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FASEB Journal : Official Publication of... Jul 2024To investigate the effects of heavy-load strength training during (neo-)adjuvant chemotherapy in women with breast cancer on muscle strength, body composition, muscle... (Randomized Controlled Trial)
Randomized Controlled Trial
Effects of heavy-load strength training during (neo-)adjuvant chemotherapy on muscle strength, muscle fiber size, myonuclei, and satellite cells in women with breast cancer.
To investigate the effects of heavy-load strength training during (neo-)adjuvant chemotherapy in women with breast cancer on muscle strength, body composition, muscle fiber size, satellite cells, and myonuclei. Women with stage I-III breast cancer were randomly assigned to a strength training group (ST, n = 23) performing supervised heavy-load strength training twice a week during chemotherapy, or a usual care control group (CON, n = 17). Muscle strength and body composition were measured and biopsies from m. vastus lateralis collected before the first cycle of chemotherapy (T0) and after chemotherapy and training (T1). Muscle strength increased significantly more in ST than in CON in chest-press (ST: +10 ± 8%, p < .001, CON: -3 ± 5%, p = .023) and leg-press (ST: +11 ± 8%, p < .001, CON: +3 ± 6%, p = .137). Both groups reduced fat-free mass (ST: -4.9 ± 4.0%, p < .001, CON: -5.2 ± 4.9%, p = .004), and increased fat mass (ST: +15.3 ± 16.5%, p < .001, CON: +16.3 ± 19.8%, p = .015) with no significant differences between groups. No significant changes from T0 to T1 and no significant differences between groups were observed in muscle fiber size. For myonuclei per fiber a non-statistically significant increase in CON and a non-statistically significant decrease in ST in type I fibers tended (p = .053) to be different between groups. Satellite cells tended to decrease in ST (type I: -14 ± 36%, p = .097, type II: -9 ± 55%, p = .084), with no changes in CON and no differences between groups. Strength training during chemotherapy improved muscle strength but did not significantly affect body composition, muscle fiber size, numbers of satellite cells, and myonuclei compared to usual care.
Topics: Humans; Female; Muscle Strength; Breast Neoplasms; Resistance Training; Satellite Cells, Skeletal Muscle; Middle Aged; Adult; Chemotherapy, Adjuvant; Body Composition; Muscle Fibers, Skeletal; Neoadjuvant Therapy; Aged
PubMed: 38953567
DOI: 10.1096/fj.202400634R -
Small (Weinheim An Der Bergstrasse,... Jul 2024Abdominal aortic aneurysm (AAA) represents a critical cardiovascular condition characterized by localized dilation of the abdominal aorta, carrying a significant risk of...
Abdominal aortic aneurysm (AAA) represents a critical cardiovascular condition characterized by localized dilation of the abdominal aorta, carrying a significant risk of rupture and mortality. Current treatment options are limited, necessitating novel therapeutic approaches. This study investigates the potential of a pioneering nanodrug delivery system, RAP@PFB, in mitigating AAA progression. RAP@PFB integrates pentagalloyl glucose (PGG) and rapamycin (RAP) within a metal-organic-framework (MOF) structure through a facile assembly process, ensuring remarkable drug loading capacity and colloidal stability. The synergistic effects of PGG, a polyphenolic antioxidant, and RAP, an mTOR inhibitor, collectively regulate key players in AAA pathogenesis, such as macrophages and smooth muscle cells (SMCs). In macrophages, RAP@PFB efficiently scavenges various free radicals, suppresses inflammation, and promotes M1-to-M2 phenotype repolarization. In SMCs, it inhibits apoptosis and calcification, thereby stabilizing the extracellular matrix and reducing the risk of AAA rupture. Administered intravenously, RAP@PFB exhibits effective accumulation at the AAA site, demonstrating robust efficacy in reducing AAA progression through multiple mechanisms. Moreover, RAP@PFB demonstrates favorable biosafety profiles, supporting its potential translation into clinical applications for AAA therapy.
PubMed: 38953313
DOI: 10.1002/smll.202402141 -
Frontiers in Immunology 2024Schistosomiasis (SM) is a parasitic disease caused by . SM causes chronic inflammation induced by parasitic eggs, with collagen/fibrosis deposition in the granuloma...
INTRODUCTION
Schistosomiasis (SM) is a parasitic disease caused by . SM causes chronic inflammation induced by parasitic eggs, with collagen/fibrosis deposition in the granuloma process in the liver, spleen, central nervous system, kidneys, and lungs. Pulmonary arterial hypertension (PAH) is a clinical manifestation characterized by high pressure in the pulmonary circulation and right ventricular overload. This study investigated the production of functional autoantibodies (fAABs) against the second loop of the G-protein-coupled receptor (GPCR) in the presence of hepatic and PAH forms of human SM.
METHODS
Uninfected and infected individuals presenting acute and chronic manifestations (e.g., hepatointestinal, hepato-splenic without PAH, and hepato-splenic with PAH) of SM were clinically evaluated and their blood was collected to identify fAABs/GPCRs capable of recognizing endothelin 1, angiotensin II, and a-1 adrenergic receptor. Human serum was analyzed in rat cardiomyocytes cultured in the presence of the receptor antagonists urapidil, losartan, and BQ123.
RESULTS
The fAABs/GPCRs from chronic hepatic and PAH SM individuals, but not from acute SM individuals, recognized the three receptors. In the presence of the antagonists, there was a reduction in beating rate changes in cultured cardiomyocytes. In addition, binding sites on the extracellular domain functionality of fAABs were identified, and IgG1 and/or IgG3 antibodies were found to be related to fAABs.
CONCLUSION
Our data suggest that fAABs against GPCR play an essential role in vascular activity in chronic SM (hepatic and PAH) and might be involved in the development of hypertensive forms of SM.
Topics: Autoantibodies; Humans; Animals; Receptors, G-Protein-Coupled; Rats; Male; Female; Adult; Hypertension, Pulmonary; Middle Aged; Myocytes, Cardiac; Schistosomiasis mansoni; Schistosoma mansoni; Schistosomiasis
PubMed: 38953035
DOI: 10.3389/fimmu.2024.1404384 -
The Canadian Veterinary Journal = La... Jul 2024An 8-year-old castrated male Maltese dog was presented with a urinary bladder mass, urolithiasis, and hematuria. A solitary, pedunculated, intraluminal mass on the...
An 8-year-old castrated male Maltese dog was presented with a urinary bladder mass, urolithiasis, and hematuria. A solitary, pedunculated, intraluminal mass on the caudodorsal wall was identified with extensive irregular bladder wall thickening, and the mass was surgically removed. Postoperative histopathology demonstrated a submucosal lesion comprising spindle cells with marked inflammatory cell infiltration, without malignant changes. Immunohistochemical staining revealed vimentin and desmin positivity in the mass. An inflammatory myofibroblastic tumor (IMT) was definitively diagnosed. No recurrence was observed during a 43-month follow-up period. Although IMTs are rare in dogs, they should be considered a differential diagnosis for mass-like urinary bladder lesions accompanying a chronic inflammatory disease process. Key clinical message: Canine IMT should be included in the differential diagnoses of bladder masses, especially when dogs exhibit chronic irritation and inflammation.
Topics: Dogs; Animals; Male; Dog Diseases; Urinary Bladder Neoplasms; Neoplasms, Muscle Tissue; Diagnosis, Differential; Inflammation
PubMed: 38952766
DOI: No ID Found -
Frontiers in Molecular Biosciences 2024The study of energy transduction in eukaryotic cells has been divided between Bioenergetics and Physiology, reflecting and contributing to a variety of Bioenergetic...
The study of energy transduction in eukaryotic cells has been divided between Bioenergetics and Physiology, reflecting and contributing to a variety of Bioenergetic myths considered here: 1) ATP production = energy production, 2) energy transduction is confined to mitochondria (plus glycolysis and chloroplasts), 3) mitochondria only produce heat when required, 4) glycolysis is inefficient compared to mitochondria, and 5) mitochondria are the main source of reactive oxygen species (ROS) in cells. These myths constitute a 'mitocentric' view of the cell that is wrong or unbalanced. In reality, mitochondria are the main site of energy dissipation and heat production in cells, and this is an essential function of mitochondria in mammals. Energy transduction and ROS production occur throughout the cell, particularly the cytosol and plasma membrane, and all cell membranes act as two-dimensional energy conduits. Glycolysis is efficient, and produces less heat per ATP than mitochondria, which might explain its increased use in muscle and cancer cells.
PubMed: 38952719
DOI: 10.3389/fmolb.2024.1402910 -
International Journal of Nanomedicine 2024Myocardial infarction, usually caused by the rupture of atherosclerotic plaque, leads to irreversible ischemic cardiomyocyte death within hours followed by impaired... (Review)
Review
Myocardial infarction, usually caused by the rupture of atherosclerotic plaque, leads to irreversible ischemic cardiomyocyte death within hours followed by impaired cardiac performance or even heart failure. Current interventional reperfusion strategies for myocardial infarction still face high mortality with the development of heart failure. Nanomaterial-based therapy has made great progress in reducing infarct size and promoting cardiac repair after MI, although most studies are preclinical trials. This review focuses primarily on recent progress (2016-now) in the development of various nanomedicines in the treatment of myocardial infarction. We summarize these applications with the strategy of mechanism including anti-cardiomyocyte death strategy, activation of neovascularization, antioxidants strategy, immunomodulation, anti-cardiac remodeling, and cardiac repair.
Topics: Myocardial Infarction; Humans; Nanomedicine; Animals; Myocytes, Cardiac; Antioxidants; Nanostructures; Neovascularization, Physiologic
PubMed: 38952676
DOI: 10.2147/IJN.S467219 -
Mechanical characterization of porcine ureter for the evaluation of tissue-engineering applications.Frontiers in Bioengineering and... 2024Clinics increasingly require readily deployable tubular substitutes to restore the functionality of structures like ureters and blood vessels. Despite extensive...
Clinics increasingly require readily deployable tubular substitutes to restore the functionality of structures like ureters and blood vessels. Despite extensive exploration of various materials, both synthetic and biological, the optimal solution remains elusive. Drawing on abundant literature experiences, there is a pressing demand for a substitute that not only emulates native tissue by providing requisite signals and growth factors but also exhibits appropriate mechanical resilience and behaviour. This study aims to assess the potential of porcine ureters by characterizing their biomechanical properties in their native configuration through ring and membrane flexion tests. In order to assess the tissue morphology before and after mechanical tests and the eventual alteration of tissue microstructure that would be inserted in material constitutive description, histological staining was performed on samples. Corresponding computational analyses were performed to mimic the experimental campaign to identify the constitutive material parameters. The absence of any damages to muscle and collagen fibres, which only compacted after mechanical tests, was demonstrated. The experimental tests (ring and membrane flexion tests) showed non-linearity for material and geometry and the viscoelastic behaviour of the native porcine ureter. Computational models were descriptive of the mechanical behaviour ureteral tissue, and the material model feasible. This analysis will be useful for future comparison with decellularized tissue for the evaluation of the aggression of cell removal and its effect on microstructure. The computational model could lay the basis for a reliable tool for the prediction of solicitation in the case of tubular substitutions in subsequent simulations.
PubMed: 38952671
DOI: 10.3389/fbioe.2024.1412136 -
Cureus Jun 2024Guillain-Barré syndrome (GBS) resulting from the use of immune checkpoint inhibitors (ICIs) is relatively uncommon but has been reported. Herein, we discuss a case of...
Guillain-Barré syndrome (GBS) resulting from the use of immune checkpoint inhibitors (ICIs) is relatively uncommon but has been reported. Herein, we discuss a case of a 67-year-old patient who received neoadjuvant ICI for treatment of non-small cell lung cancer and then presented with lower extremity weakness and areflexia, progressing to respiratory muscle and upper extremity weakness. Given the increasing use of ICI in cancer management, awareness of neurological autoimmune side effects is essential. ICI-mediated GBS can be severe and fatal if not diagnosed promptly. We discuss a case of ICI-induced GBS and review literature on current management approaches.
PubMed: 38952584
DOI: 10.7759/cureus.61489 -
Frontiers in Cardiovascular Medicine 2024In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged.... (Review)
Review
In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. However, it has been long recognized that diffuse intimal thickening (DIM), which precedes the formation of early fatty streaks in humans, primarily consists of lipid-loaded smooth muscle cells (SMCs) and their secreted proteoglycans. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques. Given that SMCs are a major component of the vascular wall, they serve as a significant source of microvesicles and exosomes, which have the potential to regulate the physiology of other vascular cells. Notably, more than half of the foam cells present in atherosclerotic lesions are of SMC origin. In this review, we describe several mechanisms underlying the formation of intimal foam-like cells in atherosclerotic plaques. Based on these mechanisms, we discuss novel therapeutic approaches that have been developed to regulate the generation of intimal foam-like cells. These innovative strategies hold promise for improving the management of atherosclerosis in the near future.
PubMed: 38952543
DOI: 10.3389/fcvm.2024.1381520 -
Renal Failure Dec 2024Abnormal renal lipid metabolism causes renal lipid deposition, which leads to the development of renal fibrosis in diabetic kidney disease (DKD). The aim of this study...
AIMS
Abnormal renal lipid metabolism causes renal lipid deposition, which leads to the development of renal fibrosis in diabetic kidney disease (DKD). The aim of this study was to investigate the effect and mechanism of chlorogenic acid (CA) on reducing renal lipid accumulation and improving DKD renal fibrosis.
METHODS
This study evaluated the effects of CA on renal fibrosis, lipid deposition and lipid metabolism by constructing and models of DKD, and detected the improvement of Notch1 and Stat3 signaling pathways. Molecular docking was used to predict the binding between CA and the extracellular domain NRR1 of Notch1 protein.
RESULTS
studies have shown that CA decreased the expression of Fibronectin, α-smooth muscle actin (α-SMA), p-smad3/smad3, alleviated lipid deposition, promoted the expression of carnitine palmitoyl transferase 1 A (CPT1A), and inhibited the expression of cholesterol regulatory element binding protein 1c (SREBP1c). The expression of Notch1, Cleaved Notch1, Hes1, and p-stat3/stat3 were inhibited. These results suggested that CA might reduce intercellular lipid deposition in human kidney cells (HK2) by inhibiting Notch1 and stat3 signaling pathways, thereby improving fibrosis. Further, studies demonstrated that CA improved renal fibrosis and renal lipid deposition in DKD mice by inhibiting Notch1 and stat3 signaling pathways. Finally, molecular docking experiments showed that the binding energy of CA and NRR1 was -6.6 kcal/mol, which preliminarily predicted the possible action of CA on Notch1 extracellular domain NRR1.
CONCLUSION
CA reduces renal lipid accumulation and improves DKD renal fibrosis by inhibiting Notch1 and stat3 signaling pathways.
Topics: STAT3 Transcription Factor; Receptor, Notch1; Diabetic Nephropathies; Animals; Signal Transduction; Fibrosis; Chlorogenic Acid; Humans; Mice; Male; Kidney; Lipid Metabolism; Molecular Docking Simulation; Mice, Inbred C57BL; Diabetes Mellitus, Experimental; Cell Line
PubMed: 38952291
DOI: 10.1080/0886022X.2024.2371988