bluuebunny/crossref_metadata_2025_split huggingface dataset:
Confocal Raman microscopy for simultaneous monitoring of partitioning and disordering of tricyclic antidepressants in phospholipid vesicle membranes
Authors: Fox Christopher B. , Harris Joel M. 
Published: September 2009

AbstractCharacterization of drug–membrane interactions is important in order to understand the mechanisms of action of drugs and to design more effective drugs and delivery vehicles. Raman spectra provide compositional and conformational information of drugs and lipid membranes, respectively, allowing membrane disordering effects and drug partitioning to be assessed. Traditional Raman spectroscopy and other widely used bioanalytical techniques such as differential scanning calorimetry (DSC) and nuclear magnetic resonance (NMR) typically require high sample concentrations. Here, we describe how temperature‐controlled, optical‐trapping confocal Raman microscopy facilitates the analysis of drug–membrane interactions using micromolar concentrations of drug, while avoiding drug depletion from solution by working at even lower lipid concentrations. The potential for confocal Raman microscopy as an effective bioanalytical tool is illustrated using tricyclic antidepressants (TCAs), which are cationic amphiphilic molecules that bind to phospholipid membranes and influence lipid phase transitions. The interaction of these drugs with vesicle membranes of differing head‐group charge is investigated while varying the ring and side‐chain structure of the drug. Changes in membrane structure are observed in Raman bands that report intra‐ and intermolecular orderversustemperature. The partitioning of drugs into the membrane can also be determined from the Raman scattering intensities. These results demonstrate the usefulness of confocal Raman microscopy for the analysis of drug–membrane systems at biologically relevant drug concentrations. Effective tools for monitoring drug–membrane interactions are crucial for rational design of new drugs. Copyright © 2009 John Wiley & Sons, Ltd.
Silver nanorods used to promote SERS as a quantitative analytical tool
Authors: Gu Geun Hoi , Suh Jung Sang 
Published: September 2009

AbstractWe have fabricated silver nanorod arrays by electrodepositing the nanorods evenly in the shallow pores of porous anodic aluminum oxide (AAO) templates. The diameter and length were 28 and 44 nm, respectively. The maxima of the transverse and longitudinal modes of the surface plasmon were near 417 and 511 nm, respectively. A good surface‐enhanced Raman scattering (SERS) spectrum was observed by excitation with the 514.5‐nm laser line. The SERS intensity increased almost linearly upon malachite green isothiocyanate adsorption on the tips of the silver nanorods as the concentration of the mother solutions increased. Our results show that silver nanorods fabricated on AAO templates could be used as an SERS substrate for quantitative analyses. Copyright © 2009 John Wiley & Sons, Ltd.
Probing antiaromaticity: resonance Raman investigation of a series of differently substituted boroles
Authors: Köhler Juliane , Lindenmeier Sonja , Fischer Ingo , Braunschweig Holger , Kupfer Thomas , Gamon Daniela , Chiu Ching‐Wen 
Published: September 2009

AbstractWe report an investigation of four differently substituted boroles by resonance Raman (RR) spectroscopy with the aim of gaining insight into the structural changes that occur upon electronic π–π* excitation in the five‐membered BC4 ring. Such boroles are prototypes for the theory of antiaromaticity, because the empty pz orbital at the boron interacts with the π system of the carbon backbone to delocalize the four π electrons. The magnitude of this interaction depends on the substituents at the boron atom. In all compounds, an intense band appears around 1600 cm−1, which can be assigned to a CC stretching vibration. The selective amplification of this mode indicates an expansion of the borole ring upon electronic excitation. The resonant enhancement of another mode at around 1300 cm−1, which can be assigned to a vibration between the boron and the substituent, gives evidence that the degree of antiaromaticity in the borole depends strongly on the interaction between the substituent at the boron atom with the empty pz orbital of the boron. When the boron is connected to a ferrocene, this band appears with high intensity, indicating a strong interaction between B and Fe. Furthermore, we studied the dependence of the excitation wavelength on the Raman intensities. In addition, we used DFT calculations to determine the vibrational wavenumbers. Copyright © 2009 John Wiley & Sons, Ltd.
Effect of thermal treatment on physicochemical composition and sensory qualities, including ‘foxy’ methyl anthranilate of interspecific variety Golden Muscat (Vitis vinifera × Vitis labrusca) fortified wine made in Taiwan
Authors: Chen Chien‐Hao , Chang Ming‐Hsu , Shih Ming‐Kwei , Jiang Chii‐Ming , Wu Ming‐Chang 
Published: September 2009

AbstractBACKGROUND: The major defect of the interspecific variety Golden Muscat (Vitis vinifera × Vitis labrusca) is the inheritance of the specific foxy off‐flavours from the parent species Vitis labrusca. Thermal treatment is a traditional method of producing fortified wine that originated from the subtropical Portuguese island of Madeira. This technique was used to treat Golden Muscat fortified wine in order to investigate the effects of thermal treatment on the physicochemical composition and sensory qualities of the wine.RESULTS: The control wine had the lowest total phenol concentration, total flavonol concentration and total acidity. Increased colour intensity in all thermal‐treated samples was detected. The amount of foxy methyl anthranilate in the wine decreased significantly (P < 0.05) after thermal treatment. Panellists indicated that, compared to the control wine, the thermal‐treated wines had higher flavour complexity, flavour intensity, persistence and balance. The control wine exhibited an unpleasant foxy flavour.CONCLUSION: These results suggest that the thermal treatment technique can be used for the production of Golden Muscat fortified wines with desirable flavour. This technique could assist local winemakers to produce an interspecific variety Golden Muscat fortified wine of acceptable quality. Copyright © 2009 Society of Chemical Industry
Visible light induces no formation in sperm and endothelial cells
Authors: Ankri Rinat , Friedman Harry , Savion Naphtali , Kotev‐Emeth Shlomo , Breitbart Haim , Lubart Rachel 
Published: September 2009

AbstractBackgroundVisible light‐based stimulation using low‐intensity lasers, LEDs, and broadband visible light devices has been recently introduced for therapy of human tissues in the absence of exogenous photosensitizers. Nitric oxide (NO) formation might be a potential mechanism for photobiomodulation because it is synthesized in cells by nitric oxide synthase (NOS), which contains both flavin and heme groups that absorb visible light. NO synthesis may also result from increased reactive oxygen species (ROS), which are found in various cell cultures following visible light illumination. NO is mainly known for inducing blood vessel dilation by endothelial cells, and in sperm cells NO is considered as an important agent in acrosome reaction and capacitation process, which are essential for successful fertilization.PurposeTo study NO formation in endothelial and sperm cells following visible light irradiation.Materials and MethodsSperm and endothelial cells were illuminated with broadband visible light, 400–800 nm, 130 mW/cm2, for 5 minutes. During illumination, the endothelial cells were incubated in PBS free of Ca+2 and Mg+2, and the sperm cells were incubated in NKM buffer, to induce “stress conditions.” NO production was quantified by using the Griess reagent which reacts with nitrite in the medium to yield an Azo compound which has an absorption band at 540 nm.ResultsVisible light illumination increased NO concentration both in sperm and endothelial cells. Blue light was more effective than red. Light‐induced NO occurred only when endothelial cells were incubated in PBS free of Ca+2 and Mg+2, and in sperm cells, only when incubated in NKM.ConclusionLight induces NO formation in endothelial and sperm cells. In endothelial cells, NO formation may explain previous results demonstrating enhanced wound healing and pain relief following illumination. In illuminated sperm cells, NO formation may account for the enhanced fertilization rate. Lasers Surg. Med. © 2009 Wiley‐Liss, Inc.
Survival after orthotopic liver transplantation: The impact of antibody against hepatitis B core antigen in the donor
Authors: Yu Lei , Koepsell Thomas , Manhart Lisa , Ioannou George 
Published: September 2009

Abstract

Liver transplantation using grafts from donors with antibody against hepatitis B core antigen (anti-HBc) increases the recipients' risk of developing hepatitis B virus (HBV) infection post-transplantation. Our aim was to assess whether using such grafts was associated with reduced posttransplantation survival and whether this association depended on recipients' prior exposure to HBV on the basis of their pretransplantation serological patterns. Data were derived from the United Network for Organ Sharing on adult, cadaveric, first-time liver transplants performed between 1994 and 2006. Among recipients who did not have HBV infection before transplantation, those with anti-HBc–positive donors had significantly worse unadjusted posttransplantation patient survival than recipients with anti-HBc–negative donors [hazard ratio, 1.35; 95% confidence interval (CI), 1.21-1.50]. However, after adjustments for other predictors of posttransplantation survival, including donor age, donor race, and recipient underlying liver diseases, patient survival was not significantly different between the 2 groups (hazard ratio, 1.09; 95% CI, 0.97-1.24). Among recipients without antibody against hepatitis B surface antigen (anti-HBs), use of anti-HBc–positive donor grafts was associated with a trend toward worse survival (adjusted hazard ratio, 1.18; 95% CI, 0.95-1.46), whereas no such trend was observed among recipients positive for anti-HBs. In conclusion, in patients without HBV infection before transplantation, using anti-HBc–positive donors was not independently associated with worse posttransplantation survival. Matching these donors to recipients with anti-HBs pre-transplantation may be especially safe. Liver Transpl 15:1343–1350, 2009. © 2009 AASLD.
Rapamycin inhibits hepatic fibrosis in rats by attenuating multiple profibrogenic pathways
Authors: Bridle Kim R. , Popa Claudia , Morgan Maelle L. , Sobbe Amy L. , Clouston Andrew D. , Fletcher Linda M. , Crawford Darrell H. G. 
Published: September 2009

Abstract

Hepatic stellate cell transdifferentiation, epithelial-mesenchymal cell transition, and the ductular reaction each contribute to the development of hepatic fibrosis in cholestatic liver diseases. Inhibitors of mammalian target of rapamycin have antifibrotic properties. We evaluated the hypothesis that the antifibrotic action of rapamycin is due to attenuated myofibroblast proliferation in addition to an inhibitory effect on epithelial-mesenchymal transition and the ductular reaction. Hepatic fibrosis was induced by bile duct ligation, and rodents received 1.5 mg/kg/day rapamycin by subcutaneous infusion for 21 days. The expression of various markers of hepatic fibrosis, stellate cell transactivation, epithelial-mesenchymal transition, and the ductular reaction was compared between treated and untreated animals. Hepatic fibrosis, hepatic procollagen type 1 messenger RNA, and alpha-smooth muscle actin expression were significantly reduced in treated animals. Hepatic stellate cell procollagen expression and proliferation were also reduced by rapamycin. The following markers of epithelial-mesenchymal transition—vimentin protein expression, S100 calcium binding protein A4 and transforming growth factor beta 1 messenger RNA, and the mothers against decapentaplegic homolog signaling pathway—were all reduced after rapamycin treatment. The intensity of the ductular reaction was reduced by rapamycin as assessed by histopathological scoring and by reduced cytokeratin 19 expression. Rapamycin caused a reduction in hepatic progenitor cell proliferation. Together, these data show that multiple profibrogenic pathways are activated in an animal model of cholestasis and that rapamycin attenuates epithelial-mesenchymal transition and the ductular reaction as well as hepatic stellate cell activation. Liver Transpl 15:1315–1324, 2009. © 2009 AASLD.
Plasma disappearance rate of indocyanine green: A tool to evaluate early graft outcome after liver transplantation
Authors: Levesque Eric , Saliba Faouzi , Benhamida Sonia , Ichaï Philippe , Azoulay Daniel , Adam René , Castaing Denis , Samuel Didier 
Published: September 2009

Abstract

Indocyanine green clearance (Cl-ICG) has been used to assess liver function and hepatic blood flow mainly before and after hepatic surgery. Cl-ICG (invasive method) has been reported to be a good marker of early graft function after liver transplantation (LT). The goal of this study was to determine if the indocyanine green plasma disappearance rate (PDR-ICG), measured by a noninvasive technique (LiMON, Impulse Medical System, Munich, Germany), is predictive of complications and graft outcome after LT. From September 2005 to June 2006, 72 LT recipients were included in the study. PDR-ICG was measured daily (from day 0 to day 5 after LT) with a digital sensor after patients were injected with 0.25 mg/kg indocyanine green. A PDR-ICG cutoff level of 12.85%/minute was predictive of the development of a serious postoperative complication. The sequential changes of PDR-ICG enabled us to differentiate 2 groups: (1) patients with early severe complications (hepatic artery thrombosis, primary graft nonfunction, or sepsis) who had a low value of PDR-ICG during the first 5 posttransplantation days (average, 8.8 ± 4.5%/minute) and (2) patients who developed acute rejection and who had a progressive reduction of PDR-ICG between days 0 and 5 (from 25.5 ± 4.8 to 10.3 ± 2.5%/minute; P < 0.002). In conclusion, after LT, PDR-ICG (a noninvasive technique), measured regularly during the first 5 postoperative days, is a safe technique that can predict early postoperative complications. Liver Transpl 15:1358–1364, 2009. © 2009 AASLD.
Role of hydrogen sulfide in hepatic ischemia-reperfusion–induced injury in rats
Authors: Kang Kai , Zhao Mingyan , Jiang Hongchi , Tan Gang , Pan Shangha , Sun Xueying 
Published: September 2009

Abstract

Hydrogen sulfide (H2S) displays anti-inflammatory and cytoprotective activities as evidenced by the inhibition of myocardial ischemia-reperfusion injury and production of lipid peroxidation. H2S also exerts many physiological or pathological effects on livers. Therefore, we designed the present study to investigate the roles of H2S in hepatic ischemia-reperfusion (HIR)–induced injury in rats by measuring H2S levels, H2S synthesizing activity, and cystathionine γ-lyase (CSE) messenger RNA (mRNA) expression. We also applied DL-propargyl glycine (PAG) and sodium hydrosulfide (NaHS) to investigate their effects on the severity of liver injury induced by HIR. The levels of H2S, H2S production activity, and CSE mRNA expression in livers were increased by HIR. Administration of NaHS significantly attenuated the severity of liver injury and inhibited the production of lipid peroxidation, serum inflammatory factors [including nitric oxide, tumor necrosis factor α (TNF-α), interleukin 10, and intercellular cell adhesion molecule 1], cell apoptosis, and apoptosis-related proteins (including caspase-3, Fas, Fas ligand, and TNF-α), which were caused or elevated by HIR, whereas PAG aggravated them. However, NaHS or PAG did not show significant effects on the activation of caspase-9, which was also increased by HIR. Although further investigation is required, this study may indicate that H2S plays a protective role in HIR-induced injury. Liver Transpl 15:1306–1314, 2009. © 2009 AASLD.
Enfuvirtide: A safe and effective antiretroviral agent for human immunodeficiency virus–infected patients shortly after liver transplantation
Authors: Teicher Elina , Abbara Chadi , Duclos-Vallée Jean-Charles , Antonini Teresa , Bonhomme-Faivre Laurence , Desbois Delphine , Samuel Didier , Vittecoq Daniel 
Published: September 2009

Abstract

The aim of this study was to evaluate the impact of an enfuvirtide-based antiretroviral (ARV) regimen on the management of immunosuppression and follow-up in hepatitis C virus (HCV)/hepatitis B virus (HBV)/human immunodeficiency virus (HIV)–coinfected liver transplant patients in comparison with a lopinavir/ritonavir-based ARV regimen. Tacrolimus and cyclosporine trough concentrations were determined at a steady state during 3 periods: after liver transplantation without ARV treatment (period 1), at the time of ARV reintroduction (period 2), and 2 to 3 months after liver transplantation (period 3). The findings for 22 HIV-coinfected patients were compared (18 with HCV and 4 with HBV); 11 patients were treated with enfuvirtide and were matched with 11 lopinavir/ritonavir–exposed patients. During period 1, tacrolimus and cyclosporine A doses were 8 and 600 mg/day, respectively, and the trough concentrations were within the therapeutic range in both groups. In period 2, the addition of lopinavir/ritonavir to the immunosuppressant regimen enabled a reduction in the dose of immunosuppressants required to maintain trough concentrations within the therapeutic range (to 0.3 mg/day for tacrolimus and 75 mg/day for cyclosporine). Immunosuppressant doses were not modified by the reintroduction of enfuvirtide, there being no change in the mean trough concentrations over the 3 periods. CD4 cell counts remained at about 200 cells/mm. The HIV RNA viral load remained undetectable. Both groups displayed signs of mild cytolysis and cholestasis due to the recurrence of HCV, whereas no renal insufficiency was observed. Enfuvirtide is an attractive alternative to standard ARV therapy, facilitating the management of drug-drug interactions shortly after liver transplantation. Moreover, the lack of liver toxicity renders this drug valuable in the event of a severe HCV recurrence. Liver Transpl 15:1330–1335, 2009. © 2009 AASLD.
Prevalence of hepatitis E virus infection in liver transplant recipients
Authors: Haagsma Elizabeth B. , Niesters Hubert G. M. , van den Berg Arie P. , Riezebos-Brilman Annelies , Porte Robert J. , Vennema Harry , Reimerink Johan H. J. , Koopmans Marion P. G. 
Published: September 2009

Abstract

Hepatitis E virus (HEV) infection is known to run a self-limited course. Recently, chronic hepatitis E has been described in several immunosuppressed patients after solid organ transplantation. The prevalence of HEV infection after transplantation, however, is unknown. We studied HEV parameters [HEV RNA, HEV immunoglobulin M (IgM), and HEV immunoglobulin G (IgG) by enzyme-linked immunosorbent assay and confirmatory immunoblotting] in a cohort of 285 adult liver transplant recipients. The most recent freeze-stored sera were investigated, and if they were positive, a retrospective analysis was performed. Samples from 274 patients (96.1%) tested negative for all HEV parameters. This included a patient described earlier as having experienced an episode of chronic HEV hepatitis in the past. One patient was found positive for HEV RNA without HEV antibodies. She presently suffers from chronic HEV hepatitis and has also been described before. Sera from 9 patients tested positive for HEV IgG without HEV IgM or HEV RNA. Six of these 9 patients (2.1% of the total) were found to have HEV IgG antibodies in retrospect related to an HEV infection at some time pre-transplant as they also tested positive in a pretransplant serum sample. One of these 9 patients suffered in retrospect from a chronic HEV infection with mild hepatitis between 2 and 5 years after liver transplantation on the basis of the course of HEV RNA, IgM, and IgG, aminotransferases, and liver histology. Overall, the prevalence of acquired HEV hepatitis after liver transplantation was 1% in this cohort. We conclude that liver transplant recipients have a risk for chronic HEV infection, but the prevalence is low. Liver Transpl 15:1225–1228, 2009. © 2009 AASLD.
Severe left-sided heart failure early after liver transplantation
Authors: Schnell Frédéric , Donal Erwan , Lorho Richard , Lavoué Sylvain , Gacouin Arnaud , Compagnon Philippe , Boudjema Karim , Mabo Philippe , Tulzo Yves Le , Camus Christophe 
Published: September 2009

Abstract

Left-sided heart failure (LHF) after liver transplantation (LT) is rare and poorly understood. We performed a case-control study. We reviewed the data of all patients with LHF after LT at our center from November 2000 to July 2007. Each case was matched to 1 LT control without LHF for age, sex, date of transplantation, and liver disease. Twenty of 599 patients developed LHF (3.3%). Pretransplant cardiovascular characteristics and risk factors were similar in cases and controls, except for the prevalence of left ventricular enlargement, which was greater in controls. At the time of diagnosis, the median left ventricular ejection fraction was 25% in cases, and increased afterload was documented by markedly elevated vascular resistances. The prevalence of infection at the time of LHF in cases was higher (55%) than in controls (10%, P = 0.02). The reported causes of LHF were infection [bacterial (n = 1) or viral (n = 7)], intraoperative cardiac arrest (n = 2), and unknown (n = 10). In comparison with their controls, cases with immediate postoperative LHF (day 0) did not have a higher Model for End-Stage Liver Disease (MELD) score (15 versus 21.5) or infection prevalence rate (17% versus 34%), whereas those with later onset LHF had a significantly higher MELD score (25.5 versus 17, P = 0.01) and infection prevalence rate (71% versus 0%, P = 0.002). Mortality was 45% in cases versus 0% in controls (P = 0.004), and the 11 cases who survived recovered from LHF. In conclusion, LHF after LT carries a high mortality risk and may have different causes. Except for immediate postoperative cases, an infection and an elevated MELD score appear to be determinant. Liver Transpl 15:1296–1305, 2009. © 2009 AASLD.