Publications by authors named "No M"

Shape memory alloys (SMAs) are functional materials with a wide range of applications, from the aerospace sector to the biomedical field. Nowadays, there is a worldwide interest in developing SMAs through powder metallurgy like additive manufacturing (AM), which allows innovative building processes. However, producing SMAs using AM techniques is particularly challenging because of the microstructure required to obtain optimal functional properties.

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Additive manufacturing (AM) constitutes the new paradigm in materials processing and its use on metals and alloys opens new unforeseen possibilities, but is facing several challenges regarding the design of the microstructure, which is particularly awkward in the case of functional materials, like shape memory alloys (SMA), as they require a robust microstructure to withstand the constraints appearing during their shape change. In the present work, the attention is focused on the AM of the important Fe-Mn-Si-based SMA family, which is attracting a great technological interest in many industrial sectors. Initially, an overview on the design concepts of this SMA family is offered, with special emphasis to the problems arising during AM.

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Cu-Al-Ni is a high-temperature shape memory alloy (HTSMA) with exceptional thermomechanical properties, making it an ideal active material for engineering new technologies able to operate at temperatures up to 200 °C. Recent studies revealed that these alloys exhibit a robust superelastic behavior at the nanometer scale, making them excellent candidates for developing a new generation of micro-/nano-electromechanical systems (MEMS/NEMS). The very large-scale integration (VLSI) technologies used in microelectronics are based on thin films.

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An accurate knowledge of the optical properties of β-GaO is key to developing the full potential of this oxide for photonics applications. In particular, the dependence of these properties on temperature is still being studied. Optical micro- and nanocavities are promising for a wide range of applications.

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Adverse effects of spaceflight on the human body are attritubuted to microgravity and space radiation. One of the most sensitive organs affected by them is the eye, particularly the retina. The conditions that astronauts suffer, such as visual acuity, is collectively called a spaceflight-associated neuro-ocular syndrome (SANS); however, the underlying molecular mechanism of the microgravity-induced ocular pathogenesis is not clearly understood.

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Shape memory alloys (SMAs) are functional materials that are being applied in practically all industries, from aerospace to biomedical sectors, and at present the scientific and technologic communities are looking to gain the advantages offered by the new processing technologies of additive manufacturing (AM). However, the use of AM to produce functional materials, like SMAs, constitutes a real challenge due to the particularly well controlled microstructure required to exhibit the functional property of shape memory. In the present work, the design of the complete AM processing route, from powder atomization to laser powder bed fusion for AM and hot isostatic pressing (HIP), is approached for Cu-Al-Ni SMAs.

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Anticancer nucleoside analogs produce adverse, and at times, dose-limiting hematological toxicities that can compromise treatment efficacy, yet the mechanisms of such toxicities are poorly understood. Recently, cellular nucleoside transport has been implicated in normal blood cell formation with studies from nucleoside transporter-deficient mice providing additional insights into the regulation of mammalian hematopoiesis. Furthermore, several idiopathic human genetic disorders have revealed nucleoside transport as an important component of mammalian hematopoiesis because mutations in individual nucleoside transporter genes are linked to various hematological abnormalities, including anemia.

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Article Synopsis
  • Chronic cerebral hypoperfusion (CCH) leads to decreased blood flow to the brain, resulting in cognitive decline and neuronal death due to mitochondrial dysfunction.
  • The study investigated the neuroprotective effects of low-intensity treadmill exercise (LITE) on cognitive impairment in an animal model, specifically in Wistar rats with induced CCH.
  • Findings showed that LITE improved mitochondrial function, preserved cerebellar Purkinje cells, and helped maintain spatial working memory, suggesting that exercise could be a potential intervention for cognitive issues related to CCH.
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Remote temperature sensing at the micro- and nanoscale is key in fields such as photonics, electronics, energy, or biomedicine, with optical properties being one of the most used transducing mechanisms for such sensors. Ga O presents very high chemical and thermal stability, as well as high radiation resistance, becoming of great interest to be used under extreme conditions, for example, electrical and/or optical high-power devices and harsh environments. In this work, a luminescent and interferometric thermometer is proposed based on Fabry-Perot (FP) optical microcavities built on Cr-doped Ga O nanowires.

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The purpose of this study is to determine whether moderate aerobic exercise training improves high-fat diet-induced alterations in mitochondrial function and structure in the skeletal muscle. Male 4-week-old C57BL/6 mice were randomly divided into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and high-fat diet plus exercise (HFD + EX). After obesity was induced by 20 weeks of 60% HFD, treadmill exercise training was performed at 13-16 m/min, 40-50 min/day, and 6 days/week for 12 weeks.

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In this Letter, we report optical confinement in the near-ultraviolet (near-UV) range in nanowires (NWs) by distributed Bragg reflector (DBR) nanopatterned cavities. High-contrast DBRs, which act as the end mirrors of the cavities of the desired length, are designed and fabricated by focused ion beam etching. The resonant modes of the cavities are analyzed by micro-photoluminescence measurements, analytical models, and simulations, which show very good agreement between each other.

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Sarcopenia, a syndrome commonly seen in elderly populations, is often characterized by a gradual loss of skeletal muscle, leading to the decline of muscle strength and physical performance. Growing evidence suggests that the prevalence of sarcopenia increases in patients with heart failure (HF), which is a dominant pathogenesis in the aging heart. HF causes diverse metabolic complications that may result in sarcopenia.

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Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart.

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Article Synopsis
  • Statins, like atorvastatin, can help prevent heart disease but may cause muscle issues and mitochondrial problems.
  • A study with Wistar rats found that combining atorvastatin treatment with aerobic exercise improved glucose tolerance, muscle strength, and reduced muscle damage compared to rats only on atorvastatin.
  • Exercise training also appears to help preserve mitochondrial function and increase certain protective proteins in the muscles affected by atorvastatin.
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Sarcopenia is defined as the involuntary loss of skeletal muscle mass and function with aging and is associated with several adverse health outcomes. Recently, the disruption of regular circadian rhythms, due to shift work or nocturnal lifestyle, is emerging as a novel deleterious factor for the development of sarcopenia. The underlying mechanisms responsible for circadian disruption-induced sarcopenia include molecular circadian clock and mitochondrial function associated with the regulation of circadian rhythms.

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Aging is associated with vulnerability to cardiovascular diseases, and mitochondrial dysfunction plays a critical role in cardiovascular disease pathogenesis. Exercise training is associated with benefits against chronic cardiac diseases. The purpose of this study was to determine the effects of aging and treadmill exercise training on mitochondrial function and apoptosis in the rat heart.

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This study aimed to determine the effects of a single bout exercise on mitochondria-mediated apoptotic signaling in cardiac and skeletal muscles. Fischer 344 rats (4 months old) were randomly divided into the control or a single bout of exercise group (n=10 each). The rats performed a single bout of treadmill exercise for 60 min.

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Purpose: Chemotherapy is associated with the side effects including damage to the mitochondrial DNA. Doxorubicin (DOX) serves as a chemotherapeutic agent for the patients with breast cancer or prostate cancer. DOX causes muscle weakness and fatigue.

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Article Synopsis
  • - This study examined how a single session of exercise impacts mitochondrial function, dynamics, and mitophagy in the heart and skeletal muscles of Fischer 344 rats.
  • - The rats that exercised showed improved mitochondrial oxygen respiration and calcium retention, but mitochondrial fusion and fission were unchanged, with varied effects on mitophagy across different muscle types.
  • - The findings suggest that aerobic exercise enhances certain aspects of mitochondrial function without affecting the overall dynamics or the process of cleaning up damaged mitochondria.
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Article Synopsis
  • * This study examined how aging affects mitochondrial function in the hearts of different age groups of male Fischer 344 rats.
  • * Results showed that aging reduces essential mitochondrial proteins and increases reactive oxygen species production, while decreasing calcium retention capacity, indicating that mitochondrial dysfunction is a key factor in age-related heart issues.
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Article Synopsis
  • Obesity leads to changes in skeletal muscle and increased apoptosis (cell death) associated with mitochondria, which can negatively affect muscle function.
  • A study used four groups of mice to examine how exercise influences muscle structure and cell death in the context of obesity induced by a high-fat diet.
  • The findings indicate that exercise helps improve muscle structure and reduces apoptosis in obese mice, highlighting its potential protective effects on skeletal muscle health.
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Sarcopenia is an age-associated decline of skeletal muscle mass and function and is known to lead to frailty, cachexia, osteoporosis, metabolic syndromes, and death. Notwithstanding the increasing incidence of sarcopenia, the molecular and cellular mechanisms driving age-related sarcopenia are not completely understood. This article reviews current definitions of sarcopenia, its potential mechanisms, and effects of exercise on sarcopenia.

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Ursolic acid (UA) is a natural triterpene compound found in various fruits and vegetables. There is a growing interest in UA because of its beneficial effects, which include anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-carcinogenic effects. It exerts these effects in various tissues and organs: by suppressing nuclear factor-kappa B signaling in cancer cells, improving insulin signaling in adipose tissues, reducing the expression of markers of cardiac damage in the heart, decreasing inflammation and increasing the level of anti-oxidants in the brain, reducing apoptotic signaling and the level of oxidants in the liver, and reducing atrophy and increasing the expression levels of adenosine monophosphate-activated protein kinase and irisin in skeletal muscles.

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Although chemotherapy increases the survival rate of patients with various cancers, such treatment can induce acute or long-term cognitive dysfunction a phenomenon known as post-chemotherapy cognitive impairment (PCCI) or "chemobrain." Exercise is known to positively affect brain function. Thus, the present study aimed to determine whether symptoms of chemobrain and disruptions in the neuroplasticity and functioning of hippocampal mitochondria can be prevented or relieved by exercise.

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Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes.

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