bluuebunny/crossref_metadata_2025_split huggingface dataset:
Angiotensin converting enzyme inhibitor induced angio‐oedema: a review of the pathophysiology and risk factors
Authors: Hoover T. , Lippmann M. , Grouzmann E. , Marceau F. , Herscu P. 
Published: July 2009

SummaryAngio‐oedema (AE) is a known adverse effect of angiotensin converting enzyme inhibitor (ACE‐I) therapy. Over the past several decades, evidence of failure to diagnose this important and potentially fatal reaction is commonly found in the literature. Because this reaction is often seen first in the primary care setting, a review was undertaken to analyse and document the keys to both diagnostic criteria as well as to investigate potential risk factors for ACE‐I AE occurrence. A general review of published literature was conducted through Medline, EMBASE, and the Cochrane Database, targeting ACE‐I‐related AE pathomechanism, diagnosis, epidemiology, risk factors, and clinical decision making and treatment. The incidence and severity of AE appears to be on the rise and there is evidence of considerable delay in diagnosis contributing to significant morbidity and mortality for patients. The mechanism of AE due to ACE‐I drugs is not fully understood, but some genomic and metabolomic information has been correlated. Additional epidemiologic data and clinical treatment outcome predictors have been evaluated, creating a basis for future work on the development of clinical prediction tools to aid in risk identification and diagnostic differentiation. Accurate recognition of AE by the primary care provider is essential to limit the rising morbidity associated with ACE‐I treatment‐related AE. Research findings on the phenotypic indicators relevant to this group of patients as well as basic research into the pathomechanism of AE are available, and should be used in the construction of better risk analysis and clinical diagnostic tools for ACE‐I AE.Cite this as: T. Hoover, M. Lippmann, E. Grouzmann, F. Marceau and P. Herscu,Clinical & Experimental Allergy, 2010 (40) 50–61.
BAFF: a local and systemic target in autoimmune diseases
Authors: Moisini I , Davidson A 
Published: July 2009

SummaryBAFF (B lymphocyte activating factor of the tumour necrosis factor family) is a vital homeostatic cytokine for B cells that helps regulate both innate and adaptive immune responses. Increased serum levels of BAFF are found in a number of different autoimmune diseases, and BAFF is found in inflammatory sites in which there is lymphoid neogenesis. BAFF antagonism has been used in several autoimmune disease models, resulting in B cell depletion, decreased activation of T cells and dendritic cells (DC) and a reduction in the overall inflammatory burden. BAFF, through its interaction with BAFF-R, is required for survival of late transitional, marginal zone and mature naive B cells, all of which are depleted by BAFF blockade. Through their interactions with TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor) and BCMA (B cell maturation protein), BAFF and its homologue APRIL (a proliferation-inducing ligand), support the survival of at least some subsets of plasma cells; blockade of both cytokines results in a decrease in serum levels of immunoglobulin (Ig)G. In contrast, neither BAFF nor APRIL is required for the survival or reactivation of memory B cells or B1 cells. BAFF also helps DC maturation and interleukin (IL)-6 release and is required for proper formation of a follicular dendritic cell (FDC) network within germinal centres, although not for B cell affinity maturation. The clinical efficacy of BAFF blockade in animal models of autoimmunity may be caused both by the decline in the number of inflammatory cells and by the inhibition of DC maturation within target organs. Blockade of BAFF and its homologue APRIL are being explored for human use; several Phase I and II clinical trials of BAFF inhibitors for autoimmunity have been completed and Phase III trials are in progress.
Ecosystem engineering by tubificid worms stimulates macrophyte growth in poorly oxygenated wetland sediments
Authors: Mermillod‐Blondin Florian , Lemoine Damien G. 
Published: July 2009

Summary 1. Positive interactions driven by ecosystem engineers have been determined to be important community forces in stressed environments. By ameliorating habitat conditions, ecosystem engineering can create available ecological niches for other species. In poorly oxygenated sediments of freshwater wetlands, small invertebrates such as tubificid worms and chironomid larvae are known to function as active bioturbators; however, their effects on the growth and physiology of organisms which are constrained by low oxygenation of sediments have never been studied. 2. We examined whether the common bioturbator, Tubifex tubifex, significantly influences the growth and the physiological state of two plant species, Elodea canadensis and Myriophyllum spicatum, in experimental systems simulating a water–sediment interface of wetlands. We also quantified the influence of plant–animal interactions on biogeochemical processes (fluxes of oxygen and nitrogen at the water–sediment interface) and microbial compartment in sediments. 3. Tubificid worms stimulated growth of aboveground and belowground biomasses of the two plants through reduction in the anoxic stress in sediments. Myriophyllum spicatum, which was the best adapted to sedimentary anaerobic conditions, essentially increased its biomass whereas E. canadensis, less adapted to anaerobic conditions, shifted its root metabolism from anaerobic to aerobic. 4. Biogeochemical processes were not significantly influenced by plant–animal interactions: (i) oxygen flux from overlying water to sediments probably reached a threshold that could not be raised by the increased plant biomass induced by worms and (ii) nitrogen fluxes were essentially linked to bioturbation activities of worms. 5. Our study confirmed that the reduction in constraining variables by physical habitat modifications (ecosystem engineering) may play a crucial role in community and ecosystem processes. The fact that positive interactions measured between ecosystem engineers and plant species in anoxic wetland sediments were highly dependent on the ecophysiology of plant species suggests an extension of this first study to a wide range of macrophytes in order to determine the main plant functional traits driving plant–animal interactions in wetland sediments.
Pharmacokinetic study of a high‐purity factor IX concentrate (Factor IX Grifols®) with a 6‐month follow up in previously treated patients with severe haemophilia B
Authors: AZNAR J. A. , CABRERA N. , MATYSIAK M. , ZAWILSKA K. , GERCHEVA L. , ANTONOV A. , MONTAÑÉS M. , PÁEZ A. M. , LISSITCHKOV T. 
Published: July 2009

Summary.  Optimal replacement treatment in haemophilia B patients requires a good understanding of the pharmacokinetics of factor IX (FIX).The aim of this study was to compare the pharmacokinetic profile of Factor IX Grífols®, a highly purified human FIX concentrate with two specific pathogen inactivation/removal steps, to that of available FIX preparations.The study was an open, non‐randomized trial including 25 male subjects older than 12 years of age with severe haemophilia B. Pharmacokinetic profile of the FIX preparation regularly used by the subjects was determined as control. Pharmacokinetic profile of Factor IX Grifols® was determined twice, one 7–15 days after control assessment and second after a 6 months period had elapsed.Results showed that all products had peak plasma levels of FIX:C within 30 min. Mean recovery was 1.3 ± 0.3 IU dL−1 per IU kg−1 for Factor IX Grifols® and 1.0 ± 0.3 IU dL−1 per IU kg−1 for control products (P < 0.001). The mean terminal half‐life (t1/2) for Factor IX Grifols® was 26.7 h and 26.8 h for control product. Pharmacokinetic parameters after 6 months of treatment with Factor IX Grifols® did not statistically differ from the parameters obtained with the first infusion. There were no adverse events related to Factor IX Grifols® for the duration of the study.In conclusion, Factor IX Grifols® has adequated pharmacokinetic properties comparable to the control plasma‐derived FIX and these parameters remain stable after 6 months of treatment. Factor IX Grifols® can be an effective and safe plasma‐derived FIX concentrate for replacement therapy in haemophilia B patients.
Histopathological work‐up and interpretation of sentinel lymph nodes removed for vulvar squamous cell carcinoma
Authors: Regauer Sigrid 
Published: July 2009

Aims: To evaluate the work‐up of sentinel lymph nodes (SLNs) removed for vulvar pT1–pT2 squamous cell carcinoma (SCC). Inguinal lymphadenectomy yields metastases in only 30% of cases. Patients with missed inguinal disease, however, have a risk of dying from systemic disease. SLN dissections reduce morbidity, but work‐up should reliably identify metastatic disease.Methods and results: All SLNs removed from 38 patients with pT1–pT2 SCC and clinically negative inguinal lymph nodes were submitted for frozen section analysis. When negative, SLN were formalin‐fixed, sectioned entirely at 330‐μm intervals to produce three slides per millimetre [two haematoxylin and eosin (H&E) stained slides; one slide for immunohistochemistry]. If screening of H&E‐stained sections was negative, all remaining slides were subjected to immunohistochemistry with an antibody to cytokeratin. Twenty‐five of 38 patients (66%) were pN0, 7/38 (18%) had metastases on frozen sections/H&E stains. Immunohistochemistry detected micrometastases in two patients and single tumour cells and anucleate cell structures in four patients. In 12/13 patients the SLN metastases, including all single‐cell deposits, were from lichen sclerosus (LS)‐associated SCC. Twelve of 13 patients with metastases had a pT2 SCC.Conclusions: Micrometastases and single tumour cell deposits in SLNs are typical of LS‐associated vulvar SCC. Single tumour cell deposits in SNLs should be regarded as ‘positive’. Identification requires serial sectioning and immunohistochemical analysis of all removed SLNs.
Immunohistochemical and molecular genetic profiling of acquired cystic disease‐associated renal cell carcinoma
Authors: Pan Chin‐Chen , Chen Yann‐Jang , Chang Liang‐Che , Chang Yen‐Hwa , Ho Donald M‐T 
Published: July 2009

Aims:  Acquired cystic disease‐associated renal cell carcinoma (ACD‐associated RCC) is a unique neoplasm that specifically develops in the background of acquired cystic disease of the kidney. The aim was to analyse nine ACD‐associated RCCs from three patients to determine their immunohistochemical and molecular characteristics using immunohistochemistry, comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH).Methods and results:  ACD‐associated RCC preferentially expressed proximal nephron phenotype (CD10+/RCC marker+/α‐methylacyl‐CoA racemase+/glutathione S‐transferase‐α+/BerEP4+/cytokeratin 7–/E‐cadherin–/high‐molecular‐weight cytokeratin−/MOC31−). CGH combined with FISH demonstrated non‐random chromosomal gains clustering on chromosomes 3 (8/9), 7 (6/9), 16 (7/9), 17 (4/9) and Y (5/9). Chromosomal losses were uncommon. The chromosomal aberrations in all multifocal tumours were not identical for the same kidney or for the same patient, indicating a ‘field effect’ that induces multiple independent clones.Conclusions:  Although the genetic profiles of ACD‐associated RCC showed some similarity to those of papillary RCC, ACD‐associated RCC distinctly revealed frequent gains on chromosomes 3 and Y. ACD‐associated RCC is characterized not only by its particular clinical setting and histology, but also by its unique immunohistochemical and molecular genetic profiles.
Wolf survival and population trend using non‐invasive capture–recapture techniques in the Western Alps
Authors: Marucco Francesca , Pletscher Daniel H. , Boitani Luigi , Schwartz Michael K. , Pilgrim Kristy L. , Lebreton Jean‐Dominique 
Published: July 2009

Summary1. Reliable estimates of population parameters are often necessary for conservation management but these are hard to obtain for elusive, rare and wide‐ranging species such as wolvesCanis lupus.This species has naturally recolonized parts of its former habitat in Western Europe; however, an accurate and cost‐effective method to assess population trend and survival has not been implemented yet.2. We used open‐model capture–recapture (CR) sampling with non‐invasive individual identifications derived from faecal genotyping to estimate survival and trend in abundance for wolves in the Western Alps between 1999 and 2006. Our sampling strategy reduced individual heterogeneity in recaptures, thus minimizing bias and increasing the precision of the estimates.3. Young wolves had lower apparent annual survival rates (0·24 ± 0·06) than adult wolves (0·82 ± 0·04); survival rates were lower in the summer than in the winter for both young and adults. The wolf population in the study area increased from 21 ± 9·6 wolves in 1999 to 47 ± 11·2 wolves in late winter 2005; the population growth rate (λ = 1·04 ± 0·27) was lower than that recorded for other recolonizing wolf populations.4. We found a positive trend in wolf abundance, regardless of the method used. However, the abundance estimate based on snow‐tracking was on average 36·2% (SD = 13·6%) lower than that from CR modelling, because young dispersing wolves are likely to have lower sign detection rates in snow‐track surveys, a problem adequately addressed by CR sampling.5. Synthesis and applications.We successfully implemented a new method to assess large carnivore population trend and survival at large spatial scales. These are the first such estimates for wolves in Italy and in the Alps and have important management implications. Our approach can be widely applied to broader spatial and temporal scales for other elusive and wide‐ranging species in Europe and elsewhere.
Clinical spectrum of gram‐positive infections in lung transplantation
Authors: Gupta M.R. , Valentine V.G. , Walker Jr J.E. , Lombard G.A. , LaPlace S.G. , Seoane L. , Taylor D.E. , Dhillon G.S. 
Published: July 2009

Purpose. Gram‐positive (GP) organisms are among the most common cause of infections in early postsurgical and immunocompromised populations. Patients recovering from lung transplantation (LT) are particularly susceptible owing to the physiologic stress imposed by surgery and induction with intense immunosuppression. Sites, types, and timing of GP infections following LT  are not well documented. This report describes the clinical spectrum of GP infections and their effects on surgical airway complications (SAC) and bronchiolitis obliterans syndrome (BOS) following LT.Methods and materials. Data were collected from 202 patients undergoing 208 LT procedures at a single institution between November 1990 and November 2005. Data were retrospectively analyzed according to timing, location, and causative pathogen.Results. In the median follow‐up period of 2.7 years (range, 0–13.6 years), 137 GP infections were confirmed in 72 patients. Sites of infection included respiratory tract (42%), blood (27%), skin, wound and catheter (21%), and other (10%). GP pathogens identified were Staphylococcus species (77%), Enterococcus species (12%), Streptococcus species (6%), Pneumococcus (4%), and Eubacterium lentum (1%). The likelihood of SAC and BOS was increased in lung allograft recipients with GP pneumonia as compared with those without (hazard ratio 2.1; 95% confidence interval=1.5–3.1).Conclusions. GP organisms were responsible for infections in 40% of lung allograft recipients and most commonly isolated from the respiratory tract and blood stream. Staphylococcal species were most frequently identified, 42% of which were methicillin‐resistant Staphylococcus aureus (MRSA). Given the strong association of respiratory tract infections with the development of SAC and BOS, empiric antimicrobial strategies after LT should include agents directed against GP organisms, especially MRSA.
Long‐term prognosis of patients with endoscopically treated postoperative bile duct stricture and bile duct stricture due to chronic pancreatitis
Authors: Sakai Yuji , Tsuyuguchi Toshio , Ishihara Takeshi , Yukisawa Seigo , Sugiyama Harutoshi , Miyakawa Kaoru , Kuroda Yasuhisa , Yamaguchi Taketo , Ozawa Shinichi , Yokosuka Osamu 
Published: July 2009

AbstractAim:  To compare the outcome of endoscopic therapy for postoperative benign bile duct stricture and benign bile duct stricture due to chronic pancreatitis, including long‐term prognosis.Methods:  The subjects were 20 patients with postoperative benign bile duct stricture and 13 patients with bile duct stricture due to chronic pancreatitis who were 2 years or more after initial therapy. The patients underwent transpapillary drainage with tube exchange every 3 to 6 months until being free from the tube. Successful therapy was defined as a stent‐free condition without hepatic disorder.Results:  Endoscopic therapy was successful in 90% (18/20) of the patients with postoperative bile duct stricture. The stent was removed (stent free) in 100% (20/20) of the patients, but jaundice resolved in only 10% (2/20) of patients while biliary enzymes kept increasing. Restricture occurred in 5% (1/20) of the patients, but after repeat treatment the stent could be removed. In patients with bile duct stricture due to chronic pancreatitis the therapy was successful in only 7.7% (1/13) of the patients; the stent was retained in 92.3% (12/13) of the patients during a long period. Severe acute pancreatitis occurred in 3.0% (1/33) of the patients as an accidental symptom attributable to endoscopic retrograde cholangiopancreatography (ERCP); however, it remitted after conservative treatment.Conclusion:  Our results further confirm the usefulness of endoscopic therapy for postoperative benign bile duct strictures and good long‐term prognosis of the patients.
Comparison of p.o. or i.v. proton pump inhibitors on 72‐h intragastric pH in bleeding peptic ulcer
Authors: Javid Gul , Zargar Showkat Ali , Riyaz‐u‐saif.  , Khan Bashir Ahmad , Yatoo Ghulam Nabi , Shah Altaf Hussain , Gulzar Ghulam Mohammad , Sodhi Jaswinder Singh , Khan Mushtaq Ahmad 
Published: July 2009

AbstractBackground and Aims:  After successful endoscopic hemostasis in bleeding peptic ulcer, addition of proton pump inhibitors reduce the rate of recurrent bleeding by maintaining intragastric pH at neutral level. The aim of the present study was to evaluate the effect of various proton pump inhibitors given through different routes on intragastric pH over 72 h after endoscopic hemostasis in bleeding peptic ulcer.Methods:  Ninety consecutive patients who had successful endoscopic therapy of bleeding peptic ulcer underwent 72‐h continuous ambulatory intragastric pH study, were randomly assigned to receive p.o. omeprazole 80 mg bolus followed by 40 mg every 12 h for 72 h or i.v. 80 mg omeprazole followed by infusion 8 mg/h for 72 h. Oral pantoprazole 80 mg bolus followed by 80 mg every 12 h for 72 h or i.v. 80 mg pantoprazole followed by infusion of 8 mg/h for 72 h. Oral rabeprazole 80 mg bolus followed by 40 mg every 12 h for 72 h or i.v. 80 mg rabeprazole followed by infusion 8 mg/h for 72 h. Five patients received no treatment after successful endoscopic therapy and underwent 72‐h pH study.Results:  Mean 72‐h intragastric pH for p.o. omeprazole was 6.56 versus 6.93 for omeprazole infusion (P = 0.48). Mean 72‐h intragastric pH for p.o. pantoprazole was 6.34 versus 6.32 for pantoprazole infusion (P = 0.62). Mean 72‐h intragastric pH for rabeprazole p.o. was 6.11 versus 6.18 rabeprazole i.v. (P = 0.55). Mean 72‐h pH for the no proton pump inhibitor group was 2.04.Conclusion:  There was no significant difference among various proton pump inhibitors given through different routes on raising intragastric pH above 6 for 72 h after successful endoscopic hemostasis in bleeding peptic ulcer.
Delayed endoscopy as a risk factor for in‐hospital mortality in cirrhotic patients with acute variceal hemorrhage
Authors: Hsu Yao‐Chun , Chung Chen‐Shuan , Tseng Cheng‐Hao , Lin Tzu‐Ling , Liou Jyh‐Ming , Wu Ming‐Shiang , Hu Fu‐Chang , Wang Hsiu‐Po 
Published: July 2009

AbstractBackground and Aims:  Risk factors for mortality in acute variceal hemorrhage remain incompletely understood. Whether endoscopy timing is associated with risk of mortality has not been investigated. We aimed to investigate risk factors for in‐hospital mortality in cirrhotic patients with acute variceal hemorrhage, with emphasis on endoscopy timing.Methods:  Three hundred and eleven (73% male and 23% female) consecutive cirrhotic patients presenting with acute variceal hemorrhage from July 2004 to July 2007 were investigated. The univariate association of endoscopy timing as the predictor for in‐hospital mortality was examined. Independent risk factors for mortality were determined by multivariate logistic regression analysis consisting of clinical, laboratory and endoscopic parameters.Results:  Twenty‐five (8.04%) patients died within admission. By plotting the receiver operating curve of endoscopy timing for mortality, we selected 15 h as the optimal cut‐off point to define delayed endoscopy. Multivariate regression analysis revealed that independent risk factors predictive for in‐hospital mortality included delayed endoscopy performed 15 h after admission (adjusted odds ratio [aOR] = 3.67; 95% confidence interval [CI], 1.27–10.39), every point increment of model for end‐stage liver disease (MELD) score (aOR = 1.16; 95% CI, 1.07–1.25), failure of the first endoscopy (aOR = 4.36; 95% CI, 1.54–12.30) and hematemesis as the chief complaint (compared with melena, aOR = 8.66; 95% CI, 1.06–70.94).Conclusion:  Delayed endoscopy for more than 15 h, high MELD score, failure of the first endoscopy and hematemesis are independent risk factors for in‐hospital mortality in cirrhotic patients with acute variceal hemorrhage.
Non‐invasive model predicting clinically‐significant portal hypertension in patients with advanced fibrosis
Authors: Park Seung Ha , Park Tae Eun , Kim Young Mook , Kim Sung Jung , Baik Gwang Ho , Kim Jin Bong , Kim Dong Joon 
Published: July 2009

AbstractBackground and Aims:  Hepatic venous pressure gradient (HVPG) has been established as a predictor for the development of varices, clinical decompensation and death. In the present study, the primary objectives were to determine the diagnostic accuracy of the model developed by using readily‐available data in predicting the presence of significant portal hypertension and esophageal varices.Methods:  This study included a total of 61 consecutive treatment‐naive patients with advanced fibrosis (METAVIR F3, F4), established by liver biopsy. All patients underwent subsequent HVPG measurement and upper gastrointestinal endoscopy within 1 week of liver biopsy.Results:  Seventeen patients (F3, 2/26; F4, 15/35) had clinically‐significant portal hypertension (HVPG ≥ 10 mmHg). The Risk Score for predicting significant portal hypertension was 14.2 − 7.1 × log10 (platelet [109/L]) + 4.2 × log10 (bilirubin [mg/dL]). The area under the receiver–operator curve (AUC) curve was 0.91 (95% confidence interval [CI], 0.84–0.98). The optimized cut‐off value (Risk Score = −1.0) offered a sensitivity of 88% (95% CI, 62–98%) and a specificity of 86% (95% CI, 72–94%). The AUC of the Risk Score in predicting varices was 0.82 (95% CI, 0.67–0.98). The cut‐off had a sensitivity of 82% (95% CI, 48–97%) and a specificity of 76% (95% CI, 62–86%).Conclusion:  A predictive model that uses readily‐available laboratory results may reliably identify advanced fibrosis patients with clinically‐significant portal hypertension as well as esophageal varices. However, before accepted, the results of the current study certainly should be validated in larger prospective cohorts.