bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epigenetic salt accumulation and water movement in the active layer of central Yakutia in eastern Siberia
Authors: Lopez C. M. Larry , Brouchkov A. , Nakayama H. , Takakai F. , Fedorov A. N. , Fukuda M. 
Published: September 2006

AbstractObservations of soil moisture and salt content were conducted from May to August at Neleger station in eastern Siberia. Seasonal changes of salt and soil moisture distribution in the active layer of larch forest (undisturbed) and a thermokarst depression known as an alas (disturbed) were studied. Electric conductivity ECeof the intact forest revealed higher concentrations that increased with depth from the soil surface into the active layer and the underlying permafrost: 1 mS cm−1at 1·1 m, to 2·6 mS cm−1at 160 cm depth in the permafrost. However, a maximum value of 5·4 mS cm−1at 0·6 m depth was found in the dry area of the alas. The concentration of ions, especially Na+, Mg2+, Ca2+, SO42−and HCO3−in the upper layers of this long‐term disturbed site, indicates the upward movement of ions together with water. A higher concentration of solutes was found in profiles with deeper seasonal thawing. The accumulation of salts in the alas occurs from spring through into the growing season. The low concentration of salt in the surface soil layers appears to be linked to leaching of salts by rainfall. There are substantial differences between water content and electric conductivity of soil in the forest and alas. Modern salinization of the active layer in the alas is epigenetic, and it happens in summer as a result of spring water collection and high summer evaporation; the gradual salt accumulation in the alas in comparison with the forest is controlled by the annual balance of water and salts in the active layer. Present climatic trends point to continuous permafrost degradation in eastern Siberia increasing the risk of surface salinization, which has already contributed to changing the landscape by hindering the growth of forest. Copyright © 2006 John Wiley & Sons, Ltd.
Effect of bedrock permeability on subsurface stormflow and the water balance of a trenched hillslope at the Panola Mountain Research Watershed, Georgia, USA
Authors: Tromp‐van Meerveld H. J. , Peters N. E. , McDonnell J. J. 
Published: September 2006

AbstractThe effect of bedrock permeability on subsurface stormflow initiation and the hillslope water balance is poorly understood. Previous hillslope hydrological studies at the Panola Mountain Research Watershed (PMRW), Georgia, USA, have assumed that the bedrock underlying the trenched hillslope is effectively impermeable. This paper presents a series of sprinkling experiments where we test the bedrock impermeability hypothesis at the PMRW. Specifically, we quantify the bedrock permeability effects on hillslope subsurface stormflow generation and the hillslope water balance at the PMRW. Five sprinkling experiments were performed by applying 882–1676 mm of rainfall over a ∼5·5 m × 12 m area on the lower hillslope during ∼8 days. In addition to water input and output captured at the trench, we measured transpiration in 14 trees on the slope to close the water balance. Of the 193 mm day−1 applied during the later part of the sprinkling experiments when soil moisture changes were small, <14 mm day−1 was collected at the trench and <4 mm day−1 was transpired by the trees, with residual bedrock leakage of >175 mm day−1 (91%). Bedrock moisture was measured at three locations downslope of the water collection system in the trench. Bedrock moisture responded quickly to precipitation in early spring. Peak tracer breakthrough in response to natural precipitation in the bedrock downslope from the trench was delayed only 2 days relative to peak tracer arrival in subsurface stormflow at the trench. Leakage to bedrock influences subsurface stormflow at the storm time‐scale and also the water balance of the hillslope. This has important implications for the age and geochemistry of the water and thus how one models this hillslope and watershed. Copyright © 2006 John Wiley & Sons, Ltd.
Evolution study of a regional groundwater system using hydrochemistry and stable isotopes in Songnen Plain, northeast China
Authors: Zhang Guangxin , Deng Wei , Yang Y. S. , Salama R. B. 
Published: September 2006

AbstractGroundwater is often a critical source of water for municipal, industrial and agricultural uses, especially in arid and semi‐arid environments. Songnen Plain, located in the central part of northeast China, is such a region, it being an important productive base of commodity grain in this country. In the past two decades, groundwater quality in the region, especially salinization, has deteriorated under natural changes and human activities, and has become a crucial factor restricting sustainable eco‐environmental and socio‐economic development. In this paper, The Taoer River catchment, situated in the middle of the region, was selected as the study area for the groundwater quality evolution study using hydrochemistry and stable isotopes to obtain a better understanding of the system. Fifty‐two groundwater samples were collected with systematic design during the low‐water and high‐water periods in 2003. A series of comprehensive quality data interpretations, e.g. statistics, ratios of ions and Piper diagrams, together with stable isotope data, have been used to gain an insight into the spatial and temporal variations and evolution laws of groundwater hydrochemistry. The following main hydrochemical processes were identified as controlling the water quality of the groundwater system: weathering–dissolution, evaporation–condensation, ion‐exchange reactions and groundwater salinization. This latter process, salinization, is the most important process and is caused by the leaching of superficial or near‐surface salts from the saline–alkaline soil into shallow groundwater. Copyright © 2006 John Wiley & Sons, Ltd.
Comparison analysis of the summer monsoon precipitation between northern and southern slopes of Tanggula Mountains, Qinghai–Xizang (Tibetan) Plateau: a case study in summer 1998
Authors: Yang Meixue , Yao Tandong , Gou Xiaohua , Wang Huijun , Hao Lisheng 
Published: September 2006

AbstractBased on the precipitation data obtained through GEWEX Asian Monsoon Experiment–Tibet fieldwork from May to September 1998, this study investigated the features of the summer monsoon precipitation on the northern and southern slopes of the huge Tanggula Mountains in the Qinghai–Xizang (Tibetan) Plateau. The results show that the precipitation on the southern slope is about 50% higher than on the northern slope, whereas the frequency and diurnal pattern of the precipitation are very similar. The mean precipitation intensity on the southern slope is larger than on the northern slope. In most cases, the daily precipitation showed similar variation on both slopes, demonstrating that the precipitation processes might be similar. In the summer monsoon period, the local convective precipitation contributed to the total precipitation on both slopes and such a contribution on the southern slope is larger. Copyright © 2006 John Wiley & Sons, Ltd.
Tumor–stromal cell interaction under hypoxia increases the invasiveness of pancreatic cancer cells through the hepatocyte growth factor/c‐Met pathway
Authors: Ide Takao , Kitajima Yoshihiko , Miyoshi Atsushi , Ohtsuka Takao , Mitsuno Mayumi , Ohtaka Kazuma , Koga Yasuo , Miyazaki Kohji 
Published: September 2006

AbstractThe hypoxic environment in tumor is reported to play an important role in pancreatic cancer progression. The interaction between stromal and cancer cells also contributes to the malignant behavior of pancreatic cancer. In the present study, we investigated whether hypoxic stimulation affects stromal as well as pancreatic cancer cells. Our findings demonstrated that hypoxia remarkably elevated the HIF‐1α expression in both pancreatic cancer (PK8) and fibroblast cells (MRC5). Hypoxic stimulation accelerated the invasive activity of PK8 cells, and invasiveness was thus further accelerated when the hypoxic PK8 cells were cultured with conditioned medium prepared from hypoxic MRC5 cells (hypoxic conditioned medium). MMP‐2, MMP‐7, MT1‐MMP and c‐Met expressions were increased in PK8 cells under hypoxia. Hypoxic stimulation also increased the hepatocyte growth factor (HGF) secretion from MRC5 cells, which led to an elevation of c‐Met phosphorylation in PK8 cells. Conversely, the elevated cancer invasion, MMP activity and c‐Met phosphorylation of PK8 cells were reduced by the removal of HGF from hypoxic conditioned medium. In immunohistochemical study, the HIF‐1α expression was observed in surrounding stromal as well as pancreatic cancer cells, thus indicating hypoxia exists in both of cancer and stromal cells. Moreover, the stromal HGF expression was found to significantly correlate with not only the stromal HIF‐1α expression but also the c‐Met expression in cancer cells. These results indicate that the hypoxic environment within stromal as well as cancer cells activates the HGF/c‐Met system, thereby contributing to the aggressive invasive features of pancreatic cancer. © 2006 Wiley‐Liss, Inc.
Use of hormone replacement therapy before and after ovarian cancer diagnosis and ovarian cancer survival
Authors: Mascarenhas Chantal , Lambe Mats , Bellocco Rino , Bergfeldt Kjell , Riman Tomas , Persson Ingemar , Weiderpass Elisabete 
Published: September 2006

AbstractUse of hormone replacement therapy (HRT) has been hypothesized to affect survival of epithelial ovarian cancer (EOC). We studied 5‐year survival in patients with invasive EOC and borderline ovarian tumors (BOT) according to HRT use before and after diagnosis in a prospective nation‐wide cohort study of 799 women diagnosed with EOC (n = 649) and BOT (n = 150) aged 50–74 years in 1993–1995 in Sweden. Cox regression was used to obtain multivariate age‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Multivariate models included indicator variables for age, tumor stage, grade and histological subtype. After 5 years of follow‐up, 45% of the patients with EOC and 93% of the patients with BOT were alive. For women with BOT there were no associations between HRT‐use pre‐ or postdiagnosis and survival. There was no overall difference in 5‐year EOC survival according to use HRT before diagnosis (multivariate HR = 0.83, 95% CI = 0.65–1.08), except for serous EOC (HR = 0.69, 95% CI = 0.48–0.98). Analyses of different HRT preparations, duration and recency of use did not reveal any variations in pattern of survival. We observed a better survival for EOC‐patients who used HRT after diagnosis (multivariate HR = 0.57, 95% CI = 0.42–0.78). We conclude that HRT‐use prior to diagnosis of EOC does not affect 5‐year survival, except for a possible survival advantage in serous EOC. Women using HRT after diagnosis had a better survival than women with no use, but we cannot rule out that this latter finding may reflect a subtle selection process. © 2006 Wiley‐Liss, Inc.
Soluble N‐cadherin in human biological fluids
Authors: Derycke Lara , De Wever Olivier , Stove Veronique , Vanhoecke Barbara , Delanghe Joris , Depypere Herman , Bracke Marc 
Published: September 2006

AbstractClassical cadherins such as E‐, P‐ and N‐cadherin are transmembrane proteins that mediate cell–cell adhesion, and are important in embryogenesis, maintenance of tissue integrity and cancer. Proteolytic shedding of the extracellular domain results in the generation of soluble E‐, P‐ or N‐cadherin ectodomains. Circulating soluble E‐ and P‐cadherin have been described in the serum, and elevated levels were detected in cancer patients when compared with healthy persons. Here we report the presence of soluble N‐cadherin, a 90‐kD protein fragment, in the serum of both healthy persons and cancer patients, using a direct ELISA and immunoprecipitation. A correlation was found between prostate specific antigen and soluble N‐cadherin, and significantly elevated levels were detected in prostate cancer follow‐up patients. The N‐cadherin protein is neo‐expressed by carcinomas of the prostate, and is responsible for epithelial to fibroblastic transition. This is reflected by the higher concentrations of soluble N‐cadherin in prostate cancer patients than in healthy persons. © 2006 Wiley‐Liss, Inc.
Increased frequencies of CD8+ T lymphocytes recognizing wild‐type p53‐derived epitopes in peripheral blood correlate with presence of epitope loss tumor variants in patients with hepatocellular carcinoma
Authors: Cicinnati Vito R. , Zhang Xia , Yu Zhengya , Ferencik Stanislav , Schmitz Klaus J. , Dworacki Grzegorz , Kaczmarek Elzbieta , Oldhafer Karl , Frilling Andrea , Baba Hideo A. , Schmid Kurt W. , Grosse‐Wilde Hans , Broelsch Christoph E. , DeLeo Albert B. , Gerken Guido , Beckebaum Susanne 
Published: September 2006

AbstractWild‐type (WT) sequence p53 peptides are attractive candidates for broadly applicable cancer vaccines. The aim of this study was to evaluate the potential of a WT p53‐based immunotherapeutic approach for patients with hepatocellular carcinoma (HCC). Circulating CD8+ T cells specific for WT p53149–157 and WT p53264–272 HLA‐A*0201 restricted epitopes were directly identified in the peripheral blood by the use of peptide/HLA‐A2.1 tetramers in 24 HCC patients. Cytotoxic T lymphocyte (CTL) activity after WT p53 peptide‐specific stimulation was assessed by analysis of granzyme B and interferon‐gamma mRNA transcription, using a quantitative real‐time polymerase chain reaction assay. Tumor immunophenotyping was performed to evaluate the p53 status, the expression of major histocompatibility complex (MHC) and costimulatory molecules in freshly isolated tumor cells. HCC patients exhibited significantly higher frequencies of WT p53‐specific memory CD8+ T cells and stronger WT p53‐specific CTL activity, when compared with healthy controls. Increased frequencies of p53‐specific CD8+ T cells and their activity correlated with selective HLA‐A2 allele loss and reduced costimulatory molecule expression of tumor cells. Moreover, augmented numbers of p53‐specific T cells coincided with high MHC class II expression in tumor cells but were inversely related to the T status of the tumor node metastasis staging system. Our results indicate the existence of natural immunosurveillance and tumor immune evasion, involving a T cell response against WT p53 tumor antigen in patients with HCC. These findings may have important implications for the future development of cancer vaccines. © 2006 Wiley‐Liss, Inc.
Differential expression and activation of NF‐κB family proteins during oral carcinogenesis: Role of high risk human papillomavirus infection
Authors: Mishra Alok , Bharti Alok C. , Varghese Prishla , Saluja Daman , Das Bhudev C. 
Published: September 2006

AbstractOral cancer is one of the most common cancers in India and south‐east Asian region consisting of more than 50% of all malignant tumors. Along with many known risk factors, infection of Human Papillomavirus (HPV) has been associated with the development of oral cancer and is suggested to modulate host cell transcription. Reciprocally, cellular transcription factors, such as NF‐κB and AP‐1 are known to modulate the expression of viral and other genes involved in the development of cancer. In the absence of data on NF‐κB in relation to HPV in oral cancer, we studied the DNA binding activity and expression pattern of NF‐κB family of proteins in different stages of oral cancer and correlated with HPV infection that has been associated with better prognosis of the disease. A total of 110 fresh oral tissue biopsies were collected comprising 10 normal controls, 34 precancer and 66 oral cancer lesions prior to chemotherapy/radiotherapy. Diagnosis of HPV was done by both consensus and type‐specific PCR. Electrophoretic mobility shift assays, western blots and immunohistochemical analysis were performed to assess the binding activity and expression pattern of NF‐κB family of proteins (p50, p65, p52, c‐Rel, RelB and Bcl‐3) in oral tissue biopsies. Twenty seven percent (18/66) of the oral cancer biopsies showed the presence of HPV infection exclusively of high risk HPV type 16, which was primarily associated with the well differentiated squamous cell carcinomas (WDSCC). We observed a high constitutive activation of NF‐κB with concomitant upregulated expression of all the NF‐κB members in oral cancer tissues. Expression of NF‐κB components gradually increased as the severity of lesion increased from precancer to invasive cancer. NF‐κB p50 was found to be the major DNA binding component, which is indicative of homodimerization of p50 subunits. Interestingly, in HPV16 infected oral cancers although p50 showed high binding activity, p65 also showed a partial involvement as evidenced in supershift assay. Both by western blotting and immunohistochemistry, a differential overexpression and nuclear localization of p50, p65 and partially of Bcl‐3 were observed in HPV16 positive oral cancer patients that also showed an over‐expression of p21. We therefore, demonstrate a constitutive activation and differential expression of NF‐κB proteins, which change as a function of severity of oral lesions during development of oral cancer. The NF‐κB DNA binding is primarily due to homodimerization of p50 but infection of high risk HPV promotes participation of p65 in NF‐κB complex formation, leading to heterodimerization of p50/p65. We propose that the involvement of p65 in HPV infected oral cancer may be linked to improved differentiation and better prognosis of the disease when treated. © 2006 Wiley‐Liss, Inc.
Melanoma cells interfere with the interaction of dendritic cells with NK/LAK cells
Authors: Capobianco Annalisa , Rovere‐Querini Patrizia , Rugarli Claudio , Manfredi Angelo A. 
Published: September 2006

AbstractDendritic cells (DCs) and natural killer (NK) cells are key players at the interface between innate resistance and acquired immunity. NK cells can induce DC maturation, a differentiation process whereby DCs respond to a environmental stimulus and acquire the ability of eliciting adaptive immunity. Conversely, maturing DCs promote NK functions in vivo and in vitro. This interplay has important consequences on the immune response to pathogens and possibly to neoplastic cells. Here, we show that B16 melanoma cells actively modulate the interaction between DCs derived from bone marrow precursors and NK/LAK cells propagated from the spleen of C57BL/6 mice. DCs increased in a dose‐dependent manner the ability of NK/LAK cells to kill melanoma cells and to produce cytokines. This activatory cross‐talk entailed the production of IL‐18 by DCs and of IFN‐γ by NK/LAK cells. Melanoma cells were not a passive target of NK activity; they regulated the outcome of the interaction between DCs and NK/LAK cells, inhibiting the in vitro production of cytokines as effectively as the genetic deletion of IL‐18 or IFN‐γ. Interference with the NK/DC interaction possibly represents a mechanism used by growing tumors to evade the immune response. © 2006 Wiley‐Liss, Inc.
Prostaglandin E2 protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP2 receptor activation
Authors: Sugiura Hisatoshi , Liu Xiangde , Togo Shinsaku , Kobayashi Tetsu , Shen Lei , Kawasaki Shin , Kamio Koichiro , Wang Xing Qi , Mao Li Jun , Rennard Stephen I. 
Published: September 2006

AbstractProstaglandin E2 (PGE2) has been shown to have a strong cytoprotective effect, inhibiting apoptosis. In the present study, we evaluated whether PGE2 has a protective effect on cigarette smoke extract (CSE)‐induced apoptosis in human lung fibroblasts. Apoptosis was assessed by various methods, including DNA content analysis. CSE (15%–20%) led to apoptosis and induced imbalance in favor of pro‐ over anti‐apoptotic protein expression and activated caspases. PGE2 blocked CSE‐induced apoptosis and modulated the balance of pro‐ and anti‐apoptotic proteins and decreased the activation of caspases. This anti‐apoptotic effect was mediated via EP2 receptor activation as the EP2 agonist butaprost mimicked PGE2 activity and siRNA for the EP2 receptor blocked it. An adenylyl cyclase inhibitor was found to abolish the PGE2‐mediated cytoprotective effect. Correspondingly, c‐AMP analogs blocked CSE‐induced apoptosis. Consistently, the protein kinase A (PKA) inhibitor KT‐5720 abolished PGE2‐mediated protection. PGE2 and butaprost phosphorylated Bad and KT‐5720 blocked phosphorylation. These results suggest that PGE2 inhibits CSE‐induced apoptosis via EP2 receptor activation and activation of PKA, which leads to an alteration in the balance between pro‐ and anti‐apoptotic factors. Through such a mechanism, PGE2 may alter survival of cells in the smoke‐exposed lungs, thus affecting the pathogenesis of cigarette smoke‐induced disease. J. Cell. Physiol. 210: 99–110, 2007. © 2006 Wiley‐Liss, Inc.
Cyclophilin C‐associated protein is up‐regulated during wound healing
Authors: Kong Wuyi , Li Shaowei , Longaker Michael T. , Lorenz H. Peter 
Published: September 2006

AbstractCyclophilin C‐associated protein (CyCAP) is identified from macrophages. It locates in intracellular, membrane bound and extracellular, suggesting it has an important role, however both of its regulation and function have not been elucidated. The expression of CyCAP in skin and during wound healing is also unknown. We demonstrate that CyCAP is expressed in both dermal fibroblasts and keratinocytes. In the dermis, the majority of CyCAP protein is located intracellular in a filamentous protein form while a lesser amount is in the extracellular matrix (ECM). CyCAP gene and protein expression is increased 1 day after skin wound healing in both fetal and adult rats and remains elevated level up to 1 week in adult rats. Immunohistochemistry studies demonstrate that the increased CyCAP expression locates mainly to inflammatory cells, including macrophages, monocytes and lymphocytes during wound healing. Interferon‐γ increases CyCAP gene and protein expression in cultured rat fibroblasts. We also found that wound healing is slower and less collagen is expressed in skin of CyCAP null mice. These data are the first observations of CyCAP expression in skin and during wound repair. Our data indicates that CyCAP is regulated by IFNγ and may function on immune defense in macrophages, lymphocytes, dermal fibroblasts and keratinocytes during wound healing. J. Cell. Physiol. 210: 153–160, 2007. © 2006 Wiley‐Liss, Inc.