Inhibition of biofilm formation and preformed biofilm in by resveratrol, chlorhexidine and benzalkonium: modulation of efflux pump activity.

Introduction: The persistence of in the contaminated environment is sustained by tolerance to biocides and ability to growth as biofilm. The aim of the study was to analyze the susceptibility of biofilms to chlorhexidine (CHX) and benzalkonium (BZK) biocides and the ability of natural monomeric stilbenoid resveratrol (RV) to modulate the phenomenon.

Methods: Biofilm formation and preformed biofilm were tested by Crystal violet and tetrazolium salt reduction assay, respectively.

Corrigendum: Estrogens modulate somatostatin receptors expression and synergize with the somatostatin analog pasireotide in prostate cells.

[This corrects the article DOI: 10.3389/fphar.2019.

Structure-based targeting of the lipid A-modifying enzyme PmrC to contrast colistin resistance in .

Introduction: Antimicrobial-resistant pathogens are an ongoing threat to human and animal health. According to the World Health Organization (WHO), colistin is considered the last resort antibiotic against human infections due to multidrug-resistant Gram-negative organisms-including , a priority-1 pathogen. Despite colistin being considered a last resort antibiotic, transferable bacterial resistance to this drug has been reported in humans and animals.

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent.

Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared: (1) levels of expression and nuclear content of BCL11A in adult erythroid cells upon GC stimulation; (2) response to GC of CD34+ cells from patients with BCL11A microdeletions and reduced BCL11A expression, and; (3) response to GC of 2 cellular models (HUDEP-2 and adult CD34+ cells) before and after reduction of BCL11A expression by shRNA.

KLHL14 is a tumor suppressor downregulated in undifferentiated thyroid cancer.

KLHL14 is a substrate-binding subunit of Cullin-RING ligase 3 ubiquitin ligase complex, highly enriched in thyroid since early embryonic development, together with its antisense RNA KLHL14-AS. We have previously demonstrated that Klhl14-AS is a competing endogenous RNA regulating several differentiation and survival factors in thyroid cancer, acting as tumor suppressor. Recently, also KLHL14 has been shown to function as tumor suppressor in diffuse large B-cell lymphoma and in malignant mesothelioma.

Erythropoietin: A Personal Alice in Wonderland Trip in the Shadow of the Giants.

The identification of the hormone erythropoietin (EPO), which regulates red blood cell production, and its development into a pharmaceutical-grade product to treat anemia has been not only a herculean task but it has also been the first of its kind. As with all the successes, it had "winners" and "losers", but its history is mostly told by the winners who, over the years, have published excellent scientific and divulgate summaries on the subject, some of which are cited in this review. In addition, "success" is also due to the superb and dedicated work of numerous "crew" members, who often are under-represented and under-recognized when the story is told and often have several "dark sides" that are not told in the polished context of most reviews, but which raised the need for the development of the current legislation on biotherapeutics.

Chromatin looping links gene expression to the assembly of transcription factories (Review).

Genes are not randomly dispersed within the nuclear space, instead they occupy precise sites either with respect to the nuclear lamina as well as to each other. This observation stands at the basis of the today well accepted concept of nuclear territories where any chromosome shows reproducible spatial connections with a selection of others in a general picture that meets a functional criterion where genes that answer the same stimuli are grouped in the same sites. In fact, transcription is not visible widely dispersed throughout the nucleus but is gathered in several 'granules', called transcription factories that accommodates ~10 genes concurrently transcribed.

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent.

Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared: levels of expression and nuclear content of BCL11A in adult erythroid cells upon GC stimulation; response to GC of CD34+ cells from patients with microdeletions and reduced expression, and; response to GC of two cellular models (HUDEP-2 and adult CD34+ cells) before and after reduction of expression by shRNA.

Filamin A in triple negative breast cancer.

Triple-negative breast cancer is a rare but highly heterogeneous breast cancer subtype with a limited choice of specific treatments. Chemotherapy remains the only efficient treatment, but its side effects and the development of resistance consolidate the urgent need to discover new targets. In TNBC, filamin A expression correlates to grade and TNM stage.

Advanced Magnetic Resonance Imaging to Define the Microvascular Injury Driven by Neuroinflammation in the Brain of a Mouse Model of Hypertension.

Background: Hypertension is one of the main risk factors for dementia and cognitive impairment.

Methods: We used the model of transverse aortic constriction to induce chronic pressure overload in mice. We characterized brain injury by advanced translational applications of magnetic resonance imaging.

Pathogenicity and virulence of : Factors contributing to the fitness in healthcare settings and the infected host.

is a common cause of healthcare-associated infections and hospital outbreaks, particularly in intensive care units. Much of the success of relies on its genomic plasticity, which allows rapid adaptation to adversity and stress. The capacity to acquire novel antibiotic resistance determinants and the tolerance to stresses encountered in the hospital environment promote spread among patients and long-term contamination of the healthcare setting.

Filamin A cooperates with the androgen receptor in preventing skeletal muscle senescence.

Aging induces a slow and progressive decrease in muscle mass and function, causing sarcopenia. Androgens control muscle trophism and exert important anabolic functions through the binding to the androgen receptor. Therefore, analysis of the androgen receptor-mediated actions in skeletal muscle might provide new hints for a better understanding of sarcopenia pathogenesis.

Phylogenomics of species and analysis of antimicrobial resistance genes.

Introduction: Non- species are increasingly isolated in the clinical setting and the environment. The aim of the present study was to analyze a genome database of 837 spp. isolates, which included 798 non- genomes, in order to define the concordance of classification and discriminatory power of 7-gene MLST, 53-gene MLST, and single-nucleotide polymorphism (SNPs) phylogenies.

Exosomes: Emerging Modulators of Pancreatic Cancer Drug Resistance.

Pancreatic cancer (PaC) is one of the most lethal tumors worldwide, difficult to diagnose, and with inadequate therapeutical chances. The most used therapy is gemcitabine, alone or in combination with nanoparticle albumin-bound paclitaxel (nab-paclitaxel), and the multidrug FOLFIRINOX. Unfortunately, PaC develops resistance early, thus reducing the already poor life expectancy of patients.

Efficacy of Novel Combinations of Antibiotics against Multidrug-Resistant-New Delhi Metallo-Beta-Lactamase-Producing Strains of .

The emergence of multidrug-resistance (MDR)-New Delhi metallo-beta-lactamase (NDM)-producing microorganisms-has become a serious concern for treating such infections. Therefore, we investigated the effective antimicrobial combinations against multidrug-resistant New Delhi metallo-beta-lactamase-producing strains of . The tests were carried out using the 2D(two-dimensional) checkerboard method.

A Phase Ib Trial of AVID200, a TGFβ 1/3 Trap, in Patients with Myelofibrosis.

Purpose: Myelofibrosis (MF) is a clonal myeloproliferative neoplasm characterized by systemic symptoms, cytopenias, organomegaly, and bone marrow fibrosis. JAK2 inhibitors afford symptom and spleen burden reduction but do not alter the disease course and frequently lead to thrombocytopenia. TGFβ, a pleiotropic cytokine elaborated by the MF clone, negatively regulates normal hematopoiesis, downregulates antitumor immunity, and promotes bone marrow fibrosis.

Single cell analysis of the localization of the hematopoietic stem cells within the bone marrow architecture identifies niche-specific proliferation dynamics.

Introduction: Hematopoietic stem cells (HSC) reside in the bone marrow (BM) in specialized niches which provide support for their self-replication and differentiation into the blood cells. Recently, numerous studies using sophisticated molecular and microscopic technology have provided snap-shots information on the identity of the BM niches in mice. In adults, HSC are localized around arterioles and sinusoids/venules whereas in juvenile mice they are in close to the osteoblasts.

The vergence-mediated gain increase: Physiology and clinical relevance.

Background: During near-viewing, the vestibulo-ocular reflex (VOR) response/gain increases to compensate for the relatively larger translation of the eyes with respect to the target.

Objective: To review vergence-mediated gain increase (VMGI) testing methods stimuli and responses (latency and amplitude), peripheral/central pathways and clinical relevance.

Methods: The authors discuss publications listed in PUBMED since 1980 in the light of their own studies.

The nerve growth factor-delivered signals in prostate cancer and its associated microenvironment: when the dialogue replaces the monologue.

Prostate cancer (PC) represents the most diagnosed and the second most lethal cancer in men worldwide. Its development and progression occur in concert with alterations in the surrounding tumor microenvironment (TME), made up of stromal cells and extracellular matrix (ECM) that dynamically interact with epithelial PC cells affecting their growth and invasiveness. PC cells, in turn, can functionally sculpt the TME through the secretion of various factors, including neurotrophins.

Inhibition of CXCR1/2 reduces the emperipolesis between neutrophils and megakaryocytes in the Gata1 model of myelofibrosis.

Emperipolesis between neutrophils and megakaryocytes was first identified by transmission electron microscopy. Although rare under steady-state conditions, its frequency greatly increases in myelofibrosis, the most severe of myeloproliferative neoplasms, in which it is believed to contribute to increasing the transforming growth factor (TGF)-β microenvironmental bioavailability responsible for fibrosis. To date, the challenge of performing studies by transmission electron microscopy has hampered the study of factors that drive the pathological emperipolesis observed in myelofibrosis.

CXCL8/CXCR2 signaling mediates bone marrow fibrosis and is a therapeutic target in myelofibrosis.

Proinflammatory signaling is a hallmark feature of human cancer, including in myeloproliferative neoplasms (MPNs), most notably myelofibrosis (MF). Dysregulated inflammatory signaling contributes to fibrotic progression in MF; however, the individual cytokine mediators elicited by malignant MPN cells to promote collagen-producing fibrosis and disease evolution are yet to be fully elucidated. Previously, we identified a critical role for combined constitutive JAK/STAT and aberrant NF-κB proinflammatory signaling in MF development.