Emergency BU Alert BU Medical Campus OPEN Jan. 28, 2015 Boston University Medical Campus will be open Wednesday, Jan. 28, 2015. BUSM classes will be held as scheduled. Staff should check with their managers regarding work schedules. Medical, PA and GMS students who are assigned to inpatient services or clinics are expected to be present, if possible. Students who are assigned to outpatient services should check with their course director or the policy at the clinical site. GMS classes are canceled. Staff should check with their manager regarding their work schedules. The Henry M. Goldman School of Dental Medicine will follow normal school hours. All Patient Treatment Centers will be open for patient care and all classes will be held as scheduled. BU School of Public Health classes are canceled; SPH non-essential staff may telecommute. Employees who are part of the BUMC parking program should park in your assigned lot or garage. The Boston parking ban is still in effect. For updated information, please call the weather/emergency hotline at 617-638-6886 or visit the BU Emergency Communications website at http://www.bu.edu/ehs/comm/

Archive: 2011

Assistant Professor Kevin Wilson and colleagues report in The American Journal of Respiratory and Critical Care Medicine that the data are less than compelling for many clinical practices used as performance measures in treatment of community-acquired pneumonia, questioning their utility as indicators for assessing quality of care.
Associate Professor Darrell Kotton and colleagues report in The Journal of Clinical Investigation that cells induced to become pluripotent stem cells have a similar capacity as embryonic stem cells to transition through development to become lung progenitors, supporting further research into the potential of cell-based therapies for lung disease.
Professor Alan Fine and colleagues report in The Journal of Biological Chemistry that an unusual cell signaling pathway involving autocrine Notch activation contributes to the normal development of the pulmonary artery, with implications for vascular remodeling such as in pulmonary arterial hypertension.
Professor George O’Connor and colleagues report in Nature Genetics the results of a major international collaboration identifying genetic loci associated with pulmonary function, analyzing results from nearly 50,000 individuals to implicate 16 gene regions as potential modifiers of lung disease.
Professor Wellington Cardoso and colleagues report in Development that the transcription factor Notch prevents cells in the airway from becoming goblet cells which secrete mucus, identifying a signaling pathway which may contribute to the pathophysiology of COPD, asthma, and other chronic lung diseases.
Assistant Professor Renda Wiener and colleagues report in the Annals of Internal Medicine that transthoracic needle lung biopsy confers considerable risks of pneumothorax and chest tube placement, of especial significance since CT chest screening is anticipated to increase demand for such biopsies.
Several PhD students have recently accomplished the critical milestone of thesis defense, including Dan Green (mentored by Bill Cruikshank), Constantina Christodoulou (mentored by Darrell Kotton), and Matt Blahna (mentored by Jay Mizgerd). Congratulations to the new doctors!
Assistant Professor Karin Sloan and her husband are featured in a Boston Globe article about gender issues and work-life balance, discussing spousal roles and the sometimes differing expectations for men and women with family responsibilities.
Assistant Professor Allan Walkey and colleagues report in the Journal of the American Medical Association (JAMA) that the onset of atrial fibrillation during sepsis associates with significantly increased risks of stroke and of death, identifying a major new factor for prognostication and management of sepsis patients.
Professor William Cruikshank and colleagues report in the Journal of Clinical Investigation that patients with cutaneous T cell lymphoma have defects in the pro-IL-16 protein that increase proliferation of T cells, suggesting that pro-IL-16 and its downstream factors are potential new drug targets for this disease.
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April 5, 2012
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