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doi：10.3969/j.issn.1672⁃6731.2021.10.013

The study aimed to evaluate the effects of an expressive writing intervention on quality of life (QoL) among mainland Chinese breast cancer patients. A total of 118 Chinese breast cancer patients were randomly assigned to one of four groups: a cancer-facts writing condition (CTL group), an emotional disclosure writing condition (EMO group), a self-regulation writing condition (SR group), or a neutral control condition with no writing tasks (CON group). QoL was assessed by FACT-B at baseline, 3-, and 6-month follow-ups. A repeated measure analysis of variance revealed significant effects of time (F = 13.9, P < 0.001, [eta].sup.2 = 0.20) and the time x group interaction (F = 3.5, P < 0.01, [eta].sup.2 = 0.08) on QoL. Residualized change models showed that the CTL, EMO and SR groups reported higher levels of QoL than the CON group at the 6-month follow-up. The EMO group had a higher level of QoL than the SR group. The CTL group had higher level of physical well-being compared to the SR group. Mainland Chinese breast cancer patients shortly after diagnosis benefit from expressive writing. They benefited more from cancer-facts and emotional disclosure compared to self-regulation. The study indicated that the impact of expressive writing may differ due to stage of cancer survivorship, social, and cultural context., Author(s): Li-li Ji [sup.1] , Qian Lu [sup.2] [sup.3] , Li-juan Wang [sup.4] , Xiang-lian Sun [sup.4] , Hui-dong Wang [sup.4] , Bing-xue Han [sup.5] , Yu-feng Ma [sup.5] , [...]

Butyrate (BU), a gut microbiota‐derived metabolite, has been reported to play a neuroprotective role in Parkinson's disease (PD). However, the specific molecular mechanism of BU has not been fully interpreted. This work aimed to verify the protective effects of BU against MPTP/MPP+‐induced neurotoxicity and explore the mechanisms involved. The results showed that BU protected against MPTP‐induced motor dysfunction and decreased tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels. Additionally, BU pretreatment improved PC12 cell viability and reduced MPP+‐induced PC12 cell apoptosis. BU treatment also attenuated MPP+‐stimulated oxidative stress and inflammatory response in PC12 cells. Furthermore, BU inhibited MPTP/MPP+‐induced hyperactivation of the JAK2/STAT3 signaling in mice and PC12 cells. Besides, a JAK2 agonist, Coumermycin A1 (C‐A1), substantially reversed BU‐mediated inhibition on JAK2/STAT3 phosphorylation in MPP+‐challenged PC12 cells and abated BU‐induced repression on MPP+‐triggered apoptosis, oxidative stress, and inflammatory response in PC12 cells. To sum up, BU might exert neuroprotective effects against MPP+/MPTP‐induced neurotoxicity by inactivating the JAK2/STAT3 signaling. [ABSTRACT FROM AUTHOR]

Skeletal muscle contraction is associated with the production of ROS due to altered O[subscript 2] distribution and flux in the cell. Despite a highly efficient antioxidant defense, a small surplus of ROS, such as hydrogen peroxide and nitric oxide, may serve as signaling molecules to stimulate cellular adaptation to reach new homeostasis largely due to the activation of redox-sensitive signaling pathways. Recent research has highlighted the important role of NF-?B, MAPK, and peroxisome proliferator-activated receptor-? coactivator-1a, along with other newly discovered signaling pathways, in some of the most vital biological functions, such as mitochondrial biogenesis, antioxidant defense, inflammation, protein turnover, apoptosis, and autophagy. There is evidence that the inability of the cell to maintain proper redox signaling underlies some basic mechanisms of biological aging, during which inflammatory and catabolic pathways eventually predominate. Physical exercise has been shown to activate various redox signaling pathways that control the adaptation and remodeling process. Although this stimulatory effect of exercise declines with aging, it is not completed abolished. Thus, aged people can still benefit from regular physical activity in the appropriate forms and at proper intensity to preserve muscle function.

Post-traumatic stress disorder (PTSD), gaining increasing attention, is a multifaceted psychiatric disorder that occurs following a stressful or traumatic event or series of events. Recently, several studies showed a close relationship between PTSD and neuroinflammation. Neuroinflammation, a defense response of the nervous system, is associated with the activation of neuroimmune cells such as microglia and astrocytes and with changes in inflammatory markers. In this review, we first analyzed the relationship between neuroinflammation and PTSD: the effect of stress-derived activation of the hypothalamic–pituitary–adrenal (HPA) axis on the main immune cells in the brain and the effect of stimulated immune cells in the brain on the HPA axis. We then summarize the alteration of inflammatory markers in brain regions related to PTSD. Astrocytes are neural parenchymal cells that protect neurons by regulating the ionic microenvironment around neurons. Microglia are macrophages of the brain that coordinate the immunological response. Recent studies on these two cell types provided new insight into neuroinflammation in PTSD. These contribute to promoting comprehension of neuroinflammation, which plays a pivotal role in the pathogenesis of PTSD. [ABSTRACT FROM AUTHOR]

Similar to other subdisciplines in kinesiology, exercise physiology (EP) as a field is facing challenges in both research (creation and dissemination of new knowledge) and education (classroom instruction and student mentoring). In the current communication, we will learn from the history, analyze the current status of the field, and provide some perspectives based primarily on our knowledge and experience working as faculty members at the University of Wisconsin-Madison. (Contains 1 figure.)

The pivotal observation that muscular exercise is associated with oxidative stress in humans was first reported over 45 years ago. Soon after this landmark finding, it was discovered that contracting skeletal muscles produce oxygen radicals and other reactive species capable of oxidizing cellular biomolecules. Importantly, the failure to eliminate these oxidant molecules during exercise results in oxidation of cellular proteins and lipids. Fortuitously, muscle fibers and other cells contain endogenous antioxidant enzymes capable of eliminating oxidants. Moreover, it is now established that several modes of exercise training (e.g., resistance exercise and endurance exercise) increase the expression of numerous antioxidant enzymes that protect myocytes against exercise-induced oxidative damage. This review concisely summarizes the impact of endurance, high-intensity interval, and resistance exercise training on the activities of enzymatic antioxidants within skeletal muscles in humans and other mammals. We also discuss the evidence that exercise-induced up-regulation of cellular antioxidants reduces contraction-induced oxidative damage in skeletal muscles and has the potential to delay muscle fatigue and improve exercise performance. Finally, in hopes of stimulating further research, we also discuss gaps in our knowledge of exercise-induced changes in muscle antioxidant capacity. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NALFD), characterized by an abnormal accumulation of triglycerides in hepatocytes, is closely linked to insulin resistance, metabolic syndrome, and changes in lipogenesis in the liver. The accumulation of hepatic lipids can lead to a range of pathologies from mild steatosis to severe cirrhosis. Endurance exercise is known to ameliorate the adverse health effects of NAFLD. Therefore, we aimed to investigate the effect of voluntary wheel running (VWR) on the metabolic changes in the livers of high-fat diet (HFD)-induced NAFLD mice and used LC-MS/MS (Liquid chromatography–mass spectrometry) to determine whether the tested intervention affected the protein expression profiles of the mouse livers. Male C57BL/6 mice were randomly divided into three groups: control (CON), high-fat diet sedentary group (HFD), high-fat diet VWR group (HFX). HFX group performed voluntary wheel running into individually cages, given a high-fat diet for 12 weeks. Food consumption, body weight, and running distance were measured every week. Using 2D (2-dimensional)-gel electrophoresis, we detected and quantitatively analyzed the protein expression with >2.0-fold change in the livers of HFD-fed mice, HFD-fed exercise (HFX) mice, and chow-fed mice. Body weight was significantly increased in HFD compared to CON (P < 0.05). The 2D-gel electrophoresis analysis indicated that there was a difference between CON and HFD groups, showing 31 increased and 27 decreased spots in the total 302 paired spots in the HFD group compared to CON. The analysis showed 43 increased and 17 decreased spots in the total 258 spots in the HFX group compared to CON. Moreover, 12 weeks of VWR showed an increase of 35 and a decrease of 8 spots in a total of 264 paired spots between HFD and HFX. LC-MS/MS of HFD group revealed that proteins involved in ketogenesis, lipid metabolism, and the metabolism of drugs and xenobiotics were upregulated, whereas detoxifying proteins, mitochondrial precursors, transport proteins, proteasomes, and proteins involved in amino acid metabolism were downregulated. On the other hand, VWR counteracted the protein expression profile of HFD-fed mice by upregulating molecular chaperones, gluconeogenesis-, detoxification-, proteasome-, and energy metabolism-related proteins. This study provided a molecular understanding of the HFD- and exercise-induced protein marker expression and presented the beneficial effects of exercise during pathophysiological conditions. [ABSTRACT FROM AUTHOR]

Eccentric contraction (EC) is known to elicit inflammation and damage in skeletal muscle. Proinflammatory cytokine TNF-[alpha] plays an important role in this pathogenesis, but the time course of its response to EC and the regulatory mechanisms involved are not clear. The purpose of the study is twofold: 1) to investigate the gene expression of TNF-[alpha] in rat muscle during and after an acute bout of downhill running and the associated oxidoreductive (redox) changes; and 2) to examine whether EC activates muscle ubiquitin-proteolytic pathway resulting in necrosis and oxidative damage. Female Sprague-Dawley rats (age 3 mo) were randomly divided into five groups (n = 6) that ran on treadmill at 25 m/min at - 10% grade for 1 h (group 1) or 2 h (group 2) and were killed immediately; ran for 2 h and killed at 6 h after exercise (group 3), ran for 2 h and killed at 24 h after exercise (group 4); and killed at rest as controls (group 5). TNF-[alpha] mRNA and protein content showed progressive increases in the deep portion of vastus lateralis (DVL) and gastrocnemius muscles during and after EC. These changes were accompanied by a progressive decrease of mitochondrial aconitase activity and NF-[kappa]B activation. After 2 h of exercise, elevated levels of serum TNF-[alpha], endotoxin, creatine kinase, and lipid peroxidation marker were evident and persisted through 24 h postexercise. At 24 h, there were marked increases in [H.sub.2][O.sub.2] concentration, myleoperoxidase activity, and endotoxin level, along with nuclear accumulation of p65, in both muscles, mRNA level of ubiquitin-conjugating enzymes ([E.sub.2])-14k was progressively upregulated during exercise and recovery, whereas the expression of the Toll-like receptor 4 (TLR4) in DVL was downregulated in both muscles. We conclude that prolonged EC induces TNF-[alpha] expression possibly due to NF-[kappa]B activation stimulated by increased reactive oxygen species generation and endotoxin release. These inflammatory and prooxidative responses may underlie the processes of muscle proteolysis and oxidative damage. inflammation; rat; reactive oxygen species; skeletal muscle; TNF-[alpha] doi:10.1152/ajpregu.00480.2009

Contraction-induced production of reactive oxygen and nitrogen species has been shown to cause oxidative stress to skeletal muscle, heart and other organs. As an adaptive response, muscle antioxidant defense systems are upregulated in response to exercise to restore intracellular prooxidant-antioxidant homeostasis. Thus, both young and old animals and humans involved in regular exercise have shown reduced oxidative damage during acute physical exertion at accustomed or excessive intensity, or under oxidative challenges otherwise deemed detrimental. The current article provides a brief review of this exercise-induced hormesis with the emphasis on the role of redox sensitive signal transduction pathways (mainly nuclear factor kB and mitogen-activated protein kinase) that can activate the gene expression of antioxidant enzymes and proteins. Molecular mechanisms and gene targets for these signaling pathways, as well as the biological significance of the adaptations, are discussed. Key words: Antioxidant, exercise, oxidative stress, reactive oxygen species, signaling, INTRODUCTION Maintenance of oxidative -antioxidant homeostasis is critical for cell survival and normal function [1]. In the field of free radical biochemistry, one paradox continues to puzzle both researchers and [...]