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Understanding the Technologies Involved in Gene Therapy
Published in Yashwant V. Pathak, Gene Delivery Systems, 2022
Manish P. Patel, Jayvadan K. Patel, Mukesh Patel, Govind Vyas
The HIV virus requires the expression of co-receptors C-C chemokine receptor type 5 (CCR5) for adhesion onto T cells. Thus, CCR5 is a promising target for the control of HIV entry into the host cell. Humans who are homozygous for a particular variation in the CCR5 gene are naturally resistant to HIV infection by blocking entry of the virus. Additionally, in clinical use the transplantation of ex vivo expanded CCR5 (-/-) primary human CD4+ T cells to HIV patients was found to be beneficial. In light of this evidence, ZFNs were also tested as a potential option for the treatment of HIV infection. The primary aim of this was to disrupt CCR5 in both primary CD4+ human T cells and human hematopoietic stem cells. Reconstitution of the patients’ immune systems using stem cells with an engineered “CCR5-negative genome” may render their T cells immune to HIV infection (Akçay et al. 2014).
PPH-Based Dendrimers as HIV Entry Inhibitors
Published in Anne-Marie Caminade, Cédric-Olivier Turrin, Jean-Pierre Majoral, Phosphorus Dendrimers in Biology and Nanomedicine, 2018
Cedric-Olivier Turrin, Muriel Blanzat
The recognition of HIV involves the viral protein gp120, and cellular receptors such as DC-SIGN, CD4, or GalCer, and co-receptors such as CXCR4 and CCR5. The recognition of DC-SIGN involves multivalent interaction with mannose-rich glycoproteins of pathogens [74]; dendrimers and other multivalent scaffolds have been successfully used to target these interactions [75–77]. Although some mannose-capped dendrons have been shown in microarray binding assays to inhibit the gp120 DC-SIGN interaction in the nanomolar range [78], these promising results have not been confirmed in vitro.
Review on the current treatment status of vein of Galen malformations and future directions in research and treatment
Published in Expert Review of Medical Devices, 2021
Panagiotis Primikiris, Georgios Hadjigeorgiou, Maria Tsamopoulou, Alessandra Biondi, Christina Iosif
Interestingly, as already mentioned, defective Smad signaling in the endothelium is associated with hereditary hemorrhagic telangiectasia, which is characterized by the development of arteriovenous malformations [173] and rarely VOGMs [110]. More specifically, approximately 85% of HHT cases are associated with heterozygous mutations in activin receptor-like kinase 1 (ACVRL1 or Alk1;type 2 HHT) or its co-receptor, Endoglin (ENG; type 1 HHT) and 4% are linked to mutations in their downstream effector Smad4 [172,174].
Applications and hazards associated with carbon nanotubes in biomedical sciences
Published in Inorganic and Nano-Metal Chemistry, 2020
Ali Hassan, Afraz Saeed, Samia Afzal, Muhammad Shahid, Iram Amin, Muhammad Idrees
Spermatogenesis may also be affected by the environmental toxicants.[96] The number of such environmental effects caused by toxicants like the nanoparticles is continuously increasing and is known to affect many organs including the testis.[67,97,98] When the nanoparticles enter the systematic circulation, they can easily penetrate many capillaries, epithelia, and biological membranes and they can comprehensively alter functioning of any animal cell.[99,100] It is said that the nanoparticles not only can cross the blood-brain barrier but can also evade the blood-testis barrier and get distributed in the gonads.[97,101,102] Spermatogonial stem cells (SSCs) are the progenitors that are necessary for differentiation and self-renewal of the sperm cells and maintaining permanent spermatogenesis. These stem cells are controlled and regulated partly by a small peptide GDNF which was first discovered in the brain cells.[103,104] The GDNF belongs to the transforming growth factor-β which works on its specific cell by binding to its receptor c-Ret and a co-receptor GFR-α releasing secondary messengers. Removing out any of these factors can cause the decline in the SSCs proliferation and activity. GDNF phosphorylates the c-Ret and Src kinase family proteins (SFK) the phosphorylation of SFK is very significant in maintaining the SSC population. SFK causes the phosphorylation of the PI3K and AKT and all this cascade of reaction ends at the N-Myc which is a transcription factor which was first said to be the tumor inducer but now said to have role in the maintaining the SSC populations.[74,104–107]