Relevant bibliographies by topics / Hypertrophy

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Hypertrophy'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Hypertrophy"

1

Maron, Barry J., and Carolyn Y. Ho. "Hypertrophic Cardiomyopathy Without Hypertrophy." JACC: Cardiovascular Imaging 2, no. 1 (January 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, Frank Stensgaard-Hansen, Thomas E. N. Jonassen, Torben F. Ørntoft, Stig Haunsø, and Søren P. Sheikh. "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 hypertrophic signalling. From gene expression analyses (8740 probe sets,n= 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61 genes whose altered expression had previously been reported. We identified a single common gene program underlying hypertrophic remodelling, regardless of how the hypertrophy was induced. These genes constitute the molecular basis for the existence of one main form of cardiac hypertrophy and may be useful for prediction of a common therapeutic approach. Supplementary material for this article can be found at: http://www.interscience.wiley.com/jpages/1531-6912/suppmat
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Li, Wei-ming, Yi-fan Zhao, Guo-fu Zhu, Wen-hui Peng, Meng-yun Zhu, Xue-jing Yu, Wei Chen, Da-chun Xu, and Ya-wei Xu. "Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload." Clinical Science 131, no. 2 (December 23, 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 expression in hypertrophic hearts and cardiomyocytes. Using a genetic loss-of-function murine model, we demonstrated that DUSP12 deficiency apparently aggravated pressure overload-induced cardiac hypertrophy and fibrosis as well as impaired cardiac function, whereas cardiac-specific overexpression of DUPS12 was capable of reversing this hypertrophic and fibrotic phenotype and improving contractile function. Furthermore, we demonstrated that JNK1/2 activity but neither ERK1/2 nor p38 activity was increased in the DUSP12 deficient group and decreased in the DUSP12 overexpression group both in vitro and in vivo under hypertrophic stress conditions. Pharmacological inhibition of JNK1/2 activity (SP600125) is capable of reversing the hypertrophic phenotype in DUSP12 knockout (KO) mice. DUSP12 protects against pathological cardiac hypertrophy and related pathologies. This regulatory role of DUSP12 is primarily through c-Jun N-terminal kinase (JNK) inhibition. DUSP12 could be a promising therapeutic target of pathological cardiac hypertrophy. DUSP12 is down-regulated in hypertrophic hearts. An absence of DUSP12 aggravated cardiac hypertrophy, whereas cardiomyocyte-specific DUSP12 overexpression can alleviate this hypertrophic phenotype with improved cardiac function. Further study demonstrated that DUSP12 inhibited JNK activity to attenuate pathological cardiac hypertrophy.
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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 (June 19, 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 polymerase chain reaction showed that silencing circCacna1c inhibited hypertrophic gene expression in ISO-induced H9c2 cells. Mechanistically, circCacna1c competitively bound to miR-29b-2-5p in a dual-luciferase reporter assay, which was downregulated in ISO-induced hypertrophic heart tissue and H9c2 cells. MiR-29b-2-5p inhibited the nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) to control hypertrophic gene expression. After silencing circCacna1c, the expression of miR-29b-2-5p increased, which reduced hypertrophic gene expression by inhibiting NFATc1 expression. Together, these experiments indicate that circCacna1c promotes ISO-induced pathological hypertrophy through the miR-29b-2-5p/NFATc1 axis.
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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 (April 28, 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 on genetics, morphology and pathogenesis of HCM.
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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 (January 10, 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 there is a boundary between pathological and normal hypertrophy. This zone contained four athletes, one of whom had hypertrophic cardiomyopathy. Numerous variables led to the diagnosis, including the patient's history, electrical anomalies, septal thickness, and a diastolic diameter of less than 45 mm. Deconditioning further supported the diagnosis.
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Morita, Kozo, Takeshi Miyamoto, Nobuyuki Fujita, Yoshiaki Kubota, Keisuke Ito, Keiyo Takubo, Kana Miyamoto, et al. "Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification." Journal of Experimental Medicine 204, no. 7 (June 18, 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 levels induce chondrocyte hypertrophy. Elevated ROS levels are detected in hypertrophic chondrocytes. In vivo and in vitro treatment with N-acetyl cysteine, which enhances endogenous antioxidant levels and protects cells from oxidative stress, inhibits chondrocyte hypertrophy. In ataxia telangiectasia mutated (Atm)–deficient (Atm−/−) mice, ROS levels were elevated in chondrocytes of growth plates, accompanied by a proliferation defect and stimulation of chondrocyte hypertrophy. Decreased proliferation and excessive hypertrophy in Atm−/− mice were also rescued by antioxidant treatment. These findings indicate that ROS levels regulate inhibition of proliferation and modulate initiation of the hypertrophic changes in chondrocytes.
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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 (February 21, 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 protein synthesis. By contrast, Phf19 overexpression promoted Ang II-induced cardiomyocyte hypertrophy in vitro. We also knocked down Phf19 expression in mouse hearts in vivo. The results demonstrated that Phf19 knockdown reduced Ang II-induced decline in cardiac fraction shortening and ejection fraction. Phf19 knockdown also inhibited Ang II-mediated increase in heart weight, reduced cardiomyocyte size, and repressed the expression of hypertrophic marker genes in mouse hearts. Further mechanism studies showed that PHF19 suppressed the expression of SIRT2, which contributed to the function of PHF19 during cardiomyocyte hypertrophy. PHF19 bound the promoter of SIRT2 and regulated the balance between H3K27me3 and H3K36me3 to repress the expression of SIRT2 in vitro and in vivo. In human hypertrophic hearts, the overexpression of PHF19 and downregulation of SIRT2 were observed. Of importance, PHF19 expression was positively correlated with hypertrophic marker genes ANP and BNP but negatively correlated with SIRT2 in human hypertrophic hearts. Therefore, our findings demonstrated that PHF19 promoted the development of cardiac hypertrophy via epigenetically regulating SIRT2.
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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 (August 16, 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 severity, localization and extent of myocardial hypertrophy, the maximum thickness of the hypertrophied segment, left ventricular myocardial mass, left ventricular myocardial mass index, the presence and severity of mid-ventricular and left ventricular outflow tract obstruction were evaluated. Depending on the predominant localization and extent of hypertrophy, patients were divided into 8 groups according to the recommendations for hypertrophic cardiomyopathy of the Ministry of Health of the Russian Federation. The analysis and comparison of the obtained results are carried out.Results. The average duration of the disease is 10.5±7.52 years. The mean values of the body mass index in patients — 28.2±2.82 kg/m2. The phenotype with basal hypertrophy of the septum (n=130, 44.1 %), group 1 was most often noted. In 47 (15.9 %) patients, hypertrophy of the septum of “reverse curve” (2 group) was detected, in 41 (13.9 %) — “neutral septum” (3 group), in 36 (12.2 %) — symmetrical hypertrophy of the left ventricle (8 group), 11 (3.7 %) of patients had combined hypertrophy of the septum and other parts of the left or right ventricle (4 group) and the free left ventricular wall (7 group), in 10 (3.4 %) — middle ventricular hypertrophy of the left ventricle (6 group) and in 9 (3.1 %) — apical hypertrophy (5 group). The highest value of the maximum thickness of the myocardium was noted in patients of the 6th group 19.3 (1920.4 mm). Mid-ventricular obstruction was detected in group 6 (90 %), left ventricular outflow tract obstruction was more often registered in groups 4 and 8 (81.8 % and 77.8 %), and less often in group 5 (22.2 %) (p <0.01). In group 7, there were no cases of rest obstruction of left ventricular outflow tract. The maximum values of myocardial mass and left ventricular myocardial mass index were noted in group 8 — 402 (356-439) g and 195 (173218) g/m2, respectively (p <0.01).Conclusion. Echocardiography is an informative tool for assessing the presence, severity myocardial hypertrophy and determination of the phenotypic variant of hypertrophic cardiomyopathy. Variants of septal hypertrophy are most commonly registered one, among which the most frequent is the phenotype of basal septal hypertrophy. Each phenotype of hypertrophic expression is characterized by its echocardiographic parameters.
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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 (August 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 incorporation and stimulation of two markers of cardiac hypertrophy, ANF-luc and αSK-actin-luc reporter genes. Experiments using 1 μM 5-HT showed that hypertrophic response occurred independently from MAO-A. Using pharmacological inhibitors (M100907 and ketanserin), we identified a novel mechanism of action involving 5-HT2A receptors and requiring Ca2+/calcineurin/nuclear factor of activated T-cell activation. The activation of this hypertrophic pathway was fully prevented by 5-HT2A inhibitors and was unaffected by MAO inhibition. When 10 μM 5-HT was used, an additional hypertrophic response, prevented by the MAO inhibitors pargyline and RO 41-1049, was observed. Unlike the 5-HT2A-receptor-mediated H9C2 cell hypertrophy, MAO-A-dependent hypertrophic response required activation of extracellular-regulated kinases. In conclusion, our results show the existence of a dose-dependent shift of activation of distinct intracellular pathways involved in 5-HT-mediated hypertrophy of cardiac cells.
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Dissertations / Theses on the topic "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.
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 molecular mechanisms underlying LVH development. LVH, in the absence of increased external loading conditions, is its quintessential clinical feature, resulting from mutations in genes encoding sarcomeric proteins. The LVH phenotype in HCM exhibits marked variability even amongst family members who carry the same disease-causing mutation. Phenotypic expression is thus determined by the causal mutation and additional determinants including the environment, epigenetics and modifier genes. Thus far, factors investigated as potential hypertrophy modifiers in HCM have been relatively removed from the primary stimulus for LVH; and the few studies that have been replicated yielded inconsistent results. We hypothesized that the factors that closely interact with the primary stimulus of faulty sarcomeric functioning, have a greater capacity to modulate it, and ultimately the LVH phenotype in HCM. Plausible candidate modifiers would include factors relating to the structure or function of the sarcomere, including known HCM-causal genes; and the enzymes that function in sarcomere-based energetics. Indeed, the literature highlights the relevance of sarcomeric proteins, Ca2+-handling and myocardial energetics in the development of LVH in HCM. This study, therefore, set out to evaluate the hypertrophy-modifying capacity of such factors by means of family-based genetic association testing in 27 South African HCM families in which one of three unique HCM-causing founder mutations segregates. Moreover, the single and combined effects of 76 variants within 26 candidate genes encoding sarcomeric or sarcomere-associated proteins were investigated. The study identified a modifying role in the development of hypertrophy in HCM for each of the candidate genes investigated with the exception of the metabolic protein-encoding gene, PRKAG1. More specifically, single variant association analyses identified a modifying role for variants within the genes MYH7, TPM1 and MYL2, which encode proteins of the sarcomere, as well as the genes CPT1B, CKM, ALDOA and PRKAB2, which encode metabolic proteins. Haplotype-based association analyses identified combined modifying effects for variants within the genes ACTC, TPM1, MYL2, MYL3 and MYBPC3, which encode proteins of the sarcomere, as well as the genes CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 and PRKAG3, which encode metabolic proteins. Moreover, a number of variants and haplotypes showed statistically significant differences in effect amongst the three HCM founder mutation groups. The HCM-modifier genes identified were prioritised for future studies according to the number of significant results obtained for the four tests of association performed. The genes TPM1 and MYBPC3, which encode sarcomeric proteins, as well as the genes PFKM and PRKAG2, which encode metabolic proteins, were identified as stronger candidates for future studies as they delivered multiple significant results for various statistical tests. This study makes a novel contribution to the field of hypertrophy research as it tested the hypothesis that structural or energy-related factors located within the sarcomere may act as modifiers of cardiac hypertrophy in HCM, and succeeded in identifying a modifying role for many of the candidate genes selected. The significant results include substantial single and within-genecontext variant effects; and identified sizeable variation in the risk of developing LVH owing to the compound effect of the modifier and the individual founder mutations. Collectively, these findings enhance the current understanding of genotype/phenotype correlations and may, as consequence, improve patient risk stratification and choice of treatment. Moreover, these findings emphasize the potential for modulation of disease by further elucidation of some of the avenues identified.
AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) is ‘n onafhanklike voorspeller van kardiovaskulêre morbiditeit en van mortaliteit weens alle oorsake. Van belang is dat dit ‘n wysigbare kardiovaskulêre risiko faktor is, aangesien die afname daarvan algehele oorlewing verhoog en die frekwensie van nadelige kardiale voorvalle verlaag. ‘n Duidelike begrip van LVH patogenese is dus noodsaaklik om verbeterde risiko stratifikasie en terapeutiese intervensie te fasiliteer. Hipertrofiese kardiomiopatie (HKM), ‘n oorerflike hart-siekte, is ‘n model-siekte vir die uitpluis van die molekulêre meganismes onderliggend aan die ontwikkeling van LVH. LVH, in die afwesigheid van verhoogde eksterne lading, is die kern kliniese simptoom van HKM en die gevolg van mutasies in die gene wat kodeer vir sarkomeriese proteïene. Die LVH fenotiepe in HKM toon merkbare veranderlikheid selfs in familie-lede wat dieselfde siekte-veroorsakende mutasie dra. Die fenotiepe word dus bepaal deur die siekte-veroorsakende mutasie asook addisionele determinante insluitend die omgewing, epigenetika en modifiserende gene. Potensiële hipertrofie-modifiseerders wat tot dusver bestudeer is, is betreklik verwyder van die primêre stimulus vir LVH en die paar studies wat gerepliseer is, het teenstrydige resultate gelewer. Ons hipoteseer dat die faktore wat in noue interaksie met die primêre stimulus van foutiewe sarkomeriese funksionering is, ‘n groter kapasitieit het om dit en uiteindelik die LVH fenotiepe in HKM, te moduleer. Aanneemlike kandidaat-modifiseerders sou insluit faktore wat betrekking het tot die struktuur en funksie van die sarkomeer insluitend HKM-oorsaaklike gene en die ensieme wat funksioneer in sarkomeer-gebaseerde energetika. Die literatuur beklemtoon inderdaad die relevansie van sarkomeriese proteïene, Ca2+-hantering en miokardiese energetika in die ontwikkeling van LVM in HKM. Hierdie studie het beoog om die hipertrofie-modifiserende kapasiteit van sulke faktore te evalueer deur middel van familie-gebaseerde genetiese assosiasie toetse in 27 Suid-Afrikaanse HKM families waarin een van drie unieke HKM-stigter mutasies segregeer. Verder was die enkel en gekombineerde effekte van 76 variante binne 26 kandidaat gene wat kodeer vir sarkomeer en sarkomeer-geassosieerde proteïene, ondersoek. Hierdie studie het ‘n modifiserende rol in die ontwikkeling van hipertrofie in HKM geïdentifiseer vir elk van die kandidaat gene wat ondersoek is, met uitsluiting van die PRKAG1, wat kodeer vir ‘n metaboliese proteïen. Meer spesifiek, enkel variant assosiasie analises het ‘n modifiserende rol geïdentifiseer vir variante in die gene MYH7, TPM1 en MYL2, wat kodeer vir sarkomeriese proteïene, asook die gene CPT1B, CKM, ALDOA en PRKAB2, wat kodeer vir metabolise proteïene. Haplotipe-gebaseerde assosiasie-analises het gekombineerde modifiserende effekte geïdentifiseer vir variante in die gene ACTC, TPM1, MYL2, MYL3 en MYBPC3, wat kodeer vir strukturele proteïene van die sarkomeer asook die gene CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 en PRKAG3, wat kodeer vir metabolise proteïene. Verder het ‘n aantal variante en haplotipes statisties betekenisvolle verskille in effek tussen die drie HKM-stigter mutasie groepe getoon. Die HKM-modifiserende gene wat geïdentifiseer is, is verder geprioritiseer vir toekomstige studies volgens die aantal beduidende resultate wat vir die vier assosiasie toetse verkry is. Die gene TPM1 and MYBPC3, wat kodeer vir sarkomeriese proteïene, asook die gene PFKM and PRKAG2, wat kodeer vir metaboliese proteïene, is geïdentifiseer as sterker kandidate vir verdere studies omdat veelvuldige beduidende resultate vir die verskeie statistiese toetse deur hulle gelewer is. Hierdie studie maak ‘n nuwe bydrae tot die veld van hipertrofie navorsing omdat dit die hipotese dat strukturele en energie-verwante faktore, wat binne die sarkomeer geposisioneer is, potensieel as modifiseerders van kardiale hipertropfie in HKM kan optree, ondersoek het. Dit slaag ook daarin om ‘n modifiserende rol vir baie van die geselekteerde kandidaatgene te identifiseer. Die beduidende resultate sluit in aansienlike enkel en binne-geen-konteks variant-effekte en aansienlike variasie in die risiko vir LVH ontwikkeling verskuldig aan die gekombineerde effek van modifiseerder en individuele stigter mutasies. Gesamentlik verbeter hierdie bevindinge die huidige begrip van genotipe/fenotipe korrelasies en dit mag tot gevolg hê verbeterde pasiënt risiko stratifikasie en keuse van behandeling. Verder beklemtoon hierdie bevindinge die potensiaal vir siekte modulering deur verdere uitpluis van sekere van hierdie geïdentifiseerde navorsingsrigtings.
National Research Foundation
Dr. Paul van Helden
Stellenbosch University
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2

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 of the molecular changes associated with each condition. The thesis also examined the effect of dietary supplementation of L-arginine to the pathological model, a treatment that has been shown to ameliorate/prevent many of the cardiovascular impairments. Studies examined selected candidate genes (qRT-PCR), including conventional biomarkers of hypertrophy and exploratory analysis of adenosine-related genes (given adenosine’s established regulatory and protective role in the heart, yet minimally studied in cardiac hypertrophy), and explored global transcriptomic shifts via microarrays. The hypothesis of this work was that cardiac hypertrophy lies on a continuum, with similarities existing at the cardiac transcriptional level between early (adaptive) stages of pathological hypertrophy (DOCA-salt rat) and later stages of physiological hypertrophy (endurance run-trained rat). Examination of ten biomarkers of hypertrophy (ANF, BNP, -MHC, -MHC, cardiac -actin, skeletal -actin, SERCA2, PPAR, Coll I and III) revealed that the pathological model displayed alterations in the expression of many of these molecules in line with the literature. These changes were not observed in the physiological model. This therefore reinforces the value of conventional biomarkers in delineating pathological vs. physiological hypertrophies, and reveals fundamental differences in genesis of these two forms of hypertrophy. The adenosine system (receptors and purine handling molecules) was altered in the pathological hypertrophy model as evidenced by the modulation of genes corresponding to A3AR, Ada, and Adk, with a potential shift from purine salvage towards degradation of adenosine to inosine. Furthermore, this study represents the first report of altered regulation of the nucleoside transporter ENT3 in a pathological condition. None of these changes were seen in the physiological model with only modulation of the A2aAR evident. Examination of the transcriptional response to physiological hypertrophy revealed that short (6 week) and long (12 week) training programmes resulted in different profiles, likely reflecting progression of the hypertrophy process. The short programme stimulated genes associated with the mitochondria, oxidoreductase, receptor binding and coenzymemetabolismand repressed the expression of transcripts associated with phosphorylation, catalytic activity, defence/immunity and energy pathways. Thus, initial changes observed are primarily of a metabolic and signalling nature. In contrast, the longer programme resulted in shifts in protein handling and synthesis, and genes involved in structural molecule activity, nucleotide binding and cellular homeostasis. These patterns support a progression with time from initial metabolic adaptations to longer term shifts in protein phenotype and structural adaptations, consistent with longer term changes in heart structure. Similarly, the pathologicalmodel displayed different time-dependent gene expression profiles. Overall, the pattern of changewith early (2week) treatment is suggestive of changes in intracellular signalling and increasing transcriptional capacity with the later changes (at 4 weeks) indicative of structural adaptations (intra- and extracellularly) togetherwith an inflammation response. Genes coding for calciumhandling, ion channels, and gap junctions were altered throughout themodel andmay contribute to electrical conduction defects and cardiac dysfunction. The adrenergic signalling pathway was modulated as associated signalling molecules were down-regulated. The study revealed many expected and novel changes, of which further study should focus on: calcium regulation, metabolic regulation, gap junctions, and (as might be exii pected) signalling via the adrenergic pathway, insulin-like growth factor, PI3K, and Jak/STAT. L-Arginine modulated biomarker expression in pathological hypertrophy, with stimulation of PPAR and SERCA2 with little or no effect on the adenosine-related genes. L-Arginine affected the overall transcriptional response to DOCA-salt treatment, stimulating genes involved in cell growth andmaintenance, nerve transmission, heparin and glycosaminoglycan binding, peptide binding and protein targeting, as well as the repression of genes related to apoptosis (favouring a pro-apoptotic state), intracellular organisation and biogenesis, and enzyme inhibitor activity. The beneficial effects of L-arginine in the setting of pathological hypertrophy may be due to modulation of metabolism, improving calcium handling and overall enhancing cellular functioning. This work demonstrates that cardiac hypertrophy is clearly different at the transcriptional level depending upon the aetiology. This repudiated the hypothesis of the thesis that cardiac hypertrophy lies on a continuum with similarities existing at the cardiac transcriptional level between early (adaptive) stages of pathological hypertrophy and later stages of physiological hypertrophy. Whilst some of the data was in accordance with current knowledge of these states, novel changes were also discovered, contributing to our understanding of the molecular aspects of cardiac hypertrophy.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
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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 programme justifies the stringent criteria set by Wilson and Jungner (1968) to evaluate any proposed programme, could be tested. The hypothesis has to be rejected after taking all the criteria into account. BPH was a major health problem among apparently well middle-age and elderly men in the community. It imposed significant interference in men's daily routine as well as influenced on their psychological general well-being. Although there was a detectable asymptomatic stage, the natural history of BPH from asymptomatic to a clinical stage was not clear. Because of the obscurity of the natural history, the optimum interval between repeated screens of a continuous screening process was unknown. The facilities for diagnosis and treatment could not be met by the present health services. The economic implications of a screening programme could be enormous, though a systemic analysis to evaluate the worthwhileness of the screening programme in economic terms was not conducted.
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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 reduced functional capacity by becoming hypertrophic, but eventually becomes fibrotic and develops dilated cardiomyopathy. Several proposed therapies have now reached clinical trial phase, but there is still no cure available for all DMD patients. Some of these therapies target skeletal muscle better than the heart. Sample availability restricts research into cardiac mechanisms of disease and testing treatments. This thesis presents a model that can potentially be used as an in vitro outcome measure for testing DMD therapies. Cardiomyocytes isolated from hearts collected from the DMD mouse model (mdx) embryos became larger than control mouse embryo-derived cardiomyocytes in response to serum starvation in culture. Control and mdx cardiomyocytes were collected at five timepoints of serum starvation and RNA-Seq was performed on the samples to identify pathways responsible for this hypertrophic response observed in dystrophic cells. Several pharmacological compounds as well as a proposed gene therapy method were trialled for their ability to reduce the hypertrophic response. Serum starved cardiomyocytes from mdx mouse embryos were transduced with adeno-associated viruses containing a gene construct expressing a functional internally truncated version of dystrophin. The viral rescue therapy and some pharmacological compounds significantly reduced the dystrophic hypertrophy caused by serum starvation. This model of mdx cardiomyocyte hypertrophy could therefore be used for testing therapies in pre-clinical trials.
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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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Books on the topic "Hypertrophy"

1

J, Sheridan Desmond, ed. Left ventricular hypertrophy. London: 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. Washington, D.C: 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. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3.

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Sever, Peter S. Left ventricular hypertrophy. London: 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. Boston, MA: 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.l: s.n., 1985.

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

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

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

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

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Book chapters on the topic "Hypertrophy"

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Capinera, John L., Thomas O. Crist, John B. Heppner, Minos E. Tzanakakis, Severiano F. Gayubo, Aurélien Tartar, Pauline O. Lawrence, et al. "Hypertrophy." In Encyclopedia of Entomology, 1901. Dordrecht: 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, 1760. Cham: 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, 1123. Cham: 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, Jeffrey S. Gonzalez, Jeffrey S. Gonzalez, Erica Shreck, Abigail Batchelder, et al. "Hypertrophy." In Encyclopedia of Behavioral Medicine, 1013–14. New York, NY: 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, 1. Cham: 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, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble, et al. "Hypertrophy." In Encyclopedia of Exercise Medicine in Health and Disease, 424. Berlin, Heidelberg: 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, 169–76. London: 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, 1284. New York, NY: 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, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Hypertrophy." In Encyclopedia of Molecular Mechanisms of Disease, 955–56. Berlin, Heidelberg: 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, 123–33. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5385-4_14.

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Conference papers on the topic "Hypertrophy"

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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 between NHE1 and SGLT1/SGLT2 in a non-diabetic in vitro model. We characterized H9c2 cardiomyoblasts stimulated with Angiotensin II (ANG II) 100nM in the presence and absence of EMPA (500nM) and measured cardiomyocyte hypertrophy and the expression of NHE1 and SGLT1/2. Stimulation of H9c2 cardiomyoblasts with ANG II (100nM) resulted in cardiomyocyte hypertrophy, an effect that was regressed in the presence of EMPA (500nM). No changes in SGLT2 and NHE1 protein expression were detected in H9c2 cardiomyoblasts. However, stimulation with ANG II in the presence of EMPA reduced the expression of SGLT1. We demonstrate that the inhibition of SGLT using EMPA following stimulation with ANG II, a hypertrophic stimulator of cardiomyocyte hypertrophy and NHE1, regressed the hypertrophic response of H9c2 cardiomyoblasts and SGLT1 protein expression. The inhibition of SGLT1 protein expression may be contributing to the anti-hypertrophic effect of EMPA. Whether EMPA reduces NHE1 activity remains to be elucidated.
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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 growth will lead to a better understanding of the disease mechanisms, which in turn has the potential to lead to better treatment strategies.
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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. Southampton, UK: 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 can influence chondrogenesis of MSCs and neocartilage formation [3]. Recent studies have also demonstrated that dynamic compression enhances the expression of chondrogenic markers and cartilage matrix synthesis by MSCs encapsulated in various hydrogels, including agarose [4], alginate [5] and fibrin [6]. Furthermore, mechanical signals also regulate growth plate and articular cartilage chondrocyte hypertrophy via the IHH-PTHrP (India hedgehog, Parathyroid hormone-related protein) pathway [7]. In contrast to biologically inert scaffold materials, HA is capable of interacting with cells (including MSCs) via cell surface receptors (CD44, CD54, and CD168) [8; 9]. Therefore the objectives of this study were to (i) evaluate the effects of both hydrogel crosslinking and dynamic compressive loading on (i) chondrogenesis and cartilage matrix production/distribution of human MSCs encapsulated in HA gels and (ii) hypertrophic differentiation of human MSCs using an in vitro MSC hypertrophy model [10].
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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)). Paris, France: 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, Andreas Seraphim, George Joy, Saidi Mohiddin, Gabriella Captur, Luis R. Lopes, Peter Kellman, and James C. Moon. "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, Nasibeh Farahani, Moein Enayati, Jeffrey B. Geske, Michael J. Ackerman, 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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Tozatto Zago, Gabriel, Rodrigo Varejão Andreão, and Mario Sarcinelli Filho. "ECG-based Detection of Left Ventricle Hypertrophy." In International Congress on Cardiovascular Technologies. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0005069600170021.

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Sutar, Rajendra G., and A. G. Kothari. "Detection of cardiac hypertrophy by ECG analysis." In 2012 International Conference on Communication, Information & Computing Technology (ICCICT). IEEE, 2012. http://dx.doi.org/10.1109/iccict.2012.6398192.

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Reports on the topic "Hypertrophy"

1

Kraemer, William J. Strategies for Optimizing Strength, Power, and Muscle Hypertrophy in Women. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada348669.

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

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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, February 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 studies that met the inclusion criteria.
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Currier, Brad, Maria Fiatarone Singh, Caroline Lowisz, Eric Rawson, Brad Schoenfeld, Abbie Smith-Ryan, Jeremy Steen, 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, June 2023. http://dx.doi.org/10.37766/inplasy2023.6.0071.

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Leblanc, Samuel. The optimal range of motion for hypertrophy:<br>A review of the literature. ResearchHub Technologies, Inc., August 2022. http://dx.doi.org/10.55277/researchhub.56zv24z4.

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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, February 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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Kraemer, William J. Strategies for Optimizing Strength, Power, and Muscle Hypertrophy in Women: Contribution of Upper Body Resistance Training. Fort Belvoir, VA: Defense Technical Information Center, November 1999. http://dx.doi.org/10.21236/ada371349.

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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, May 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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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, November 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 driven by higher rates of feed intake and metabolism, resulting in elevated internal heat production. Hot rearing conditions negatively affect broiler growth by hindering dissipation of heat and may lead to a lethal elevation in body temperature. To avoid heat-induced mortality, broilers reduce feed intake, leading to depressed growth rate, lower weight gain, reduce breast meat yield and quality. Thus, the genetic potential of contemporary commercial broilers (CCB) is not fully expressed under hot conditions. Major conclusions, solutions, and achievementsResearch conducted in Israel focused on three broiler strains – CCB, Featherless, Feathered sibs (i.e., sharing similar genetic background). Complimentary research trials conducted at Auburn utilized CCB (Cobb 500, Cobb 700, Ross 308, Ross 708), contrasting their performance to slow growing strains. Warm rearing conditions consistently reduced feed intake, growth rate, feed efficiency, body weight uniformity and breast muscle yield, especially pronounced with CCB and magnified with age. Breast meat quality was also negatively affected, as measured by higher drip loss and paler meat color. Exposure to continuous or short-term heat stress induced respiratory alkalosis. Breast muscle histomorphometrics confirmed enhanced myofiber hypertrophy in CCB. Featherless broilers exhibited a significant increase in blood-vessel density under warm conditions. Rapid growth and muscle accretion rate was correlated to various myopathies (white striping, woody and necrotic) as well as to increases in plasma creatinekinase levels. Whether the trigger(s) of muscle damage is loss of cellular membrane integrity due to oxidative damage or tissue lactate accumulation, or to loss of inter-compartmental cation homeostasis is yet to be determined. Based on genome-wide single-nucleotide polymorphism array genotyping, identification of the gene with the recessive mutation Scaleless (sc) facilitated the development a dCAPS assay to discriminate between sc carrier (sc/+) and non-carrier (+/+) individuals. ImplicationsThis project confirmed that featherless broiler strains grow efficiently with high yield and quality of breast meat, even under warm rearing conditions that significantly depress the overall performance of CCB. Therefore, broiler meat production in hot regions and climates can be substantially improved by introducing the featherless gene into contemporary commercial broiler stocks. This approach has become more feasible with the development of dCAPS assay. A novel modification of the PCR protocol (using whole blood samples instead of extracted DNA) may contribute to the efficient development of commercial featherless broiler strains. Such strains will allow expansion of the broiler meat production in developing countries in warm climates, where energy intensive environmental control of rearing facilities are not economical and easily achievable.
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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, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0128.

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