Inevitable Evolutionary Temporal Elements in Neural Processing: A Study Based on Evolutionary Simulations

Recent studies have suggested that some neural computational mechanisms are based on the fine temporal structure of spiking activity. However, less effort has been devoted to investigating the evolutionary aspects of such mechanisms. In this paper we explore the issue of temporal neural computation from an evolutionary point of view, using a genetic simulation of the evolutionary development of neural systems. We evolve neural systems in an environment with selective pressure based on mate finding, and examine the temporal aspects of the evolved systems. In repeating evolutionary sessions, there was a significant increase during evolution in the mutual information between the evolved agent's temporal neural representation and the external environment. In ten different simulated evolutionary sessions, there was an increased effect of time -related neural ablations on the agents' fitness. These results suggest that in some fitness landscapes the emergence of temporal elements in neural computation is almost inevitable. Future research using similar evolutionary simulations may shed new light on various biological mechanisms

Evolving Synaptic Plasticity with an Evolutionary Cellular Development Model

Since synaptic plasticity is regarded as a potential mechanism for memory formation and learning, there is growing interest in the study of its underlying mechanisms. Recently several evolutionary models of cellular development have been presented, but none have been shown to be able to evolve a range of biological synaptic plasticity regimes. In this paper we present a biologically plausible evolutionary cellular development model and test its ability to evolve different biological synaptic plasticity regimes. The core of the model is a genomic and proteomic regulation network which controls cells and their neurites in a 2D environment. The model has previously been shown to successfully evolve behaving organisms, enable gene related phenomena, and produce biological neural mechanisms such as temporal representations. Several experiments are described in which the model evolves different synaptic plasticity regimes using a direct fitness function. Other experiments examine the ability of the model to evolve simple plasticity regimes in a task -based fitness function environment. These results suggest that such evolutionary cellular development models have the potential to be used as a research tool for investigating the evolutionary aspects of synaptic plasticity and at the same time can serve as the basis for novel artificial computational systems

Wafer-Scale, Sub-5 nm Junction Formation by Monolayer Doping and Conventional Spike Annealing

We report the formation of sub-5 nm ultrashallow junctions in 4 inch Si wafers enabled by the molecular monolayer doping of phosphorous and boron atoms and the use of conventional spike annealing. The junctions are characterized by secondary ion mass spectrometry and non-contact sheet resistance measurements. It is found that the majority (~70%) of the incorporated dopants are electrically active, therefore, enabling a low sheet resistance for a given dopant areal dose. The wafer-scale uniformity is investigated and found to be limited by the temperature homogeneity of the spike anneal tool used in the experiments. Notably, minimal junction leakage currents (<1 uA/cm2) are observed which highlights the quality of the junctions formed by this process. The results clearly demonstrate the versatility and potency of the monolayer doping approach for enabling controlled, molecular-scale ultrashallow junction formation without introducing defects in the semiconductor.Comment: 21 pages, 5 figure

Magnetic Resonance Enterography Cannot Replace Upper Endoscopy in Pediatric Crohn Disease: An Imagekids Sub-study

Objectives: Although magnetic resonance enterography (MRE) can accurately reflect ileal inflammation in pediatric Crohn disease (CD), there are no pediatric data on the accuracy of MRE to detect upper gastrointestinal tract (UGI) lesions. We aimed to compare MRE and esophagogastroduodenoscopy (EGD) in detecting the spectrum and severity of UGI disease in children. Methods: This is an ancillary study of the prospective multi-center ImageKids study focusing on pediatric MRE. EGD was performed within 2 weeks of MRE (at disease onset or thereafter) and explicitly scored by SES-CD modified for the UGI and physician global assessment. Local and central radiologists scored the UGI region of the MRE blinded to the EGD. Accuracy of MRE compared with EGD was examined using correlational coefficients (r) and area under receiver operating characteristic curves (AUC). Results: One hundred and eighty-eight patients were reviewed (mean age 14 +/- 1 years, 103 [55%] boys);66 of 188 (35%) children had macroscopic ulcerations on EGD (esophagus, 13 [7%];stomach, 34 [18%];duodenum, 45 [24%]). Most children had aphthous ulcers, but 10 (5%) had larger ulcers (stomach, 2 [1%];duodenum, 8 [4%]). There was no agreement between local and central radiologists on the presence or absence of UGI inflammation on MRE (Kappa=0.02, P - 0.71). EGD findings were not accurately detected by MRE, read locally or centrally (r=-0.03 to 0.11, P = 0.18-0.88;AUC - 0.47-0.55, P = 0.53-1.00).No fistulae or narrowings were identified on either EGD or MRE. Conclusions: MRE cannot reliably assess the UGI in pediatric CD and cannot replace EGD for this purpose

Engineering the Controlled Assembly of Filamentous Injectisomes in E. coli K-12 for Protein Translocation into Mammalian Cells.

Bacterial pathogens containing type III protein secretion systems (T3SS) assemble large needle-like protein complexes in the bacterial envelope, called injectisomes, for translocation of protein effectors into host cells. The application of these molecular syringes for the injection of proteins into mammalian cells is hindered by their structural and genomic complexity, requiring multiple polypeptides encoded along with effectors in various transcriptional units (TUs) with intricate regulation. In this work, we have rationally designed the controlled expression of the filamentous injectisomes found in enteropathogenic Escherichia coli (EPEC) in the nonpathogenic strain E. coli K-12. All structural components of EPEC injectisomes, encoded in a genomic island called the locus of enterocyte effacement (LEE), were engineered in five TUs (eLEEs) excluding effectors, promoters and transcriptional regulators. These eLEEs were placed under the control of the IPTG-inducible promoter Ptac and integrated into specific chromosomal sites of E. coli K-12 using a marker-less strategy. The resulting strain, named synthetic injector E. coli (SIEC), assembles filamentous injectisomes similar to those in EPEC. SIEC injectisomes form pores in the host plasma membrane and are able to translocate T3-substrate proteins (e.g., translocated intimin receptor, Tir) into the cytoplasm of HeLa cells reproducing the phenotypes of intimate attachment and polymerization of actin-pedestals elicited by EPEC bacteria. Hence, SIEC strain allows the controlled expression of functional filamentous injectisomes for efficient translocation of proteins with T3S-signals into mammalian cells

Lactate concentration in breast cancer using advanced magnetic resonance spectroscopy

Acknowledgements We would like to thank Dr. Nicholas Senn for conducting data auditing, Dr. Matthew Clemence (Philips Healthcare Clinical Science, UK) for clinical scientist support, Dr. Tim Smith for biologist support, Mr. Gordon Buchan for technician support, Ms Bolanle Brikinns for patient recruitment support, Ms Dawn Younie for logistic support, Prof. Andrew M. Blamire for advice on MRS. We would also like to thank Mr Roger Bourne and Ms Mairi Fuller for providing access to the patients. Data availability Data supporting this publication are stored at Institute of Medical Sciences and available upon request. Funding information This project was funded by Friends of Aberdeen and North Centre for Haematology, Oncology and Radiotherapy (ANCHOR) (RS2015 004). Sai Man Cheung’s PhD study was jointly supported by Elphinstone scholarship, Roland Sutton Academic Trust and John Mallard scholarship.Peer reviewedPublisher PD