Notes

TMEM119 makes it possible for ovarian cancers cell proliferation, attack, as well as migration via the PDGFRB/PI3K/AKT signaling walkway.
BACKGROUND We sought to determine the association of dysmetabolic iron overload syndrome (DIOS) with metabolic syndrome (MetS). METHODS-RESULTS Several studies have shown that DIOS is associated with Mets, mainly through the pathogenesis of its components type 2 diabetes melitus (T2DM), essential hypertension, non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (POS). Serum ferritin levels increase proportionally according to the degree of insulin resistance (IR) and the number of components of Mets [5]. Moreover, DIOS predictis the onset of T2DM and NAFLD. Dysregulation of iron metabolism in DIOS is due to a multifactorial and dynamic process triggered by unhealthy diet, facilitated by environmental and genetic cofactors, and resulting in a bidirectional relation between the liver and visceral adipose tissue (VAT). Iron removal combined with healthy diet improved both insulin sensitivity and beta cell function, but had no significant effect on blood glucose; phlebotomy therapy might be considered with conflicting results however. CONCLUSIONS Iron overload is closely associated with the metabolic syndrome and its components; however, it remains under-appreciated in everyday clinical practice. Diet and lifestyle modification offer some clinical benefit; however, it is not adequate for the successful management of the disease. The results of phlebotomy remain controversial, underlying the necessity of further efforts in this field. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] spite of therapeutic modalities such as surgical resection, chemotherapy and radiotherapy, glioblastoma multiforme (GBM) remains an incurable fatal disease. This necessitates further therapeutic options that could enhance the efficacy of existing modalities. Nitric oxide (NO), a short-lived small molecule, has been revealed to play a crucial role in the pathophysiology of GBM. Several studies have demonstrated that NO is involved in apoptosis, metastasis, cellular proliferation, angiogenesis, invasion and many other processes implicated in GBM pathobiology. Herein, we elaborate on the role of NO as a therapeutic target in GBM and discuss some natural products affecting the NO signaling pathway. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] is a good alternative to traditional methods of cancer treatment, but does not solve all the limitations of oncology. Nanoparticles used in anticancer therapy can work as carriers of drugs, nucleic acids, imaging agents or they can sensitize cells to radiation. The present review focuses on the application of nanoparticles to treating cancer, as well as on its problems and limitations. Using nanoparticles as drug carriers, significant improvement in the efficiency of transport of compounds and their targeting directly to the tumour has been achieved; it also reduces the side effects of chemotherapeutic drugs on the body. However, nanoparticles do not significantly improve the effectiveness of the chemotherapeutic agent itself. Most nanodrugs can reduce toxicity of chemotherapy, but do not significantly affect the effectiveness of treatment. Nanodrugs should be developed that can be effective as an anti-metastatic treatment, e.g. by enhancing the ability of nanoparticles to transport chemotherapeutic loads to sentinel lymph nodes using the immune system, and developing chemotherapy in specific metastatic areas. Gene therapy, however, is the most modern method of treating cancer, the cause of cancer being tackled by altering genetic material. Other applications of nanoparticles for radiotherapy and diagnostics are discussed. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] carcinoma (HCC) is a common gastrointestinal malignancy with leading incidence of cancer-related mortality worldwide. Despite the progress of therapeutic treatment, it remains low efficacy for patients with intermediate-advanced HCC, due to tumor metastasis, recurrence and chemoresistance. Increasing evidence suggests that exosomes in the tumor microenvironment (TME), along with other extracellular vesicles (EVs) and cytokines, contribute to the drug chemosensitivity of cancer cells. Exosomes, the intercellular communicators in various biological activities, have shown to play important roles in HCC progression. This review summarized the underlying associations between exosomes and chemoresistance of HCC cells. selleck chemicals llc The exosomes derived from distinct cell types mediate the drug resistance by regulating drug efflux, epithelial-mesenchymal transition (EMT), cancer stem cell (CSC) properties, autophagic phenotypes, as well as the immune response. In summary, TME-related exosomes can be a potential target to reverse chemoresistance and a candidate biomarker of drug efficacy in HCC patients. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] We compared serum levels of chemokines between male elders with major depressive disorder (MDD) and healthy controls, verifying whether any difference exists in the levels of these mediators between those with and without current suicidal ideation (SI). METHODS We enrolled 145 male elders aged 65 or older and analyzed 40 chemokines in patients with MDD with SI (n = 24) and without SI (n = 23), as well as healthy controls (n = 98). RESULTS The patients with MDD with SI presented higher levels of MCP-2/CCL8 (p  less then  0.001) compared with the patients with MDD without SI and the healthy controls. CONCLUSIONS Current findings suggest a potential role of MCP-2/CCL8 in suicidality among elderly males with depression.Aortic aneurysms were the primary cause of nearly 10,000 deaths in 2014 according to data from the Centers for Disease Control and may involve segments of the thoracic or abdominal aorta. Thoracic aortic aneurysms and dissections are more commonly associated with an underlying genetic etiology. In the past several decades, in parallel with the burst of new genome sequencing technologies, a number of genetic aortopathies have been identified. These have provided important insights into the molecular mechanisms of aneurysmal disease, but pose challenges in clinical practice as there are limited consensus recommendations at this time. In this review, we aim to address the pathophysiology, clinical presentation, and treatment considerations in the key heritable thoracic aortopathies.
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