has been written so that ‘you can hear our voices’, and with the overarching intent of being logical, clear and comprehensible. The style will therefore be perceived as less formal than many other texts – and we trust more readable. Furthermore, we have sought to avoid phrases such as ‘it may be shown that...’, and ‘clearly, it follows that...’. If ‘it may be shown’, we show it; and we don’t use ‘clearly’ when things aren’t clear at all. Thermodynamics is notoriously difficult. This book does not make an intrinsically deep science ‘easy’. But it does make it intelligible.

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Books on the topic 'Oxidative state of protein'

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