bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased incidence of another cancer in myeloproliferative neoplasms patients at the time of diagnosis
Authors: Pettersson Helna , Knutsen Håvar , Holmberg Erik , Andréasson Björn 
Published: July 2014

AbstractSeveral studies have reported an increased incidence of coexistent cancer in patients with myeloproliferative neoplasms (MPN), and myelosuppressive treatment has been speculated to be one of the causes. In this study, we have concentrated on malignancies diagnosed before the MPN diagnosis to eliminate the possible influence of MPN treatment. The patients were recruited from the Swedish and Norwegian cancer registries. One thousand seven hundred and 45 patients from the Swedish MPN Quality Registry and 468 patients from the Norwegian National Cancer Registry were included in this study covering a 3‐yr period. The results show that primary concurrent cancer is higher among patients with MPN compared to the general population. When pooled together, the Swedish and the Norwegian cohort showed increased prevalence of all types of cancer in general compared with the general population, standard prevalence ratio (SPR) of 1.20 (95% CI 1.07–1.34). Significantly high SPRs were reached for skin malignant melanoma [1.89 (95% CI 1.33–2.62)], prostate cancer [1.39 (95% CI 1.11–1.71)], and hematologic cancer [1.49 (95% CI 1.00–2.12)]. In the polycythemia vera group, the risk of having prior malignant melanoma of the skin was significant, with an SPR of 2.20 (95% CI 1.17–3.77). For patients with essential thrombocythemia and primary myelofibrosis, no significant risks were found. Coexisting cancers have a high impact on the treatment strategies of MPN, as it narrows down the treatment options. Chronic inflammation, as a common denominator of MPN with other cancers, can catalyze each other's existence and progression.
The control of complex finger movements by directional information flow between mesial frontocentral areas and the primary motor cortex
Authors: Boenstrup M. , Feldheim J. , Heise K. , Gerloff C. , Hummel F. C. 
Published: July 2014

AbstractComplex movements require the interplay of local activation and interareal communication of sensorimotor brain regions. This is reflected in a decrease of task‐related spectral power over the sensorimotor cortices and an increase in functional connectivity predominantly in the upper alpha band in the electroencephalogram (EEG). In the present study, directionality of information flow was investigated using EEG recordings to gain better understanding about the network architecture underlying the performance of complex sequential finger movements. This was assessed by means of Granger causality‐derived directed transfer function (DTF). As DTF measures the influence one signal exerts on another based on a time lag between them, it allows implications to be drawn on causal relationships. To reveal causal connections between brain regions that are specifically modulated by task complexity, we contrasted the performance of right‐handed sequential finger movements of different complexities (simple, scale, complex) that were either pre‐learned (memorized) or novel instructed. A complexity‐dependent increase in information flow from mesial frontocentral to the left motor cortex and, less pronounced, also to the right motor cortex specifically in the upper alpha range was found. Effective coupling during sequences of high complexity was larger for memorized sequences compared with novel sequences (P = 0.0037). These findings further support the role of mesial frontocentral areas in directing the primary motor cortex in the process of orchestrating complex movements and in particular learned sequences.
Increased burst‐firing of ventral tegmental area dopaminergic neurons in d‐amino acid oxidase knockout mice in vivo
Authors: Schweimer Judith V. , Coullon Gaelle S. L. , Betts Jill F. , Burnet Philip W. J. , Engle Sandra J. , Brandon Nicholas J. , Harrison Paul J. , Sharp Trevor 
Published: July 2014

Abstractd‐Amino acid oxidase (DAO) degrades the N‐methyl‐d‐aspartate (NMDA) receptor co‐agonist d‐serine, and is implicated in schizophrenia as a risk gene and therapeutic target. In schizophrenia, the critical neurochemical abnormality affects dopamine, but to date there is little evidence that DAO impacts on the dopamine system. To address this issue, we measured the electrophysiological properties of dopaminergic (DA) and non‐DA neurons in the ventral tegmental area (VTA) of anaesthetised DAO knockout (DAO−/−) and DAO heterozygote (DAO+/−) mice as compared with their wild‐type (DAO+/+) littermates. Genotype was confirmed at the protein level by western blotting and immunohistochemistry. One hundred and thirty‐nine VTA neurons were recorded in total, and juxtacellular labelling of a subset revealed that neurons immunopositive for tyrosine hydroxylase had DA‐like electrophysiological properties that were distinct from those of neurons that were tyrosine hydroxylase‐immunonegative. In DAO−/− mice, approximately twice as many DA‐like neurons fired in a bursting pattern than in DAO+/− or DAO+/+ mice, but other electrophysiological properties did not differ between genotypes. In contrast, non‐DA‐like neurons had a lower firing rate in DAO−/− mice than in DAO+/− or DAO+/+ mice. These data provide the first direct evidence that DAO modulates VTA DA neuron activity, which is of interest for understanding both the glutamatergic regulation of dopamine function and the therapeutic potential of DAO inhibitors. The increased DA neuron burst‐firing probably reflects increased availability of d‐serine at VTA NMDA receptors, but the site, mechanism and mediation of the effect requires further investigation, and may include both direct and indirect processes.
Induction of interleukin‐1β by activated microglia is a prerequisite for immunologically induced fatigue
Authors: Ifuku Masataka , Hossain Shamim M. , Noda Mami , Katafuchi Toshihiko 
Published: July 2014

AbstractWe previously reported that an intraperitoneal (i.p.) injection of synthetic double‐stranded RNA, polyriboinosinic:polyribocytidylic acid (poly‐I:C), produced prolonged fatigue in rats, which might serve as a model for chronic fatigue syndrome. The poly‐I:C‐induced fatigue was associated with serotonin transporter (5‐HTT) overexpression in the prefrontal cortex (PFC), a brain region that has been suggested to be critical for fatigue sensation. In the present study, we demonstrated that microglial activation in the PFC was important for poly‐I:C‐induced fatigue in rats, as pretreatment with minocycline, an inhibitor of microglial activation, prevented the decrease in running wheel activity. Poly‐I:C injection increased the microglial interleukin (IL)‐1β expression in the PFC. An intracerebroventricular (i.c.v.) injection of IL‐1β neutralising antibody limited the poly‐I:C‐induced decrease in activity, whereas IL‐1β (i.c.v.) reduced the activity in a dose‐dependent manner. 5‐HTT expression was enhanced by IL‐1β in primary cultured astrocytes but not in microglia. Poly‐I:C injection (i.p.) caused an increase in 5‐HTT expression in astrocytes in the PFC of the rat, which was inhibited by pretreatment with minocycline (i.p.) and rat recombinant IL‐1 receptor antagonist (i.c.v.). Poly‐I:C injection (i.p.) led to a breakdown of the blood–brain barrier and enhanced Toll‐like receptor 3 signaling in the brain. Furthermore, direct application of poly‐I:C enhanced IL‐1β expression in primary microglia. We therefore propose that poly‐I:C‐induced microglial activation, which may be at least partly caused by a direct action of poly‐I:C, enhances IL‐1β expression. Then, IL‐1β induces 5‐HTT expression in astrocytes, resulting in the immunologically induced fatigue.
Steroid Hormones and Facial Traits in The Recognition of A Potential Rival in Men
Authors: Borráz‐León Javier Iván , Cerda‐Molina Ana Lilia , Hernández‐López Leonor , Chavira‐Ramírez Roberto , de la O‐Rodríguez Claudio 
Published: July 2014

AbstractThere is evidence that the cognitive skills that enable an individual to evaluate their own physical characteristics and those of others are an important strategy for recognizing a potential rival in intrasexual competition in humans. It has been shown that these strategies are facilitated by steroid hormones such as testosterone (T) and cortisol (C). This study examines whether men recognize as attractive some facial characteristics of other men that the literature reports as attractive to women when observing the faces of other men, under the hypothesis that the presence of these features indicates a potential rival. The characteristics evaluated were facial fluctuating asymmetry (FA), dominance (D), and assertiveness (A). In addition, we investigated whether the recognition of these facial characteristics depended upon the characteristics of the evaluator, that is, of the man's ownFA,D, andA, or on the concentration ofTandCin saliva. We found that evaluators with greaterFA(asymmetric faces) and lower concentrations of C rated the faces of more symmetrical men as more attractive to women and as the most likely to represent potential rivals. Men with asymmetric faces exhibited higher levels of T than lowFAmales, although the difference was not significant. Conversely, men with low levels ofFA(symmetric) identified the faces of more assertive men as the most attractive to women and the most likely to represent potential rivals. We concluded that men with highFAlevels are more prone to recognize a potential rival in others according to female preferences, and this identification enables them to reduce the cost of competition.
The newly characterized Pl‐jun is specifically expressed in skeletogenic cells of the Paracentrotus lividus sea urchin embryo
Authors: Russo Roberta , Pinsino Annalisa , Costa Caterina , Bonaventura Rosa , Matranga Valeria , Zito Francesca 
Published: July 2014

Growing evidence suggests that the transcription factors belonging to the Jun family are involved in many important cellular events, such as the control of bone development in mammalians. We have characterized, for the first time, a member of the Jun family from embryos of the sea urchin Paracentrotus lividus. The Pl‐jun protein sequence includes all the functional domains characteristic of members of the Jun family (i.e. the basic leucine zipper, the basic DNA‐binding and the c‐Jun N‐terminal kinase docking‐like domains), which are evolutionarily conserved. Moreover, all the key serine and threonine residues, which are phosphorylation targets for different kinases necessary for jun activation, appear to be well preserved. A model of the monomeric protein provides a simulation of the three‐dimensional structure and shows the potential sites for dimerization and DNA binding. Pl‐jun mRNA is expressed in the unfertilized egg and throughout sea urchin embryo development. As the development proceeds, Pl‐jun mRNA becomes exclusively expressed in the skeletogenic cells. Intriguingly, these cells contain significant amounts of the phosphorylated active protein entirely localized into their nuclei. These findings strengthen our hypothesis that suggests an active role for Pl‐jun in skeletogenic cells, thus indicating that this transcription factor is a novel component of the gene regulatory networks controlling skeletogenesis.DatabaseNucleotide sequence data have been deposited in the EMBL databases under the accession number: HE817756.
Proline‐serine‐threonine phosphatase interacting protein 1 inhibition of T‐cell receptor signaling depends on its SH3 domain
Authors: Marcos Tamara , Ruiz‐Martín Virginia , de la Puerta María Luisa , Trinidad Antonio G. , Rodríguez María del Carmen , de la Fuente Miguel Angel , Sánchez Crespo Mariano , Alonso Andrés , Bayón Yolanda 
Published: July 2014

Proline‐serine‐threonine phosphatase interacting protein 1 (PSTPIP1) is an adaptor protein associated with the cytoskeleton that is mainly expressed in hematopoietic cells. Mutations in PSTPIP1 cause the rare autoinflammatory disease called pyogenic arthritis, pyoderma gangrenosum, and acne. We carried out this study to further our knowledge on PSTPIP1 function in T cells, particularly in relation to the phosphatase lymphoid phosphatase (LYP), which is involved in several autoimmune diseases. LYP–PSTPIP1 binding occurs through the C‐terminal homology domain of LYP and the F‐BAR domain of PSTPIP1. PSTPIP1 inhibits T‐cell activation upon T‐cell receptor (TCR) and CD28 engagement, regardless of CD2 costimulation. This function of PSTPIP1 depends on the presence of an intact SH3 domain rather than on the F‐BAR domain, indicating that ligands of the F‐BAR domain, such as the PEST phosphatases LYP and PTP‐PEST, are not critical for its negative regulatory role in TCR signaling. Additionally, PSTPIP1 mutations that cause the pyogenic arthritis, pyoderma gangrenosum and acne syndrome do not affect PSTPIP1 function in T‐cell activation through the TCR.Structured digital abstract

LYP physically interacts with PSTPIP1 by pull down (View interaction)

PSTPIP1 physically interacts with LYP by anti tag coimmunoprecipitation (1, 2, 3, 4)

LYP physically interacts with PSTPIP1 by anti bait coip (View interaction)
Contrasting above‐ and belowground sensitivity of three Great Plains grasslands to altered rainfall regimes
Authors: Wilcox Kevin R. , von Fischer Joseph C. , Muscha Jennifer M. , Petersen Mark K. , Knapp Alan K. 
Published: July 2014

AbstractIntensification of the global hydrological cycle with atmospheric warming is expected to increase interannual variation in precipitation amount and the frequency of extreme precipitation events. Although studies in grasslands have shown sensitivity of aboveground net primary productivity (ANPP) to both precipitation amount and event size, we lack equivalent knowledge for responses of belowground net primary productivity (BNPP) andNPP. We conducted a 2‐year experiment in threeUSGreat Plains grasslands – the C4‐dominated shortgrass prairie (SGP; lowANPP) and tallgrass prairie (TGP; highANPP), and the C3‐dominated northern mixed grass prairie (NMP; intermediateANPP) – to test three predictions: (i) bothANPPandBNPPresponses to increased precipitation amount would vary inversely with mean annual precipitation (MAP) and site productivity; (ii) increased numbers of extreme rainfall events during high‐rainfall years would affect high and lowMAPsites differently; and (iii) responses belowground would mirror those aboveground. We increased growing season precipitation by as much as 50% by augmenting natural rainfall via (i) many (11–13) small or (ii) fewer (3–5) large watering events, with the latter coinciding with naturally occurring large storms. BothANPPandBNPPincreased with water addition in the two C4grasslands, with greaterANPPsensitivity inTGP, but greaterBNPPandNPPsensitivity inSGP.ANPPandBNPPdid not respond to any rainfall manipulations in the C3‐dominatedNMP. Consistent with previous studies, fewer larger (extreme) rainfall events increasedANPPrelative to many small events inSGP, but event size had no effect inTGP. Neither system responded consistently above‐ and belowground to event size; consequently, totalNPPwas insensitive to event size. The diversity of responses observed in these three grassland types underscores the challenge of predicting responses relevant to C cycling to forecast changes in precipitation regimes even within relatively homogeneous biomes such as grasslands.
Amplification and overexpression of CMET is a common event in brain metastases of non‐small cell lung cancer
Authors: Preusser Matthias , Streubel Berthold , Berghoff Anna S , Hainfellner Johannes A , von Deimling Andreas , Widhalm Georg , Dieckmann Karin , Wöhrer Adelheid , Hackl Monika , Zielinski Christoph , Birner Peter 
Published: July 2014

BackgroundCMET represents an emerging therapy target for monoclonal antibodies and tyrosine kinase inhibitors in non‐small cell lung cancer (NSCLC).MethodsWe investigated CMET gene amplification status by fluorescence in‐situ hybridization (FISH) and CMET protein expression by immunohistochemistry in a large series of 209 NSCLC brain metastases (BM; 165 adenocarcinoma, 20 squamous cell carcinoma, 11 adenosquamous carcinomas, 11 large cell carcinomas and two large cell neuroendocrine carcinomas) and correlated our results to clinic‐pathological parameters and molecular data from previous studies.ResultsWe found CMET gene amplification in 36/167 (21.6%) and CMET protein expression in 87/196 (44.4%) of evaluable BM. There was a strong correlation between the presence of CMET gene amplification and CMET protein expression (P < 0.001, chi‐square test). Furthermore, presence of CMET amplification correlated positively with presence of ALK amplifications (P = 0.039, chi‐square test) and high HIF1 alpha index (P = 0.013, Mann–Whitney U‐test). Neither CMET expression nor CMET gene amplification status correlated with patient outcome parameters or known prognostic factors.ConclusionsCMET overexpression and CMET amplification are commonly found in NSCLC BM and may represent a promising therapeutic target.
Management of breast papillary lesions diagnosed in ultrasound‐guided vacuum‐assisted and core needle biopsies
Authors: Yamaguchi Rin , Tanaka Maki , Tse Gary M , Yamaguchi Miki , Terasaki Hiroshi , Hirai Yoshitake , Nonaka Yasuhide , Morita Michi , Yokoyama Toshiro , Kanomata Naoki , Naito Yoshiki , Akiba Jun , Yano Hirohisa 
Published: July 2014

AimsTo assess the outcome of breast papillary lesions diagnosed by ultrasound‐guided core needle biopsy (CB) or vacuum‐assisted ‘mammotome’ biopsy (MT), the accuracy of these diagnoses, and whether it is justified not to undertake surgical excision of non‐malignant papillary lesions so diagnosed.Methods and resultsAmong 3219 (MT, 2195; CB, 1024) breast biopsies spanning 5 years, 185 (5.7%) papillary lesions [MT, 162 (88%); CB, 23 (12%)] were identified. Of these, 142 cases (77%; MT/CB, 125/17) were benign, 24 (13%, 23/1) were atypical, and 19 (10%; 14/5) were malignant. Of the 142 benign cases, 114 had imaging follow‐up (FU) (FU period 2–81 months); 17 of 114 cases were excised, and four were malignant (3.5%) (FU period 4–57 months). Of the 24 atypical cases (23 had FU), 19 were excised: six were benign (32%) and 13 malignant (68%). The remaining four cases were considered to be non‐malignant (FU period 7–54 months).ConclusionsBenign papillary lesions diagnosed by MT or CB might not require immediate excision, but should receive imaging FU for at least 5 years. Excision should be performed in cases showing changes in imaging features, as the possibilities of carcinoma coexisting with papilloma or carcinoma developing from papilloma cannot be excluded, as illustrated by the 4% upgrade rate at excision in this study.
Maspin expression patterns differ in the invasive versus lepidic growth pattern of pulmonary adenocarcinoma
Authors: Lonardo Fulvio , Guan Hui , Dzinic Sijana , Sheng Shijie 
Published: July 2014

AimsTo test whether changes in the subcellular localization of maspin parallel morphological progression in pulmonary adenocarcinoma, we compared its expression between lepidic and invasive growth patterns.MethodsApplying immunohistochemistry, we compared maspin expression in lepidic and invasive growth patterns occurring in different tumours (series #1, n = 86) as well as within the same tumour and in the same section (series #2, n = 29).ResultsIn both series, the lepidic growth pattern (n = 45) was significantly associated with nuclear maspin, while the invasive (n = 70) with combined nuclear and cytoplasmic maspin (P < 0.05). In the second series, transition from a lepidic to an invasive pattern in the same tumour was associated predominantly with a shift respectively from a nuclear to a combined nuclear and cytoplasmic maspin (15/29) or preservation of nuclear expression (8/29). A shift from nuclear maspin to negative expression (3/29) or other patterns (3/29) were also observed.ConclusionsNuclear maspin is a typical but not exclusive feature of the lepidic growth pattern of pulmonary adenocarcinoma, whereas combined nuclear and cytoplasmic maspin characterizes invasion. These data show that changes of expression and subcellular localization of maspin may constitute an important biological end point of tumour progression and aid in the classification of lung adenocarcinoma.
Intestinal metaplasia in Barrett's oesophagus may be an epiphenomenon rather than a preneoplastic condition, and CDX2‐positive cardiac‐type epithelium is associated with minute Barrett's tumour
Authors: Watanabe Gen , Ajioka Yoichi , Takeuchi Manabu , Annenkov Alexey , Kato Takashi , Watanabe Kaori , Tani Yusuke , Ikegami Kikuo , Yokota Yoko , Fukuda Mutsumi 
Published: July 2014

AimsAlthough intestinal‐type epithelium in Barrett's oesophagus has been traditionally recognized as having a distinct malignant potential, whether this also holds true for cardiac‐type epithelium remains controversial. The aim of this study was to identify a type of epithelium that is highly associated with Barrett's tumour.Methods and resultsWe analysed tumours and the corresponding background mucosa with special regard to tumour size in 40 cases of superficial Barrett's tumour by using immunohistochemical staining for CDX2, CD10, MUC2, MUC5AC, and MUC6. Intestinal metaplasia in tumour‐adjacent mucosa was not associated with tumour size, but was significantly correlated with the extent of Barrett's oesophagus (P < 0.001). The majority (69.2%, 9/13) of small tumours (≤10 mm) had no intestinal metaplasia in adjacent non‐neoplastic mucosae. Minute (≤5 mm) tumours were significantly associated with a gastric immunophenotype (P < 0.001). Purely gastric‐immunophenotype tumour cells expressed CDX2, and cardiac‐type epithelium adjacent to small tumours also showed low‐level CDX2 expression.ConclusionsOur data suggest that intestinal metaplasia in Barrett's oesophagus is an epiphenomenon rather than a preneoplastic condition, and that CDX2‐positive cardiac‐type epithelium is highly associated with minute Barrett's tumour. Further prospective studies are needed to evaluate the risk of malignancy of cardiac‐type epithelium with regard to sub‐morphological intestinalization.
Granular cell tumours of the colorectum: histopathological and immunohistochemical evaluation of 30 cases
Authors: Na Jong‐In , Kim Hye‐Jeong , Jung Jong‐Jae , Kim Young , Kim Sung‐Sun , Lee Jae‐Hyuk , Lee Kyung‐Hwa , Park Jong‐Tae 
Published: July 2014

AimsGranular cell tumours (GCTs) are uncommon in the gastrointestinal tract, particularly in the colorectum. Herein, we report a series of 30 colorectal GCTs and discuss the properties of colorectal GCTs based on histopathological and immunohistochemical studies.Methods and resultsSearching the surgical pathology files identified 30 cases of colorectal GCTs for 2005–2013. A broad panel of antibodies including neural and macrophage markers were used for immunohistochemical evaluation. Colorectal GCTs predominantly involved the right colon and showed increased nuclear atypia including nuclear pleomorphism and nuclear spindling. All 24 cases with mucosal tumour components had infiltrative growth patterns within the mucosa. In all available cases, diffuse strong immunopositivity was observed for S100 and SOX10 of schwannian differentiation markers, as well as for CD68. Other neuronal lineage markers, including CD56, neuron‐specific enolase, nestin, and synaptophysin showed consistently high expression rates. The immunohistochemical results are suggestive for a neural origin of GCTs.ConclusionHistopathological and immunohistochemical features of colorectal GCTs were delineated in this large series of 30 colorectal GCTs. Although the incidence of GCTs is relatively low, clinicians and pathologists need to be aware of GCT in the differential diagnosis.