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Aquatic Plants Native to America
Published in Namrita Lall, Aquatic Plants, 2020
Bianca D. Fibrich, Jacqueline Maphutha, Carel B. Oosthuizen, Danielle Twilley, Khan-Van Ho, Chung-Ho Lin, Leszek P. Vincent, T. N. Shilpa, N. P. Deepika, B. Duraiswamy, S. P. Dhanabal, Suresh M. Kumar, Namrita Lall
Synonyms:Nymphaea odorata var. gigantea Tricker, Nymphaea odorata var. glabra Casp., Nymphaea odorata var. godfreyi D. B. Ward, Nymphaea odorata var. minor Sims, Nymphaea odorata var. rosea Pursh, Nymphaea odorata var. rubra Guillon, Nymphaea odorata var. stenopetala Fernald, Nymphaea odorata var. villosa Casp.
Reviewing the literature systematically
Published in Jeremy Jolley, Introducing Research and Evidence-Based Practice for Nursing and Healthcare Professionals, 2020
A PICO chart does not tell us how ‘good’ each research study is. The good news is that ready-made charts exist for this purpose too. The Critical Appraisal Skills Programme (CASP) website, at https://casp-uk.net/casp-tools-checklists/, has check lists for just about any kind of research article one may wish to review. Table 3.2 provides an example of the use of CASP for a qualitative study.
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
Two main signaling pathways, the TNF (Tumor Necrosis Factor)- TNF receptor (TNFR) and the Fas-Fas ligand (FasL), have been well-characterized in the extrinsic or cell receptor pathway of apoptotic mechanisms. Both involve receptors of the family coupled to extrinsic signals [32]. These pathways activate CASP-8. CASP-8 in turn activates CASP-3, which is responsible for proteolysis of cellular factors and finally creating the morphological signs of apoptosis (Fig. 3.1). All death receptors (DR) in cell surface are distinguished by their specific ligands. They translocate the death signal to the cytosol by their death domain. There are at least six members of DR family: TNF-R1, TRAILR 1 and 2 (TNF-Related Apoptosis-Inducing Ligand Receptor 1 and 2), CD95 (Fas), DR3, and DR6, which will be discussed below [33].
In silico and in vivo demonstration of the regulatory mechanism of Qi-Ge decoction in treating NAFLD
Published in Annals of Medicine, 2023
Chong Peng, Jing Li, Xuehong Ke, Fengbin Liu, Ke-er Huang
Activation of the transcription factor and myelocytomatosis oncogene MYC allows it to stably interact with sirtuin 7 on the ribosomal protein promoter to induce the ER stress response and cause liver damage in mice that looks similar to that in humans. Caspase (CASP)-3 is a critical molecule involved in cell apoptosis [47]. Palmitic acid-induced liver cell lipotoxicity not only causes excessive lipid deposition and ER stress, but also leads to liver cell apoptosis [48]. This is because the polymer formed by the activation of factor-1 under palmitic acid stress binds to the caspase precursor protein to generate apoptotic bodies and activate CASP9, which further activates CASP3 and ultimately leads to liver cell apoptosis. Additionally, studies have found that HFD feeding significantly increases the expression of CASP3 in mouse liver cells [49]. Mitogen-activated protein kinase 8 (MAPK8, also known as JNK1) has been shown to induce accelerated liver regeneration in mice. This is mainly achieved by mediating the reversal of the inadequate regenerative capacity of hepatic stellate cells through the MAPK8-Indian hedgehog axis [50], which may represent a unique mechanism by which MAPK8 protects the liver from damage.
Understanding the facilitators and barriers of stroke survivors’ adherence to recovery-oriented self-practice: a thematic synthesis
Published in Disability and Rehabilitation, 2022
Dor Vadas, Kirsten Prest, Amadea Turk, Stephanie Tierney
Results from using the CASP tool are presented in Supplementary Appendix 1. The key reason for papers losing marks was a failure to mention the nature of the relationship between researcher and participants (n = 6 when the relationship was not discussed). In addition, the appropriateness of the data collection approach used was unclear in five of the studies. One study failed to reflect many of the components of the CASP tool [33]. Despite the flaws, its findings were taken into consideration as they still provided valuable insights. Collecting qualitative data for synthesis is in essence a search for a variety of thoughts and experiences. It is better to use each found quote or segment than not to use it, as it may add to this variety. That is also the reason for the related protocol decision to not exclude studies based on their quality appraisal.
The Mechanical Autophagy as a Part of Cellular Immunity; Facts and Features in Treating the Medical Disorders
Published in Immunological Investigations, 2022
Hany Khalil, Amira Abd ElHady, Khaled A. Elawdan, Dalia Mohamed, Doaa D. Mohamed, Ahmed I Abd El Maksoud, Farha A. El-Chennawi, Bhgat El-Fikiy, Ibrahim H. El-Sayed
Programmed cell death (PCD) or apoptosis refers to the changes that occur in the cells that aim to self-kill in response to intrinsic or extrinsic events to maintain the molecular balance that is required to prevent diseases. These changes begin with a series of cellular pathways known as apoptotic signaling that leads to serious damage in cellular DNA and characteristic cell changes. The characteristic morphology of apoptosis includes nuclear condensation, cell shrinking, membrane blebbing, and DNA fragmentation. The apoptotic signaling is activated by a family of cytosine proteases namely caspases (casps) that converge on a common protocol of cell destruction. The conjugation and association between initiator casps including casp-2, casp-8, casp-9, casp-10, casp-11, and casp-12, is required for the pro-apoptotic signals. Subsequently, the activation of these casps cleaves and activates the downstream targets of other casps including casp-3, casp-6, and casp-7 which in turn approve the PCD by cleaving cellular proteins (Kurokawa and Kornbluth 2009; Plati et al. 2011).