Treatment and control for IBD are

Treatment and control for IBD are targeted to identify and eliminate the cause if possible, decrease intestinal inflammation, reduce diarrhea and vomiting, improve appetite, and promote weight gain. Methods include dietary manipulation with or without concurrent medical therapy such as corticosteroids, azathioprine, sulfasalazine, metronidazole, and tylosin. A typical treatment protocol begins with an antiparasitic medication, followed by dietary modification for 3-4 weeks, then an antibacterial trial for 3-4 weeks, and lastly immunosuppressive therapy. Treatment for IBD in ferrets is similar to that of other small animals and includes immunosuppressive therapy and elimination of possible causes of gastrointestinal inflammation. Immunosuppression may be achieved by using prednisolone, cyclosporine, or azathioprine.
Acknowledgments
Introduction Despite advancements in preclinical and clinical research, cancer incidence remains in full view due to a range of heterogeneous risk factors including location, ethnicity, gender, dietary habits, genetic predisposition, environmental exposure and socio-economic factors. Therefore, cancer research is still one of the top research subjects, with current interest focusing on personalized and targeted therapeutic approaches, novel diagnosis and prognosis methods and improved clinical management [1]. The installation and development of malignant entities is governed by a high number of interconnected pathological signaling pathways such as the extracellular signaling Wingless-type (Wnt) and Hedgehog (Hh) pathways, linked to direct embryonic growth and modeling and abnormally synchronized in cancer [2]. In fact, the Hh signaling pathway is fundamental in regulating cell growth and differentiation, as well as maintaining homeostasis in several tissues and organs, by influencing the activity of stem Safingol in vertebrates and invertebrate organisms [[2], [3], [4]]. It is well-known that stem cells possess the capacity for continuous division, being able to shift into different cell types through differentiation mediated by a number of cell signaling pathways including Wnt, Hh, and Notch [5]. Sonic hedgehog (SHh), Indian hedgehog (IHh), and Desert hedgehog (DHh) comprise the three mammalian Hh genes playing major roles in designing and modeling many tissues and organs [6]. Of these tissues, the Hh gene was characterized as an obligatory signaling protein for the specification of positional distinctiveness in the Drosophila embryo [7]. Porter et al. [8] reported that the peptide formed through intramolecular cleavage and lipid modification reactions in the secretory pathway is responsible for the total signaling actions of the Hh gene. Zhu et al. [2] recently showed that the expression of Hh canonical pathway genes, namely Smoothened (Smo) and Gli1, are mediated by fibroblast growth factor (bFGF) which in turn accelerates fibroblast migration. On the other hand, when the Hh pathway is activated in an unusual manner, it may facilitate a number of tumor types, by favoring the process of tumorigenesis, and metastasis [5,9]. Actually, cancer stem cells are quite similar to regular stem cells, in terms of their self-renewal capacity. Several studies have demonstrated that the Hh pathway is actively involved in cancer and can control self-renewal pathways within cancer stem cells, particularly in leukemia, other blood cancers, and breast cancer [[10], [11], [12]]. Since a significant number of molecules targeting said pathway are already at the clinical testing stage, especially for the niche of hematological malignancies, we aimed to review the Hh signaling pathway in detail as one of the key targets for cancer therapy and development of more effective and promising cancer inhibitory strategies. Therefore, this review covers all mechanistic and functional details related to Hh pathway along with its inhibitors and clinical potential.