Biochemistry with clinical correlations pdf


Textbook of Biochemistry with Clinical Correlations Edited by Thomas M Devlin. pp John Wiley & Sons, New York. £ ISBN 0 - 4 7 1. 5-DEVLIN'S Textbook of Biochemistry with Clinical ehab Aboueladab. This document is currently being converted. Please check back in a few. These are very exciting times for biochemistry and especially for that part that pertains to human biology and human medicine. The much discussed Human.

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Biochemistry With Clinical Correlations Pdf

Textbook of biochemistry with clinical correlations (4th edn). edited by Biochemical Underpinnings of Immune Cell Metabolic Phenotypes Full-Text · PDF. Textbook of Biochemistry with Clinical Correlations, 7th Edition PDF MB Password: Help · Download. Report This. Please complete the. Request PDF on ResearchGate | On Jul 1, , James Zimmerman and others published Textbook of biochemistry: With clinical correlations.

Translational research Abstract Antenatal corticosteroids ANS are the major intervention to decrease respiratory distress syndrome and mortality from premature birth and are standard of care. The use of ANS is expanding to include new indications and gestational ages, although the recommended dosing was never optimized. The most widely used treatment is two intramuscular doses of a mixture of betamethasone-phosphate Beta-P and betamethasone-acetate Beta-Ac — the clinical drug. We tested in a primate model the efficacy of the slow release Beta-Ac alone for enhancing fetal lung maturation and to reduce fetal corticosteroid exposure and potential toxic effects. Beta-Ac alone increased lung compliance and surfactant concentration in the fetal lung equivalently to the clinical drug. By transcriptome analyses the early suppression of genes associated with immune responses and developmental pathways were less affected by Beta-Ac than the clinical drug.

Adenosine Triphosphate ATP is the intermediate molecule that drives the exergonic transfer of energy to switch to endergonic anabolic reactions used in muscle contraction. This is what causes muscles to work which can require a breakdown, and also to build in the rest period, which occurs during the strengthening phase associated with muscular contraction.

ATP is composed of adenine, a nitrogen containing base, ribose, a five carbon sugar collectively called adenosine , and three phosphate groups. ATP is a high energy molecule because it stores large amounts of energy in the chemical bonds of the two terminal phosphate groups.

The breaking of these chemical bonds in the Krebs Cycle provides the energy needed for muscular contraction. Glucose[ edit ] Because the ratio of hydrogen to oxygen atoms in all carbohydrates is always the same as that in water—that is, 2 to 1—all of the oxygen consumed by the cells is used to oxidize the carbon in the carbohydrate molecule to form carbon dioxide.

Textbook of biochemistry with clinical correlations

Consequently, during the complete oxidation of a glucose molecule, six molecules of carbon dioxide and six molecules of water are produced and six molecules of oxygen are consumed. When listed on nutritional information tables, fats are generally divided into six categories: total fats, saturated fatty acid , polyunsaturated fatty acid , monounsaturated fatty acid , dietary cholesterol , and trans fatty acid.

From a basal metabolic or resting metabolic perspective, more energy is needed to burn a saturated fatty acid than an unsaturated fatty acid.

The fatty acid molecule is broken down and categorized based on the number of carbon atoms in its molecular structure. The chemical equation for metabolism of the twelve to sixteen carbon atoms in a saturated fatty acid molecule shows the difference between metabolism of carbohydrates and fatty acids.

Palmitic acid is a commonly studied example of the saturated fatty acid molecule. Unlike fat the body has no storage deposits of protein. All of it is contained in the body as important parts of tissues, blood hormones, and enzymes.

5-DEVLIN'S Textbook of Biochemistry with Clinical | ehab Aboueladab -

The structural components of the body that contain these amino acids are continually undergoing a process of breakdown and replacement.

This process could severely degrade the protein structures needed to maintain survival such as contractile properties of proteins in the heart, cellular mitochondria, myoglobin storage, and metabolic enzymes within muscles. The oxidative system aerobic is the primary source of ATP supplied to the body at rest and during low intensity activities and uses primarily carbohydrates and fats as substrates.

Protein is not normally metabolized significantly, except during long term starvation and long bouts of exercise greater than 90 minutes. Following the onset of activity, as the intensity of the exercise increases, there is a shift in substrate preference from fats to carbohydrates.

These results have given us first insights into the possible functions of adropin but were primarily explored in mouse models or human association studies. There is one study showing that circulating adropin declines with obesity in nonhuman primates 6 , but it is not otherwise known whether adropin biology can be translated from rodents to primates, and particularly humans. To fill this gap, Butler and colleagues 1 set out to data mine the expression profile of ENHO in baboon tissues.

They utilized a recently published database to probe tissue-specific and diurnal patterns of ENHO gene expression in baboons. It is known that ENHO is expressed in the brain and liver in mice.

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Whereas this is true in baboon tissues, surprisingly, brain regions involved in metabolic regulation, such as amygdala, ventromedial hypothalamus, and lateral hypothalamus, express the highest levels of ENHO. This study demonstrates that the expression profile of ENHO in baboons is consistent with those in mice and humans. Next, Butler and colleagues 1 explored the association of circulating adropin with cardiometabolic biomarkers in a rhesus monkey model of metabolic syndrome.

Rhesus monkeys were fed for 3 months with a high-fructose beverage diet, which rapidly induces weight gain, hyperinsulinemia, and dyslipidemia.

Plasma was sampled at baseline and after 1 and 3 months of the diet. Simple modeling of the data revealed a negative correlation between levels of adropin and those of leptin, glucose, ApoA1 a major high-density lipoprotein HDL 2 apoprotein , and ApoC3 a key component of triglyceride-rich lipoproteins , but a positive correlation between plasma adropin and HDL-C Fig.

All diabetic monkeys exhibit a low plasma adropin level. The authors then performed multiple linear regression analysis to find correlates of plasma adropin based on age, body weight, and measures of insulin resistance and dyslipidemia. The results showed that plasma adropin is strongly correlated with measures of adiposity e.

Grouping of the monkeys based on plasma adropin levels produced similar results. This shows that a low level of adropin in circulation signals the risks of cardiometabolic diseases in a nonhuman primate model of metabolic syndrome.

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