Tissue engineering and regeneration
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
Advances in both the biological and physical sciences underpin the fields of tissue engineering and regenerative therapy (Figure4.1). In the biological sciences, new discoveries in stem cell biology have been key, particularly an understanding of the different types of stem cell, and how these can be derived and directed in vitro to differentiate into specialised cell types. In material sciences, major advances in the manufacture of scaffolds, on which to seed cells or to encourage specific interaction with host cells, have been key. In particular, design goals relate to scaffolds that possess both the physical and the biological characteristics that allow cells to create tissues, and potentially even organs, for therapeutic purposes. Key also have been engineering advances in the development of the many different types of bioreactors that provide an appropriate physical environment for growing engineered tissues in vitro, outside the body in the laboratory.
Social medicine and international expert networks in Latin America, 1930–1945
Emily E. Vasquez, Amaya Perez-Brume, Richard G. Parker in Social Inequities and Contemporary Struggles for Collective Health in Latin America, 2020
During the 1930s, the Geneva Institutions became increasingly focused on the problem of adequate nutrition. Because of its ‘clear connections with broader social and economic processes related to the production and consumption of food,’ nutritional research was often caught between the integrative approach of social medicine and the reductionist tendencies of physiology and cell biology (Packard, 2016). Corinne Pernet (2013) contends that, compared to the ILO’s broad social vision, the LNHO supported ‘pure science’ research in nutrition, with priority placed on defining international nutrition standards and tracing the health impacts of malnutrition, while largely neglecting how underlying social and economic conditions contributed to malnutrition. Even with this integrative approach, the ILO valued scientific research on nutrition to establish baseline standards for nutritional needs of workers and their families, a key component for calculating a ‘living wage’ (Pernet, 2013).
Neuromuscular disorders
Angus Clarke, Alex Murray, Julian Sampson in Harper's Practical Genetic Counselling, 2019
Both genetic counselling and our general understanding of myotonic dystrophy have been entirely transformed as a result of the identification of the specific mutation in the gene on chromosome 19. An unstable trinucleotide repeat sequence is involved, with expansion in a specific CTG repeat found in virtually all cases so far studied. The expansion correlates broadly with severity of phenotype, and tends to increase from generation to generation, thus explaining the progressively earlier onset and greater severity (anticipation) characteristic of this disorder. The gene itself codes for a previously unknown protein, which shows protein kinase activity. Unlike DMD, there does not appear to be absence of the protein in patients – the mutation is in an untranslated part of the gene and its effects are related to its size. An effect on the function of other genes at the RNA level is involved, and the cell biology of the disorder is complex.
Accounting for robustness in modeling signal transduction responses
Published in Journal of Receptors and Signal Transduction, 2018
Mohammad Omid Oftadeh, Sayed-Amir Marashi
Cellular response to external signals is often mediated through a complex protein signaling network. Such an intricate network determines the behavior of a cell type when a certain set of signals are encountered. A detailed understanding of cell behavior has a central role in cell biology and bioengineering. Although the outcome of applying the external stimuli can be determined by conducting experiments on a certain cell type, the number of experiments required to screen various combinations of the input signals tremendously rises when the number of the stimulators increases. In practice, it is necessary to construct a model to enable us predicting the cell responses by using a limited set of experimental data. Furthermore, such a model is inherently an enabling framework to elucidate the underlying mechanism of signal transduction.
MiR-144-3p inhibits the proliferation, migration and invasion of lung adenocargen cancer cells by targeting COL11A1
Published in Journal of Chemotherapy, 2021
Yahong Sun, Zhihao Liu, Lifei Huang, Yan Shang
In order to verify the effect of miR-144-3p on the proliferation, migration and invasion of LUAD cells by targeting COL11A1, rescue experiments were carried out. First of all, the cells are divided into NC simulators plus oe-NC, miR-144-3p simulators with oe-NC and miR-144-3p simulators with oe-COL11A1 groups. QRT-PCR was performed to detect levels of miR-144-3p and COL11A1 mRNA in each treatment group. Figure 6A shown, as shown, miR-144-3p imitation plus oe-NC and miR-144-3p imitation plus oe-COL11A1 group miR-1 144-3p is significantly raised, and there is no difference between the significant miR-144-3p simulator plus oe-NC and the miR-144-3p simulator plus oe-COL11A1 group. At the same time, COL11A1 decreased significantly when miR-144-3p over-expressed, while COL11A1 increased slightly when miR-144-3p and COL11A1 over-expressed at the same time. In addition, cell biology behavior was evaluated through a series of experiments. CCK-8, wound healing test and Transwell invasive test showed that the cell proliferation, migration and invasive ability of miR-144-3p imitation plus oe-NC group decreased significantly compared to NC imitation plus oe-NC group, Figure 6B-D). Together, these results show that the over-expression of miR-144-3p inhibits the proliferation, migration and invasion of LUAD cells, while the elevation of COL11A1 partially counteracts the inhibition of over-expression of miR-144-3p on cancer cells.
Current perspectives on the clinical management of cryptogenic stroke
Published in Expert Review of Neurotherapeutics, 2023
Dixon Yang, Mitchell S. V. Elkind
Looking ahead, molecular cell biology and specialized imaging may be two areas that particularly hold promise. Several studies have examined cellular and histological clot compositions of large vessel occlusions extracted during endovascular thrombectomy. Quantifying the relative proportion of red blood cells, fibrin, platelets, and leukocytes may provide clues on the source of the thromboembolism in cryptogenic stroke [8,127]. In a similar thread, emerging data have suggested that RNA may serve as a precision biomarker in the determination of stroke etiology [128–130]. Various circulating cells that may contribute to thromboembolism formation in the peripheral blood can express different RNA signatures and these differences have been preliminarily applied to classify probable etiology of cryptogenic stroke in conjunction with neuroimaging [131]. On the imaging front, high-resolution MRI with vessel wall imaging has become increasingly popular as an adjunctive tool in the assessment of extra- and intracranial arterial stenosis as it offers information beyond the degree of luminal stenosis like markers of plaque vulnerability [132]. Advanced ultrasound techniques such as elastography may provide an alternative and cheaper avenue to assessing plaque vulnerability [133]. Together, these promising diagnostic modalities would need validation of their findings with pathology and demonstration of feasibility in routine clinical practice.