MiR-20b Tissue Expression Level Displays the Diagnostic Value in Papillary Thyroid Carcinoma.

Background: Detection of cancer in patients with thyroid nodules requires sensitive and specific diagnostic modalities that are accurate and inexpensive. This study aimed to identify a potential microRNA(miRNA) panel to detect papillary thyroid carcinoma (PTC). Methods: Following a comprehensive literature review as well as miRNA target predictor databases, Real-time PCR was used to quantify the expression of candidate miRNAs in 59 tissue specimens from 30 patients with PTC and 29 patients with benign nodules. A receiver operating characteristic (ROC) curve analysis was used to assess the accuracy of miRNA expression levels compared to the pathology report as the gold standard. Based on prediction results, four miRNAs, including miR-9, miR-20b, miR-221, and miR-222, were selected to evaluate their expression level in Iranian thyroid samples. Results: A significant difference between the tissue expression level of miR-20b, miR-9, miR-222, and miR-221 was detected in the PTC group compared with non-PTC (P < 0.05). The area under the curves for the included miRs were 1, 0.98, 0.99, 0.98, and 1, respectively. Conclusion: Our results confirmed deregulations of miR-20b as well as miR-222, miR-221, and miR-9 in PTC and, therefore, could be used as a helpful miRNA panel to differentiate PTC from benign nodules, which results in the more efficient clinical management of PTC patients.

Hs-CRP and TNF-α Effects on Postnatal Umbilical Coiling: Impact Assessment of the Gestational Diabetes Mellitus.

Background: No study has been conducted to specifically demonstrate the relationship between gestational diabetes mellitus (GDM) status, inflammatory factors, and postnatal umbilical coiling index (pUCI). Understanding this relationship could help select the best interventions to save the fetus. To evaluate the effects of maternal venous and umbilical cord blood levels of high sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-alpha (TNF-alpha) on pUCI in GDM and non-GDM groups. Methods: This prospective observational study included 40 participants in each of the GDM and non-GDM groups, matched for maternal age, ethnicity, and parity. The GDM diagnosis was confirmed by 24 to 28 weeks of gestation (WOG) and a 2-step strategy. The covariates of interest were maternal hs-CRP and TNF-α, measured at 37 to 40 WOG, and their UC analogous was measured during delivery. The gross morphologies were assessed immediately after delivery. The UC coiling was quantitatively assessed by the pUCI. To compare the GDM and non-GDM groups, the t test and the Mann-Whitney test were used for normal and non-normal variables, respectively. Results: There was not a significant difference in hs-CRP and TNF-a levels in maternal venous blood or UC blood between the GDM and non-GDM groups. The mean (SD) of pUCI in the GDM and non-GDM groups were 0.28 (0.15) and 0.24 (0.21) (P = 0.441), respectively. In the GDM group, none of the 4 covariates of interest had significant effects on the UCI. Among the non-GDM participants, merely the UC hs-CRP had a direct association with the pUCI, with a Pearson correlation of 0.54 (P = 0.001). Impacts of hs-CRP and TNF-α on the pUCI were assessed using Poisson regression models and no significant findings were detected (95% CI, 0.999-1.001, for all parameters). Conclusion: In the GDM group, no apparent association was observed between inflammatory factors and pUCI, although a direct association was detected between UC hs-CRP and pUCI in the non-GDM.

Wnt Network: A Brief Review of Pathways and Multifunctional Components.

The Wnt signaling pathway appears to activate intracellular signaling transduction in embryonic development, cell migration, hematopoiesis, and several diseases. Wnt signaling is basically recognized as a canonical ß-catenin-dependent signaling pathway. However, in recent years, generally three Wnt-mediated pathways have been investigated, which operate independently of ß-catenin and include calcium/calmodulin-dependent kinase II and protein kinase C, planar cell polarity, and a third one recruits hetrotrimeric GTP-binding proteins to stimulate phospholipase C and phosphodiesterase. We provide an overview of the noncanonical Wnt signaling pathway and then will focus on canonical Wnt signaling components, Wnt ligands, agonists, and antagonist. This review will also discuss ß-catenin, both cytoplasmic and nuclear mechanisms, through signaling transduction, and, as a consequence, we have briefly highlighted potential implications of Wnt/ß-catenin in some cancers.

Resolvins: Emerging Players in Autoimmune and Inflammatory Diseases.

Resolvins, belonging to the group of specialized proresolving mediators (SPMs), are metabolic products of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) and are synthesized during the initial phases of acute inflammatory responses to promote the resolution of inflammation. Resolvins are produced for termination of neutrophil infiltration, stimulation of the clearance of apoptotic cells by macrophages, and promotion of tissue remodeling and homeostasis. Metabolic dysregulation due to either uncontrolled activity of pro-inflammatory responses or to inefficient resolution of inflammation results in chronic inflammation and may also lead to atherosclerosis or other chronic autoimmune diseases such as rheumatoid arthritis, psoriasis, systemic lupus erythematosus, vasculitis, inflammatory bowel diseases, and type 1 diabetes mellitus. The pathogenesis of such diseases involves a complex interplay between the immune system and, environmental factors (non-infectious or infectious), and critically depends on individual susceptibility to such factors. In the present review, resolvins and their roles in the resolution of inflammation, as well as the role of these mediators as potential therapeutic agents to counteract specific chronic autoimmune and inflammatory diseases are discussed.

Atherosclerosis and immunity: A perspective.

Atherosclerosis is an inflammatory and multifaceted disorder resulting from the accumulation of lipid droplets and several types of immune cells, including macrophages, T and B lymphocytes in the arterial walls. A wide variety of macrophage subtypes with different functions is implicated in the development and progression of atherosclerotic lesions. The prevalence of specific macrophage subtypes, which is influenced by cytokines, mediators, and substances composing atherosclerotic lesions, has been suggested to be an appropriate indicator of transition from a stable to an unstable plaque phenotype. Thus, a better understanding of the mechanisms underlying the differentiation of macrophage subpopulations in relation to the plaque phenotype would help to develop novel approaches aiming at slowing-down the progression of atherosclerotic disease by modulating the polarization of these cells. In addition, many arms of the adaptative immune system, which are regulated by different subtypes of T and B lymphocytes, are involved in atherosclerosis progression and there is an increasing effort to identify immune-modulating therapies targeting either T or B cells with a potential anti-atherosclerotic impact. This paper summarizes the pathophysiology of atherosclerotic disease as it relates to the contribution from the immune system, reviewing the crucial role of macrophages, T and B lymphocytes.

The Role of Efferocytosis in Autoimmune Diseases.

Apoptosis happens continuously for millions of cells along with the active removal of apoptotic debris in order to maintain tissue homeostasis. In this respect, efferocytosis, i.e., the process of dead cell clearance, is orchestrated through cell exposure of a set of "find me," "eat me," and "tolerate me" signals facilitating the engulfment of dying cells through phagocytosis by macrophages and dendritic cells. The clearance of dead cells via phagocytes is of utmost importance to maintain the immune system tolerance to self-antigens. Accordingly, this biological activity prevents the release of autoantigens by dead cells, thus potentially suppressing the undesirable autoreactivity of immune cells and the appearance of inflammatory autoimmune disorders as systemic lupus erythematous and rheumatoid arthritis. In the present study, the apoptosis pathways and their immune regulation were reviewed. Moreover, efferocytosis process and its impairment in association with some autoimmune diseases were discussed.