bluuebunny/crossref_metadata_2025_split huggingface dataset:
Design and Development of an Optimal CO2 Separation Process for the Oxidative Coupling of Methane in Mini Plant Scale
Authors: Stünkel Steffen , Martini Walter , Arellano‐Garcia Harvey , Wozny Günter 
Published: March 2011

AbstractDie katalytische oxidative Kopplung von Methan zu höheren Kohlenwasserstoffen (OCM) ist für die Produktion von Ethylen oder flüssigen Brennstoffen von großem Interesse. Neben der Katalysatorentwicklung werden auch reaktionstechnische Untersuchungen durchgeführt, um den OCM‐Prozess und die Produktaufarbeitung technisch durchführbar zu gestalten. Hierbei spielt die Aufbereitung der Prozessgase eine entscheidende Rolle. CO2 fällt als unerwünschtes Neben‐ bzw. Abfallprodukt an und sollte daher frühzeitig entfernt werden. Energiebedarf und Kostenaufwand müssen möglichst klein gehalten werden. Am Beispiel der OCM wird die Entwicklung eines integrierten Aufbereitungsprozesses für die CO2‐Abtrennung im Miniplant‐Maßstab vorgestellt.
Comparison of the Coalescence Behavior of Stagnant and Dynamic Water‐in‐Oil‐in‐Water Single Drops
Authors: Gaitzsch Friedemann , Kamp Johannes , Kraume Matthias , Gäbler Ansor 
Published: March 2011

AbstractDie Phaseninversion einer Wasser‐in‐Öl‐Emulsion zu einer Wasser‐in‐Öl‐in‐Wasser‐Doppelemulsion wird technisch zur Flüssig/flüssig‐Separation eingesetzt. Für eine erfolgreiche Trennung im Wasserteil des Separators ist die Koaleszenz der inneren Wassertropfen mit der umgebenden kontinuierlichen Wasserphase ausschlaggebend. Die Untersuchung dieses Koaleszenzphänomens dient zur Auslegung des Separationsprozesses. Hierzu werden einzelne Wasser‐in‐Öl‐in‐Wasser‐Tropfen unter statischen und dynamischen Bedingungen mittels einer Hochgeschwindigkeitskamera untersucht. Der Einfluss stofflicher und geometrischer Parameter auf die Koaleszenzzeit und das Verhalten bezüglich auftretender partieller Koaleszenz wird bestimmt.
Phase 2 trial of a novel capecitabine dosing schedule in combination with bevacizumab for patients with metastatic breast cancer
Authors: Gajria Devika , Feigin Kim , Tan Lee K. , Patil Sujata , Geneus Stephanie , Theodoulou Maria , Norton Larry , Hudis Clifford A. , Traina Tiffany A. 
Published: March 2011

AbstractBACKGROUND:Capecitabine has antitumor activity in metastatic breast cancer (MBC); however, its optimal dose and schedule remain unclear. Mathematical modeling predicts that a capecitabine schedule 7 days of treatment followed by 7 days of rest (7—7) will improve efficacy and minimize toxicity. Bevacizumab has demonstrated the ability to improve outcomes when it is added to chemotherapy, including capecitabine, in the first‐line and second‐line settings.METHODS:Patients with measurable MBC received oral capecitabine (2000 mg twice daily; 7—7), and intravenous bevacizumab (10 mg/kg every 2 weeks). The primary endpoint was the response rate. Secondary endpoints included toxicity, the clinical benefit rate, and progression‐free survival (PFS).RESULTS:Forty‐one patients were treated. After a median of 7 cycles (range, 1‐32 cycles), partial responses were observed in 20% of patients, and stable disease for ≥6 months was noted in 35% patients. The median PFS was 8 months. The most common treatment‐related toxicities were hand‐foot syndrome (49% grade 2, 20% grade 3/4) hypertension (12% grade 2, 10% grade 3/4), and fatigue (12% grade 2, 2% grade 3/4). Diarrhea (5% grade 2, 0% grade 3/4), nausea (0% grade 2‐4), and vomiting (0% grade 2‐4) were rare.CONCLUSIONS:Capecitabine administered for 7 days followed by a 7‐day rest in combination with bevacizumab had modest efficacy and an acceptable toxicity profile in patients with MBC. Gastrointestinal toxicity with this schedule was minimal. Cancer 2011;. © 2011 American Cancer Society.
Limitations in small intestinal neuroendocrine tumor therapy by mTor kinase inhibition reflect growth factor–mediated PI3K feedback loop activation via ERK1/2 and AKT
Authors: Svejda Bernhard , Kidd Mark , Kazberouk Alexander , Lawrence Ben , Pfragner Roswitha , Modlin Irvin M. 
Published: March 2011

AbstractBACKGROUND:Treatment of small intestinal neuroendocrine tumors (SINETs) with mammalian target of rapamycin (mTOR) inhibitors alone or with somatostatin analogs has been proposed as effective therapy, because both agents have been reported to exhibit antiproliferative activity. Because adenocarcinomas escape mTOR inhibition, we examined whether the escape phenomenon occurred in SINETs and whether usage of somatostatin analogs with mTOR inhibitors surmounted loss of inhibition.METHODS:The effects of the somatostatin analog octreotide (OCT), the mTOR inhibitor RAD001 (RAD), or the combination were evaluated in SINET cell lines (KRJ‐I, H‐STS) using cell viability assays, western blotting, enzyme‐linked immunosorbent assay, and reverse‐transcription polymerase chain reaction to assess antiproliferative signaling pathways and feedback regulation.RESULTS:RAD (10−9 M) incompletely decreased cell viability (−40% to +15%); growth escape (P < .001) was noted at 72 hours in both cell lines. Phosphorylated (p)mTOR/mTOR and pp70S6K/p70S6K ratios were decreased but were associated with increases in phosphorylated extracellular signal‐regulated kinase (pERK)/ERK and pAKT/AKT in both cell lines, whereas phosphorylated insulin‐like growth factor 1 receptor (pIGF‐1R)/IGF‐1R levels were elevated only in H‐STS cells. Increased (P < .05) transcript levels for AKT1, MAPK, mTOR, IGF‐1R, IGF‐1, and TGFβ1 were evident. OCT (10−6 M) itself had no significant effect on growth signaling in either cell line. An antiproliferative effect (66 ± 5%) using OCT+RAD was only noted in the KRJ‐I cells (P < .05).CONCLUSIONS:SINET treatment with the mTOR inhibitor RAD had no antiproliferative effect based on activation of pAKT and pERK1/2. A combinatorial approach using OCT and RAD failed to overcome this escape phenomenon. However, differences in RAD response rates in individual NET cell lines suggested that pretreatment identification of different tumor sensitivity to mTOR inhibitors could provide the basis for individualized treatment. Cancer 2011;. © 2011 American Cancer Society.
Deceased‐donor kidney transplant following ethylene glycol‐induced brain death
Authors: Sifontis Nicole , Kim Richard , Birkenbach Mark , Lee Iris , Constantinescu Serban , Karachristos Andreas , Silva Patricio , Daller John 
Published: March 2011

AbstractWe report on a deceased‐donor kidney transplant following ethylene glycol‐induced brain death. The donor was a 53‐year‐old man with a history of depression who presented to the emergency department after drinking a “cocktail amount” of windshield wiper ﬂuid each day for the past 3 weeks. Upon presentation he became unresponsive and suffered a seizure. Fomepizole 1.2 g IV followed by emergent hemodialysis was initiated as indicated for acute treat‐ment of ethylene glycol poisoning. Unfortunately, the patient never regained consciousness and progressed to brain death. At the time of procurement his urine output was over 250 mL/h, and serum creatinine was 2.2 mg/dL. Renal biopsy following procurement revealed minimal tubule injury without evidence of intratubular oxalate crystals. The kidney recipient was a 76‐year‐old woman with end‐stage renal disease secondary to diabetes and hypertension. Cold ischemia time was 31 hours, 45 minutes. The only postoperative complication was delayed graft function and one episode of mild acute cellular rejection 7 weeks post transplant that resolved with IV methylprednisolone. Two years post transplant the patient continues to do well clinically with a baseline serum creatinine of 2.5 mg/dL.
Post‐renal transplant plasma cell dyscrasia presenting as retroperitoneal plasmacytoma: A case report and literature review
Authors: Muzaffar Mahvish , Chaudhary Rekha , Li Xin , Ratnam Shobha 
Published: March 2011

AbstractPost‐transplant lymphoproliferative disease (PTLD) is a rare but potentially fatal complication of organ transplanta‐tion. Most cases of PTLD represent Epstein Barr virus (EBV)‐related B‐cell disease in a setting of pharmacological immunosuppression. Post‐transplant plasma cell dyscrasia is very rare, and post‐transplant plasma cell dyscrasia with extramedullary plasmacytoma is extremely rare. We report here a case of the latter, which to our knowledge is the fourth such reported case in the English literature. A 22‐year‐old man developed post‐transplant plasma cell dyscrasia 20 years after a renal transplant while on immunosuppression. His presentation included retroperitoneal plasmacytoma, which is very rare and is probably the ﬁrst case in a renal transplant patient. The patient is in complete remission 1 year after receiving ﬁve cycles of bortezomib and dexamethasone.
Analysis of some risk factors of coronary and valvular calcification in peritoneal dialysis
Authors: Janicka Lucyna , Duma Dariusz , Grzebalska Agnieszka M. , Czekajska‐Chehab Elzbieta , Drop Andrzej , Staskiewicz Grzegorz , Janicki Krzysztof , Solski Janusz , Książek Andrzej 
Published: March 2011

AbstractOBJECTIVEOur study was performed to analyze risk factors for coronary artery calcification (CAC) and valvular calcification (VC) in peritoneally dialyzed patients, as well as the frequency of fatal cardiovascular complications.METHODSThe study was performed on 102 peritoneal dialyzed patients (mean time of dialysis: 37.3 ± 23 months). Patients were divided depending on the severity of calcification into three groups: A, lack of calcification; B, CAC up to 400 mm3; and C, CAC >400 mm3. CAC and VC were measured by means of computed tomography. The following risk factors for CAC and VC were analyzed: age, gender, time of peritoneal dialysis, and levels of calcium, phosphates, calcium × phosphorus product (Ca × P), C‐reactive protein (CRP), fibrinogen, fetuin‐A, and parathormone (PTH).RESULTSPositive correlation was found between CAC and VC expressed by Agatston and volumetric score, and serum levels of CRP and fibrinogen and patient age. In patients with CAC and VC, serum levels of phosphorus and Ca × P were significantly higher; however, such significance was not observed in patients with CAC only. Serum fetuin‐A was decreased in all study groups, and was significantly lower in patients with CAC and VC than in patients with CAC only. Cardiovascular complications were significantly more frequent and mortality was higher in group C than in groups A and B.CONCLUSIONSIn peritoneally dialyzed patients, CAC accompanied by VC is a high risk factor for mortality resulting from cardiovascular complications.
Dispositional optimism and loneliness in older men
Authors: Rius‐Ottenheim Nathaly , Kromhout Daan , van der Mast Roos C. , Zitman Frans G. , Geleijnse Johanna M. , Giltay Erik J. 
Published: March 2011

BackgroundDispositional optimism, defined as a generalized tendency to positive outcome expectancies, is associated with well‐being and successful aging. However, it remains unclear whether optimism is also correlated to less feelings of loneliness over time. We aimed to determine whether dispositional optimism is prospectively associated with less feelings of loneliness, independently of potential confounders inherent to the aging process.MethodsWe observed 416 older men aged between 70 and 89 years (mean 74.9 years, standard deviation [SD] 4.7 years) within the population‐based Zutphen Elderly Study during 10 years of follow‐up. Baseline dispositional optimism was assessed using a four‐item questionnaire. The presence of feelings of loneliness, the main outcome of our study, was assessed using the 11‐item loneliness scale of De Jong Gierveld in the years 1990, 1993, 1995, and 2000. The association between baseline dispositional optimism and loneliness over time was tested by using multilevel regression analysis and by adjusting for potential confounders (i.e. age, living arrangement, social contacts, widowhood, memberships, self‐rated health, and depressive symptoms).ResultsFeelings of loneliness significantly increased during 10 years of follow‐up but showed temporal stability (reliability coefficient 0.78). Low baseline dispositional optimism was strongly associated with loneliness over time, also in the adjusted analysis. A 1 SD increase in baseline dispositional optimism was associated with a 0.14 SD (95% confidence interval 0.04–0.23) lower level of loneliness (F1,320 = 7.8; p = 0.006).ConclusionsDispositional optimism is correlated to lower feelings of loneliness over time in older men, independently of depression or changes in social network. Copyright © 2011 John Wiley & Sons, Ltd.
The effect of waiting time and distance on hospital choice for English cataract patients
Authors: Sivey Peter 
Published: March 2011

SUMMARYThis paper applies latent‐class multinomial logit models to the choice of hospital for cataract operations in the UK NHS. We concentrate on the effects of travel time and waiting time and especially on estimating the waiting time elasticity of demand. Models including hospital fixed effects rely on changes over time in waiting time to indentify coefficients. We show how using a latent‐class multinomial logit model characterises the unobserved heterogeneity in GP practices' choice behaviour and affects the estimated elasticities of travel time and waiting time. The models estimate waiting time elasticities of demand of approximately −0.1, comparable with previous waiting time‐demand models. For the average waiting time elasticity, the simple multinomial logit models are good approximations of the latent‐class logit results. Copyright © 2011 John Wiley & Sons, Ltd.
Does managed care affect the diffusion of psychotropic medications?
Authors: Domino Marisa E. 
Published: March 2011

SUMMARYNewer technologies to treat many mental illnesses have shown substantial heterogeneity in diffusion rates across states. In this paper, I investigate whether variation in the level of managed care penetration is associated with changes in state‐level diffusion of three newer classes of psychotropic medications in fee‐for‐service Medicaid programs from 1991 to 2005. Three different types of managed care programs are examined: capitated managed care, any type of managed care and behavioral health carve‐outs. A fourth‐order polynomial fixed effect regression model is used to model the diffusion path of newer antidepressant and antipsychotic medications controlling for time‐varying state characteristics. Substantial differences are found in the diffusion paths by the degree of managed care use in each state Medicaid program. The largest effect is seen through spillover effects of capitated managed care programs; states with greater capitated managed care have greater initial shares of newer psychotropic medications. The influence of carve‐outs and of all types of managed care combined on the diffusion path was modest. Copyright © 2011 John Wiley & Sons, Ltd.
Inhibition of hyaluronan synthesis in breast cancer cells by 4‐methylumbelliferone suppresses tumorigenicity in vitro and metastatic lesions of bone in vivo
Authors: Urakawa Hiroshi , Nishida Yoshihiro , Wasa Junji , Arai Eisuke , Zhuo Lisheng , Kimata Koji , Kozawa Eiji , Futamura Naohisa , Ishiguro Naoki 
Published: March 2011

AbstractHyaluronan (HA) has been shown to play crucial roles in the tumorigenicity of malignant tumors. Previous studies demonstrated that inhibition of HA suppressed the tumorigenicity of various malignant tumors including breast cancer. 4‐methylumbelliferone (MU) has been reported to inhibit HA synthesis in several cell types. However, few studies have focused on the effects of HA inhibition in breast cancer cells by MU, nor the effects on bone metastasis. We hypothesized that MU would suppress the progression of bone metastasis via inhibition of HA synthesis. Here, we investigated the effects of MU on HA expression in MDA‐MB‐231 breast cancer cell line in addition to their tumorigenicity in vitro and in vivo. HAS2 mRNA expression was downregulated after 6 and 24 hr treatment with MU. Quantitative analysis of HA revealed that MU significantly inhibited the intracellular and cell surface HA. MU significantly inhibited cell growth and induced apoptosis as determined by cell proliferation and TUNEL assays, respectively. Phosphorylation of Akt was suppressed after 12 and 24 hr treatment with MU. MU treatment also inhibited cell motility as well as cell invasiveness. MU also inhibited cell growth and motility in murine fibroblast cell line NIH3T3. In vivo, administration of MU inhibited the expansion of osteolytic lesions on soft X‐rays in mouse breast cancer xenograft models. HA accumulation in bone metastatic lesions was perturbed peripherally. These data suggest that MU might be a therapeutic candidate for bone metastasis of breast cancer via suppression of HA synthesis and accumulation.
Expression of epithelial–mesenchymal transition‐inducing transcription factors in primary breast cancer: The effect of neoadjuvant therapy
Authors: Mego Michal , Mani Sendurai A. , Lee Bang‐Ning , Li Changping , Evans Kurt W. , Cohen Evan N. , Gao Hui , Jackson Summer A. , Giordano Antonio , Hortobagyi Gabriel N. , Cristofanilli Massimo , Lucci Anthony , Reuben James M. 
Published: March 2011

AbstractEpithelial cancer cells are likely to undergo epithelial–mesenchymal transition (EMT) prior to entering the peripheral circulation. By undergoing EMT, circulating tumor cells (CTCs) lose epithelial markers and may escape detection by conventional methods. Therefore, we conducted a pilot study to investigate mRNA transcripts of EMT‐inducing transcription factors (TFs) in tumor cells from the peripheral blood (PB) of patients with primary breast cancer (PBC). PB mononuclear cells were isolated from 52 patients with stages I–III PBC and 30 healthy donors (HDs) and were sequentially depleted of EpCAM+ cells and CD45+ leukocytes, henceforth referred to as CD45−. The expression levels of EMT‐inducing TFs (TWIST1, SNAIL1, SLUG, ZEB1 and FOXC2) in the CD45− cells were determined using quantitative real‐time polymerase chain reaction. The highest level of expression by the CD45− cell fraction of HD was used as “cutoff” to determine if samples from patients with PBC overexpressed any EMT‐inducing TFs. In total, 15.4% of patients with PBC overexpressed at least one of the EMT‐inducing TF transcripts. Overexpression of any EMT‐inducing TF transcripts was more likely to be detected in patients with PBC who received neoadjuvant therapies (NAT) than patients who received no NAT (p = 0.003). Concurrently, CTCs were detected in 7 of 38 (18.4%) patients by CellSearch® and in 15 of 42 (35.7%) patients by AdnaTest™. There was no association between the presence of CTCs measured by CellSearch® or AdnaTest™. In summary, our results demonstrate that CTCs with EMT phenotype may occur in the peripheral circulation of patients with PBC and that NAT is unable to eliminate CTCs undergoing EMT.
Aberrant DNA methylation and tumor suppressive activity of the EBF3 gene in gastric carcinoma
Authors: Kim Jin , Min Sun Young , Lee Hee Eun , Kim Woo Ho 
Published: March 2011

AbstractThe early B‐cell factors (EBFs) are a group of four highly conserved DNA‐binding transcription factors with an atypical zinc‐finger and a helix‐loop‐helix domain. The EBF3 locus on chromosome 10q26.3 is epigenetically silenced or deleted in several types of cancers. In addition, EBF3 activates genes involved in cell cycle arrest and inhibits cell survival. However, inactivation of EBF3 gene expression was not fully studied in gastric carcinoma and the functions of EBF3 that underlie EBF3‐regulated tumor suppression have not been identified. In our study, we found that inactivation of the EBF3 gene is frequently accompanied by promoter region hypermethylation in several gastric cancer cell lines and that the gene is reactivated by 5‐aza‐2′‐deoxycytidine (5‐aza‐dc) and/or trichostatin A (TSA) in all ten gastric cancer cell lines. We performed functional analysis using small interfering RNA or expressional cDNA transfection in gastric cancer cell lines and demonstrate that EBF3 represses gastric cancer cell growth and migration, but activates cell cycle arrest and apoptosis. Promoter methylation of EBF3 was detected in 42/104 (40.4%) gastric cancer tissues but not in normal gastric tissues. Furthermore, promoter methylation of EBF3 was found to be significantly correlated with lymphatic invasion (p = 0.013) and poor survival (p = 0.038) in gastric carcinoma. These results suggest that EBF3 tumor suppressor is epigenetically silenced and that it serves as an independent prognostic marker in gastric carcinoma.
A fast, cost‐efficient and sensitive approach for KRAS mutation detection using multiplexed primer extension with IP/RP‐HPLC separation
Authors: Tierling Sascha , Sers Christine , Lehmann Annika , Walter Jörn 
Published: March 2011

AbstractMutations in the KRAS gene are very important diagnostic and prognostic markers in cancer. Particularly, KRAS mutations at codons 12 and 13 have a high prognostic value for EGFR‐directed antibody therapies. Several methods are available to detect the most common mutations, some of them are commercialized. The most frequently used techniques, allele‐specific PCR or direct sequencing, are not standardized and often lack sensitivity to detect low amounts of mutated tumor cells in paraffin‐embedded tissue‐blocks leading to a high number of false‐negatives. Here we present a reliable, fast, cost‐effective and sensitive approach for KRAS mutation detection that has a high potential for standardized large scale screening. The method is based on multiplexed primer extension reactions coupled to HPLC separation. The highly sensitive assay gives easily interpretable and reproducible results at affordable costs. We describe the method and an application example for diagnosis in early colorectal cancer screening.
Genetic variation in bone morphogenetic protein and colon and rectal cancer
Authors: Slattery Martha L. , Lundgreen Abbie , Herrick Jennifer S. , Kadlubar Susan , Caan Bette J. , Potter John D. , Wolff Roger K. 
Published: March 2011

AbstractBone morphogenetic proteins (BMP) are part of the TGF‐β‐signaling pathway; genetic variation in these genes may be involved in colorectal cancer. In this study, we evaluated the association between genetic variation in BMP1 (11 tagSNPs), BMP2 (5 tagSNPs), BMP4 (3 tagSNPs), BMPR1A (9 tagSNPs), BMPR1B (21 tagSNPs), BMPR2 (11 tagSNPs) and GDF10 (7 tagSNPs) with risk of colon and rectal cancer and tumor molecular phenotype. We used data from population‐based case‐control studies (colon cancer n = 1,574 cases, 1,970 controls; rectal cancer n = 791 cases, 999 controls). We observed that genetic variation in BMPR1A, BMPR1B, BMPR2, BMP2 and BMP4 was associated with risk of developing colon cancer, with 20 to 30% increased risk for most high‐risk genotypes. A summary of high‐risk genotypes showed over a twofold increase in colon cancer risk at the upper risk category (OR = 2.49 95% CI = 1.95, 3.18). BMPR2, BMPR1B, BMP2 and GDF10 were associated with rectal cancer. BMPR2 rs2228545 was associated with an almost twofold increased risk of rectal cancer. The risk associated with the highest category of the summary score for rectal cancer was 2.97 (95% CI = 1.87, 4.72). Genes in the BMP‐signaling pathway were consistently associated with CIMP+ status in combination with both KRAS‐mutated and MSI tumors. BMP genes interacted statistically significantly with other genes in the TGF‐β‐signaling pathway, including TGFβ1, TGFβR1, Smad 3, Smad 4 and Smad 7. Our data support a role for genetic variation in BMP‐related genes in the etiology of colon and rectal cancer. One possible mechanism is via the TGF‐β‐signaling pathway.