Aims Our aim was to investigate the skin‐homing T‐cell immune responses triggered in patients with Demodex infestation and/or rosacea. Methods Collected whole blood samples were divided into four groups: control subjects; nonrosacea patients with Demodex infestation (Demodex group); papulopustular rosacea (PPR) patients without Demodex infestation (Rosacea group); and PPR patients with Demodex infestation (Rosacea/Demodex group). Following ex vivo activation, skin‐homing CLA+CD4+ T‐cell subset levels were monitored by flow cytometry. Results When compared with control subjects, among skin‐homing CD4+ T‐cell subsets analysed, Demodex patients had higher TH9 and Treg cell levels; Rosacea subjects displayed elevated TH1 cell levels; and Rosacea/Demodex patients exhibited increased frequencies of TH9 and TH22 cells. In contrast to Rosacea subjects, Rosacea/Demodex group members displayed higher TH2 cell levels; and when compared with Demodex groups, they had higher TH1 and TH2 but lower Treg cell levels. Demodex group members also exhibited higher Treg but lower TH1 and TH22 levels than Rosacea/Demodex group subjects. Conclusions The skin‐homing T‐cell responses associated with Demodex infestation and rosacea formation seem to influence each other. The present as well as future studies could contribute to the development of effective treatment strategies for demodicosis and rosacea.

Lichens and their secondary metabolite are still among the many unexamined natural sources in the drug industry. This study was designed to evaluate the cytotoxic effects of vulpinic acid lichen secondary metabolite and 6. 25, 12.5, 25, 50, 100, 200 and 400 µM concentrations that treat cancer cell lines (CaCo2, HepG2, Hep2C, RD Wehi) and normal cells (Vero and L929) by MTT assay. The aim of this study was to determine the apoptotic effect of vulpinic acid on a molecular level. The determination of apoptotic molecular patterns of vulpinic acid was performed on western blot and quantitative realtime PCR (qRT-PCR) analysis. In our study, transcriptome changes on both gene and protein levels showed similar results. The determination of, mRNA levels of Bax, Bcl-2 and P53 genes were showed by qRT-PCR in cancer and normal cell lines. The results of the study showed that IC 50 value of vulpinic acid altered the mRNA levels of Bax, Bcl-2 and P53 genes in all examined cancer cells when compared to the untreated cells. When the mRNA levels of the examined genes were compared, it was observed that Bax gene showed more expression increase in all cell lines when compared to Bcl-2 and P53 genes. This is the first evaluation of the apoptotic effect of vulpinic acid secondary metabolite on mRNA levels. The current study highlights some points regarding vulpinic acid and its use for cancer treatment.

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The modulation of cardiac functions by nitric oxide (NO) was established. This study examined the influences of phosphodiesterase (PDE) inhibitors on the action of NO in the different regions of the rat heart. NO donor diethylamine nonoate (DEA/NO) (0.1-100 μM) decreased functions of the right atrium. DEA/NO-induced depression of the developed tension of the right atrium was inhibited by [erythro-9-(2-hydroxy-3-nonyl)adenine] (PDE2 inhibitor), augmented by milrinone (PDE3 inhibitor), and upturned by rolipram (PDE4 inhibitor). A DEA/NO-induced decrease in the resting tension was inhibited by vinpocetine (PDE1 inhibitor) and [erythro-9-(2-hydroxy-3-nonyl)adenine] but reversed by rolipram. The decreased sinus rate by DEA/NO was prevented by vinpocetine and rolipram. DEA/NO increased cyclic guanosine monophosphate and cyclic adenosine monophosphate (cAMP) concentrations in the right atrium, and rolipram enhanced increased cAMP level. DEA/NO had no effect on the contraction of the papillary muscle. However, unchanged contraction under DEA/NO stimulation was decreased by vinpocetine, milrinone, and rolipram. DEA/NO increased cyclic guanosine monophosphate concentration but has no effect on cAMP in the papillary muscle. However, in the presence of vinpocetine and milrinone, DEA/NO reduced cAMP level. The PDE5 inhibitor sildenafil has no effect on DEA/NO actions. This study indicates that a variety of PDE activities in different regions of the rat heart shapes the action of NO on the myocardium.

Leishmaniasis, a deadly parasitic infection, threatens many people worldwide. Since the high cost, toxicity, and resistance are drawbacks of current treatment options, it is necessary to find safer and more effective new antileishmanial drugs. The aim of this study was to determine the antileishmanial activity of usnic acid and its apoptotic mechanism on spp. promastigotes. The antileishmanial activity was evaluated by MTT assay and apoptosis-related gene expression was investigated by qRT-PCR. Usnic acid was to be effective against, and promastigotes at IC = 10.76 µg/ml, 13.34 µg/ml, and 21.06 µg/ml, respectively. We also demonstrated a novel mechanism by which usnic acid inhibited proliferation and caused apoptosis; usnic acid upregulated , and gene expression and downregulated the level of gene expression. Accordingly, the expression level of the P53 gene increased in and by 14.4-, 11.8-, and 9.5-fold, respectively, and in contrast, the gene expression decreased in all three leishmaniasis by 0.8-, 0.8-, and 0.7-fold, respectively. The present study, therefore, revealed that usnic acid played a critical role in the usnic acid-induced apoptotic process in species. Usnic acid is easily accessible and an inexpensive agent, and can be considered as an alternative therapeutic agent for infections subject to further tests in animal models.

Our results suggest that spleen is important, but not essential, for survival and/or generation of memory IgG B cells. In contrast, it seems to be indispensable for PCV-13-specific memory T 1-cell levels. Studies enhancing the levels of vaccine-induced memory cells and further enlightening the immune responses in asplenic individuals are required to develop more effective vaccination strategies against OPSI.