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Infectious Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Susanna J. Dunachie, Hanif Esmail, Ruth Corrigan, Maria Dudareva
Disease manifests as a spectrum influenced by the host's cell-mediated immune response. Lepromatous leprosy occurs with poor cellular immunity and high pathogen numbers, resulting in tissue thickening and damage. Tuberculoid leprosy occurs with substantial cellular immunity and is usually localized within an area of hypopigmented anaesthetic skin supplied by a thickened nerve.
Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
It was recently observed that the endogenous free C-terminal fragment localizes to Purkinje's cell nuclei. In addition, C-terminal fragments cleaved from recombinant a1A subunits or expressed as isolated C-termini localize to nuclei in cultured cell lines and primary granule cell cultures. Cleavage and nuclear localization are not however affected by polyglutamine length. The relevance of the cleaved fragment to disease pathogenesis is unclear.
Short-Term Exercise and Immune Function
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
At rest — In the previously sedentary women, moderate exercise training (in the form of a 15-week walking program — five 45-min sessions per week), had no significant effect on total numbers of helper cells, suppressor cells or the H/S cell ratio.21 In the highly trained athletes, regimens of normal training did not effect the percentages of helper cells, suppressor cells, or the H/S ratio observed in blood samples taken at rest.10,22 However, there is evidence to suggest that when athletes engage in periods of heavy training, the proportion of helper cells may decrease and the proportion of suppressor cells increase, thus, decreasing the H/S ratio at rest.22 Three weeks of recovery following a regimen of heavy training resulted in a significant increase in the H/S ratio, primarily due to a significant decrease in the percentage of suppressor cells.22
Repurposing Natural Dietary Flavonoids in the Modulation of Cancer Tumorigenesis: Decrypting the Molecular Targets of Naringenin, Hesperetin and Myricetin
Published in Nutrition and Cancer, 2022
Carolina Sousa, Denise Duarte, Beatriz Silva-Lima, Mafalda Videira
Proteins underlying DNA repair, such as BRCA2 and PARP, are frequently downregulated during tumorigenesis. Inhibition of two or more of these genes result in synthetic lethally and, consequently, cell death. This strategy has been used in BRCA2-deficient cells, with PARP as an enticing molecular target. HESP and NAR can block PARP’s activity in a very similar manner (103). The pair has been described by (59) as being capable of inhibiting growth in positive HER2 breast cancer cells, by acting as an inhibitor of this receptor. Their administration also changed the mitochondrial membrane potential, leading to activation of caspase-8 and −3 and G2/S cell cycle arrest (59). Another pathway behind NAR-induced apoptosis was observed in B16F10 melanoma cells, specifically for those arrested in sub-G0/G1 phase, while triggering melanin synthesis as a result of activation of cyclic AMP-protein kinase A (104). More importantly, a dose-effect behavior established for NAR can temper apoptosis in TNBC, owing to the recovery of the expression of caspase-3 and −9 (57) (Figure 3).
circYap inhibits oral squamous cell carcinoma by arresting cell cycle
Published in Acta Odontologica Scandinavica, 2022
Xiao-Yun Zhang, Huifang Tang, Yanping Liu, Nan Du, Songbo Tian, Yong-Qing Dou
The active proliferative ability of tumor cells is closely related to the mitosis process. We then examined the effect of circYap on the cell cycle of OSSC cells. The results showed that overexpression of circYap inhibited G1/S transformation in CAL-27 cells, while knockdown of circYap promoted G1/S transformation in SCC-4 cells. Rb protein regulates the G1/S cell cycle by regulating the transcription factor E2F1, which induces the expression of S phase genes. In particular, low-phosphorylated Rb can bind to E2F1, thus blocking its ability to activate S phase genes, leading to G1-S stagnation [15]. Akt and phosphorylated Akt (p-Akt) are also known to be important regulators of the cell cycle. We detected the effect of circYap on the changes of Rb and Akt proteins and their phosphorylation levels. The results showed that overexpression of circYap inhibited the two proteins and their phosphorylation levels, reducing the phosphorylation ratio, respectively. Knocking down circYap yielded the opposite result. The above experimental results confirmed that circYap inhibited the G1/S phase transformation of OSSC cells and then inhibited cell proliferation.
Demonstration of treatment planning software for hyperthermic intraperitoneal chemotherapy in a rat model
Published in International Journal of Hyperthermia, 2021
Daan R. Löke, Roxan F. C. P. A. Helderman, Hans M. Rodermond, Pieter J. Tanis, Geert J. Streekstra, Nicolaas A. P. Franken, Arlene L. Oei, Johannes Crezee, H. Petra Kok
The chemotherapy is delivered to the organ surface via convection. The chemotherapy diffuses freely into the organs where it is subject to vascular and cellular absorption. Therefore, the total drug sink term Sdrug drug can be written as Scell is the cellular uptake and Sv is the vascular uptake transferred to the central compartment. The sink term is incorporated in the chemotherapy dynamics via ρ, U, D are the fluid density, fluid velocity and diffusion constant. For more detail, we refer to [26]. We know from experimental in vivo data that the systemic concentration decreases for higher temperatures resulting in a higher cellular uptake [19]. Therefore, we write the cellular uptake as β a first-order elimination constant (s−1), y(T) is a temperature-dependent enhancement function and C is the drug concentration in the cell. Due to diffusion of the chemotherapy, the chemotherapy concentration C becomes non-zero after some treatment time, and Equation (18) functions as a sink to model cellular uptake. The enhancement function is based on data from [19], which represents the temperature-dependent change in systemic uptake. A first-order approximation was fitted to these data to obtain a continuous function across the hyperthermic temperature range. The function reads: