Selenium: 48-year journey of global clinical trials.

Selenium, an essential trace mineral for health, has seen a rise in clinical trials over the past nearly 5 decades. Our aim here is to provide a comprehensive and concise overview of selenium clinical trials from 1976 to 2023. Overall, the evolution of selenium clinical trials over 48 years has advanced through phases of emergence, prosperity, and either stability or transition.

Circular RNAs: key players in tumor immune evasion.

Immune responses against tumor antigens play a role in confining tumor growth. In response, cancer cells developed several mechanisms to bypass or defeat these anti-tumor immune responses-collectively referred to as "tumor immune evasion". Recent studies have shown that a group of non-coding RNAs, namely circRNAs affect several aspects of tumor immune evasion through regulation of activity of CD8 + T cells, regulatory T cells, natural killer cells, cytokine-induced killer cells or other immune cells.

Crocin and gallic acid attenuate ethanol-induced mitochondrial dysfunction via suppression of ROS formation and inhibition of mitochondrial swelling in pancreatic mitochondria.

Chronic/heavy exposure with ethanol is associated with risk of type 2 diabetes, due to β-cells dysfunction. It has been reported that ethanol can induce oxidative stress directly or indirectly by involvement of mitochondria. We aimed to explore the protective effects of the crocin/gallic acid/L-alliin as natural antioxidants separately on ethanol-induced mitochondrial damage.

L3MBTL3 and STAT3 collaboratively upregulate SNAIL expression to promote metastasis in female breast cancer.

The STAT3 pathway promotes epithelial-mesenchymal transition, migration, invasion and metastasis in cancer. STAT3 upregulates the transcription of the key epithelial-mesenchymal transition transcription factor SNAIL in a DNA binding-independent manner. However, the mechanism by which STAT3 is recruited to the SNAIL promoter to upregulate its expression is still elusive.

PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.

Colorectal cancer (CRC) ranks third for morbidity and second for mortality among all digestive malignant tumors worldwide, but its pathogenesis remains not entirely clear. Bioinformatic analyses were performed to find out important biomarkers for CRC. For validation, reverse transcription-quantitative PCR, western blotting, and immunohistochemistry were performed.

Angiogenic Markers in Gestational Diabetes and their Association with Placental Dimensions.

GDM is an increasing global concern, with its etiology not fully understood, though altered placental function is likely to play a role. Placental angiogenesis, essential for sufficient blood flow and nutrient exchange between mother and fetus, may be affected by GDM. However, the role of angiogenic markers in GDM remains unclear.

Accumulation of microtubule-associated protein tau promotes hepatocellular carcinogenesis through inhibiting autophagosome-lysosome fusion.

Dysregulated expression of microtubule-associated protein tau (MAPT) has been reported in a variety of human cancers. However, whether and how Tau influences hepatocellular carcinogenesis remains elusive. This study was aimed to investigate the role and the underlying mechanism of Tau in the proliferation, invasion, migration and sorafenib sensitivity of hepatocellular carcinoma (HCC) cells.

The highs and lows of monoamine oxidase as molecular target in cancer: an updated review.

The global burden of cancer as a major cause of death and invalidity has been constantly increasing in the past decades. Monoamine oxidases (MAO) with two isoforms, MAO-A and MAO-B, are mammalian mitochondrial enzymes responsible for the oxidative deamination of neurotransmitters and amines in the central nervous system and peripheral tissues with the constant generation of hydrogen peroxide as the main deleterious ancillary product. However, given the complexity of cancer biology, MAO involvement in tumorigenesis is multifaceted with different tumors displaying either an increased or decreased MAO profile.

Short-chain fatty acids as a novel intervention for high-fat diet-induced metabolic syndrome.

Metabolic syndrome (MetS) is driven by a complex interplay of genetic, lifestyle, and dietary factors, leading to weight gain, insulin resistance, dyslipidemia, and chronic inflammation. Gut microbiota dysbiosis has been recently recognized as a key contributor to MetS, leading to advancements in gut microbiome-based interventions to improve health outcomes. Considering the unique challenges associated with the use of pre/probiotics, short-chain fatty acids (SCFA), also known as postbiotics, have emerged as promising therapeutic agents due to their role in modulating host metabolism and physiology.

Pre-ribosomal WDR74 module coordinates the early and late pre-rRNA processing stages for the NVL2-mediated regulation of 60S ribosome biogenesis.

WD repeat domain 74 (WDR74) is a nucleolar protein involved in the early stages of pre-60S maturation in the ribosome biogenesis pathway. In later stages, WDR74 interacts with MTR4, an RNA helicase that functions with the exosome nuclease complex, and is dissociated upon ATP hydrolysis by the chaperone-like nuclear VCP-like 2 (NVL2) AAA-ATPase. We previously reported that ATP hydrolysis-defective NVL2 causes aberrant accumulation of WDR74 on the MTR4-exosome complex at the nucleolar periphery and in the nucleoplasm and that this nuclear redistribution of WDR74 leads to the unusual cleavage of the early rRNA precursor within the internal transcribed spacer 1 sequence.

Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease.

Obesity, diabetes, and their cardiovascular and hepatic comorbidities are alarming public health issues of the twenty-first century, which share mitochondrial dysfunction, oxidative stress, and chronic inflammation as common pathophysiological mechanisms. An increasing body of evidence links the combined exposure to multiple environmental toxicants with the occurrence and severity of metabolic diseases. Endocrine disruptors (EDs) are ubiquitous chemicals or mixtures with persistent deleterious effects on the living organisms beyond the endocrine system impairment; in particular, those known as metabolism-disrupting chemicals (MDCs), increase the risk of the metabolic pathologies in adult organism or its progeny.

A mammary gland secretion function exploratory study based on a quantitative comparison between milk and serum.

Lactation is a complex physiological process, and the knowledge about the secretion of many milk components is limited. The objective of this study was to explore the secretory function of human mammary glands through a comparative analysis of common clinical indicators in serum and milk. Milk and serum samples were collected from lactating women simultaneously, and titers of common biochemical components were determined using an automated biochemical analyzer.

C-Peptide Ameliorates Particulate Matter 2.5-Induced Skin Cell Apoptosis by Inhibiting NADPH Oxidation.

Connecting peptide (C-peptide), a byproduct of insulin biosynthesis, has diverse cellular and biological functions. Particulate matter 2.5 (PM) adversely affects human skin, leading to skin thickening, wrinkle formation, skin aging, and inflammation.

Interleukin-22 promotes endometrial carcinoma cell proliferation and cycle progression via ERK1/2 and p38 activation.

Endometrial carcinoma (EC) is one of the most common gynecological malignant tumors, but its underlying pathogenic mechanisms are largely obscure. Interleukin-22 (IL-22), one cytokine in the tumor immune microenvironment, was reported to be associated with carcinoma progression. Here, we aimed to investigate the regulation of IL-22 in endometrial carcinoma.

Immune dysregulation of decidual NK cells mediated by GRIM19 downregulation contributes to the occurrence of recurrent pregnancy loss.

In patients with recurrent pregnancy loss (RPL), excessive activation of decidual natural killer (dNK) cells has been widely observed, yet the precise underlying mechanisms remain to be elucidated. We collected decidual specimens from RPL patients and controls to assess GRIM19 expression, activation phenotype, cytotoxic function, inflammatory cytokine secretion, and mitochondrial homeostasis in dNK cells. Furthermore, we established a GRIM19-knockout NK-92MI cell line and a GRIM19 ± C57BL/6J mouse model to investigate the relationship between GRIM19 downregulation and dNK immune dysregulation, ultimately contributing to pregnancy loss.

Activated TREM1-mediated MAPK signaling in endothelial cells caused by highly expressed STAT1 is associated with intracranial aneurysms occurrence and rupture.

Intracranial aneurysm (IA) poses significant health risks, yet the specific mRNA profiles and regulatory mechanisms distinguishing unruptured IA (UIA) from ruptured IA (RIA) remain unclear. This study aimed to elucidate these differences through comprehensive mRNA analysis. We employed RNA sequencing to compare mRNA expression patterns among control individuals, UIA patients, and RIA patients.

Conjugated fatty acids drive ferroptosis through chaperone-mediated autophagic degradation of GPX4 by targeting mitochondria.

Conjugated fatty acids (CFAs) have been known for their anti-tumor activity. However, the mechanism of action remains unclear. Here, we identify CFAs as inducers of glutathione peroxidase 4 (GPX4) degradation through chaperone-mediated autophagy (CMA).

Histone variants: The bricks that fit differently.

Histone proteins organize nuclear DNA in eukaryotic cells and play crucial roles in regulating chromatin structure and function. Histone variants are produced by distinct histone genes and are produced independently of their canonical counterparts throughout the cell cycle. Even though histone variants may differ by only one or a few amino acids relative to their canonical counterparts, these minor variations can profoundly alter chromatin structure, accessibility, dynamics, and gene expression.

Autophagy-related gene BECN1 single nucleotide polymorphisms in diseases.

Autophagy is a cytoprotective process that operates within a cell to maintain cellular homeostasis. An array of multiple proteins is involved to mediate this conserved cellular process. Among these, Beclin 1 protein encoded by BECN1 gene plays a crucial role during the initiation of autophagy.