Science’s ‘Gollum effect’: PhDs bear brunt of territorial behaviour

Ecologists were among the researchers surveyed about the prevalence of territorial behaviours such as data hoarding.Credit: Tomas Munita/Bloomberg/GettyAlmost half of the scientists who responded to a survey have experienced territorial and undermining behaviours from other scientists — most commonly during their PhD studies1. Of those affected, nearly half said that the perpetrator was a high-profile researcher, and one-third said it was their own supervisor.Most of the survey respondents were ecologists, but the study’s organizers suspect that surveys focusing on other disciplines would yield similar results.The gatekeeping behaviours that the study documents “damage careers, particularly of early-career and marginalized researchers”, says lead author Jose Valdez, an ecologist at the German Centre for Integrative Biodiversity Research in Leipzig. “Most alarming was that nearly one in five of those affected left academia or science entirely.”Why we quit: how ‘toxic management’ and pandemic pressures fuelled disillusionment in higher educationValdez and his colleagues call the possessiveness shown by many researchers the ‘Gollum effect’, after the character Gollum in The Lord of the Rings (1954–55), whose one goal in life is to hoard an object of great power for himself. The study was published today in One Earth.“It makes something tangible that all researchers probably have experienced one way or another: the territoriality of other researchers and fear of being ‘scooped’,” says computational social scientist Jana Lasser at the University of Graz in Austria, who co-founded the Network against Abuse of Power in Science and was not involved in the study.Unnamed hazardThat academic workplaces are often toxic environments is hardly news. But “despite growing attention to issues such as bullying, harassment and mental health in academia”, Valdez says, “the root cause of many of these problems — the toxic possessiveness and gatekeeping — didn’t have a name or formal recognition”. Enter the Gollum effect, which Valdez defines as including possessive behaviours, attempts to undermine others, and efforts to restrict access to data, resources or opportunities.Valdez and his colleagues distributed their survey through professional conservation and ecology societies and social media. To reduce self-selection bias, they presented it as a survey about experiences at different career stages, not mentioning the Gollum effect until the survey was underway. The survey drew 563 responses, representing 64 nationalities.Familiar monsterThe Gollum effect was common: 44% of respondents said they had experienced it. Of these, 18% had experienced it many times. In 46% of cases, scientists said that the perpetrator was a high-profile researcher, and 35% said it was their supervisor.Among those who experienced the Gollum effect, 54% said it happened during their PhD studies, 32% during their master’s studies, 31% as a postdoctoral researcher and 27% as an undergraduate. But independent researchers, senior researchers and even professors experienced it, too.“The most surprising finding was the profound impact of the Gollum effect on career trajectories,” says Valdez. More than two-thirds of those affected said that the experience had had a moderate or large effect on their career path, and some 20% had left academia or science completely as a result (see ‘Toll of territorial behaviours’).Source: Ref. 1.

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NSF plan to slash ‘indirect’ science funding: will it stick?

The National Science Foundation has suspended its plans to set a blanket rate for all overhead-cost funding on research grants.Credit: B Christopher/AlamyThe US National Science Foundation (NSF) has paused a policy that threatened to cost universities hundreds of millions of dollars a year in ‘research overhead’ payments. The suspension, announced last Friday, follows freezes of similar policies at the US National Institutes of Health (NIH) and the US Department of Energy (DoE).The NSF announced on 2 May that it would cap overhead payments on new research grants at 15% and was swiftly sued by a coalition of 13 US universities and 3 academic associations seeking to stop the policy. The newly announced pause will last until 13 June, when a judge will hear the case. The decision allows the agency to skip a preliminary hearing.NIH cuts triggered a host of lawsuits: Nature’s guide to what’s nextSince US President Donald Trump took office in January, the NIH, NSF and DoE have all announced that they would cap overhead payments. Groups of academic organizations also sued the NIH and DoE; judges have blocked both agencies from implementing their caps.Universities argue that the caps are not only illegal, but also devastating to science. The NSF’s cap would threaten the country’s “status as a global leader in scientific research and innovation”, the plaintiffs say.A spokesperson for the NSF declined to comment on the lawsuit, but acknowledged that the agency has paused the cap. Here, Nature looks at what’s at stake and whether the administration is likely to prevail.What are overhead costs?Research grants pay for staff salaries and new laboratory equipment — the direct costs of doing science. But agencies such as the NSF and NIH also fund overhead, or indirect costs, including the electricity consumed by research facilities, information-technology support and more.In 1965, Congress mandated that universities negotiate their overhead rate with either the US Department of Health and Human Services (HHS) or the US Office of Naval Research (ONR). Each university’s rate typically applies to all federal grants it receives.University rates generally range from 40% to 70% and depend mainly on the institution’s location and the type of research being supported. For a university with a 50% indirect cost rate, for example, a US$100,000 NIH grant would provide $50,000 in further funding for indirect costs.Where does the 15% number come from?The NSF did not provide a rationale. Some wealthy private foundations provide an overhead rate of 15%, but say that they pay lower indirect rates than the government does because they expect the government to support overhead. Some foundations, such as the Gates Foundation in Seattle, Washington, often consider overhead to be part of direct costs.Why did the NSF cap indirect costs?On its website, the NSF justifies the policy by saying it will force universities to reduce overhead costs, thereby improving efficiency. The agency also argues that the change would increase its own efficiency “by eliminating the need for individualized indirect cost negations” and its own effectiveness by devoting more funds to direct research costs.The latter argument about effectiveness is “not plausible”, says John Walsh, a science-policy researcher at the Georgia Institute of Technology in Atlanta, because any increase of direct expenditures creates more indirect costs. He likens it to a chicken franchise trying to cook twice as much chicken. “You’d need a second fryer,” he says.Hundreds more NSF grants terminated after agency director resignsIn the lawsuit, universities argue that a 15% cap is simply much too low and would prevent them from carrying out crucial research.

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NSF plan to slash ‘indirect’ science funding: will it stick?

The National Science Foundation has suspended its plans to set a blanket rate for all overhead-cost funding on research grants.Credit: B Christopher/AlamyThe US National Science Foundation (NSF) has paused a policy that threatened to cost universities hundreds of millions of dollars a year in ‘research overhead’ payments. The suspension, announced last Friday, follows freezes of similar policies at the US National Institutes of Health (NIH) and the US Department of Energy (DoE).The NSF announced on 2 May that it would cap overhead payments on new research grants at 15% and was swiftly sued by a coalition of 13 US universities and 3 academic associations seeking to stop the policy. The newly announced pause will last until 13 June, when a judge will hear the case. The decision allows the agency to skip a preliminary hearing.NIH cuts triggered a host of lawsuits: Nature’s guide to what’s nextSince US President Donald Trump took office in January, the NIH, NSF and DoE have all announced that they would cap overhead payments. Groups of academic organizations also sued the NIH and DoE; judges have blocked both agencies from implementing their caps.Universities argue that the caps are not only illegal, but also devastating to science. The NSF’s cap would threaten the country’s “status as a global leader in scientific research and innovation”, the plaintiffs say.A spokesperson for the NSF declined to comment on the lawsuit, but acknowledged that the agency has paused the cap. Here, Nature looks at what’s at stake and whether the administration is likely to prevail.What are overhead costs?Research grants pay for staff salaries and new laboratory equipment — the direct costs of doing science. But agencies such as the NSF and NIH also fund overhead, or indirect costs, including the electricity consumed by research facilities, information-technology support and more.In 1965, Congress mandated that universities negotiate their overhead rate with either the US Department of Health and Human Services (HHS) or the US Office of Naval Research (ONR). Each university’s rate typically applies to all federal grants it receives.University rates generally range from 40% to 70% and depend mainly on the institution’s location and the type of research being supported. For a university with a 50% indirect cost rate, for example, a US$100,000 NIH grant would provide $50,000 in further funding for indirect costs.Where does the 15% number come from?The NSF did not provide a rationale. Some wealthy private foundations provide an overhead rate of 15%, but say that they pay lower indirect rates than the government does because they expect the government to support overhead. Some foundations, such as the Gates Foundation in Seattle, Washington, often consider overhead to be part of direct costs.Why did the NSF cap indirect costs?On its website, the NSF justifies the policy by saying it will force universities to reduce overhead costs, thereby improving efficiency. The agency also argues that the change would increase its own efficiency “by eliminating the need for individualized indirect cost negations” and its own effectiveness by devoting more funds to direct research costs.The latter argument about effectiveness is “not plausible”, says John Walsh, a science-policy researcher at the Georgia Institute of Technology in Atlanta, because any increase of direct expenditures creates more indirect costs. He likens it to a chicken franchise trying to cook twice as much chicken. “You’d need a second fryer,” he says.Hundreds more NSF grants terminated after agency director resignsIn the lawsuit, universities argue that a 15% cap is simply much too low and would prevent them from carrying out crucial research.

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Who was M R Srinivasan? Veteran nuclear scientist passes away at 95; PM Modi condoles demise

Dr. M R Srinivasan, the former Chairman of India’s Atomic Energy Commission, passed away on Tuesday, 20 May 2025, at the age of 95. The veteran scientist suddenly fell ill overnight in Ooty and peacefully passed away in the local hospital at 4 a.m. on Tuesday.“My father suddenly took ill in Ooty over last night and passed away peacefully in hospital at 4 am in hospital, my mother is with him.. we are going from Bangalore now..,” said Sharada Srinivasan, the daughter of the veteran scientist according to a social media post on Facebook post.Also Read

Who was M R Srinivasan? Veteran nuclear scientist passes away at 95; PM Modi condoles demise

Dr. M R Srinivasan, the former Chairman of India’s Atomic Energy Commission, passed away on Tuesday, 20 May 2025, at the age of 95. The veteran scientist suddenly fell ill overnight in Ooty and peacefully passed away in the local hospital at 4 a.m. on Tuesday.“My father suddenly took ill in Ooty over last night and passed away peacefully in hospital at 4 am in hospital, my mother is with him.. we are going from Bangalore now..,” said Sharada Srinivasan, the daughter of the veteran scientist according to a social media post on Facebook post.Also Read

SK Life Science starts TV ad campaign to drive patients to seizure drug Xcopri

SK Life Science is encouraging patients beetling down the long and winding road toward seizure-free life to switch gears. In a new nationwide direct-to-consumer (DTC) ad, the Xcopri manufacturer asks partial-onset seizure patients to consider switching to a new treatment.

Xcopri sales beat expectations last year, climbing more than 50% to hit $322 million. SK is aiming to keep sales on an upward trajectory this year and turn the medicine into a blockbuster toward the end of the decade. But with Xenon Pharmaceuticals aiming to publish phase 3 data on a rival molecule early next year, a potential branded competitor for the generic-focused market is on the horizon.

SK is therefore stepping up promotion of Xcopri with a campaign that is now running across streaming TV, digital, social and healthcare platforms. The “Road to Reduction” campaign includes a one-minute ad that shows a young man sitting in the passenger seat of a car on a road trip with his father. 

“The road to partial-onset seizure reduction can be long and winding. You feel like you’re not in the driver’s seat, afraid to try a new medicine because of side effects or going backwards. But doing nothing means you won’t get anywhere,” the voiceover says. “Try switching gears to Xcopri.”

The visuals mirror the voiceover, with the car variously taking bends, needing to reverse because a tree is blocking the road and spinning its wheels in the mud, going nowhere. 

The journey improves once the car takes a turnoff signposted “Significant Seizure Reduction.” The young man then visits a physician, and the road trip ends with father and son enjoying the view across a vast expanse of forested hills.

“At SK Life Science, we’ve always been committed to elevating the voices of people living with epilepsy and advocating for patient voices to be heard when choosing a treatment option,” Chris Fanale, SK’s executive director of marketing, said in a statement. “This campaign reflects a deeply authentic understanding of what patients and caregivers face daily—and encourages them to talk with their doctors about options that may help reduce seizures, even in people who have been living with uncontrolled seizures for a long time.”

The TV spot is the latest in a series of actions intended to boost awareness of Xcopri among patients and healthcare professionals. In 2021, SK ran a DTC campaign, aiming one ad at patients and another at physicians, and also enlisted social media influencers to an awareness push. The company got even more creative in 2022 and 2023, sending reps out with men’s work boots to tell a patient’s story and creating a simulated rainstorm at a conference. 

SK Life Science starts TV ad campaign to drive patients to seizure drug Xcopri

SK Life Science is encouraging patients beetling down the long and winding road toward seizure-free life to switch gears. In a new nationwide direct-to-consumer (DTC) ad, the Xcopri manufacturer asks partial-onset seizure patients to consider switching to a new treatment.

Xcopri sales beat expectations last year, climbing more than 50% to hit $322 million. SK is aiming to keep sales on an upward trajectory this year and turn the medicine into a blockbuster toward the end of the decade. But with Xenon Pharmaceuticals aiming to publish phase 3 data on a rival molecule early next year, a potential branded competitor for the generic-focused market is on the horizon.

SK is therefore stepping up promotion of Xcopri with a campaign that is now running across streaming TV, digital, social and healthcare platforms. The “Road to Reduction” campaign includes a one-minute ad that shows a young man sitting in the passenger seat of a car on a road trip with his father. 

“The road to partial-onset seizure reduction can be long and winding. You feel like you’re not in the driver’s seat, afraid to try a new medicine because of side effects or going backwards. But doing nothing means you won’t get anywhere,” the voiceover says. “Try switching gears to Xcopri.”

The visuals mirror the voiceover, with the car variously taking bends, needing to reverse because a tree is blocking the road and spinning its wheels in the mud, going nowhere. 

The journey improves once the car takes a turnoff signposted “Significant Seizure Reduction.” The young man then visits a physician, and the road trip ends with father and son enjoying the view across a vast expanse of forested hills.

“At SK Life Science, we’ve always been committed to elevating the voices of people living with epilepsy and advocating for patient voices to be heard when choosing a treatment option,” Chris Fanale, SK’s executive director of marketing, said in a statement. “This campaign reflects a deeply authentic understanding of what patients and caregivers face daily—and encourages them to talk with their doctors about options that may help reduce seizures, even in people who have been living with uncontrolled seizures for a long time.”

The TV spot is the latest in a series of actions intended to boost awareness of Xcopri among patients and healthcare professionals. In 2021, SK ran a DTC campaign, aiming one ad at patients and another at physicians, and also enlisted social media influencers to an awareness push. The company got even more creative in 2022 and 2023, sending reps out with men’s work boots to tell a patient’s story and creating a simulated rainstorm at a conference. 

LJI Scientists Identify Critical Mechanisms Linking Viral Infection to Arthritis-Like Disease

In recent research emerging from the La Jolla Institute for Immunology (LJI), scientists have unveiled a critical insight into how Chikungunya virus (CHIKV) infections may precipitate long-lasting joint pain reminiscent of autoimmune arthritis. CHIKV, a mosquito-borne alphavirus, has now established a presence in over 110 countries worldwide and often manifests as an acute febrile illness accompanied by severe joint discomfort. However, for a subset of infected individuals, symptoms progress into a debilitating, chronic arthritic condition that mimics the pathophysiology of rheumatoid arthritis, prompting researchers to investigate underlying immunological mechanisms. At the core of this investigation lies the body’s adaptive immune system, particularly the role of CD4+ T cells. These lymphocytes are known to orchestrate immune responses against various pathogens, including viruses, by producing a broad repertoire of cytokines that modulate inflammation and immune cell activity. Using blood samples obtained from a cohort of CHIKV patients in Colombia, the LJI team employed peptide stimulation assays to dissect the specificity and functionality of T cell responses against viral epitopes. Remarkably, their data revealed an unexpectedly predominant expansion of CD4+ T cells directed specifically against CHIKV antigens, accompanied by comparatively low levels of CD8+ T cell responses. This skewed T cell profile contrasts with classical antiviral immunity, where CD8+ cytotoxic T cells typically exert a leading role by directly killing infected cells. Instead, in CHIKV infection, the persistence of virus-specific memory CD4+ T cells was notable, with these cells persisting in 87% of patients even six years post-infection. In stark contrast, memory CD8+ T cells specific to CHIKV were detectable in only 13% of these individuals. Such an immune signature aligns closely with those observed in autoimmune diseases, suggesting that these CD4+ T cells might contribute not only to viral control but also to chronic inflammatory sequelae. Diving deeper into the functional attributes of these cells, the investigators found that the CD4+ T cells from patients suffering chronic joint pain predominantly exhibited a “monofunctional” cytokine secretion profile, producing primarily tumor necrosis factor-alpha (TNF-α). TNF-α is a potent pro-inflammatory cytokine implicated in the pathogenesis of autoimmune arthritis. Typically, effective antiviral CD4+ T cells are polyfunctional, simultaneously producing multiple cytokines such as interferon-gamma (IFN-γ), interleukin-2 (IL-2), and TNF-α; this multifaceted secretion enhances viral clearance and limits immune-mediated damage. The predominance of monofunctional TNF-α-secreting CD4+ T cells in CHIKV patients points to a maladaptive immune response that may drive sustained synovial inflammation and joint degradation. These findings offer the first direct human evidence linking CD4+ T cell-driven inflammation to the chronic arthritic manifestations observed after CHIKV infection. They underscore a pathogenic mechanism whereby CD4+ T cells, while initially protective, transition into a phenotype that promotes persistent inflammation even after viral clearance. This phenomenon illuminates a possible molecular pathway that underpins the virus-induced trigger of autoimmune-like pathology. Furthermore, by elucidating this immunological profile, the study opens potential therapeutic avenues targeting TNF-α to ameliorate post-viral arthritis symptoms and improve patient quality of life. Importantly, this research also touches upon demographic disparities observed in CHIKV-induced chronic arthritis. Epidemiological data show that middle-aged women disproportionately develop severe, long-lasting joint pain after infection, a sex-specific vulnerability echoing broader patterns in autoimmune diseases. Current investigations, supported by LJI’s SPARK funding program, aim to dissect whether sex hormones or genetic factors influence the aberrant CD4+ T cell responses and contribute to this predisposition. Understanding these variables could refine treatment strategies and enable personalized therapeutic interventions. From a broader perspective, the study adds to the mounting evidence that viral infections can initiate or exacerbate autoimmune diseases through molecular mimicry, bystander activation, or persistent immune activation. Viruses like dengue and now SARS-CoV-2 have also been implicated in triggering chronic immune dysregulation and inflammatory syndromes. The parallels drawn between CHIKV and other viral infections highlight an urgent need for comprehensive longitudinal studies that monitor immune responses well beyond the acute infectious phase. Central to these investigations is the characterization of viral epitopes that elicit robust immune responses. By mapping these key CD4+ T cell epitopes within CHIKV, researchers can better understand viral antigenicity and immune evasion strategies, offering insights relevant to vaccine design. LJI’s work, therefore, not only advances fundamental immunological knowledge but also carries translational potential for developing vaccines or immunotherapies aimed at modulating deleterious T cell responses. Given the global expansion of CHIKV and the absence of specific antiviral treatments or licensed vaccines, these findings could dramatically shift the clinical approach to managing post-chikungunya arthritis. Targeting monofunctional, TNF-α-secreting CD4+ T cells pharmacologically might curb chronic inflammation. Anti-TNF biologics, already in use for rheumatoid arthritis, present a promising therapeutic option, potentially repurposable for CHIKV-associated arthritis pending rigorous clinical evaluation. In conclusion, this groundbreaking study led by LJI Assistant Professor Daniela Weiskopf sheds light on the immunopathology of chronic Chikungunya disease, revealing how the virus manipulates host T cell responses to provoke persistent inflammation and joint damage. Such mechanistic clarity propels the field toward novel interventions and fuels further studies on the intricate interface between infectious agents and autoimmune disease development. Subject of Research: Cells Article Title: Chikungunya virus-specific CD4+ T cells are associated with chronic chikungunya viral arthritic disease in humans News Publication Date: 20-May-2025 Web References: For further reading on related topics in immunology and viral pathogenesis, visit La Jolla Institute for Immunology’s site at lji.org.Immune Matters Magazine article “For some women, one mosquito bite leads to chronic pain”: https://mag.lji.org/spring2025/for-some-women-one-mosquito-bite-leads-to-chronic-pain/ References:Weiskopf D, Agarwal R, Chang J, Côrtes FHC, Ha C, Villalpando J, Castillo IN, Gálvez RI, Grifoni A, Sette A, Romero Vivas CM, Heise MT, Premkumar L, Falconar AK. Chikungunya virus-specific CD4+ T cells are associated with chronic chikungunya viral arthritic disease in humans. Cell Reports Medicine. 2025 May 20. Image Credits: La Jolla Institute for Immunology Tags: adaptive immune response in viral infectionsarthritis-like disease progressionautoimmune arthritis pathophysiologyCD4+ T cell role in immunityChikungunya virus infection mechanismschronic arthritic conditions post-infectionchronic joint pain after viral infectioncytokine production in immune responseimmunological mechanisms of arthritisLa Jolla Institute for Immunology research findingsmosquito-borne virus health impactsT cell responses to viral epitopes