bluuebunny/crossref_metadata_2025_split huggingface dataset:
IFN-Induced Protein with Tetratricopeptide Repeats 2 Inhibits Migration Activity and Increases Survival of Oral Squamous Cell Carcinoma
Authors: Lai Kuo-Chu , Chang Kuo-Wei , Liu Chung-Ji , Kao Shou-Yen , Lee Te-Chang 
Published: September 2008

AbstractThe function of the IFN-stimulated gene family protein, IFN-induced protein with tetratricopeptide repeats 2 (IFIT2), is poorly understood. Here, we report that IFIT2 colocalizes with cytokeratin 18 in oral squamous cell carcinoma (OSCC) cells. Treatment of OSCC cells with IFN-β significantly increased the expression of IFIT2 and remarkably inhibited cell migration. To further explore the effect of IFIT2 on cell migration, IFIT2 expression was either silenced with a small interfering RNA or increased by ectopic expression. IFIT2 knockdown in OSCC cells led to a significantly higher level of migration in vitro (P &lt; 0.05) compared with control cells; by contrast, IFIT2 overexpression led to a significantly lower level of migration in vitro (P &lt; 0.05). Immunohistochemically, 71.4% of OSCC tissues had elevated IFIT2 protein levels compared with noncancerous matched tissues. Elevated IFIT2 protein expression was positively associated with tumor differentiation status and inversely associated with nodal stage in OSCC specimens (P &lt; 0.05). Higher IFIT2 protein levels in tumor tissues were also associated with better patient survival (P &lt; 0.01). Our present study shows an inverse correlation between IFIT2 expression and cell migration, suggesting that IFIT2 plays an important role in inhibiting this process and that its expression may be associated with better prognosis in patients with OSCC. (Mol Cancer Res 2008;6(9):1431–9)
Mercantile Networks, Port Cities, and “Pirate” States: Conflict and Competition in the Indian Ocean World of Trade before the Sixteenth Century
Authors: Margariti Roxani Eleni 
Published: September 2008

AbstractThe prevailing image of the Indian Ocean world of trade before the arrival of western Europeans and Ottomans in the region in the sixteenth century is one of a generally peaceful, conflict-free realm dominated by cosmopolitan traders who moved easily across boundaries of geography, ethnicity, language, and religion. This paper modifies this picture by examining the evidence for conflict and competition between pre-modern maritime polities in the western end of the Indian Ocean. In the fifth/eleventh and sixth/twelfth centuries maritime polities on the islands of Kish in the Persian Gulf and Dahlak in the Red Sea antagonized Aden's supremacy as the region's most frequented entrepot. In the subsequent three centuries, the Ayyubids and Rasulids of Yemen also strove to control maritime routes and networks.L'historiographie en vigueur de l'Océan Indien à l'époque précédant la venue des Ottomans et des Européens au XVIème siècle, décrit une aire commerciale généralement paisible parcourue aisément par des négociants cosmopolites par-delà les obstacles géographiques, ethniques, religieux et linguistiques. Cette contribution modifie cette image par un examen des témoignages des Vème/XIème et VIème/XIIe siècles qui attestent les conflits et rivalités des cités portuaires de Kish en la Golfe de Perse, de Dahlak en la Mer Rouge contestant la suprématie d'Aden, l'entrepôt le plus fréquenté. Durant les trois siècles suivants, les Ayyûbides et Rasûlides du Yémen s'efforcèrent également de contrôler les routes et réseaux maritimes.
The Nature and Role of Phenomenological Psychology in Alfred Schutz
Authors: Embree Lester 
Published: September 2008

AbstractThe essay reviews how phenomenological psychology can draw on Edmund Husserl's transcendental phenomenology in order to clarify the foundations of the cultural sciences and then explicates the theory of this psychology implicit in Schutz's oeuvre.Max Weber has shown that all phenomena of the socio-cultural world originate in social interaction and can be referred to it. According to him, it is the central task of sociology to understand the meaning which the actor bestows on his action (the “subjective meaning” in his terminology). But what is action, what is meaning, and how is the understanding of such meaning by a fellow-man possible, be he a partner of the social interaction, or merely an observer in everyday life, or a social scientist? I submit that any attempt to answer these questions leads immediately to questions with which Husserl was concerned and which he has to a certain extent solved. (Schutz, 1962, p. 145)
The CD34-like protein PODXL and α6-integrin (CD49f) identify early progenitor MSCs with increased clonogenicity and migration to infarcted heart in mice
Authors: Lee Ryang Hwa , Seo Min Jeong , Pulin Andrey A. , Gregory Carl A. , Ylostalo Joni , Prockop Darwin J. 
Published: September 2008

AbstractWe screened for surface proteins expressed only by the early progenitor cells present in low-passage, low-density cultures of the adult stem/progenitor cells from bone marrow referred to as mesenchymal stem cells or multipotent stromal cells (MSCs). Six proteins were identified that were selectively expressed in the early progenitors: podocalyxin-like protein (PODXL), α6-integrin (CD49f), α4-integrin (CD49d), c-Met, CXCR4, and CX3CR1. All were previously shown to be involved in cell trafficking or tumor progression. Antibodies to CD49f and PODXL, a sialomucin in the CD34 family, were the most robust for FACScan assays. PODXLhi/CD49fhi MSCs were more clonogenic and differentiated more efficiently than PODXLlo/CD49flo cells. Inhibition of expression of PODXL with RNA interference caused aggregation of the cells. Furthermore, PODXLhi/CD49fhi MSCs were less prone to produce lethal pulmonary emboli, and larger numbers were recovered in heart and kidney after intravenous infusion into mice with myocardial infarcts.
Defective Notch activation in microenvironment leads to myeloproliferative disease
Authors: Kim Young-Woong , Koo Bon-Kyoung , Jeong Hyun-Woo , Yoon Mi-Jeong , Song Ran , Shin Juhee , Jeong Dae-Chul , Kim Sun-Hee , Kong Young-Yun 
Published: September 2008

AbstractDespite the great importance of nonhematopoietic cells constituting the microenvironment for normal hematopoiesis, the cellular interactions between nonhematopoietic cells themselves are largely unknown. Using the Cre-loxP system in mice to inactivate Mind bomb-1 (Mib1), an essential component for Notch ligand endocytosis, here we show that the development of an MPD is dependent on defective Notch activation in the microenvironment. Our 2 independent Mib1 conditional knockout (CKO) mouse lines each developed a myeloproliferative disease (MPD), with gradual accumulations of immature granulocytes. The mutant mice showed hepatosplenomegaly, anemia, granulocytosis, and leukocyte infiltration in multiple organs and finally died at approximately 20 weeks of age. We were surprised to find that the transplantation of wild-type bone marrow cells into the Mib1-null microenvironment resulted in a de novo MPD. Moreover, by introducing the constitutively active intracellular domain of Notch1 in the Mib1-null background, we show that active Notch1 expression in the Mib1-null microenvironment significantly suppressed the disease progression, suggesting that the MPD development in the Mib1 CKO mice is due to defective Notch activation in the nonhematopoietic cells. These findings demonstrate that normal hematopoiesis absolutely requires Notch activation through the Notch ligand-receptor interaction between microenvironmental cells themselves and shed light on the microenvironment that fosters hematopoietic disorders.
An L-selectin ligand distinct from P-selectin glycoprotein ligand-1 is expressed on endothelial cells and promotes neutrophil rolling in inflammation
Authors: Shigeta Akiko , Matsumoto Masanori , Tedder Thomas F. , Lowe John B. , Miyasaka Masayuki , Hirata Takako 
Published: September 2008

AbstractNeutrophils recruited from the blood are key players in the innate immune response. Selectins play critical roles in neutrophil recruitment by mediating their tethering and rolling in inflamed venules. While the roles of P- and E-selectin in this process are well established, the mechanisms of L-selectin–mediated neutrophil recruitment remain elusive. One proposal is that tethering is mediated by L-selectin on flowing neutrophils interacting with P-selectin glycoprotein ligand-1 (PSGL-1) on adherent neutrophils. To clarify whether L-selectin–mediated neutrophil recruitment depends entirely on PSGL-1, we examined the impact of L-selectin deficiency in mice with a PSGL-1–deficient background. L-selectin and PSGL-1 double-knockout mice exhibited a higher increase in their peripheral blood neutrophil count and a worse defect in neutrophil recruitment into the inflamed peritoneum than PSGL-1–deficient mice. Intravital microscopy of inflamed cremaster muscle venules showed that L-selectindeficiency or antibody blockade of L-selectin reduced the residual leukocyte rolling in PSGL-1–deficient mice. Flow cytometric analyses showed that the endothelial cells from the cremaster muscle bound L-selectin in a PSGL-1–independent manner. These results provide evidence for the existence of an L-selectin ligand distinct from PSGL-1 in inflammation and indicate that such a ligand is expressed on endothelial cells, promoting neutrophil rolling in vivo.
Mll5 contributes to hematopoietic stem cell fitness and homeostasis
Authors: Zhang Yan , Wong Jasmine , Klinger Mark , Tran Mary T. , Shannon Kevin M. , Killeen Nigel 
Published: September 2008

Abstract
MLL5 is a novel trithorax group gene and a candidate tumor suppressor gene located within a 2.5-Mb interval of chromosome band 7q22 that frequently is deleted in human myeloid malignancy. Here we show that inactivation of the Mll5 gene in mice results in a 30% reduction in the average representation of hematopoietic stem cells and in functional impairment of long-term hematopoietic repopulation potential under competitive conditions. Bone marrow cells from Mll5-deficient mice were defective in spleen colony-forming assays, and the mutant mice showed enhanced susceptibility to 5-fluorouracil–induced myelosuppression. Heterozygous and homozygous Mll5 mutant mice did not spontaneously develop hematologic cancers, and loss of Mll5 did not alter the phenotype of a fatal myeloproliferative disorder induced by oncogenic Kras in vivo. Collectively, the data reveal an important role for Mll5 in HSC homeostasis and provide a basis for further studies to explore its role in leukemogenesis.
Aurora-A kinase: a novel target of cellular immunotherapy for leukemia
Authors: Ochi Toshiki , Fujiwara Hiroshi , Suemori Koichiro , Azuma Taichi , Yakushijin Yoshihiro , Hato Takaaki , Kuzushima Kiyotaka , Yasukawa Masaki 
Published: September 2008

Abstract
Aurora-A kinase (Aur-A) is a member of the serine/threonine kinase family that regulates the cell division process, and has recently been implicated in tumorigenesis. In this study, we identified an antigenic 9–amino-acid epitope (Aur-A207-215: YLILEYAPL) derived from Aur-A capable of generating leukemia-reactive cytotoxic T lymphocytes (CTLs) in the context of HLA-A*0201. The synthetic peptide of this epitope appeared to be capable of binding to HLA-A*2402 as well as HLA-A*0201 molecules. Leukemia cell lines and freshly isolated leukemia cells, particularly chronic myelogenous leukemia (CML) cells, appeared to express Aur-A abundantly. Aur-A–specific CTLs were able to lyse human leukemia cell lines and freshly isolated leukemia cells, but not normal cells, in an HLA-A*0201–restricted manner. Importantly, Aur-A–specific CTLs were able to lyse CD34+ CML progenitor cells but did not show any cytotoxicity against normal CD34+ hematopoietic stem cells. The tetramer assay revealed that the Aur-A207-215 epitope–specific CTL precursors are present in peripheral blood of HLA-A*0201–positive and HLA-A*2402–positive patients with leukemia, but not in healthy individuals. Our results indicate that cellular immunotherapy targeting Aur-A is a promising strategy for treatment of leukemia.
Mitochondrial oxidative phosphorylation in autosomal dominant optic atrophy
Authors: Mayorov Vladimir I , Lowrey Angela J , Biousse Valerie , Newman Nancy J , Cline Susan D , Brown Michael D 
Published: September 2008

Abstract

Background
Autosomal dominant optic atrophy (ADOA), a form of progressive bilateral blindness due to loss of retinal ganglion cells and optic nerve deterioration, arises predominantly from mutations in the nuclear gene for the mitochondrial GTPase, OPA1. OPA1 localizes to mitochondrial cristae in the inner membrane where electron transport chain complexes are enriched. While OPA1 has been characterized for its role in mitochondrial cristae structure and organelle fusion, possible effects of OPA1 on mitochondrial function have not been determined.

Results
Mitochondria from six ADOA patients bearing OPA1 mutations and ten ADOA patients with unidentified gene mutations were studied for respiratory capacity and electron transport complex function. Results suggest that the nuclear DNA mutations that give rise to ADOA in our patient population do not alter mitochondrial electron transport.

Conclusion
We conclude that the pathophysiology of ADOA likely stems from the role of OPA1 in mitochondrial structure or fusion and not from OPA1 support of oxidative phosphorylation.
Evidence for positive selection acting on microcystin synthetase adenylation domains in three cyanobacterial genera
Authors: Tooming-Klunderud Ave , Fewer David P , Rohrlack Thomas , Jokela Jouni , Rouhiainen Leo , Sivonen Kaarina , Kristensen Tom , Jakobsen Kjetill S 
Published: September 2008

Abstract

Background
Cyanobacteria produce a wealth of secondary metabolites, including the group of small cyclic heptapeptide hepatotoxins that constitutes the microcystin family. The enzyme complex that directs the biosynthesis of microcystin is encoded in a single large gene cluster (mcy). mcy genes have a widespread distribution among cyanobacteria and are likely to have an ancient origin. The notable diversity within some of the Mcy modules is generated through various recombination events including horizontal gene transfer.

Results
A comparative analysis of the adenylation domains from the first module of McyB (McyB1) and McyC in the microcystin synthetase complex was performed on a large number of microcystin-producing strains from the Anabaena, Microcystis and Planktothrix genera. We found no decisive evidence for recombination between strains from different genera. However, we detected frequent recombination events in the mcyB and mcyC genes between strains within the same genus. Frequent interdomain recombination events were also observed between mcyB and mcyC sequences in Anabaena and Microcystis. Recombination and mutation rate ratios suggest that the diversification of mcyB and mcyC genes is driven by recombination events as well as point mutations in all three genera. Sequence analysis suggests that generally the adenylation domains of the first domain of McyB and McyC are under purifying selection. However, we found clear evidence for positive selection acting on a number of amino acid residues within these adenylation domains. These include residues important for active site selectivity of the adenylation domain, strongly suggesting selection for novel microcystin variants.

Conclusion
We provide the first clear evidence for positive selection acting on amino acid residues involved directly in the recognition and activation of amino acids incorporated into microcystin, indicating that the microcystin complement of a given strain may influence the ability of a particular strain to interact with its environment.
Accelerated evolutionary rates in tropical and oceanic parmelioid lichens (Ascomycota)
Authors: Lumbsch H Thorsten , Hipp Andrew L , Divakar Pradeep K , Blanco Oscar , Crespo Ana 
Published: September 2008

Abstract

Background
The rate of nucleotide substitutions is not constant across the Tree of Life, and departures from a molecular clock have been commonly reported. Within parmelioid lichens, the largest group of macrolichens, large discrepancies in branch lengths between clades were found in previous studies. Using an extended taxon sampling, we test for presence of significant rate discrepancies within and between these clades and test our a priori hypothesis that such rate discrepancies may be explained by shifts in moisture regime or other environmental conditions.

Results
In this paper, the first statistical evidence for accelerated evolutionary rate in lichenized ascomycetes is presented. Our results give clear evidence for a faster rate of evolution in two Hypotrachyna clades that includes species occurring in tropical and oceanic habitats in comparison with clades consisting of species occurring in semi-arid and temperate habitats. Further we explore potential links between evolutionary rates and shifts in habitat by comparing alternative Ornstein-Uhlenbeck models.

Conclusion
Although there was only weak support for a shift at the base of a second tropical clade, where the observed nucleotide substitution rate is high, overall support for a shift in environmental conditions at cladogenesis is very strong. This suggests that speciation in some lichen clades has proceeded by dispersal into a novel environment, followed by radiation within that environment. We found moderate support for a shift in moisture regime at the base of one tropical clade and a clade occurring in semi-arid regions and a shift in minimum temperature at the base of a boreal-temperate clade.
Chromosomal evolution of the PKD1 gene family in primates
Authors: Kirsch Stefan , Pasantes Juanjo , Wolf Andreas , Bogdanova Nadia , Münch Claudia , Pennekamp Petra , Krawczak Michael , Dworniczak Bernd , Schempp Werner 
Published: September 2008

Abstract

Background
The autosomal dominant polycystic kidney disease (ADPKD) is mostly caused by mutations in the PKD1 (polycystic kidney disease 1) gene located in 16p13.3. Moreover, there are six pseudogenes of PKD1 that are located proximal to the master gene in 16p13.1. In contrast, no pseudogene could be detected in the mouse genome, only a single copy gene on chromosome 17. The question arises how the human situation originated phylogenetically. To address this question we applied comparative FISH-mapping of a human PKD1-containing genomic BAC clone and a PKD1-cDNA clone to chromosomes of a variety of primate species and the dog as a non-primate outgroup species.

Results
Comparative FISH with the PKD1-cDNA clone clearly shows that in all primate species studied distinct single signals map in subtelomeric chromosomal positions orthologous to the short arm of human chromosome 16 harbouring the master PKD1 gene. Only in human and African great apes, but not in orangutan, FISH with both BAC and cDNA clones reveals additional signal clusters located proximal of and clearly separated from the PKD1 master genes indicating the chromosomal position of PKD1 pseudogenes in 16p of these species, respectively. Indeed, this is in accordance with sequencing data in human, chimpanzee and orangutan. Apart from the master PKD1 gene, six pseudogenes are identified in both, human and chimpanzee, while only a single-copy gene is present in the whole-genome sequence of orangutan. The phylogenetic reconstruction of the PKD1-tree reveals that all human pseudogenes are closely related to the human PKD1 gene, and all chimpanzee pseudogenes are closely related to the chimpanzee PKD1 gene. However, our statistical analyses provide strong indication that gene conversion events may have occurred within the PKD1 family members of human and chimpanzee, respectively.

Conclusion

PKD1 must have undergone amplification very recently in hominid evolution. Duplicative transposition of the PKD1 gene and further amplification and evolution of the PKD1 pseudogenes may have arisen in a common ancestor of Homo, Pan and Gorilla ~8 MYA. Reticulate evolutionary processes such as gene conversion and non-allelic homologous recombination (NAHR) may have resulted in concerted evolution of PKD1 family members in human and chimpanzee and, thus, simulate an independent evolution of the PKD1 pseudogenes from their master PKD1 genes in human and chimpanzee.
Heat stress-responsive transcriptome analysis in heat susceptible and tolerant wheat (Triticum aestivum L.) by using Wheat Genome Array
Authors: Qin Dandan , Wu Haiyan , Peng Huiru , Yao Yingyin , Ni Zhongfu , Li Zhenxing , Zhou Chunlei , Sun Qixin 
Published: September 2008

AbstractBackgroundWheat is a major crop in the world, and the high temperature stress can reduce the yield of wheat by as much as 15%. The molecular changes in response to heat stress are poorly understood. Using GeneChip®Wheat Genome Array, we analyzed genome-wide gene expression profiles in the leaves of two wheat genotypes, namely, heat susceptible 'Chinese Spring' (CS) and heat tolerant 'TAM107' (TAM).ResultsA total of 6560 (~10.7%) probe sets displayed 2-fold or more changes in expression in at least one heat treatment (falsediscoveryrate, FDR, α = 0.001). Except for heat shock protein (HSP) and heat shock factor (HSF) genes, these putative heat responsive genes encode transcription factors and proteins involved in phytohormone biosynthesis/signaling, calcium and sugar signal pathways, RNA metabolism, ribosomal proteins, primary and secondary metabolisms, as well as proteins related to other stresses. A total of 313 probe sets were differentially expressed between the two genotypes, which could be responsible for the difference in heat tolerance of the two genotypes. Moreover, 1314 were differentially expressed between the heat treatments with and without pre-acclimation, and 4533 were differentially expressed between short and prolonged heat treatments.ConclusionThe differences in heat tolerance in different wheat genotypes may be associated with multiple processes and mechanisms involving HSPs, transcription factors, and other stress related genes. Heat acclimation has little effects on gene expression under prolonged treatments but affects gene expression in wheat under short-term heat stress. The heat stress responsive genes identified in this study will facilitate our understanding of molecular basis for heat tolerance in different wheat genotypes and future improvement of heat tolerance in wheat and other cereals.