The following are recent instances of the Wellman Center for Photomedicine and Wellman Center researchers being covered by the media.

Maiman Student Paper Competition
Sheldon Kwok of Andy Yun's lab was awarded an Honorable Mention of OSA Maiman Student Award for the Maiman Student Paper Competition. This competition began in 2008 and acknowledges students who have excelled in innovation as well as research and in their presentation skill in the fields of laser technology and electro-optics.

Congratulations Sheldon!

Second Endowed MGH Research Institute Chair Established
The MGH recently celebrated the second endowed chair established within the Research Institute. Thanks to a generous gift from the Remondi Family Foundation, the Remondi Family Endowed MGH Research Institute Chair will support – in perpetuity – research that improves patient care through innovation. We salute Guillermo (Gary) Tearney, MD, PhD, of the Department of Pathology and the Wellman Center for Photomedicine, who has been named the inaugural incumbent of this chair. We are confident that Gary's passion for pioneering approaches to early diagnosis and treatment of disease will accelerate our ability to deliver the very best care to patients here in Boston and around the world.

2018 ASLMS Research Grant Award
Congratulations to Leon Leanse, PhD along with his mentor Tianhong Dai, PhD on receiving the 2018 ASLMS Research Grant Award.

Project Title: Elucidating the molecular mechanisms involved in antimicrobial blue light (aBL) therapy and its synergistic action within quinine.

Source and type of award: American Society for Laser Medicine and Surgery (ASLMS) Research Grant

Brief summary of specific aims:
With the rise in antimicrobial resistance, it is essential that we look to other, 'non-antibiotic' strategies, e.g. antimicrobial blue light (aBL), as alternative methods to treat infections. aBL therapy is a novel and effective approach for the treatment of infections caused by different pathogens. Although aBL has been shown to be highly effective in inactivating pathogens, varied sensitivities are often observed between microbial species, with some eliciting significantly high relative resistances. Therefore, it is vital that approaches, such as aBL combination therapies, are investigated, so we may improve microbial inactivation while simultaneously providing safer and more timely care to patients. This proposal represents the first instance where the synergistic effect of aBL and quinine will be investigated. Our hypotheses are (1): aBL-quinine therapy will offer an improved inactivation efficacy of numerous microbial species; (2): elucidating the transcriptional portrait of bacteria exposed to aBL or aBL-quinine will reveal novel mediators of their respective activities. Therefore, the following aims will be completed:

Aim 1: Investigate the synergistic effect of aBL-Q-HCL therapy against numerous bacteria: in vitro and in vivo. Gram-negative and Gram-positive bacteria will be treated with aBL-Q-HCL to determine whether any improvement in the antimicrobial efficacy is observed (against aBL or Q-HCL alone). Inactivatoon of planktonic cells and cells within biofilms (monomicrobial and polymicrobial) will be tested, with different aBL irradiances and Q-HCL concentrations. Superficial mouse skin infections caused by different Gram-positive and Gram-negative bacteria will be treated (after a 3 or 24-hour incubation) with aBL-Q-HCL to establish any improvement in the treatment efficacy (against aBL or Q-HCL alone). Scanning and transmission electron microscopy will be performed on cells treated with aBL-QHCL to predict the mechanism of action. Any cytotoxic effect of aBL-Q-HCL therapy to host cells will be determined using the MTT tetrazolium assay.

Aim 2: Elucidate the transcriptional portrait of P. aeruginosa, when exposed to aBL or aBL-Q-HCL, in vitro, using RNA-seq. We will elucidate the transcriptional portrait of, P. aeruginosa, when exposed to aBL or aBL-Q-HCL, in vitro. Highly differentially expressed genes will be targets of defined mutagenesis. Up-regulated genes will be deleted from the chromosome, using a sacB markerless mutation strategy. Mutants found to be significantly more resistant/sensitive to aBL or aBL-Q-HCL will be heterologously complemented with the native gene using pUCP19. Complemented strains that regain wild-type sensitivity to aBL or aBL-Q-HCL, represent mediators of aBL or aBL-QHCL activity.

Congratualtion Leon!