China
Africa
Explore chapters and articles related to this topic
Leukaemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
The FAB classification of acute leukaemias first described in 1976 relied solely on morphological and cytochemical studies to identify the lineage of the leukaemic cells and the degree of differentiation present. The annotated version proposed in 1985, divides AML into 10 distinct subtypes that differ morphologically and histochemically; immunological and genetic differences are also used to define some subtypes, in particular the M3 subtype. Despite its limitation, this version of the FAB classification remains popular amongst many haematologists. The WHO classification was introduced in 2001 to improve diagnostic concordance and is based on the cytogenetic and molecular genetic abnormalities as well as clinical, morphological and surface membrane abnormalities.12 It recognizes four major categories: (1) AML with recurring genetic abnormalities; (2) AML with multi-lineage dysplasia; (3) AML that is therapy-related and (4) AML not otherwise categorized. Table 28.1 depicts the FAB 1976 and WHO 2001 classifications of AML. The current (2008) WHO classification encompasses a greater number of entities with recurrent chromosomal translocations and also included two (newer) entities characterized by gene mutations: AML with cytoplasmic/mutated nucleophosmin 1 gene (NPM1) and AML with CCAAT/enhancer binding protein alpha (CEBPA) mutations;13 other changes include a refinement in diagnosis of MDS-related AML and AML-related to Down’s syndrome is now a separate subtype (Table 28.2). Importantly, any myeloid neoplasm with 20% or more blasts in the peripheral blood or bone marrow is diagnosed as AML. In patients a granulocytic sarcoma or demonstrating any of the following cytogenetic abnormalities: inv (16), t(8;21), t(16;16) or t(15;17), a diagnosis of AML is proposed irrespective of the blast count.
Diet as a Potential Modulator of Body Fat Distribution
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Sofia Laforest, Geneviève B. Marchand, André Tchernof, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Conjugated linoleic acid (CLA) supplements have been of interest following reports of their anticancer and anti-inflammatory properties as well as a potential role in modulating body fat mass (Pariza 2004, Silveira et al. 2007). CLA occurs naturally and is found primarily in ruminant meat and dairy products (Steinhart, Rickert, and Winkler 2003). It is synthetically produced from sunflower and safflower oils in supplements (Pariza, Park, and Cook 2001). The estimated daily intake of CLA is 0.36 g/day for women and 0.43 g/day for men, according to the German Nutrition Study (Steinhart, Rickert, and Winkler 2003). CLA comprises a group of 28 isomers that present two conjugated cis or trans dienes, primarily on positions C9 and C11 or C10 and C12. CLA is well absorbed in free FA form or as digested triglycerides when compared to ethyl ester (Fernie et al. 2004). Poor palatability was reported when CLA was ingested as free FA (Fernie et al. 2004). CLA has multiple effects on adipose tissue metabolism. It has been linked to decreased fat cell size and preadipocyte proliferation (Tsuboyama-Kasaoka et al. 2000, Evans, Brown, and McIntosh 2002, Brown and McIntosh 2003). Other reports showed adverse effects of CLA such as a decrease of preadipocyte differentiation via reduced peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha activity C/EBPα (Brown et al. 2003, Kang et al. 2003), and activation of the nuclear factor-kappa B (NF-κB) pathway and subsequent expression of tumor necrosis factor alpha (TNFα) (Chung et al. 2005). Impaired insulin signaling after CLA supplementation was also reported in animal models and was linked to the impact of TNFα on the expression of key adipogenic genes such as glucose transporter type 4 (GLUT-4), lipoprotein lipase (LPL), and adipocyte Protein 2 (aP2) (Chung et al. 2005). Reports (Evans, Brown, and McIntosh 2002) suggested differential effects of the two most studied CLA isomers, trans10cis12 and cis9trans11, the latter being associated with body composition (reduction in body fat and increase of lean body mass) and the other with anticarcinogenic properties.
Lipogenesis inhibition and adipogenesis regulation via PPARγ pathway in 3T3-L1 cells by Zingiber cassumunar Roxb. rhizome extracts
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Natthawut Wong-a-nan, Kewalin Inthanon, Aroonchai Saiai, Angkhana Inta, Wutigri Nimlamool, Siriwadee Chomdej, Prasat Kittakoop, Weerah Wongkham
In this study, we focused on 4 groups of genes i.e. those involved in the following processes: 1) adipocyte differentiation (C/EBPα (CCAAT/enhancer binding protein alpha), PPARγ (Peroxisome proliferator-activated receptor gamma), ADD-1 (Adipocyte determination and differentiation-dependent factor 1) and Pref-1 (Pre-adipocyte factor 1)); 2) glucose uptake (IRS-1 (Insulin receptor substrate 1), GLUT4 (Glucose transporter type 4) and Adiponectin); 3) lipid metabolism (FAS (Fatty acid synthase) and aP2 (Adipocyte protein 2)) and 4) fatty acid oxidation (ATGL (Adipose triglyceride lipase), HSL (Hormone sensitive lipase) and PGC-1β (PPARγ coactivator 1 beta)). The relative mRNA expression of real-time PCR products was evaluated. ZCE and ZCW extracts were chosen in this work, since other solvents pose human health hazards and are not used in traditional medicine.
Combined effect of retinoic acid and calcium on the in vitro differentiation of human adipose-derived stem cells to adipocytes
Published in Archives of Physiology and Biochemistry, 2018
Farjam Goudarzi, Arash Sarveazad, Maryam Mahmoudi, Adel Mohammadalipour, Reza Chahardoli, Obeid M. Malekshah, Shiva Karimi Gorgani, Ali Akbar Saboor-Yaraghi
Among them, various transcriptional factors such as CCAAT-enhancer-binding protein alpha (C/EBPA) and CCAAT-enhancer-binding protein beta (C/EBPB) are important to regulate all pro-adipogenic cell signaling pathways and differentiation of the preadipocytes into the mature cells (Morrison and Farmer 2000, Guo et al. 2015). Their regulatory function is accomplished with the participation of genes such as peroxisome proliferator-activated receptor gamma (PPARG), a master regulator of adipogenesis (Tzameli et al. 2004).
The effect of homocysteine on the expression of CD36, PPARγ, and C/EBPα in adipose tissue of normal and obese mice
Published in Archives of Physiology and Biochemistry, 2021
Ahmet Mentese, Seniz Dogramaci, Selim Demir, Serap Ozer Yaman, Imran Ince, Diler Us Altay, Mehmet Erdem, Ibrahim Turan, Ahmet Alver
Homocysteine (2-amino-4-mercapto butyric acid) (Hcy) is a sulfur-containing non-essential amino acid forming during intracellular demethylation of methionine and a known risk factor for fatty liver disease, hypertension, diabetes, obesity, and cardiovascular diseases (Mentese et al.2016). It has been suggested that an increased plasma Hcy level increases the risk of cardiovascular disease and causes early atherosclerosis and foam cell formation (Cook et al.2002, Mentese et al.2016). This has been attributed to Hcy increasing free radicals, endothelial damage, and low-density lipoprotein (LDL) oxidation (Cook et al.2002). Levels of oxidised LDL (ox-LDL) in the circulation have been reported to increase in chronic diseases, such as atherosclerosis, type 2 diabetes, and obesity (Coburn et al.2000). Cluster of differentiation 36 (CD36) class B scavenger receptor has been shown to be involved in the uptake of ox-LDL and long-chain fatty acids in monocytes, macrophages, platelets, capillary endothelial cells, and adipocytes (Endemann et al.1993). Hcy has been shown to increase LDL oxidisation under in vitro conditions (Tzotzas et al.2011, Mentese et al.2016). Hcy ingested through diet has been shown to trigger the formation of atherosclerotic lesions by raising ox-LDL levels, and increasing ox-LDL regulates CD36 expression (Thampi et al.2008). As a result of transportation of ox-LDL into the cell by CD36, lipid side-products increase CD36 expression by activating peroxisome proliferator activated receptor gamma (PPARγ), a member of the type II nuclear receptor family. PPARγ contributes to the regulation of the expression of several target genes involved in adipocyte differentiation, lipid metabolism, and glucose homeostasis (Zhang and Chawla 2004). CCAAT/enhancer binding protein alpha (C/EBPα) is known to be synthesised in the early stages of adipocyte differentiation together with PPARγ, and these together contribute to the development of obesity. C/EBPα is necessary for both adipogenesis and for normal adipocyte differentiation. C/EBPα stimulates adipogenesis by increasing PPARγ expression (Kim et al. 2018). Under hypercholesterolemic conditions, adipocytes remove ox-LDLs from the circulation by means of CD36 and reduce levels of ox-LDLs in blood. Due to this characteristic, adipose tissue is considered a buffering pool for cholesterol in the circulation. This has led the majority of researchers to regard adipocytes as a potential target in the treatment of atherosclerosis. Although Hcy reduced adipocyte differentiation but had no effect on CD36 gene expression in one study of the 3T3-L1 cell line under in vitro conditions (Mentese et al.2016), we encountered no previous studies investigating the relationship between Hcy and CD36 in adipose tissue under in vivo conditions.