Effects of Transport and Feeding Strategies Before Transportation on Redox Homeostasis and Gastric Ulceration in Horses.

Transportation may lead to oxidative stress (OS) and gastric ulceration in horses, and optimal feed management before, or during, transportation is unclear. This study aimed to evaluate the effects of transportation after three different feeding strategies on OS and to explore possible associations between OS and equine gastric ulcer syndrome (EGUS). Twenty-six mares were transported by truck for 12 hours without food or water. Horses were randomly divided into 3 groups; (1) fed 1 hour before departure (BD), (2) fed 6 hours BD, (3) fed 12 hours BD. Clinical examinations and blood collections were performed at approximately 4 hours BD (T0), at unloading (T1), 8 hours (T2) and 60 hours (T3) after unloading. Gastroscopy was conducted prior to departure, and at T1 and T3. Although OS parameters remained in the normal range, transportation was associated with increased reactive oxygen metabolites (ROMS) at unloading (P=0.004), with differences between horses fed 1 hour and 12 hours BD (P < .05). The level of total antioxidant (PTAS) was affected by both transportation and feeding strategy (P = 0.019), with horses fed 1 hour BD demonstrating greater PTAS at T = 0, and a different response in comparison with the other groups and the literature. Nine horses demonstrated clinically significant ulceration of the squamous mucosa at T1 but, although weak correlations were evident between OS parameters and ulcer scores, univariate logistic regression showed no associations. This study suggests that feed management prior to a long journey (12 hours) may affect oxidative balance. Further studies are needed to understand the nexus between feed management before and during transport, transport-related OS and EGUS.

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects.

Molecular signaling pathways play a significant role in the regulation of biological mechanisms, and their abnormal expression can provide the conditions for cancer development. The signal transducer and activator of transcription 3 (STAT3) is a key member of the STAT proteins and its oncogene role in cancer has been shown. STAT3 is able to promote the proliferation and invasion of cancer cells and induces chemoresistance. Different downstream targets of STAT3 have been identified in cancer and it has also been shown that microRNA (miR), long non-coding RNA (lncRNA) and other molecular pathways are able to function as upstream mediators of STAT3 in cancer. In the present review, we focus on the role and regulation of STAT3 in gastric cancer (GC). miRs and lncRNAs are considered as potential upstream mediators of STAT3 and they are able to affect STAT3 expression in exerting their oncogene or onco-suppressor role in GC cells. Anti-tumor compounds suppress the STAT3 signaling pathway to restrict the proliferation and malignant behavior of GC cells. Other molecular pathways, such as sirtuin, stathmin and so on, can act as upstream mediators of STAT3 in GC. Notably, the components of the tumor microenvironment that are capable of targeting STAT3 in GC, such as fibroblasts and macrophages, are discussed in this review. Finally, we demonstrate that STAT3 can target oncogene factors to enhance the proliferation and metastasis of GC cells.