bluuebunny/crossref_metadata_2025_split huggingface dataset:
Permissibility and use of options for hedging purposes in Islamic Finance
Authors: Smolarski Jan , Schapek Michael , Tahir Mohammad Iqbal 
Published: April 2006

AbstractThe debate concerning permissibility and use of options in Islamic finance is ongoing, and the issue is far from settled. Current analyses on this issue appear to focus on taking of unnecessary risks ( gharar), the perceived lack of a physical asset in an options contract, and the possibility of exploitation of the ignorant. To the extent that these factors are involved, options are not permitted under Islamic teachings (the Shariah).In this article, we investigate whether options may be permitted for hedging purposes in Islamic finance. We use equity options as an example in our analysis. After providing a brief overview of options markets, we review the existing literature and critically examine other work such as the religious decrees (fatwas). We also provide two examples, one each of call and put options, to illustrate the managerial issue of use of options for hedging purposes.Our analysis shows that options may be permitted for hedging purposes in Islamic finance as long as the underlying economic activities are themselves permissible (halal) from an Islamic point of view. The analysis also indicates that one of the key issues is related to unnecessary risk taking. The avoidance or reduction of such risks in hedging situations is largely dependent on the settlement and clearing function of the exchanges trading options, which effectively provides a guarantee of delivery. Mutual consent for entering into or canceling contracts and the issue of intangible assets also play a role in determining if options are permissible under the Shariah. We conclude the article by urging experts of Islamic jurisprudence to understand the theory and mechanics of options and use group ijitihad (consensus opinion of Islamic scholars) in conjunction with academics and experts in financial markets and instruments on this vital issue in contemporary finance for the benefit of the Islamic world as well as those trading with the Islamic world. © 2006 Wiley Periodicals, Inc.
Staphylococcus AureusColonization and the Risk of Infection in Critically Ill Patients
Authors: Keene Adam , Vavagiakis Peter , Lee Mei-Ho , Finnerty Kathryn , Nicolls Deborah , Cespedes Christian , Quagliarello Bianca , Chiasson Mary Ann , Chong David , Lowy Franklin D. 
Published: April 2006

AbstractObjective:To evaluate the relationship betweenStaphylococcus aureusnasal and tracheal colonization and infection in medical intensive care unit (MICU) patients. The primary outcome was the incidence ofS. aureusinfection in colonized versus non-colonized patients.Design:Prospective, observational cohort study. Patients admitted to the MICU during the study period were screened forS. aureusnasal and tracheal colonization by culture and a PCR assay twice weekly. Demographic, clinical, and microbiologic data were collected in the MICU and for 30 days after discharge. PFGE and antibiotic susceptibility testing were performed on allS. aureusnasal, tracheal, and clinical isolates.Results:Twenty-three percent of patients (47 of 208) were nasally colonized withS. aureus. Twenty-four percent of these patients developedS. aureusinfections versus 2% of noncolonized patients (P< .01). Nine of 11 patients with both nasal colonization and infection were infected by their colonizing strain. Two of 47 nasally colonized patients developed an infection with a different strain ofS. aureus. Fifty-three percent of intubated patients with nasal colonization (10 of 19) had tracheal colonization withS. aureusas opposed to 4.9% of intubated, non-colonized patients (3 of 61) (P< .01). Parenteral antibiotics were ineffective at clearing nasal colonization. PCR detectedS. aureuscolonization (nasal and tracheal) within 6.5 hours with a sensitivity of 83% and a specificity of 99%.Conclusions:The incidence ofS. aureusinfection was significantly elevated in nasally colonized MICU patients. Techniques to rapidly detect colonization in this population may make targeted topical prevention strategies feasible. (Infect Control Hosp Epidemiol 2005;26:622-628)
The Effects of Prolonged Ethanol Exposure on the Mechanical Properties of Polyurethane and Silicone Catheters Used for Intravascular Access
Authors: Crnich Christopher J. , Halfmann Jeremy A. , Crone Wendy C. , Maki Dennis G. 
Published: April 2006

AbstractBackground:Products containing alcohol are commonly used with intravascular devices at insertion, to remove lipids from occluded intravascular devices used during parenteral nutrition, and increasingly for the prevention and treatment of intravascular device-related bloodstream infection. The effects of alcohol on the integrity of intravascular devices remain unknown.Methods:Two types of widely used commercial peripherally inserted central catheters, one made of polyether-urethane and one made of silicone, were exposed to a 70% etha-nol lock solution for up to 10 weeks. Mechanical testing was performed to identify force-at-break, stress, strain, modulus of elasticity, modulus of toughness, and wall area of ethanol-exposed and control catheters.Results:No significant differences between exposed and unexposed catheters were identified for any of the mechanical parameters tested except for a marginal reduction in the modulus of elasticity for both polyetherurethane and silicone catheters and minor increases in the wall area of polyetherurethane catheters.Conclusions:These data indicate that exposure to a 70% ethanol lock solution does not appreciably alter the integrity of selected commercial polyetherurethane and silicone catheters. Given the greatly expanded use of alcoholic solutions with intravascular devices of all types, we believe that manufacturers would be well advised to subject their catheters and other intravascular devices to formal testing of the type employed in this study.
A Large Nosocomial Outbreak of Hepatitis C Virus Infections at a Hemodialysis Center
Authors: Savey Anne , Simon Fernando , Izopet Jacques , Lepoutre Agnès , Fabry Jacques , Desenclos Jean-Claude 
Published: April 2006

AbstractObjective:To identify modes of HCV transmission during an outbreak of HCV infection in a hemodialysis unit.Design:An epidemiologic study, virologie analysis, assessment of infection control practices and procedures, and technical examination of products and dialysis machines.Setting:A private hemodialysis unit treating approximately 70 patients.Patients:Detection of HCV RNA by PCR was performed among patients receiving dialysis in 2001. Case-patients were patients who had a first positive result for HCV RNA between January 2001 and January 2002 and either acute hepatitis, a seroconversion for HCV antibodies, or a previous negative result. Three control-patients were randomly selected per case-patient.Results:Of the 61 patients treated in the unit in 2001 and not infected with HCV, 22 (36.1%) became case-patients with onset from May 2001 to January 2002 for an incidence density rate of 70 per 100 patient-years. Phylogenic analysis identified four distinct HCV groups and an index case-patient for each with a similar virus among patients already known to be infected. No multidose medication vials or material was shared between patients. Connection to a dialysis machine by a nurse who had connected an HCV-infected patient “just before” or “one patient before” increased the risk of HCV infection, whereas using the same dialysis machine after a patient infected with HCV did not. Understating, lack of training, and breaches in infection control were documented. Direct observation of practices revealed frequent flooding of blood into the double filter on the arterial pressure tubing set.Conclusions:During this outbreak, HCV transmission was mainly patient to patient via healthcare workers' hands. However, transmission via dialysis machines because of possible contamination of internal components could not be excluded.
Usefulness of a Rapid Human Immunodeficiency Virus-1 Antibody Test for the Management of Occupational Exposure to Blood and Body Fluid
Authors: Landrum Michael L. , Wilson Clarissa H. , Perii Luci P. , Hannibal Sandra L. , O'Connell Robert J. 
Published: April 2006

AbstractObjective:To describe the usefulness of the OraQuick Rapid HIV-1 Antibody Test (OraSure Technologies, Bethlehem, PA) in cases of occupational exposure regarding its use with source-patient sera, effects on post-exposure prophylaxis (PEP) use, potential cost savings, and effects on healthcare worker (HCW) stress reaction symptoms.Design:Before-and-after analysis.Setting:A 269-bed, tertiary-care medical center with adjacent clinics.Participants:All source-patients and HCWs experiencing an occupational exposure during the study period.Methods:Use of the OraQuick test with patient sera was validated prior to its use for occupational exposures. Exposures from January 1 through July 10, 2003 (enzyme immunoassay [EIA] group) and July 11 through December 31, 2003 (OraQuick group) were retrospectively reviewed and the use and cost of PEP was compared for each group. Randomly selected HCWs from both groups completed a survey to assess their stress reaction symptoms.Results:After exclusion, there were 71 exposures in the EIA group and 79 in the OraQuick group. OraQuick results were 100% concordant with the reference standard of EIA and Western blot using patient sera. The mean number of doses ingested per course of PEP was significantly higher for HCWs in the EIA group (3.8; range, 0 to 6) compared with the OraQuick group (1.2; range, 0 to 3; P = .016). Cost analysis revealed a mean savings of $6.62 with the OraQuick test per occupational exposure. Although the survey failed to detect an overall reduction in HCW stress reaction symptoms using OraQuick for source-patient testing, 11 HCWs in the EIA group had repetitive thoughts of the exposure compared with 5 in the OraQuick group (P= .049).Conclusion:Because of the reduction in ingested doses of unnecessary PEP and reduced cost of occupational exposure management with their use, rapid HJV-antibody tests should be the preferred method for source-patient testing following an occupational exposure.
Differential Functional Activation of Chemokine Receptor CXCR4 Is Mediated by G Proteins in Breast Cancer Cells
Authors: Holland Jane D. , Kochetkova Marina , Akekawatchai Chareeporn , Dottore Mara , Lopez Angel , McColl Shaun R. 
Published: April 2006

AbstractCXCR4 is a G protein–coupled receptor of considerable biological significance, and among its numerous functions, it is suggested to play a critical role in cancer metastasis. We have investigated the expression and function of CXCR4 in a range of breast cancer cell lines covering a spectrum of invasive phenotypes and found that, while surface levels of CXCR4 were uniform across the entire panel, only highly invasive cells that are metastatic in immunocompromised mice expressed functional receptors. CXCL12/SDF-1 induced cellular responses such as calcium mobilization, actin polymerization, and chemotaxis in metastatic cells, whereas noninvasive cells were unresponsive. Moreover, CXCL12 activated multiple signaling pathways downstream of G proteins in highly invasive cells but failed to activate any of the examined kinase cascades in noninvasive cell lines. This blockade in nonmetastatic cell lines seems to be due to the inability of G protein α and β subunits to form a heterotrimeric complex with CXCR4. Gα and Gβ were able to bind to CXCR4 independently in all cell lines, but the association of G protein αβγ heterotrimers with the receptor, a prerequisite for signal transduction downstream from G protein–coupled receptors, was only observed in the highly invasive cell lines. Our findings show, for the first time, that CXCR4 function is subject to complex and potentially tightly controlled regulation in breast cancer cells via differential G protein–receptor complex formation, and this regulation may play a role in the transition from nonmetastatic to malignant tumors. (Cancer Res 2006; 66(8): 4117-24)
Growth-Regulated Oncogene Is Pivotal in Thrombin-Induced Angiogenesis
Authors: Caunt Maresa , Hu Liang , Tang Thomas , Brooks Peter C. , Ibrahim Sherif , Karpatkin Simon 
Published: April 2006

Abstract
The mechanism of thrombin-induced angiogenesis is poorly understood. Using a gene chip array to investigate the pro-malignant phenotype of thrombin-stimulated cells, we observed that thrombin markedly up-regulates growth-regulated oncogene-α (GRO-α) in several tumor cell lines as well as endothelial cells by mRNA and protein analysis. Thrombin enhanced the secretion of GRO-α from tumor cells 25- to 64-fold. GRO-α is a CXC chemokine with tumor-associated angiogenic as well as oncogenic activation following ligation of its CXCR2 receptor. GRO-α enhanced angiogenesis in the chick chorioallantoic membrane assay 2.2-fold, providing direct evidence for GRO-α as an angiogenic growth factor. Anti-GRO-α antibody completely inhibited the 2.7-fold thrombin-induced up-regulation of angiogenesis, as well as the 1.5-fold thrombin-induced up-regulation of both endothelial cell cord formation in Matrigel and growth in vitro. Thrombin as well as its PAR-1 receptor activation peptide [thrombin receptor activation peptide (TRAP)] as well as GRO-α all markedly increased vascular regulatory proteins and growth factors: matrix metalloproteinase (MMP)-1, MMP-2, vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang-2), CD31, and receptors KDR and CXCR2 in human umbilical vein endothelial cells. All of the thrombin/TRAP gene up-regulations were completely inhibited by anti-GRO-α antibody and unaffected by irrelevant antibody. Similar inhibition of gene up-regulation as well as thrombin-induced chemotaxis was noted with small interfering RNA (shRNA) GRO-α KD 4T1 breast tumor and B16F10 melanoma cells. In vivo tumor growth studies in wild-type mice with shRNA GRO-α KD cells revealed 2- to 4-fold impaired tumor growth, metastasis, and angiogenesis, which was not affected by endogenous thrombin. Thus, thrombin-induced angiogenesis requires the up-regulation of GRO-α. Thrombin up-regulation of GRO-α in tumor cells as well as endothelial cells contributes to tumor angiogenesis. (Cancer Res 2006; 66(8): 4125-32)
Brain-Derived Neurotrophic Factor Activation of TrkB Induces Vascular Endothelial Growth Factor Expression via Hypoxia-Inducible Factor-1α in Neuroblastoma Cells
Authors: Nakamura Katsuya , Martin Kelly C. , Jackson Jennifer K. , Beppu Kiichiro , Woo Chan-Wook , Thiele Carol J. 
Published: April 2006

AbstractThe extent of angiogenesis and/or vascular endothelial growth factor (VEGF) expression in neuroblastoma tumors correlates with metastases, N-myc amplification, and poor clinical outcome. Recently, we have shown that insulin-like growth factor-I and serum-derived growth factors stimulate VEGF expression in neuroblastoma cells via induction of hypoxia-inducible factor-1α (HIF-1α). Because another marker of poor prognosis in neuroblastoma tumors is high expression of brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor, TrkB, we sought to evaluate the involvement of BDNF and TrkB in the regulation of VEGF expression. VEGF mRNA levels in neuroblastoma cells cultured in serum-free media increased after 8 to 16 hours in BDNF. BDNF induced increases in VEGF and HIF-1α protein, whereas HIF-1β levels were unaffected. BDNF induced a 2- to 4-fold increase in VEGF promoter activity, which could be abrogated if the hypoxia response element in the VEGF promoter was mutated. Transfection of HIF-1α small interfering RNA blocked BDNF-stimulated increases in VEGF promoter activity and VEGF protein expression. The BDNF-stimulated increases in HIF-1α and VEGF expression required TrkB tyrosine kinase activity and were completely blocked by inhibitors of phosphatidylinositol 3-kinase (PI3K) and mammalian target of rapamycin (mTOR) pathways. These data indicate that BDNF plays a role in regulating VEGF levels in neuroblastoma cells and that targeted therapies to BDNF/TrkB, PI3K, mTOR signal transduction pathways, and/or HIF-1α have the potential to inhibit VEGF expression and limit neuroblastoma tumor growth. (Cancer Res 2006; 66(8): 4249-55)
Nitric Oxide–Donating Aspirin Prevents Pancreatic Cancer in a Hamster Tumor Model
Authors: Ouyang Nengtai , Williams Jennie L. , Tsioulias George J. , Gao Jianjun , Iatropoulos Michael J. , Kopelovich Levy , Kashfi Khosrow , Rigas Basil 
Published: April 2006

AbstractTo evaluate the chemopreventive effect of nitric oxide–donating aspirin (NO-ASA), an ASA bearing a NO-releasing moiety, against pancreatic cancer, we studied six groups of female Syrian golden hamsters: groups 1 to 3 (n = 12 each) were given saline and groups 4 to 6 (n = 17) the carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) s.c. in five weekly injections (the first, 70 mg/kg, and the remaining, 20 mg/kg each). Control and BOP-treated hamsters were fed a NO-ASA 3,000 ppm or conventional ASA 3,000 ppm or control diet for 19 weeks. Groups 1 to 3 had no tumors. Compared with the BOP/vehicle group, NO-ASA reduced the incidence (88.9%, P &lt; 0.003) and multiplicity (94%, P &lt; 0.05) of pancreatic cancer; ASA had no statistically significant effect. NO-ASA arrested the transition from PanIN2 to PanIN3 and carcinoma. The proliferation (proliferating cell nuclear antigen) / apoptosis (terminal deoxyribonucleotide transferase–mediated nick-end labeling) ratio of ductal cells increased with the histologic severity of the ductal lesion; NO-ASA suppressed it significantly during all stages except PanIN1A. p21WAF1/CIP1, undetectable in normal cells, was progressively induced in neoplastic cells and suppressed by NO-ASA up to PanIN3. Nuclear factor-κB activation, absent in normal tissue, increased progressively (17-fold in cancer); NO-ASA suppressed it throughout and significantly in PanIN1B and PanIN2. Cyclooxygenase-2 expression, absent during early stages, was induced 6-fold in carcinoma and suppressed by NO-ASA in PanIN3 and carcinoma. Conventional ASA had no effect on these molecular markers. Thus, NO-ASA profoundly prevented pancreatic cancer and modulated multiple molecular targets in this model system; conventional ASA had no such effects. NO-ASA merits further evaluation as a chemopreventive agent against pancreatic cancer. (Cancer Res 2006; 66(8): 4503-11)
Subtractive Transcriptomics: Establishing Polarity Drives In vitro Human Endothelial Morphogenesis
Authors: Glesne David A. , Zhang Wen , Mandava Suneeta , Ursos Lyann , Buell Margaret E. , Makowski Lee , Rodi Diane J. 
Published: April 2006

Abstract
Although investigations of mature normal and tumor-derived capillaries have resulted in characterization of these structures at the phenotypic level, less is known regarding the initial molecular cues for cellular assembly of endothelial cells into human capillaries. Here, we employ a novel combination of microenvironmental manipulation and microarray data filtration over narrowly delineated temporal data series to identify the morphogenesis component apart from the proliferation component, as pooled human microvascular-derived endothelial cells are induced to form capillary-like structures in vitro in a murine tumor-derived matrix. The 217 morphogenesis-specific genes identified using this subtractive transcriptomics approach are mostly independent of the angiogenic proteins currently used as therapeutic targets for aberrant angiogenesis. Quantitative real-time PCR was used to validate 20% of these transcripts. Immunofluorescent analysis of proliferating and tube-forming cells validates at the protein level the morphogenesis-specific expression pattern of 16 of the 217 gene products identified. The transcripts that are selectively up-regulated in tube-forming endothelial cells reveal a temporal expression pattern of genes primarily associated with intracellular trafficking, guided migration, cytoskeletal reorganization, cellular adhesion, and proliferation inhibition. These data show that a sequential up-regulation of genes that establish and maintain polarity occurs during migration and morphogenesis of in vitro human endothelial cells undergoing tubulogenesis; some of which may well be effective as novel antiangiogenic drug targets. (Cancer Res 2006; 66(8): 4030-40)
Inhibition of Mammalian Thioredoxin Reductase by Some Flavonoids: Implications for Myricetin and Quercetin Anticancer Activity
Authors: Lu Jun , Papp Laura V. , Fang Jianguo , Rodriguez-Nieto Salvador , Zhivotovsky Boris , Holmgren Arne 
Published: April 2006

Abstract
The thioredoxin system, composed of thioredoxin reductase (TrxR), thioredoxin (Trx), and NADPH, exerts a wide range of activities in cellular redox control, antioxidant function, cell viability, and proliferation. Recently, the selenocysteine (Sec)-containing mammalian TrxR has emerged as a new target for anticancer drug development because TrxR and Trx are overexpressed in many aggressive tumors and the tumor cells seem to be more dependent on Trx system than normal cells. Here we have investigated the inhibition of mammalian TrxR by flavonoids which have been presumed to be cancer chemoprevention agents because of their antioxidant activities. Myricetin and quercetin were found to have strong inhibitory effects on mammalian TrxRs with IC50 values of 0.62 and 0.97 μmol/L, respectively. The inhibition was shown to be concentration, NADPH, and time dependent and involved an attack on the reduced COOH-terminal -Cys-Sec-Gly active site of TrxR. Oxygen-derived superoxide anions enhanced the inhibitory effect whereas anaerobic conditions attenuated inhibition. Spectral analysis suggested that the flavonols might perform their inhibitory effects via semiquinone radicals. Additionally, the flavonols had the potential to inhibit the growth of A549 cells with the same potency as inhibition of TrxR. TrxR activity in the cell lysates was reduced on treatment with myricetin &gt;50 μmol/L, which coincided with the oxidization of Trx. The cell cycle was arrested in S phase by quercetin and an accumulation of cells in sub-G1 was observed in response to myricetin. Thus, the anticancer activity of quercetin and myricetin may be due to inhibition of TrxR, consequently inducing cell death. (Cancer Res 2006; 66(8): 4410-8)