Toll-like receptors (TLRs) are a family of pattern recognition receptors involved in cardiovascular diseases. Notably, numerous studies have demonstrated that TLR4 activates the expression of several of pro-inflammatory cytokine genes that play pivotal roles in myocardial inflammation, particularly myocarditis, myocardial infarction, ischemia-reperfusion injury, and heart failure. In addition, TLR4 is an emerging target for anti-inflammatory therapies. Given the significance of TLR4, it would be useful to summarize the current literature on the molecular mechanisms and roles of TLR4 in myocardial inflammation. Thus, in this review, we first introduce the basic knowledge of the TLR4 gene and describe the activation and signaling pathways of TLR4 in myocardial inflammation. Moreover, we highlight the recent progress of research on the involvement of TLR4 in myocardial inflammation. The information reviewed here may be useful to further experimental research and to increase the potential of TLR4 as a therapeutic target.

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Antimicrobial resistance is an urgent global health challenge in human and veterinary medicine. Wild animals are not directly exposed to clinically relevant antibiotics; however, antibacterial resistance in wild animals has been increasingly reported worldwide in parallel to the situation in human and veterinary medicine. This underlies the complexity of bacterial resistance in wild animals and the possible interspecies transmission between humans, domestic animals, the environment, and wildlife. This review summarizes the current data on expanded-spectrum β-lactamase (ESBL), AmpC β-lactamase, carbapenemase, and colistin resistance genes in Enterobacteriaceae isolates of wildlife origin. The aim of this review is to better understand the important role of wild animals as reservoirs and vectors in the global dissemination of crucial clinical antibacterial resistance. In this regard, continued surveillance is urgently needed worldwide.

Worldwide spread of antibiotic resistance genes among Enterobacteriaceae isolates is of great concern. F33:A−:B− plasmids are important vectors of resistance genes, such as blaCTX-M-55/-65, blaNDM-1, fosA3, and rmtB, among E. coli isolates from various sources in China. We determined and compared the complete sequences of 17 F33:A−:B− plasmids from various sources. These plasmids appear to have evolved from the same ancestor by mobile element-mediated rearrangement, acquisition, and/or loss of resistance modules and similar IncN1, IncI1, and/or IncX1 plasmid backbone segments. Our findings highlight the evolutionary potential of F33:A−:B− plasmids as efficient vectors to capture and diffuse clinically relevant resistance genes.

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