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Published online 19 March 2008 | Nature 452, 258-259 (2008) | doi:10.1038/452258a
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222 NIH grants: 22 researchers
Grandee grantees are sitting pretty through agency cash crisis.
A whopping 200 scientists received six or more grants each from the US National Institutes of Health (NIH) in 2007, according to data analysed by Nature. One principal investigator was awarded 32 grants, the data reveal, and many others got eight or nine (see Table).
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There is a big question of oversight when a PI has multiple research grants. The possibility of fraud/mistakes increases when less time is available for direct supervision of each post-doc, graduate student, lab assistant, etc. Does a PI really know what post-doc #5, 6 or 7 are doing?
The chances are almost nil for fresh Ph.Ds to get grants. It is so sad to hear that most of the money were given to the older researchers. However my suggestion is that NIH should put a limit on number of grants depending on the appliacnt's age. This does not mean that NIH should support "junk" grant applications from junior researchers. To me every deserved person should be given a chance to get funding to prove themselves. Most of the time "inner loop" of known people gets funded or scored lower. It is hard for me to understand how someone would manage more than 3-4 grants. Mannaging the grants can be easily overcome by recuriting senoir people in the lab to manage each project. However most of the time this does not happen. PI thinks 'economical' on this issue and hire many low paid junior fellows to do the job. Another suggestion is that the senior PI should be only be a consultant for junior PI. This way the junior PI gets his experience with senior PI and also senior PI gets his credit for the contribution. It is true that we can not put a age limit for research, but at the same time it is equally unimaginable to expect NIH to support all the applications so we need to draw a line and all the senior PIs should have a bigger heart on this and give way for younger people.
I agree completely with both of the previous posts. Giving more than 3 or 4 major grants to single established PI's at the cost of funding a new PhD/postdoc is insane even if that establish PI is producing great quantities of quality research. That quality research is being produced by PhD students and postdocs, so they should be rewarded more than the established PI. I like the idea of more mentor-based post-doc to PI grants because they would also reward the established PI for training the next generation of PI's. At the moment establish PI's only get rewarded for their publication output. This model is flawed if we are to nurture new talent for the future.
I've worked in labs which are huge (number of personnel and amount of funding, and not so huge (fewer personnel and lower funding). No matter how "great" the PI, the fact of the matter is that there will always be an inverse relationship between the number of grants in a lab and the time the PI can devote to them. Consequently, what often happens in a huge lab is that there is a duplication of efforts on projects, unbeknownst to the PI, ideas are stolen and overall there is a stench in terms of collegiality in the lab (note, I said it often happens, *not* always). This is counterproductive on so many levels, I wouldn't know where to start enumerating them! I think what the NIH should do is put more money into programs focused on funding NON-TENURED scientist. What will this do? Well, for starters, it will give opportunities to under served sections of researchers - the people who often have those eureka moments only to find them stolen by unscrupulous PIs, resulting in an ultimate stagnation of their careers.
you have to wonder how the grant review process goes such that certain researchers monopolize the field--who is scratching whose back at these NIH study sections? while these guys with all of the money might be brilliant scientists, the NIH is hurting itself by not letting young, fresh ideas into the game.
The list of publications and the quality of the work performed does not always correlate with the amount of money granted. Check out the papers published within the next 3 years by some researchers mentioned in the article: hem... well. It is ok work, but nothing that justifies $13 or $14 millions, even if some projects are very expensive. We all know that getting NIH grants depends mainly on "Who You Know" and not on "What You Do". I salute the recommendation that each PI should dedicate 20% of their time to each major project, but how can we make sure that this will be the case? Why not limiting the number of major grants awarded to each PI? If you need more money, why not having your favorite post-doc as a Principal Investigator on a grant application? The money would end up in the same lab, right? This should help young researchers getting a job faster. After all, wasn't that the purpose of post-doctoral training (years ago?).
Does the monopoly grant enrich science or slavery?--- I have no doubt that there are some very brilliant scientists who deserve all the grant support that can be used for their OWN investigations. I also admire those dedicated scientists who are sacrificing their own leisure time to work harder for the society. However, from my direct and indirect observations, I must say these kinds of brilliant and dedicated scientists are some endangered species that are hard to find in this real world./// Many PIs today are not even qualified as a principal INVESTIGATOR because they do not do the INVESTIGATION or, at least, not the data-acquisition investigation. Their principal roles are money-acquisition and impact-dissemination. These PIs normally spend more time out of the lab but in the meetings. You may not be able to find them near the bench but will find them constantly hooked to the phone line. They may talk more with reporters than with their students. They may review more of others' papers and grants than read manuscripts from their own labs./// Certainly, these PIs will become smarter and smarter as they not only collect all the intelligence from others' work in their own labs but also absorb novel ideas from others' finished or planned work outside their labs but nevertheless under their surveillance. If necessary, some of them will even make some "extra" efforts to ensure that their lab will remain the leaders in his/her field. To see how this can be achieved, please visit the Nilsson-Science Gate (http://www.the-scientist.com/news/home/53081/)./// The "figurehead" PIs can be revealed if you ask them the technical INVESTIGATION questions or when their paper got retracted. Then their only role may be the "designing" of the study and the writing of manuscript. I actually saw some PIs disclosed their contribution as the recipient of the grant but made no other intellectual contribution to a specific paper./// What usually happens when a paper is retracted? Has any PI actually got a principal responsibility for their "great" contribution? How could only one of the "co-first" authors who contributed "equally" before now collect all the blame because he alone actually contributed all the data and figures to the paper authors by a team including a Nobel Prize winner (http://www.nature.com/news/2008/080305/full/452013a.html)?/// Finally, I do not like any one-size-fits-all rule in limiting how many grants a PI can get. However, I strongly urge the implementation of a one-principle-governs-all standard in assigning credit and condemnation for scientific discovery and fakery. This standard should be based on whoever make the INVESTIGATIONAL discovery should collect the SCIENTIFIC credit. Those principal investors should not be entitled with scientific credit even though they may deserve an acknowledgment of financial support (with public grant money given to them for support the assumed their OWN investigations). --- Shi V. Liu (http://im1.biz) SVL@logibio.com
No real criticism but just a casual observation--- S Basu and H E Varmus/// Retraction. Moloney murine leukemia virus integration protein produced in yeast binds specifically to viral att sites. /// J Virol. 1991 December; 65(12): 7086. /// "Some of the data shown in Fig. 4 were not obtained from the reactions indicated ...†--- Shi V. Liu (http://im1.biz) SVL@logibio.com
Again no real criticism but just another casual observation--- Irene M. Pedersen, Juan M. Zapata, Temesgen Samuel, Fiona L. Scott, Guy S. Salvesen, Tadashi Honda, Gordon W. Gribble, Nanjoo Suh, Michael B. Sporn, Thomas J. Kipps, and John C. Reed/// Retraction: The triterpenoid CDDO-Imidazolide induces apoptosis and enhances fludarabine-induced apoptosis of CLL B-cells./// Blood, 15 August 2004, Vol. 104, No. 4, pp. 932./// "Upon analysis of additional CLL patient specimens since the original submission, the effects of CDDO-IM on fludarabine-induced apoptosis have proven to be highly variable..." --- Shi V. Liu (http://im1.biz) SVL@logibio.com
Grant!Grants!!--- I was given the following information that is worthy of sharing with scientific communities and public supporting scientific research. ------- Three "similar" proposals from one "grandee grantee" David Rawlings 1) Lentiviral Gene Therapy for Wiskott-Aldrich Syndrome; 2) Lentiviral Gene Therapy of X-linked Agammaglobulinemia; 3) Model for Gene Therapy in X-linked Agammaglobulinemia (in which the major aims were to use lentiviral vectors to introduce genes to correct genetic defects in Agammaglobulinemia). Two "overlapping" proposals from another "grandee grantee" Jennifer Grandis, Proposal 1: TARGETING ACTIVATED STAT3 IN HN CANCER (HN stands for head and neck) Proposal 2: Stat3 as a Therapeutic Target in Head and Neck Cancer ---------- The above information can be found at http://crisp.cit.nih.gov/ which stands for "Computer Retrieval of Information on Scientific Projects" that includes NIH grant information. ---- Shi V. Liu (http://im1.biz) SVL@logibio.com
It is interesting how the comments are all directed to the problem, which is clearly well known among most people who have been involved with grant writing in any field and any funding agency not only NIH. Of course the ones who wanted to fix the problem are worthy of the great thanks from the entire scientific community. Dr. Zerhouni’s goal on the limitation is right on target and should be supported by everyone without angry responses or finger pointing. The mechanisms that allow the well connected and those who have excellent salesperson talents will always have a better chance. Those same people are the ones who decide and implement the mechanisms by which funding is awarded. Real democratic means for peer review, policy establishment and implementing, and most importantly oversight of these mechanism and procedures need the involvement of the largest number of scientists, which can only be done if we remove these study groups and use similar mechanism to reviews of papers for publication (even though the latter is not perfect, but is clearly fairer than the current grant review). To those who have the means to decide, please consider the millions wasted in redundant projects from well known or well connected PIs. And for those who are angry, please start participating in a true democratic talk in surveys, feed back and the likes such as the last initiative from NIH itself to improve grant review. Without both efforts, we will be talking about the same issues years from now.
Erwin Chargaff's "In Praise of Smallness" seems quite prescient.(see: http://post.queensu.ca/~forsdyke/peerrev0.htm#IN%20PRAISE%20OF%20SMALLNESS
Well I agree with all the comments and the observations posted here. But no where have I found any reference to a simple idea of blind Author and Referee, i.e. the authors and the referees should never know each others identity. The referees should not be revealed the identity of the authors. This though not a full proof method but should provide some insulation from preset notion and leverage that some people enjoy both in publication and proposal accepectance
The global health expenditures to treat or prevent diabetes and its sequences amount to hundreds of billions of dollars every year (international diabetes federation, 2007). On the basis of evidence, autoimmune reactions, reactive, inflammatory mediators and oxygen species (ROS) have been emerged to be the major possible underling mechanisms for diabetes incidence. Several studies have been confirmed that vitamin D is a potential modifier against diabetes. In comparison with the other therapeutic agents the economic impact of vitamin D supplementations is nothing when compare with the other commercial therapeutics. The steroidal hormone form of 1α,25(OH)2D3 has at least in part, three important properties or functions through which it could reduce or totally prevent risk of diabetes. Firstly, 1α,25(OH)2D3 is the major regulator for calcium levels, thus it could indirectly induce insulin secretion through activation of β-cell calciumdependent endopeptidases to produce the cleavage that facilitates the conversion of proinsulin to insulin (Palomer X et al., 2007; Chiu KC et al., 2004, Boucher BJ, 1998). Additionally, it could directly enhance insulin action by stimulating the expression of insulin receptors and regulating insulin-mediated intra cellular processes via regulation of the calcium pool (Seenia V Peechakara and Anastassios G Pittas, 2008). Secondly, 1α,25(OH)2D3 acts as a potent immunosuppressive effector, since it could inhibit CD4+ T-lymphocyte proliferation and suppresses the release of typical Th-1-type cytokines, i.e. interleukin (IL)-2, IFN-γ or TNF-α (Mathieu C, Adorini L, 2002; Lemire JM et al., 1995; Rausch-Fan X et al., 2002). Several studies reported the occurrence of these inflammatory changes many years before diabetes onset; they are regarded as contributors rather than a consequence of the disease (Kolb H, Mandrup-Poulsen T, 2005; Palomer X et al., 2007). Suppress the release of typical IL-12 and TNF-α by vitamin D could mediate an immune response in the Th2 direction (Rabinovitch A, Suarez-Pinzon WL, 1998; Cameron MJ et al., 1997) and mediate humeral immunity. Thirdly, 1α,25(OH)2D3 acts as a potential antioxidant to scavenging ROS, thus reduces the stringent destructive effect of ROS on insulin producing B-cells, so prevents incidence of type 2 diabetes. On the other hand, through our search, there are two possible reasons for why obese individual is chronically vitamin D deficient. Firstly, vitamin D is a fat soluble, and it is efficiently deposited in the large body fat stores and is not bioavailable, or seizor in the fat cells. Secondly, obesity is associated with hyperparathyroidism which in turn leads to decrease vitamin D synthesis, since there is a reverse relationship between each. Up to date, several studies that conducted in the early stage of gestation that conclusively confirmed that there is no association between maternal 25(OH)D and gestational diabetes. Furthermore, maternal 25(OH)D concentrations is unrelated to neonate’s anthropometry or cord plasma variables (Farrant HJW et al., 2008; Hollis and Wagner., 2006). Further prospective studies in alter pregnancy are important, since most of these studies have been conducted during the earlier pregnancy. However, the mechanisms controlling biphasic insulin release develop during the late fetal life in the rat and human (Farrant HJW et al., 2008; Hellerstrom and Swenne, 1991; Kervran A and Randon J, 1980). Finally, It is no doubt that vitamin D appears a propitious effects merit to set it as a potential therapeutic agent to treat or prevent diabetes. Daily regular sun exposure or alternatively sun-beds using could assist to decrease or prevent risk of diabetes.
The global health expenditures to treat or prevent diabetes and its sequences amount to hundreds of billions of dollars every year (International Diabetes Federation, 2007). On the basis of evidence, autoimmune reactions, inflammatory mediators and reactive oxygen species (ROS) have been emerged to be the major possible underling mechanisms for diabetes incidence. Several studies have been confirmed that vitamin D is a potential modifier against diabetes. In comparison with the other therapeutic agents the economic impact of vitamin D supplementations is nothing when compare with the other commercial therapeutics. The steroidal hormone form of 1-alpha,25(OH)2D3 has at least in part, three important properties or functions through which it could reduce or totally prevent risk of diabetes. Firstly, 1-alpha,25(OH)2D3 is the major regulator for calcium levels, thus it could indirectly induce insulin secretion through activation of beta-cell calciumdependent endopeptidases to produce the cleavage that facilitates the conversion of proinsulin to insulin (Palomer X et al., 2007; Chiu KC et al., 2004, Boucher BJ, 1998). Additionally, it could directly enhance insulin action by stimulating the expression of insulin receptors and regulating insulin-mediated intra cellular processes via regulation of the calcium pool (Seenia V Peechakara and Anastassios G Pittas, 2008). Secondly, 1-alpha,25(OH)2D3 acts as a potent immunosuppressive effector, since it could inhibit CD4+ T-lymphocyte proliferation and suppresses the release of typical Th-1-type cytokines, i.e. interleukin (IL)-2, IFN-gamma or TNF-alphaï€ (Mathieu C, Adorini L, 2002; Lemire JM et al., 1995; Rausch-Fan X et al., 2002). Several studies reported the occurrence of these inflammatory changes many years before diabetes onset; they are regarded as contributors rather than a consequence of the disease (Kolb H, Mandrup-Poulsen T, 2005; Palomer X et al., 2007). Suppress the release of typical IL-12 and TNF-alpha by vitamin D could mediate an immune response in the Th2 direction (Rabinovitch A, Suarez-Pinzon WL, 1998; Cameron MJ et al., 1997) and mediate humeral immunity. Thirdly, 1-alpha,25(OH)2D3 acts as a potential antioxidant to scavenging ROS, thus reduces the stringent destructive effect of ROS on insulin producing B-cells, so prevents incidence of type 2 diabetes. On the other hand, through our search, there are two possible reasons for why obese individual is chronically vitamin D deficient. Firstly, vitamin D is a fat soluble, and it is efficiently deposited in the large body fat stores and is not bioavailable, or seizor in the fat cells. Secondly, obesity is associated with hyperparathyroidism which in turn leads to decrease vitamin D synthesis, since there is a reverse relationship between each. Up to date, several studies that conducted in the early stage of gestation that conclusively confirmed that there is no association between maternal 25(OH)D and gestational diabetes. Furthermore, maternal 25(OH)D concentrations is unrelated to neonates anthropometry or cord plasma variables (Farrant HJW et al., 2008; Hollis and Wagner., 2006). Further prospective studies in alter pregnancy are important, since most of these studies have been conducted during the earlier pregnancy. However, the mechanisms controlling biphasic insulin release develop during the late fetal life in the rat and human (Farrant HJW et al., 2008; Hellerstrom and Swenne, 1991; Kervran A and Randon J, 1980). Finally, It is no doubt that vitamin D appears a propitious effects merit to set it as a potential therapeutic agent to treat or prevent diabetes. Daily regular sun exposure or alternatively sun-beds using could assist to decrease or prevent risk of diabetes.
Could you re-run your analysis looking only at R01 or R01-like grants. This type of analysis would be the most informative for this discussion. There are many grants offered by NIH that fund research teams or research infrastructure. Although one person may be the "PI" for such a grant, you can be sure that they are not the only investigators receiving support. In other words, sometimes one investigator's grant may be supporting a number of PIs at his institution. However, if a significant number of NIH investigators have more than 5 R01-type grants this would be cause for concern. At this level, most people would find this a bit unfair, especially in times of tight budgets and increasing ages for first R01...
Fair, unfair who knows? But, without a doubt, it is corrupt and will be the downfall of science. I am sick of the big grand PI who never lifts a finger do an experiment or teach a grad student or postdoc. I don't want to be apart of that. Soon, all we will have is foriegn labor.