The Yin and Yang of hsa-miR-1244 expression levels during activation of the UPR control cell fate.

Regulation of endoplasmic reticulum (ER) homeostasis plays a critical role in maintaining cell survival. When ER stress occurs, a network of three pathways called the unfolded protein response (UPR) is activated to reestablish homeostasis. While it is known that there is cross-talk between these pathways, how this complex network is regulated is not entirely clear.

The lipid side of unfolded protein response.

Although our current knowledge of the molecular crosstalk between the ER stress, the unfolded protein response (UPR), and lipid homeostasis remains limited, there is increasing evidence that dysregulation of either protein or lipid homeostasis profoundly affects the other. Most research regarding UPR signaling in human diseases has focused on the causes and consequences of disrupted protein folding. The UPR itself consists of very complex pathways that function to not only maintain protein homeostasis, but just as importantly, modulate lipid biogenesis to allow the ER to adjust and promote cell survival.

Activity of Novel Ultrashort Cyclic Lipopeptides against Biofilm of Isolated from VVC in the Ex Vivo Animal Vaginal Model and BioFlux Biofilm Model-A Pilot Study.

In recent years, clinicians and doctors have become increasingly interested in fungal infections, including those affecting the mucous membranes. Vulvovaginal candidiasis (VVC) is no exception. The etiology of this infection remains unexplained to this day, as well as the role and significance of asymptomatic vaginal colonization.

Virulence Factors of spp. and Host Immune Response Important in the Pathogenesis of Vulvovaginal Candidiasis.

Vulvovaginal candidiasis (VVC) is one of the most common types of vaginal infections in women around the world and is often underestimated by both patients and doctors. Research on the pathogenesis of fungal vaginal infections over the last 20 years has resulted in a closer understanding of the virulence factors involved in epithelial invasion and their mechanisms of action. Recently, attention was drawn to the enormous complexity of the interaction between yeast-like fungi and host cells, as well as the level of complexity of the host's response to infection and their impact on the course and treatment of VVC.

Antifungal Activity of Linear and Disulfide-Cyclized Ultrashort Cationic Lipopeptides Alone and in Combination with Fluconazole against Vulvovaginal spp.

Vulvovaginal candidiasis (VVC) occurs in over 75% of women at least once during their lifetime and is an infection that significantly affects their health. strains resistant to standard azole antifungal therapy and relapses of VVC are more and more common. Hypothetically, biofilm is one of the main reasons of relapses and failure of the therapy.

The Antimicrobial Activity of Omiganan Alone and In Combination against Isolated from Vulvovaginal Candidiasis and Bloodstream Infections.

Fungi from the genus are widespread commensals and, at the same time, are the leading cause of fungal infections worldwide. For instance, vulvovaginal candidiasis (VVC) affects approximately 75% of women at least once in their lifetime, remaining the second most common gynecological infection. On the contrary, hospital-acquired fungal bloodstream infections (BSIs), although less frequent, are characterized by a high mortality rate.

Anticandidal Activity of Omiganan and Its Retro Analog Alone and in Combination with Fluconazole.

Vulvovaginal candidiasis (VVC) is a vaginal infection that manifests itself as several symptoms which can lead to various life-threatening complications. The majority of VVC is caused by Candida albicans strains, and it is estimated that approximately 75% of women worldwide would suffer from this condition at least once during their lifetime. Surprisingly, the detailed pathomechanism of yeast-like fungi invasions in vagina is not yet fully understood.

Polymorphisms of the MTHFR gene in mothers of children with trisomy 21 (Down syndrome) in a Polish population.

Background: Down syndrome (DS) is the most frequent cause of intellectual disability. In 95% of cases, it is caused by simple trisomy of chromosome 21 resulting from nondisjunction of chromosomes in meiotic division. Currently, the molecular and cellular mechanisms responsible for the phenomenon of nondisjunction are unknown.