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  • Additionally molecular imaging has great potential for nonin

    2022-07-30

    Additionally, molecular imaging has great potential for noninvasive and quantitative imaging of pancreatic β-cells, but each single imaging modality has its own intrinsic strengths and limitations. Functional imaging modalities have high sensitivity (such as SPECT and PET) and anatomical imaging techniques have high spatial resolution (such as CT and MRI) [266]. Therefore, a bimodal or multimodal approach may provide complementary quantitative and spatial information [165].
    CRTH2 – history and clinical potential Ironically, the purported TP antagonist ramatroban (BAY u 3405) which had already been marketed in Japan as a treatment of allergic rhinitis, was also revealed to be a potent CRTH2 antagonist [34].
    CRTH2 beyond allergy and asthma Meanwhile, CRTH2 has been found to be expressed on several additional cell types and in different tissues suggesting that the PGD2/CRTH2 axis might be of potential relevance beyond allergy and asthma. Although the role of PGD2 in a Th2-biased inflammation is well established, investigation of its function in other groups of inflammatory reactions in experimental mouse models is confounded by differential expression patterns of CRTH2 in mice and humans: While CRTH2 can be used as an exclusive marker for Th2 ARQ197 in humans, CRTH2-positive Th1 cells as well as neutrophils are present in mice. These differences have to be taken into consideration when drawing conclusions from studies exclusively based on mouse data. A detailed summary of the presence or absence of CRTH2 on various cells types can be found in Table 1.
    Conclusion With a plethora of actions, CRTH2-mediated effects are apparent in almost every tissue of the human body (Fig. 1). There is growing evidence that CRTH2 plays important roles in allergic inflammation of the respiratory tract and the skin; however, this does not exclude it from being a potential therapeutic target in other conditions, too. These might comprise inflammatory bowel disease, mood disturbances or even cognitive dysfunction on the one hand, and autoimmune disease such as rheumatoid arthritis, and lung and kidney fibrosis, on the other hand. In male-type baldness, CRTH2 antagonists might already be on the crossroads to becoming available for patients, soon. Supported by the Austrian Science Fund FWF (grant P22521-B18 to A.H.) and the Austrian National Bank (grant 14263 to A.H.). K.J. was funded by the PhD Program DK-MOLIN (FWF-W1241).
    Acknowledgements
    Introduction Androgenetic alopecia (AGA) and alopecia areata (AA) are common forms of hair loss. AGA is caused by the heightened sensitivity of scalp follicles to dihydrotestosterone (DHT) whereas AA is induced by an autoimmune reaction [1]. Various synthetic medicines are available for hair loss treatment. Among them are minoxidil, finasteride and spironolactone used for AGA treatment, as well as minoxidil, anthralin (dithranol), corticosteroids and tretinoin used for AA therapy [1], [2], [3]. The mechanisms by which synthetic drugs promotes hair growth are partially understood. Minoxidil has a specific direct effect on the proliferation and differentiation of follicular keratinocytes which leads to prolongation of the anagen phase. Many mechanisms of action of minoxidil have been proposed [4], including (1) minoxidil metabolised by the enzyme sulphotranspherase to minoxidil sulfate in the hair follicles, acts as a potassium channel agonist to reduce the cytoplasmic free Ca concentration and then prevents epidermal growth factor (EGF) from inhibiting hair formation [5], [6], (2) minoxidil increased expression of VEGF and its receptors in the dermal papilla which subsequently stimulates angiogenesis in the hair anagen phase [7], (3) minoxidil stimulates regrowth in hair follicle cultures where a blood supply is absent [8], (4) minoxidil is a potent activator of prostaglandin endoperoxide synthase-1, a cytoprotective enzyme that stimulates hair growth [9], (5) minoxidil induce hair growth through the activation of Wnt/β-catenin pathway [10], (6) minoxidil increases the number of DNA synthesising cells in the dermal papilla, bulbar matrix, outer root sheath and perifollicular fibrocytic cells, what result in the prolongation of anagen phase and the conversion of vellus hairs to terminal hairs [11], [12]. In turn, finasteride is a competitive inhibitor of type II 5α-reductase. This intracellular enzyme converts testosterone into the biologically more active metabolite dihydrotestosterone (DHT) which binds to androgenic receptors in the hair follicle and then activates the genes responsible for hair follicle regression. By reducing scalp tissue levels of DHT, finasteride treatment suppresses male pattern hair shedding [13], [14]. Dutasteride mechanism of action is similar to finasteride, with one difference, dutasteride is a competitive inhibitor both of type I and II 5α-reductase [15]. Spironolactone has potent anti-androgenic properties resulting from dual mechanisms: reduction of androgen production and competitive blockage of androgen receptors in target tissues [16]. The mechanism of anthralin action is unknown, but in mouse studies anthralin has been shown to decrease the expression of tumor necrosis factor-α (TNF-α) and -β (TNF-β) in the treated area [17].