bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of Heat
Transfer in Consecutive Variable Cross-Sectional Domains: Applications in Biological Media and
Thermal Management
Authors: Mahjoob Shadi , Vafai Kambiz 
Published: October 2010

Abstract
Temperature prescription and control is important within biological media and in bioheat transport applications such as in hyperthermia cancer treatment in which the unhealthy tissue/organ is subject to an imposed heat flux. Thermal transport investigation and optimization is also important in designing heat management devices and small-scale porous-filled-channels utilized in electronic and biomedical applications. In this work, biological media or the stated heat management devices with a nonuniform geometry are modeled analytically as a combination of convergent, uniform and/or divergent configurations. The biological media is represented as blood saturated porous tissue matrix while incorporating cells and interstices. Two primary models, namely, adiabatic and constant temperature boundary conditions, are employed and the local thermal nonequilibrium and an imposed heat flux are fully accounted for in the presented analytical expressions. Fluid and solid temperature distributions and Nusselt number correlations are derived analytically for variable cross-sectional domain represented by convergent, divergent, and uniform or any combination thereof of these geometries while also incorporating internal heat generation in fluid and/or solid. Our results indicate that the geometrical variations have a substantial impact on the temperature field within the domain and on the surface with an imposed heat flux. It is illustrated that, the temperature distribution within a region of interest can be controlled by a proper design of the multisectional domain as well as proper selection of the porous matrix. These comprehensive analytical solutions are presented for the first time, to the best of the authors' knowledge in literature.
Apophysomyces elegans
: Epidemiology, Amplified Fragment Length Polymorphism Typing, and
In Vitro
Antifungal Susceptibility Pattern
Authors: Chakrabarti A. , Shivaprakash M. R. , Curfs-Breuker I. , Baghela A. , Klaassen C. H. , Meis J. F. 
Published: September 2010

ABSTRACT

Apophysomyces elegans
is an emerging pathogen in India. We planned the present study to analyze the clinical pattern of the disease, to perform molecular strain typing, and to determine the
in vitro
activities of eight antifungal drugs against
A. elegans.
A total of 16 clinical and two environmental
A. elegans
isolates were included in the study. The clinical histories of the patients were noted. MICs or minimum effective concentrations (MECs) were determined for antifungal drugs by microdilution testing in accordance with CLSI standard M38-A2 guidelines. Of 16 patients, seven had rhino-cerebral, five had cutaneous, and three had renal zygomycosis. One patient had osteomyelitis. Uncontrolled diabetes was observed in 63% of the patients. Amplified fragment length polymorphism (AFLP) analysis divided the strains into two clearly different clades. The fingerprints of the environmental strains (including the type strain) were clearly different from those of the clinical strains. The MIC
50
s and MIC
90
s for amphotericin B, itraconazole, posaconazole, and isavuconazole were 2 and 4, 1 and 2, 0.5 and 1, and 2 and 4 μg/ml, respectively. The strains had high MICs for fluconazole, voriconazole, and echinocandins. The study indicates a possible change in the clinical pattern of zygomycosis due to
A. elegans
in India. The fungus caused not only cutaneous or subcutaneous infection but also other deep-seated infections, and the disease is commonly associated with uncontrolled diabetes. The AFLP patterns show a clear difference between environmental and clinical strains. Posaconazole is the most active drug against the isolates, followed by itraconazole. The MICs of amphotericin B against
A. elegans
were higher than those of the other drugs.
Reliability of the BD GeneOhm Methicillin-Resistant
Staphylococcus aureus
(MRSA) Assay in Detecting MRSA Isolates with a Variety of Genotypes from the United States and Taiwan
Authors: Boyle-Vavra Susan , Daum Robert S. 
Published: September 2010

ABSTRACT

The BD GeneOhm methicillin-resistant
Staphylococcus aureus
(MRSA) assay is a molecular screening test for detection of MRSA in nasal colonization. This assay coamplifies the extremity of staphylococcal chromosome cassette
mec
(SCC
mec
) and adjacent chromosomal DNA at the SCC
mec
insertion site. Increasing reports of novel SCC
mec
types and the diverse genetic backgrounds of MRSA strains prompted us to test the accuracy of the BD GeneOhm MRSA kit with 914 MRSA isolates with a variety of SCC
mec
types harbored in 21 genetic backgrounds, as determined by the multilocus sequence type (ST). The BD GeneOhm MRSA assay was performed on colony lysates; purified genomic DNA (0.2 pg/μl and 0.2 ng/μl) was tested to confirm negative results from lysates. Of 914 MRSA isolates tested, 911 tested positive (detection rate, 99.7%). The SCC
mec
types carried by assay-positive isolates were I, II, III, IV, V, V
(5C2&5)
, VI, and VIII and SCC
mec
composite islands with
mec
class A and
ccr
complexes 2 and 4. One of the assay-negative isolates had a community-associated genotype: ST8, SCC
mec
type IV. However, this was an outlier among the 99.8% (434/435) ST8, SCC
mec
type IV-containing isolates that tested positive. The two other assay-negative isolates had a health care-associated genotype (ST5); both carried a distinct, uncommon, composite SCC
mec
type. In summary, the BD GeneOhm MRSA assay had a high rate of detection of MRSA isolates harboring common and uncommon SCC
mec
types from the United States and Taiwan.
Vaccination Reduces Simian-Human Immunodeficiency Virus Sequence Reversion through Enhanced Viral Control
Authors: Manuel Edwin R. , Yeh Wendy W. , Balachandran Harikrishnan , Clarke Ryon H. , Lifton Michelle A. , Letvin Norman L. 
Published: September 2010

ABSTRACTIt has been suggested that vaccination prior to infection may direct the mutational evolution of human immunodeficiency virus type 1 (HIV-1) to a less fit virus, resulting in an attenuated course of disease. The present study was initiated to explore whether prior immunization might prevent the reversion of the virus to the wild-type form. Mamu-A*01 monkeys were vaccinated to generate a cytotoxic T-lymphocyte response to the immunodominant Gag p11C epitope and were then challenged with a cloned pathogenic CXCR4-tropic simian-human immunodeficiency virus (SHIV) expressing a mutant Gag p11C sequence (Δp11C SHIV). The epitopic and extraepitopic compensatory mutations introduced intogagof Δp11C SHIV resulted in attenuated replicative capacity and eventual reversions to the wild-type Gag p11C sequence in naïve rhesus monkeys. However, in vaccinated rhesus monkeys, no reversions of the challenge virus were observed, an effect that may have been a consequence of significantly decreased viral replication rather than a redirection of the mutational evolution of the virus. These findings highlight the multifactorial pressures that affect the evolution of primate immunodeficiency viruses.
In search of database consistency
Authors: Stonebraker Michael 
Published: October 2010

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Michael Stonebraker discusses the implications of the CAP theorem on database management system applications that span multiple processing sites.
Dysregulation of the Mitogen Granulin in Human Cancer through the miR-15/107 microRNA Gene Group
Authors: Wang Wang-Xia , Kyprianou Natasha , Wang Xiaowei , Nelson Peter T. 
Published: October 2010

Abstract
Granulin (GRN) is a potent mitogen and growth factor implicated in many human cancers, but its regulation is poorly understood. Recent findings indicate that GRN is regulated strongly by the microRNA miR-107, which functionally overlaps with miR-15, miR-16, and miR-195 due to a common 5′ sequence critical for target specificity. In this study, we queried whether miR-107 and paralogs regulated GRN in human cancers. In cultured cells, anti-argonaute RNA coimmunoprecipitation with downstream microarray analyses indicates that GRN mRNA is directly targeted by numerous miR-15/107 miRNAs. We further tested this association in human tumors. MiR-15 and miR-16 are known to be downregulated in chronic lymphocytic leukemia (CLL). Using pre-existing microarray datasets, we found that GRN expression is higher in CLL relative to nonneoplastic lymphocytes (P &lt; 0.00001). By contrast, other prospective miR-15/miR-16 targets in the dataset (BCL-2 and cyclin D1) were not upregulated in CLL. Unlike in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralogs are not known to be dysregulated. Prior studies have shown that GRN is also upregulated, and miR-107 downregulated, in prostate carcinoma. Our results indicate that multiple members of the miR-107 gene group indeed repress GRN protein levels when transfected into prostate cancer cells. At least a dozen distinct types of cancer have the pattern of increased GRN and decreased miR-107 expression. These findings indicate for the first time that the mitogen and growth factor GRN is dysregulated via the miR-15/107 gene group in multiple human cancers, which may provide a potential common therapeutic target. Cancer Res; 70(22); 9137–42. ©2010 AACR.
Improved Clinical Outcome in Indolent B-Cell Lymphoma Patients Vaccinated with Autologous Tumor Cells Experiencing Immunogenic Death
Authors: Zappasodi Roberta , Pupa Serenella M. , Ghedini Gaia C. , Bongarzone Italia , Magni Michele , Cabras Antonello D. , Colombo Mario P. , Carlo-Stella Carmelo , Gianni Alessandro M. , Di Nicola Massimo 
Published: October 2010

AbstractIncreasing evidence argues that the success of an anticancer treatment may rely on immunoadjuvant side effects including the induction of immunogenic tumor cell death. Based on the assumption that this death mechanism is a similar prerequisite for the efficacy of an active immunotherapy using killed tumor cells, we examined a vaccination strategy using dendritic cells (DC) loaded with apoptotic and necrotic cell bodies derived from autologous tumors. Using this approach, clinical and immunologic responses were achieved in 6 of 18 patients with relapsed indolent non–Hodgkin's lymphoma (NHL). The present report illustrates an impaired ability of the neoplastic cells used to vaccinate nonresponders to undergo immunogenic death on exposure to a cell death protocol based on heat shock, γ-ray, and UVC ray. Interestingly, when compared with doxorubicin, this treatment increased surface translocation of calreticulin and cellular release of high-mobility group box 1 and ATP in histologically distinct NHL cell lines. In contrast, treated lymphoma cells from responders displayed higher amounts of calreticulin and heat shock protein 90 (HSP90) compared with those from nonresponders and boosted the production of specific antibodies when loaded into DCs for vaccination. Accordingly, the extent of calreticulin and HSP90 surface expression in the DC antigenic cargo was significantly associated with the clinical and immunologic responses achieved. Our results indicate that a positive clinical effect is obtained when immunogenically killed autologous neoplastic cells are used for the generation of a DC-based vaccine. Therapeutic improvements may thus be accomplished by circumventing the tumor-impaired ability to undergo immunogenic death and prime the antitumor immune response. Cancer Res; 70(22); 9062–72. ©2010 AACR.
Synergistic Killing Effect between Vorinostat and Target of CD146 in Malignant Cells
Authors: Ma Xiaoli , Liu Jia , Wu Jiang , Yan Xiyun , Wu Peng , Liu Yong , Li Shuang , Tian Yuan , Cao Yang , Chen Gang , Meng Li , Xu Gang , Wang Shixuan , Lu Yunping , Ma Ding , Zhou Jianfeng 
Published: October 2010

Abstract

Purpose:
Although histone deacetylase inhibitors (HDACi) are emerging as a new class of anticancer agents, one of the most significant concerns is that interactions with a wide array of substrates using these agents might initiate both therapeutic and undesired protective responses. Here, we sought to identify the potential protective reactions initiated by HDACi and determine whether targeting these reactions would enhance the antitumoral activity of HDACi.

Experimental Design:
Gene expression profiles were analyzed by cDNA microarray in Molt-4 cells before and after treatment of vorinostat. Induction of CD146 by vorinostat was examined in a wide range of tumors and nonmalignant cells. AA98, an anti-CD146 monoclonal antibody, was used to target CD146 function. Synergistic antitumoral and antiangiogenic effects between AA98 and vorinostat were examined both in vitro and in vivo. The potential effect of combined AA98 and vorinostat treatment on the AKT pathway was determined by Western blotting.

Results:
The induction of CD146 is a common phenomenon in vorinostat-treated cancer but not in nonmalignant cells. Targeting of CD146 with AA98 substantially enhanced vorinostat-induced killing via the suppression of activation of AKT pathways in cancer cells. Moreover, AA98 in combination with vorinostat significantly inhibited angiogenesis. In vivo, AA98 synergized with vorinostat to inhibit tumor growth and metastasis.

Conclusion:
The present study provided the first evidence that an undesired induction of CD146 could serve as a protective response to offset the antitumor efficacy of vorinostat. On the other hand, targeting CD146 in combination with vorinostat could be exploited as a novel strategy to more effectively kill cancer cells. Clin Cancer Res; 16(21); 5165–76. ©2010 AACR.
EGFR Fluorescence In situ Hybridization Pattern of Chromosome 7 Disomy Predicts Resistance to Cetuximab in KRAS Wild-type Metastatic Colorectal Cancer Patients
Authors: Li Yu-Hong , Wang Fang , Shen Lin , Deng Yan-Ming , Shao Qiong , Feng Fen , An Xin , Wang Feng-Hua , Wang Zhi-Qiang , Xu Rui-Hua , Shao Jian-Yong 
Published: October 2010

Abstract
Purpose: Metastatic colorectal cancer patients with low epidermal growth factor receptor (EGFR) gene copy number are unlikely to respond to anti-EGFR monoclonal antibody (mAb) treatment. The objective of this study was to investigate EGFR fluorescence in situ hybridization (FISH) patterns of chromosome 7 disomy with efficacy of cetuximab therapy in metastatic colorectal cancer patients.
Experimental Design: We detected the EGFR FISH patterns and KRAS status in 74 tumors from cetuximab-treated metastatic colorectal cancer patients and analyzed with response rate (RR) and progression-free survival (PFS).
Results: One of the 16 (6.25%) patients with chromosome 7 homogeneous disomy (defined as FISH negative) had objective response to cetuximab. A total of 53(76.8%) patients with chromosome 7 pattern of variable ratios of disomy versus polysomy (defined as FISH positive) had a significantly higher RR (37.7% versus 6.25%; P = 0.01), a trend towards longer PFS (4.5 versus 2.9 months; P = 0.07). Among 54 KRAS wild-type patients, EGFR FISH-positive patients had significantly higher RR (51.3% versus 9%; P = 0.01) and longer PFS (5.0 versus 2.3 months; P = 0.02) than EGFR FISH-negative patients. However, among 20 KRAS mutant-type patients, there was no difference in RR (0% versus 0%) and PFS (2.5 versus 3.8 months; P = 0.51) between EGFR FISH-positive and -negative patients.
Conclusion: Our results show firstly that patients with EGFR FISH pattern of chromosome 7 disomy have a very low chance to benefit from cetuximab-based therapy. EGFR FISH pattern of chromosome 7 disomy may be as a negative predicative factor for cetuximab response in KRAS wild-type metastatic colorectal cancer patients. Clin Cancer Res; 17(2); 382–90. ©2011 AACR.
A Randomized Trial ofEx vivoCD40L Activation of a Dendritic Cell Vaccine in Colorectal Cancer Patients: Tumor-Specific Immune Responses Are Associated with Improved Survival
Authors: Barth Richard J. , Fisher Dawn A. , Wallace Paul K. , Channon Jacqueline Y. , Noelle Randolph J. , Gui Jiang , Ernstoff Marc S. 
Published: October 2010

AbstractPurpose: To determine whether an autologous dendritic cell (DC) vaccine could induce antitumor immune responses in patients after resection of colorectal cancer metastases and whether these responses could be enhanced by activating DCs with CD40L.Experimental Design: Twenty-six patients who had undergone resection of colorectal metastases were treated with intranodal injections of an autologous tumor lysate– and control protein [keyhole limpet hemocyanin (KLH)]–pulsed DC vaccine. Patients were randomized to receive DCs that had been either activated or not activated with CD40L. All patients were followed for a minimum of 5.5 years.Results: Immunization induced an autologous tumor-specific T-cell proliferative or IFNγ enzyme-linked immunospot response in 15 of 24 assessable patients (63%) and a tumor-specific DTH response in 61%. Patients with evidence of a vaccine-induced, tumor-specific T-cell proliferative or IFNγ response 1 week after vaccination had a markedly better recurrence-free survival (RFS) at 5 years (63% versus 18%, P = 0.037) than nonresponders. In contrast, no association was observed between induction of KLH-specific immune responses and RFS. CD40L maturation induced CD86 and CD83 expression on DCs but had no effect on immune responses or RFS.Conclusion: Adjuvant treatment of patients after resection of colorectal metastases with an autologous tumor lysate–pulsed, DC vaccine–induced, tumor-specific immune responses in a high proportion of patients. There was an association between induction of tumor-specific immune responses and RFS. Activation of this DC vaccine with CD40L did not lead to increased immune responses. Clin Cancer Res; 16(22); 5548–56. ©2010 AACR.
Daunorubicin induces procoagulant activity of cultured endothelial cells through phosphatidylserine exposure and microparticles release
Authors: Li Huibo , Cao Fenglin , Su Yanhua , Fan Shengjin , Li Yinghua , Wang Shuye , Li Limin , Gilbert Gary E. , Fu Yueyue , Zhou Jin , Shi Jialan 
Published: October 2010

SummaryAdministration of various chemotherapeutic agents is associated with an increased risk of thrombotic events. Although vascular endothelium plays a predominant role in blood coagulation and fibrinolysis, the effect of cytotoxic drugs on the procoagulant activity (PCA) of endothelial cells has not been well evaluated. Our study aims to investigate the possibility that daunorubicin, a chemotherapeutic agent, exerts prothrombotic effect on endothelial cells. We tested the impact of daunorubicin on phosphatidylserine (PS) exposure, endothelial microparticles (EMPs) release and consequent PCA. Human umbilical vein endothelial cells (HUVECs) were treated with daunorubicin (0.1, 0.2, 0.5, 1, 2 μM) for 24 hours. PCA of HUVECs was measured using clotting time and purified coagulation complex assays. Counts and PCA of EMPs were evaluated by flow cytometry and clotting time assay, respectively. Lactadherin was used as a novel probe for detection of PS exposure and EMPs release. We found that daunorubicin dose-dependently increased the PS exposure and consequent PCA of HUVECs. Moreover, daunorubicin treatment also enhanced the release of EMPs which were highly procoagulant. This increment was especially significant at 0.2 μM of daunorubicin or more. Blockade of PS with lactadherin inhibited over 90% of HUVECs and EMPs PCA. However, anti-TF antibody had no significant inhibition effect. Our results demonstrate that daunorubicin treatment enhanced PCA of HUVECs through PS exposure and shedding of procoagulant EMPs. Lactadherin acts as an efficient anticoagulant in this process.
Optimisation of the diagnostic strategy for suspected deep-vein thrombosis in primary care
Authors: van der Velde Eit , ten Cate Arina , Prins Martin , van Weert Henk , Stoffers H. E. Jelle , Buller Harry , Oudega Ruud , Hoes Arno , Janssen Kristel , Toll Diane , Moons Karel 
Published: October 2010

SummaryRecently, a diagnostic score was developed to safely exclude deep-vein thrombosis (DVT) in primary care. A large prospective study, in which general practitioners used this diagnostic score to decide which patients needed referral, revealed that the number of referrals for ultra-sound measurements was reduced by almost 50%, at the cost of an acceptably low risk (1.4%, 95% confidence interval [CI] 0.6% to 2.9%) of venous thromboembolic events in non-referred patients. However, simple adjustments to the diagnostic score (so-called updating) might further improve the accuracy; i.e. reduce the proportion of missed diagnoses (safety) or increase the proportion of patients who do not need to be referred (efficiency). We applied two updating methods to determine whether adjusting the weights of the predictors or adding new predictors could further improve the accuracy of the diagnostic score. The weights of the predictors did not need to be adjusted, but inclusion of ‘history of DVT’ and ‘prolonged travelling’ significantly added predictive value (p-values 0.014 and 0.023, respectively). However, adding these predictors to the diagnostic score did not improve the safety and efficiency: at equal safety (1.4% missed diagnoses among the non-referred patients), the efficiency was lower (43.5%, 95% CI 40.4% to 46.6% compared to 49.4%, 95% CI 46.3% to 52.5%). The diagnostic score for excluding DVT in primary care has good accuracy in its original form and could not be improved by including additional predictors. This suggests that the original diagnostic score can be used to safely exclude clinically suspected DVT in primary care.
Prospective study of ABO blood type and the risk of pulmonary embolism in two large cohort studies
Authors: Kabrhel Christopher , Varraso Raphaëlle , Kraft Peter , Rimm Eric , Goldhaber Samuel , Camargo Carlos , Fuchs Charles , Wolpin Brian 
Published: October 2010

SummaryPrior studies have suggested an association of ABO blood type and the risk of venous thromboembolism; however, most studies were retrospective and lacked important covariates or validated endpoints. Moreover, risk estimates varied widely across studies. Therefore, we prospectively examined the association of blood type and the risk of incident pulmonary embolism (PE) in two large cohort studies, the Nurses’ Health Study and Health Professionals Follow-up Study. During 1,010,378 person-years of follow-up among 77,025 women and 30,105 men, 499 participants developed PE. Compared to those with O-blood type, participants with non-O blood type had multivariable-adjusted hazard ratios (HR) of 1.86 (95% CI, 1.35–2.57) for idiopathic PE, 1.29 (95% CI, 1.03–1.62) for non-idiopathic PE, and 1.46 (95% CI, 1.22–1.76) for any PE. Hazard ratios were similar for participants with blood types A, B, and AB. Age-adjusted absolute rates of idiopathic PE over 10 years of follow-up differed by blood type: 0.11% for O, 0.20% for A, 0.19% for AB, and 0.21% for B. For idiopathic PE, the population attributable fraction was 33% for inheritance of non-O blood type. Among past and current smokers, participants with non-O vs. O-blood type had a HR for idiopathic PE of 2.56 (95% CI, 1.61–4.08). Among never smokers, the HR for idiopathic PE was 1.30 (95% CI, 0.82–2.05; Pinteraction=0.04). In two large, prospective cohorts, ABO blood type was significantly associated with the risk of idiopathic and non-idiopathic PE, with even greater risk for idiopathic PE among current and past smokers with non-O blood type.