scholarly journals The Increasing Importance of Fellowships and Career Development Awards in the Careers of Early-Stage Biomedical Academic Researchers

2019 ◽  
Author(s):  
Christopher L. Pickett

AbstractExcessive competition for biomedical faculty positions has ratcheted up the need to accumulate some mix of high-quality publications and prestigious grants to move from a training position to university faculty. How universities value each of these attributes when considering faculty candidates is critical for understanding what is needed to succeed as academic faculty. In this study, I analyzed publicly available NIH grant information to determine the grants first-time R01 (FTR01) awardees held during their training period. Increases in the percentage of the FTR01 population that held a training award demonstrate these awards are becoming a more common component of a faculty candidate’s resume. The increase was largely due to an expansion of NIH K-series career development awards between 2000 and 2017. FTR01 awardees with a K01, K08, K23, or K99 award were overrepresented in a subset of institutions, whereas FTR01 awardees with F32 fellowships and those with no training award were evenly distributed across institutions. Finally, training awardees from top institutions were overrepresented in the faculty of the majority of institutions, echoing data from other fields where a select few institutions supply an overwhelming majority of the faculty for the rest of the field. These data give important insight into how trainees compete for NIH funding and faculty positions and how institutions prefer those with or without training awards.

2020 ◽  
pp. 1-9
Author(s):  
Russell R. Lonser ◽  
Luke G. F. Smith ◽  
Michael Tennekoon ◽  
Kavon P. Rezai-Zadeh ◽  
Jeffrey G. Ojemann ◽  
...  

OBJECTIVETo increase the number of independent National Institutes of Health (NIH)–funded neurosurgeons and to enhance neurosurgery research, the National Institute of Neurological Disorders and Stroke (NINDS) developed two national comprehensive programs (R25 [established 2009] for residents/fellows and K12 [2013] for early-career neurosurgical faculty) in consultation with neurosurgical leaders and academic departments to support in-training and early-career neurosurgeons. The authors assessed the effectiveness of these NINDS-initiated programs to increase the number of independent NIH-funded neurosurgeon-scientists and grow NIH neurosurgery research funding.METHODSNIH funding data for faculty and clinical department funding were derived from the NIH, academic departments, and Blue Ridge Institute of Medical Research databases from 2006 to 2019.RESULTSBetween 2009 and 2019, the NINDS R25 funded 87 neurosurgical residents. Fifty-three (61%) have completed the award and training, and 39 (74%) are in academic practice. Compared to neurosurgeons who did not receive R25 funding, R25 awardees were twice as successful (64% vs 31%) in obtaining K-series awards and received the K-series award in a significantly shorter period of time after training (25.2 ± 10.1 months vs 53.9 ± 23.0 months; p < 0.004). Between 2013 and 2019, the NINDS K12 has supported 19 neurosurgeons. Thirteen (68%) have finished their K12 support and all (100%) have applied for federal funding. Eleven (85%) have obtained major individual NIH grant support. Since the establishment of these two programs, the number of unique neurosurgeons supported by either individual (R01 or DP-series) or collaborative (U- or P-series) NIH grants increased from 36 to 82 (a 2.3-fold increase). Overall, NIH funding to clinical neurological surgery departments between 2006 and 2019 increased from $66.9 million to $157.3 million (a 2.2-fold increase).CONCLUSIONSTargeted research education and career development programs initiated by the NINDS led to a rapid and dramatic increase in the number of NIH-funded neurosurgeon-scientists and total NIH neurosurgery department funding.


2021 ◽  
Vol 266 ◽  
pp. 6-12
Author(s):  
Mary Smithson ◽  
M. Chandler McLeod ◽  
Dan I. Chu ◽  
Greg Kennedy ◽  
Melanie Morris ◽  
...  

Author(s):  
Т.А. Богумил

В статье предлагается концепция жизни и творческого роста В.М. Шукшина сквозь призму тезаурусного и кластерного подходов. Объяснительными «персональными моделями» для интерпретации биографического текста писателя являются кластеры Мартина Идена, Гамлета и Степана Разина. Ранее биографы и литературоведы указывали на важность этих персон для Шукшина, но разрозненно. Впервые предпринята попытка свести указанные персональные модели воедино, в целостный сюжет становления писателя в пространстве культуры. На разных этапах эволюции автора доминирует одна из указанных моделей, последовательно сменяя друг друга, но не вытесняя, а «внахлест». Ранний этап творчества, ориентированный на стратегию Мартина Идена, является попыткой «вписаться» в наличный культурный мейнстрим. Выражено это в следовании поэтике соцреализма. Второй этап подспудно начинается с реабилитации отца Шукшина в 1956 года, когда актуализируется «гамлетовский комплекс», проявляющийся в чувстве вины перед отцом, через стратегию утаивания подлинного «я», мотивы чудаковатости. Третий этап связан с личностью реального исторического лица, Степана Разина, и выражается в открытом протесте против власти. Все важные для В.М. Шукшина поведенческие модели объединены мотивом одинокого противостояния враждебному социуму и имеют трагический финал, что обусловило ранний уход писателя и порождение мифов о насильственном характере его смерти. В.М. Шукшин одновременно был фигурой неординарной и типичной, что позволило его биографии стать «персональной моделью» для последующих авторов, выходцев из сельской глубинки. The article proposes the concept of life and creative growth of V.M. Shukshin through the prism of the thesaurus and cluster approach. The explanatory "personal models" for interpreting the biographical text of the writer are clusters of Martin Eden, Hamlet and Stepan Razin. Earlier, biographers and literary critics pointed out the importance of these people for Shukshin, but it was scattered. For the first time, an attempt was made to bring these personal models together into an integral plot of the formation of the writer in the space of culture. At different stages of the writer’s evolution, one of these models dominates, successively replacing each other, but not crowding out, but “overlapping”. The early stage of creativity, focused on Martin Eden’s strategy, is an attempt to “fit in” the current cultural mainstream. This is expressed in following the poetics of socialist realism. The second stage implicitly begins with the rehabilitation of Shukshin’s father in 1956, when the “Hamletian complex” is actualized. It is manifested in a sense of guilt towards his father, the strategy of concealing the true “I”, eccentricities. The third stage is connected with the personality of a real historical person, Stepan Razin, and is expressed in an open protest against the authorities. All important for V.M. Shukshin's behavioral models are united by the motive of a lonely confrontation with a hostile society and have a tragic ending, which led to the early departure of the writer and the generation of myths about the violent nature of his death. V.M. Shukshin was an extraordinary and typical figure at the same time. That allowed his biography to become a “personal model” for subsequent authors who came from the rural outback.


2020 ◽  
Author(s):  
María A. Duque-Correa ◽  
David Goulding ◽  
Claire Cormie ◽  
Catherine Sharpe ◽  
Judit Gali Moya ◽  
...  

ABSTRACTHundreds of millions of people are infected with whipworms (Trichuris trichiura), large metazoan parasites that live in the caecum and proximal colon. Whipworms inhabit distinct multi-intracellular epithelial burrows that have been described as syncytial tunnels. However, the interactions between first-stage (L1) larvae and the host epithelia that determine parasite invasion and establishment in the syncytium remain unclear. In vivo experiments investigating these events have been severely hampered by the limited in situ accessibility to intracellular infective larvae at the bottom of the crypts of Lieberkühn, and the lack of genetic tools such as fluorescent organisms that are readily available for other pathogens but not parasitic nematodes. Moreover, cell lines, which do not mimic the complexity of the intestinal epithelium, have been unsuccessful in supporting infection by whipworm larvae. Here, we show that caecaloids grown in an open crypt-like conformation recapitulate the caecal epithelium. Using this system, we establish in vitro infections with T. muris L1 larvae for the first-time, and provide clear evidence that syncytial tunnels are formed at this early stage. We show that larval whipworms are completely intracellular but woven through multiple cells. Using the caecaloids, we are able to visualise the pathways taken by the larvae as they burrow through the epithelial cells. We also demonstrate that larvae degrade the mucus layers overlaying the epithelium, enabling them to access the cells below. We show that early syncytial tunnels are composed of enterocytes and goblet cells that are alive and actively interacting with the larvae during the first 24 h of the infection. Progression of infection results in damage to host cells and by 72 h post-infection, we show that desmosomes of cells from infected epithelium widen and some host cells appear to become liquified. Collectively, our work unravels processes mediating the intestinal epithelium invasion by whipworms and reveals new specific interactions between the host and the parasite that allow the whipworm to establish on its multi-intracellular niche. Our study demonstrates that caecaloids can be used as a relevant in vitro model to investigate the infection biology of T. muris during the early colonisation of its host.


2008 ◽  
Vol 294 (3) ◽  
pp. E568-E575 ◽  
Author(s):  
Johannes Erdmann ◽  
Bianca Kallabis ◽  
Ulrich Oppel ◽  
Oleg Sypchenko ◽  
Stefan Wagenpfeil ◽  
...  

Obesity is associated with insulin resistance and hyperinsulinemia, which is considered to be a core component in the pathophysiology of obesity-related comorbidities. As yet it is unknown whether insulin resistance and hyperinsulinemia already develop during weight gain within the normal range. In 10 healthy male subjects the effect of intentional weight gain by 2 BMI points was examined on insulin. C-peptide and glucose levels following a meal, 75 g of glucose, and a two-step hyperglycemic clamp increased plasma glucose by 1.38 and 2.75 mmol/l, respectively. Baseline insulin, C-peptide, and glucose concentrations were significantly higher after weight gain from 21.8 to 23.8 kg/m2 BMI within 41/2 mo. Calculations of insulin secretion and clearance indicate that reduced insulin clearance contributes more to post-weight gain basal hyperinsulinemia than insulin secretion. Following oral or intravenous stimulation insulin concentrations were significantly higher post-weight gain during all three test conditions, whereas C-peptide and glucose levels did not differ. Calculations of insulin secretion and clearance demonstrated that higher stimulated insulin concentrations are entirely due to clearance but not secretion. Despite significantly higher insulin levels, the rate of intravenous glucose required to maintain the defined elevation of glucose levels was either identical (1.38 mmol/l) or even significantly lower (2.75 mmol/l) following weight gain. The present study demonstrates for the first time that insulin resistance already develops during weight gain within the normal range of body weight. The associated basal and stimulated hyperinsulinemia is the result of differentiated changes of insulin secretion and clearance, respectively.


Author(s):  
David Edward Jones ◽  
Chris Snider ◽  
Lee Kent ◽  
Ben Hicks

ABSTRACTWhile extensive modelling - both physical and virtual - is imperative to develop right-first-time products, the parallel use of virtual and physical models gives rise to two interrelated issues: the lack of revision control for physical prototypes; and the need for designers to manually inspect, measure, and interpret modifications to either virtual or physical models, for subsequent update of the other. The Digital Twin paradigm addresses similar problems later in the product life-cycle, and while these digital twins, or the “twinning” process, have shown significant value, there is little work to date on their implementation in the earlier design stages. With large prospective benefits in increased product understanding, performance, and reduced design cycle time and cost, this paper explores the concept of using the Digital Twin in early design, including an introduction to digital twinning, examination of opportunities for and challenges of their implementation, a presentation of the structure of Early Stage Twins, and evaluation via two implementation cases.


2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Kathryn E. Cherny ◽  
Karin Sauer

ABSTRACT The dispersion of biofilms is an active process resulting in the release of planktonic cells from the biofilm structure. While much is known about the process of dispersion cue perception and the subsequent modulation of the c-di-GMP pool, little is known about subsequent events resulting in the release of cells from the biofilm. Given that dispersion coincides with void formation and an overall erosion of the biofilm structure, we asked whether dispersion involves degradation of the biofilm matrix. Here, we focused on extracellular genomic DNA (eDNA) due to its almost universal presence in the matrix of biofilm-forming species. We identified two probable nucleases, endA and eddB, and eddA encoding a phosphatase that were significantly increased in transcript abundance in dispersed cells. However, only inactivation of endA but not eddA or eddB impaired dispersion by Pseudomonas aeruginosa biofilms in response to glutamate and nitric oxide (NO). Heterologously produced EndA was found to be secreted and active in degrading genomic DNA. While endA inactivation had little effect on biofilm formation and the presence of eDNA in biofilms, eDNA degradation upon induction of dispersion was impaired. In contrast, induction of endA expression coincided with eDNA degradation and resulted in biofilm dispersion. Thus, released cells demonstrated a hyperattaching phenotype but remained as resistant to tobramycin as biofilm cells from which they egress, indicating EndA-dispersed cells adopted some but not all of the phenotypes associated with dispersed cells. Our findings indicate for the first time a role of DNase EndA in dispersion and suggest weakening of the biofilm matrix is a requisite for biofilm dispersion. IMPORTANCE The finding that exposure to DNase I impairs biofilm formation or leads to the dispersal of early stage biofilms has led to the realization of extracellular genomic DNA (eDNA) as a structural component of the biofilm matrix. However, little is known about the contribution of intrinsic DNases to the weakening of the biofilm matrix and dispersion of established biofilms. Here, we demonstrate for the first time that nucleases are induced in dispersed Pseudomonas aeruginosa cells and are essential to the dispersion response and that degradation of matrix eDNA by endogenously produced/secreted EndA is required for P. aeruginosa biofilm dispersion. Our findings suggest that dispersing cells mediate their active release from the biofilm matrix via the induction of nucleases.


2020 ◽  
Vol 8 (2) ◽  
pp. 228 ◽  
Author(s):  
Lilibeth Arias ◽  
Paula Cardona ◽  
Martí Català ◽  
Víctor Campo-Pérez ◽  
Clara Prats ◽  
...  

Cording was the first virulence factor identified in Mycobacterium tuberculosis (Mtb). We aimed to ascertain its role in the induction of active tuberculosis (TB) in the mouse strain C3HeB/FeJ by testing the immunopathogenic capacity of the H37Rv strain. We have obtained two batches of the same strain by stopping their growth in Proskauer Beck liquid medium once the mid-log phase was reached, in the noncording Mtb (NCMtb) batch, and two days later in the cording Mtb (CMtb) batch, when cording could be detected by microscopic analysis. Mice were challenged with each batch intravenously and followed-up for 24 days. CMtb caused a significant increase in the bacillary load at an early stage post-challenge (day 17), when a granulomatous response started, generating exudative lesions characterized by neutrophilic infiltration, which promoted extracellular bacillary growth together with cording formation, as shown for the first time in vivo. In contrast, NCMtb experienced slight or no bacillary growth and lesions could barely be detected. Previous Bacillus Calmette-Guérin (BCG) vaccination or low dose aerosol (LDA) Mtb infection were able to delay the progression towards active TB after CMtb challenge. While BCG vaccination also reduced bacillary load when NCMtb was challenged, LDA did not, and its proliferative lesions experienced neutrophil infiltration. Analysis of lung cytokine and chemokine profiles points to their capacity to block the production of CXCL-1 and further amplification of IL-1β, IL-17 and neutrophilic extracellular trap formation, all of which are essential for TB progression. These data highlight the key role of cording formation in the induction of active TB.


Sign in / Sign up

Export Citation Format

Share Document