bluuebunny/crossref_metadata_2025_split huggingface dataset:
Marxism and Kazantzakis
Authors: Georgopoulos N. 
Published: June 2013

I fight to embrace the entire circle of human activity to the full extent of my ability, to divine which wind is urging all these waves of mankind upward. I bend over the age in which I live, that tiny, imperceptible arc of the vast circle, and struggle to attain a clear view of today’s duty. Perhaps this is the only way man can carry out something immortal within the ephemeral moment of his life: immortal because he collaborates with an immortal rhythm.Report to GrecoThe name of Nikos Kazantzakis continues to arouse controversy. Much of it, especially in Greece, is political in nature and revolves around the confusion concerning Kazantzakis’ relation to Marxism. The confusion arises because of the ways Kazantzakis’ activities and writings have been interpreted. For example, even before the latest military regime in Greece and while he was still alive, Kazantzakis was anathema to the royalists. Consecutive right wing governments, both before and after World War II, waged war against him and his books; he was called immoral, red, and a Bolshevik troublemaker. In the fall of 1924, in his native Crete, he was actually arrested. In the spring of 1928, in Athens, he was accused of being a Russian agent. Yet his books were banned in Russia—particularly those he wrote about that country—and the Greek Communist party refused to include him in its ranks, labelling him bourgeois, decadent and even fascist. In fact, his offer to join the communist controlled resistance in the 1940s was rejected. Such responses neidier prevented the International Peace Committee from offering him the Peace Award in Vienna in 1956 nor did it bar the Chinese communists from inviting him to the Peoples’ Republic of China as one of their ‘chosen Foreigners’ and, upon the occasion of his death in 1957, from praising him: ‘Kazantzakis was not only a great writer. He was actively interested in social and political issues. He was also a devotee of peace’. More recently, views about him have ranged from those in which he is considered an egomaniac, oblivious to the fate of others, a man whom ‘the really important things—political tyranny, social injustice, economic exploitation—interested … the least’, to those in which he is seen as an advocate of equality, peace and the cooperation of the world’s people, one who to the end of his career sided with the ‘ideas of genuine Democracy and Socialism’.
Novel mechanisms for activated protein C cytoprotective activities involving noncanonical activation of protease-activated receptor 3
Authors: Burnier Laurent , Mosnier Laurent O. 
Published: June 2013

Key PointsAPC activates PAR3 in the presence of EPCR by noncanonical cleavage at Arg41. APC-derived PAR3 tethered-ligand peptides induced APC-like vascular barrier protective effects in vitro and in vivo.
Platelet protein disulfide isomerase is required for thrombus formation but not for hemostasis in mice
Authors: Kim Kyungho , Hahm Eunsil , Li Jing , Holbrook Lisa-Marie , Sasikumar Parvathy , Stanley Ronald G. , Ushio-Fukai Masuko , Gibbins Jonathan M. , Cho Jaehyung 
Published: June 2013

Key PointsPlatelet PDI regulates αIIbβ3 integrin activation without affecting platelet activation and inside-out integrin signaling. Platelet PDI is essential for platelet accumulation but not for fibrin generation and hemostasis in mice.
MetaPathways: a modular pipeline for constructing pathway/genome databases from environmental sequence information
Authors: Konwar Kishori M , Hanson Niels W , Pagé Antoine P , Hallam Steven J 
Published: June 2013

Abstract

Background
A central challenge to understanding the ecological and biogeochemical roles of microorganisms in natural and human engineered ecosystems is the reconstruction of metabolic interaction networks from environmental sequence information. The dominant paradigm in metabolic reconstruction is to assign functional annotations using BLAST. Functional annotations are then projected onto symbolic representations of metabolism in the form of KEGG pathways or SEED subsystems.

Results
Here we present MetaPathways, an open source pipeline for pathway inference that uses the PathoLogic algorithm to map functional annotations onto the MetaCyc collection of reactions and pathways, and construct environmental Pathway/Genome Databases (ePGDBs) compatible with the editing and navigation features of Pathway Tools. The pipeline accepts assembled or unassembled nucleotide sequences, performs quality assessment and control, predicts and annotates noncoding genes and open reading frames, and produces inputs to PathoLogic. In addition to constructing ePGDBs, MetaPathways uses MLTreeMap to build phylogenetic trees for selected taxonomic anchor and functional gene markers, converts General Feature Format (GFF) files into concatenated GenBank files for ePGDB construction based on third-party annotations, and generates useful file formats including Sequin files for direct GenBank submission and gene feature tables summarizing annotations, MLTreeMap trees, and ePGDB pathway coverage summaries for statistical comparisons.

Conclusions
MetaPathways provides users with a modular annotation and analysis pipeline for predicting metabolic interaction networks from environmental sequence information using an alternative to KEGG pathways and SEED subsystems mapping. It is extensible to genomic and transcriptomic datasets from a wide range of sequencing platforms, and generates useful data products for microbial community structure and function analysis. The MetaPathways software package, installation instructions, and example data can be obtained from http://hallam.microbiology.ubc.ca/MetaPathways.
Proposal of a quantitative PCR-based protocol for an optimal Pseudomonas aeruginosa detection in patients with cystic fibrosis
Authors: Le Gall Florence , Le Berre Rozenn , Rosec Sylvain , Hardy Jeanne , Gouriou Stéphanie , Boisramé-Gastrin Sylvie , Vallet Sophie , Rault Gilles , Payan Christopher , Héry-Arnaud Geneviève 
Published: June 2013

Abstract

Background
The lung of patients with cystic fibrosis (CF) is particularly sensitive to Pseudomonas aeruginosa. This bacterium plays an important role in the poor outcome of CF patients. During the disease progress, first acquisition of P. aeruginosa is the key-step in the management of CF patients. Quantitative PCR (qPCR) offers an opportunity to detect earlier the first acquisition of P. aeruginosa by CF patients. Given the lack of a validated protocol, our goal was to find an optimal molecular protocol for detection of P. aeruginosa in CF patients.

Methods
We compared two formerly described qPCR formats in early detection of P. aeruginosa in CF sputum samples: a qPCR targeting oprL gene, and a multiplex PCR targeting gyrB and ecfX genes.

Results
Tested in vitro on a large panel of P. aeruginosa isolates and others gram-negative bacilli, oprL qPCR exhibited a better sensitivity (threshold of 10 CFU/mL versus 730 CFU/mL), whereas the gyrB/ecfX qPCR exhibited a better specificity (90% versus 73%). These results were validated ex vivo on 46 CF sputum samples positive for P. aeruginosa in culture. Ex vivo assays revealed that qPCR detected 100 times more bacterial cells than culture-based method did.

Conclusion
Based on these results, we proposed a reference molecular protocol combining the two qPCRs, which offers a sensitivity of 100% with a threshold of 10 CFU/mL and a specificity of 100%. This combined qPCR-based protocol can be adapted and used for other future prospective studies.
Myopericarditis and exertional rhabdomyolysis following an influenza A (H3N2) infection
Authors: Tseng Guo-Shiang , Hsieh Chung-Yueh , Hsu Ching-Tsai , Lin Jung-Chung , Chan Jenq-Shyong 
Published: June 2013

Abstract

Background
Acute myopericarditis and exertional rhabdomyolysis, two uncommon but well-described diseases with potentially life-threatening effects, are generally considered as independent clinical entities. However, they may in fact be pathophysiologically related under certain circumstances. This is the first ever report of influenza myopericarditis provoked by exertional rhabdomyolysis to the best of our knowledge.

Case presentation
A 25-year-old immunocompetent Chinese man presented with bilateral leg pain, dizziness, and shortness of breath on admission soon after completing vigorous training comprising running drills. Exertional rhabdomyolysis was diagnosed with 44 fold high serum creatine phosphokinase. Then he developed chest pain, pericardial effusion, changes of electrocardiography and positive troponin I suggestive of myopericarditis. Influenza A (H3N2) virus infection was confirmed by polymerase chain reaction analysis of nasopharyngeal wash samples. Other possible infective and autoimmune causes were excluded. Patient recovered completely with anti-inflammatory therapy and the supportive care.

Conclusion
This case suggests that clinicians who treat patients with exertional rhabdomyolysis should be aware of the potential vulnerability to acute myopericarditis, especially in the presence of recent influenza A infection.
Inherited KIF21A and PAX6 gene mutations in a boy with congenital Fibrosis of extraocular muscles and aniridia
Authors: Ying Ming , Han Ruifang , Hao Peng , Wang Liming , Li Ningdong 
Published: June 2013

Abstract

Background
Mutations in the KIF21A gene are detected in the patients with congenital fibrosis of the extraocular muscles. Mutations in the PAX6 gene are detected in the patients with congenital aniridia.

Case presentation
Herein we report a boy with both congenital fibrosis of extraocular muscles and aniridia. Sequence analysis of his KIF21A and PAX6 genes reveals a 1-bp deletion (c.745delC) in the PAX6 gene and a missense mutation of c.2860C > T (p.Arg954Trp) in KIF21A.

Conclusions
This study demonstrates that the occurrence of independent mutations in more than a single gene in a patient may lead to a complex phenotype.
Ultrasonic spectrum analysis for in vivo characterization of tumor microstructural changes in the evaluation of tumor response to chemotherapy using diagnostic ultrasound
Authors: Lin Chun-yi , Cao Long-hui , Wang Jian-wei , Zheng Wei , Chen Yao , Feng Zi-zhen , Li An-hua , Zhou Jian-hua 
Published: June 2013

Abstract

Background
There is a strong need for early assessment of tumor response to chemotherapy in order to avoid the adverse effects of unnecessary chemotherapy and to allow early transition to second-line therapy. The purpose of this study was to determine the feasibility of ultrasonic spectral analysis for the in vivo characterization of changes in tumor microstructure in the evaluation of tumor response to chemotherapy using diagnostic ultrasound.

Methods
Experiments were approved by the regional animal care committee. Twenty-four MCF-7 breast cancer bearing nude mice were treated with adriamycin or sterile saline administered by intraperitoneal injection. Ultrasonic radio-frequency (RF) data was collected using a clinically available ultrasound scanner (6-MHz linear transducer). Linear regression parameters (spectral slope and midband-fit) regarding the calibrated power spectra from the RF signals were tested to monitor tumor response to treatment. The section equivalent to the ultrasound imaging plane was stained with hematoxylin and eosin to allow for assessment of the density of tumor cell nuclei.

Results
Treatment with adriamycin significantly reduced tumor growth in comparison with the control group (p = 0.003). Significant changes were observed in the ultrasonic parameters of the treated relative to the untreated tumors (p < 0.05). The spectral slope increased by 48.5%, from −10.66 ± 2.96 to −5.49 ± 2.69; the midband-fit increased by 12.8%, from −57.10 ± 7.68 to −49.81 ± 5.40. Treated tumors were associated with a significant decrease in the density of tumor cell nuclei as compared with control tumors (p < 0.001).

Conclusions
Ultrasonic spectral analysis can detect changes in tumor microstructure after chemotherapy, and this will be helpful in the early evaluation tumor response to chemotherapy.
Association of arterial stiffness with single nucleotide polymorphism rs1333049 and metabolic risk factors
Authors: Phababpha Suphawadee , Kukongviriyapan Upa , Pakdeechote Poungrat , Senggunprai Laddawan , Kukongviriyapan Veerapol , Settasatian Chatri , Tatsanavivat Pyatat , Intharaphet Phongsak , Senthong Vichai , Komanasin Nantarat , Settasatian Nongnuch , Greenwald Stephen E 
Published: June 2013

Abstract

Background
Increased arterial stiffness is a cardiovascular outcome of metabolic syndrome (MetS). The chromosome 9p21 locus has been identified as a major locus for risk of coronary artery disease (CAD). The single nucleotide polymorphism (SNP), rs1333049 on chromosome 9p21.3 has been strongly associated with CAD and myocardial infarction. Increased arterial stiffness could be the link between the 9p21 polymorphism and increased cardiovascular risk. Since the impact of a genetic polymorphism on arterial stiffness especially in Asian populations has not been well defined, we aimed to investigate the association of arterial stiffness with rs 1333049 variant on chromosome 9p21.3 in Thai subjects with and without MetS risk factors.

Methods
A total of 208 Thai subjects, aged 35–75 years, 135 with and 73 without MetS, according to IDF and NCEP-ATPIII criteria, were included in this study. Aortic-femoral pulse wave velocity (afPWV), brachial-ankle pulse wave velocity (baPWV) and aortic ankle pulse wave velocity (aaPWV) were measured and used as markers of arterial stiffness. The chromosome 9p21.3 locus, represented by the rs 1333049 variant and blood biochemistry were evaluated.

Results
Arterial stiffness was elevated in subjects with MetS when compared with nonMetS subjects. PWV, especially afPWV increased progressively with increasing number of MetS risk factors (r = 0.322, P <0.001). We also found that the frequency distribution of the rs1333049 genotypes is significantly associated with the afPWV (P <0.05). In multivariate analyses, there was an association between homozygous C allele and afPWV (Odds ratio (OR), 8.16; 95% confidence interval (CI), 1.91 to 34.90; P = 0.005), while the GC genotype was not related to afPWV (OR, 1.79; 95% CI, 0.84 to 3.77; P = 0.129) when compared with the GG genotype.

Conclusions
Our findings demonstrate for the first time that arterial stiffness is associated with genetic polymorphism in 9p21 and metabolic risk factors in a Thai population.
CYP450 phenotyping and metabolite identification of quinine by accurate mass UPLC-MS analysis: a possible metabolic link to blackwater fever
Authors: Marcsisin Sean R , Jin Xiannu , Bettger Theresa , McCulley Nicholas , Sousa Jason C , Shanks G Dennis , Tekwani Babu L , Sahu Rajnish , Reichard Gregory A , Sciotti Richard J , Melendez Victor , Pybus Brandon S 
Published: June 2013

Abstract

Background
The naturally occurring alkaloid drug, quinine is commonly used for the treatment of severe malaria. Despite centuries of use, its metabolism is still not fully understood, and may play a role in the haemolytic disorders associated with the drug.

Methods
Incubations of quinine with CYPs 1A2, 2C9, 2C19, 2D6, and 3A4 were conducted, and the metabolites were characterized by accurate mass UPLC-MSE analysis. Reactive oxygen species generation was also measured in human erythrocytes incubated in the presence of quinine with and without microsomes.

Results
The metabolites 3-hydroxyquinine, 2’-oxoquininone, and O-desmethylquinine were observed after incubation with CYPs 3A4 (3-hydroxyquinine and 2’-oxoquininone) and 2D6 (O-desmethylquinine). In addition, multiple hydroxylations were observed both on the quinoline core and the quinuclidine ring system. Of the five primary abundance CYPs tested, 3A4, 2D6, 2C9, and 2C19 all demonstrated activity toward quinine, while 1A2 did not. Further, quinine produced robust dose-dependent oxidative stress in human erythrocytes in the presence of microsomes.

Conclusions
Taken in context, these data suggest a CYP-mediated link between quinine metabolism and the poorly understood haemolytic condition known as blackwater fever, often associated with quinine ingestion.
TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson’s disease
Authors: Rayaprolu Sruti , Mullen Bianca , Baker Matt , Lynch Timothy , Finger Elizabeth , Seeley William W , Hatanpaa Kimmo J , Lomen-Hoerth Catherine , Kertesz Andrew , Bigio Eileen H , Lippa Carol , Josephs Keith A , Knopman David S , White Charles L , Caselli Richard , Mackenzie Ian R , Miller Bruce L , Boczarska-Jedynak Magdalena , Opala Grzegorz , Krygowska-Wajs Anna , Barcikowska Maria , Younkin Steven G , Petersen Ronald C , Ertekin-Taner Nilüfer , Uitti Ryan J , Meschia James F , Boylan Kevin B , Boeve Bradley F , Graff-Radford Neill R , Wszolek Zbigniew K , Dickson Dennis W , Rademakers Rosa , Ross Owen A 
Published: June 2013

Abstract

Background
A rare variant in the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) gene has been reported to be a genetic risk factor for Alzheimer’s disease by two independent groups (Odds ratio between 2.9-4.5). Given the key role of TREM2 in the effective phagocytosis of apoptotic neuronal cells by microglia, we hypothesized that dysfunction of TREM2 may play a more generalized role in neurodegeneration. With this in mind we set out to assess the genetic association of the Alzheimer’s disease-related risk variant in TREM2 (rs75932628, p.R47H) with other related neurodegenerative disorders.

Results
The study included 609 patients with frontotemporal dementia, 765 with amyotrophic lateral sclerosis, 1493 with Parkinson’s disease, 772 with progressive supranuclear palsy, 448 with ischemic stroke and 1957 controls subjects free of neurodegenerative disease. A significant association was observed for the TREM2 p.R47H substitution in susceptibility to frontotemporal dementia (OR = 5.06; p-value = 0.001) and Parkinson’s disease (OR = 2.67; p-value = 0.026), while no evidence of association with risk of amyotrophic lateral sclerosis, progressive supranuclear palsy or ischemic stroke was observed.

Conclusions
Our results suggest that the TREM2 p.R47H substitution is a risk factor for frontotemporal dementia and Parkinson’s disease in addition to Alzheimer’s disease. These findings suggest a more general role for TREM2 dysfunction in neurodegeneration, which could be related to its role in the immune response.
Metal-free synthesis of polysubstituted oxazoles via a decarboxylative cyclization from primary α-amino acids
Authors: Li Yunfeng , Guo Fengfeng , Zha Zhenggen , Wang Zhiyong 
Published: June 2013

Abstract

Background
The ubiquitous oxazoles have attracted more and more attention in both industrial and academic fields for decades. This interest arises from the fact that a variety of natural and synthetic compounds which contain the oxazole substructure exhibit significant biological activities and antiviral properties. Although various synthetic methodologies for synthesis of oxazols have been reported, the development of milder and more general procedure to access oxazoles is still desirable.

Results
In this manuscript, a novel method for synthesis of polysubstituted oxazoles was developed from metal-free decarboxylative cyclization of easily available primary α-amino acids with 2-bromoacetophenones.

Conclusions
The method was simple, and this reaction could be carried out smoothly under mild and metal-free conditions. By virtue of this method, various polysubstituted oxazoles were obtained from the primary α-amino acids with moderate yields.
pKa determination of oxysophocarpine by reversed - phase high performance liquid chromatography
Authors: Huo Huiling , Li Tingting , Zhang Lei 
Published: June 2013

Abstract

Background
In this study, a RP - HPLC method was applied for determination of pKa value by using the dependence of the capacity factor (k) on the pH of the mobile phase for oxysophocarpine (OSP).

Findings
The effect of the mobile phase composition on the ionization constant was studied by measuring the pKa value at different MeOH concentrations, ranging from 10 to 20% (v/v). Based on all pH - k curves plotted and pH values at inflection point calculated, experimental pKa value obtained for oxysophocarpine was 6.5.

Conclusion
This method was successfully applied to realize low sample consumption, rapid sample throughput, high sensitivity and precision.
Endogenous progesterone levels and frontotemporal dementia: modulation of TDP-43 and Tau levelsin vitroand treatment of the A315TTARDBPmouse model
Authors: Dang Theresa N. T. , Dobson-Stone Carol , Glaros Elias N. , Kim Woojin S. , Hallupp Marianne , Bartley Lauren , Piguet Olivier , Hodges John R. , Halliday Glenda M. , Double Kay L. , Schofield Peter R. , Crouch Peter J. , Kwok John B. J. 
Published: June 2013

SummaryFrontotemporal dementia (FTD) is associated with motor neurone disease (FTD-MND), corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). Together, this group of disorders constitutes a major cause of young-onset dementia. One of the three clinical variants of FTD is progressive nonfluent aphasia (PNFA), which is focused on in this study. The steroid hormone progesterone (PROG) is known to have an important role as a neurosteroid with potent neuroprotective and promyelination properties. In a case-control study of serum samples (39 FTD, 91 controls), low serum PROG was associated with FTD overall. In subgroup analysis, low PROG levels were significantly associated with FTD-MND and CBS, but not with PSP or PNFA. PROG levels of &gt;195 pg/ml were significantly correlated with lower disease severity (frontotemporal dementia rating scale) for individuals with CBS. In the human neuroblastoma SK-N-MC cell line, exogenous PROG (9300-93,000 pg/ml) had a significant effect on overall Tau and nuclear TDP-43 levels, reducing total Tau levels by ~1.5-fold and increasing nuclear TDP-43 by 1.7- to 2.0-fold. Finally, elevation of plasma PROG to a mean concentration of 5870 pg/ml in an Ala315Thr (A315T) TARDBP transgenic mouse model significantly reduced the rate of loss of locomotor control in PROG-treated, compared with placebo, mice. The PROG treatment did not significantly increase survival of the mice, which might be due to the limitation of the transgenic mouse to accurately model TDP-43-mediated neurodegeneration. Together, our clinical, cellular and animal data provide strong evidence that PROG could be a valid therapy for specific related disorders of FTD.