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Books on the topic 'Corn – Metabolsim'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

C, Shannon Jack, Knievel Daniel P. 1943-, Boyer Charles D, and Pennsylvania State University. Intercollege Graduate Program in Plant Physiology., eds. Regulation of carbon and nitrogen reduction and utilization in maize: Proceedings of the first annual Penn State Symposium in Plant Physiology (May 22-23, 1986), The Pennsylvania State University. Rockville, Md: American Society of Plant Physiologists, 1986.

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2

Nadjmi, Maschallah, ed. Imaging of Brain Metabolism Spine and Cord Interventional Neuroradiology Free Communications. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74337-5.

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3

Genevieve, Morgan, ed. The core balance diet: 4 weeks to boost your metabolism and lose weight for good. Carlsbad, Calif: Hay House, 2009.

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4

Genevieve, Morgan, ed. The core balance diet: 28 days to boost your metabolism and lose weight for good. 5th ed. Carlsbad, CA: Hay House, 2013.

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5

Congress, European Society of Neuroradiology. Imaging of brain metabolism, spine and cord interventional neuroradiology free communications: XVth Congress of the European Society of Neuroradiology, Würzburg, September 13th-17th, 1988. Berlin: Springer-Verlag, 1989.

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6

Marzok, Mohamed Ahmed Tony Ahmed. Detection of genetically modified soybeans and maize in Egypt as well as comparative nutritional safety investigations of isogenic and transgenic (Bt) maize in broiler nutrition: Broiler performance, degradation and metabolic fate of maize DNA in some tissues and organs. Berlin: Mensch & Buch Verlag, 2004.

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7

Mohamed Ahmed Tony Ahmed Marzok. Detection of genetically modified soybeans and maize in Egypt as well as comparative nutritional safety investigations of isogenic and transgenic (Bt) maize in broiler nutrition: Broiler performance, degradation and metabolic fate of maize DNA in some tissues and organs. Berlin: Mensch & Buch Verlag, 2004.

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8

V, Khotyleva L., Instytut henetyki i tsytalohii (Akadėmii͡a︡ navuk Belarusi), and Belorusskoe obshchestvo genetikov i selekt͡s︡ionerov., eds. Bioėnergeticheskie prot͡s︡essy pri geterozise. Minsk: "Navuka i tėkhnika", 1991.

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9

Miller, Keith Douglas. The effects of the herbicide safener benoxacor on glutathione s-transferase activity and the metabolism of benoxacor in suspension cultures of Zea mays. 1994.

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10

Kjelgaard, James F. Comparison of models for estimating evapotranspiration from maize. 1993.

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11

Outlines of biochemistry [by] Eric E. Conn and P.K. Stumpf. the mucmillan press ltd, 1987.

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12

Fraser, Jamie L., Frédéric Sedel, and Charles P. Vendetti. Disorders of Cobalamin and Folate Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0027.

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Cobalamin C deficiency (cblC) and related disorders of intracellular cobalamin metabolism may present at any time from the prenatal period through adolescence/adulthood and are due to deficiency of the cobalamin cofactors adenosylcobalamin and methylcobalamin. Chronic complications of cblC depend on the age at presentation and may include poor growth, renal dysfunction, neuropsychiatric manifestations, intellectual disability, strokes, progressive leukoencephalopathy and spinal cord degeneration, psychiatric manifestations and executive function deficits, and optic nerve and retinal anomalies. While less common than in isolated MMA, acute metabolic decompensation may occur in cblC patients due to accumulation of methylmalonic acid and associate metabolites and should be managed as in isolated MMA in conjunction with a metabolic consultant. The most common inborn error of folate (vitamin B9) metabolism relevant for adult patients is methylenetetrahydrofolate reductase (MTHFR) deficiency. Manifestations are primarily neurological, but the disorder may present in a substantial number of adults with psychiatric symptoms. Early recognition with adequate treatment is crucial.

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13

Nadjmi, Maschallah. Imaging of Brain Metabolism Spine and Cord Interventional Neuroradiology Free Communications. Springer-Verlag, 1990.

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14

Bates, David. Spinal cord disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0650.

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Non-traumatic spinal cord disease may be caused by compression due to tumour, infection or haematoma, inflammation, infection or post-infection, metabolic disturbances, infarction, and degeneration. The diagnosis is often made easier by the clinical assessment: the patient’s age, the speed of onset of the disease, severity of the deficits, the pattern of motor and sensory involvement, and presence of pain and sphincter symptoms are all important in making an assessment of the site and likely nature of the spinal disease.Investigations are obligatory to confirm a diagnosis and to direct therapy. MRI is the most useful investigation. It has largely replaced myelography which should now only be considered in patients with indwelling cardiac pacing wires. Additional investigations including examination of the cerebrospinal fluid, evoked potentials, and specific blood tests may be required and the value of plain X-rays, CT scan, and, in some instances, angiography should not be overlooked.The remainder of this chapter will consider specific disorders, identifying pathology, clinical presentation, investigation, and management. Acute and chronic conditions are considered separately and those affecting the cauda equina, spinal root, and sphincters are considered in Chapter 29.

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15

Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.

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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.

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16

Rho, Jong M. Overview. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0011.

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After nearly a century of clinical use, the ketogenic diet is firmly established as an efficacious treatment for medically intractable epilepsy. Intriguingly, there is growing experimental evidence that the ketogenic diet and its metabolites also render neuroprotective and potentially disease-modifying effects. Hence, dietary and metabolic therapies have been attempted in a variety of neurological disorders other than epilepsy, including brain cancer, cognitive disorders, autism, neurotrauma, pain, and multiple sclerosis. This section, “Ketogenic Diet: Emerging Clinical Applications and Future Potential,” explores the current preclinical and clinical evidence for metabolism-based treatments designed to counter the myriad disease processes seen in many neurological conditions. Specific attention has been given to the effects of the ketogenic diet in malignant brain cancer, autism spectrum disorder, Alzheimer’s disease, traumatic brain and spinal cord injury, pain, and multiple sclerosis.

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17

Benton, Richard Lee. The effect of methylprednisolone treatment on astroglial activation and glutamate metabolism following spinal cord injury. [s.n.], 2000.

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18

Core Balance Diet: A 4-Week Plan for Women to Boost Their Metabolism and Lose Weight. Hay House UK, Limited, 2011.

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19

Dietrich, W. Dalton. Physiologic Modulators of Neural Injury After Brain and Spinal Cord Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0001.

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Brain and spinal cord injury are leading causes of death and long-term disability, producing diverse burdens for the affected individuals, their families, and society. Such injuries, including traumatic brain injury, stroke, subarachnoid hemorrhage, and spinal cord injury, have common patterns of neuronal cell vulnerability that are associated with a complex cascade of pathologic processes that trigger the propagation of tissue damage beyond the acute injury. Secondary injury mechanisms, including oxidative stress, edema formation, changes in cerebral blood flow and vessel reactivity, metabolic and blood–brain barrier disruption, and neuroinflammation, are therefore important therapeutic targets. Several key physiological parameters require monitoring and intensive management during various phases of treatment to ameliorate secondary injury mechanisms and potentially protect against further neuronal injury. This chapter reviews the core physiological targets in the management of brain and spinal cord injury and relates them to secondary injury mechanisms and outcomes.

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20

Lozano, Adriana, Cecilia Bacca, Vilma Pinzón, and Claudia Rozo. Bioquímica -Metabolismo energético, conceptos y aplicaciones. Universidad de Bogotá Jorge Tadeo Lozano, 2011. http://dx.doi.org/10.21789/9789587250879.

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El grupo de docentes de la cátedra de bioquímica del Departamento de Ciencias Básicas de la Facultad de Ciencias Naturales e Ingeniería de la Universidad de Bogotá Jorge Tadeo Lozano, presenta a la comunidad universitaria un material didáctico para los alumnos que cursan el espacio académico de Bioquímica. El objetivo de este grupo de ejercicios es formar parte del trabajo continuado en pro del mejoramiento permanente de la calidad, en el proceso de aprendizaje de los estudiantes como apoyo al trabajo independiente. La primera entrega se enfocó en la bioquímica estructural y descriptiva de las principales biomoléculas; en esta segunda parte se abordan los principios básicos de las interacciones y transformaciones entre ellas, que permiten obtener energía a los seres vivos. Se trata principalmente del metabolismo humano, y aunque ocasionalmente se abordan estrategias metabólicas propias de otras especies, se hace especial énfasis en las rutas de las tres fases del metabolismo intermediario aerobio, tanto catabólico como anabólico, y los capítulos de bioenergética se complementan con los de la bioquímica estructural de lípidos y carbohidratos de importancia biológica o en las industrias: alimentaria, farmacéutica y cosmética.

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21

Carbohydrate and lipid disorders and relevant considerations in persons with spinal cord injury. Rockville, MD: Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services, 2008.

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22

Healthstream. Core Curriculum in Primary Care: Part I Metabolic Diseases (CD-ROM for Windows & Macintosh, Individual Version). Healthstream Inc., 1997.

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23

Campbell, Ian Gordon. The influence of spinal cord injury on the physiological and metabolic responses to exercise and performance. 1992.

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24

Cheng, Ning, Susan A. Masino, and Jong M. Rho. Metabolic Therapy for Autism Spectrum Disorder and Comorbidities. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0014.

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Autism spectrum disorder (ASD) is a heretogenous developmental disorder characterized by deficits in sociability and communication and by repetitive and/or restrictive behaviors. Currently, only comorbid manifestations can be alleviated (such as seizures and sleep disturbance) not core behavioral symptoms. Recent studies have increasingly implicated mitochondrial dysfunction as a cause of ASD. Mitochondria play an integral role in many cellular functions and are susceptible to many pathophysiological insults. Derangements in mitochondrial structure and function provide a scientific rationale for experimental therapeutics. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD) has been shown to enhance mitochondrial function through a multiplicity of mechanisms. Reviewed herein is clinical and basic laboratory evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD, as well as emerging comorbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying novel mechanistic targets are discussed.

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25

Streijger, Femke, Ward T. Plunet, and Wolfram Tetzlaff. Ketogenic Diet and Ketones for the Treatment of Traumatic Brain and Spinal Cord Injury. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0016.

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Ketogenic diets (KD)—high in fat, adequate in protein, and very low in carbohydrates—were developed almost a century ago and are still used clinically for drug-resistant epilepsy and some rare metabolic disorders. Possible new indications for cancers, diabetes, obesity, and neurodegenerative disorders are being trialed in humans based on a growing body of preclinical data showing efficacy. However the underlying mechanisms of KD remain incompletely understood. This chapter focuses on the neuroprotective effects of KD after spinal cord injury (SCI) and traumatic brain injury (TBI), and discusses possible mechanisms of action. It considers the possible role of ketone bodies as alternative fuels for mitochondrial energy utilization and the actions of ketones outside the mitochondria as agonists of antioxidant and anti-inflammatory pathways. It places these into context with the known pathophysiology of SCI and TBI, and discusses possible roles of KD and ketone bodies for their treatment.

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26

Chávez Vivas, Mónica, Mónica Cabrera Tello, Alfonsina del Cristo Martínez Gutiérrez, Romel Fabian Gómez Naranjo, Harold Rivas Mosquera, Vanessa Quintana Ordoñez, Juan David Diago Yusti, et al. Avances en el estudio de marcadores moleculares en el diagnóstico y pronóstico de sepsis bacteriana en la ciudad de Cali. Editorial Universidad Santiago de Cali, 2021. http://dx.doi.org/10.35985/9789585147577.

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El presente libro Marcadores moleculares avances en el estudio de sepsis bacteriana en la ciudad de Cali nace como una iniciativa de socializar los resultados obtenidos en los trabajos de investigación más recientes de los miembros del grupo de investigación en genética, fisiología y metabolismo- GEFIME de la Universidad Santiago de Cali en asociación con otras universidades de la Región. Estos trabajos de investigación se han desarrollado con la finalidad de dar a conocer los resultados que se han obtenido en el estudio de las características epidemiológicas de la sepsis en la ciudad de Cali y cómo la investigación en torno a la búsqueda de marcadores comunes en la población caleña que la hacen susceptible a desarrollar sepsis como complicación de una enfermedad infecciosa de origen bacteriano. Algunos de estos trabajos se realizaron en colaboración con otras instituciones nacionales fortaleciendo las alianzas inter-institucionales en las investigaciones biomédicas. Este libro de investigación comprende trabajos de gran interés en el área de las Ciencias de la Salud con especial interés en la prevención de las complicaciones generadas por enfermedades causadas por agentes infecciosos bacterianos.

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27

Banerjee, Ashis, and Clara Oliver. Haematology and oncological emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0020.

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This chapter covers both the common haematological and oncological emergencies that may present to the emergency department. It includes an overview of blood group type including transfusion reactions, as well haemoglobinopathies such as sickle cell disease. There is also a section on bleeding disorders and their associated management. In addition, this chapter also covers common oncological emergencies which may present to the emergency department. The chapter is subdivided by type of oncological emergency to aid revision; metabolic, cardiovascular, and neurological, the latter of which includes metastatic spinal cord compression and the management of raised intracranial pressure related to cerebral metastases.

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28

Frawley, Geoff. Mucopolysaccharidoses. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0064.

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The mucopolysaccharidoses (MPS) are a group of seven chronic progressive diseases caused by deficiencies of 11 different lysosomal enzymes required for the catabolism of glycosaminoglycans (GAGs). Hurler syndrome (MPS IH) is an autosomal recessive storage disorder caused by a deficiency of α‎-L-iduronidase. Hunter syndrome (MPS II) is an X-linked recessive disorder of metabolism involving the enzyme iduronate-2-sulfatase. Many of the MPS clinical manifestations have potential anesthetic implications. Significant airway issues are particularly common due to thickening of the soft tissues, enlarged tongue, short immobile neck, and limited mobility of the cervical spine and temporomandibular joints. Spinal deformities, hepatosplenomegaly, airway granulomatous tissue, and recurrent lung infections may inhibit pulmonary function. Odontoid dysplasia and radiographic subluxation of C1 on C2 is common and may cause anterior dislocation of the atlas and spinal cord compression.

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29

Endocrine and metabolic disorders sourcebook: Basic consumer health information about hormonal and metabolic disorders that affect the body's growth, development, and functioning, including disorders of the pancreas, ovaries and testes, and pituitary, thyroid, parathyroid, and adrenal glands, with facts about growth disorders, addison disease, cushing syndrome, conn syndrome, diabetic disorders, multiple endocrine neoplasia, inborn errors of metabolism, and more along with information about endocrine functioning, diagnostic and screening tests, a glossary of related terms, and directories of additional resources. Detroit, MI: Omnigraphics, 2017.

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30

Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0182_update_001.

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AbstractSchistosomiasis is a parasitic disease that affects millions of people in 78 countries, where it is held responsible for considerable morbidity and mortality. It is caused by a blood fluke, which provokes an immunological response to hundreds of its antigens. This induces multi-organ pathology through the formation of tissue granulomata or circulating immune complexes. In addition, it is amyloidogenic and carcinogenic, through the interaction of immunological perturbation with confounding metabolic and genetic factors. The primary targets of schistosomiasis are urinary and hepatointestinal.The lower urinary tract is mainly affected in S. haematobium infection, and may lead to chronic pyelonephritis and/or obstructive nephropathy. The colon and liver are the targets of S. mansoni and S. japonicum infection, leading to hepatic fibrosis, portal hypertension, and liver failure. S. mansoni may also lead to immune complex glomerulonephritis, which is discussed elsewhere. Both S. haematobium and S. mansoni ova may be carried with the venous circulation to the lungs, where they provoke granulomatous and immune-mediated endothelial injury leading to cor-pulmonale. Ova may be subsequently carried with the arterial circulation to form ‘metastatic’ granulomas in other tissues, notably the brain (S. japonicum), spinal cord (S. haematobium), skin, conjunctiva, and genital organs.Schistosomiasis is preventable. World Health Organization programmes have successfully eradicated or reduced the incidence of infection in many countries, particularly Egypt and China. Prevention strategies include health education, raising hygiene standards, and interruption of the parasite’s life cycle by snail control and mass treatment. The search for a vaccine continues. Effective antiparasitic treatment is now possible with high elimination rates. Available agents include praziquantel and artemether for all species, metrifonate for S. haematobium, and oxamniquine for S. mansoni. Successful outcome correlates with early intervention, before fibrosis has occurred.

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31

Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.

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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.

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32

Bouchama, Abderrezak. Pathophysiology and management of hyperthermia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0353.

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Hyperthermia is a state of elevated core temperature that rises rapidly above 40°C, secondary to failure of thermoregulation. Hyperthermia has many causes, but it is the hallmark of three conditions—heatstroke, malignant hyperthermia, and neuroleptic malignant syndrome. The clinical and metabolic alterations of hyperthermia, if left untreated, can culminate in multiple organ system failure and death. High temperature causes direct cellular death and tissue damage. The extent of tissue injury is a function of the degree and duration of hyperthermia. Heat-induced ischaemia-reperfusion injury, and exacerbated activation of inflammation and coagulation are also contributory. Hyperthermia is a true medical emergency with rapid progression to multiple organ system failure and death. The primary therapeutic goal is to reduce body temperature as quickly as possible using physical cooling methods, and if indicated, the use of pharmacological treatment to accelerate cooling. There is no evidence of the superiority of one cooling technique over another. Non-invasive techniques that are easy to use and well-tolerated are preferred. Pharmacological cooling with Dantrolene sodium is crucial in the treatment of malignant hyperthermia.

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33

Taljanovic, Mihra S., Imran M. Omar, Kevin B. Hoover, and Tyson S. Chadaz, eds. Musculoskeletal Imaging Volume 1. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190938161.001.0001.

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This volume meets the needs of radiology residents to become adept at interpreting musculoskeletal (MSK) imaging studies. It does so by presenting core knowledge and fundamentals that must be learned to accurately and effectively interpret MSK studies by the trainee and non-specialist. The goal is to impart to residents, as well as to refresh for practitioners, essential facts in a concise and readable format so the reader becomes conversant with all imaging modalities used and the essentials of interpretation and technique. Other resources are at too high a level for the resident in training or contain far more information than a resident can easily assimilate during a rotation. The book is part of the Rotations in Radiology series for residents, which defines and encapsulates core knowledge for areas within Radiology, offering a guided, structured approach to imaging diagnosis. It contains sections on 10 key topics in MSK radiology: trauma; arthritis; tumors and tumor-like conditions; metabolic, hematopoietic, endocrine, and deposition diseases; infectious diseases; arthrography; internal derangements of the joints; congenital diseases; and ultrasound. Each section begins with an overview chapter, orienting the reader to the specific concerns and issues related to imaging that anatomic region or category of problem. Each clinical problem or diagnosis is concisely covered to provide a targeted discussion and highlight salient points. For each topic, concise chunks of text will review: definition; clinical features; anatomy and physiology; how to appraoch the image; what not to miss; differential diagnosis; common variants if pertinent; clinical issues; key points; high yield references.

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34

Taljanovic, Mihra S., Imran M. Omar, Kevin B. Hoover, and Tyson S. Chadaz, eds. Musculoskeletal Imaging Volume 2. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190938178.001.0001.

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This volume meets the needs of radiology residents to become adept at interpreting musculoskeletal (MSK) imaging studies. It does so by presenting core knowledge and fundamentals that must be learned to accurately and effectively interpret MSK studies by the trainee and non-specialist. The goal is to impart to residents, as well as to refresh for practitioners, essential facts in a concise and readable format so the reader becomes conversant with all imaging modalities used and the essentials of interpretation and technique. Other resources are at too high a level for the resident in training or contain far more information than a resident can easily assimilate during a rotation. The book is part of the Rotations in Radiology series for residents, which defines and encapsulates core knowledge for areas within Radiology, offering a guided, structured approach to imaging diagnosis. It contains sections on 10 key topics in MSK radiology: trauma; arthritis; tumors and tumor-like conditions; metabolic, hematopoietic, endocrine, and deposition diseases; infectious diseases; arthrography; internal derangements of the joints; congenital diseases; and ultrasound. Each section begins with an overview chapter, orienting the reader to the specific concerns and issues related to imaging that anatomic region or category of problem. Each clinical problem or diagnosis is concisely covered to provide a targeted discussion and highlight salient points. For each topic, concise chunks of text will review: definition; clinical features; anatomy and physiology; how to appraoch the image; what not to miss; differential diagnosis; common variants if pertinent; clinical issues; key points; high yield references.

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35

Foster, Helen E., and Paul A. Brogan, eds. Paediatric Rheumatology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738756.001.0001.

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Paediatric Rheumatology, second edition is an indispensable resource for the identification and management of rheumatological diseases of children and young people. As well as covering common and rare musculoskeletal problems, there are also chapters on rheumatological emergencies designed for quick reference, and essential core clinical skills of relevance to the full spectrum of paediatric rheumatological disease. This second edition is fully updated, including state-of-the-art descriptions of new autoinflammatory diseases, advances in genetics in paediatric rheumatology, up-to-date guidance on the treatment of JIA, vasculitis, SLE, JDM, and other connective tissue diseases. Highlights of the second edition include alignment of management approaches for paediatric rheumatological diseases with recent evidence-based / consensus European guidelines; a description of North American treatment approaches to JIA; updated chapters on more specialist interventions including immunization in the immunosuppressed, and haematopoietic stem cell transplantation; and sections describing approaches to the management of rheumatological diseases in developing countries. Bone diseases are also described in detail including CRMO, skeletal dysplasias, and metabolic bone diseases. The second edition also includes a colour plate depicting rashes presenting in paediatric rheumatological conditions. This second edition is fully endorsed by the British Society for Paediatric and Adolescent Rheumatology (BSPAR), and many members of BSPAR have contributed most of the chapters. This second edition thus provides fully updated clinical guidelines and supporting information needed to successfully manage children and young people with rheumatological conditions.

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36

Ellinson, Michelle, and Tommy Rampling. Normal nutritional function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0331.

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Normal nutritional function requires a healthy diet. Healthy eating incorporates a variety of nutrients that are essential for energy expenditure, prevention of disease, and maintenance of normal physiological function. An unhealthy diet can result in malnutrition, and this contributes to illness and death throughout the world. The core principle of healthy eating is obtaining an adequate balance, and the diseases resulting from overnourishment differ greatly from those resulting from undernourishment. In the third world, diets tend to rely heavily on staple crops, and can be very seasonal. Energy sources are predominantly cereals, whereas meat and fish are limited. Malnutrition tends to occur from a lack of essential nutrients, leading to conditions such as vitamin deficiencies, kwashiorkor, and iodine deficiency syndromes. In first-world countries, people have more freedom to choose what they eat. Thus, diets tend to be high in fat and dense in energy. Obesity, diabetes, coronary heart disease, cancer, and hypertension are major contributors to morbidity and mortality. A healthy diet should contain adequate proportions of carbohydrates, fats, proteins, vitamins, and trace elements. The intake of these constituents is sporadic, with meals constituting major boluses of potential energy. Energy expenditure, conversely, is continuous. The human body has, therefore, developed complex mechanisms directing nutrients into storage when in excess, and mobilizing these stores as they are needed, and it is essential that sufficient energy is always available to maintain the basal metabolic rate, which is the amount of energy expended while at rest in a neutrally temperate environment. This energy is sufficient only for the functioning of the vital organs, such as the heart, the lungs, the liver, the kidneys, and the CNS.

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37

Jara Orellana,, Claudia. Efectos de la proteína Tau sobre la disfunción mitocondrial y el deterioro cognitivo en el envejecimiento. Universidad Autónoma de Chile, 2018. http://dx.doi.org/10.32457/20.500.12728/87452018dcbm6.

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El envejecimiento es un proceso complejo e irreversible que afecta el funcionamiento del cerebro y se considera el principal factor de riesgo para las patologías neurodegenerativas. Las mitocondrias son organelos fundamentales para la generación de energía, el equilibrio oxidativo y la regulación del calcio. Actualmente, se considera a la disfunción mitocondrial como un factor importante que contribuye al envejecimiento cerebral y a la patogénesis de diversas enfermedades neurodegenerativas. Este daño mitocondrial se ve reflejado en una disminución del metabolismo cerebral, aumentando el daño oxidativo y disminuyendo la formación de ATP. Estos daños alteran el normal funcionamiento neuronal y juegan un papel importante en la pérdida de la función cognitiva. Durante el envejecimiento, una serie de agregados proteicos se acumulan regularmente en el cerebro, como por ejemplo la proteína tau. Interesantemente, investigaciones de nuestro grupo y otros han determinado que bajo condiciones patológicas tau puede afectar la función sináptica debido a su capacidad para facilitar la falla mitocondrial. Dentro de este contexto, nuestro grupo recientemente ha encontrado que la ausencia de la proteína tau mejora la salud mitocondrial y las capacidades cognitivas en ratones jóvenes. Ya que las modificaciones patológicas de tau pueden afectar la función mitocondrial y la falla mitocondrial contribuye al envejecimiento cerebral, es interesante poder estudiar los efectos que la ausencia de tau podría tener sobre la función mitocondrial y las habilidades cognitivas durante el envejecimiento. En el desarrollo de esta tesis, observamos que la ausencia de tau previene la disfunción mitocondrial y el deterioro cognitivo asociado al envejecimiento. Se realizaron pruebas cognitivas, bioquímicas e histológicas utilizando ratones Wild Type (WT) y Knockout para la proteína tau (tau-/-) de 18 meses de edad. Nuestros resultados indican que la ausencia de tau previene la pérdida de la función cognitiva durante el envejecimiento, incluido la memoria de reconocimiento, la memoria espacial y las capacidades sociales. Además, los ratones tau-/- mostraron una mejor bioenergética mitocondrial, que fue evidenciada por una mayor producción de ATP y una menor sensibilidad a la sobrecarga de calcio en mitocondrias aisladas. También observamos elevados niveles de proteína ciclofilina-D(CypD) en el cerebro de ratones WT; de manera interesante, los ratones tau-/- envejecidos mostraron una disminución significativa de esta proteína en comparación con los ratones WT. CypD es una proteína fundamental en la formación del poro de transición de permeabilidad mitocondrial (mPTP). Para determinar si la disminución de CypD jugó un papel en la bioenergética mitocondrial mejorada de ratones tau-/- envejecidos, se realizó la sobreexpresión de CypD en el hipocampo de estos ratones utilizando la técnica de inyección estereotáxica de vectores lentivirales que codifican para CypD. Tres semanas después de la infección hipocampal, se realizaron pruebas conductuales y, posteriormente, se utilizó el hipocampo para evaluar la función mitocondrial. En estos estudios observamos que la expresión de CypD en ratones tau -/- redujo la producción de ATP y afecto la regulación del calcio produciendo un aumento de la sensibilidad al calcio mitocondrial, lo que sugiere apertura del mPTP. Más interesante es que los ratones tau-/- envejecidos infectados con lentivirus CypD mostraron una disminución significativa en sus capacidades cognitivas en comparación con los ratones tau-/- no infectados. En conclusión, nuestros resultados sugieren que la ausencia de tau previene la pérdida de habilidades cognitivas a través de la mejora de la función mitocondrial durante el envejecimiento. Estos efectos beneficiosos implican la regulación de la expresión de CypD y posiblemente la formación de mPTP. Esto también propone un nuevo y potencial objetivo terapéutico para prevenir alteraciones relacionadas con la edad.

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38

Ringuelet, Jorge Abel, and Sonia Zulma Viña, eds. Productos naturales vegetales. Editorial de la Universidad Nacional de La Plata (EDULP), 2013. http://dx.doi.org/10.35537/10915/27885.

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El mundo vegetal es, quizás, el que muestra un abanico de moléculas más diverso y del cual el hombre ha hecho y hace una provechosa utilización. La maquinaria química de un vegetal es tan ingeniosa que asombra al estudiar en su profundidad la estructura, función, metabolismo y regulación de cada molécula identificada y de los innumerables procesos en que participan a nivel celular. Por otra parte, al no contar con el mecanismo de evasión y encontrarse ancladas al suelo o algún otro sustrato, las variadas especies vegetales han necesitado desarrollar mecanismos químicos de defensa que posibilitan su supervivencia frente al ataque de parásitos y herbívoros. A dichos mecanismos ha contribuido, sin lugar a dudas, el amplio espectro de sustancias orgánicas propias de los organismos vegetales. A toda esa diversidad de compuestos que el hombre extrae de un vegetal y aprovecha o intenta darle alguna utilización los denominamos productos naturales vegetales. En la elaboración de este texto hemos tratado de describir los más importantes, agrupándolos para un estudio ordenado. Se ha iniciado la obra abarcando una serie de consideraciones generales sobre dichos productos. Seguidamente se han descripto las características estructurales, propiedades, distribución en la naturaleza, funciones en las plantas, actividades biológicas, biosíntesis y métodos de extracción y/o cuantificación de los diferentes productos naturales vegetales. Los grupos a los que se ha hecho referencia son: metabolitos secundarios nitrogenados y/o azufrados, sustancias fenólicas y compuestos terpénicos. Se ha incluido, finalmente, un capítulo donde se trata, en particular, la vinculación entre distintos productos naturales vegetales y la adaptación de las plantas al medio ambiente, como así también su participación en las relaciones bióticas observadas en diferentes sistemas naturales y/o agroecosistemas. El objetivo principal de la obra es resumir los aspectos más importantes de esta área para quien quiera profundizar en el estudio de diversas moléculas orgánicas distribuidas en el mundo vegetal. La misma es el resultado de la experiencia acumulada durante varios años por los docentes del curso Bioquímica y Fitoquímica de la Facultad de Ciencias Agrarias y Forestales de la Universidad Nacional de La Plata. Pretendemos modestamente que sirva de base y guía para los estudiantes de grado en áreas biológicas, como la Ingeniería Agronómica, Ingeniería Forestal, Biología, Ciencias Farmacéuticas y otras que pudieran estar relacionadas a este interesante campo de estudio.

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39

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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40

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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