bluuebunny/crossref_metadata_2025_split huggingface dataset:
A novel neural response algorithm for protein function prediction
Authors: Yalamanchili Hari Krishna , Xiao Quan-Wu , Wang Junwen 
Published: December 2012

Abstract

Background
Large amounts of data are being generated by high-throughput genome sequencing methods. But the rate of the experimental functional characterization falls far behind. To fill the gap between the number of sequences and their annotations, fast and accurate automated annotation methods are required. Many methods, such as GOblet, GOFigure, and Gotcha, are designed based on the BLAST search. Unfortunately, the sequence coverage of these methods is low as they cannot detect the remote homologues. Adding to this, the lack of annotation specificity advocates the need to improve automated protein function prediction.

Results
We designed a novel automated protein functional assignment method based on the neural response algorithm, which simulates the neuronal behavior of the visual cortex in the human brain. Firstly, we predict the most similar target protein for a given query protein and thereby assign its GO term to the query sequence. When assessed on test set, our method ranked the actual leaf GO term among the top 5 probable GO terms with accuracy of 86.93%.

Conclusions
The proposed algorithm is the first instance of neural response algorithm being used in the biological domain. The use of HMM profiles along with the secondary structure information to define the neural response gives our method an edge over other available methods on annotation accuracy. Results of the 5-fold cross validation and the comparison with PFP and FFPred servers indicate the prominent performance by our method. The program, the dataset, and help files are available at http://www.jjwanglab.org/NRProF/.
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle – an update
Authors: Konold Timm , Arnold Mark E , Austin Anthony R , Cawthraw Saira , Hawkins Steve AC , Stack Michael J , Simmons Marion M , Sayers A Robin , Dawson Michael , Wilesmith John W , Wells Gerald AH 
Published: December 2012

Abstract

Background
To provide information on dose–response and aid in modelling the exposure dynamics of the BSE epidemic in the United Kingdom groups of cattle were exposed orally to a range of different doses of brainstem homogenate of known infectious titre from clinical cases of classical bovine spongiform encephalopathy (BSE). Interim data from this study was published in 2007. This communication documents additional BSE cases, which occurred subsequently, examines possible influence of the bovine prion protein gene on disease incidence and revises estimates of effective oral exposure.

Findings
Following interim published results, two further cattle, one dosed with 100 mg and culled at 127 months post exposure and the other dosed with 10 mg and culled at 110 months post exposure, developed BSE. Both had a similar pathological phenotype to previous cases. Based on attack rate and incubation period distribution according to dose, the dose estimate at which 50% of confirmed cases would be clinically affected was revised to 0.15 g of the brain homogenate used in the experiment, with a 95% confidence interval of 0.03–0.79 g. Neither the full open reading frame nor the promoter region of the prion protein gene of dosed cattle appeared to influence susceptibility to BSE, but this may be due to the sample size.

Conclusions
Oral exposure of cattle to a large range of doses of a BSE brainstem homogenate produced disease in all dose groups. The pathological presentation resembled natural disease. The attack rate and incubation period were dependent on the dose.
A unified phylogeny-based nomenclature for histone variants
Authors: Talbert Paul B , Ahmad Kami , Almouzni Geneviève , Ausió Juan , Berger Frederic , Bhalla Prem L , Bonner William M , Cande W Zacheus , Chadwick Brian P , Chan Simon W L , Cross George A M , Cui Liwang , Dimitrov Stefan I , Doenecke Detlef , Eirin-López José M , Gorovsky Martin A , Hake Sandra B , Hamkalo Barbara A , Holec Sarah , Jacobsen Steven E , Kamieniarz Kinga , Khochbin Saadi , Ladurner Andreas G , Landsman David , Latham John A , Loppin Benjamin , Malik Harmit S , Marzluff William F , Pehrson John R , Postberg Jan , Schneider Robert , Singh Mohan B , Smith M Mitchell , Thompson Eric , Torres-Padilla Maria-Elena , Tremethick David John , Turner Bryan M , Waterborg Jakob Harm , Wollmann Heike , Yelagandula Ramesh , Zhu Bing , Henikoff Steven 
Published: December 2012

Abstract
Histone variants are non-allelic protein isoforms that play key roles in diversifying chromatin structure. The known number of such variants has greatly increased in recent years, but the lack of naming conventions for them has led to a variety of naming styles, multiple synonyms and misleading homographs that obscure variant relationships and complicate database searches. We propose here a unified nomenclature for variants of all five classes of histones that uses consistent but flexible naming conventions to produce names that are informative and readily searchable. The nomenclature builds on historical usage and incorporates phylogenetic relationships, which are strong predictors of structure and function. A key feature is the consistent use of punctuation to represent phylogenetic divergence, making explicit the relationships among variant subtypes that have previously been implicit or unclear. We recommend that by default new histone variants be named with organism-specific paralog-number suffixes that lack phylogenetic implication, while letter suffixes be reserved for structurally distinct clades of variants. For clarity and searchability, we encourage the use of descriptors that are separate from the phylogeny-based variant name to indicate developmental and other properties of variants that may be independent of structure.
MicroRNA-203 suppresses cell proliferation and migration by targeting BIRC5 and LASP1 in human triple-negative breast cancer cells
Authors: Wang Chen , Zheng Xiangqian , Shen Chunyan , Shi Yurong 
Published: December 2012

Abstract

Background
This study was performed to investigate the effect of microRNA-203 (miR-203) on cell proliferation and migration in triple-negative breast cancer (TNBC).

Methods
Real-time PCR was performed to detect the expression of miR-203 in TNBC cell lines. miR-203 precursor and control microRNA (miRNA) were transfected into triple-negative breast cancer (TNBC) cell lines and the effects of miR-203 up-regulation on the proliferation and migration of cells were investigated. Meanwhile, the mRNA and protein levels of baculoviral IAP repeat-containing protein 5 (BIRC5) and Lim and SH3 domain protein 1 (LASP1) were measured. Luciferase assays were also performed to validate BIRC5 and LASP1 as miR-203 targets.

Results
Both miR-203 and BIRC5 siRNA signicantly inhibited cell proliferation in TNBC cells. Both miR-203 and LASP1 siRNA signicantly inhibited cell migration in TNBC cells, also. Moreover, up-regulated of BIRC5 and LASP1 was able to abrogate the effects induced by transfection with the miR-203 precursor.

Conclusions
These data suggest that miR-203 may function as a tumor suppressor in TNBC cells. Thus, miR-203 could be a potential therapeutic target for this disease.
Intravascular CNS lymphoma: Successful therapy using high-dose methotrexate-based polychemotherapy
Authors: Kebir Sied , Kuchelmeister Klaus , Niehusmann Pitt , Nelles Michael , Kim Young , Thanendrarajan Sharmilan , Schäfer Niklas , Stuplich Moritz , Mack Frederic , Scheffler Björn , Urbach Horst , Glas Martin , Herrlinger Ulrich 
Published: December 2012

Abstract
Intravascular diffuse large B-cell lymphoma limited to the CNS (cIVL) is a very rare malignant disorder characterized by a selective accumulation of neoplastic lymphocytes (usually B cells) within the lumen of CNS blood vessels but not in the brain parenchyma. In the past, treatment of cIVL with anthracycline-based regimens was unsatisfactory with very short survival times. In the case of cIVL presented here, high-dose methotrexate-based polychemotherapy according to the Bonn protocol plus rituximab therapy was successful and led to a complete clinical and MRI remission which is ongoing 29 months after diagnosis.
An interval mixed-integer non-linear programming model to support regional electric power systems planning with CO2 capture and storage under uncertainty
Authors: Wang XQ , Huang GH , Lin QG 
Published: December 2012

Abstract

Background
Electric generating capacity expansion has been always an essential way to handle the electricity shortage, meanwhile, greenhouse-gas (GHG) emission, especially CO2, from electric power systems becomes crucial considerations in recent years for the related planners. Therefore, effective approach to dealing with the tradeoff between capacity expansion and carbon emission reduction is much desired.

Results
In this study, an interval mixed-integer non-linear programming (IMINLP) model was developed to assist regional electric power systems planning under uncertainty. CO2 capture and storage (CCS) technologies had been introduced to the IMINLP model to help reduce carbon emission. The developed IMINLP model could be disassembled into a number of ILP models, then two-step method (TSM) was used to obtain the optimal solutions. A case study was provided for demonstrating applicability of the developed method.

Conclusions
The results indicated that the developed model was capable of providing alternative decisions based on scenario analysis for electricity planning with consideration of CCS technologies. The IMINLP model could provide an effective linkage between carbon sequestration and electric generating capacity expansion with the aim of minimizing system costs.
Parasite manipulation of host personality and behavioural syndromes
Authors: Poulin Robert 
Published: December 2012

SummaryThe past decades have seen mounting evidence that parasites alter their host’s behaviour in ways that benefit transmission, based on differences in the expression of behavioural traits between infected and control individuals, or on significant correlations between trait expression and infection levels. The multidimensional nature of host manipulation has only recently been recognised: parasites do not target single host traits, but instead suites of interrelated traits. Here, I use recent research on animal personality (behavioural differences among individuals consistent across time and situations) and behavioural syndromes (correlations at the population level among distinct behavioural traits, or between the same trait expressed in different contexts) to provide a framework from which simple testable patterns of host behavioural changes can be predicted. Following infection, a manipulative parasite could (i) change the temporal consistency of its host’s behavioural responses, (ii) change the slope of a host reaction norm, i.e. the way host behavioural traits are expressed as a function of an environmental gradient, or (iii) decouple two or more host behavioural traits and/or change the way in which they correlate with each other. Two case studies involving trematode parasites and their freshwater hosts are used to provide empirical illustrations of the above scenarios. These clearly illustrate the full richness of behavioural alterations induced by parasites, and how these effects would go unnoticed using the classical trait-by-trait comparisons of mean values between parasitised and non-parasitised individuals. However, the power of animal personality and behavioural syndromes to inform research on host manipulation by parasites will only be fully realised when underlying mechanisms are elucidated and linked to their phenotypic impacts.
Immune–neural connections: how the immune system’s response to infectious agents influences behavior
Authors: McCusker Robert H. , Kelley Keith W. 
Published: December 2012

Summary
Humans and animals use the classical five senses of sight, sound, touch, smell and taste to monitor their environment. The very survival of feral animals depends on these sensory perception systems, which is a central theme in scholarly research on comparative aspects of anatomy and physiology. But how do all of us sense and respond to an infection? We cannot see, hear, feel, smell or taste bacterial and viral pathogens, but humans and animals alike are fully aware of symptoms of sickness that are caused by these microbes. Pain, fatigue, altered sleep pattern, anorexia and fever are common symptoms in both sick animals and humans. Many of these physiological changes represent adaptive responses that are considered to promote animal survival, and this constellation of events results in sickness behavior. Infectious agents display a variety of pathogen-associated molecular patterns (PAMPs) that are recognized by pattern recognition receptors (PRRs). These PRR are expressed on both the surface [e.g. Toll-like receptor (TLR)-4] and in the cytoplasm [e.g. nucleotide-binding oligomerization domain (Nod)-like receptors] of cells of the innate immune system, primarily macrophages and dendritic cells. These cells initiate and propagate an inflammatory response by stimulating the synthesis and release of a variety of cytokines. Once an infection has occurred in the periphery, both cytokines and bacterial toxins deliver this information to the brain using both humoral and neuronal routes of communication. For example, binding of PRR can lead to activation of the afferent vagus nerve, which communicates neuronal signals via the lower brain stem (nucleus tractus solitarius) to higher brain centers such as the hypothalamus and amygdala. Blood-borne cytokines initiate a cytokine response from vascular endothelial cells that form the blood–brain barrier (BBB). Cytokines can also reach the brain directly by leakage through the BBB via circumventricular organs or by being synthesized within the brain, thus forming a mirror image of the cytokine milieu in the periphery. Although all cells within the brain are capable of initiating cytokine secretion, microglia have an early response to incoming neuronal and humoral stimuli. Inhibition of proinflammatory cytokines that are induced following bacterial infection blocks the appearance of sickness behaviors. Collectively, these data are consistent with the notion that the immune system communicates with the brain to regulate behavior in a way that is consistent with animal survival.
Parasites: evolution’s neurobiologists
Authors: Adamo Shelley Anne 
Published: December 2012

SummaryFor millions of years, parasites have altered the behaviour of their hosts. Parasites can affect host behaviour by: (1) interfering with the host’s normal immune–neural communication, (2) secreting substances that directly alter neuronal activity via non-genomic mechanisms and (3) inducing genomic- and/or proteomic-based changes in the brain of the host. Changes in host behaviour are often restricted to particular behaviours, with many other behaviours remaining unaffected. Neuroscientists can produce this degree of selectivity by targeting specific brain areas. Parasites, however, do not selectively attack discrete brain areas. Parasites typically induce a variety of effects in several parts of the brain. Parasitic manipulation of host behaviour evolved within the context of the manipulation of other host physiological systems (especially the immune system) that was required for a parasite’s survival. This starting point, coupled with the fortuitous nature of evolutionary innovation and evolutionary pressures to minimize the costs of parasitic manipulation, likely contributed to the complex and indirect nature of the mechanisms involved in host behavioural control. Because parasites and neuroscientists use different tactics to control behaviour, studying the methods used by parasites can provide novel insights into how nervous systems generate and regulate behaviour. Studying how parasites influence host behaviour will also help us integrate genomic, proteomic and neurophysiological perspectives on behaviour.
Comparing mechanisms of host manipulation across host and parasite taxa
Authors: Lafferty Kevin D. , Shaw Jenny C. 
Published: December 2012

SummaryParasites affect host behavior in several ways. They can alter activity, microhabitats or both. For trophically transmitted parasites (the focus of our study), decreased activity might impair the ability of hosts to respond to final-host predators, and increased activity and altered microhabitat choice might increase contact rates between hosts and final-host predators. In an analysis of trophically transmitted parasites, more parasite groups altered activity than altered microhabitat choice. Parasites that infected vertebrates were more likely to impair the host’s reaction to predators, whereas parasites that infected invertebrates were more likely to increase the host’s contact with predators. The site of infection might affect how parasites manipulate their hosts. For instance, parasites in the central nervous system seem particularly suited to manipulating host behavior. Manipulative parasites commonly occupy the body cavity, muscles and central nervous systems of their hosts. Acanthocephalans in the data set differed from other taxa in that they occurred exclusively in the body cavity of invertebrates. In addition, they were more likely to alter microhabitat choice than activity. Parasites in the body cavity (across parasite types) were more likely to be associated with increased host contact with predators. Parasites can manipulate the host through energetic drain, but most parasites use more sophisticated means. For instance, parasites target four physiological systems that shape behavior in both invertebrates and vertebrates: neural, endocrine, neuromodulatory and immunomodulatory. The interconnections between these systems make it difficult to isolate specific mechanisms of host behavioral manipulation.
Host–parasite molecular cross-talk during the manipulative process of a host by its parasite
Authors: Biron David G. , Loxdale Hugh D. 
Published: December 2012

SummaryMany parasite taxa are able to alter a wide range of phenotypic traits of their hosts in ways that seem to improve the parasite’s chance of completing its life cycle. Host behavioural alterations are classically seen as compelling illustrations of the ‘extended phenotype’ concept, which suggests that parasite genes have phenotype effects on the host. The molecular mechanisms and the host–parasite cross-talk involved during the manipulative process of a host by its parasite are still poorly understood. In this Review, the current knowledge on proximate mechanisms related to the ‘parasite manipulation hypothesis’ is presented. Parasite genome sequences do not themselves provide a full explanation of parasite biology nor of the molecular cross-talk involved in host–parasite associations. Recently, first-generation proteomics tools have been employed to unravel some aspects of the parasite manipulation process (i.e. proximate mechanisms and evolutionary convergence) using certain model arthropod-host–parasite associations. The pioneer proteomics results obtained on the manipulative process are here highlighted, along with the many gaps in our knowledge. Candidate genes and biochemical pathways potentially involved in the parasite manipulation are presented. Finally, taking into account the environmental factors, we suggest new avenues and approaches to further explore and understand the proximate mechanisms used by parasite species to alter phenotypic traits of their hosts.
The significance of cerebral toxocariasis: a model system for exploring the link between brain involvement, behaviour and the immune response
Authors: Holland Celia V. , Hamilton Clare M. 
Published: December 2012

SummaryToxocara canis is a parasitic nematode that infects canines worldwide, and as a consequence of the widespread environmental dissemination of its ova in host faeces, other abnormal hosts including mice and humans are exposed to infection. In such abnormal or paratenic hosts, the immature third-stage larvae undergo a somatic migration through the organs of the body but fail to reach maturity as adult worms in the intestine. The presence of the migrating larvae contributes to pathology that is dependent upon the intensity of infection and the location of the larvae. A phenomenon of potential public health significance in humans and of ecological significance in mice is that T. canis larvae exhibit neurotrophic behaviour, which results in a greater concentration of parasites in the brain, as infection progresses. Toxocara larval burdens vary between individual outbred mice receiving the same inocula, suggesting a role for immunity in the establishment of cerebral infection. Although the systemic immune response to T. canis has been widely reported, the immune response in the brain has received little attention. Differential cytokine expression and other brain injury-associated biomarkers have been observed in infected versus uninfected outbred and inbred mice. Preliminary data have also suggested a possible link between significant memory impairment and cytokine production associated with T. canis infection. Mice provide a useful, replicable animal model with significant applicability and ease of manipulation. Understanding the cerebral host–parasite relationship may shed some light on the cryptic symptoms of human infection where patients often present with other CNS disorders such as epilepsy and mental retardation.
CD200 Expression in Plasma Cells of Nonmyeloma Immunoproliferative Disorders
Authors: Olteanu Horatiu , Harrington Alexandra M. , Kroft Steven H. 
Published: December 2012

AbstractThe majority of plasma cell myelomas (PCMs) are positive for CD200, a membrane protein with immunosuppressive function. There are no flow cytometry data in the literature on plasma cell CD200 expression in other immunoproliferative disorders. Therefore we used flow cytometry to study the expression of CD200 on plasma cells in diagnostic bone marrow aspirates from 61 patients with monoclonal gammopathy of undetermined significance (MGUS) and 10 patients with lymphoplasmacytic lymphoma (LPL). For comparison, we evaluated CD200 expression in 74 PCM bone marrow biopsies. Thirty-three (54.1%) of 61 MGUS cases and 2 (20.0%) of 10 LPL cases were CD200+. Comparative clinicopathologic parameters for MGUS cases, based on CD200 expression status, showed no differences between the 2 groups. The proportion of CD200+ PCMs (73.0%) in our series was significantly higher than that of CD200+ MGUS (P = .030) and CD200+ LPL (P = .002) cases.
Comparison of Monoclonal Napsin A, Polyclonal Napsin A, and TTF-1 for Determining Lung Origin in Metastatic Adenocarcinomas
Authors: Mukhopadhyay Sanjay , Katzenstein Anna-Luise A. 
Published: December 2012

Abstract
Thyroid transcription factor 1 (TTF-1) is currently the best immunohistochemical marker for carcinomas of lung origin. Our aim was to compare napsin A to TTF-1 for identifying pulmonary origin in metastatic adenocarcinoma and its mimics. One hundred fifty-five metastatic carcinomas (55 pulmonary, 100 nonpulmonary) were stained with monoclonal napsin A and TTF-1, and most also with polyclonal napsin A. The sensitivity of monoclonal napsin A, polyclonal napsin A, and TTF-1 for metastatic adenocarcinomas of pulmonary origin was 76%, 81%, and 82%, respectively. Two lung carcinomas were diffusely positive for monoclonal napsin A, but negative or equivocal for TTF-1. TTF-1 stained 9 of 100 nonpulmonary carcinomas (all thyroid), monoclonal napsin A stained 12 of 100 (4 sites), and polyclonal napsin A stained 27 of 91 (8 sites). Napsin A is expressed in a wider variety of metastatic nonpulmonary carcinomas than TTF-1, and the monoclonal antibody is more specific. Napsin A is a useful adjunct to TTF-1, because occasional lung adenocarcinomas are TTF-1 negative but napsin A positive.