NIH funding data reveals dramatic shifts in award rates last year even for highly ranked proposals – yet another warning sign for the state of American science.
This is a mess. Another element that is often lost on people is the positive impact that researchers receiving new NIH grants have on simply keeping people employed. Efficiency on teams is great, but hiring a research manager or a postdoc also means that the local businesses will have new patrons.
The scientific loss is harder to feel for everyday people immediately, but job loss and hollowing out cities who built up infrastructure to do really cool work is felt quickly.
NIH support catalyzes local, near-term economic activities and long-term discovery. Our SCIMaP work (scienceimpacts.org) focuses on the near-term risk to job loss in a vital sector. Unfortunately, this is a yes-and situation as you suggest.
Is it my perception that they invented a virtual third axis to your plot that is the actual appropriation for the CURRENT fiscal year of the multi-year awards? That is, the comparison to the previous years should be on a current FY basis.
Boo hoo. In the summer of 1963 I accepted a summer cancer research fellowship at McArdle Labs in MSN, WI, and received a crash course in molecular biology research. The lead researcher cooked the data and the glow was gone. I've written about cancer in my 2018 "Stress R Us" 51 chapter ("Topic") monograph, a free downloadable PDF is out at Stanford. I'm 80yo and am being treated for prostate cancer, like 1/8 American men, but our great cancer research establishment has no opinion on the etiology of this and many other cancers. So far, I've not been given so much as an "informed consent" for treatments, especially Lupron, which suppresses testosterone production, and that made my life not worth living. I'm getting a consultation with the local Marietta Memorial Cancer Center and will NOT take anymore Lupron. I do not wish to live a bit longer but be miserable with many side-effects, etc. Have a blessed day, but don't cry for me, government researchers. Read my book, it's free!
I wish you the best in your treatment and hope you can find the support you need. As additional context, the federal government cancelled over 180 grants from NIH's National Cancer Institute last year, spanning basic to translational research and clinical trials & award rates within NCI dropped significantly last year as they did for NIH more broadly.
Ugly blame and accusations - Prostate cancer is a heterogeneous group of diseases. Many tumors grow very slowly while others are aggressive. Initiating mutations, hormonal environments, and immune responses vary widely between individuals.
Genetic mutations that accumulate in prostate epithelial cells that alter growth control. Commonly involved genes include:
BRCA2 and BRCA1 (DNA repair genes), HOXB13 (a prostate-development gene with inherited risk variants), PTEN tumor suppressor loss, TP53 mutations in advanced disease, Gene fusions such as TMPRSS2–ERG, driven by androgen signaling. These mutations allow cells to proliferate and resist apoptosis.
Then, abnormal androgen receptor signaling promotes tumor growth. The prostate is highly dependent on androgens such as testosterone and dihydrotestosterone, which helps explain why androgen-deprivation therapy is effective for many patients.
Evidence also suggests possible contributions from:
This is a mess. Another element that is often lost on people is the positive impact that researchers receiving new NIH grants have on simply keeping people employed. Efficiency on teams is great, but hiring a research manager or a postdoc also means that the local businesses will have new patrons.
The scientific loss is harder to feel for everyday people immediately, but job loss and hollowing out cities who built up infrastructure to do really cool work is felt quickly.
NIH support catalyzes local, near-term economic activities and long-term discovery. Our SCIMaP work (scienceimpacts.org) focuses on the near-term risk to job loss in a vital sector. Unfortunately, this is a yes-and situation as you suggest.
Is it my perception that they invented a virtual third axis to your plot that is the actual appropriation for the CURRENT fiscal year of the multi-year awards? That is, the comparison to the previous years should be on a current FY basis.
Boo hoo. In the summer of 1963 I accepted a summer cancer research fellowship at McArdle Labs in MSN, WI, and received a crash course in molecular biology research. The lead researcher cooked the data and the glow was gone. I've written about cancer in my 2018 "Stress R Us" 51 chapter ("Topic") monograph, a free downloadable PDF is out at Stanford. I'm 80yo and am being treated for prostate cancer, like 1/8 American men, but our great cancer research establishment has no opinion on the etiology of this and many other cancers. So far, I've not been given so much as an "informed consent" for treatments, especially Lupron, which suppresses testosterone production, and that made my life not worth living. I'm getting a consultation with the local Marietta Memorial Cancer Center and will NOT take anymore Lupron. I do not wish to live a bit longer but be miserable with many side-effects, etc. Have a blessed day, but don't cry for me, government researchers. Read my book, it's free!
I wish you the best in your treatment and hope you can find the support you need. As additional context, the federal government cancelled over 180 grants from NIH's National Cancer Institute last year, spanning basic to translational research and clinical trials & award rates within NCI dropped significantly last year as they did for NIH more broadly.
https://jamanetwork.com/journals/jamaoncology/fullarticle/2841870?guestAccessKey=8e0ca9d5-0f67-4a24-9a97-c26dd8757378&utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=112625
Ugly blame and accusations - Prostate cancer is a heterogeneous group of diseases. Many tumors grow very slowly while others are aggressive. Initiating mutations, hormonal environments, and immune responses vary widely between individuals.
Genetic mutations that accumulate in prostate epithelial cells that alter growth control. Commonly involved genes include:
BRCA2 and BRCA1 (DNA repair genes), HOXB13 (a prostate-development gene with inherited risk variants), PTEN tumor suppressor loss, TP53 mutations in advanced disease, Gene fusions such as TMPRSS2–ERG, driven by androgen signaling. These mutations allow cells to proliferate and resist apoptosis.
Then, abnormal androgen receptor signaling promotes tumor growth. The prostate is highly dependent on androgens such as testosterone and dihydrotestosterone, which helps explain why androgen-deprivation therapy is effective for many patients.
Evidence also suggests possible contributions from:
Diet high in animal fat
Obesity and metabolic factors
Chronic prostate inflammation or infection
Exposure to certain chemicals