44 research outputs found
How citation boosts promote scientific paradigm shifts and Nobel Prizes
Nobel Prizes are commonly seen to be among the most prestigious achievements
of our times. Based on mining several million citations, we quantitatively
analyze the processes driving paradigm shifts in science. We find that
groundbreaking discoveries of Nobel Prize Laureates and other famous scientists
are not only acknowledged by many citations of their landmark papers.
Surprisingly, they also boost the citation rates of their previous
publications. Given that innovations must outcompete the rich-gets-richer
effect for scientific citations, it turns out that they can make their way only
through citation cascades. A quantitative analysis reveals how and why they
happen. Science appears to behave like a self-organized critical system, in
which citation cascades of all sizes occur, from continuous scientific progress
all the way up to scientific revolutions, which change the way we see our
world. Measuring the "boosting effect" of landmark papers, our analysis reveals
how new ideas and new players can make their way and finally triumph in a world
dominated by established paradigms. The underlying "boost factor" is also
useful to discover scientific breakthroughs and talents much earlier than
through classical citation analysis, which by now has become a widespread
method to measure scientific excellence, influencing scientific careers and the
distribution of research funds. Our findings reveal patterns of collective
social behavior, which are also interesting from an attention economics
perspective. Understanding the origin of scientific authority may therefore
ultimately help to explain, how social influence comes about and why the value
of goods depends so strongly on the attention they attract.Comment: 6 pages, 6 figure
Autologous microsurgical breast reconstruction and coronary artery bypass grafting: an anatomical study and clinical implications
OBJECTIVE: To identify possible avenues of sparing the internal mammary artery (IMA) for coronary artery bypass grafting (CABG) in women undergoing autologous breast reconstruction with deep inferior epigastric artery perforator (DIEP) flaps. BACKGROUND: Optimal autologous reconstruction of the breast and coronary artery bypass grafting (CABG) are often mutually exclusive as they both require utilisation of the IMA as the preferred arterial conduit. Given the prevalence of both breast cancer and coronary artery disease, this is an important issue for women's health as women with DIEP flap reconstructions and women at increased risk of developing coronary artery disease are potentially restricted from receiving this reconstructive option should the other condition arise. METHODS: The largest clinical and cadaveric anatomical study (n=315) to date was performed, investigating four solutions to this predicament by correlating the precise requirements of breast reconstruction and CABG against the anatomical features of the in situ IMAs. This information was supplemented by a thorough literature review. RESULTS: Minimum lengths of the left and right IMA needed for grafting to the left-anterior descending artery are 160.08 and 177.80 mm, respectively. Based on anatomical findings, the suitable options for anastomosis to each intercostals space are offered. In addition, 87-91% of patients have IMA perforator vessels to which DIEP flaps can be anastomosed in the first- and second-intercostal spaces. CONCLUSION: We outline five methods of preserving the IMA for future CABG: (1) lowering the level of DIEP flaps to the fourth- and fifth-intercostals spaces, (2) using the DIEP pedicle as an intermediary for CABG, (3) using IMA perforators to spare the IMA proper, (4) using and end-to-side anastomosis between the DIEP pedicle and IMA and (5) anastomosis of DIEP flaps using retrograde flow from the distal IMA. With careful patient selection, we hypothesize using the IMA for autologous breast reconstruction need not be an absolute contraindication for future CABG
Lessons from non-canonical splicing
Recent improvements in experimental and computational techniques that are used to study the transcriptome have enabled an unprecedented view of RNA processing, revealing many previously unknown non-canonical splicing events. This includes cryptic events located far from the currently annotated exons and unconventional splicing mechanisms that have important roles in regulating gene expression. These non-canonical splicing events are a major source of newly emerging transcripts during evolution, especially when they involve sequences derived from transposable elements. They are therefore under precise regulation and quality control, which minimizes their potential to disrupt gene expression. We explain how non-canonical splicing can lead to aberrant transcripts that cause many diseases, and also how it can be exploited for new therapeutic strategies
Molecular cloning of multiple splicing variants of JIP-1 preferentially expressed in brain
Stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) is activated by a variety of cellular or environmental stresses. Proper regulation of the SAPK/JNK pathway may be critical for cell survival or death under various conditions. In this study, we report the molecular cloning of novel isoforms of JIP-1, which harbor a putative phosphotyrosine interaction domain and a helix-loop-helix domain, as well as an SH3 homologous region in the C terminus. Northern analysis indicates that transcription variant jip-1 is expressed in brain and kidney and transcription variants jip-2 and jip-3 are specifically expressed in brain. In situ hybridization data showed that the hybridized jip messages were heavily concentrated in adult brain, and were particularly enriched in the cerebral cortex and hippocampus, the brain regions vulnerable to pathological states such as hypoxia-ischemia, epilepsy, and Alzheimer's disease. All the deduced protein products of the jip transcription variants appear to have a similar property in that they inhibit the SAPK/JNK stimulation when overexpressed. Inhibition of SAPK activation by overexpression of the novel isoform JIP-2a resulted in suppression of etoposide-induced cell death in a neuroglioma cell line, N18TG. These findings suggest that JIP may play an important role in regulation of the SAPK pathway that is involved in stress-induced cellular responses.X1145sciescopu
An Analytical Research on Determination of Beam and Column Contribution to Plastic Energy Dissipation of RC Frames
Determination of capacities of structural members, both in terms of strength and deformation, and estimation of seismic demand are essential issues in earthquake-resistant design. In energy-based design and evaluation, both the structural capacity and the demand imposed by earthquake are considered in terms of energy and accordingly energy dissipation capacity of the structure is associated with seismic energy demand. Plastic energy dissipation of structures under monotonic lateral loading may be obtained by using the resultant pushover curves of nonlinear static analyses. However, the time variation of individual contribution of structural members to the dissipated plastic energy cannot be determined. In this study, the contribution of beam and column deformations to the plastic energy dissipated in multistory reinforced concrete (RC) frames is determined by using nonlinear time history (NLTH) analysis. It is found that rotational deformations of beams are dominant in plastic energy dissipation. Accordingly, some linear relations considering the contribution of dissipated plastic energy in beam plastic hinges to the total plastic energy dissipation of RC frames are derived. Pushover analysis of frames in conducted and the area under the resultant pushover curve is determined to satisfy the mean value of the maximum plastic energy dissipated in frames during the selected earthquakes. The interstory drift ratios are calculated and compared with the interstory drift ratios directly obtained from NLTH analyses. The results are evaluated and presented by graphs and tables