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Background: Inflammation can result in the development of breast cancer in women with overweight and obese, and also affects the outcome and prognosis of breast cancer patients, thereby decreasing the cure and survival rates of breast cancer patients. Exercise may benefit breast cancer patients as a supplement to conventional treatments. However, research on the effects of exercise on inflammatory markers in women with breast cancer who are overweight and obese remains incomplete. Objective: A systematic review and meta-analysis were used to study the effects of exercise on inflammatory markers in women with breast cancer who are overweight and obese. Method: Literature up to May 2024 was searched from databases such as Cochrane, Embase, Pubmed, Web of Science, and EBSCO, and English-language randomized controlled trials (RCTs) that met the inclusion criteria were screened. The screening criteria were as follows (A) written in English; (B) RCT; (C) studied in women with overweight obese and breast cancer; (D) outcome measures: inflammatory markers; (E) the duration of the exercise intervention was unlimited. Results: A total of 14 articles and 1064 participants were included. Exercise significantly reduced C-reactive protein (CRP) (MD: −0.52, 95 % CI: −0.94 to −0.11; p = 0.01; heterogeneity p

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, and the most prevalent form of dementia. The main hallmarks for the diagnosis of AD are extracellular amyloid-beta (Aβ) plaque deposition and intracellular accumulation of highly hyperphosphorylated Tau protein as neurofibrillary tangles. The brain consumes more oxygen than any other organs, so it is more easily to be affected by hypoxia. Hypoxia has long been recognized as one of the possible causes of AD and other neurodegenerative diseases, but the exact mechanism has not been clarified. In this review, we will elucidate the connection between hypoxia-inducible factors-1α and AD, including its contribution to AD and its possible protective effects. Additionally, we will discuss the relationship between oxidative stress and AD as evidence show that oxidative stress acts on AD-related pathogenic factors such as mitochondrial dysfunction, Aβ deposition, inflammation, etc. Currently, there is no cure for AD. Given the close association between hypoxia, oxidative stress, and AD, along with current research on the protective effects of antioxidants against AD, we speculate that antioxidants could be a potential therapeutic approach for AD and worth further study.

Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-a), and IL-1? levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-a, and IL-1? levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a neurodegenerative disorder, which has become the leading cause of dementia cases globally. Synaptic failure is an early pathological feature of AD. However, the cause of synaptic failure in AD, especially the GABAergic synaptic activity remains unclear. Extensive evidence indicates that the presence of soluble amyloid-ß is an early pathological feature in AD, which triggers synaptic dysfunction and cognitive decline. Our recent study explored the relation of GABAergic transmission and soluble Aß in early APP/PS1 mice. Firstly, we found soluble Aß42 levels were significantly increased in serum, hippocampus and prefrontal cortex in 3-4 months APP/PS1 mice, which was much earlier than Aß plagues formation. In addition, we found TNF-a and BDNF expression levels were increased, while KCC2 and GABAAR expression were decreased in 3-4 months APP/PS1 hippocampus. When we treated 3-4 months APP/PS1 mice with a potent ?-secretase inhibitor, LY411575, which can reduce the soluble Aß42 levels, the TNF-a and BDNF protein levels were decreased, while KCC2 and GABAAR levels were increased. In conclusion, our study suggested soluble Aß may impaired the GABA inhibition by mediating KCC2 levels in early APP/PS1 mice. KCC2 may be served as a potential biomarker for AD. [ABSTRACT FROM AUTHOR]