University research and knowledge transfer: A dynamic view of ambidexterity in british universities

This paper examines the dynamic interlinkages between the two pillars of ambidexterity in universities, research and knowledge transfer. We propose a theoretical model linking these two pillars at the organisational level. The model is tested using the longitudinal HE-BCI survey data juxtaposed against two consecutive rounds of research evaluation in the UK higher education sector. Results indicate that a university's past performance along the research pillar strengthens the knowledge transfer pillar over time, through both commercialisation and academic engagement channels. This positive impact is negatively moderated by the university's size and reputation, in the sense that in larger or more reputed universities, the marginal impact of research on knowledge transfer declines significantly. Additionally, we find that knowledge transfer reinforces the research pillar through positive mediation between past and future research, but only through academic engagement channels. The results also indicate that contract research routes provide the maximum benefit for most universities in enhancing their ambidexterity framework, both in the short and the long run. For the relatively more reputed universities, it is the collaboration route which provides the maximum benefit. Interestingly, no such reinforcement could be detected in the case of the research commercialisation channels

Antitumor activity and safety of the PARP inhibitor rucaparib in patients with high grade ovarian carcinoma and a germline or somatic BRCA1 or BRCA2 mutation: integrated analysis of data from Study 10 and ARIEL2

Objective: An integrated analysis was undertaken to characterize the antitumor activity and safety profile of the oral poly(ADP-ribose) polymerase inhibitor rucaparib in patients with relapsed high-grade ovarian carcinoma (HGOC). Methods: Eligible patients from Study 10 (NCT01482715) and ARIEL2 (NCT01891344) who received a starting dose of oral rucaparib 600 mg twice daily (BID) with or without food were included in these analyses. The integrated efficacy population included patients with HGOC and a deleterious germline or somatic BRCA1 or BRCA2 (BRCA1/2) mutation who received at least two prior chemotherapies and were sensitive, resistant, or refractory to platinum-based chemotherapy. The primary endpoint was investigator-assessed confirmed objective response rate (ORR). Secondary endpoints included duration of response (DOR) and progression-free survival (PFS). The integrated safety population included patients with HGOC who received at least one dose of rucaparib 600 mg BID, irrespective of BRCA1/2 mutation status and prior treatments. Results: In the efficacy population (n = 106), ORR was 53.8% (95% confidence interval [CI], 43.8–63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median DOR was 9.2 months (95% CI, 6.6–11.6). In the safety population (n = 377), the most frequent treatment-emergent adverse events (AEs) were nausea, asthenia/fatigue, vomiting, and anemia/hemoglobin decreased. The most common grade ≥ 3 treatment-emergent AE was anemia/hemoglobin decreased. Treatment-emergent AEs led to treatment interruption, dose reduction, and treatment discontinuation in 58.6%, 45.9%, and 9.8% of patients, respectively. No treatment-related deaths occurred. Conclusions: Rucaparib has antitumor activity in advanced BRCA1/2-mutated HGOC and a manageable safety profile

Dynamic Critical Behavior of the Chayes-Machta Algorithm for the Random-Cluster Model. I. Two Dimensions

We study, via Monte Carlo simulation, the dynamic critical behavior of the Chayes-Machta dynamics for the Fortuin-Kasteleyn random-cluster model, which generalizes the Swendsen-Wang dynamics for the q-state Potts ferromagnet to non-integer q \ge 1. We consider spatial dimension d=2 and 1.25 \le q \le 4 in steps of 0.25, on lattices up to 1024^2, and obtain estimates for the dynamic critical exponent z_{CM}. We present evidence that when 1 \le q \lesssim 1.95 the Ossola-Sokal conjecture z_{CM} \ge \beta/\nu is violated, though we also present plausible fits compatible with this conjecture. We show that the Li-Sokal bound z_{CM} \ge \alpha/\nu is close to being sharp over the entire range 1 \le q \le 4, but is probably non-sharp by a power. As a byproduct of our work, we also obtain evidence concerning the corrections to scaling in static observables.Comment: LaTeX2e, 75 pages including 26 Postscript figure

Dhyani, Veerendra Georgiev, Yordan M. Gangnaik, Anushka S. Biswas, Subhajit Holmes, Justin D. Das, Amit K. Ray, Samit K. Das, Samaresh

Here, we report the observation of negative photoconductance (NPC) effect in highly arsenic-doped germanium nanowires (Ge NWs) for the infrared light. NPC was studied by light-assisted Kelvin probe force microscopy, which shows the depletion of carriers in n-Ge NWs in the presence of infrared light. The trapping of photocarriers leads to high recombination of carriers in the presence of light, which is dominant in the n-type devices. Furthermore, a carrier trapping model was used to investigate the trapping and detrapping phenomena and it was observed that the NPC in n-Ge occurred, because of the fast trapping of mobile charge carriers by interfacial states. The performance of n-type devices was compared with p-type NW detectors, which shows the conventional positive photoconductive behavior with high gain of 104. The observed results can be used to study the application of Ge NWs for various optoelectronic applications involving light tunable memory device applications

Avelumab Alone or in Combination With Chemotherapy Versus Chemotherapy Alone in Platinum-Resistant or Platinum-Refractory Ovarian Cancer (JAVELIN Ovarian 200): An Open-Label, Three-Arm, Randomised, Phase 3 Study

The majority of patients with ovarian cancer will experience relapse and develop platinum-resistant disease after being treated with frontline platinum-based chemotherapy. Treatment options for platinum-resistance or platinum-refractory disease are very limited, usually involving nonplatinum chemotherapy, and they are associated with poor objective response rates and life expectancy

Clinical research in ovarian cancer: consensus recommendations from the Gynecologic Cancer InterGroup

The Gynecologic Cancer InterGroup (GCIG) sixth Ovarian Cancer Conference on Clinical Research was held virtually in October, 2021, following published consensus guidelines. The goal of the consensus meeting was to achieve harmonisation on the design elements of upcoming trials in ovarian cancer, to select important questions for future study, and to identify unmet needs. All 33 GCIG member groups participated in the development, refinement, and adoption of 20 statements within four topic groups on clinical research in ovarian cancer including first line treatment, recurrent disease, disease subgroups, and future trials. Unanimous consensus was obtained for 14 of 20 statements, with greater than 90% concordance in the remaining six statements. The high acceptance rate following active deliberation among the GCIG groups confirmed that a consensus process could be applied in a virtual setting. Together with detailed categorisation of unmet needs, these consensus statements will promote the harmonisation of international clinical research in ovarian cancer

Genomic and epigenomic EBF1 alterations modulate TERT expression in gastric cancer

Transcriptional reactivation of telomerase catalytic subunit (TERT) is a frequent hallmark of cancer, occurring in 90% of human malignancies. However, specific mechanisms driving TERT reactivation remain obscure for many tumor types and in particular gastric cancer (GC), a leading cause of global cancer mortality. Here, through comprehensive genomic and epigenomic analysis of primary GCs and GC cell lines, we identified the transcription factor early B cell factor 1 (EBF1) as a TERT transcriptional repressor and inactivation of EBF1 function as a major cause of TERT upregulation. Abolishment of EBF1 function occurs through 3 distinct (epi)genomic mechanisms. First, EBF1 is epigenetically silenced via DNA methyltransferase, polycomb-repressive complex 2 (PRC2), and histone deacetylase activity in GCs. Second, recurrent, somatic, and heterozygous EBF1 DNA–binding domain mutations result in the production of dominant-negative EBF1 isoforms. Third, more rarely, genomic deletions and rearrangements proximal to the TERT promoter remobilize or abolish EBF1-binding sites, derepressing TERT and leading to high TERT expression. EBF1 is also functionally required for various malignant phenotypes in vitro and in vivo, highlighting its importance for GC development. These results indicate that multimodal genomic and epigenomic alterations underpin TERT reactivation in GC, converging on transcriptional repressors such as EBF1