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Topic Review
Great Green Wall
The Great Green Wall or Great Green Wall of the Sahara and the Sahel (French: Grande Muraille Verte pour le Sahara et le Sahel) is Africa's flagship initiative to combat the increasing desertification. Led by the African Union, the initiative aims to transform the lives of millions of people by creating a mosaic of green and productive landscapes across North Africa. From the initial idea of a line of trees from east to west bordering the Saharan Desert, the vision of a Great Green Wall has evolved into that of a mosaic of interventions addressing the challenges facing the people in the Sahel and the Sahara. As a programming tool for rural development, the overall goal of this partnership is to strengthen regional resilience and natural systems with sound ecosystem management, protection of rural heritage, and improved living conditions. The project is a response to the combined effect of natural resources degradation and drought in rural areas. It is a partnership that supports communities working towards sustainable management and use of forests, rangelands and other natural resources. It seeks to help communities mitigate and adapt to climate change, as well as improve food security. It is expected that the population in the Sahel would double by 2039, adding urgency to the project.
  • 930
  • 14 Nov 2022
Topic Review
Open MHC Class I Conformers
Open MHC-I conformers are mature fully glycosylated plasma membrane molecules (HLA-A, HLA-B, HLA-C, HLA-E, HLA-G, HLA-E, and CD1d in humans; H-2D, H-2L, and H-2K in mice) that have dissociated from the β2m light chain and the peptide. Given the flexibility and mobility of the α1 domain of the heavy chain, the open MHC-I conformers are free to interact with any nearby complementary amino acid sequences or peptides in a covalent and a non-covalent manner. Open MHC-I conformers are functional cis-trans structures capable of establishing physical cis-associations with themselves (i.e., homodimers), with other surface receptors (i.e., heterodimers), and shed into the extracellular milieu (i.e., soluble open conformers). In turn, the open conformers and the homodimers trans-interact with several receptors expressed by lymphomyeloid cells. Overall, the open MHC-I conformers impact cellular physiology and clinical and biomedical settings, including autoimmune responses, tumor escape, graft rejection, and neuronal development and cognition. 
  • 930
  • 27 Oct 2021
Topic Review
The Relation of KLF11 to Cancers
KLF11 (Krüppel-like factor 11) belongs to the family of Sp1/Krüppel-like zinc finger transcription factors that play important roles in a variety of cell types and tissues. In carcinogenesis, KLF11 can show diverse effects. Its function as a tumor suppressor gene can be suppressed by phosphorylation of its binding domains via oncogenic pathways. However, KLF 11 itself can also show tumor-promoting effects and seems to have a crucial role in the epithelial-mesenchymal transition (EMT) process. 
  • 930
  • 29 Apr 2020
Topic Review
Potocki-Lupski Syndrome
Potocki-Lupski syndrome is a condition that results from having an extra copy (duplication) of a small piece of chromosome 17 in each cell. The duplication occurs on the short (p) arm of the chromosome at a position designated p11.2. This condition is also known as 17p11.2 duplication syndrome.
  • 930
  • 24 Dec 2020
Topic Review
Single-Cell RNA Sequencing
Single-cell RNA sequencing (scRNA-seq) technology is a powerful, rapidly developing tool for characterizing individual cells and elucidating biological mechanisms at the cellular level. Cardiovascular disease is one of the major causes of death worldwide and its precise pathology remains unclear. scRNA-seq has provided many novel insights into both healthy and pathological hearts. In this review, we summarize the various scRNA-seq platforms and describe the molecular mechanisms of cardiovascular development and disease revealed by scRNA-seq analysis. We then describe the latest technological advances in scRNA-seq. Finally, we discuss how to translate basic research into clinical medicine using scRNA-seq technology.
  • 929
  • 19 Nov 2020
Topic Review
Lipoprotein Lipase Regulation in Atherosclerosis
Lipoprotein lipase (LPL) plays a major role in the lipid homeostasis mainly by mediating the intravascular lipolysis of triglyceride rich lipoproteins. Impaired LPL activity leads to the accumulation of chylomicrons and very low-density lipoproteins (VLDL) in plasma, resulting in hypertriglyceridemia. While low-density lipoprotein cholesterol (LDL-C) is recognized as a primary risk factor for atherosclerosis, hypertriglyceridemia has been shown to be an independent risk factor for cardiovascular disease (CVD) and a residual risk factor in atherosclerosis development.
  • 930
  • 01 Aug 2021
Topic Review
STAT3 and STAT5
A central characteristic of many types of cancer is altered energy metabolism processes such as enhanced glucose uptake and glycolysis and decreased oxidative metabolism. The regulation of energy metabolism is an elaborate process involving regulatory proteins such as HIF (pro-metastatic protein), which reduces oxidative metabolism, and some other proteins such as tumour suppressors that promote oxidative phosphorylation. In recent years, it has been demonstrated that signal transducer and activator of transcription (STAT) proteins play a pivotal role in metabolism regulation. STAT3 and STAT5 are essential regulators of cytokine- or growth factor-induced cell survival and proliferation, as well as the crosstalk between STAT signalling and oxidative metabolism. Several reports suggest that the constitutive activation of STAT proteins promotes glycolysis through the transcriptional activation of hypoxia-inducible factors and therefore, the alteration of mitochondrial activity. It seems that STAT proteins function as an integrative centre for different growth and survival signals for energy and respiratory metabolism.
  • 929
  • 16 Jun 2021
Topic Review
Delayed Contralateral Nephrectomy
Background: Successful treatment of acute kidney injury (AKI)-induced chronic kidney disease (CKD) is unresolved. We aimed to characterize the time-course of changes after contralateral nephrectomy (Nx) in a model of unilateral ischemic AKI-induced CKD with good translational utility. (2) Methods: Severe (30 min) left renal ischemia-reperfusion injury (IRI) or sham operation (S) was performed in male Naval Medical Research Institute (NMRI) mice followed by Nx or S one week later. Expression of proinflammatory, oxidative stress, injury and fibrotic markers was evaluated by RT-qPCR. (3) Results: Upon Nx, the injured kidney hardly functioned for three days, but it gradually regained function until day 14 to 21, as demonstrated by the plasma urea. Functional recovery led to a drastic reduction in inflammatory infiltration by macrophages and by decreases in macrophage chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) mRNA and most injury markers. However, without Nx, a marked upregulation of proinflammatory (TNF-α, IL-6, MCP-1 and complement-3 (C3)); oxidative stress (nuclear factor erythroid 2-related factor 2, NRF2) and fibrosis (collagen-1a1 (Col1a1) and fibronectin-1 (FN1)) genes perpetuated, and the injured kidney became completely fibrotic. Contralateral Nx delayed the development of renal failure up to 20 weeks. (4) Conclusion: Our results suggest that macrophage activation is involved in postischemic renal fibrosis, and it is drastically suppressed by contralateral nephrectomy ameliorating progression.
  • 929
  • 02 Nov 2020
Topic Review
Mutant p53
The p53 tumor suppressor plays a pivotal role in cancer and infectious disease. Many oncology treatments are now calling on immunotherapy approaches, and scores of studies have investigated the role of p53 antibodies in cancer diagnosis and therapy. This review summarizes the current knowledge from the preliminary evidence that suggests a potential role of p53 as an antigen in the adaptive immune response and a monitoring key role of the innate immune system, thereby speculating on the idea that mutant p53 antigens serve as a druggable target in immunotherapy. Except in a few cases, the vast majority of published work on p53 antibodies in cancer patients use wild-type p53 as the antigen to detect these antibodies and it is unclear that they can recognize p53 mutants carried by cancer patients at all. We envision that an antibody targeting a specific mutant p53 will be effective therapeutically against the cancer carrying the exact mutant p53. Thus, novel antibodies targeting mutant p53, but not the wild-type isoform, should be pursued in preclincial and clinical studies.
  • 929
  • 27 Oct 2020
Topic Review
KMT2A (Lysine Methyltransferase 2A)
KMT2A (Lysine methyltransferase 2A) is a member of the epigenetic machinery, encoding a lysine methyltransferase responsible for the transcriptional activation through lysine 4 of histone 3 (H3K4) methylation. KMT2A has a crucial role in gene expression, thus it is associated to pathological conditions when found mutated. KMT2A germinal mutations are associated to Wiedemann–Steiner syndrome and also in patients with initial clinical diagnosis of several other chromatinopathies (i.e., Coffin–Siris syndromes, Kabuki syndrome, Cornelia De Lange syndrome, Rubinstein–Taybi syndrome), sharing an overlapping phenotype. On the other hand, KMT2A somatic mutations have been reported in several tumors, mainly blood malignancies. Due to its evolutionary conservation, the role of KMT2A in embryonic development, hematopoiesis and neurodevelopment has been explored in different animal models, and epigenetic treatments for disorders linked to KMT2A dysfunction have been extensively investigated. 
  • 928
  • 06 Apr 2022
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