China
Africa
Explore chapters and articles related to this topic
Body
Published in Lisa Zammit, Georgeanne Schopp, Relational Care, 2022
Lisa Zammit, Georgeanne Schopp
The anatomical definition of the Body is the physical structure of a human being, excluding head and limbs. The body is technically limited to the trunk. Medically, the body is the material of the human. It comprises the anatomical structures as well as its physiological functioning – from the corporeal to the cellular level.
Lipids and Lipid Metabolism in Postnatal Gut Development and Risk of Intestinal Injury
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Utilization of fatty acids at the cellular level begins with internalization of the fatty acid into the cell via fatty acid transporters. Once within the cell, the fatty acid is converted to fatty acyl-CoA via fatty acyl-CoA synthase (Figure 49.2). At the outer membrane of the mitochondria, carnitine palmitoyltransferase 1 converts the fatty acid-CoA to fatty acyl carnitine. Fatty acyl carnitine then crosses the inner mitochondrial membrane through a carnitine exchange via carnitine-acyl carnitine translocase. Once inside the mitochondrial matrix, the fatty acyl carnitine is converted back to fatty acyl-CoA via carnitine palmitoyltransferase 2, allowing for entry into the β-oxidation pathway generating acetyl-CoA. Acetyl-CoA is utilized by the tricarboxylic acid cycle (TCA) cycle to form NADH and FADH2.
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Understanding how to care for people safely and effectively requires the nurse to appreciate both the microscopic and macroscopic aspects of the human. Studying the human at a cellular level, as described in this chapter, will help you to recognise factors that impact on health and on a person’s vulnerability to illness. Observing the person at a cellular level is only one aspect of a wider understanding, as this chapter sets the scene for the following chapters, providing a detailed introduction to the chemical foundations of life and how the body’s cells are built and operate. The chapter then explores how the body’s tissues function, allowing you to appreciate what occurs when cells, tissues and organ systems fail.
Approaches to discern if microbiome associations reflect causation in metabolic and immune disorders
Published in Gut Microbes, 2022
Marijana Basic, Dominique Dardevet, Peter Michael Abuja, Silvia Bolsega, Stéphanie Bornes, Robert Caesar, Francesco Maria Calabrese, Massimo Collino, Maria De Angelis, Philippe Gérard, Miguel Gueimonde, François Leulier, Eva Untersmayr, Evelien Van Rymenant, Paul De Vos, Isabelle Savary-Auzeloux
Although similarities exist between species, digestive tract morphology, physiology as well as the amount and type of microbiota may vary (Table 2). Animals adapt to their environment and in particular to their food pattern.54 Omnivore species such as humans depend on food digestion and nutrient absorption in the foregut and midgut54 and on hindgut bacterial fermentation of food components that are not digestible by host enzymes. Anatomical differences of the hindgut exist between animal models used (Table 2). These differences need to be considered for translation of concepts to humans. In addition, physiological/biochemical discrepancies in the lumen environment (digestion rate, transit time, physical pressures, pH, osmolarity, enzymes, bile acids, metabolites) impact the metabolic fate of ingested nutrients and induce various selective pressure on microbiota present in the different segments of the intestine. If these concerns can be addressed partially in mammal models that present physiological similarities with humans, this is less the case in invertebrate models such as C. elegans or D. melanogaster where gut physiology, digestive processes, and nutritional habits are quite different from humans. Nevertheless, at cellular level, hydrolysis of lumen molecules by proteases, processes of metabolites absorption, lipids accumulation, endocytosis mechanisms and regulation of some metabolic pathways are partially preserved, and represent a complement, alternative and potentially more powerful option to investigate these mechanisms.55,56
Stereotaxic-assisted gene therapy in Alzheimer’s and Parkinson’s diseases: therapeutic potentials and clinical frontiers
Published in Expert Review of Neurotherapeutics, 2022
Samar O. El Ganainy, Tony Cijsouw, Mennatallah A. Ali, Susanne Schoch, Amira Sayed Hanafy
As previously mentioned, gene-based biotherapeutics hold substantial promise in the treatment of neurodegenerative disorders. However, the systemic administration of bare gene-editing therapeutics is practically challenging as they are prone to rapid degradation by nucleases in the blood stream. Moreover, they are mostly cleared from the body via renal filtration, rendering their biological half-life too short and their biodistribution extremely unfavorable [7]. On a cellular level, the molecules used for gene therapy are electrostatically repulsed by cell membranes, hindering their cellular uptake. Therefore, it is necessary to package gene-editing tools into viral or non-viral vectors before systemic administration. In principle, these vectors can stabilize gene therapeutics in the blood circulation, minimize their clearance by renal filtration, extend their half-lives and improve their targetability and cellular uptake [133].
PTGS1 gene variations associated with bleeding and platelet dysfunction
Published in Platelets, 2021
Verónica Palma-Barqueros, Natalia Bohdan, Nuria Revilla, Vicente Vicente, José M. Bastida, José Rivera
The PTGS1 gene lacks a TATA box and exhibits features of a housekeeping gene [4]. Thus, COX-1 is constitutively expressed in most human cells and tissues at a constant level, although its expression in endothelial cells may be induced [5]. Mammalian cells also display an inducible COX-2 isoform, which is encoded by PTGS2 gene and is very similar to the COX-1 in structure (60% sequence similarity) and catalytic activity [5]. In platelets, COX-1 is the mainly expressed isoform but traces of COX-2 are present, possibly derived from the precursor megakaryocytes [6]. At the cellular level, COX-1 is embedded in the luminal membrane of the endoplasmic reticulum (ER) and in the nucleus envelope. As well as housing the enzyme, ER modulates the structure and function of COX-1, as it mediates its N-glycosylation and allows the formation of disulfide bonds [1]. In platelets, COX-1 is located in the dense tubular membrane system preferentially. Consequently this is the main platelet place for prostanoid synthesis [7].