bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does Seed Priming Induce Changes in the Levels of Some Endogenous Plant Hormones in Hexaploid Wheat Plants Under Salt Stress?
Authors: Iqbal Muhammad , Ashraf Muhammad , Jamil Amer , Ur‐Rehman Shafiq 
Published: January 2006

AbstractIn order to assess whether salt tolerance could be improved in spring wheat (Triticum aestivum L.), the present study was performed by soaking the seeds of two cultivars, namely MH‐97 (salt sensitive) and Inqlab‐91 (salt tolerant), for 12 h in distilled water or 100 mol/m3 CaCl2, KCl, or NaCl. Primed seeds from each treatment group and non‐primed seeds were sown in a field in which NaCl salinity of 15 dS/m was developed. Priming of seeds with CaCl2, followed by priming with KCl and NaCl, was found to be effective in alleviating the adverse effects of salt stress on both wheat cultivars in terms of shoot fresh and dry weights and grain yield. Priming with CaCl2 alleviated the adverse effects of salt stress on hormonal balance in plants of both cultivars. In MH‐97 plants, CaCl2 pretreatment considerably reduced leaf abscisic acid (ABA) concentrations and increased leaf free salicylic acid (SA) concentrations under both saline and non‐saline conditions. In contrast, in the Inqlab‐91 plant, CaCl2 increased free indoleacetic acid (IAA) and indolebutyric acid (IBA) content. However, priming of seeds with CaCl2 did not alter free polyamine levels in either cultivar, although spermidine levels were considerably lower in plants raised from seeds treated with CaCl2 for both cultivars under saline conditions. Priming with KCl increased growth in Inqlab‐91 plants, but not in MH‐97 plants, under saline conditions. The salinity induced reduction in auxins (IAA and IBA) was alleviated by NaCl priming in both cultivars under saline conditions. However, NaCl increased leaf free ABA content and lowered leaf SA and putrescine levels in Inqlab‐91 plants under saline conditions. In conclusion, although all three priming agents (i.e. CaCl2, KCl, and NaCl) were effective in alleviating the adverse effects of salt stress on wheat plants, their effects on altering the levels of different plant hormones were different in the two cultivars.(Managing editor: Ping He)
Disruption of Cortical Microtubules by Overexpression of Green Fluorescent Protein‐Tagged α‐Tubulin 6 Causes a Marked Reduction in Cell Wall Synthesis
Authors: Burk David H. , Zhong Ruiqin , Morrison W. Herbert , Ye Zheng‐Hua 
Published: January 2006

AbstractIt has been known that the transverse orientation of cortical microtubules (MTs) along the elongation axis is essential for normal cell morphogenesis, but whether cortical MTs are essential for normal cell wall synthesis is still not clear. In the present study, we have investigated whether cortical MTs affect cell wall synthesis by direct alteration of the cortical MT organization in Arabidopsis thaliana. Disruption of the cortical MT organization by expression of an excess amount of green fluorescent protein‐tagged α‐tubulin 6 (GFP‐TUA6) in transgenic Arabidopsis plants was found to cause a marked reduction in cell wall thickness and a decrease in the cell wall sugars glucose and xylose. Concomitantly, the stem strength of the GFP‐TUA6 overexpressors was markedly reduced compared with the wild type. In addition, expression of excess GFP‐TUA6 results in an alteration in cell morphogenesis and a severe effect on plant growth and development. Together, these results suggest that the proper organization of cortical MTs is essential for the normal synthesis of plant cell walls.(Managing editor: Wei Wang)
Gene Discovery and Functional Analyses in the Model Plant Arabidopsis
Authors: Feng Cai‐Ping , Mundy John 
Published: January 2006

AbstractThe present mini‐review describes newer methods and strategies, including transposon and T‐DNA insertions, TILLING, Deleteagene, and RNA interference, to functionally analyze genes of interest in the model plant Arabidopsis. The relative advantages and disadvantages of the systems are also discussed.(Managing editor: Ping He)
Analysis of Global Expression Profiles of Arabidopsis Genes Under Abscisic Acid and H2O2 Applications
Authors: Wang Peng‐Cheng , Du Yan‐Yan , An Guo‐Yong , Zhou Yun , Miao Chen , Song Chun‐Peng 
Published: January 2006

AbstractTo gain insight into the coordination of gene expression profiles under abscisic acid (ABA) and H2O2 applications, global changes in gene expression in response to ABA and H2O2 in Arabidopsis seedlings were investigated using GeneChip (Santa Clara, CA, USA) arrays. Among over 24 000 genes present in the arrays, 459 transcripts were found to be significantly increased, whereas another 221 decreased following H2O2 treatment compared with control. Similar to treatment with H2O2, ABA treatment elevated the transcription of 391 genes and repressed that of 322 genes. One hundred and forty‐three upregulated genes and 75 downregulated genes were shared between the two treatments and these genes were mainly involved in metabolism, signal transduction, transcription, defense, and resistance. Only two genes, which encode an APETALA2/dehydration‐responsive element binding protein (AP2/DREBP) family transcriptional factor and a late embryogenesis‐abundant protein, were downregulated by H2O2, but upregulated by ABA. These results suggest that, similar to ABA, H2O2 plays a global role in gene transcription of Arabidopsis seedlings. The transcriptional responses induced by the application of exogenous ABA and H2O2 overlapped substantially. These two treatments regulated most of the downstream genes in a coordinated manner.(Managing editor: Li‐Hui Zhao)
Improving Reverse Supply Chain Operational Performance: A Transshipment Application Study for Not‐for‐Profit Organizations
Authors: Reyes Pedro M. , Meade Laura M. 
Published: January 2006

SUMMARYThis paper describes an approach for improving the operational performance in the reverse supply chain in a not‐for‐profit environment. The authors present a model based on risk pooling through preventive lateral transshipment as a method for improving the responsiveness of not‐for‐profit core business practice of redistributing donated products in order to increase revenues. The model considers a three‐echelon structure consisting of three collection centers, one sorting and disposition center, and three retail stocking locations. The ensuing simulation indicates a favorable response of the model. Results indicated that while the daily average inventories slightly increased, the frequency of lost sales significantly decreased, thus offering the potential increased revenues.
Effect of spontaneous exercise on antioxidant capacity in rat muscles determined by electron spin resonance
Authors: Tanabe K. , Masuda K. , Hirayama A. , Nagase S. , Kono I. , Kuno S. 
Published: January 2006

AbstractAims:  The effect of physical activity on antioxidant capacity in muscle remains unknown. This study investigated the effect of spontaneous exercise on antioxidant capacity in rat muscles determined by electron spin resonance (ESR), which is a technique for the direct detection of free radicals.Methods:  Ten‐week‐old male Wistar rats were housed individually in cages with a running wheel. Rats were classified as high activity (HA), middle activity (MA) or low activity group (LA), based on an assessment of running distance covered over a 23‐week period. After 23 weeks of housing, soleus (Sol), plantaris (Pl), gastrocnemius [deep/surface portions (GasD/GasS)] and heart (Hrt) muscles were isolated, and scavenging activity against superoxide anions () and hydroxyl radicals (HO·) was determined by ESR using a spin‐trap chemical. The citrate synthase (CS) activity was used as a marker of mitochondrial oxidative phosphorylation capacity.Results:  Among the parameters measured, only scavenging activity in GasD significantly correlated with the running distance. The highest scavenging activity was observed in Hrt of HA rats. The scavenging activity in Pl of MA rats was significantly higher than that of LA rats. The scavenging activity of Sol and GasS was not significantly different between the three groups. Furthermore, the HO· scavenging activity of any muscle specimens was similar among the three groups and did not correlate with running distance at all. CS activity did not significantly differ between the three groups.Conclusion:  These data suggest that scavenging activity in specific types of muscle tissues would increase especially in spontaneously active animals. However, HO· scavenging activity would not.
Metabolic cost, mechanical work, and efficiency during walking in young and older men
Authors: Mian O. S. , Thom J. M. , Ardigò L. P. , Narici M. V. , Minetti A. E. 
Published: January 2006

AbstractAim:  To investigate mechanical work, efficiency, and antagonist muscle co‐activation with a view to better understand the cause of the elevated metabolic cost of walking (CW) in older adults.Methods:  Metabolic, mechanical and electromyographic measurements were made as healthy young (YOU; n = 12, age = 27 ± 3 years) and older (OLD; n = 20, age = 74 ± 3 years) men of equivalent body mass and leg length walked on a treadmill at four speeds (ranging from 0.83 to 1.67 m s−1).Results:  Net (above resting) CW, determined by indirect calorimetry was 31% higher (average across speeds) in OLD (P < 0.05). The integrity of the passive pendulum like interchange of mechanical energies of the centre of mass (COMB), an energy‐saving mechanism, was maintained in OLD. Furthermore, total mechanical work, determined from fluctuations in mechanical energy of COMB and of body segments relative to COMB, was not significantly elevated in OLD. This resulted in a lower efficiency in OLD (−17%, P < 0.05). Co‐activation, temporally quantified from electromyography recordings, was 31% higher in OLD for antagonist muscles of the thigh (P < 0.05). Thigh co‐activation was moderately correlated with CW at three speeds (r = 0.38–0.52, P < 0.05).Conclusion:  Healthy septuagenarians with no gait impairment have an elevated CW which is not explained by an elevation in whole body mechanical work. Increased antagonist muscle co‐activation (possibly an adaptation to ensure adequate joint stability) may offer partial explanation of the elevated CW.
Diagnostic Markers of Ovarian Cancer by High-Throughput Antigen Cloning and Detection on Arrays
Authors: Chatterjee Madhumita , Mohapatra Saroj , Ionan Alexei , Bawa Gagandeep , Ali-Fehmi Rouba , Wang Xiaoju , Nowak James , Ye Bin , Nahhas Fatimah A. , Lu Karen , Witkin Steven S. , Fishman David , Munkarah Adnan , Morris Robert , Levin Nancy K. , Shirley Natalie N. , Tromp Gerard , Abrams Judith , Draghici Sorin , Tainsky Michael A. 
Published: January 2006

Abstract
A noninvasive screening test would significantly facilitate early detection of epithelial ovarian cancer. This study used a combination of high-throughput selection and array-based serologic detection of many antigens indicative of the presence of cancer, thereby using the immune system as a biosensor. This high-throughput selection involved biopanning of an ovarian cancer phage display library using serum immunoglobulins from an ovarian cancer patient as bait. Protein macroarrays containing 480 of these selected antigen clones revealed 65 clones that interacted with immunoglobulins in sera from 32 ovarian cancer patients but not with sera from 25 healthy women or 14 patients having other benign or malignant gynecologic diseases. Sequence analysis data of these 65 clones revealed 62 different antigens. Among the markers, we identified some known antigens, including RCAS1, signal recognition protein-19, AHNAK-related sequence, nuclear autoantogenic sperm protein, Nijmegen breakage syndrome 1 (Nibrin), ribosomal protein L4, Homo sapiens KIAA0419 gene product, eukaryotic initiation factor 5A, and casein kinase II, as well as many previously uncharacterized antigenic gene products. Using these 65 antigens on protein microarrays, we trained neural networks on two-color fluorescent detection of serum IgG binding and found an average sensitivity and specificity of 55% and 98%, respectively. In addition, the top 6 of the most specific clones resulted in an average sensitivity and specificity of 32% and 94%, respectively. This global approach to antigenic profiling, epitomics, has applications to cancer and autoimmune diseases for diagnostic and therapeutic studies. Further work with larger panels of antigens should provide a comprehensive set of markers with sufficient sensitivity and specificity suitable for clinical testing in high-risk populations. (Cancer Res 2006; 66(2): 1181-90)
c-Myc Overexpression Causes Anaplasia in Medulloblastoma
Authors: Stearns Duncan , Chaudhry Aneeka , Abel Ty W. , Burger Peter C. , Dang Chi V. , Eberhart Charles G. 
Published: January 2006

AbstractBoth anaplasia and increased c-myc gene expression have been shown to be negative prognostic indicators for survival in medulloblastoma patients. myc gene amplification has been identified in many large cell/anaplastic medulloblastoma, but no causative link between c-myc and anaplastic changes has been established. To address this, we stably overexpressed c-myc in two medulloblastoma cell lines, DAOY and UW228, and examined the changes in growth characteristics. When analyzed in vitro, cell lines with increased levels of c-myc had higher rates of growth and apoptosis as well as significantly improved ability to form colonies in soft agar compared with control. When injected s.c. into nu/nu mice, flank xenograft tumors with high levels of c-myc in DAOY cell line background were 75% larger than those derived from control. Overexpression of c-myc was required for tumor formation by UW228 cells. Most remarkably, the histopathology of the Myc tumors was severely anaplastic, with large areas of necrosis/apoptosis, increased nuclear size, and macronucleoli. Indices of proliferation and apoptosis were also significantly higher in Myc xenografts. Thus, c-myc seems to play a causal role in inducing anaplasia in medulloblastoma. Because anaplastic changes are often observed in recurrent medulloblastoma, we propose that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms. (Cancer Res 2006; 66(2): 673-81)
Profiling Genetic Variation along the Androgen Biosynthesis and Metabolism Pathways Implicates Several Single Nucleotide Polymorphisms and Their Combinations as Prostate Cancer Risk Factors
Authors: Mononen Nina , Seppälä Eija H. , Duggal Priya , Autio Ville , Ikonen Tarja , Ellonen Pekka , Saharinen Juha , Saarela Janna , Vihinen Mauno , Tammela Teuvo L.J. , Kallioniemi Olli , Bailey-Wilson Joan E. , Schleutker Johanna 
Published: January 2006

Abstract
Several candidate genes along androgen pathway have been suggested to affect prostate cancer risk but no single gene seems to be overwhelmingly important for a large fraction of the patients. In this study, we first screened for variants in candidate genes and then chose to explore the association between 18 variants and prostate cancer risk by genotyping DNA samples from unselected (n = 847) and familial (n = 121) prostate cancer patients and population controls (n = 923). We identified a novel single nucleotide polymorphism (SNP) in the CYP19A1 gene, T201M, with a mild significant association with prostate cancer [odds ratio (OR), 2.04; 95% confidence interval (95% CI), 1.03-4.03; P = 0.04]. Stratified analysis revealed that this risk was most apparent in patients with organ-confined (T1-T2) and low-grade (WHO grade 1) tumors (OR, 5.42; 95% CI, 2.33-12.6; P &lt; 0.0001). In contrast, CYP17A1 −34T&gt;C alteration was associated with moderate to poorly differentiated (WHO grade 2-3) organ-confined disease (OR, 1.42; 95% CI, 1.09-1.83; P = 0.007). We also tested a multigenic model of prostate cancer risk by calculating the joint effect of CYP19A1 T201M with five other common SNPs. Individuals carrying both the CYP19A1 and KLK3 −252A&gt;G variant alleles had a significantly increased risk for prostate cancer (OR, 2.87; 95% CI, 1.10-7.49; P = 0.03). In conclusion, our results suggest that several SNPs along the androgen pathway, especially in CYP19A1 and CYP17A1, may influence prostate cancer development and progression. These genes may have different contributions to distinct clinical subsets as well as combinatorial effects in others illustrating that profiling and joint analysis of several genes along each pathway may be needed to understand genetic contributions to prostate cancer etiology. (Cancer Res 2006; 66(2): 743-7)
Efficient Inhibition of Intra-Peritoneal Tumor Growth and Dissemination of Human Ovarian Carcinoma Cells in Nude Mice by Anti-L1-Cell Adhesion Molecule Monoclonal Antibody Treatment
Authors: Arlt Matthias J.E. , Novak-Hofer Ilse , Gast Daniela , Gschwend Verena , Moldenhauer Gerhard , Grünberg Jürgen , Honer Michael , Schubiger P. August , Altevogt Peter , Krüger Achim 
Published: January 2006

AbstractThe L1 cell adhesion molecule is implicated in the control of proliferation, migration, and invasion of several tumor cell types in vitro. Recently, L1 overexpression was found to correlate with tumor progression of ovarian carcinoma, one of the most common causes of cancer-related deaths in gynecologic malignant diseases. To evaluate L1 as a potential target for ovarian cancer therapy, we investigated the effects of anti-L1 monoclonal antibodies (chCE7 and L1-11A) on proliferation and migration of L1-positive human SKOV3ip ovarian carcinoma cells in vitro and the therapeutic efficacy of L1-11A against i.p. SKOV3ip tumor growth in nude mice. In vitro, both anti-L1 antibodies efficiently inhibited the proliferation of SKOV3ip cells as well as other L1-expressing tumor cell lines (renal carcinoma, neuroblastoma, and colon carcinoma). On two cell lines, hyper-cross-linking of L1-11A with a secondary antibody was necessary for significant inhibition of proliferation, indicating that cross-linking of L1 is required for the antiproliferative effect. L1-negative prostate carcinoma cells were not influenced by antibody treatment. Biweekly treatment of ovarian carcinoma-bearing mice with L1-11A led to a dose-dependent and significant reduction of tumor burden (up to −63.5%) and ascites formation (up to −75%). This effect was associated with reduced proliferation within the tumors. L1-directed antibody-based inhibition of peritoneal growth and dissemination of human ovarian carcinoma cells represents important proof-of-principle for the development of a new therapy against one of the leading gynecologic malignant diseases. (Cancer Res 2006; 66(2): 936-43)
Restoring E-Cadherin Expression Increases Sensitivity to Epidermal Growth Factor Receptor Inhibitors in Lung Cancer Cell Lines
Authors: Witta Samir E. , Gemmill Robert M. , Hirsch Fred R. , Coldren Christopher D. , Hedman Karla , Ravdel Larisa , Helfrich Barbara , Dziadziuszko Rafal , Chan Daniel C. , Sugita Michio , Chan Zeng , Baron Anna , Franklin Wilbur , Drabkin Harry A. , Girard Luc , Gazdar Adi F. , Minna John D. , Bunn Paul A. 
Published: January 2006

Abstract
The epidermal growth factor receptor (EGFR) is overexpressed in the majority of non–small cell lung cancers (NSCLC). EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib, produce 9% to 27% response rates in NSCLC patients. E-Cadherin, a calcium-dependent adhesion molecule, plays an important role in NSCLC prognosis and progression, and interacts with EGFR. The zinc finger transcriptional repressor, ZEB1, inhibits E-cadherin expression by recruiting histone deacetylases (HDAC). We identified a significant correlation between sensitivity to gefitinib and expression of E-cadherin, and ZEB1, suggesting their predictive value for responsiveness to EGFR-tyrosine kinase inhibitors. E-Cadherin transfection into a gefitinib-resistant line increased its sensitivity to gefitinib. Pretreating resistant cell lines with the HDAC inhibitor, MS-275, induced E-cadherin along with EGFR and led to a growth-inhibitory and apoptotic effect of gefitinib similar to that in gefitinib-sensitive NSCLC cell lines including those harboring EGFR mutations. Thus, combined HDAC inhibitor and gefitinib treatment represents a novel pharmacologic strategy for overcoming resistance to EGFR inhibitors in patients with lung cancer. (Cancer Res 2006; 66(2); 944-50)
The Synthetic Compound CC-5079 Is a Potent Inhibitor of Tubulin Polymerization and Tumor Necrosis Factor-α Production with Antitumor Activity
Authors: Zhang Ling-Hua , Wu Lei , Raymon Heather K. , Chen Roger S. , Corral Laura , Shirley Michael A. , Krishna Narla Rama , Gamez Jim , Muller George W. , Stirling David I. , Bartlett J. Blake , Schafer Peter H. , Payvandi Faribourz 
Published: January 2006

AbstractWe have found that the synthetic compound CC-5079 potently inhibits cancer cell growth in vitro and in vivo by a novel combination of molecular mechanisms. CC-5079 inhibits proliferation of cancer cell lines from various organs and tissues at nanomolar concentrations. Its IC50 value ranges from 4.1 to 50 nmol/L. The effect of CC-5079 on cell growth is associated with cell cycle arrest in G2-M phase, increased phosphorylation of G2-M checkpoint proteins, and apoptosis. CC-5079 prevents polymerization of purified tubulin in a concentration-dependent manner in vitro and depolymerizes microtubules in cultured cancer cells. In competitive binding assays, CC-5079 competes with [3H]colchicine for binding to tubulin; however, it does not compete with [3H]paclitaxel (Taxol) or [3H]vinblastine. Our data indicate that CC-5079 inhibits cancer cell growth with a mechanism of action similar to that of other tubulin inhibitors. However, CC-5079 remains active against multidrug-resistant cancer cells unlike other tubulin-interacting drugs, such as Taxol and colchicine. Interestingly, CC-5079 also inhibits tumor necrosis factor-α (TNF-α) secretion from lipopolysaccharide-stimulated human peripheral blood mononuclear cells (IC50, 270 nmol/L). This inhibitory effect on TNF-α production is related to its inhibition of phosphodiesterase type 4 enzymatic activity. Moreover, in a mouse xenograft model using HCT-116 human colorectal tumor cells, CC-5079 significantly inhibits tumor growth in vivo. In conclusion, our data indicate that CC-5079 represents a new chemotype with novel mechanisms of action and that it has the potential to be developed for neoplastic and inflammatory disease therapy. (Cancer Res 2006; 66(2): 951-9)
Overexpression of c-Maf Contributes to T-Cell Lymphoma in Both Mice and Human
Authors: Morito Naoki , Yoh Keigyou , Fujioka Yuki , Nakano Takako , Shimohata Homare , Hashimoto Yuko , Yamada Akiko , Maeda Atsuko , Matsuno Fumihiko , Hata Hiroyuki , Suzuki Atsushi , Imagawa Shigehiko , Mitsuya Hiroaki , Esumi Hiroyasu , Koyama Akio , Yamamoto Masayuki , Mori Naoyoshi , Takahashi Satoru 
Published: January 2006

Abstract
c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin β7, and ARK5 were up-regulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin β7, might be downstream target genes of c-Maf leading to malignant transformation. (Cancer Res 2006; 66(2): 812-9)