scholarly journals Rescue of thyroid cells from antibody induced cell death via induction of autophagy

2022 ◽  
Vol 126 ◽  
pp. 102746
Author(s):  
Syed Morshed ◽  
Rauf Latif ◽  
Terry F. Davies
Keyword(s):  
2013 ◽  
Vol 134 (2) ◽  
pp. 276-290 ◽  
Author(s):  
Florencia Chiappini ◽  
Carolina Pontillo ◽  
Andrea S. Randi ◽  
Laura Alvarez ◽  
Diana L. Kleiman de Pisarev

2017 ◽  
Vol 43 (12) ◽  
pp. 2387
Author(s):  
Beverley Yu ◽  
Vicky Green ◽  
James England ◽  
Anand Goomany ◽  
John Greenman

2021 ◽  
Author(s):  
Aisyah Elliyanti

Radioiodine-131 (RAI) is an isotope of the chemical element iodine and is commonly used for hyperthyroidism, including Graves’ disease. It is given orally, and its concentration in the thyroid gland. The RAI transport involves a natrium iodide symporter (NIS) role that brings two cations sodium (Na+) and one anion of iodide (I-) across the membrane. The process is facilitated by the enzyme Na+/K+ ATPase. RAI is a beta (β) and gamma (γ) particles emitter. β particle is used for therapy and γ particle for imaging (theranostic). β particle inhibits cell growth by inducing cell death through apoptosis or necrosis of some of the sufficient thyroid cells. The aim of RAI therapy in Graves’ disease is to control hyperthyroidism and render the patient hypothyroidism. It is easier to manage patients with hypothyroidism with levothyroxine and fewer complications. This review will focus on RAI’s therapeutic approach in Graves’ disease, including patient preparation, selecting activity dose, adverse events, contraindication, controversies issues such as malignancy and fertility, the follow-up to ensuring the patient remains euthyroid or need a replacement therapy if they become hypothyroidism. RAI therapy is safe as definitive therapy and cost-effective for Graves’ disease therapy.


1995 ◽  
Vol 214 (3) ◽  
pp. 819-824 ◽  
Author(s):  
B. Dijeso ◽  
L. Ulianich ◽  
L. Racioppi ◽  
F. Darmiento ◽  
A. Feliciello ◽  
...  

Author(s):  
Anne F. Bushnell ◽  
Sarah Webster ◽  
Lynn S. Perlmutter

Apoptosis, or programmed cell death, is an important mechanism in development and in diverse disease states. The morphological characteristics of apoptosis were first identified using the electron microscope. Since then, DNA laddering on agarose gels was found to correlate well with apoptotic cell death in cultured cells of dissimilar origins. Recently numerous DNA nick end labeling methods have been developed in an attempt to visualize, at the light microscopic level, the apoptotic cells responsible for DNA laddering.The present studies were designed to compare various tissue processing techniques and staining methods to assess the occurrence of apoptosis in post mortem tissue from Alzheimer's diseased (AD) and control human brains by DNA nick end labeling methods. Three tissue preparation methods and two commercial DNA nick end labeling kits were evaluated: the Apoptag kit from Oncor and the Biotin-21 dUTP 3' end labeling kit from Clontech. The detection methods of the two kits differed in that the Oncor kit used digoxigenin dUTP and anti-digoxigenin-peroxidase and the Clontech used biotinylated dUTP and avidinperoxidase. Both used 3-3' diaminobenzidine (DAB) for final color development.


Author(s):  
S. Trachtenberg ◽  
P.M. Steinert ◽  
B.L. Trus ◽  
A.C. Steven

During terminal differentiation of vertebrate epidermis, certain specific keratin intermediate filament (KIF) proteins are produced. Keratinization of the epidermis involves cell death and disruption of the cytoplasm, leaving a network of KIF embedded in an amorphous matrix which forms the outer horny layer known as the stratum corneum. Eventually these cells are shed (desquamation). Normally, the processes of differentiation, keratinization, and desquamation are regulated in an orderly manner. In psoriasis, a chronic skin disease, a hyperkeratotic stratum corneum is produced, resulting in abnormal desquamation of unusually large scales. In this disease, the normal KIF proteins are diminished in amount or absent, and other proteins more typical of proliferative epidermal cells are present. There is also evidence of proteolytic degradation of the KIF.


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