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Books on the topic 'Muscles Genes'

Author: Grafiati

Published: 6 September 2023

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1

1933-, Pette Dirk, and Symposium "The Dynamic State of Muscle Fibers" (1989 : University of Konstanz), eds. The Dynamic state of muscle fibers: Proceedings of the international symposium, October 1-6, 1989, Konstanz, Federal Republic of Germany. De Gruyter, 1990.

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2

Duan, Dongsheng. Muscle gene therapy. Springer, 2010.

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3

Muscle gene therapy: Methods and protocols. Humana, 2011.

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4

C, Strohman Richard, Wolf Stewart 1914-, and Muscular Dystrophy Association, eds. Gene expression in muscle. Plenum Press, 1985.

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5

Muscular, Dystrophy Association-UCLA Symposium (1988 Steamboat Springs Colo ). Cellular and molecular biology of muscle development: Proceedings of a Muscular Dystrophy Association-UCLA Symposium, held at Steamboat Springs, Colorado, April 3-10, 1988. Liss, 1989.

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6

rdh-Nilsson, Anna Hultga. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. Kongl. Carolinska Medico Chirurgiska Institutet, 1991.

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7

M, Kelly Alan, and Blau Helen M, eds. Neuromuscular development and disease. Raven Press, 1992.

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8

Yu, Sŭng-gwŏn. So ŭi kŭnyuk kwa chibang kwallyŏn kyŏngje hyŏngjil yuyong yujŏnja ŭi kinŭng punsŏk ŭl wihan model sisŭt'em ŭi kaebal kwa sanŏpchŏk hwaryong pangan kuch'uk =: Development of high-throughput screening system to evaluate the fuctional role of various genes related in muscle and adipose growth and differentiation in bovine. Nongch'on Chinhŭngch'ŏng, 2009.

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9

Reggiani, Carlo, and Roberto Bottinelli. Skeletal Muscle Plasticity in Health and Disease: From Genes to Whole Muscle. Springer London, Limited, 2010.

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10

(Editor), Roberto Bottinelli, and Carlo Reggiani (Editor), eds. Skeletal Muscle Plasticity in Health and Disease: From Genes to Whole Muscle (Advances in Muscle Research). Springer, 2006.

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11

Tissue-engineered skeletal muscle organoids for reversible gene therapy: Brief report. National Aeronautics and Space Administration, 1996.

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12

photographer, Varney Jason, ed. Zero belly cookbook: 150+ delicious recipes to flatten your belly, turn off your fat genes, and help keep you lean for life! 2015.

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13

Cellular and molecular biology of muscle development: Proceedings of a Muscular Dystrophy Association-UCLA Symposium, held at Steamboat Springs, Colorado, ... symposia on molecular and cellular biology). Liss, 1989.

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14

Mendell, Jerry R., and Dongsheng Duan. Muscle Gene Therapy. Springer, 2019.

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15

Duan, Dongsheng. Muscle Gene Therapy. Springer New York, 2014.

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16

Wolf, Stewart. Gene Expression in Muscle. Springer, 2012.

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17

Duan, Dongsheng. Muscle Gene Therapy: Methods and Protocols. Humana Press, 2016.

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18

Elliott, Perry, Kristina H. Haugaa, Pio Caso, and Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently cau

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19

Syrris, Petros, and Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0359.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder of the heart muscle which is typically inherited in an autosomal dominant manner. It is believed to be familial in over 50% of cases. A recessive mode of inheritance has also been reported in syndromic cases with cardiocutaneous features. The classic form of the disorder is considered to be ‘a disease of the desmosome’ as pathogenic variants have been identified in five genes encoding key desmosomal proteins: plakoglobin, desmoplakin, plakophilin-2, desmoglein-2, and desmocollin-2. Mutations in these genes account for 30–50%

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20

Cellular and molecular biology of muscle development: Proceedings of a Muscular Dystrophy Association-UCLA Symposium, held at Steamboat Springs, Colorado, ... symposia on molecular and cellular biology). Liss, 1989.

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21

Pozio, Edoardo. Trichinellosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0068.

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Trichinellosis is caused by nematodes of the genus Trichinella. These zoonotic parasites show a cosmopolitan distribution in all the continents, but Antarctica. They circulate in nature by synanthropic-domestic and sylvatic cycles. Today, eight species and four genotypes are recognized, all of which infect mammals, including humans, one species also infects birds, and two other species infect also reptiles.Parasites of the genus Trichinella are unusual among the other nematodes in that the worm undergoes a complete developmental cycle, from larva to adult to larva, in the body of a single host

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22

Stafstrom, Carl E. Disorders Caused by Botulinum Toxin and Tetanus Toxin. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0156.

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Anaerobic organisms of the genus Clostridia (C) can cause significant human disease. Exotoxins secreted by C botulinum and C tetani cause botulism and tetanus, respectively (summarized in Table 156.1). Botulinum neurotoxin causes neuromuscular blockade by interfering with vesicular acetylcholine release, leading to cholinergic blockade at the neuromuscular junctions of skeletal muscle, and consequently, symmetric flaccid paralysis. Tetanus toxin prevents release of inhibitory neurotransmitters at central synapses, leading to overactivity of motor neurons and muscle rigidity and spasms. This ch

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23

Mammen, Andrew L., and Jessica R. Nance. Evaluation of hyperCKaemia. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0007.

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Serum creatine kinase (CK) levels may be elevated in patients with muscle weakness or pain. In asymptomatic patients with CK elevations, the focus should be on identifying reversible causes, followed by investigation for inherited muscle diseases. In asymptomatic patients with an incidental finding of elevated CK, clinicians should look for reversible causes, then re-test the CK after 10 days of rest in the absence of potential triggers. If the CK remains markedly elevated and/or electromyography proves myopathic, a muscle biopsy should be considered. Women of childbearing age with elevation o

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24

Jinnah, H. A., Cecilia N. Prudente, Samuel J. Rose, and Ellen J. Hess. The Neurobiology of Dystonia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0010.

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The dystonias are a large group of disorders characterized by excessive muscle activity leading to abnormal movements. They are clinically diverse, affecting different parts of the body at all ages in both humans and other animals. They also are etiologically diverse, with causes that are either inherited due to specific dystonia-causing genes, or acquired because of nervous system injury or exposure to certain drugs or chemicals. Despite the clinical and etiological heterogeneity, there is an increasing appreciation that certain subgroups of dystonias share some biological abnormalities at th

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25

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 ra

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26

1932-, Kakulas Byron A., Howell J. McC, and Roses Allen D, eds. Duchenne muscular dystrophy: Animal models and genetic manipulation. Raven Press, 1992.

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27

Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Alport syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0323.

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The diagnosis of Alport syndrome is suspected from the clinical features and confirmed by identifying the almost pathognomonic ultrastructural changes to the basement membrane in a family member with early disease (so that glomeruli are not too sclerosed), or in modern times by identifying a causative mutation in one or more of the three implicated COL4 genes. Genetic testing is becoming simpler and cheaper, but is still out of the reach of many. Eighty-five per cent of cases are caused by COL4A5 mutations and 10–15% by autosomal recessive disease. A significant proportion of morbidity in X-li

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28

(Editor), Charles P. Emerson, and H. Lee Sweeney (Editor), eds. Methods in Cell Biology: Methods in Muscle Biology (Methods in Cell Biology). Academic Pr, 1997.

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29

(Editor), Charles P. Emerson, and H. Lee Sweeney (Editor), eds. Methods in Cell Biology: Methods in Muscle Biology (Methods in Cell Biology). Academic Pr, 1997.

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30

RYAN, Natasha. Sirt Diet: A Beginner's Guide to Sirt Food, Lose Weight While Eating, Like You're Not on a Diet. Burns Fat and Increases Muscle Mass by Activating Lean Genes. Independently Published, 2020.

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31

Schutte, Nienke M., Meike Bartels, and Eco JC de Geus. Genetics of physical activity and physical fitness. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0020.

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Regular physical activity and fitness are key contributors to children’s health. It is important to understand sources of variation in phenotypes seen among children and adolescents. It is important to calculate the relative importance of genetic and environmental factors to observed individual differences. Heritability estimates of physical activity vary, depending on sample size and measurement instrument, but the overall importance of environmental factors seems to decrease in adolescence, whereas genetic effects become more prominent. Twin and family studies show that individual difference

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32

Forsyth, Rob, and Richard Newton. Neurodiagnostic tools. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0002.

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This chapter explains the principles of how best to use the main diagnostic tools in paediatric neurology in the context of evidence-based medicine. The description of neuroradiology includes the principles of DWI, SWI, MRS, ASL and fMRI, and the usefulness of ultrasound, CT and PET scanning; neuroradiological anatomy, terminology, common incidental findings and normal myelination patterns. An approach to white matter and developmental brain abnormalities is depicted. Neurogenetic testing discusses the capabilities and limitations of microarray for Comparative Genomic Hybridization (copy-numbe

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33

Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.

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Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy a

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34

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly

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35

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly

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36

Hakim, Alan J., and Rodney Grahame. Hypermobility syndromes. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0159.

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Hypermobility-related syndromes constitute a family of heritable disorders of connective tissue (HDCT) that derive from abnormalities affecting genes that encode for the connective tissue matrix proteins such as collagen, fibrillin, and tenascin. They range from such commonplace though poorly recognized conditions such as the joint hypermobility syndrome (JHS) to the better-known, if more rare, eponymous syndromes such as Marfan's syndrome (MFS) and the different types of the Ehlers-Danlos syndrome (EDS). The more common presentations are with skin pathology (bruising, scaring), joint or spina

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37

Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.

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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will lear

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38

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existi

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39

Skiba, Grzegorz. Fizjologiczne, żywieniowe i genetyczne uwarunkowania właściwości kości rosnących świń. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_gs_2020.

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Bones are multifunctional passive organs of movement that supports soft tissue and directly attached muscles. They also protect internal organs and are a reserve of calcium, phosphorus and magnesium. Each bone is covered with periosteum, and the adjacent bone surfaces are covered by articular cartilage. Histologically, the bone is an organ composed of many different tissues. The main component is bone tissue (cortical and spongy) composed of a set of bone cells and intercellular substance (mineral and organic), it also contains fat, hematopoietic (bone marrow) and cartilaginous tissue. Bones a

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