scholarly journals A new record for PBDEs in people | POPs treaty targets further chemicals | Canada's research funding system works | Do male frogs naturally have female traits? | Are low levels of lead in water risky?

2005 ◽  
Vol 39 (14) ◽  
pp. 296A-298A ◽  
Author(s):  
Kellyn S. Betts ◽  
Janet Pelley ◽  
Rebecca Renner
Keyword(s):  
Research Funding ◽  
New Record ◽  
Funding System ◽  
Low Levels

scholarly journals Investigating the Performance of Japan’s Competitive Grant Grants-in-Aid for Scientific Research System

2018 ◽  
Vol 7 (5) ◽  
pp. 167 ◽  
Author(s):  
Yasunori Yamashita ◽  
Hoang Gyan Giang ◽  
Tatsuo Oyama
Keyword(s):  
Research Funding ◽  
Quantitative Characteristic ◽  
Scientific Research ◽  
Academic Disciplines ◽  
Policy Recommendations ◽  
Research System ◽  
Research Projects ◽  
Funding Allocation ◽  
Funding System ◽  
Japanese Science

We aim at investigating characteristics of Japan’s largest competitive grant Grants-in-Aid for Scientific Research (GASR) system in order to find a desirable research funding system, obtaining more applicants from various academic disciplines, researchers’ gender, and ages. Firstly, we briefly describe the Japanese competitive research funding system including the GASR system. Then we investigate the GASR system quantitatively, focusing on its funding, allocation and relationship with the Japanese Science and Technology Basic Plans. Quantitative characteristic analyses are conducted for the GASR system from various perspectives such as type of research projects, academic disciplines, researchers’ gender, and ages by investigating the data for applications, acceptances, and budgets allocated in the recent 10 years. Finally, we summarize our findings and conclude the paper by proposing policy recommendations to improve Japan’s competitive research funding system.

Toward an excellence-based research funding system: Evidence from Poland

2017 ◽  
Vol 11 (1) ◽  
pp. 282-298 ◽  
Author(s):  
Emanuel Kulczycki ◽  
Marcin Korzeń ◽  
Przemysław Korytkowski
Keyword(s):  
Research Funding ◽  
Funding System

A Failure to Start: Aborted Activation of CAR T Cells in Chronic Lymphocytic Leukemia

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 681-681
Author(s):  
McKensie Collins ◽  
Weimin Kong ◽  
Inyoung Jung ◽  
Meng Wang ◽  
Stefan M Lundh ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Research Funding ◽  
Cell Dysfunction ◽  
Car T Cells ◽  
Car T Cell ◽  
Car T ◽  
T Cell Dysfunction ◽  
Low Levels

Introduction: Chronic Lymphocytic Leukemia (CLL) is a CD19+ B-cell malignancy that accounts for approximately 25% of adult leukemia diagnoses in the developed world. While conventional therapies have some efficacy, there are few curative therapeutic options and many patients ultimately progress to relapsed or refractory disease. CD19-targeting chimeric antigen receptor (CAR) T cell therapy has provided some hope, but induces complete remission in only 26% of patients. This suboptimal response rate is believed to be due to T cell dysfunction and immune-suppression by CLL cells, the mechanisms of which are poorly understood. Results: To understand the causes of CAR T cell dysfunction in CLL we investigated the defects that CLL cells induced in normal donor CD19-targeting CAR T cells. CAR T cells were repeatedly stimulated at 5-day intervals with either primary CLL cells from patients or a CD19-expressing control cell line (aAPC). Repeat stimulation of CAR T cells with aAPCs resulted in 5.36 ± .94 population doublings after three stimulations, whereas CLL cells only evoked 2.39 ± .92 population doublings. We performed phenotyping, proliferation analysis, and cytokine analysis of stimulated CAR T cells. CLL-stimulated T cells appeared un-activated, with low levels of PD-1, LAG3, and TIM3, low levels of cytokine production, and a high proportion of non-cycling cells as measured by Ki67 staining. We first hypothesized that CLL cells induce an altered epigenetic program that prevents effector function and is stabilized by successive stimulations. To test this, we stimulated CAR T cells with CLL cells or aAPCs as indicated in Fig. 1A. CLL-stimulated CAR T cells failed to proliferate or produce cytokines, but subsequent stimulation with aAPCs rescued these functions (Fig. 1B). Further, CLL-stimulated CAR T cells did not differentiate, suggesting that CLL cells do not induce stable defects but rather insufficiently activate CAR T cells (Fig. 1C). These cells also appeared un-activated as indicated by low levels of PD-1 and Ki67. We then used flow cytometry to assess expression of costimulatory and inhibitory molecules on the primary CLL samples. We found that the levels of co-stimulatory and adhesion molecules, namely CD80/CD86 and CD54/CD58 respectively were found at low frequencies, and where present were expressed at low levels. This suggested that one mechanism behind the lack of CAR T cell effector responses may be that a lack of co-stimulation prevents proper CAR T cell targeting of these cells. Towards this, we incubated CLL cells with a murine fibroblast line expressing CD40 ligand for 24 hours with IL-4 to activate the CLL cells. We found that this activation significantly increased expression of CD80, CD86, CD54, and CD58 on the CLL cells. We then used these cells to stimulate CAR T cells in our re-stimulation assay and found that CAR T cells were able to proliferate in response to these activated CLLs (Fig. 1D). In addition, CAR T cells stimulated with activated CLL cells formed more cell-to-cell conjugates than those stimulated with un-activated CLL cells. These data suggest not only that insufficient activation of CAR T cells may be responsible for the poor response rates to CAR T cell therapy in CLL, but also implicate a need for additional co-stimulation in this CAR T cell setting. Another contributing factor may be immune suppression by CLL cells. To determine if CLL cells are immune-suppressive, we used a co-culture assay to stimulate CAR T cells with aAPCs and CLL cells mixed at known ratios. Interestingly, all mixed cultures proliferated similarly, suggesting that CLL cells did not prevent T cell activation in the presence of a strong activation signal. We also found that CLL cells are responsive to IL-2, as addition of this cytokine to culture media prolongs survival of CLL cells out to 10 days depending on the dose. This suggests that CLL cells express a functional IL-2 receptor and may be taking up IL-2 from the culture media, further impairing T cell activation. In support of this, supplementing IL-2 into our CLL/CAR T cell co-cultures rescued T cell proliferative capacity. Taken together, these data suggest that T cell dysfunction in CLL is the result of insufficient activation rather than true functional defects. Disclosures June: Novartis: Research Funding; Tmunity: Other: scientific founder, for which he has founders stock but no income, Patents & Royalties. Melenhorst:National Institutes of Health: Research Funding; Parker Institute for Cancer Immunotherapy: Research Funding; Novartis: Research Funding, Speakers Bureau; IASO Biotherapeutics, Co: Consultancy; Simcere of America, Inc: Consultancy; Shanghai Unicar Therapy, Co: Consultancy; Colorado Clinical and Translational Sciences Institute: Membership on an entity's Board of Directors or advisory committees; Genentech: Speakers Bureau; Stand Up to Cancer: Research Funding; Incyte: Research Funding.

Iron Chelation Therapy in Transfusion Dependent Patients with Thalassemia and Minimal Liver Iron Load

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4270-4270
Author(s):  
Antonios Kattamis ◽  
Konstantinos Stokidis ◽  
Theoni Petropoulou ◽  
Dimitra Kyriacopoulou ◽  
Polyxeni Delaporta ◽  
...  
Keyword(s):  
Combination Therapy ◽  
Iron Overload ◽  
Research Funding ◽  
Chelation Therapy ◽  
Combined Therapy ◽  
Iron Chelation ◽  
Thalassemia Major ◽  
Liver Iron ◽  
Iron Load ◽  
Low Levels

Abstract Abstract 4270 Background: Recent advances in the treatment of iron overload in patients with transfusion- dependent thalassemia have dramatically changed iron related morbidity and mortality. Intensive chelation therapy by using combination therapy or monotherapy at high doses had led to total clearing of the iron in many patients. The best approach for chelation treatment in patients with low levels of iron overload is debatable. Patients and Methods This study included all the patients with thalassemia major with minimal liver iron overload, followed in our unit. More precisely, to be eligible for this observational study, the patients needed to have liver iron concentration (LIC) <1.5 mg Fe/gram dry weight tissue, defined by MRI, and to have at least a subsequent MRI evaluation after this time. The mean observation time, which was the time between the two MRIs, was 16.9±5.2 months. Results Fourty five patients (22 females, 30 non-splemectomized, 21 HCV seropositive, mean age: 31±5.6 years) have reached minimal levels of iron overload in any time point after 2004. Thirty one of them have been treated with combined therapy of desferrioxamine (DFO) and deferiprone (DFP) and 5, 6 and 3 with monotherapy of deferasirox (DFX), DFP and DFO, respectively. After reaching these levels, 42% of the patients changed therapy, with the most frequent change being from combined therapy to monotherapy (15 patients). Baseline ferritin levels at the time of the first MRI range from 43 to 4336 ng/ml (median 230 ng/ml) and they were not affected by spleen, gender or HCV status. Baseline LIC (mean 1.2 ± 1.7 mgFe/g.d.w.) correlated well with ferritin levels (Spearman's rho = 0.47, p<0.005), as did ferritin changes to LIC changes (Spearman's rho = 0.67, p<0.005). The results on the follow up evaluation, stratified according to the actual treatment, are shown in the table Deferiprone was less efficacious in controlling both LIC and ferritin levels compared to combination therapy (p=0.016 and 0.031, respectively). Fifteen out of 17 patients treated with DFP showed an increase in LIC, despite using the recommended dose. Six out of 9 patients treated with DFX, most at a low dose, showed an increase in LIC. There were no differences in changes in the cardiac parameters (LVEF, cardiac T2*) in between treatment groups. The efficiency of DFP and DFX, which represents the ratio of iron excreted to the theoretical maximum of iron that could be bound by the chelators, was calculated at 1.8±0.9 % and 15.2 ± 3.6 %, respectively. Conclusions Current iron chelation therapy regimens are able to render iron load-free many patients with thalassemia major. As iron accumulation from transfusions continues, a fine balance needs to be found in which neither worsening of iron overload nor toxicity from excessive dose of iron chelators will occur. This study showed that at low levels of iron overload both combination therapy and DFX can control iron accumulation, whether monotherapy with DFP may be insufficient to achieve iron balance in many patients. The dose of the chelators needs to be adjusted according to the needs and the clinical course of the patients, which can be predicted by the trend of the ferritin levels. Furthermore, it should be kept in mind that at low levels of iron overload, the iron chelators' efficiency may be lower than previously described. Disclosures: Kattamis: NOVARTIS ONCOLOGY: Honoraria, Research Funding, Speakers Bureau; APOPHARMA: Honoraria. Ladis:NOVARTIS ONCOLOGY: Honoraria, Research Funding; APOPHARMA: Honoraria, Research Funding.

Prevalence of Thrombophilia In Patients with Sickle Cell Disease and Osteonecrosis

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3184-3184
Author(s):  
Murtadha K. Al-Khabori ◽  
Anil Pathare ◽  
Khalil Al Farsi ◽  
Mohammed Al Huneini ◽  
Salam Alkindi
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Research Funding ◽  
Protein C ◽  
Dna Analysis ◽  
White Cell Count ◽  
Protein S ◽  
Cell Disease ◽  
High Prevalence ◽  
Low Levels

Abstract Abstract 3184 Background: Osteonecrosis (ON) of the femoral and humeral heads is frequently seen in patients with sickle cell disease (SCD). Earlier studies reported a high prevalence of thrombophilia in patients with ON. Aims: To study the prevalence of thrombophilia in patients of SCD with ON. Methods: Case records of SCD patients with ON were retrospectively reviewed for protein S, protein C, and anti-thrombin deficiency, along with activated protein C resistance (APCR). Results: A total of sixty-three patients were identified, 35 of whom were males, with a median age of 21 years (range 15to 46). Median haemoglobin, total white cell count and platelet counts were 10 g/dL (range 7.7to 13.3), 7.5 ×109/L (range 3.4 to 16.7) and 302 ×109/L (range 72 to 1101) respectively. Twenty-eight patients were on hydroxyurea. Thrombophilia testing showed that 29% (95% confidence interval: 17–40), 47% (95% CI: 29–64) and 79% (95% CI: 65–93) of the patients had low levels of functional (<60 unit/dl), total antigenic (<70 unit/dl) and free antigenic (<70 unit/dl) protein S respectively, while 21% (95% CI: 10–31) and 67% (95% CI: 46–87) had low levels of functional (<70 unit/dl) and antigenic (<70 unit/dl) protein C respectively. In addition, 14% (95% CI: 5–23) and 22% (95% CI: 0–56) of the patients had low levels of functional (<80 unit/dl) and antigenic (<80 unit/dl) anti-thrombin levels respectively. Only 2% (95% CI: 0–5) of these patients had an abnormally low APCR (APCR ratio ≤2.3). Summary/Conclusions: Patients with SCD and ON have a high prevalence of thrombophilia. These results indicate that a prospective study with more detailed thrombophilia work-up, along with confirmatory DNA analysis, as well as a study of the role of prophylactic anticoagulation in such patients is highly warranted. Disclosures: Pathare: Sultan Qaboos University: Employment, Research Funding. Alkindi:Sultan Qaboos University: Employment, Research Funding.

Treatment With Minihepcidin Peptide Improves Anemia and Iron Overload In a Mouse Model Of Thalassemia Intermedia

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 431-431 ◽  
Author(s):  
Carla Casu ◽  
Adam Goldberg ◽  
Elizabeta Nemeth ◽  
Tomas Ganz ◽  
Sara Gardenghi ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Iron Overload ◽  
Research Funding ◽  
Erythroid Cell ◽  
Beta Thalassemia ◽  
Thalassemia Intermedia ◽  
Iron Restriction ◽  
Liver And Kidney ◽  
Equity Ownership ◽  
Low Levels

Abstract Introduction Beta-thalassemia is a inherited disorder characterized by mutations in the beta-globin gene that lead to reduced or absent beta-globin synthesis. As a consequence, in erythroid cells there is a relative excess of alpha globin chains and heme forming toxic hemichromes, which lead to oxidative damage, impaired erythroid cell maturation, premature cell death and anemia. Under these conditions, the anemia and the elevated erythropoietin levels increase the proliferation of the erythroid progenitors, suppressing the expression of the iron master regulator hepcidin. Hepcidin targets the iron exporter ferroportin present on enterocytes and macrophages. High levels of hepcidin limit iron absorption and iron recycling but low levels of hepcidin increase iron absorption. Chronic low levels of hepcidin, as in β-thalassemia, eventually lead to iron overload. The th3/+ mouse model of thalassemia intermedia (Non-Transfusion Dependent Thalassemia or NTDT), reproduces the main features of the disease including anemia, increased erythropoiesis, splenomegaly and iron overload due to low levels of hepcidin. It has been previously demonstrated that modestly increasing hepcidin levels in these mice ameliorates both anemia and iron overload (Gardenghi et al, JCI, 2010). Methods We used minihepcidin M004, a modified peptide analog of the 9 N-terminal amino acids of hepcidin, to reproduce the biological effects of hepcidin. In a dose-ranging study, we treated th3/+ animals with daily intraperitoneal (ip) injections of M004 at doses of 6.25-100 µg/day for 2-6 weeks or with subcutaneous (sc) dosing of 52.5 μg twice a week for 6 weeks. Results In animals treated with the lower ip doses of M004 (6.25-25 μg/day for 2-4 weeks), mild iron restriction was observed (Tf sat ≥15%). Flow cytometry studies using the markers CD44 and Ter119 demonstrated an increase in the proportion of mature erythroid cells. Consistent with the flow cytometry findings, a 30% increase in peripheral red cells (rbc) was observed associated with a reduction in reticulocyte count (>62%) and a reduction in spleen size (>40%), reflecting improved erythropoietic efficiency. At the 12.5 and 25 µg doses, Hb level increased by 1.8-2.5 g/dL. Longer treatment (6 weeks) with 12.5-25 µg/day led to greater iron restriction and the loss of therapeutic effect at 6 weeks. In the same animals, measurement of total organ iron concentrations demonstrated no changes in the liver and kidney, but a 4-fold iron increase in the spleen. Prussian blue staining confirmed increased sequestration of iron in splenic macrophages and Kupffer cells. At high ip doses of M004 (100 μg/day for 2 weeks) the mice developed severe iron restriction (Tf sat = 6%) and exacerbation of anemia (Hb reduction of 4.5 g/dL). Accumulation of immature erythroid precursors was observed by flow cytometry studies, reflecting the erythroid maturation block caused by lack of iron for hemoglobin generation. Subsequent pharmacokinetic studies in rats indicated that plasma levels of M004 increased gradually with sc dosing and were still increasing 24h after dosing, indicating accumulation of drug levels and iron restriction with daily administration. We therefore explored whether less frequent dosing may be preferable to achieve sustained improvement in anemia and normalization of tissue iron. Sc dosing of M004 at 52.5 µg twice weekly was associated with an increase in rbc at 6 weeks to levels observed in WT animals, and an Hb increase of almost 3 g/dL. Reduced spleen weight (-51%) and reticulocyte count (-61%) reflected improved erythropoietic efficiency, further corroborated by flow cytometry studies. Reduction in hemichrome and ROS formation coupled with improvement in rbc morphology and reduced RDW indicated that hematological improvement was likely caused by improved erythroid cell survival as a result of reduced oxidative damage secondary to decreased erythroid iron uptake. Evaluation of total organ iron concentrations showed a reduction of 77% and 54% in the liver and kidney, respectively. Remarkably, the liver iron values were normalized compared to WT animals. Splenic iron increased only ∼1.5 times or 148%. However, when the total weight of the spleen was taken in account, the total splenic iron was reduced (-39%). Conclusion Minihepcidin peptides may be beneficial for the treatment of beta thalassemia intermedia by improving anemia and reducing tissue iron burden. Disclosures: Casu: Merganser: Research Funding. Goldberg:Merganser: Research Funding. Nemeth:Merganser: Equity Ownership. Ganz:Merganser: Equity Ownership. MacDonald:Merganser : Employment, Equity Ownership, Membership on an entity’s Board of Directors or advisory committees. Rivella:Alexion: Consultancy; Biomarin: Consultancy; Merganser: Equity Ownership, Research Funding; Isis: Consultancy, Research Funding; Bayer: Consultancy; Novartis: Consultancy; Imago: Consultancy.

scholarly journals Counting quality? The Czech performance-based research funding system

2015 ◽  
Vol 24 (2) ◽  
pp. 91-105 ◽  
Author(s):  
B. Good ◽  
N. Vermeulen ◽  
B. Tiefenthaler ◽  
E. Arnold
Keyword(s):  
Research Funding ◽  
Funding System

scholarly journals The Flemish Performance-based Research Funding System: A Unique Variant of the Norwegian Model

2018 ◽  
Vol 3 (4) ◽  
pp. 45-60 ◽  
Author(s):  
Tim C. E. Engels ◽  
Raf Guns
Keyword(s):  
Higher Education ◽  
Research Funding ◽  
Web Of Science ◽  
Historical Background ◽  
Funding Allocation ◽  
Current Form ◽  
Funding System ◽  
System A ◽  
Current Design

Abstract The BOF-key is the performance-based research funding system that is used in Flanders, Belgium. In this paper we describe the historical background of the system, its current design and organization, as well as its effects on the Flemish higher education landscape. The BOF-key in its current form relies on three bibliometric parameters: publications in Web of Science, citations in Web of Science, and publications in a comprehensive regional database for SSH publications. Taken together, the BOF-key forms a unique variant of the Norwegian model: while the system to a large extent relies on a commercial database, it avoids the problem of inadequate coverage of the SSH. Because the bibliometric parameters of the BOF-key are reused in other funding allocation schemes, their overall importance to the Flemish universities is substantial.

scholarly journals Hypovitaminosis D Is Prevalent in Patients with Renal AL Amyloidosis and Associated with Non-t(11;14)

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5523-5523
Author(s):  
Eli Muchtar ◽  
Matthew T. Drake ◽  
Angela Dispenzieri ◽  
Martha Q. Lacy ◽  
Francis K. Buadi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Research Funding ◽  
Renal Involvement ◽  
Hypovitaminosis D ◽  
Al Amyloidosis ◽  
Advisory Committees ◽  
Heavy Proteinuria ◽  
Vitamin D Levels ◽  
Low Levels ◽  
Low Serum

Introduction: Vitamin D deficiency is common, with 25-50% of the population having levels below the optimal range (<20 ng/mL). Aside from its role in maintaining serum calcium and skeletal homeostasis, vitamin D has been shown to play an important role in regulation of differentiation, proliferation, apoptosis, metastatic potential and angiogenesis in a variety of malignancies. Low serum 25(OH)D levels have been associated with a worse prognosis in several malignancies, including colorectal and breast cancer, chronic lymphocytic leukemia and non-Hodgkin's lymphoma. Almost no data have been reported on vitamin D levels in light chain (AL) amyloidosis. We therefore measured vitamin D levels among AL patients and correlated levels at presentation to explore if vitamin D deficiency has any effect or association in this disease. Methods: Stored serum samples from 90 patients with newly diagnosed AL amyloidosis were obtained for vitamin D studies, which included 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin D binding protein (DBP). All vitamin D measurements were made by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Total 25(OH)D and 1,25(OH)2D was assessed as the additive sum of the 25(OH)D2/25(OH)D3 and 1,25(OH)2D2/1,25(OH)2D3 components, respectively. Clinical data was extracted from the electronic medical records. All calculations were made using JMP software (SAS, Cary, NC). Results: All patients were seen between June 2004 and September 2013. Median age was 63 [IQR 57-70]. Heart, kidney, nerve, liver and gastrointestinal amyloidosis was seen in 80%, 60%, 19%, 17% and 13% of patients, respectively. The median dFLC and bone marrow plasma cells were 28 (IQR 12-84) mg/dL and 10% (IQR 5-20%), respectively. The median serum 25(OH)D level was 20 ng/mL (IQR 10-29; normal >20 ng/mL), while the median serum level of 1,25(OH)2D was 23 pg/mL (IQR 14-37; normal 16-64 pg/mL for men; 16-78 pg/mL for women). 25(OH)D levels <20 ng/mL were strongly associated with renal involvement (84% renal involvement vs 42% of renal involvement for levels ≥20 ng/dL, P<0.001; Table). No other association with organ involvement was seen. Among all patients, heavy proteinuria (>5 gr/24-h) was strongly associated with low 25(OH)D, (P<0.001, Table). A weaker association was seen between 25(OH)D levels and estimated glomerular filtration rate (eGFR) (P=0.06). Seventy-eight percent of patients with 1,25(OH)2D levels below 20 pg/mL had renal involvement versus 48% in those with levels above 20 pg/mL (P=0.01). While heavy proteinuria was associated with 1,25(OH)2D (P=0.008), the association was stronger for eGFR, as no patient with an eGFR <30 ml/min/1.73 m2 had a 1,25(OH)2D level above 20 pg/mL (P<0.001). An association between vitamin D levels and low serum albumin was also seen, mainly in relation to 25(OH)D (Table). The median level of serum DBP was 58 μg/mL (IQR 36 - 120 μg/mL), significantly lower than the normal range (168-367 μg/mL). Low levels of 25(OH)D or 1,25(OH)2D were not associated with lower DBP levels. Surprisingly, patients with renal involvement had higher levels of DBP versus those without renal involvement (median 70.9 vs 48 μg/mL; P=0.03), although median levels were below normal in both groups. FISH data was available in 47 of patients (52%). Patients with 25(OH)D levels <20 ng/dL were less likely to harbor t(11;14) versus patients with 25(OH)D levels above this threshold (26% vs 64%, respectively; P=0.0095). A similar, but less significant association was seen between 1,25(OH)2D levels at a 20 pg/mL threshold and t(11;14) (35% vs 59%, P=0.09). Other associations between vitamin D and FISH abnormalities were not seen. Conclusions: Hypovitaminosis D is common among AL amyloidosis patients with renal involvement. In the general cohort, heavy proteinuria, reduced eGFR and low serum albumin were all associated with low circulating vitamin D levels. Although the majority of AL patients had low levels of DBP, urinary loss of DBP does not explain the low levels of vitamin D. Hypovitaminosis D is associated with non-t(11;14) disease, a finding which warrants further exploration. Disclosures Dispenzieri: Akcea: Consultancy; Intellia: Consultancy; Janssen: Consultancy; Pfizer: Research Funding; Takeda: Research Funding; Celgene: Research Funding; Alnylam: Research Funding. Lacy:Celgene: Research Funding. Dingli:Rigel: Consultancy; Karyopharm: Research Funding; Millenium: Consultancy; Janssen: Consultancy; alexion: Consultancy. Kapoor:Cellectar: Consultancy; Celgene: Honoraria; Sanofi: Consultancy, Research Funding; Amgen: Research Funding; Takeda: Honoraria, Research Funding; Janssen: Research Funding; Glaxo Smith Kline: Research Funding. Leung:Omeros: Research Funding; Aduro: Membership on an entity's Board of Directors or advisory committees; Prothena: Membership on an entity's Board of Directors or advisory committees; Takeda: Research Funding. Russell:Imanis: Equity Ownership. Kumar:Celgene: Consultancy, Research Funding; Janssen: Consultancy, Research Funding; Takeda: Research Funding. Gertz:Ionis/Akcea: Consultancy; Alnylam: Consultancy; Janssen: Consultancy; Celgene: Consultancy; Annexon: Consultancy; Prothena Biosciences Inc: Consultancy; Spectrum: Consultancy, Research Funding.

scholarly journals The Uptake and Impact of a Label for Peer-Reviewed Books

2022 ◽  
Vol 6 ◽  
Author(s):  
Eline Vandewalle ◽  
Raf Guns ◽  
Tim C. E. Engels
Keyword(s):  
Social Sciences ◽  
Peer Review ◽  
Research Funding ◽  
Quantitative Methods ◽  
Peer Review Process ◽  
Formal System ◽  
Social Sciences And Humanities ◽  
Funding System ◽  
The Social ◽  
Book Publishers

This article presents an analysis of the uptake of the GPRC label (Guaranteed Peer Reviewed Content label) since its introduction in 2010 until 2019. GPRC is a label for books that have been peer reviewed introduced by the Flemish publishers association. The GPRC label allows locally published scholarly books to be included in the regional database for the Social Sciences and Humanities which is used in the Flemish performance-based research funding system. Ten years after the start of the GPRC label, this is the first systematic analysis of the uptake of the label. We use a mix of qualitative and quantitative methods. Our two main data sources are the Flemish regional database for the Social Sciences and Humanities, which currently includes 2,580 GPRC-labeled publications, and three interviews with experts on the GPRC label. Firstly, we study the importance of the label in the Flemish performance-based research funding system. Secondly, we analyse the label in terms of its possible effect on multilingualism and the local or international orientation of publications. Thirdly, we analyse to what extent the label has been used by the different disciplines. Lastly, we discuss the potential implications of the label for the peer review process among book publishers. We find that the GPRC label is of limited importance to the Flemish performance-based research funding system. However, we also conclude that the label has a specific use for locally oriented book publications and in particular for the discipline Law. Furthermore, by requiring publishers to adhere to a formalized peer review procedure, the label affects the peer review practices of local publishers because not all book publishers were using a formal system of peer review before the introduction of the label and even at those publishers who already practiced peer review, the label may have required the publishers to make these procedures more uniform.

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