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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
An increase in the size of an organ or tissue due to an enlargement of its component cells is known as hypertrophy (Figure 5.7). Parasite-induced hypertrophy is a well-known phenomenon. For example, monocytes infected with Leishmania become hypertrophic. In Chagas disease patients, cardiac muscle cells undergo hypertrophy in response to Trypanosoma cruzi infection. During the hypertrophic response, there is an increased expression for contractile proteins in the host cells, followed by a doubling of cell size. Interleukin 1β, which is expressed rapidly upon the initial establishment of a T. cruzi infection, appears to promote the hypertrophic response.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
HFpEF refers to a failure of diastolic function; the heart is unable to adequately fill with blood during diastole, but is still able to eject a good proportion of this reduced amount as stroke volume. HFpEF can be due to: Stenosis of the mitral or tricuspid valve, preventing blood from flowing into the ventricle during diastole.Changes in the compliance (or distensibility) of the ventricular myocardium, so that it does not expand as the ventricle fills with blood. A poorly compliant ventricle will have a reduced volume of blood at the end of diastole, and therefore will eject a smaller amount during systole, leading to a reduced cardiac output.Ventricular hypertrophy may occur in response to some heart problems; the ventricular wall becomes thicker and less compliant. Hypertrophy can occur in patients with a history of hypertension, valve problems and/or renal failure, as the myocardium adapts to increased stress on the ventricular wall.
Reducing Aging-associated Risk of Sarcopenia
Published in James M. Rippe, Lifestyle Medicine, 2019
Resistance training is the most effective approach known for increasing muscle hypertrophy and strength at all stages of life, including in frail, elderly individuals.7,74 However, the increase in muscle mass and strength with resistance training is specific to the muscle groups involved in the training and is less effective in older, as compared with younger people, and in older women as compared with men of the same age. Furthermore, a larger volume of exercise is required for maintenance of induced hypertrophy in older as compared with younger adults.74 As discussed later in the section on nutritional support, there is evidence accumulating that an increase in protein intake in proximity to an exercise session can enhance training-induced muscle hypertrophy. The associated training-induced muscle fiber hypertrophy appears to primarily affect the type IIb slow twitch fibers, which are primarily affected by aging. There is a concern, however, based on recent studies, that simultaneous sessions of aerobic and resistance training may blunt the hypertrophy response to resistance training.75 This observation required confirmation, and if it is correct, there is a need to establish the optimal period between sessions of these two forms of exercise.
Comparison between stromal vascular fraction and adipose derived stem cells in a mouse lymphedema model
Published in Journal of Plastic Surgery and Hand Surgery, 2020
Amar Bucan, Pratibha Dhumale, Mads Gustaf Jørgensen, Farima Dalaei, Alexander Wiinholt, Christian Rønn Hansen, Svend Hvidsten, Christina Baun, Eva Kildall Hejbøl, Henrik Daa Schrøder, Jens Ahm Sørensen
The mean volume of the operated hindlimbs after 8 weeks in the NS (control) group was less than our previous study [13]. This difference could be due to a number of factors such as differences in operating technique, experience, animals, radiation delivery and the scar releasing treatment. It is possible that by using three different surgeons our operating technique would slightly differ resulting in various lymphedema volumes. However, as the mice were randomized, any difference in surgery should, therefore, be diminished. It is further speculated that the mice were more inclined to use their unoperated hindlimb post-surgery, and that it might have induced hypertrophy leading to a higher volume in the unoperated hindlimb, hence decreasing the difference between the lymphedema hindlimb and the control hindlimb. In fact, there was a statistically significant difference between the volumes of the unoperated hindlimbs of the mice in week eight vs. week one (Table 4) (p = 0.0115) 95% CI [2.3605, 18.1595]. Whether the difference is due to hypertrophy is unclear.
Masked hypertension is associated with end organ damage in geriatric age: Geriatric MASked Hypertension and End organ damage (G-MASH-End organ Study)
Published in Blood Pressure, 2020
Mert Esme, Serkan Asil, Bunyamin Yavuz, Cafer Balci, Mustafa Kemal Kılıç, Muhammed Cemal Kızılarslanoğlu, Hacer Doğan Varan, Rana Tuna Doğrul, Meltem Halil, Mustafa Cankurtaran, Burcu Balam Yavuz
One of the parameters showing end organ damage and showing the negative effect of hypertension on the heart is the LVMI. LVMI calculated according to the formula was 86 (60–127)g/m2 in all patients. It was calculated as 91 (63–121) g/m2 in the MH group and 83.5 (60–127)g/m2 in the normal group. Among the two groups, LVMI of MH group was significantly higher (p = .017). The relationship between MH and LVMI is shown in Figure 2. LVMI value above 115 g/m2 was accepted as hypertrophy in men. In women, LVMI value above 95 g/m2 was accepted as hypertrophy. Accordingly, there were 3 patients above the reference value in men and 11 patients in women. A total of 14 patients had hypertrophy. There was no significant difference between patients with and without MH regarding hypertrophy.
The role of Thymosin β4 in angiotensin II-induced cardiomyocytes growth
Published in Expert Opinion on Biological Therapy, 2018
Cardiac hypertrophy is an adaptive response to hemodynamic stress and has a compensatory role to trigger cardiac performance [1]; however, it poses a risk for the development of heart failure. At the cellular level, cardiomyocytes hypertrophy is characterized by an increase in cell size and not in cell numbers, enhanced protein synthesis, and sarcomere organization [2–4]. At the molecular level, hypertrophic growth of the myocardium is associated with increased fetal gene expression (ANF and β-MHC), multiple protein signal transduction cascade activation that demonstrates a high degree of cellular and molecular coordination [5]. Although the initial adaptive mechanism is beneficial, prolonged hypertrophy is potentially disastrous, leading to heart failure and death. Additionally, inadequate supply–demand of the myocardium secondary to increased myocardial oxygen consumption of the hypertrophic heart further predisposes to associated cardiovascular ailments, such as arrhythmias, myocardial infarction (MI), and sudden death [6]. The requirement for insight in cardiac hypertrophy is therefore essential as there is no specific therapeutic agent that can be used to treat this disease.