The National Academy of Medicine is a part of the National Academies of Sciences, Engineering, and Medicine, along with the National Academy of Sciences (NAS), National Academy of Engineering (NAE), and the National Research Council (NRC).The National Academy of Medicine provides national and international advice on issues relating to health, medicine, health policy, and biomedical science. It aims to provide unbiased, evidence-based, and authoritative information and advice concerning health and science policy to policy-makers, professionals, leaders in every sector of society, and the public at large.Operating outside the framework of the U.S. federal government, it relies on a volunteer workforce of scientists and other experts, operating under a formal peer-review system. As a national academy, the organization annually elects new members with the help of its current members; the election is based on the members' distinguished and continuing achievements in a relevant field as well as for their willingness to participate actively.
Key PointsMulticentric carpotarsal osteolysis, a rare disorder, causes progressive osteolysis and kidney failure because of v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) gene mutations.A genome-edited mouse model carrying the multicentric carpotarsal osteolysis mutation was used to obtain a deeper understanding of this rare disease.Targeting MAFB/IGF-1/PI3K/AKT signaling may provide new treatments for multicentric carpotarsal osteolysis-related nephropathy.BackgroundMulticentric carpotarsal osteolysis (MCTO) is a rare condition characterized by progressive osteolysis and often kidney failure. It is caused by autosomal dominant mutations in the transcription factor v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB).MethodsGiven the absence of efficacious therapeutic interventions for MCTO and the obscurity of its pathophysiologic mechanisms, we used mice with the MCTO mutation (MafbMCTO/MCTO mice) to explore the role of MAFB.ResultsMafbMCTO/MCTO mice displayed FSGS, mirroring the manifestations seen in patients with MCTO. These mice showed that the MCTO mutation leads to the accumulation of MAFB protein. Heterozygous MafbMCTO/- mice, generated by crossbreeding to reduce MAFB levels, neither exhibited albuminuria nor showed any histologic abnormalities in the kidney, suggesting that excess MAFB was detrimental. We subsequently conducted RNA-seq on the glomeruli from MafbMCTO/MCTO mice and detected pronounced upregulation of the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway through IGF-1. Given that receptor tyrosine kinases activate PI3K/AKT, we treated MafbMCTO/MCTO mice with the inhibitor imatinib. This led to a significant decline in urinary albumin levels compared with the control group.ConclusionsOur findings demonstrate that the MCTO mutation resulted in MAFB protein accumulation and led to the development of FSGS in mice.
The National Cancer Policy Forum (NCPF) of the National Academies of Sciences, Engineering, and Medicine was founded in 2006 to serve as a trusted venue for identifying and addressing high-priority policy issues in cancer research and care. NPCF takes a comprehensive, multisectoral, and multidisciplinary approach to strategically consider the entire continuum of cancer research and cancer care. Over the past two decades, the Forum has served a uniquely important role in examining both long-standing and emerging policy issues that are relevant to reducing the burden of cancer, both through prevention and by improving the care and outcomes for those diagnosed with cancer, and exploring solutions from multiple perspectives. The Forum has fostered actionable dialogue among a broad range of participants, including patient advocacy organizations, federal agencies, academia, professional organizations, nonprofits, and industry. NCPF activities inform the cancer community and the general public about a wide range of scientific, clinical, and policy issues through workshops, webinars, and the proceedings published after these convenings. Forum activities have influenced policy through the resulting publications and by providing input to National Academies consensus studies, which provide consensus recommendations. This commentary summarizes the breadth of topics addressed by the Forum over the years and examples of the impact of the Forum activities on policies and procedures, programs and practices, and participants and people around the globe.
The field of academic medicine, through its tripartite mission, has for decades driven scientific achievement, translated biomedical research into improved clinical outcomes, and educated the next generation of researchers and medical practitioners. Throughout its history, it has remained resilient in the face of changing political and funding environments and evolving attitudes toward science and medicine. However, rarely has academic medicine confronted changes as abrupt and destabilizing as those unfolding today. To successfully navigate this moment and preserve its essential mission of advancing research, patient care, and medical training, the authors propose a roadmap for leadership at academic medical centers(AMCs). AMCs must stand firm in the face of political and policy pressures, defend core principles, and remain committed to the mission. They should bolster financial stewardship through increased operational efficiency, prioritization of mission-critical programs and core academic functions, and consolidation of nonaligned activities. This will include developing strategic partnerships, especially with philanthropy and industry, to unlock new opportunities and diversify funding, as well as remodeling research and education and innovating with artificial intelligence. Importantly, AMCs must strengthen commitment to the workforce, particularly through support for vulnerable early-career trainees and faculty. Finally, AMCs should align research and clinical priorities with public priorities to strengthen the social compact between medicine and the communities it serves and increase public trust.
Background: Direct laryngoscopy and intubation is invariably associated with hemodynamic changes (Hypertension, tachycardia and arrhythmias) which may be hazardous to patient especially if they have cardiac morbidity. Lignocaine is regularly used to attenuate these changes although the evidence supporting its use is not well established. Moreover, there is scarcity of study regarding usefulness of lignocaine when etomidate, a cardiac stable drugs, is used for induction. Materials and Methods: Total 104 patients undergoing CABG were randomized in two groups, lignocaine was given in one group, the other received normal saline. In this double blind controlled clinical trial etomidate induction was performed. Heart rate(HR), Systolic blood pressure(SBP), Diastolic blood pressure(DBP) and mean blood pressure(MBP)collected at 0, 1, 3, 5, and 10 minutes of intubation. Results: There was no significant difference between the demographic profile between two groups. Our results showed no significant differences between Baseline, SBP, DBP and MBP at 1,3,5 and 10 minutes after laryngoscopy and endotracheal intubation. Baseline HR, HR at 1,3,5 and 10 minutes after laryngoscopy and endotracheal intubation were also not significantly different between the two groups. Conclusions: Lignocaine has no attenuating effect on hemodynamic response to laryngoscopy and Intubation withEtomidate induction for CABG surgery
