bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chiral inversion of RS‐8359: A selective and reversible MAO‐A inhibitor via oxido‐reduction of keto‐alcohol
Authors: Itoh Kunio , Hoshino Kouichi , Endo Asuka , Asakawa Tasuku , Yamakami Kazumi , Noji Chisa , Kosaka Toshiyuki , Tanaka Yorihisa 
Published: July 2006

AbstractRS‐8359, (±)‐4‐(4‐cyanoanilino)‐5,6‐dihydro‐7‐hydroxy‐7H‐cyclopenta[d]‐pyrimidine is a selective and reversible MAO‐A inhibitor. The (S)‐enantiomer of RS‐8359 has been demonstrated to be inverted to the (R)‐enantiomer after oral administration to rats. In the current study, we investigated the chiral inversion mechanism and the properties of involved enzymes using rat liver subcellular fractions. The 7‐hydroxy function of RS‐8359 was oxidized at least by the two different enzymes. The cytosolic enzyme oxidized enantiospecifically the (S)‐enantiomer with NADP as a cofactor. On the other hand, the microsomal enzyme catalyzed more preferentially the oxidation of the (S)‐enantiomer than the (R)‐enantiomer with NAD as a cofactor. With to product enantioselectivity of reduction of the 7‐keto derivative, it was found that only the alcohol bearing (R)‐configuration was formed by the cytosolic enzyme with NADPH and the microsomal enzyme with NADH at almost equal rate. The reduction rate was much larger than the oxidation rate of 7‐hydroxy group. The results suggest that the chiral inversion might occur via an enantioselectivity of consecutive two opposing reactions, oxidation and reduction of keto‐alcohol group. In this case, the direction of chiral inversion from the (S)‐enantiomer to the (R)‐enantiomer is governed by the enantiospecific reduction of intermediate 7‐keto group to the alcohol with (R)‐configuration. The enzyme responsible for the enantiospecific reduction of the 7‐keto group was purified from rat liver cytosolic fractions and identified as 3α‐hydroxysteroid dehydrogenase (3α‐HSD) via database search of peptide mass data obtained by nano‐LC/MS/MS. Chirality, 2006. © 2006 Wiley‐Liss, Inc.
Nickel‐catalyzed Electrochemical Coupling of Phenyl Halide and Study of Mechanism
Authors: Zhao Peng , Luo Yi‐Wen , Xue Teng , Zhang Ai‐Jian , Lu Jia‐Xing 
Published: July 2006

AbstractElectrochemical coupling of phenyl halide catalyzed by NiCl2bpy in DMF has been investigated in this paper. Stainless steel was used as cathode and zinc as anode. Effects of potential, temperature and catalyst on electrolyses were studied to optimize the electrolytic conditions, with the maximal isolated yield under potentiostatic electrolysis to be 85%. Cyclic voltammetry of NiCl2bpy in the presence of phenyl bromide has been studied and mechanisms, concerned with several kinds of nickel complex, have been summarized.
The relation between hypoxia‐inducible factor (HIF)‐1α and HIF‐2α expression with anemia and outcome in surgically treated head and neck cancer
Authors: Winter Stuart C. , Shah Ketan A. , Han Cheng , Campo Leticia , Turley Helen , Leek Russell , Corbridge Rogan J. , Cox Graham J. , Harris Adrian L. 
Published: July 2006

AbstractBACKGROUND.Hypoxia promotes tumorigenesis through the hypoxia‐inducible factor (HIF) pathway. There are 2 main homologues of the regulatory proteins, HIF‐1α and HIF‐2α, which have different effects in genetic knock‐out experiments. Anemia may contribute to hypoxia by reducing oxygen delivery, but it is not known whether this influences HIF‐α expression in tumors.METHODS.The expression of HIF‐1α, HIF‐2α, carbonic anhydrase‐9 (CA‐9), and peripheral hemoglobin (Hb) levels in 151 patients who underwent surgery for head and neck squamous cell carcinoma (HNSCC) were analyzed and related to outcome.RESULTS.High HIF‐1α was expressed in 45 of 140 tumors (30%), HIF‐2α was expressed in 21 of 139 tumors (14%), and CA‐9 was expressed in 56 of 149 tumors (62%). There was a positive correlation between HIF‐1α expression and HIF‐2α expression (P = .0001). HIF‐1α alone was associated with a worse disease‐specific survival (DSS) (P = .05) and disease‐free survival (DFS) (P = .03) in multivariate analyses. Nine percent of tumors expressed both high HIF‐1α and high HIF‐2α. High HIF‐1α/high HIF‐2α expression was an independent prognostic factors in DSS (P = .04) and DFS (P = .005) in multivariate analyses. There was no correlation noted between Hb and HIF‐1α, HIF‐2α, or CA‐9.CONCLUSIONS.HIF‐1α alone was correlated with DSS and DFS. The additive effect of HIF‐2α on poor prognosis suggested that different pathways may be regulated by HIF‐2α. Anemia that was not related to HIF‐α expression suggests that tumor intrinsic factors regulate HIF‐α; therefore, anemia may be a surrogate marker for other factors that affect outcome. Cancer 2006. © 2006 American Cancer Society.
Inhibition of survivin reduces cell proliferation and induces apoptosis in human endometrial cancer
Authors: Ai Zhihong , Yin Lianhua , Zhou Xianrong , Zhu Ying , Zhu Dongmei , Yu Yinhua , Feng Youji 
Published: July 2006

AbstractBACKGROUNDEndometrial cancer is a common gynecologic malignancy among women. The molecular mechanisms involved in the progression of endometrial cancer are unclear, which has hampered the development of an effective treatment. Survivin, a newly identified member of the inhibitor of apoptosis (IAP) family, regulates 2 critical processes in neoplastic transformation: cell proliferation and apoptosis.METHODSSurvivin mRNA and protein expression levels were analyzed in human normal cycling endometrium, atypical endometrium, and endometrial adenocarcinoma by immunohistochemical, reverse‐transcriptase polymerase chain reaction (RT‐PCR), and Western blot analyses. To study the biological function of survivin in endometrial cancer, RNA interference was applied to knock down survivin expression in the Ishikawa endometrial cancer cell line by recombinant plasmids producing survivin small hairpin RNA. Furthermore, the signal pathway that regulates survivin expression was investigated.RESULTSHigher levels of survivin mRNA and protein expression were observed in endometrial adenocarcinomas than in atypical or normal endometrium. Immunohistochemical staining revealed that 83.3% (50 of 60) of endometrial adenocarcinoma samples, 55.0% (11 of 20) of atypical endometrium samples, and 25.0% (5 of 20) of normal endometrium samples were positive for survivin protein. Inhibition of survivin by RNA interference reduced cell proliferation and induced apoptosis in Ishikawa cells by down‐regulating cyclin D1 and phosphorylated RB and activating caspase‐3 and caspase‐8. The authors also found that the MAPK pathway was a signal transduction pathway upstream of survivin. Epidermal growth factor (EGF) and transforming growth factor‐α (TGF‐α) up‐regulated survivin protein expression by activating the MAPK pathway in endometrial cancer cells.CONCLUSIONSSurvivin is an attractive target for endometrial cancer treatment. Growth factors could regulate survivin expression by activating the MAPK pathway. Cancer 2006. © 2006 American Cancer Society.
A phase II study of irinotecan plus cisplatin for patients with advanced stage IIIB or IV NSCLC previously treated with nonplatinum‐based chemotherapy
Authors: Kim Heung T. , Han Ji‐Youn , Lee Dae H. , Chun Jong H. , Lee Hong G. , Lee Jae J. , Kim Hyae Y. , Lee Sung Y. , Lee Jin S. 
Published: July 2006

AbstractBACKGROUND.Irinotecan (I) and cisplatin (P) are active chemotherapy agents with clinical synergy in non–small‐cell lung cancer (NSCLC). We evaluated the efficacy of IP regimen as a salvage treatment of patients with NSCLC that progressed after nonplatinum‐containing regimen(s).METHODS.Eligibility required histologically confirmed NSCLC, bidimensionally measurable disease, ECOG PS 0‐2, and progressive disease after nonplatinum‐based chemotherapy. Treatment consisted of I (65 mg/m2) and P (30 mg/m2) i.v. on Days 1 and 8 of a 21‐day cycle, for a maximum of 6 cycles. An informed consent was obtained from all patients.RESULTS.Between August 2002 and May 2004, 32 patients with median age of 56 years (range, 42–74) were enrolled. Twenty‐four (75%) patients were men, and 28 (88%) had ECOG PS 0 or 1. Twenty‐five patients had adenocarcinoma and 6 had squamous‐cell carcinoma. All patients were evaluated for response and toxicity, and the response rate was 40.6%. After a median follow‐up of 18.5 months, the median survival time was found to be 9.3 months, with a 1‐year survival rate of 43.8%. Toxicities were moderate and manageable, with 47% G3 and 9% G4 neutropenia, 19% G3 diarrhea, and 22% G3 asthenia. There was no G4 nonhematologic toxicity.CONCLUSIONS.The irinotecan and cisplatin combination is an active and well‐tolerated regimen for the patients with advanced NSCLC that progressed after nonplatinum‐containing regimen(s). Cancer 2006. © 2006 American Cancer Society.
Recommendations for the use of Yttrium‐90 ibritumomab tiuxetan in malignant lymphoma
Authors: Weigert Oliver , Illidge Tim , Hiddemann Wolfgang , Dreyling Martin 
Published: July 2006

AbstractRadioimmunotherapy (RIT) with Yttrium‐90 (90Y) ibritumomab tiuxetan (Zevalin®) combines the tumor targeting attributes of a monoclonal antibody against the CD20 antigen and the pure β‐radiation of 90Y. High efficacy and a favorable safety profile have been demonstrated in Phase II and III clinical trials enrolling patients with CD20+ B‐cell non‐Hodgkin lymphoma (B‐NHL). On the basis of these results, 90Y‐ibritumomab tiuxetan was approved in the United States for the treatment of patients with follicular lymphoma (FL) or transformed B‐NHL. In the European Union its use was restricted to FL, refractory to or relapsed after rituximab. There are a number of important clinical trials currently evaluating 90Y‐ibritumomab tiuxetan in other subtypes of lymphoma such as diffuse large‐cell and mantle‐cell lymphoma, as consolidation therapy or as part of myeloablative regimens. In light of the constantly increasing clinical experience with RIT, clinicians face the challenge of how to best integrate this promising new treatment option into existing established treatment algorithms. By incorporating the most recent data in this rapidly developing field, this review article focuses on current recommendations for the use of 90Y‐ibritumomab tiuxetan in patients with malignant lymphoma, outlines future perspectives, and provides practical recommendations for patient management. Cancer 2006. © 2006 American Cancer Society.
Iridium Metal Thin Films and Patterned IrO2 Nanowires Deposited Using Iridium(I) Carbonyl Precursors
Authors: Chen Y.‐L. , Hsu C.‐C. , Song Y.‐H. , Chi Y. , Carty A. J. , Peng S.‐M. , Lee G.‐H. 
Published: July 2006

AbstractHighly volatile iridium(I) carbonyl complexes (1–5) with three anionic fluorinated chelates, namely ketoiminate, aminoalkoxide, or iminoalkoxide, have been synthesized and their physical properties relevant to CVD are evaluated. A single‐crystal X‐ray diffraction (XRD) study on Ir(CO)2(amakNMe2) (3) confirms a square‐planar geometry with two cis‐orientated carbonyl ligands. Metallic iridium, polycrystalline IrO2 thin films, or even patterned IrO2 nanowires are deposited using Ir(CO)2(hfdaNnPr) (5) as the CVD precursor. A systematic investigation of the deposition of IrO2 nanowires is conducted, showing a close correlation of observed crystallite morphology with applied system pressure, underlying growth surface, and deposition temperature. Of particular importance, tilted and vertically aligned IrO2 nanowires are obtained on LiTaO3(012) and LiNbO3(100) surfaces under a pressure of 30 Torr of oxygen at 425 °C. The morphology and structural composition of the IrO2 are confirmed by scanning electron microscopy, transmission electron microscopy, X‐ray photoelectron spectroscopy, and XRD analyses.
Numerical modelling of complex turbulent free‐surface flows with the SPH method: an overview
Authors: Violeau D. , Issa R. 
Published: July 2006

AbstractThe gridless smoothed particle hydrodynamics (SPH) method is now commonly used in computational fluid dynamics (CFD) and appears to be promising in predicting complex free‐surface flows. However, increasing flow complexity requires appropriate approaches for taking account of turbulent effects, whereas some authors are still working without any turbulence closure in SPH. A review of recently developed turbulence models adapted to the SPH method is presented herein, from the simplistic point of view of a one‐equation model involving mixing length to more sophisticated (and thus realistic) models like explicit algebraic Reynolds stress models (EARSM) or large eddy simulation (LES). Each proposed model is tested and validated on the basis of schematic cases for which laboratory data, theoretical or numerical solutions are available in the general field of turbulent free‐surface incompressible flows (e.g. open‐channel flow and schematic dam break). They give satisfactory results, even though some progress should be made in the future in terms of free‐surface influence and wall conditions. Recommendations are given to SPH users to apply this method to the modelling of complex free‐surface turbulent flows. Copyright © 2006 John Wiley & Sons, Ltd.
Taphonomy and site formation on California's Channel Islands
Authors: Rick Torben C. , Erlandson Jon M. , Vellanoweth René L. 
Published: July 2006

AbstractInhabited by humans for over 12,000 calendar years, California's Channel Islands contain thousands of archaeological sites, ranging from dense shell middens and villages to small lithic scatters and camps. Similar to many islands around the world, the Channel Islands have a dearth of burrowing animals and limited historical development leading to generally good preservation of archaeological constituents and relatively high stratigraphic integrity. Despite these favorable preservation conditions, numerous natural and cultural processes have impacted the island's archaeological record. Channel Islands archaeologists, however, have given relatively limited attention to the effects of taphonomic and formation processes. The authors provide an overview of taphonomic and formation processes affecting Channel Islands archaeology, illustrating the importance of regional taphonomic syntheses in the management, preservation, and interpretation of archaeological sites. These data also demonstrate the significance of detailing formation processes in islands and other areas where burrowing rodents and other disturbances are thought to be absent or limited. © 2006 Wiley Periodicals, Inc.
Intraoperative parathyroid hormone assay for management of patients undergoing total thyroidectomy
Authors: Roh Jong‐Lyel , Il Park Chan 
Published: July 2006

AbstractBackground.Rapid parathyroid hormone (PTH) assay has been applied to predict hypocalcemia after thyroidectomy compared with conventional close monitoring of serum calcium levels. We evaluated the reliability of intraoperative intact PTH (ioPTH) assay to predict hypocalcemia after total thyroidectomy and sought to develop an algorithm for the management of postthyroidectomy patients.Methods.Rapid PTH assays were performed before and after thyroidectomy for 92 new patients receiving total thyroidectomy. Preoperative and postoperative serum calcium and standard PTH levels were serially obtained to 6 months after surgeryResults.Postoperative hypocalcemia developed in 34 of 92 patients (37%), who showed significantly lower ioPTH values compared with those of normocalcemic patients (mean 9.2 pg/mL vs 31.3 pg/mL). The ioPTH levels were significantly correlated with standard PTH levels (p < .001, r > 0.62), but not with early serum calcium levels within 8 hours after the operation. Sensitivity and specificity of ioPTH levels of <15.0 pg/mL for the prediction of postoperative hypocalcemia were 85% and 84%, respectively. A value of >15.0 pg/mL and <70% decline in ioPTH after thyroidectomy can reliably identify normocalcemic patients during thyroidectomy or patients requiring close monitoring and early calcium supplementConclusions.Rapid ioPTH assay can reliably monitor parathyroid function after thyroidectomy and predict postoperative hypocalcemia. The proposed algorithm based on rapid PTH levels will lead to improved prediction of normocalcemic patients. © 2006 Wiley Periodicals, Inc. Head Neck, 2006
Retracted: Down‐regulation of Jagged‐1 induces cell growth inhibition and S phase arrest in prostate cancer cells
Authors: Zhang Yuxiang , Wang Zhiwei , Ahmed Fakhara , Banerjee Sanjeev , Li Yiwei , Sarkar Fazlul H. 
Published: July 2006

AbstractThis article has been retracted at the request of: Editor‐in‐Chief and Co‐author‘Down‐regulation of Jagged‐1 induces cell growth inhibition and S phase arrest in prostate cancer cells’ by Zhang, Y., Wang, Z., Ahmed, F., Banerjee, S., Li, Y. and Sarkar, F. H.The above article, published online on 5 July 2006, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor‐in‐Chief, Professor Peter Lichter, and Wiley Periodicals, Inc. A university investigation involving the second and the corresponding author determined that histone bands in Fig. 4 in this paper were manipulated and that β‐actin bands in Fig. 1C were duplicated from another publication. Therefore, the authors are retracting the paper in its entirety although they maintain that these issues did not affect the major conclusions. They apologize for any inconvenience this may have caused.ReferenceZhang, Y., Wang, Z., Ahmed, F., Banerjee, S., Li, Y. and Sarkar, F. H. (2006), Down‐regulation of Jagged‐1 induces cell growth inhibition and S phase arrest in prostate cancer cells. Int. J. Cancer, 119: 2071–2077. doi: 10.1002/ijc.22077
Expression of the hemochromatosis gene modulates the cytotoxicity of doxorubicin in breast cancer cells
Authors: Chitambar Christopher R. , Kotamraju Srigiridhar , Wereley Janine P. 
Published: July 2006

AbstractThe antineoplastic agent doxorubicin inhibits cell growth through mechanisms that include an interaction with iron, resulting in the generation of cytotoxic reactive oxygen species (ROS). Prior studies have shown that the wild‐type hemochromatosis gene (wt HFE) may downregulate iron uptake and alter iron homeostasis in cells. We therefore tested the hypothesis that expression of wt HFE would affect the cytotoxicity of doxorubicin. Human breast cancer MCF‐7 cells were transfected with an expression plasmid for a FLAG‐tagged wt HFE gene [fwtHFE(+) cells], to examine the impact of wt HFE expression on doxorubicin‐induced apoptosis. Our results show that, in MCF‐7 cells, fwtHFE expression resulted in a reduction in cellular iron uptake and a decrease in the growth inhibitory effects of doxorubicin. Two micromolar doxorubicin inhibited the growth of fwtHFE(+) and fwtHFE(−) MCF‐7 cells by 34% and 61%, respectively. In parallel, doxorubicin induced caspase‐3‐like activity in fwtHFE(−) cells, but not in fwtHFE(+) cells. On analysis with a DCF fluorescence assay, ROS could be detected in fwtHFE(−) cells but not in fwtHFE(+) cells exposed to doxorubicin. Western blot analysis of breast biopsy samples from patients revealed immunoreactive HFE and transferrin receptor proteins in both normal and malignant breast tissues. Our studies suggest that HFE expression and its consequent effect on cellular iron homeostasis may modulate doxorubicin‐induced oxidative stress and apoptosis in breast cancer cells. Further investigation is warranted to determine whether HFE expression in tumor cells impacts on the clinical efficacy of doxorubicin. © 2006 Wiley‐Liss, Inc.
Hypermethylation of the GATA gene family in esophageal cancer
Authors: Guo MingZhou , House Michael G. , Akiyama Yoshimitsu , Qi Yu , Capagna Domenico , Harmon John , Baylin Stephen B. , Brock Malcolm V. , Herman James G. 
Published: July 2006

AbstractThe GATA family of transcription factors promotes the normal development of the gastrointestinal tract during embryogenesis and determines tissue differentiation in adult gut epithelium. Loss of GATA‐4 and GATA‐5 has been reported in human gastric and colon cancer. We examined GATA‐4,‐5 and ‐6 gene expression in established esophageal squamous cancer cell lines and the relationship to DNA methylation in the promoter region of these genes. GATA‐4 and GATA‐5 expression was absent in most esophageal cancer cell lines, but was restored upon treatment with the demethylating agent 5‐aza‐2′‐deoxycytidine. For each of the cell lines without detectable GATA gene expression, aberrant methylation of the promoter region CpG‐island was detected by methylation specific PCR. We confirmed these results with genomic bisulfite sequencing. GATA‐6 expression was found in each of the cell lines. GATA‐4/‐5 promoter methylation was not detected in normal esophageal mucosa, but GATA‐4 methylation was present in 27 of 44 (61%) squamous carcinomas and 31 of 44 (71%) adenocarcinoma of the esophagus, while GATA‐5 methylation was present in 14 of 44 (32%) squamous carcinomas and 24 of 44 (55%) adenocarcinoma of the esophagus. Our studies demonstrate frequent silencing of GATA‐4 and GATA‐5, but not GATA‐6, in human esophageal neoplasia associated with gene promoter hypermethylation. © 2006 Wiley‐Liss, Inc.
Adult height, age at attained height, and incidence of breast cancer in premenopausal women
Authors: Baer Heather J. , Rich‐Edwards Janet W. , Colditz Graham A. , Hunter David J. , Willett Walter C. , Michels Karin B. 
Published: July 2006

AbstractAdult height has been positively associated with breast cancer risk in epidemiologic studies, and recent evidence suggests that the timing and rate of growth may also influence risk. We examined both adult height and age at attained height, an indicator of the timing of the pubertal growth spurt, in relation to incidence of premenopausal breast cancer in the Nurses' Health Study II. Participants were 108,829 premenopausal women who reported their height in 1989; of these, 37,572 provided information on their age at attained height on a later supplementary questionnaire. During 12 years of follow‐up, 1,041 cases of invasive breast cancer were identified (402 with age at attained height). Cox proportional hazards models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs). Adult height was positively associated with breast cancer incidence; the multivariate RR for participants 1.75 m or taller compared to those shorter than 1.60 m was 1.57 (95% CI: 1.23–2.01, p trend < 0.0001), and each 5‐cm increment corresponded to an 11% increase in risk (95% CI: 6–17%). There was no overall association for age at attained height, however, with a multivariate RR of 0.96 (95% CI: 0.66–1.39) for women who attained their maximum height at age 18 or older compared to those who reached it before age 14 (p trend = 0.65). These results confirm previous findings that taller adult height is associated with increased risk of premenopausal breast cancer but do not provide evidence that age at attained height is related to risk. © 2006 Wiley‐Liss, Inc.