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Clinical Aspects on the Role of Prolactin in Human Breast Cancer
Published in Nagasawa Hiroshi, Prolactin and Lesions in Breast, Uterus, and Prostate, 2020
According to current concepts, the action of a hormone on the target cell requires the presence of a hormone receptor. In the murine breast cancer model, the degree of stimulation of tumor growth by PRL correlates with the PRL receptor content.9 PRL receptors are also demonstrated in human breast cancers.10 In about 30% of carcinomas, there is a specific PRL binding. The clinical relevance of the PRL receptor in human breast cancer is still unknown.
The chemistry of the Body
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
Hormones (from the Greek word hormon, meaning to excite or to set in motion) are chemical signals. They are released into the blood by endocrine cells (the building blocks of the endocrine system, which include the hypothalamus, pituitary, and thyroid glands) and neurosecretory cells, which are specialized nerve cells that also make hormones. These cells sometimes release the hormones directly, but they also often store them in a gland for later release (for example, the digestive glands or the pancreas). Once something gets into the bloodstream, it will reach every cell in the body, because that is what the blood is designed to do—to take oxygen and nutrients to every single cell and take away waste products, such as carbon dioxide and nitrogenous waste. However, although the hormones will get to every cell, only certain types of cells, the target cells for that particular hormone, will respond. The other cells will ignore it. Changes in hormone response could therefore be caused by the hormone itself, by the cells that produce it, or by the target cells’ ability to respond.
The Pituitary Gland Eva Nagy
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
The number and perhaps the affinity of hormone receptors on target cells is regulated by the specific hormone itself. For example, elevation of circulating insulin levels causes a decrease in the number of insulin receptors in target tissues,59,60 In the obese-hyperglycemic mice, there is a marked resistance to insulin action, hyperinsulinemia, and the plasma membranes have a marked decrease in the capacity for insulin binding. However, when such obese mice are fasted and insulin levels decrease, insulin receptors increase toward normal.61,62 The mechanism of this autoregulation can now be explained easily by assuming that cells exposed to excess hormone internalize and degrade rapidly hormone-receptor complexes, in order to avoid over-responding to the hormone. On the other hand, they gain receptors when there is little hormone around, in order to make it more likely that they will pick up the hormones required. In addition to autoregulation, coordinated regulation (interaction of a steroid and peptide hormone to effect the number of receptors for the same or a different peptide hormone) and heteroregulation (regulation by one hormone of receptors for an entirely different hormone) of hormone receptors has been postulated with some supporting experimental evidence.42,43
Current approaches to evaluate the function of cytotoxic T-cells in non-human primates
Published in Journal of Immunotoxicology, 2023
Cris Kamperschroer, Brendon Frank, Caroline Genell, Hervé Lebrec, Shermaine Mitchell-Ryan, Brigitte Molinier, Courtni Newsome, Marie-Soleil Piche, Daniel Weinstock, Mark Collinge, Wendy Freebern, Daniel Rubio
Historically, a chromium release assay has been used to monitor the level of target cell killing by CTL (Brunner et al. 1968). In brief, antigen-expressing target cells labeled with radio-labeled chromium (51Cr) are co-cultured with effector cells (e.g. purified T-cells or peripheral blood mononuclear cells [PBMC]) in vitro for a set period of time at various ratios of effector cell to target cell. The effector cells consist of mature CTL that have been previously exposed to the specific antigen. Target cells typically are cancer cell lines or virally-infected cells. The bioactivity of the CTL is then monitored by detecting the radioactive release of 51Cr from the lysed target cells. Over time, the chromium release assay has been replaced by other methods to reduce use of radioactive materials and increase the throughput of the assays. Modern methods include labeling target cells with chromogenic or fluorescent dyes and measuring cytotoxicity via colorimetric or fluorescence changes in supernatants following CTL and target cell incubation using a spectrometer or fluorimeter. If flow cytometry is used, target killing can be measured by identification of labeled target cells with a unique fluorescing dye, such as carboxyfluorescein succinimidyl ester (CFSE) dye followed by analysis of membrane integrity of the target cells using a viability stain to assess the proportion of live cells to dead cells (Figure 1).
The applications of targeted delivery for gene therapies in hearing loss
Published in Journal of Drug Targeting, 2023
Melissa Jones, Bozica Kovacevic, Corina Mihaela Ionescu, Susbin Raj Wagle, Christina Quintas, Elaine Y. M. Wong, Momir Mikov, Armin Mooranian, Hani Al-Salami
The research of this review primarily offers focus on the prospect of using targeted delivery in order to offer gene delivery to the inner ear with reduced off target effects. Currently, gene therapies are being investigated as potential treatments for a wide array of conditions, including hearing loss. Following the discovery of the benefits of specific genes in the inner ear, a key requirement is their delivery. Targeted delivery is a vital prospect to deliver genes to aid in the prevention of their action in areas of the inner ear which are not the intended target. This therapy has the potential for life changing positive impacts on patients who experience hearing loss. However, in order for this technology to be implemented, there are multiple barriers which first must be overcome. Such include the discovery of the ideal gene for use in hearing recovery, which will be dependent based upon the type of hearing loss and genes involved in the condition. In addition, the target cells must be identified, and an antibody for targeting will be required to be determined. Following such discoveries, a formulated nanoparticle is required, which will envelope the gene and be conjugated to the targeting antibodies. Such discoveries must then be effectively delivered to the target cells in the inner ear. Hence, the implementation of this technology is multi-fold, with all elements crucial to its success.
Determination of cytokine profile and associated genes of the signaling pathway in HNSCC
Published in Journal of Receptors and Signal Transduction, 2022
Aysel Kalayci Yigin, Ali Azzawri, Kayhan Ozturk, Tulin Cora, Mehmet Seven
Cytokines, chemokines and growth factors are important immunmodulators and prognostic markers which have a complex regulatory effect in the control of cellular processes. They act over short distances and at very low concentrations and are also coordinate intercellular signal transduction pathways [8]. To trigger these signal transduction pathways, they bind to receptors (receptor tyrosine kinases) on the membranes of responsive target cells and induce gene expression in target cells. Many cellular activities associated with survival, activation, proliferation, and differentiation of cells are under the control of intracellular signal transduction pathways. Aberrant activations of these components in the signal transduction pathways play a major role in the malignant transformation of many cancers [6]. Therefore, determining these activators involved in the etiopathogenesis of the HNSCC can be notable molecular targets for novel therapeutic approaches. The study aims to evaluate the cytokine, chemokine and growth factor profiling of HNSCC patients, and the relationship of genes involved in the pathway related to these cytokines.