bluuebunny/crossref_metadata_2025_split huggingface dataset:
Geoarchaeological studies in Nara, Japan: The integrated findings
Authors: Barnes Gina L. , Nishida Shiro , Okita Masaaki 
Published: November 2005

AbstractIn this article, the authors summarize 20 years of scholarship and two field projects on geoarchaeology in Nara, Japan, carried out by researchers from 12 different institutions in 4 countries. The research goal was to test an aerial photographic reconstruction of surface landforms in the Nara Basin with subsurface data. Project A was conducted at Asawa; it tested, through geological coring, whether a suspected swampy backmarsh in the eastern basin existed and whether it would yield data on the transition to wet rice agriculture in the mid‐1st millennium B.C. Project B was conducted at Miwa; it tested, through geological coring and subsequent excavation, the nature of upland agricultural terrace formation in the southeastern basin and whether the suspected existence of a 4th‐century palace site could be confirmed.Two layers of carbonaceous clay at Asawa were dated to the Early (˜5000–3500 B.C.) and Final (˜1000‐300 B.C.) phases of the Jomon period. Pollen data revealed the establishment of an evergreen oak forest from 5,000 years ago and anthropogenic changes in forest cover from 2,000 years ago. Phytoliths from rice, millets, reeds, and bamboo were recovered in layers postdating the Final Jomon carbonaceous clay. A fault scarp with anthropogenic modification of the terraces was identified at Miwa. It was discovered that an incised stream valley had been infilled in the Medieval period at the same time surface layers were razed; the front of the terrace was extended in the premodern period. Remains were recovered from the Middle Yayoi (˜100 B.C.–A.D. 100) and the Medieval (˜A.D. 1185–1603) periods. However, as the terracing involved razing the early historic levels, no data were recovered on the alleged 4th‐century palace site.The significance of these findings lies in the identification of (a) a swampy backmarsh at Asawa, where initial agricultural efforts in growing wet rice in the basin may have occurred, confirming the aerial photographic reconstruction; and (b) hillside terracing activities at Miwa, from the Medieval period onwards, which have radically changed the configuration of the natural topography. © 2005 Wiley Periodicals, Inc.
Generation of a conditional allele of the B‐myb gene
Authors: García Paloma , Berlanga Oscar , Watson Roger , Frampton Jon 
Published: November 2005

AbstractB‐Myb is an essential transcription factor involved in control of the cell cycle and the regulation of tissue‐specific gene expression in a wide range of cell types. Loss of both alleles results in early embryonic lethality at E4.5–6.5. To address the function of B‐Myb in later stages of embryogenesis and in specific adult tissues, a floxed B‐myb allele (B‐mybF) was generated. Cre‐mediated deletion in vivo was demonstrated by breeding with a transgenic GATA‐Cre mouse line. An intermediate allele produced in the creation of the floxed allele, in which the PGK‐neoR cassette is present in intron 3 (B‐mybloxneo), was deduced to be a weak hypomorph based on the later embryonic death of homozygotes compared to B‐myb−/− embryos. To demonstrate the efficiency and possible consequences of B‐myb inactivation, we performed conditional deletion in cultured MEFs and observed decreased growth that correlated with aberrant nuclear DNA replication. genesis 43:189–195, 2005. © 2005 Wiley‐Liss, Inc.
Protection of corticospinal tract neurons after dorsal spinal cord transection and engraftment of olfactory ensheathing cells
Authors: Sasaki Masanori , Hains Bryan C. , Lankford Karen L. , Waxman Stephen G. , Kocsis Jeffery D. 
Published: November 2005

AbstractTransplantation of olfactory ensheathing cells (OECs) into the damaged rat spinal cord leads to directed elongative axonal regeneration and improved functional outcome. OECs are known to produce a number of neurotrophic molecules. To explore the possibility that OECs are neuroprotective for injured corticospinal tract (CST) neurons, we transplanted OECs into the dorsal transected spinal cord (T9) and examined primary motor cortex (M1) to assess apoptosis and neuronal loss at 1 and 4 weeks post‐transplantation. The number of apoptotic cortical neurons was reduced at 1 week, and the extent of neuronal loss was reduced at 4 weeks. Biochemical analysis indicated an increase in BDNF levels in the spinal cord injury zone after OEC transplantation at 1 week. The transplanted OECs associated longitudinally with axons at 4 weeks. Thus, OEC transplantation into the injured spinal cord has distant neuroprotective effects on descending cortical projection neurons. © 2005 Wiley‐Liss, Inc.
Human attachment security is mediated by the amygdala: Evidence from combined fMRI and psychophysiological measures
Authors: Lemche Erwin , Giampietro Vincent P. , Surguladze Simon A. , Amaro Edson J. , Andrew Christopher M. , Williams Steven C.R. , Brammer Michael J. , Lawrence Natalia , Maier Markus A. , Russell Tamara A. , Simmons Andrew , Ecker Christine , Joraschky Peter , Phillips Mary L. 
Published: November 2005

AbstractThe neural basis of human attachment security remains unexamined. Using event‐related functional magnetic resonance imaging (fMRI) and simultaneous recordings of skin conductance levels, we measured neural and autonomic responses in healthy adult individuals during a semantic conceptual priming task measuring human attachment security “by proxy”. Performance during a stress but not a neutral prime condition was associated with response in bilateral amygdalae. Furthermore, levels of activity within bilateral amygdalae were highly positively correlated with attachment insecurity and autonomic response during the stress prime condition. We thereby demonstrate a key role of the amygdala in mediating autonomic activity associated with human attachment insecurity. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.
Neural bases of categorization of simple speech and nonspeech sounds
Authors: Husain Fatima T. , Fromm Stephen J. , Pursley Randall H. , Hosey Lara A. , Braun Allen R. , Horwitz Barry 
Published: November 2005

AbstractCategorization is fundamental to our perception and understanding of the environment. However, little is known about the neural bases underlying the categorization of sounds. Using human functional magnetic resonance imaging (fMRI) we compared the brain responses to a category discrimination task with an auditory discrimination task using identical sets of sounds. Our stimuli differed along two dimensions: a speech–nonspeech dimension and a fast–slow temporal dynamics dimension. All stimuli activated regions in the primary and nonprimary auditory cortices in the temporal cortex and in the parietal and frontal cortices for the two tasks. When comparing the activation patterns for the category discrimination task to those for the auditory discrimination task, the results show that a core group of regions beyond the auditory cortices, including inferior and middle frontal gyri, dorsomedial frontal gyrus, and intraparietal sulcus, were preferentially activated for familiar speech categories and for novel nonspeech categories. These regions have been shown to play a role in working memory tasks by a number of studies. Additionally, the categorization of nonspeech sounds activated left middle frontal gyrus and right parietal cortex to a greater extent than did the categorization of speech sounds. Processing the temporal aspects of the stimuli had a greater impact on the left lateralization of the categorization network than did other factors, particularly in the inferior frontal gyrus, suggesting that there is no inherent left hemisphere advantage in the categorical processing of speech stimuli, or for the categorization task itself. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.
Protective mechanisms of head and neck squamous cell carcinomas from immune assault
Authors: Young M. Rita I. 
Published: November 2005

AbstractHead and neck squamous cell carcinoma (HNSCC) is an aggressive malignancy that is the sixth most common neoplasm in the world. Despite advances in treatments involving surgery, radiation, and chemotherapy, the 5‐year survival has remained at less than 50% for the past 30 years, primarily because of local recurrences. Thus, the possibility of immunotherapeutic approaches for patients with HNSCC has gained interest. Unfortunately, patients with HNSCC have profound immune defects that are associated with increased recurrence. This review aims to provide an overview of both the defensive and immune subversive mechanisms by which patients with HNSCC can protect themselves from immune antitumor assault. © 2005 Wiley Periodicals, Inc. Head Neck 27: 462–470, 2006
Risk of malignancy in Filipinos with thyroid nodules—A matched pair analysis
Authors: Clark Jonathan R. , Eski Spiro J. , Freeman Jeremy L. 
Published: November 2005

AbstractBackground.Ethnicity is an infrequently cited risk factor for thyroid cancer. This study aims to determine whether patients of Filipino origin assessed at a tertiary referral center are at increased risk of thyroid cancer and to quantify that risk.Methods.This is a retrospective analysis of 72 Filipino patients with thyroid nodules undergoing thyroidectomy individually matched to 72 controls according to demographics, risk factors, and pre‐referral investigations.Results.Thyroid cancer was found in 50 (69.4%) Filipino patients compared with 28 (38.9%) controls. Odds ratio for malignancy in Filipinos was 3.57 (95% confidence interval, 1.79–7.12). Pathologic characteristics of thyroid cancer were not significantly different in the two groups. The median follow‐up for Filipino patients was 14.1 months (range, 1.4 months–19.7 years). Recurrence occurred in four Filipino patients, and one patient with anaplastic thyroid cancer died of the disease.Conclusions.Filipino patients with thyroid nodules are at significantly increased risk of thyroid cancer compared with matched controls, and hence the index of suspicion for malignancy should be high when evaluating these patients. © 2005 Wiley Periodicals, Inc. Head Neck 27: 427–431, 2006
Does cognitive function influence alaryngeal speech rehabilitation?
Authors: Ho T. P. , Gray J. , Ratcliffe A. A. , Rees S. , Rockey J. , Wight R. G. 
Published: November 2005

AbstractBackground.We sought to define the cognitive domains that influence valved speech rehabilitation.Methods.Sixteen laryngectomees with primary tracheoesophageal punctures were randomly recruited from one head and neck unit. They were assessed by a consultant neuropsychologist and a speech therapist. Speech therapy time was determined from speech therapy notes.Results.The Digit Symbol Substitution Test, assessing learning speed and processing speed, correlated significantly with speech therapy time in the first (p = .002) and third (p = .014) postoperative years, respectively. Categorical fluency assessment correlated positively with speech therapy time in the first year (p = .009). Learning speed (p = .007) and categorical fluency (p = .041) correlated positively with the fall in speech therapy input between the first and third year after laryngectomy.Conclusions.Learning speed, processing speed, and categorical fluency strongly influence alaryngeal speech rehabilitation. This study highlights the potential for pre‐laryngectomy cognitive assessment to help plan alaryngeal speech rehabilitation. This has significant resource implications. © 2005 Wiley Periodicals, Inc. Head Neck 27: 413–419, 2006
Acute myeloid leukemia with concurrent myeloid sarcoma treated with autologous bone marrow transplantation: two illustrative cases and a literature review
Authors: Finnegan DPJ , Jones FGC , McMullin MF 
Published: November 2005

AbstractMyeloid sarcoma (MS) is an invasive extramedullary solid tumor composed of immature cells of the myeloid series. It complicates the clinical course of a minority of patients with acute myeloid leukemia (AML). Traditionally its presence has been regarded as an indicator of aggressive disease. Currently, the optimal treatment of AML with concurrent MS remains to be determined. We report two cases of autologous bone marrow transplantation (auto‐BMT) for AML with concurrent MS followed by a review of the literature. Copyright © 2005 John Wiley & Sons, Ltd.
Biallelic deletion within 16p13.13 including SOCS‐1 in Karpas1106P mediastinal B‐cell lymphoma line is associated with delayed degradation of JAK2 protein
Authors: Melzner Ingo , Weniger Marc A. , Bucur Alexandra J. , Brüderlein Silke , Dorsch Karola , Hasel Cornelia , Leithäuser Frank , Ritz Olga , Dyer Martin J.S. , Barth Thomas F.E. , Möller Peter 
Published: November 2005

AbstractActivity of Janus kinase 2 (JAK2) in the JAK2/STAT5 signaling pathway is critically controlled by suppressor of cytokine signaling‐1 (SOCS‐1). We have previously shown that SOCS‐1 is biallelically mutated in the primary mediastinal B‐cell lymphoma (PMBL) cell line MedB‐1, resulting in impaired JAK2 degradation and sustained phospho‐JAK2 action. SOCS‐1 is frequently mutated in PMBL tumor primaries. Here, we report that the PMBL cell line Karpas1106P has a biallelic deletion of the SOCS‐1 region on chromosome 16p13.13. By fluorescence in situ hybridization and microsatellite analysis, this deletion was narrowed down to a range of 650 kb to 1.48 Mb. Like MedB‐1, Karpas1106P harbors gains of the JAK2 gene on chromosomal region 9p24 and elevated levels of JAK2 mRNA. Nevertheless, JAK2 protein was not increased but constitutively phosphorylated in Karpas1106P cells. In analogy to MedB‐1 cells, Karpas1106P cells exhibited a retarded degradation of de novo synthesized JAK2 protein revealed by pulse/chase experiments. Therefore, we conclude that loss of SOCS‐1 function either by mutation or by the complete deletion of the gene plays an important role in the dysregulation of JAK/STAT signaling in Karpas1106P and PMBL. © 2005 Wiley‐Liss, Inc.
Circulating EM66 is a highly sensitive marker for the diagnosis and follow‐up of pheochromocytoma
Authors: Guillemot Johann , Anouar Youssef , Montero‐Hadjadje Maïté , Grouzmann Eric , Grumolato Luca , Roshmaninho‐Salgado Joana , Turquier Valérie , Duparc Céline , Lefebvre Hervé , Plouin Pierre‐François , Klein Marc , Muresan Mihaela , Chow Billy K.C. , Vaudry Hubert , Yon Laurent 
Published: November 2005

AbstractWe have previously demonstrated that measurement of tissue concentration of the novel secretogranin II‐derived peptide EM66 may help to discriminate between benign and malignant pheochromocytomas. The aim of the present study was to characterize EM66 in plasma and urine of healthy volunteers and pheochromocytoma patients, in order to further evaluate the usefulness of this peptide as a circulating marker for the management of the tumors. HPLC analysis of plasma and urine samples demonstrated that the EM66‐immunoreactive material coeluted with the recombinant peptide. In healthy volunteers, plasma and urinary EM66 levels were, respectively, 2.6 (1.9–3.7) ng/ml and 2.9 (1.9–4.6) ng/ml. In patients with pheochromocytoma, plasma EM66 levels were 10‐fold higher than those of healthy volunteers (26.9 (7.3–44) ng/ml), and returned to normal values after removal of the tumor. In contrast, urinary EM66 levels were not significantly different from those of healthy volunteers (3.2 (2.2–3.9) ng/ml). Measurement of total or free plasma metanephrines and 24 hr urinary metanephrines in our series of patients revealed that these tests, taken separately, are less sensitive than the EM66 determination. Pheochromocytes in primary culture secreted high levels of EM66, suggesting that the chromaffin tumor was actually responsible for the increased plasma peptide concentrations in the patients. These data indicate that EM66 is secreted in the general circulation and that elevated plasma EM66 levels are correlated with the occurrence of pheochromocytoma. Thus, EM66 is a sensitive plasma marker that should be considered as a complementary tool in the management of pheochromocytoma. © 2005 Wiley‐Liss, Inc.
Dominant‐negative Rac increases both inherent and ionizing radiation‐induced cell migration in C6 rat glioma cells
Authors: Hwang So‐Young , Jung Jae‐Won , Jeong Jae‐Seob , Kim Yun‐Jung , Oh Eok‐Soo , Kim Tae‐Hyun , Kim Joo‐Young , Cho Kwan‐Ho , Han Inn‐Oc 
Published: November 2005

AbstractRho‐like GTPases, including Cdc42, Rac1 and RhoA, regulate distinct actin cytoskeleton changes required for cell adhesion, migration and invasion. In the present study, we examined the role of Rac signaling in inherent migration, as well as radiation‐induced migration, of rat glioma cells. Stable overexpression of dominant‐negative Rac1N17 in a C6 rat glioma cell line (C6‐RacN17) promoted cell migration, and ionizing radiation further increased this migration. Migration was accompanied by decreased expression of the focal adhesion molecules FAK and paxillin. Focal contacts and actin stress fibers were also reduced in C6‐RacN17 cells. Downstream effectors of Rac include JNK and p38 MAP kinases. Irradiation transiently activated p38, JNK and ERK1/2 MAP kinases in C6‐RacN17 cells, while p38 and JNK were constitutively activated in C6 control cells. Blocking JNK activity with JNK inhibitor SP600125 inhibited migration, suggesting that the JNK pathway may regulate radiation‐induced, as well as inherent, migration of C6‐RacN17 cells. Additionally, the radiation‐induced migration increase was also inhibited by SB203580, a specific inhibitor of p38 MAP kinase. However, PD98059, a MEK kinase 1 inhibitor, failed to influence migration. This is the first evidence that suppression of Rac signaling may be involved in invasion or metastasis of glioma cells before and/or after radiotherapy. These data further suggest that radiotherapy for malignant glioma needs to be used with caution because of the potential for therapy‐induced cell migration or invasion and that pharmacological inhibition of cell migration and invasion through targeting the Rac signaling pathway may represent a new approach for improving the therapeutic efficacy of radiotherapy for malignant glioma. © 2005 Wiley‐Liss, Inc.
Mantle cell lymphomas acquire increased expression of CCL4, CCL5 and 4‐1BB‐L implicated in cell survival
Authors: Ek Sara , Björck Erik , Högerkorp Carl‐Magnus , Nordenskjöld Magnus , Porwit‐MacDonald Anna , Borrebaeck Carl A.K. 
Published: November 2005

AbstractWe have analyzed mantle cell lymphomas (MCLs), using high‐density DNA microarrays, and confirmed the expression of differentially regulated antigens, using flow cytometry and immunohistochemistry. The results show that MCLs acquire expression of molecules that normally are involved in interaction with other immune cells and, thus, might affect the ability of the tumor to survive. The MCL signature is represented by the overexpression of the chemokine CCL4 (MIP‐1β), implicated in the recruitment of regulatory T cells, as well as CCL5 and 4‐1BB‐L. The latter molecules are normally involved in chemotaxis of T cells and B cell activation, respectively. Signaling through 4‐1BB‐L allows B cells to proliferate and the expression of its ligand, by the intra‐tumoral mesh of follicular dendritic cells (FDC), could thus serve as a paracrine loop facilitating growth and survival of MCL cells. © 2005 Wiley‐Liss, Inc.
Molecular profiling of platinum resistant ovarian cancer
Authors: Helleman Jozien , Jansen Maurice P.H.M. , Span Paul N. , van Staveren Iris L. , Massuger Leon F.A.G. , Meijer‐van Gelder Marion E. , Sweep Fred C.G.J. , Ewing Patricia C. , van der Burg Maria E.L. , Stoter Gerrit , Nooter Kees , Berns Els M.J.J. 
Published: November 2005

AbstractThe aim of this study is to discover a gene set that can predict resistance to platinum‐based chemotherapy in ovarian cancer. The study was performed on 96 primary ovarian adenocarcinoma specimens from 2 hospitals all treated with platinum‐based chemotherapy. In our search for genes, 24 specimens of the discovery set (5 nonresponders and 19 responders) were profiled in duplicate with 18K cDNA microarrays. Confirmation was done using quantitative RT‐PCR on 72 independent specimens (9 nonresponders and 63 responders). Sixty‐nine genes were differentially expressed between the nonresponders (n = 5) and the responders (n = 19) in the discovery phase. An algorithm was constructed to identify predictive genes in this discovery set. This resulted in 9 genes (FN1, TOP2A, LBR, ASS, COL3A1, STK6, SGPP1, ITGAE, PCNA), which were confirmed with qRT‐PCR. This gene set predicted platinum resistance in an independent validation set of 72 tumours with a sensitivity of 89% (95% CI: 0.68–1.09) and a specificity of 59% (95% CI: 0.47–0.71)(OR = 0.09, p = 0.026). Multivariable analysis including patient and tumour characteristics demonstrated that this set of 9 genes is independent for the prediction of resistance (p < 0.01). The findings of this study are the discovery of a gene signature that classifies the tumours, according to their response, and a 9‐gene set that determines resistance in an independent validation set that outperforms patient and tumour characteristics. A larger independent multicentre study should further confirm whether this 9‐gene set can identify the patients who will not respond to platinum‐based chemotherapy and could benefit from other therapies. © 2005 Wiley‐Liss, Inc.
Diabetes mellitus and cancer risk in a population‐based case–controlstudy among men from Montreal, Canada
Authors: Rousseau Marie‐Claude , Parent Marie‐Élise , Pollak Michael N. , Siemiatycki Jack 
Published: November 2005

AbstractDiabetics may have a higher risk of cancer, notably liver and pancreatic cancers. Evidence about other cancer types remains sparse. The authors examined potential associations between diabetes and several types of cancer in a large multicancer case–control project carried out in Montreal, Canada, in the 1980s. This report, based on 3,107 male cancer cases and 509 population controls, uses information on diabetes and several covariates collected by interview. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) were estimated for the associations between diabetes and each of 12 cancer types. Risks of pancreatic and liver cancers were increased among diabetics: adjusted ORs were 2.1 (95% CI: 1.0, 4.3) for pancreatic and 3.1 (95% CI: 1.1, 8.8) for liver cancer. The increased risk of pancreatic cancer was completely restricted to those with recent onset of diabetes; this was likely a manifestation of reverse causality. Conversely, the increased risk of liver cancer was independent of the interval between diabetes and cancer diagnoses. No associations were observed with melanoma, non‐Hodgkin's lymphoma, cancers of the esophagus, stomach, colon, rectum, lung, prostate, bladder and kidney. In conclusion, diabetes was associated with an increased risk of liver cancer among men, but with no other cancer type including pancreatic cancer. © 2005 Wiley‐Liss, Inc.