Scholar : ΦΩΝΗΤΙΚΕΣ ΧΟΡΔΕΣ - νέα αποτελέσματα

[PDF] Το μοιρολόι του Πόντου. Βιβλιογραφία & ηχογραφήσεις.

Γ Αμπερίδης - 2017

Page 1. ΤΕΙ ΗΠΕΙΡΟΥ ΣΧΟΛΗ ΚΑΛΛΙΤΕΧΝΙΚΩΝ ΣΠΟΥΔΩΝ ΤΜΗΜΑ ΛΑΪΚΗΣ ΚΑΙ ΠΑΡΑΔΟΣΙΑΚΗΣ
ΜΟΥΣΙΚΗΣ ΠΤΥΧΙΑΚΗ ΕΡΓΑΣΙΑ ΤΟ ΜΟΙΡΟΛΟΙ ΤΟΥ ΠΟΝΤΟΥ ΒΙΒΛΙΟΓΡΑΦΙΑ & ΗΧΟΓΡΑΦΗΣΕΙΣ
Φοιτητής: Αμπερίδης Γεώργιος Επιβλέπων: Γεώργιος Κοκκώνης …

[PDF] Ιορδάνης Τσομίδης: ένας «μάγος» της πενιάς. Το πορτραίτο του καλλιτέχνη μέσα από τα ταξίμια του.

ΙΣ Αγγελινάς - 2017

Page 1. ΤΕΙ ΗΠΕΙΡΟΥ ΣΧΟΛΗ ΜΟΥΣΙΚΗΣ ΤΕΧΝΟΛΟΓΙΑΣ ΤΜΗΜΑ ΛΑΙΚΗΣ ΚΑΙ
ΠΑΡΑΔΟΣΙΑΚΗΣ ΜΟΥΣΙΚΗΣ ΠΤΥΧΙΑΚΗ ΕΡΓΑΣΙΑ ΘΕΜΑ Ιορδάνης Τσομίδης: ένας
«μάγος» της πενιάς Το πορτραίτο του καλλιτέχνη μέσα από τα ταξίμια του …

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Αυτή η Ειδοποίηση του Μελετητή Google σας προσφέρεται από τη Google

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Factors impacting hearing aid performance outcomes for Egyptian hearing impaired children

Publication date: Available online 15 December 2017
Source:Egyptian Journal of Ear, Nose, Throat and Allied Sciences
Author(s): Eman Abdel-Fattah Said
Despite recent technological advances in the audiologic assessment of children, their hearing aid fitting remains a daunting task.Aims of studyTo assess effectiveness of amplification in children using aided sound field tests and Auditory Behavior in Everyday Life (ABEL) questionnaire and to elucidate factors contributing to poor outcomes.MethodsDetailed medical history, otoscopic examination, basic audiological evaluation, aided sound field tests and ABEL questionnaire for 114 hearing impaired children aged 4–16 years.ResultsCongenital HL considered the commonest cause of HL (55.3%), 36% had unknown cause and 8.8% of HI had acquired cause. Profound loss in 67.5%, severe in 17% and 54.4% of them (54.4%) were fitted around the age of 3 years. Binaural HA in 88.6% and digital type for 61.4%. There were statistically significant differences between unaided and aided values in sound field tests for HI children.Poor performance in direct measures and ABEl in children with congenital and profound degree of hearing loss, better response when they were fitted earlier with digital aids. ABEL scores showed negative correlations with aided tonal sound field test and positive with aided speech discrimination score.ConclusionsInappropriate amplification, late age of fitting with no speech therapy were clinical red flags for poor outcomes. ABEL questionnaire was a valid procedure to assess the hearing aids appropriateness.



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Progestin-primed ovarian stimulation with or without clomiphene citrate supplementation in normal ovulatory women undergoing IVF/ICSI: a prospective randomized controlled trial

Abstract

Objective

To compare the endocrinological profiles, cycle characteristics and pregnancy outcomes of progestin-primed ovarian stimulation (PPOS) with or without clomiphene citrate (CC) supplementation in normal ovulatory women undergoing in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI).

Design

Prospective randomized controlled study.

Patient(s)

A total of 320 infertile women undergoing IVF/ICSI. Medroxyprogesterone acetate (MPA) and human menopausal gonadotropin (hMG) were simultaneously administered on menstrual cycle day 3. The women were randomized into two equal groups with or without CC supplementation.

Measures

The primary outcome measure was the percentage of women with profound pituitary suppression (luteinizing hormone (LH) < 1.0 IU/L on the trigger day). The secondary outcomes were endocrinological profiles, cycle characteristics and pregnancy outcomes.

Results

The percentage of women with profound pituitary suppression was significantly lower in the study group (hMG + MPA + CC) than in the control group (hMG + MPA) (1.9% vs. 33.1%, P < 0.001). The mean LH level during controlled ovarian stimulation (COS) was higher in the study group than in the control group (P < 0.001), but none of the patients in either group exhibited a premature LH surge. The doses of Gn in the study group were significantly lower than those in the control group (1334.06 ± 212.53 IU vs. 1488.28 ± 325.08 IU, P < 0.001). The number of oocytes retrieved was similar between the two groups (10.03 ± 5.97 vs. 10.34 ± 7.52, P > 0.05). No significant differences were observed in either the number of viable embryos or the pregnancy outcomes between the two groups.

Conclusion(s)

CC is an effective adjuvant to alleviate pituitary suppression in the PPOS protocol; however, it has no impact on clinical outcomes.

This article is protected by copyright. All rights reserved.

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Genetic Overview of Syndactyly and Polydactyly

Summary: Syndactyly and polydactyly—respectively characterized by fused and supernumerary digits—are among the most common congenital limb malformations, with syndactyly presenting at an estimated incidence of 1 in 2,000–3,000 live births and polydactyly at a frequency of 1 in approximately 700–1,000 live births. Despite their relatively regular manifestation in the clinic, the etiologies of syndactyly and polydactyly remain poorly understood because of their phenotypic and genetic diversity. Further, even though concrete knowledge of genotypic links has been established for some variants of syndactyly and polydactyly, there appears to be no single comprehensive published summary of all syndromic and nonsyndromic syndactyly and polydactyly presentations, and there is decidedly no resource that maps all syndromic and nonsyndromic syndactylies and polydactylies to their genetic bases. This gap in the literature problematizes comprehensive carrier screening and prenatal diagnosis and complicates novel diagnostic attempts. This review thus attempts to collect all that is known about the genetic bases of syndromic and nonsyndromic syndactylies and polydactylies, as well as to highlight the dactyly manifestations for which no genetic bases are as yet known. Then, having established a summation of existing and missing knowledge, this work briefly outlines the diagnostic techniques that a genetics-reinforced understanding of syndactyly and polydactyly could inform.

http://ift.tt/2j0AM86

Activation of thyroid antigen-reactive B cells in recent onset autoimmune thyroid disease patients

Publication date: Available online 9 December 2017
Source:Journal of Autoimmunity
Author(s): Mia J. Smith, Marynette Rihanek, Brianne M. Coleman, Peter A. Gottlieb, Virginia D. Sarapura, John C. Cambier
Autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis (HT) and Graves' disease (GD), is the most common autoimmune disorder in the United States, affecting over 20 million people. At the time of diagnosis, both HD and GD are characterized by the accumulation of B and T lymphocytes in the thyroid gland and production of autoantibodies targeting the thyroid, indicating that a breach in tolerance of autoreactive lymphocytes has occurred. However, few studies have sought to understand the underlying pathogenesis of AITD that ultimately leads to production of autoantibodies and loss of thyroid function. In this study, we analyzed the phenotype of thyroid antigen-reactive B cells in the peripheral blood of recent onset and long standing AITD patients. We found that in recent onset patients thyroid antigen-reactive B cells in blood no longer appear anergic, rather they express CD86, a marker of activation. This likely reflects activation of these cells leading to their production of autoantibodies. Hence, this study reports the early loss of anergy in thyroid antigen-reactive B cells, an event that contributes to development of AITD.



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Allele-specific methylation of type 1 diabetes susceptibility genes

Publication date: Available online 8 December 2017
Source:Journal of Autoimmunity
Author(s): Alida S.D. Kindt, Rainer W. Fuerst, Jan Knoop, Michael Laimighofer, Tanja Telieps, Markus Hippich, Maria A. Woerheide, Simone Wahl, Rory Wilson, Eva-Maria Sedlmeier, Angela Hommel, John A. Todd, Jan Krumsiek, Anette-G. Ziegler, Ezio Bonifacio
The susceptibility to autoimmune diseases is influenced by genes encoding major histocompatibility complex (MHC) proteins. By examining the epigenetic methylation maps of cord blood samples, we found marked differences in the methylation status of CpG sites within the MHC genes (cis-metQTLs) between carriers of the type 1 diabetes risk haplotypes HLA-DRB1*03-DQA1*0501-DQB1*0201 (DR3-DQ2) and HLA-DRB1*04-DQA1*0301-DQB1*0302 (DR4-DQ8). These differences were found in children and adults, and were accompanied by reduced HLA-DR protein expression in immune cells with the HLA-DR3-DQ2 haplotype. Extensive cis-metQTLs were identified in all 45 immune and non-immune type 1 diabetes susceptibility genes analyzed in this study. We observed and validated a novel association between the methylation status of CpG sites within the LDHC gene and the development of insulin autoantibodies in early childhood in children who are carriers of the highest type 1 diabetes risk genotype. Functionally relevant epigenetic changes in susceptibility genes may represent therapeutic targets for type 1 diabetes.



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Innately versatile: γδ17 T cells in inflammatory and autoimmune diseases

Publication date: Available online 6 December 2017
Source:Journal of Autoimmunity
Author(s): Pedro H. Papotto, Annika Reinhardt, Immo Prinz, Bruno Silva-Santos
IL-17-producing γδ (γδ17) T cells form a versatile subset of cells that respond rapidly to innate stimuli and support the pro-inflammatory functions of different myeloid and lymphoid lineages, being particularly critical in the early stages of inflammatory and autoimmune responses. In mice, under homeostatic conditions, these innate-like lymphocytes are pre-programmed in the fetal thymus, through an intricate process involving both T cell receptor-dependent and -independent signals, which allows them to readily produce IL-17 upon stimulation. However, given their transcriptional and epigenetic wiring, γδ17 T cells are permissive to different environmental instructions, and can readily acquire the ability to co-produce multiple cytokines, such as IFN-γ, IL-22 and GM-CSF, that further propagate inflammation. Moreover, strong IL-23 signals, which are abundantly found in autoinflammatory conditions, are able to induce de novo differentiation of γδ17 T cells from uncommitted precursors, both in mice and humans. This notwithstanding, the exact mechanisms responsible for γδ17 T cell pathogenicity and multifunctionality are still poorly understood, especially in humans. The pathogenic roles attributed to γδ17 T cells in autoimmune diseases stem mainly from their ability to recruit different inflammatory myeloid populations to the target tissue, and to modulate αβ T cell function, either by enhancing inflammatory TH17 responses, or by restraining regulatory Treg cell activity. Given their capacity to link key inflammatory axes of innate and adaptive immunity, a better understanding of the molecular basis underpinning γδ17 T cell plasticity, and how much this feature accounts for their pathophysiological roles, may be critical for developing novel therapeutic approaches. In this review, we discuss the importance of γδ17 T cells in breaking tolerance and enhancing inflammation in various autoimmune diseases, such as multiple sclerosis, psoriasis and rheumatoid arthritis under the light of their basic biological traits, e.g. development, activation, effector functions and plasticity.



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Editorial Board

Publication date: December 2017
Source:Journal of Autoimmunity, Volume 85





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Immune responses to peptides containing homocitrulline or citrulline in the DR4-transgenic mouse model of rheumatoid arthritis

Publication date: Available online 11 December 2017
Source:Journal of Autoimmunity
Author(s): Patrick Lac, Sheri Saunders, Elena Tutunea-Fatan, Lillian Barra, David A. Bell, Ewa Cairns
Antibodies to proteins/peptides containing citrulline are hallmarks of Rheumatoid Arthritis (RA). These antibodies are strongly associated with the expression of the Shared Epitope (SE). RA patients also generate antibodies to homocitrulline-containing proteins/peptides (also referred to as anti-carbamylated protein antibodies (Anti-CarP)). This study was undertaken to investigate the relationship between homocitrulline and citrulline immune responses using an established mouse model of RA: DR4-transgenic (DR4tg) mice that express the human SE. C57BL/6 (B6) and DR4tg (on a B6 background) mice were immunized subcutaneously with a homocitrullinated peptide (HomoCitJED). Splenic T cell proliferation was evaluated by ³H-thymidine incorporation assay. Antibodies to homocitrullinated and citrullinated antigens were screened by enzyme-linked immunosorbent assay (ELISA). Antibody cross-reactivity was examined by inhibition with HomoCitJED and its citrullinated counterpart peptide, CitJED (the number of homocitrullines in HomoCitJED is equal to the number of citrullines in CitJED). HomoCitJED-immunized DR4tg mice developed early T and B cell responses to HomoCitJED and late responses to CitJED. These mice also developed anti-CCP2 antibodies. In some mice, antibodies to HomoCitJED were also reactive to CitJED. B6 mice immunized with HomoCitJED developed late T and B cell responses to HomoCitJED, but did not generate responses to citrullinated antigens. Unlike DR4tg mice, anti-HomoCitJED antibodies from B6 mice did not react to CitJED. In conclusion, DR4tg mice immunized with HomoCitJED developed immune responses to CitJED, indicating cross-reactivity. CitJED immune responses were dependent on the SE. HomoCitJED responses occurred in the absence of the SE (B6 mice); however, they developed earlier in DR4tg SE-expressing mice.



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Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo

Publication date: Available online 1 December 2017
Source:Journal of Autoimmunity
Author(s): Patrick Maschmeyer, Georg Petkau, Francesco Siracusa, Jakob Zimmermann, Franziska Zügel, Anja Andrea Kühl, Katrin Lehmann, Sarah Schimmelpfennig, Melanie Weber, Claudia Haftmann, René Riedel, Markus Bardua, Gitta Anne Heinz, Cam Loan Tran, Bimba Franziska Hoyer, Falk Hiepe, Sebastian Herzog, Jürgen Wittmann, Nikolaus Rajewsky, Fritz Georg Melchers, Hyun-Dong Chang, Andreas Radbruch, Mir-Farzin Mashreghi
In T lymphocytes, expression of miR-148a is induced by T-bet and Twist1, and is specific for pro-inflammatory Th1 cells. In these cells, miR-148a inhibits the expression of the pro-apoptotic protein Bim and promotes their survival. Here we use sequence-specific cholesterol-modified oligonucleotides against miR-148a (antagomir-148a) for the selective elimination of pro-inflammatory Th1 cells in vivo. In the murine model of transfer colitis, antagomir-148a treatment reduced the number of pro-inflammatory Th1 cells in the colon of colitic mice by 50% and inhibited miR-148a expression by 71% in the remaining Th1 cells. Expression of Bim protein in colonic Th1 cells was increased. Antagomir-148a-mediated reduction of Th1 cells resulted in a significant amelioration of colitis. The effect of antagomir-148a was selective for chronic inflammation. Antigen-specific memory Th cells that were generated by an acute immune reaction to nitrophenylacetyl-coupled chicken gamma globulin (NP-CGG) were not affected by treatment with antagomir-148a, both during the effector and the memory phase. In addition, antibody titers to NP-CGG were not altered. Thus, antagomir-148a might qualify as an effective drug to selectively deplete pro-inflammatory Th1 cells of chronic inflammation without affecting the protective immunological memory.



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Excessive interferon-α signaling in autoimmunity alters glycosphingolipid processing in B cells

Publication date: Available online 27 November 2017
Source:Journal of Autoimmunity
Author(s): Andy Hee-Meng Tan, Arleen Sanny, Sze-Wai Ng, Ying-Swan Ho, Nurhidayah Basri, Alison Ping Lee, Kong-Peng Lam
Excessive interferon-α (IFN-α) production by innate immune cells is a hallmark of autoimmune diseases. What other cell type secretes IFN-α and how IFN-α affects immune cell metabolism and homeostasis in autoimmunity are largely unclear. Here, we report that autoimmune B cells, arising from two different B cell-specific genetic lesions in mice, secrete IFN-α. In addition, IFN-α, found in abundance in autoimmunity, elicited profound changes in the B cell lipidome, increasing their expression of glycosphingolipids (GSLs) and leading to their CD1d-mediated depletion of iNKT cells in vitro and in vivo. IFN-α receptor blockade could reverse the loss of iNKT cells. Excessive stimulation of B cells with IFN-α altered the expression of enzymes that catalyze critical steps in GSL processing, increasing the expressions of glucosylceramide synthase (GCS) and globotrihexosylceramide synthase (Gb3S) but decreasing that of α-galactosidase A (α-galA). Inhibiting GCS or restoring α-galA expression prevented iNKT depletion by IFN-α-activated B cells. Taken together, our work indicated that excessive IFN-α perturbs GSL metabolism in B cells which in turn adversely affects iNKT homeostasis.



http://ift.tt/2yIiWJ0

Th17 cells in primary Sjögren's syndrome: Pathogenicity and plasticity

Publication date: Available online 27 November 2017
Source:Journal of Autoimmunity
Author(s): Gwenny M. Verstappen, Odilia B.J. Corneth, Hendrika Bootsma, Frans G.M. Kroese
Th17 cells play an important physiological role at mucosal barriers, and are involved in inflammatory responses to pathogens. Th17 cells and their signature cytokine IL-17 are also present in salivary gland lesions of primary Sjögren's syndrome (pSS) patients and can be elevated in their peripheral blood. In pSS patients, clear correlations between increased Th17 cell activity and symptoms of the disease have not been found, but Th17 cells may contribute to disease progression, for example by supporting autoreactive B cell responses. In mouse models of pSS, Th17 cells play an important role in pathogenesis, particularly at disease onset, when there is a disturbed balance between T effector and T regulatory cells. Studying the pathogenicity of Th17 cells in humans is complicated due to the plasticity of this cell subset, allowing them to obtain different effector functions depending on the local environment. Th17 cells can develop towards Th17.1 cells, producing both IL-17 and IFN-γ, or even towards Th1-like cells producing IFN-γ in the absence of IL-17. These effector subsets may be more pathogenic than bona fide Th17 cells. Co-expression of IFN-γ by Th17 cells has been shown to promote chronic inflammation in several autoimmune diseases and may also contribute to pSS pathogenesis. In line with the noticeable role of IL-17 in pSS mouse models, interference with Th17 cell generation, recruitment or effector functions (e.g. IL-17 inhibition) can prevent or ameliorate disease in these models. Therapies targeting Th17 cells or IL-17 have not been tested so far in pSS patients, although treatment with rituximab seems to lower local and systemic IL-17 protein levels, and to a lesser extent also chemokine receptor-defined Th17 cells. In this review we discuss current knowledge of pathogenicity and plasticity of Th17 cells in human pSS and murine models of pSS. We postulate that plasticity towards Th17.1 cells in pSS may enhance pathogenicity of Th17 cells at the main target sites of the disease, i.e. salivary and lacrimal glands.



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Tick-borne diseases and autoimmunity: A comprehensive review

Publication date: Available online 26 November 2017
Source:Journal of Autoimmunity
Author(s): Yhojan Rodríguez, Manuel Rojas, M. Eric Gershwin, Juan-Manuel Anaya
Tick-borne diseases (TBDs) are emerging and reemerging diseases transmitted by ticks, which portray wide heterogeneity and global distribution. TBDs may present acute clinical pictures that resemble those of autoimmune diseases (i.e., musculoskeletal symptoms, cutaneous involvement, neurologic impairment, renal failure, etc.), and in some cases infection is considered a triggering factor for autoimmunity (e.g., rheumatoid arthritis, autoimmune thyroid disease, vasculitides). The clinician should consider TBDs among the differential diagnoses when approaching autoimmune-like signs in areas of tick infestation. Epidemiological setting (e.g., endemic areas, seasons) and an accurate diagnostic approach (i.e., clinical history, physical examination and laboratory tests) are necessary to confirm TBDs. Further, control and prevention of TBDs is warranted. Research in the fields of ticks microbiome and vaccination (i.e., wildlife and humans) are ahead to control vector transmission and bacterial infection. This review offers a comprehensive update on TBDs and their relationship with autoimmunity.



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Decrease of galectin-3 in keratinocytes: A potential diagnostic marker and a critical contributor to the pathogenesis of psoriasis

Publication date: Available online 20 November 2017
Source:Journal of Autoimmunity
Author(s): Zhen-rui Shi, Guo-zhen Tan, Cui-xiang Cao, Yan-fang Han, Zhen Meng, Xiao-yong Man, Ze-xin Jiang, Yu-ping Zhang, Ning-ning Dang, Kai-hua Wei, Ding-fang Bu, Fu-tong Liu, Liangchun Wang
Psoriasis-specific proteins dysregulated in keratinocytes and involved in the pathophysiological process of psoriasis remains elusive. We report here that epidermal galectin-3 expression is significantly downregulated in lesional skin, but not in non-lesional skin in psoriasis patients, nor in a group of diseases known as psoriasiform dermatitis clinically and histologically similar to psoriasis. The deficiency of epidermal galectin-3 is sufficient to promote development of psoriatic lesions, as evidenced by more severe skin inflammation in galectin-3 knockout (gal3^−/−) mice, compared to wild-type mice, after imiquimod treatment, and in skin from gal3^−/− mice grafted onto wildtype mice. The development of psoriatic-like lesions is attributable to 1) the spontaneously tuning up of psoriasis signatures in keratinocytes through JNK pathway; and 2) neutrophil accumulation caused by the enhanced leukocyte-recruiting capacity associated with overexpression of S100A7-9 and CXCL-1, 8 in keratinocytes with impaired galectin-3 expression. Psoriasis-like skin inflammation is significantly improved in gal-3^−/− mice both by inhibition of neutrophils accumulation with a selective CXCR2 antagonist of SB225002, and by intracutaneous injection of recombinant galectin-3. Overall, these findings offer promising galectin-3-related diagnostic and therapeutic resolutions of psoriasis.



http://ift.tt/2yGGwFY

Scholar : ΦΩΝΗΤΙΚΕΣ ΧΟΡΔΕΣ - νέα αποτελέσματα

[PDF] Το μοιρολόι του Πόντου. Βιβλιογραφία & ηχογραφήσεις.

Γ Αμπερίδης - 2017

Page 1. ΤΕΙ ΗΠΕΙΡΟΥ ΣΧΟΛΗ ΚΑΛΛΙΤΕΧΝΙΚΩΝ ΣΠΟΥΔΩΝ ΤΜΗΜΑ ΛΑΪΚΗΣ ΚΑΙ ΠΑΡΑΔΟΣΙΑΚΗΣ
ΜΟΥΣΙΚΗΣ ΠΤΥΧΙΑΚΗ ΕΡΓΑΣΙΑ ΤΟ ΜΟΙΡΟΛΟΙ ΤΟΥ ΠΟΝΤΟΥ ΒΙΒΛΙΟΓΡΑΦΙΑ & ΗΧΟΓΡΑΦΗΣΕΙΣ
Φοιτητής: Αμπερίδης Γεώργιος Επιβλέπων: Γεώργιος Κοκκώνης …

[PDF] Ιορδάνης Τσομίδης: ένας «μάγος» της πενιάς. Το πορτραίτο του καλλιτέχνη μέσα από τα ταξίμια του.

ΙΣ Αγγελινάς - 2017

Page 1. ΤΕΙ ΗΠΕΙΡΟΥ ΣΧΟΛΗ ΜΟΥΣΙΚΗΣ ΤΕΧΝΟΛΟΓΙΑΣ ΤΜΗΜΑ ΛΑΙΚΗΣ ΚΑΙ
ΠΑΡΑΔΟΣΙΑΚΗΣ ΜΟΥΣΙΚΗΣ ΠΤΥΧΙΑΚΗ ΕΡΓΑΣΙΑ ΘΕΜΑ Ιορδάνης Τσομίδης: ένας
«μάγος» της πενιάς Το πορτραίτο του καλλιτέχνη μέσα από τα ταξίμια του …

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Αυτή η Ειδοποίηση του Μελετητή Google σας προσφέρεται από τη Google

Ακύρωση ειδοποίησης
Δημιουργία λίστας των ειδοποιήσεών μου

The key role of extracellular vesicles in the metastatic process

Publication date: Available online 24 November 2017
Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer
Author(s): Hongyun Zhao, Abhinav Achreja, Elisabetta Iessi, Mariantonia Logozzi, Davide Mizzoni, Rossella Di Raimo, Deepak Nagrath, Stefano Fais
Extracellular vesicles (EVs), including exosomes, have a key role in the paracrine communication between organs and compartments. EVs shuttle virtually all types of biomolecules such as proteins, lipids, nucleic acids, metabolites and even pharmacological compounds. Their ability to transfer their biomolecular cargo into target cells enables EVs to play a key role in intercellular communication that can regulate cellular functions such as proliferation, apoptosis and migration. This has led to the emergence of EVs as a key player in tumor growth and metastasis through the formation of "tumor niches" in target organs. Recent data have also been shown that EVs may transform the microenvironment of primary tumors thus favoring the selection of cancer cells with a metastatic behavior. The release of EVs from resident non-malignant cells may contribute to the metastatic processes as well. However, cancer EVs may induce malignant transformation in resident mesenchymal stem cells, suggesting that the metastatic process is not exclusively due to circulating tumor cells. In this review, we outline and discuss evidence-based roles of EVs in actively regulating multiple steps of the metastatic process and how we can leverage EVs to impair metastasis.

Graphical abstract

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Genetic host factors in Helicobacter pylori-induced carcinogenesis: Emerging new paradigms

Publication date: January 2018
Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Volume 1869, Issue 1
Author(s): Michiel C. Mommersteeg, Jun Yu, Maikel P. Peppelenbosch, Gwenny M. Fuhler
Helicobacter Pylori is a gram negative rod shaped microaerophilic bacterium that colonizes the stomach of approximately half the world's population. Infection with c may cause chronic gastritis which via a quite well described process known as Correas cascade can progress through sequential development of atrophic gastritis, intestinal metaplasia and dysplasia to gastric cancer. H. pylori is currently the only bacterium that is classified as a class 1 carcinogen by the WHO, although the exact mechanisms by which this bacterium contributes to gastric carcinogenesis are still poorly understood. Only a minority of H. pylori-infected patients will eventually develop gastric cancer, suggesting that host factors may be important in determining the outcome of H. pylori infection. This is supported by a growing body of evidence suggesting that the host genetic background contributes to risk of H. pylori infection and gastric carcinogenesis. In particular single nucleotide polymorphisms in genes that influence bacterial handling via pattern recognition receptors appear to be involved, further strengthening the link between host risk factors, H. pylori incidence and cancer. Many of these genes influence cellular pathways leading to inflammatory signaling, inflammasome formation and autophagy. In this review we summarize known carcinogenic effects of H. pylori, and discuss recent findings that implicate host genetic pattern recognition pathways in the development of gastric cancer and their relation with H. pylori.



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Long pentraxin 3: A novel multifaceted player in cancer

Publication date: January 2018
Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Volume 1869, Issue 1
Author(s): Arianna Giacomini, Gaia Cristina Ghedini, Marco Presta, Roberto Ronca
Since its discovery in 1992, long pentraxin 3 (PTX3) has been characterized as soluble patter recognition receptor, a key player of the innate immunity arm with non-redundant functions in pathogen recognition and inflammatory responses. As a component of the extra-cellular matrix milieu, PTX3 has been implicated also in wound healing/tissue remodeling, cardiovascular diseases, fertility, and infectious diseases. Consequently, PTX3 levels in biological fluids have been proposed as a fluid-phase biomarker in different pathological conditions.In the last decade, experimental evidences have shown that PTX3 may exert a significant impact also on different aspects of cancer biology, including tumor onset, angiogenesis, metastatic dissemination and immune-modulation. However, it remains unclear whether PTX3 acts as a good cop or bad cop in cancer. In this review, we will summarize and discuss the scientific literature data focusing on the role of PTX3 in experimental and human tumors, including its putative translational implications.



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Scholar : ΦΩΝΗΤΙΚΕΣ ΧΟΡΔΕΣ - νέα αποτελέσματα

[PDF] Το μοιρολόι του Πόντου. Βιβλιογραφία & ηχογραφήσεις.

Γ Αμπερίδης - 2017

Page 1. ΤΕΙ ΗΠΕΙΡΟΥ ΣΧΟΛΗ ΚΑΛΛΙΤΕΧΝΙΚΩΝ ΣΠΟΥΔΩΝ ΤΜΗΜΑ ΛΑΪΚΗΣ ΚΑΙ ΠΑΡΑΔΟΣΙΑΚΗΣ
ΜΟΥΣΙΚΗΣ ΠΤΥΧΙΑΚΗ ΕΡΓΑΣΙΑ ΤΟ ΜΟΙΡΟΛΟΙ ΤΟΥ ΠΟΝΤΟΥ ΒΙΒΛΙΟΓΡΑΦΙΑ & ΗΧΟΓΡΑΦΗΣΕΙΣ
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ΙΣ Αγγελινάς - 2017

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Cystic Fibrosis Transmembrane Conductance Regulator Attaches Tumor Suppressor PTEN to the Membrane and Promotes Anti Pseudomonas aeruginosa Immunity

Publication date: Available online 12 December 2017
Source:Immunity
Author(s): Sebastián A. Riquelme, Benjamin D. Hopkins, Andrew L. Wolfe, Emily DiMango, Kipyegon Kitur, Ramon Parsons, Alice Prince
The tumor suppressor PTEN controls cell proliferation by regulating phosphatidylinositol-3-kinase (PI3K) activity, but the participation of PTEN in host defense against bacterial infection is less well understood. Anti-inflammatory PI3K-Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-inflammatory responses to airway infection. We found that Ptenl^−/− mice, which lack the NH2-amino terminal splice variant of PTEN, were unable to eradicate Pseudomonas aeruginosa from the airways and could not generate sufficient anti-inflammatory PI3K activity, similar to what is observed in CF. PTEN and the CF transmembrane conductance regulator (CFTR) interacted directly and this interaction was necessary to position PTEN at the membrane. CF patients under corrector-potentiator therapy, which enhances CFTR transport to the membrane, have increased PTEN amounts. These findings suggest that improved CFTR trafficking could enhance P. aeruginosa clearance from the CF airway by activating PTEN-mediated anti-bacterial responses and might represent a therapeutic strategy.

Graphical abstract

Teaser

Anti-inflammatory PI3K-Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-inflammatory responses to airway infection. Riquelme et al. find that CFTR channel directly interacts with tumor suppressor PTEN, which regulates PI3K activity. CFTR helps position PTEN at the membrane to promote PTEN function and host immunity against Pseudomonas aeruginosa infection.


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