Publications by authors named "W Gary Bachman"

Article Synopsis
  • - The study focused on KPC-Kp bloodstream infections, which are deadly, and aimed to understand how these bacteria resist a key defense mechanism in our blood, called complement.
  • - Researchers tested various KPC-Kp isolates from patients, discovering that 27% of them resisted killing by human serum; a specific gene mutation (wcaJ) linked to capsule production contributed to this resistance.
  • - This mutation resulted in less capsule presence, paradoxically increasing the bacteria's ability to bind complement proteins while also improving their survival against immune responses, potentially allowing them to thrive in the bloodstream without being overly virulent in tissues.
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The use of race-specific reference values to evaluate pulmonary function has long been embedded into clinical practice; however, there is a growing consensus that this practice may be inappropriate and that the use of race-neutral equations should be adopted to improve access to health care. To evaluate whether the use of race-neutral equations to assess percent predicted forced vital capacity (FVC%) impacts eligibility for clinical trials, antifibrotic therapy, and referral for lung transplantation in Black, Hispanic/Latino, and White patients with interstitial lung disease (ILD). FVC% values for patients from the Pulmonary Fibrosis Foundation Patient Registry were calculated using race-specific (Hankinson and colleagues, 1999), race-agnostic (Global Lung Function Initiative [GLI]-2012), and race-neutral (GLI-2022 or GLI-Global) equations.

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β-Lactamases can accumulate stepwise mutations that increase their resistance profiles to the latest β-lactam agents. CMY-185 is a CMY-2-like β-lactamase and was identified in an clinical strain isolated from a patient who underwent treatment with ceftazidime-avibactam. CMY-185, possessing four amino acid substitutions of A114E, Q120K, V211S, and N346Y relative to CMY-2, confers high-level ceftazidime-avibactam resistance, and accumulation of the substitutions incrementally enhances the level of resistance to this agent.

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Article Synopsis
  • - This study investigated a variant of the blaCMY gene linked to resistance against the antibiotic combination ceftazidime/avibactam in a series of E. coli isolates from a patient with an intra-abdominal infection.
  • - Whole-genome sequencing showed the resistant E. coli strain, identified as ST410, carried a new CMY β-lactamase gene called blaCMY-185, which had specific amino acid changes that contributed to its resistance.
  • - The research concluded that the CMY-185 variant requires multiple amino acid mutations to effectively confer resistance, marking a significant differentiation from other similar enzymes when it comes to resisting ceftazidime/avibactam treatments.
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Article Synopsis
  • *Researchers found that 27% of KPC-Kp isolates showed increased resistance to human serum, linked to a mutation that reduces capsule content and helps the bacteria evade immune responses.
  • *The mutation allows KPC-Kp to survive better in the bloodstream while being less virulent in tissues, highlighting a complex interaction that aids the bacteria's persistence in the host.
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