Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Δευτέρα 8 Μαρτίου 2021

Integrated analysis of miRNA‐mRNA networks reveals a strong anti‐skin cancer signature in vitiligo epidermis

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Abstract

Background

Expression of microRNAs (miRNAs) is often dysregulated in several cancers, including non‐melanoma skin cancer (NMSC). Individuals with vitiligo possess a deregulated miRnome along with a lower risk of developing NMSCs.

Objectives

To understand the molecular basis underlying the lower incidence of NMSC observed in patients with vitiligo by investigating their miRNA‐regulated gene networks.

Methodology

We used data sets from our previously published studies on vitiligo epidermis to construct functional miRNA‐mRNA networks. MiRtarbase was used to fetch the experimentally validated targets of DE‐miRNAs. Protein‐protein interaction (PPI) networks were constructed with only those gene targets that demonstrated a pattern of inverse regulation with their upstream miRNAs. Oncogenic transcription factors (OTFs) that were upregulated in publicly available squamous cell carcinoma (SCC) or basal cell carcinoma (BCC) microarray data were compared with that of vitiligo to decode skin cancer‐specific molecular signatures.

Results

Two PPI networks were constructed for the miRNA–mRNA interactions (230 down‐regulated targets of 5 up‐regulated miRNAs and 47 up‐regulated mRNAs targeted by 12 down‐regulated miRNAs). Pathway enrichment analysis identified RNA biogenesis and transport as well as cell adhesion to be perturbed in vitiligo. We further identified three significantly upregulated miRNAs, miR‐31‐5p, miR‐31‐3p and miR‐194‐3p in lesional epidermis that could negatively regulate seven oncogenic transcription factors, FOXC1, AR, SP1, YY1, GLI2, TP53 and RARA, known to be overexpressed in SCC or BCC.

Conclusion

We identified a perturbed miRNA‐regulated transcriptome, which potentially confers protection to vitiligo skin from an increased incidence of NMSC.

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Serum vasohibin‐1 levels: a potential marker of dermal and pulmonary fibrosis in systemic sclerosis

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Abstract

Vasohibin‐1 (VASH‐1) is a potent anti‐angiogenic factor mainly produced by endothelial cells. In addition, VASH‐1 prevents TGF‐β‐dependent activation of renal fibroblasts. Since systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy and fibrosis of multiple organs, VASH‐1 may be involved in the development of this disease. In this study, we investigated the potential role of VASH‐1 in SSc by evaluating the clinical correlation of serum VASH‐1 levels and the expression of VASH‐1 in SSc‐involved skin. Serum VASH‐1 levels were higher in SSc patients, especially those with diffuse cutaneous involvement, than in healthy controls and positively correlated with skin score. Furthermore, SSc patients with interstitial lung disease had significantly elevated levels of serum VASH‐1 as compared to those without. Importantly, serum VASH‐1 levels correlated inversely with both the percentage of predicted vital capacity and the percentage of predicted diffusion lung capacity for carbon monoxide and positively with serum KL‐6 levels, but not serum surfactant protein‐D levels. In SSc‐involved skin, VASH1 mRNA was remarkably upregulated compared with healthy control skin, but the major source of VASH‐1 was not clear. Fli1 deficiency, a predisposing factor inducing SSc‐like endothelial properties, did not affect VASH‐1 expression in human dermal microvascular endothelial cells. Collectively, these results suggest that VASH‐1 upregulation in the skin and sera is linked to dermal and pulmonary fibrotic changes in SSc, while the contribution of VASH‐1 to SSc vasculopathy seems to be limited.

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Keratinocyte‐derived IL‐1β induces PPARG down‐regulation and PPARD up‐regulation in

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Abstract

Peroxisome proliferator‐activated receptors (PPARs) are a family of nuclear hormone receptors. In skin, PPARs modulate inflammation, lipid synthesis, keratinocyte differentiation and proliferation and thus are important for skin barrier homeostasis. Accordingly, PPAR expression is altered in various skin conditions that entail epidermal barrier impairment i.e. atopic dermatitis (AD) and psoriasis. Using human epidermal equivalents (HEEs) we established models of acute epidermal barrier impairment devoid of immune cells. We assessed PPAR and cytokine expression after barrier perturbation and examined effects of keratinocyte‐derived cytokines on PPAR expression. We show that acetone or SDS treatment causes graded impairment of epidermal barrier function. Furthermore, we demonstrate that besides IL‐1β and TNFα, IL‐33 and TSLP are highly relevant markers for acute epidermal barrier impairment. Both SDS‐ and acetone‐mediated epidermal barrier impairment reduce PPARG expression levels, whereas only SDS enhances PPARD expression. In line with findings in IL‐1β and TNFα treated HEEs, abrogation of IL‐1 signaling restores PPARG expression and limits the increase of PPARD expression in SDS‐induced epidermal barrier impairment. Thus, following epidermal barrier perturbation, keratinocyte‐derived IL‐1β and partly TNFα modulate PPARG and PPARD expression. These results emphasize a role for PPARγ and PPARβ/δ in acute epidermal barrier impairment with possible implications for diseases such as AD and psoriasis.

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Head and neck cancer and non‐steroidal anti‐inflammatory drugs: Systematic review and meta‐analysis

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Abstract

The objective was to assess the effects of non‐steroidal anti‐inflammatory drugs (NSAIDs) on head and neck cancer (HNC) outcomes. A systematic review was conducted following the PRISMA guidelines. The MEDLINE and the Cochrane Central Register databases were searched. Risk of bias was assessed by the Cochrane Collaboration's tool and by the Newcastle‐Ottawa Scale. Meta‐analyses were performed with the RevMan software. Seventeen articles met the inclusion criteria. Quality scores for observational studies ranged between 5 and 8 stars and the RCT was assessed as high risk of bias. NSAIDs use was associated with a 13% risk reduction of HNC (OR: 0.87 95% CI 0.77–0.99). NSAIDs use was associated with a 30% reduced cancer‐specific mortality and with a 40% decreased risk on disease‐recurrence. NSAIDs may have a modest protective effect on HNC risk and a positive impact on cancer‐specific survival and disease‐recurrence. The findings do not support a protective role of as pirin on HNC outcomes.

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Multi-Detector CT Instillation Dacryocystography and Its Role in the Diagnosis of Lacrimal Drainage System Blocks

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Abstract

To assess the use of Multi-detector computed tomography instillation dacryocystography (MDCT-DCG) and its role in the diagnosis of lacrimal drainage system (LDS) blocks. It is a prospective evaluation of Twenty-five cases presenting with symptoms with NLDO (nasolacrimal duct obstruction) assessed by MDCT-DCG. The study was conducted in LN medical college and JK hospital Bhopal (M.P) territory centre between January 2016 and January 2017. Various levels of LDS obstruction were detected, Lower canaliculus 12% common canaliculus in 20% patients, lacrimal sac in 12% junction between lacrimal sac and NLD in 40% and NLD obstruction in 16% patients. The most common CTDCG findings were dilated opacified lacrimal sac with no opacification of the nasolacrimal duct (NLD) in 40% patients. CTDCG is a non-invasive, quick, patient friendly, indispensable in the assessment of NLDO procedure that adds benefit in documentation and preoperative planning.

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Incidence and Clinical Analysis of Complications of Neck Dissection

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Abstract

The aim of the study was to assess and evaluate the incidence of complications related to type of neck dissection to different variables. Retrospective study was conducted on patients who reported to our craniofacial centre between 2010 and 2019 and underwent neck dissection for evaluation of complications related to it. Records of all patients were analysed for complications which were alienated into intra-operative, immediate post-operative (within 10 days) and post-operative complications. 256 patients, 141 male and 115 female aged between 25 and 70 years operated for squamous cell carcinoma were included. The overall incidence of complications was 32.8%. Intra-operative complications were haemorrhage 14%, nerve injury 5.4%, inadvertent internal jugular vein ligation 0.3%, chyle leak 0.3%. No incidence of carotid blow out. Immediate post-operative complications were hematoma formation 7%, salivary fistula in 2.3% and re-exploration was done in 1.5% c ases. Post-operative complications noted were wound dehiscence in 22.6%, infection in 20.7%, hematoma in 2.7%, salivary fistula in 11.7% and nerve injury in 0.3% cases. Neck dissection is a challenging and therapeutic procedure. Prevention of major complications like carotid blow-out, injury to brachial plexus, vagus nerve or hypoglossal nerve requires thorough knowledge of neck anatomy.

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Allergische Reaktionen auf COVID-19-Impfungen – Was HNO-Ärzte wissen sollten – Teil 1: Immunologische Grundlagen von Allergien auf Impfstoffe, Immunmechanismen von allergischen und pseudoallergischen Reaktionen; Teil 2: Charakteristika der mRNA-Impfstoffe BNT162b2- und mRNA-1273 zur Prophylaxe von COVID-19 und assoziierte Immunphänomene; Teil 3: Praktische Aspekte der Prophylaxe, Diagnostik und Therapie von Allergien auf COVID-19-Impfstoffe

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Laryngorhinootologie
DOI: 10.1055/a-1397-0754

Obwohl allergische Reaktionen auf mRNA-COVID-19-Impfstoffe selten sind, ist durch die hohe Zahl der durchzuführenden Impfungen mit Anaphylaxien bei Personen zu rechnen, die zuvor auf Impfstoffkomponenten sensibilisiert wurden. Dargelegt werden hier praktische Aspekte zu diagnostischen Möglichkeiten, zur Prävention, zum Erkennen und zur Therapie einer anaphylaktischen Reaktion. Risikopopulationen, die nicht geimpft werden sollten oder die eine allergologische Abklärung vor Impfung benötigen, werden besprochen. Patienten mit Allergien des atopischen Formenkreises sowie Insektengiftallergiker zeigen aus allergologischer Sicht kein erhöhtes Risiko für eine Anaphylaxie durch eine COVID-Impfung.
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Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany

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