Kerman 大学医学院

Silicone-coated prosthetic devices, a category of medical implants with a history spanning decades, have significantly impacted medical technology by enhancing patients’ quality of life and functional outcomes across various conditions. Since the use of these devices has been steadily rising and concerning complications have been reported, it is necessary to understand the epidemiologic characteristics, etiologies, and risk factors associated with their adverse outcomes. This study aims to provide a comprehensive overview of the survival rates and adverse effects of silicone-coated prosthetic devices. PubMed, Embase, and Scopus were systematically explored using a combination of keywords and Medical Subject Heading terms, including “silicone-coated prosthetic device”, “survival rate”, “adverse event”, “epidemiology”, “etiology”, and “risk factor”. Studies focusing on other aspects of silicone-coated prostheses or non-silicone-coated devices were excluded. Capsular contracture, infection, implant rupture, and allergic reactions are the most prevalent complications reported by the available literature. The acute inflammatory reaction against silicone-coated devices is initiated by neutrophils and monocytes activation resulting in the activation of pro-inflammatory macrophage M1 as a prominent mediator. This response is characterized by decreased interleukin (IL)-10 levels and elevated levels of IL-12, IL-23, IL-6, IL-1β, IL-17, tumor necrosis factor-α (TNF- α), and reactive nitrogen and oxygen species which leads to an increased activity of T-helper 1 and 17. IL-6, IL-8, TNF-α, and transforming growth factor-β are among the main factors involved in the chronic inflammatory response that could result in capsule contracture. Additionally, factors such as age, chronic diseases, surgical methods, and post-surgical care are identified as significant contributors to the viability of silicone-coated implants. Ongoing investigations continue to delve into the complicated aspects of the immune response to silicone-coated devices. The ultimate goal is to fully comprehend these complexities and devise strategies that minimize inflammation, ultimately enhancing the biocompatibility of these devices. Level of Evidence: not gradable.

Infertility is a crucial challenge for global health that encompasses economic, psychological, and medical aspects. Besides anatomical contributors to infertility, specific dietary components may influence reproductive outcomes in both men and women through diverse molecular and epigenetic mechanisms. This study aimed to evaluate the role of macronutrients, vitamins, and minerals in male and female infertility using a system biology approach. To address the complex interplay between infertility and nutritional factors, we focused on published studies that explore molecular and systems biology pathways, including those involving nutrigenetics, epigenetics, metabolomics, and gene expression profiling. These studies span both human and animal models and were selected based on their relevance to reproductive outcomes and mechanistic insights. Several nutrients appear to influence infertility through distinct molecular mechanisms. Polyunsaturated fatty acids (PUFAs) may exert beneficial effects by modulating the expression of fertility-related genes, while saturated fatty acids (SFAs) are associated with impaired oocyte quality and reproductive dysfunction via altered gene expression and DNA damage. Among micronutrients, increased intake of folate and vitamin D has been linked to improved gamete quality and folliculogenesis in women with infertility. Dietary glutamine and selenium may enhance fertility through their antioxidant properties. Iron demonstrates dual effects, potentially supporting or impairing fertility depending on its role in epigenetic regulation. Dietary intake may influence the risk of infertility through pathways related to nutrigenetics, nutrigenomics, and nutri-epigenomics. While current evidence suggests promising nutrient–gene interactions, most findings are derived from small-scale or preclinical studies, highlighting the need for robust human trials.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with limited treatment options that primarily offer symptomatic relief. Mesenchymal stem cells (MSCs) have shown promise in preclinical studies due to their neuroprotective, immunomodulatory, and regenerative properties. This systematic review and meta-analysis aimed to assess the effects of MSC therapy on cognitive performance and molecular pathology in animal models of AD.A systematic search was conducted in PubMed, Web of Science, Scopus, Embase, ProQuest, and gray literature sources. This study included in vivo interventional animal studies that evaluated the effects of MSCs on cognitive outcomes in Alzheimer’s disease models using the Morris Water Maze test. The standardized mean difference (SMD) was used as the effect size, and data were synthesized using a random-effects model. Study quality was assessed using the SYRCLE risk of bias tool. Publication bias was evaluated through funnel plots, Egger’s test, and the trim-and-fill method. Sensitivity analysis was performed using the leave-one-out method and further supported by a risk-of-bias–based approach.A total of 51 studies met the inclusion criteria, of which 37 were included in the meta-analysis. The findings indicated that MSC therapy significantly reduced escape latency (SMD = −1.18, 95

This study aimed to identify and characterize irlncRNAs associated with prognosis and immune modulation in breast cancer. We integrated single-cell RNA sequencing, hdWGCNA, and bulk RNA-seq differential expression analysis results to identify candidate irlncRNAs. The top candidate, SIMALR, was further investigated using immune, survival, mutation analysis, and GSEA. RT-qPCR preliminary validation was performed on patient tissues. SIMALR was linked to favorable survival and enriched in immune pathways, including T-cell receptor signaling, Natural Killer (NK) cell cytotoxicity, and antigen processing. Pearson analysis showed co-expression of SIMALR-related genes (CD8A, CD4, TNF, LCP2, ITGB2) in key immune populations. High SIMALR As per standard instruction, “Statement of Significance” section should not be captured. Hence, the “Clinical significance” section was deleted. Please check and confirm if presented correctly; otherwise, please amend. expression in tumor cells is associated with enhanced secretion of Th1-attracting chemokines (CXCL9/10/11, CCL5), recruitment of CD8 + T cells, activated dendritic cells, and both M1/M2 macrophages. RT-qPCR confirmed higher SIMALR expression in tumors. Due to limited availability of clinical specimens, the RT-qPCR analysis was performed on paired tissue samples from six patients, and therefore the results should be considered a preliminary validation. SIMALR may contribute to anti-tumor immunity, highlighting its potential as a promising biomarker and therapeutic target in breast cancer.

This study investigates the potential link between exposure to organochlorine pesticides (OCPs) and unexplained female infertility (UFI), exploring oxidative stress (OS) as a potential mechanistic pathway underlying this association. Serum samples from 113 women with UFI and 103 healthy controls were analyzed for seven OCPs: 2,4-DDT, 2,4-DDE, 4,4-DDT, 4,4-DDE, α-HCH, β-HCH, and γ-HCH. Enzymatic and non-enzymatic OS biomarkers were also measured. Associations between OCP exposure, OS markers, and UFI risk were assessed using linear and logistic regression models. Women with UFI had significantly higher serum levels of 2,4-DDT, 2,4-DDE, 4,4-DDT, 4,4-DDE, α-HCH, β-HCH, and malondialdehyde (MDA) compared to controls. Conversely, antioxidant enzyme activities (SOD3, GPx3, CAT, and AChE) and total antioxidant capacity (TAC) were significantly lower. Logistic regression analysis indicated that higher serum concentrations of several OCPs were associated with an increased risk of UFI, including α-HCH (OR = 1.13, 95