bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B35: Establishment of patient-derived xenograft models of acute leukemias.
Authors: Siegert Antje , Brzezicha Bernadette , Wulf-Goldenberg Annika , Fichtner Iduna , Hoffmann Jens 
Published: August 2015

Abstract
Acute leukemia, a hematological malignancy, is characterised by a rapid increase of functionally immature blood cells. Acute Myeloid Leukemia (AML) and Acute Lymphoblastic Leukemia (ALL) are distinguished by their cells of origin. If untreated, AML and ALL are life-threatening and patients show different responses to current standards of care (SoC) therapy. The majority of acute leukemias are genetically heterogeneous and therefore a challenge for the development of new targeted therapies. There is a need to develop robust animal models to investigate leukemia in vivo. Patient-derived xenograft (PDX) mouse models recapitulate many clinical features of cancer. They have proven to be useful tools for the evaluation of novel therapeutic strategies and biomarkers, and for the study of cancer biology.
The aim of our work was to establish PDX models of AML and ALL and to characterize their sensitivity to different therapeutic agents.
Bone marrow aspirates were obtained from primary and relapsed AML/ALL patients and were intravenously (i.v.) and/or subcutaneously (s.c.) inoculated into immunodeficient mice. Mice were sacrificed when signs of disease were obvious and single cell suspensions of spleens (i.v.) or tumor fragments (s.c.) were transferred to new recipient mice. Chemosensitivity to SoC treatments was tested.
In our study several AML-PDX and ALL-PDX were established. These models show different sensitivity to SoC treatment. The models will be used for further investigations like gene expression or mutation analysis or biomarker identification.
The established PDX models of AML and ALL are suitable tools for preclinical drug development. In order to cover the complex heterogeneity of acute leukemias, the establishment of further PDX models is currently in progress.

Citation Format: Antje Siegert, Bernadette Brzezicha, Annika Wulf-Goldenberg, Iduna Fichtner, Jens Hoffmann. Establishment of patient-derived xenograft models of acute leukemias. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr B35.
Abstract B41: Mutant U2AF1 alters hematopoiesis and pre-mRNA splicing in transgenic mice.
Authors: Shirai Cara Lunn , Ley James N. , White Brian , Tibbitts Justin , Shao Jin , Ndonwi Matthew , Kim Sanghyun , Okeyo-Owuor Theresa , Graubert Timothy A. , Walter Matthew J. 
Published: August 2015

Abstract
This abstract is being presented as a short talk. A full abstract is printed in the Proffered Abstracts section (PR06) of the Conference Proceedings.
Citation Format: Cara Lunn Shirai, James N. Ley, Brian White, Justin Tibbitts, Jin Shao, Matthew Ndonwi, Sanghyun Kim, Theresa Okeyo-Owuor, Timothy A. Graubert, Matthew J. Walter. Mutant U2AF1 alters hematopoiesis and pre-mRNA splicing in transgenic mice. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr B41.
Abstract B42: Modeling MDS in mice through precise molecular lesions in APC and mDia1.
Authors: Turner Julie Davis , Kitchen-Goosen Susan , Howard Andrew M. , Schumacher Heather , Alberts Art S. 
Published: August 2015

Abstract
While the murine equivalent to “5q– syndrome” should map to the distal arms of murine chromosomes 11 and 18, molecular attempts have been unsuccessful in generating a reliable mouse model of myelodysplasia leading to exacerbated myeloid leukemia. Genetic studies suggest interactions between individual proteins in this locus suppress tumor initiation. More specifically, cellular and biochemical studies demonstrated collaboration between two proteins in the commonly deleted regions of 5q– syndrome: mDia1 (mammalian Diaphanous-related Rho GTPase effector formin) and APC (adenomatous polypolis coli). Therefore, we generated mice compounding these two putative disease alleles. Because both mDia1 knockout [Drf1(–/–)] mice and Apcmin (min = multiple intestinal neoplasia; haploinsufficient) mice develop age-dependent myelodysplastic syndrome (MDS), we hypothesized that a mouse strain lacking both proteins will exhibit a more severe MDS phenotype than either mutant allele alone.
To define the disease caused by mutation in Drf1 and Apcmin, we monitored erythropoiesis, myelopoiesis, and overall survival. At all ages, mice with both mutant alleles exhibit granulocytosis. Anemia occurs in aged mice (&gt;270 days), exhibiting drastic differences in blood cell morphology that corresponded to differences in long-term survival in comparison to either Drf1–/– or Apcmin animals. Furthermore, immunophenotyping of all subpopulations indicate an accumulation of CD71+/TER-119+ cells in mice with both mutant alleles, however no significant differences in CD11b expression appeared among CD45+ bone marrow subpopulations.
Our studies indicate that combined loss of mDia1 and APC expression and function direct disease progression. We are currently defining the hematopoietic precursor cell responsible for anemia and bone marrow failure. This enhanced mouse model also serves as molecular laboratory to study disease progression and to test potential therapeutics under development in our laboratory.

Citation Format: Julie Davis Turner, Susan Kitchen-Goosen, Andrew M. Howard, Heather Schumacher, Art S. Alberts. Modeling MDS in mice through precise molecular lesions in APC and mDia1. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr B42.
Abstract IA29: Using mitochondria to guide leukemia therapy.
Authors: Letai Anthony , Hogdal Leah , Chonghaile Triona , Gutierrez Alejandro , Roderick Justine , Kelliher Michelle , Konopleva Marina 
Published: August 2015

Abstract
Most biomarkers in cancer rely on the study of parts of dead cells: DNA, RNA, or proteins. Studying viable functioning cells offers the opportunity to capture some of the complexity that is lost upon killing the cancer cell. BH3 profiling uses BH3 peptides derived from pro-apoptotic proteins to perturb functional mitochondria from cancer cells. The effect of these peptides on mitochondria provides very useful information to guide cancer therapy. Examples include the identification of CLL, AML, and ETP-ALL as disease that are sensitive to BCL-2 inhibition, identifications that are now being tested in the clinic. In addition BH3 profiling can guide the use of conventional chemotherapy and novel targeted pathway inhibitors in the clinic.
Citation Format: Anthony Letai, Leah Hogdal, Triona Chonghaile, Alejandro Gutierrez, Justine Roderick, Michelle Kelliher, Marina Konopleva. Using mitochondria to guide leukemia therapy. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr IA29.
Abstract IA42: Interpreting the role of acquired gene mutations in defining clinical outcome and treatment response.
Authors: Papaemmanuil Elli 
Published: August 2015

Abstract
Recent sequencing studies in MDS, have identified a diverse range of somatic mutations in genes implicated in RNA splicing, DNA modification, chromatin regulation and cell signalling. Similar to most cancers and other haematological neoplasms the genomic landscape of MDS is composed by a small number of frequently (&gt;10% of the patient population) mutated genes accompanied by a long list of genes that are infrequently mutated (&lt;3%). Importantly the majority of MDS patients have two or more oncogenic mutations (defined by gene mutation or structural variation) with evidence of specific pairwise interactions and intra-clonal heterogeneity. Whilst new gene discoveries improve our understanding of the molecular aetiology of this disease, a detailed evaluation of how the individual genetic contributions as well as the frequently observed genotype interactions and clonal relationships correlate with treatment response is warranted.
Next generation sequencing based approaches, deliver quantitative profiles of the composite genomic architecture, support the identification of the key molecular lesions and reconstruction of partial clonal phylogenies from a single sample. Profiling of sequential specimens before and after treatment allows for the first time to track response at a clonal level, providing important new insights into the molecular mechanisms of therapeutic response as well as resistance. Examples of how mutational profiling of samples before, during and after treatment allow for detailed definition of clonal response and the related genetic changes will be presented.
The complex genetic architecture, and the large proportion of infrequently mutated genes impose great challenges to the identification of robust and reliable gene-treatment interactions and overall clinical outcome predictions. Importantly, these effects can be modified by comorbidities, performance status and age amongst other demographic variables. Systematic characterisation of well-annotated and large (&gt;1000) clinical trial samples are necessary to accurately define risk contributions and support the development of molecularly guided prognostication and predictive algorithms in the future.
Citation Format: Elli Papaemmanuil. Interpreting the role of acquired gene mutations in defining clinical outcome and treatment response. [abstract]. In: Proceedings of the AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(17 Suppl):Abstract nr IA42.
Piezoelectric Nanowire toward Harvesting Energy from In-Vivo Environment
Authors: Ghareaghaji Ali 
Published: August 2015

This paper discusses technologies used to harvest energies from in-vivo environment. The discussion mainly concentrated on nanogenerators based on Piezoelectric nanowires which are employed for converting biomechanical energy (such as muscle stretching), vibration energy (such as heart rate sound, sound waves) and biohydraulic energy (such as blood flow, contraction of blood vessel) into electric energy. At the end this paper studies an approach for harvesting biomechanical and biochemical energies from living organisms simultaneously. This system, by using aligned nanowire arrays, can power medical nanosystems and nanodevices through converting vibration, biomechanical and biohydrulic energies into electricity. On the other hand by using biofuel cell structure, this hybrid cell can convert biochemical (glucose/O2) energy in biofluid into electricity. This technology can provide adequate power required for feeding nanodevices and nanosystems or at least to indirectly charge battery of the device. This technology can provide a sound basis for designing wireless self-powered nanodevices with direct energy harvesting from in-vivo environment.
Portable Biomass Gasifier Power Generation Using Non Edible Seed Cake
Authors: Vivek M , Srividhya PK , Sujatha K 
Published: August 2015

Non edible seeds are used most of the applications but the dehydration of seed cakes is too difficult. And the same time the seeds could not feed food as animal. Hence, to adopt various techniques it can be used for other applications. 1 ton crude oil yield from 3 tons of seeds and the remaining becomes seed cake. After oil extraction using screw press machine, seed cake still has 10 % to 15 % of oil. Hence this is a good combustible material with calorific value of approximately 600 Kcal/m3 and the electrical output voltage 180 – 200 at the range of 3.00 -3.5 amps. This paper deals with the power generation from Jatropha seed cake using gasification technology.
Fractal dimension (df ) as a new structural biomarker of clot microstructure in different stages of lung cancer
Authors: Davies Nia Anne , Harrison Nicholas Kim , Keith Morris Roger H. , Noble Simon , Lawrence Matthew James , D’Silva Lindsay Antonio , Broome Laura , Brown Martin Rowan , Hawkins Karl M. , Williams Phylip Rhodri , Davidson Simon , Evans Phillip Adrian 
Published: August 2015

SummaryVenous thromboembolism (VTE) is common in cancer patients, and is the second commonest cause of death associated with the disease. Patients with chronic inflammation, such as cancer, have been shown to have pathological clot structures with modulated mechanical properties. Fractal dimension (df) is a new technique which has been shown to act as a marker of the microstructure and mechanical properties of blood clots, and can be performed more readily than current methods such as scanning electron microscopy (SEM). We measured df in 87 consecutive patients with newly diagnosed lung cancer prior to treatment and 47 matched-controls. Mean group values were compared for all patients with lung cancer vs controls and for limited disease vs extensive disease. Results were compared with conventional markers of coagulation, fibrinolysis and SEM images. Significantly higher values of df were observed in lung cancer patients compared with controls and patients with extensive disease had higher values than those with limited disease (p< 0.05), whilst conventional markers failed to distinguish between these groups. The relationship between df of the incipient clot and mature clot microstructure was confirmed by SEM and computational modelling: higher df was associated with highly dense clots formed of smaller fibrin fibres in lung cancer patients compared to controls. This study demonstrates that df is a sensitive technique which quantifies the structure and mechanical properties of blood clots in patients with lung cancer. Our data suggests that df has the potential to identify patients with an abnormal clot micro-structure and greatest VTE risk.
A Conductive Polymer Hydrogel Supports Cell Electrical Signaling and Improves Cardiac Function After Implantation into Myocardial Infarct
Authors: Mihic Anton , Cui Zhi , Wu Jun , Vlacic Goran , Miyagi Yasuo , Li Shu-Hong , Lu Sun , Sung Hsing-Wen , Weisel Richard D. , Li Ren-Ke 
Published: August 2015

Background—
Efficient cardiac function requires synchronous ventricular contraction. After myocardial infarction, the nonconductive nature of scar tissue contributes to ventricular dysfunction by electrically uncoupling viable cardiomyocytes in the infarct region. Injection of a conductive biomaterial polymer that restores impulse propagation could synchronize contraction and restore ventricular function by electrically connecting isolated cardiomyocytes to intact tissue, allowing them to contribute to global heart function.

Methods and Results—

We created a conductive polymer by grafting pyrrole to the clinically tested biomaterial chitosan to create a polypyrrole (PPy)-chitosan hydrogel. Cyclic voltammetry showed that PPy-chitosan had semiconductive properties lacking in chitosan alone. PPy-chitosan did not reduce cell attachment, metabolism, or proliferation in vitro. Neonatal rat cardiomyocytes plated on PPy-chitosan showed enhanced Ca
2+
signal conduction in comparison with chitosan alone. PPy-chitosan plating also improved electric coupling between skeletal muscles placed 25 mm apart in comparison with chitosan alone, demonstrating that PPy-chitosan can electrically connect contracting cells at a distance. In rats, injection of PPy-chitosan 1 week after myocardial infarction decreased the QRS interval and increased the transverse activation velocity in comparison with saline or chitosan, suggesting improved electric conduction. Optical mapping showed increased activation in the border zone of PPy-chitosan–treated rats. Echocardiography and pressure–volume analysis showed improvement in load-dependent (ejection fraction, fractional shortening) and load-independent (preload recruitable stroke work) indices of heart function 8 weeks after injection.

Conclusions—
We synthesized a biocompatible conductive biomaterial (PPy-chitosan) that enhances biological conduction in vitro and in vivo. Injection of PPy-chitosan better maintained heart function after myocardial infarction than a nonconductive polymer.
Outcomes of Patients With Acute Type B (DeBakey III) Aortic Dissection
Authors: Afifi Rana O. , Sandhu Harleen K. , Leake Samuel S. , Boutrous Mina L. , Kumar Varsha , Azizzadeh Ali , Charlton-Ouw Kristofer M. , Saqib Naveed U. , Nguyen Tom C. , Miller Charles C. , Safi Hazim J. , Estrera Anthony L 
Published: August 2015

Background—
Aortic dissection remains the most common aortic catastrophe. In the endovascular era, the management of acute type B aortic dissection (ATBAD) is undergoing dramatic changes. The aim of this study is to evaluate the long-term outcomes of patients with ATBAD who were treated at our center over a 13-year period.

Methods and Results—

We reviewed patients with ATBAD between 2001 and 2014, analyzing variables based on status (complicated [c] versus uncomplicated [u]) and treatment modalities. We defined cATBAD as rupture, expansion of diameter on imaging during the admission, persistent pain, or clinical malperfusion leading to a deficit in cerebral, spinal, visceral, renal, or peripheral vascular territories at presentation or during initial hospitalization. Postoperative outcomes were defined as deficits not present before the intervention. Outcomes were compared between the groups by use of Kaplan-Meier and descriptive statistics. We treated 442 patients with ATBAD. Of those 442, 60.6% had uATBAD and were treated medically, and 39.4% had cATBAD, of whom 39.0% were treated medically to 30.0% with open repair, 21.3% with thoracic endovascular aortic repair, and 9.7% with other open peripheral procedures. Intervention-free survival at 1 and 5 years was 84.8% and 62.7% for uATBAD, 61.8% and 44.0% for cATBAD-medical, 69.2% and 47.2% for cATBAD-open, and 68.0% and 42.5% for cATBAD–thoracic endovascular aortic repair, respectively (
P
=0.001). Overall survival was significantly related primarily to complicated presentation.

Conclusions—
In our experience, early and late outcomes of ATBAD were dependent on the presence of complications, with cATBAD faring worse. Although uATBAD was associated with favorable early survival, late complications still occurred, mandating radiographic surveillance and open or endovascular interventions. Prospective trials are required to better determine the optimal therapy for uATBAD.
International University Education
Authors: Roberts Gethin Wyn 
Published: August 2015

In 2004, The University of Nottingham was the first Sino-Foreign University to open a campus in mainland China. Today, the University of Nottingham Ningbo, China (unnc) campus holds approximately 6,600 students and 500 staff from 40 different countries. Science and Engineering subjects are relatively new on the campus, but are all based on the long standing pedigree at the University of Nottingham in the United Kingdom. In 2012, a new msc course in Engineering Surveying and Geodesy started at unnc, which was the same as the course in the uk. All the courses at unnc are the same in learning outcomes as those on the uk campus, all the teaching is carried out in the medium of English and undergo the same stringent Quality Assurance. The University of Nottingham also has a campus in Malaysia, which makes the university truly global. Students attending any of these campuses have the opportunities of exchange at any of the other two, as well as many other international universities. unnc aspires to grow to 8,000 students by 2020, consisting of 20% international students and 15-20% postgraduate students, approximately 40% of which will be within the Faculty of Science and Engineering. This paper details the model used by the University of Nottingham in establishing and operating the msc course and research activities in Engineering Surveying and Geodesy at unnc, and gives a case study of this parallel course.
Wave-Induced Boundary Layer Separation in the Lee of the Medicine Bow Mountains. Part I: Observations*
Authors: French Jeffrey R. , Haimov Samuel J. , Oolman Larry D. , Grubišić Vanda , Serafin Stefano , Strauss Lukas 
Published: August 2015

Abstract
Two cases of mountain waves, rotors, and the associated turbulence in the lee of the Medicine Bow Mountains in southeastern Wyoming are investigated in a two-part study using aircraft observations and numerical simulations. In Part I, observations from in situ instruments and high-resolution cloud radar on board the University of Wyoming King Air aircraft are presented and analyzed. Measurements from the radar compose the first direct observations of wave-induced boundary layer separation.
The data from these two events show some striking similarities but also significant differences. In both cases, rotors were observed; yet one looks like a classical lee-wave rotor, while the other resembles an atmospheric hydraulic jump with midtropospheric gravity wave breaking aloft. High-resolution (30 × 30 m2) dual-Doppler syntheses of the two-dimensional velocity fields in the vertical plane beneath the aircraft reveal the boundary layer separation, the scale and structure of the attendant rotors, and downslope windstorms. In the stronger of the two events, near-surface winds upwind of the boundary layer separation reached 35 m s−1, and vertical winds were in excess of 10 m s−1. Moderate to strong turbulence was observed within and downstream of these regions. In both cases, the rotor extended horizontally 5–10 km and vertically 2–2.5 km. Horizontal vorticity within the rotor zone reached 0.2 s−1. Several subrotors from 500 to 1000 m in diameter were identified inside the main rotor in one of the cases.
Part II presents a modeling study and investigates the kinematic structure and the dynamic evolution of these two events.
Wave-Induced Boundary Layer Separation in the Lee of the Medicine Bow Mountains. Part II: Numerical Modeling
Authors: Grubišić Vanda , Serafin Stefano , Strauss Lukas , Haimov Samuel J. , French Jeffrey R. , Oolman Larry D. 
Published: August 2015

Abstract
Mountain waves and rotors in the lee of the Medicine Bow Mountains in southeastern Wyoming are investigated in a two-part paper. Part I by French et al. delivers a detailed observational account of two rotor events: one displays characteristics of a hydraulic jump and the other displays characteristics of a classic lee-wave rotor. In Part II, presented here, results of high-resolution numerical simulations are conveyed and physical processes involved in the formation and dynamical evolution of these two rotor events are examined.
The simulation results reveal that the origin of the observed rotors lies in boundary layer separation, induced by wave perturbations whose amplitudes reach maxima at or near the mountain top. An undular hydraulic jump that gave rise to a rotor in one of these events was found to be triggered by midtropospheric wave breaking and an ensuing strong downslope windstorm. Lee waves spawning rotors developed under conditions favoring wave energy trapping at low levels in different phases of these two events. The upstream shift of the boundary layer separation zone, documented to occur over a relatively short period of time in both events, is shown to be the manifestation of a transition in flow regimes, from downslope windstorms to trapped lee waves, in response to a rapid change in the upstream environment, related to the passage of a short-wave synoptic disturbance aloft.
The model results also suggest that the secondary obstacles surrounding the Medicine Bow Mountains play a role in the dynamics of wave and rotor events by promoting lee-wave resonance in the complex terrain of southeastern Wyoming.