https://www.selleckchem.com/products/gdc-0068.html Methane emissions from enteric fermentation in the ruminant digestive system generated by methanogenic archaea are a significant contributor to anthropogenic greenhouse gas emissions. Additionally, methane produced as an end-product of enteric fermentation is an energy loss from digested feed. To control the methane emissions from ruminants, extensive research in the last decades has been focused on developing viable enteric methane mitigation practices, particularly, using methanogen-specific inhibitors. We report here the utilization of two known inhibitors of methanogenic archaea, neomycin and chloroform, together with a recently identified inhibitor, echinomycin, to produce resistant mutants of Methanococcus maripaludis S2 and S0001. Whole-genome sequencing at high coverage (> 100-fold) was performed subsequently to investigate the potential targets of these inhibitors at the genomic level. Upon analysis of the whole-genome sequencing data, we identified mutations in a number of genetic loci pointing to potential mechanisms of inhibitor action and their underlying mechanisms of resistance.Sinusitis is a common ailment a clinician comes across in their day-to-day practice. Simple as it may sound, it may become a very debilitating condition depending on the comorbidities of the patient and the organism involved. Rhizopus and Escherichia coli are less common organisms to affect the sinuses, but they are more common in immunocompromised patients such as patients with uncontrolled diabetes. Rhizopus can be a very debilitating infection as it erodes into the bone and blood vessels resulting in tissue necrosis. However, coinfection of both of these organisms is a very rare occurrence. Psoas abscess is also a less common infection in the immunocompetent patients but it is more common among the immunocompromised patients. It is extremely rare for both of these organisms to cause sinusitis in one patient, and for E. coli