Bibliografías temáticas / Hypertrophy

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Literatura académica sobre el tema "Hypertrophy"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 25 de julio de 2025

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Artículos de revistas sobre el tema "Hypertrophy"

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Maron, Barry J., and Carolyn Y. Ho. "Hypertrophic Cardiomyopathy Without Hypertrophy." JACC: Cardiovascular Imaging 2, no. 1 (2009): 65–68. http://dx.doi.org/10.1016/j.jcmg.2008.09.008.

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Strøm, Claes C., Mogens Kruhøffer, Steen Knudsen, et al. "Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy." Comparative and Functional Genomics 5, no. 6-7 (2004): 459–70. http://dx.doi.org/10.1002/cfg.428.

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Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in h
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Li, Wei-ming, Yi-fan Zhao, Guo-fu Zhu, et al. "Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload." Clinical Science 131, no. 2 (2016): 141–54. http://dx.doi.org/10.1042/cs20160664.

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Pathological cardiac hypertrophy is an independent risk factor of heart failure. However, we still lack effective methods to reverse cardiac hypertrophy. DUSP12 is a member of the dual specific phosphatase (DUSP) family, which is characterized by its DUSP activity to dephosphorylate both tyrosine and serine/threonine residues on one substrate. Some DUSPs have been identified as being involved in the regulation of cardiac hypertrophy. However, the role of DUSP12 during pathological cardiac hypertrophy is still unclear. In the present study, we observed a significant decrease in DUSP12 expressio
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Lu, Peilei, Danyu Zhang, Fan Ding, Jialu Ma, Yang K. Xiang, and Meimi Zhao. "Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis." Cells 12, no. 12 (2023): 1667. http://dx.doi.org/10.3390/cells12121667.

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Pathological cardiac hypertrophy is one of the notable causes of heart failure. Circular RNAs (circRNAs) have been studied in association with cardiac hypertrophy; however, the mechanisms by which circRNAs regulate cardiac hypertrophy remain unclear. In this study, we identified a new circRNA, named circCacna1c, in cardiac hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated with isoprenaline hydrochloride (ISO) to establish a hypertrophy model. We found that circCacna1c was upregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. Western blot and quantitative real-time
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Abdelbaki, Mourad, A. Boureghda, and N. Hanifi. "Comparative Research Between Sportsman's Heart and Hypertrophic Cardiomyopathy." International Journal of Innovative Research in Medical Science 9, no. 01 (2024): 24–27. http://dx.doi.org/10.23958/ijirms/vol09-i01/1802.

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Physiological left ventricular hypertrophy is the result of the left ventricle having to function harder due to intense physical exercise. After exercise is stopped, this modest and reversible hypertrophy persists. Studying these structural alterations is now feasible because to cardiac echodoppler. Distinguishing this adaptive hypertrophy from the pathogenic hypertrophic cardiomyopathy might be challenging at times. We examined 212 athletes who competed and a group of hypertrophic cardiomyopathy patients who had asymmetric septal hypertrophy that was confirmed. The findings demonstrated that
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Savchenko, M. I., YU R. Kovalev, and A. P. Kuchinskiy. "HYPERTROPHIC CARDIOMYOPATHY: FIBROSIS OR HYPERTROPHY." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 2 (2013): 148–55. http://dx.doi.org/10.18705/1607-419x-2013-19-2-148-155.

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Objective.Despite the high frequency — 0,2 % (1:500) population, hypertrophic cardiomyopathy (HCM) is still considered one of the most mysterious and misunderstood diseases of myocardium. Insidious pathology has neither specific anatomical and morphological, nor clinical features which makes it a delayed-action bomb: nobody is capable to predict when and what clinical symptoms develop. The clinical phenotype of HCM varies from latent course when the symptoms are absent till rapid progress of heart failure syndrome and sudden cardiac death due to severe arrhythmia. The review covers modern view
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Morita, Kozo, Takeshi Miyamoto, Nobuyuki Fujita, et al. "Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification." Journal of Experimental Medicine 204, no. 7 (2007): 1613–23. http://dx.doi.org/10.1084/jem.20062525.

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Chondrocyte hypertrophy during endochondral ossification is a well-controlled process in which proliferating chondrocytes stop proliferating and differentiate into hypertrophic chondrocytes, which then undergo apoptosis. Chondrocyte hypertrophy induces angiogenesis and mineralization. This step is crucial for the longitudinal growth and development of long bones, but what triggers the process is unknown. Reactive oxygen species (ROS) have been implicated in cellular damage; however, the physiological role of ROS in chondrogenesis is not well characterized. We demonstrate that increasing ROS le
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Gu, Wei, Yutong Cheng, Su Wang, Tao Sun, and Zhizhong Li. "PHD Finger Protein 19 Promotes Cardiac Hypertrophy via Epigenetically Regulating SIRT2." Cardiovascular Toxicology 21, no. 6 (2021): 451–61. http://dx.doi.org/10.1007/s12012-021-09639-0.

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AbstractEpigenetic regulations essentially participate in the development of cardiomyocyte hypertrophy. PHD finger protein 19 (PHF19) is a polycomb protein that controls H3K36me3 and H3K27me3. However, the roles of PHF19 in cardiac hypertrophy remain unknown. Here in this work, we observed that PHF19 promoted cardiac hypertrophy via epigenetically targeting SIRT2. In angiotensin II (Ang II)-induced cardiomyocyte hypertrophy, adenovirus-mediated knockdown of Phf19 reduced the increase in cardiomyocyte size, repressed the expression of hypertrophic marker genes Anp and Bnp, as well as inhibited
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Ignatenko, G. I., G. G. Taradin, and T. E. Kugler. "Specifics of Left Ventricular Hypertrophy and Characteristic of Phenotypic Variants in Patients with Hypertrophic Cardiomyopathy." Russian Archives of Internal Medicine 13, no. 4 (2023): 282–93. http://dx.doi.org/10.20514/2226-6704-2023-13-4-282-293.

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Hypertrophic cardiomyopathy is characterized by genetic and phenotypic heterogeneity which manifests in different variants of localization and extent of myocardial hypertrophy.Aim: to evaluate specifics of left ventricular hypertrophy, the prevalence and characteristics of clinical and instrumental features of phenotypic variants of hypertrophic cardiomyopathy.Materials and methods. The study includes 295 patients with hypertrophic cardiomyopathy aged 18 to 88 years (60.3±13.4 years), 183 men (62 %), and women 112 (38 %). The diagnosis of which was established by 2D echocardiography. The sever
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Villeneuve, C., A. Caudrillier, C. Ordener, N. Pizzinat, A. Parini, and J. Mialet-Perez. "Dose-dependent activation of distinct hypertrophic pathways by serotonin in cardiac cells." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (2009): H821—H828. http://dx.doi.org/10.1152/ajpheart.00345.2009.

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There is substantial evidence supporting a hypertrophic action of serotonin [5-hydroxytryptamine (5-HT)] in cardiomyocytes. However, little is known about the mechanisms involved. We previously demonstrated that 5-HT-induced hypertrophy depends, in part, on the generation of reactive oxygen species by monoamine oxidase-A (MAO-A) (see Ref. 3 ). Cardiomyocytes express 5-HT2 receptors, which may also participate in hypertrophy. Here, we analyzed the respective contribution of 5-HT2 receptors and MAO-A in H9C2 cardiomyoblast hypertrophy. 5-HT induced a dose-dependent increase in [3H]leucine incorp
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Tesis sobre el tema "Hypertrophy"

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Bloem, Liezl Margaretha. "Sarcomeric modifiers of hypertrophy in hypertrophic cardiomyopathy (HCM)." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79795.

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Thesis (PhD)--Stellenbosch University, 2013.<br>ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular morbidity and allcause mortality. Significantly, it is considered a modifiable cardiovascular risk factor as its regression increases overall survival and reduces the frequency of adverse cardiac events. A clear understanding of LVH pathogenesis is thus imperative to facilitate improved risk stratification and therapeutic intervention. Hypertrophic cardiomyopathy (HCM), an inherited cardiac disorder, is a model disease for elucidating the mole
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Soana, valentina. "Ornamental Hypertrophy." Thesis, KTH, Arkitektur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-35924.

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The thesis is exploring the potential of the ornament conceived as inhabitable space, exuberant, blissfull in opulence, flamboyant. The coexistence of opposite elements sensations that are overlapping, intertwining and blurring, generates a space that breathes, perspires and froths, exceeding in its blossom.
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Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.

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Abstract :Cardiac hypertrophy has been identified as the most important independent risk factor for cardiovascular-related morbidity and mortality and is therefore regarded as a pathological condition. Despite this, beneficial physiological forms also appear to exist, such as in response to exercise, leading to maintained or improved cardiac function. The aim of this thesis was to examine two distinct rodent models, an endurance run-trained rat, and the DOCA-salt hypertensive rat, representing physiological and pathological hypertrophy, respectively, in order to develop a better understanding
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Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.

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Clarke, Samantha Jayne. "Biochemical adaptations in cardiac hypertrophy." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395503.

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Tsang, K. K. "Screening for benign prostatic hypertrophy." Thesis, University of Edinburgh, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663068.

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Benign prostatic hypertrophy (BPH) is a very common disease among men aged 50 and its economic burden on health services continues to grow. The advocation for adopting new screening procedure for BPH begins to emerge. However, a new proposal for screening should be under careful scrutiny and ineffective and inappropriate screening must be avoided. A prospective cohort study has been launched to study the frequency, distribution, and natural history of BPH in two well-defined small communities in Central Scotland. Using the data from the cohort study, the hypothesis that a BPH screening program
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Risto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.

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Duchenne Muscular Dystrophy (DMD) is an X-linked disorder, caused by mutations in the DMD gene. This gene encodes dystrophin, a structural protein that links the sarcomere to the extracellular matrix via a trans-membrane protein complex. In the absence of dystrophin the associated glycoprotein complex fails to assemble, leading to sarcolemmal instability, impaired ion handling, skeletal muscle wasting and fibrosis. Patients become non-ambulant in their teens and seldom live past their third decade. Cardiac failure is one of the leading causes of death. The heart initially compensates for reduc
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Schans, Veerle Anna Maria van de. "Wnt signaling and cardiac hypertrophy." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=14684.

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Stone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4532.

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Stone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/4544.

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Libros sobre el tema "Hypertrophy"

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J, Sheridan Desmond, ed. Left ventricular hypertrophy. Churchill Livingstone, 1998.

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1929-, Ison-Franklin Eleanor L., Sandler Harold 1929-, and Hawthorne Edward William 1922-1986, eds. Myocardial hypertrophy: A symposium. Howard University Press, 1991.

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Van der Wall, Ernst E., Arnoud Van der Laarse, Babette M. Pluim, and Albert V. G. Bruschke. Left Ventricular Hypertrophy. Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3.

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Sever, Peter S. Left ventricular hypertrophy. Current Medical Literature, 1996.

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Dhalla, Naranjan S., Grant N. Pierce, Vincenzo Panagia, and Robert E. Beamish, eds. Heart Hypertrophy and Failure. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-1237-6.

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Adami, J. George. Notes upon cardiac hypertrophy. s.n., 1985.

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B, Swynghedauw, ed. Cardiac hypertrophy and failure. Libbey, 1990.

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S, Dhalla Naranjan, and International Conference on Heart Failure (1994 : Winnipeg, Man.), eds. Heart hypertrophy and failure. Kluwer, 1995.

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World Heart Congress (17th 2001 Winnipeg, Man.). Signal transduction and cardiac hypertrophy. Edited by Dhalla Naranjan S. Kluwer Academic Pub., 2003.

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McVary, Kevin T. Management of Benign Prostatic Hypertrophy. Humana Press, 2003. http://dx.doi.org/10.1385/1592596444.

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Capítulos de libros sobre el tema "Hypertrophy"

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Capinera, John L., Thomas O. Crist, John B. Heppner, et al. "Hypertrophy." In Encyclopedia of Entomology. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1457.

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DePiero, Theslee Joy. "Hypertrophy." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_459.

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Rosenberg, Leah. "Hypertrophy." In Encyclopedia of Behavioral Medicine. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1269.

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Orbell, Sheina, Havah Schneider, Sabrina Esbitt, et al. "Hypertrophy." In Encyclopedia of Behavioral Medicine. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1269.

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DePiero, Theslee Joy. "Hypertrophy." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_459-2.

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Sainburg, Robert L., Andrew L. Clark, George E. Billman, et al. "Hypertrophy." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2514.

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Vecht, Romeo, Nicholas Peters, and Micheal A. Gatzoulis. "Hypertrophy." In ECG Diagnosis in Clinical Practice. Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-312-5_5.

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DePiero, Theslee Joy. "Hypertrophy." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_459.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "Hypertrophy." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9227.

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Mallion, Jean-Michel, Jean-Philippe Baguet, Jean-Philippe Siché, F. Tremel, and R. De Gaudemaris. "Left Ventricular Hypertrophy and Arterial Hypertrophy." In Advances in Experimental Medicine and Biology. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5385-4_14.

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Actas de conferencias sobre el tema "Hypertrophy"

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Tang, Wei, Kangning Cui, Raymond H. Chan, and Jean-Michel Morel. "Bilateral Signal Warping for Left Ventricular Hypertrophy Diagnosis." In 2025 IEEE 22nd International Symposium on Biomedical Imaging (ISBI). IEEE, 2025. https://doi.org/10.1109/isbi60581.2025.10980912.

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Ng, Wei Wen, Wan Naimah Wan Ab Naim, Yih Miin Liew, and Bee Ting Chan. "Estimation of In-Vivo Mechanical Properties of Aortic Wall in Left Ventricular Hypertrophy Patients." In 2024 8th International Conference on Biomedical Engineering and Applications (ICBEA). IEEE, 2024. http://dx.doi.org/10.1109/icbea62825.2024.00024.

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Al-Shamasi, Al-Anood, Meram Elsayed, Nabeel Abdulrahman, Jensa Joseph, and Fatima Mraiche. "The Cardiovascular benefits of Empagliflozin, a Sodium Glucose Cotransporter Inhibitor: Is NHE1 a viable target?" In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0228.

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Empagliflozin (EMPA), an SGLT2 inhibitor (with a low affinity for SGLT1) has attracted much attention due to a recent clinical trial, the Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes (EMPA-REG OUTCOME). In this trial, treatment with EMPA over 2.6 years decreased cardiovascular vascular events (14% reduction). Whether EMPA induces cardioprotection, independent of diabetes remains unclear. A previous report has demonstrated that EMPA inhibited NHE1 activity, which led to a reduction in intracellular sodium and calcium. In our study, we examine the cellular interplay b
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Farrar, G. E., and A. I. Veress. "A Coupled Model of LV Growth and Mechanics Applied to Pressure Overload Hypertrophy." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14557.

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Hypertension currently affects approximately one third the population in the United States, and represents a major economic burden on the health care system with an estimated annual direct and indirect cost of $50.6 billion [1]. In the case of systemic hypertension, the left ventricle (LV) must work against increased pressure load to pump blood to the body. Over time, this excessive work causes hypertrophy of the myocardium (thickening of the myofibers). While initially a compensatory mechanism, hypertrophy can eventually lead to heart failure (HF) [2]. Predictive modeling of the hypertrophic
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Macpherson, A. K., S. Neti, P. A. Macpherson, S. R. Houser, M. Hari, and J. Marzillier. "Mechanical stress and hypertrophy." In BIOMEDICINE 2005. WIT Press, 2005. http://dx.doi.org/10.2495/bio050171.

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Bian, Liming, Robert L. Mauck, and Jason A. Burdick. "Dynamic Compressive Loading and Crosslinking Density Influence the Chondrogenic and Hypertrophic Differentiation of Human Mesenchymal Stem Cells Seeded in Hyaluronic Acid Hydrogels." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80048.

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While hyaluronic acid (HA) hydrogels provide a stable 3D environment that is conducive to the chondrogenesis of mesenchymal stem cells (MSCs) in the presence of growth factors [1], the neocartilage that is formed remains inferior to native tissue, even after long culture durations. Additionally, MSCs eventually transit into a hypertrophic phenotype after chondrogenic induction, resulting in the calcification of the ECM after ectopic transplantation [2]. From a material design perspective, variation in the HA hydrogel scaffold crosslinking density via changes in the HA macromer concentration ca
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Pujowaskito, Prihati, Nia Melinda Pardede, Evi Sovia, and Pradiba Amadita. "Hypertension with Left Ventricular Hypertrophy." In 12th Annual Scientific Meeting, Medical Faculty, Universitas Jenderal Achmad Yani, International Symposium on "Emergency Preparedness and Disaster Response during COVID 19 Pandemic" (ASMC 2021)). Atlantis Press, 2021. http://dx.doi.org/10.2991/ahsr.k.210723.057.

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Hughes, Rebecca K., João B. Augusto, Kristopher Knott, et al. "20 Apical ischaemia is ubiquitous in apical hypertrophic cardiomyopathy and occurs before overt hypertrophy." In British Society of Cardiovascular Magnetic Resonance 2021 Annual Meeting. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bscmr.20.

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Damani, Devanshi N., Anoushka Kapoor, Priyadharshini Sivasubramaniam, et al. "Biventricular Involvement In Hypertrophic Cardiomyopathy: Preliminary Analysis Of Cardiac MRIs With Visual Right Ventricular Hypertrophy." In 2022 IEEE 10th International Conference on Healthcare Informatics (ICHI). IEEE, 2022. http://dx.doi.org/10.1109/ichi54592.2022.00031.

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Martin, DW, J. Mazer, EO Harrington, and G. Choudhary. "PKC Isoforms in Right Ventricular Hypertrophy." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4145.

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Informes sobre el tema "Hypertrophy"

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liu, menghui, yanchao zhang, and lixin li. Traditional Chinese medicine for the treatment of pediatric adenoid hypertrophy: A protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.2.0104.

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Review question / Objective: In order to verify effectiveness and safety of traditional Chinese medicine in the treatment of pediatric adenoid hypertrophy. Condition being studied: Pediatric adenoid hypertrophy. A total of 135 potential literatures were selected after extensive browsing and collection. 73 studies remained after duplicates removed. And we excluded 34 literatures that did not meet the research objects by screening the title and abstract of the literature in detail. Immediately after that, we deleted 39 literatures based on the inclusion criteria, and finally, we screened out 11
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Kraemer, William J. Strategies for Optimizing Strength, Power, and Muscle Hypertrophy in Women. Defense Technical Information Center, 1997. http://dx.doi.org/10.21236/ada348669.

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Lingle, Wilma. Centrosome Hypertrophy Induced by p53 Mutations Leads to Tumor Aneuploidy. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada392933.

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Currier, Brad, Maria Fiatarone Singh, Caroline Lowisz, et al. An umbrella review of resistance training to promote increases in muscle function and hypertrophy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.6.0071.

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Currier, Brad, Jonathan Mcleod, and Stuart Phillips. The Influence of Resistance Exercise Training Prescription Variables on Muscle Mass, Muscle Strength, and Physical Function in Healthy Adults: An Umbrella Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.2.0028.

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Review question / Objective: To determine how resistance training prescription variables (load, sets, frequency, time under tension, etc) affect muscle mass, muscle strength, and physical function in healthy adults. Condition being studied: To determine how resistance training prescription variables (load, sets, frequency, time under tension, etc) affect muscle mass (hypertrophy), muscle strength, and physical function in healthy adults. Information sources: OVID MEDLINE, SPORTDiscus, Web of Science.
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Leblanc, Samuel. The optimal range of motion for hypertrophy:<br>A review of the literature. ResearchHub Technologies, Inc., 2022. http://dx.doi.org/10.55277/researchhub.56zv24z4.

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Guede-Rojas, Francisco, Alexis Benavides-Villanueva, Sergio Salgado-González, Cristhian Mendoza, Gonzalo Arias-Álvarez, and Claudio Carvajal-Parodi. Effect of strength training on knee proprioception in patients with knee osteoarthritis. A systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.5.0102.

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Review question / Objective: To analyze the effect of strength training (ST) on knee proprioception in patients with knee osteoarthritis (KOA). Condition being studied: KOA is a chronic and degenerative joint disease characterized by articular cartilage loss, marginal bone hypertrophy, and inflammatory involvement of periarticular tissue of the knee. Symptoms of KOA are pain, stiffness, reduced range of motion, and muscle weakness, although proprioception may also be affected, contributing to the associated functional limitation.
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Kraemer, William J. Strategies for Optimizing Strength, Power, and Muscle Hypertrophy in Women: Contribution of Upper Body Resistance Training. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada371349.

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Cahaner, Avigdor, Sacit F. Bilgili, Orna Halevy, Roger J. Lien, and Kellye S. Joiner. effects of enhanced hypertrophy, reduced oxygen supply and heat load on breast meat yield and quality in broilers. United States Department of Agriculture, 2014. http://dx.doi.org/10.32747/2014.7699855.bard.

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Original objectivesThe objectives of this project were to evaluate the growth performance, meat yield and quality attributes of broiler strains widely differing in their genetic potential under normal temperature vs. warm temperature (short and long-term) conditions. Strain differences in breast muscle accretion rate, metabolic responses under heat load and, gross and histopathological changes in breast muscle under thermal load was also to be characterized. BackgroundTremendous genetic progress has been made in broiler chicken growth rate and meat yield since the 1950s. Higher growth rate is
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Laskin, Grant, Liliana Renteria, and Brad Gordon. Effects of resistance exercise load on muscle fiber type hypertrophy in the untrained: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.9.0128.

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