Nikolena Repousi

Nikolena Repousi


Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 March 2022 in Pathogens
Verified
Journal Article
Open access
PDF file
GPGethsimani Papadopoulou
Gethsimani Papadopoulou
EMEleni Manoloudi
Eleni Manoloudi
NRNikolena Repousi
Nikolena Repousi
Lemonia SkouraLemonia Skoura
Lemonia Skoura
THTara Hurst
Tara Hurst
TKTimokratis Karamitros
Timokratis Karamitros
The coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), poses several challenges to clinicians, due to its unpredictable clinical course. The identification of laboratory biomarkers, specific cellular, and molecular mediators of immune response could contribute to the prognosis and management of COVID-19 patients. Of utmost importance is also the detection of differentially expressed genes, which can serve as transcriptomic signatures, providing information valuable to stratify patients into groups, based on the severity of the disease. The role of biomarkers such as IL-6, procalcitonin, neutrophil–lymphocyte ratio, white blood cell counts, etc. has already been highlighted in recently published studies; however, there is a notable amount of new evidence that has not been summarized yet, especially regarding transcriptomic signatures. Hence, in this review, we assess the latest cellular and molecular data and determine the significance of abnormalities in potential biomarkers for COVID-19 severity and persistence. Furthermore, we applied Gene Ontology (GO) enrichment analysis using the genes reported as differentially expressed in the literature in order to investigate which biological pathways are significantly enriched. The analysis revealed a number of processes, such as inflammatory response, and monocyte and neutrophil chemotaxis, which occur as part of the complex immune response to SARS-CoV-2.

1 May 2022 in European Journal Of Dermatology
Verified
Journal Article
Closed access
PDF file
NRNikolena Repousi
Nikolena Repousi
SFStavroula Fotiadou
Stavroula Fotiadou
ECEleftheria Chaireti
Eleftheria Chaireti
GMGerasimos Makris
Gerasimos Makris
GCGiorgos Chouliaras
Giorgos Chouliaras
PPPanagiota Pervanidou
Panagiota Pervanidou
There is evidence that stress and psoriasis interact bidirectionally. Specifically, stress is not only induced by psoriasis, but it is also considered a precipitating factor for onset or exacerbation of the disease. Neuroendocrine alterations of the stress system have been implicated in this association. To assess the diurnal rhythm of the hypothalamic-pituitary-adrenal (HPA) axis and hair cortisol levels in patients with psoriasis compared to healthy controls, and further explore whether suggested alterations in HPA axis activity are related to anthropometric, psychological, and disease activity/severity indices. We assessed stress levels quantified by questionnaires, psoriasis severity, and stress system activity based on HPA axis biomarkers. The sample comprised 18 adult patients with exacerbation of non-pustular psoriasis compared to 18 healthy controls (18-65 years old). In particular, salivary cortisol diurnal profiles and hair cortisol concentration were evaluated in both groups. Five distinct salivary samples were collected during a day of rest and 3-cm hair segments were cut. A higher prevalence of self-reported anxiety, stress, and depressive symptoms was reported among psoriatic patients compared to healthy controls. Also, blunted salivary cortisol diurnal rhythm in psoriatic patients and a positive correlation of salivary cortisol concentration with state anxiety and psoriasis severity were revealed. No associations were shown between hair cortisol concentrations and disease presence/severity. We provide preliminary evidence that psoriasis patients may demonstrate a hypofunctional HPA axis, while our findings also suggest a complex interaction between HPA axis activity, psychosocial status and pathophysiological processes in psoriasis.