bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suberized Cell Walls of Cork from Cork Oak Differ from Other Species
Authors: Teixeira Rita Teresa , Pereira Helena 
Published: August 2010

AbstractPlants have suberized cells that act as protective interfaces with the environment or between different plant tissues. A lamellar structure of alternating dark and light bands has been found upon transmission electron microscopy (TEM) observation of cork cells and considered a typical feature of the suberized secondary wall. We observed cork cells from periderms ofQuercus suber,Quercus cerris, Solanum tuberosum, andCalotropis proceraby TEM after uranyl acetate and lead citrate staining. A lamellated structure was observed inS. tuberosumandC. procerabut not inQ. suberandQ. cerriswhere the suberized cell wall showed a predominantly hyaline aspect with only a dark dotted staining. Removal of suberin fromQ. subercells left a thinner secondary wall that lost the translucent aspect. We hypothesize that the species' specific chemical composition of suberin will result in different three-dimensional macromolecular development and in a different spatial location of lignin and other aromatics. A lamellated ultrastructure is therefore not a general feature of suberized cells.
No evidence of nanodiamonds in Younger–Dryas sediments to support an impact event
Authors: Daulton Tyrone L. , Pinter Nicholas , Scott Andrew C. 
Published: August 2010

The causes of the late Pleistocene megafaunal extinctions in North America, disappearance of Clovis paleoindian lithic technology, and abrupt Younger–Dryas (YD) climate reversal of the last deglacial warming in the Northern Hemisphere remain an enigma. A controversial hypothesis proposes that one or more cometary airbursts/impacts barraged North America ≈12,900 cal yr B.P. and caused these events. Most evidence supporting this hypothesis has been discredited except for reports of nanodiamonds (including the rare hexagonal polytype) in Bølling–Ållerod-YD-boundary sediments. The hexagonal polytype of diamond, lonsdaleite, is of particular interest because it is often associated with shock pressures related to impacts where it has been found to occur naturally. Unfortunately, previous reports of YD-boundary nanodiamonds have left many unanswered questions regarding the nature and occurrence of the nanodiamonds. Therefore, we examined carbon-rich materials isolated from sediments dated 15,818 cal yr B.P. to present (including the Bølling–Ållerod-YD boundary). No nanodiamonds were found in our study. Instead, graphene- and graphene/graphane-oxide aggregates are ubiquitous in all specimens examined. We demonstrate that previous studies misidentified graphene/graphane-oxide aggregates as hexagonal diamond and likely misidentified graphene as cubic diamond. Our results cast doubt upon one of the last widely discussed pieces of evidence supporting the YD impact hypothesis.
Propofol Modulates Agonist-induced Transient Receptor Potential Vanilloid Subtype-1 Receptor Desensitization via a Protein Kinase Cϵ-dependent Pathway in Mouse Dorsal Root Ganglion Sensory Neurons
Authors: Wickley Peter J. , Yuge Ryo , Russell Mary S. , Zhang Hongyu , Sulak Michael A. , Damron Derek S. 
Published: August 2010

Background
The activity of transient receptor potential vanilloid subtype-1 (TRPV1) receptors, key nociceptive transducers in dorsal root ganglion sensory neurons, is enhanced by protein kinase C epsilon (PKCepsilon) activation. The intravenous anesthetic propofol has been shown to activate PKCepsilon. Our objectives were to examine whether propofol modulates TRPV1 function in dorsal root ganglion neurons via activation of PKCepsilon.

Methods
Lumbar dorsal root ganglion neurons from wild-type and PKC& epsilon;-null mice were isolated and cultured for 24 h. Intracellular free Ca concentration was measured in neurons by using fura-2 acetoxymethyl ester. The duration of pain-associated behaviors was also assessed. Phosphorylation of PKCepsilon and TRPV1 and the cellular translocation of PKCepsilon from cytosol to membrane compartments were assessed by immunoblot analysis.

Results
In wild-type neurons, repeated stimulation with capsaicin (100 nm) progressively decreased the transient rise in intracellular free Ca concentration. After desensitization, exposure to propofol rescued the Ca response. The resensitizing effect of propofol was absent in neurons obtained from PKCepsilon-null mice. Moreover, the capsaicin-induced desensitization of TRPV1 was markedly attenuated in the presence of propofol in neurons from wild-type mice but not in neurons from PKCepsilon-null mice. Propofol also prolonged the duration of agonist-induced pain associated behaviors in wild-type mice. In addition, propofol increased phosphorylation of PKCepsilon as well as TRPV1 and stimulated translocation of PKCepsilon from cytosolic to membrane fraction.

Discussion
Our results indicate that propofol modulates TRPV1 sensitivity to capsaicin and that this most likely occurs through a PKCepsilon-mediated phosphorylation of TRPV1.
A Mouse Model of Ischemic Spinal Cord Injury with Delayed Paralysis Caused by Aortic Cross-clamping
Authors: Awad Hamdy , Ankeny Daniel P. , Guan Zhen , Wei Ping , McTigue Dana M. , Popovich Phillip G. 
Published: August 2010

Background
Spinal cord ischemia and paralysis are devastating perioperative complications that can accompany open or endovascular repair surgery for aortic aneurysms. Here, we report on the development of a new mouse model of spinal cord ischemia with delayed paralysis induced by cross-clamping the descending aorta.

Methods
Transient aortic occlusion was produced in mice by cross-clamping the descending aorta through a lateral thoracotomy. To establish an optimal surgical procedure with limited mortality, variable cross-clamp times and core temperatures were tested between experiments.

Results
The onset of paresis or paralysis and postsurgical mortality varied as a function of cross-clamp time and core temperature that was maintained during the period of cross-clamp. Using optimal surgical parameters (7.5-min cross-clamp duration at 33°C core temperature), the onset of paralysis is delayed 24-36 h after reperfusion, and more than 95% of mice survive through 9 weeks after surgery. These mice are further stratified into two groups, 70% (n = 19/27) of mice developing severe hind limb paralysis and the remaining mice showing mild, though still permanent, behavioral deficits.

Conclusion
This new model should prove useful as a preclinical tool for screening neuroprotective therapeutics and for defining the basic biologic mechanisms that cause delayed paralysis and neurodegeneration after transient spinal cord ischemia.
Perioperative Outcomes among Patients with the Modified Metabolic Syndrome Who Are Undergoing Noncardiac Surgery
Authors: Glance Laurent G. , Wissler Richard , Mukamel Dana B. , Li Yue , Diachun Carol Ann B. , Salloum Rabih , Fleming Fergal J. , Dick Andrew W. 
Published: August 2010

Background
Previous studies have demonstrated that obesity is paradoxically associated with a lower risk of mortality after noncardiac surgery. This study will determine the impact of the modified metabolic syndrome (defined as the presence of obesity, hypertension, and diabetes) on perioperative outcomes.

Methods
This study is based on data from 310,208 patients in the American College of Surgeons National Surgical Quality Improvement Program database. We estimated separate multivariate logistic regression models for 30-day mortality and for 30-day complications.

Results
Patients with the modified metabolic syndrome who are super obese had a 2-fold increased risk of death (adjusted odds ratio [AOR] 1.99; 95% CI 1.41-2.80). As stratified by body mass index, patients with the modified metabolic syndrome had a 2- to 2.5-fold higher risk of cardiac adverse events (CAE) compared with normal-weight patients: obese (AOR 1.70; 95% CI 1.40-2.07), morbidly obese (AOR 2.01; 95% CI 1.48-2.73), and super obese (AOR 2.66; 95% CI 1.68-4.19). In addition, the risk of acute kidney injury (AKI) was 3- to 7-fold higher in these patients: obese (AOR 3.30; 95% CI 2.75-3.94), morbidly obese (AOR 5.01; 95% CI 3.87-6.49), and super obese (AOR 7.29; 95% CI 5.27-10.1).

Conclusion
Patients with the modified metabolic syndrome undergoing noncardiac surgery are at substantially higher risk of complications compared with patients of normal weight.
Relationship between Normalized Adductor Pollicis Train-of-four Ratio and Manifestations of Residual Neuromuscular Block
Authors: Heier Tom , Caldwell James E. , Feiner John R. , Liu Luke , Ward Theresa , Wright Peter M. C. 
Published: August 2010

Background
Baseline acceleromyographic adductor pollicis train-of-four (TOF) ratio varies significantly between individuals and is often greater than unity. Thus, normalization of acceleromyography data is necessary. The relationship between normalized acceleromyographic TOF ratio, lung volumes, and clinical signs of residual neuromuscular block was studied.

Methods
In 12 healthy volunteers, three steady-state levels of neuromuscular block were achieved with mivacurium infusions. TOF ratio was measured acceleromyographically at the adductor pollicis using a preload. Lung volume measurements and a series of clinical tests were made at each stable block and reconciled to the normalized TOF measures.

Results
None experienced airway obstruction or arterial oxygen desaturation, even at normalized TOF ratio less than 0.4. Functional residual capacity remained unchanged whereas vital capacity decreased linearly with decreasing TOF ratio. The ability to protrude the tongue was preserved at all times. The ability to clench the teeth was lost in one volunteer at normalized TOF ratio of 0.84 but retained in four at normalized TOF ratio less than 0.4. Four volunteers lost the ability both to raise the head more than 5 s and to swallow, with the most sensitive individual demonstrating these effects at normalized TOF ratio of 0.60. At mean normalized TOF ratio of 0.42, the mean handgrip strength was approximately 20% of baseline value.

Conclusion
Lung vital capacity decreased linearly with decreasing TOF ratio. Responses to clinical tests of muscle function varied to a large extent among individuals at comparable TOF ratios. None of the volunteers had significant clinical effects of neuromuscular block at normalized acceleromyographic TOF ratio greater than 0.90.
Maintenance of clinical benefit in Crohn’s disease patients after discontinuation of infliximab: long‐term follow‐up of a single centre cohort
Authors: Waugh A. W. G. , Garg S. , Matic K. , Gramlich L. , Wong C. , Sadowski D. C. , Millan M. , Bailey R. , Todoruk D. , Cherry R. , Teshima C. W. , Dieleman L. , Fedorak R. N. 
Published: August 2010

Aliment Pharmacol Ther 2010; 32: 1129–1134SummaryBackground  Tumour necrosis factor‐blockade with infliximab has advanced the treatment of Crohn’s disease. While infliximab is efficacious, it remains to be determined whether patients who enter clinical remission with an anti‐tumour necrosis factor therapy can have their treatment stopped and retain the state of remission.Aim  To assess in patients with Crohn’s disease who obtained infliximab‐induced remission, the proportion who relapsed after infliximab discontinuation.Methods  This longitudinal cohort study examined patients from a University‐based IBD referral centre. Forty eight patients with Crohn’s disease in full clinical remission and who then discontinued infliximab were followed up for up to 7 years. Crohn’s disease relapse was defined as an intervention with Crohn’s disease medication or surgery.Results  Kaplan–Meier analysis of the proportion of patients with sustained clinical benefit demonstrated that 50% relapsed within 477 days after infliximab discontinuance. In contrast, 35% of patients remained well, and without clinical relapse, up to the end of the nearly 7‐year follow‐up.Conclusions  In patients with Crohn’s disease with an infliximab‐induced remission, stopping infliximab results in a predictable relapse in a majority of patients. Nevertheless, a small percentage of patients sustain a long‐term remission.
Meta‐analysis: reduction in hepatic events following interferon‐alfa therapy of chronic hepatitis B
Authors: Wong G. L.‐H. , Yiu K. K.‐L. , Wong V. W.‐S. , Tsoi K. K.‐F. , Chan H. L.‐Y. 
Published: August 2010

Aliment Pharmacol Ther 2010; 32: 1059–1068SummaryBackground  The long‐term benefit of interferon‐alfa (IFN‐α) treatment in preventing various hepatic complications is not certain.Aim  To study the effects of IFN‐α on reducing the risk of developing overall hepatic events (hepatocellular carcinoma, cirrhotic complications and liver‐related mortality) in chronic hepatitis B patients.Methods  Randomized controlled trials, case–control studies and cohort studies were retrieved from electronic databases and conference abstracts. Relative risks (RRs) of different hepatic complications among patients treated by IFN‐α vs. no treatment or placebo were studied.Results  Eleven studies were identified totalling 975 patients treated by IFN‐α vs. 1147 untreated controls for analysis. Patients were treated by IFN‐α for 1–24 months with a post‐treatment follow‐up of 1–13 years. Treatment by IFN‐α reduced the risk of overall hepatic events (RR 0.55, 95% confident interval or CI 0.43–0.70, P < 0.001) and cirrhotic complications (RR 0.46, 95% CI 0.32–0.67, P < 0.001) by 45% and 54% respectively. Patients who responded to IFN‐α had more profound reduction in overall hepatic events (RR 0.20, 95% CI 0.05–0.87, P = 0.03) and cirrhotic complications (RR 0.19, 95% CI 0.09–0.38, P < 0.001) vs. the untreated controls.Conclusion  Interferon‐alfa treatment reduces the risk of hepatic events particularly among responders to treatment.
Genomic lesions associated with a different clinical outcome in diffuse large B‐Cell lymphoma treated with R‐CHOP‐21
Authors: Scandurra Marta , Mian Michael , Greiner Timothy C. , Rancoita Paola M. V. , De Campos Cassio P. , Chan Wing C. , Vose Julie M. , Chigrinova Ekaterina , Inghirami Giorgio , Chiappella Annalisa , Baldini Luca , Ponzoni Maurilio , Ferreri Andres J.M. , Franceschetti Silvia , Gaidano Gianluca , Montes‐Moreno Santiago , Piris Miguel A. , Facchetti Fabio , Tucci Alessandra , Nomdedeu Josep Fr. , Lazure Thierry , Lambotte Olivier , Uccella Silvia , Pinotti Graziella , Pruneri Giancarlo , Martinelli Giovanni , Young Ken H. , Tibiletti Maria Grazia , Rinaldi Andrea , Zucca Emanuele , Kwee Ivo , Bertoni Francesco 
Published: August 2010

SummaryDespite recent therapeutic improvements, the clinical course of diffuse large B‐cell lymphoma (DLBCL) still differs considerably among patients. We conducted this retrospective multi‐centre study to evaluate the impact of genomic aberrations detected using a high‐density genome wide‐single nucleotide polymorphism‐based array on clinical outcome in a population of DLBCL patients treated with R‐CHOP‐21 (rituximab, cyclophosphamide, doxorubicine, vincristine and prednisone repeated every 21 d). 166 DNA samples were analysed using the GeneChip Human Mapping 250K NspI. Genomic anomalies were analysed regarding their impact on the clinical course of 124 patients treated with R‐CHOP‐21. Unsupervised clustering was performed to identify genetically related subgroups of patients with different clinical outcomes. Twenty recurrent genetic lesions showed an impact on the clinical course. Loss of genomic material at 8p23.1 showed the strongest statistical significance and was associated with additional aberrations, such as 17p‐ and 15q‐. Unsupervised clustering identified five DLBCL clusters with distinct genetic profiles, clinical characteristics and outcomes. Genetic features and clusters, associated with a different outcome in patients treated with R‐CHOP, have been identified by arrayCGH.
Seizures in the Jamaica cohort study of sickle cell disease
Authors: Ali Susanna B. , Reid Marvin , Fraser Raphael , MooSang Michelle , Ali Amza 
Published: August 2010

SummaryAlthough there is some evidence that epilepsy is more common in Sickle Cell Disease (SCD), we sought to establish the incidence rates, risk factors for and specific types of seizures in a SCD cohort followed from birth, and how seizure occurrence affects morbidity and mortality. We examined all records of persons in the Jamaica cohort Study of Sickle Cell Disease (JSSCD) clinically identified as having experienced a seizure during their lifetime. At first presentation, seizures were classified as Febrile Convulsion, Acute Symptomatic Seizure or Single Unprovoked Seizure. The seizure classification was revised to include Epilepsy if seizures recurred. Thirty‐eight persons in the JSSCD (N = 543) were identified with seizures. The 5‐year cumulative incidence of febrile convulsions was 2·2%. The incidence rate of epilepsy (all genotypes) was 100/100 000 person‐years, 139/100 000 for the SS genotype. Despite limited availability of diagnostic investigations, clinical seizures were associated with increased all‐cause mortality. Male gender (Odds Ratio [OR]: 4·0[95% confidence interval [CI]; 1·03–20·0]) and dactylitis in childhood (OR: 17·4 [95% CI; 4·82–62·85]) were associated with increased risk of developing epilepsy. Epilepsy in persons with SCD is 2–3 times more common than in non‐sickle populations and is associated with increased all‐cause mortality in all sickle cell genotypes.
Recent advances in the understanding of genetic defects of neutrophil number and function
Authors: Bouma Gerben , Ancliff Phil J. , Thrasher Adrian J. , Burns Siobhan O. 
Published: August 2010

SummaryNeutrophils are amongst the first immune cells to arrive at sites of infection and play an important role as the host’s first line of defence against invading pathogens. Defects of neutrophil number or function are usually recognized clinically by recurrent infections that often are life‐threatening. Over the last few years, a number of genetic mutations have been discovered to be the basis for congenital neutropenia, adding to our understanding of the molecular basis of these diseases. While many genetic mutations that cause severe congenital neutropenia result in a differentiation block at the promyelocyte stage, defects of neutrophil function are more heterogeneous on clinical, genetic and mechanistic levels. In this review we discuss recent advances in our understanding of the genetic and molecular basis of human neutrophil disorders.
‘The hard work starts now’: a glimpse into the lives of carers of community‐dwelling stroke survivors
Authors: Cecil Rosanne , Parahoo Kader , Thompson Kate , McCaughan Eilis , Power Michael , Campbell Yvonne 
Published: August 2010

Aims and objectives.  To explore the personal experiences of carers of stroke survivors and to elicit their views and opinions of what constitute the major issues and concerns of people in their situation.Background.  The unexpected nature of stroke can propel people into the role of carer with little or no warning. Some carers of stroke survivors suffer from considerable stress and a range of psychological and physical disorders.Design.  A small‐scale qualitative study of experienced carers of stroke survivors.Method.  Ten carers with experience of caring for a stroke survivor were recruited to the study through community stroke staff. Data were collected using semi‐structured interviews and a focus group.Results.  The women’s main concerns were focused around the need for information and support, including the need for some preparation and training in the necessary skills of caring.Conclusions.  To understand fully the lives that carers lead, it is necessary to explore what carers want to do, and expect to do, for the care‐recipient. There is a need to develop an understanding of factors that appear to be protective against stress, to identify how they can be enhanced and to develop ways to minimise the impact of those factors that have a detrimental impact on the well‐being of carers and on those for whom they care.Relevance to clinical practice.  Health professionals need to ensure that appropriate information is clearly provided for carers. Communication between health professionals to ensure the ‘joined up’ provision of therapeutic services is another area for continual development. Carers expressed the wish to be better prepared to take on the caring role in the home and would have welcomed some training in this area.
Chasing the unknown: predicting seed dispersal mechanisms from plant traits
Authors: Thomson Fiona J. , Moles Angela T. , Auld Tony D. , Ramp Daniel , Ren Shiquan , Kingsford Richard T. 
Published: August 2010

Summary 1. The dispersal capabilities of most plant species remain unknown. However, gaining basic dispersal information is a critical step for understanding species’ geographical distributions and for predicting the likely impacts of future climate change. Dispersal mechanisms can indicate short‐ or long‐distance dispersers, and highlight important biological interactions. 2. To predict dispersal mechanisms for species where information is limited, we used generalized linear mixed models with basic life‐history and ecological traits. Sets of models were created (using Australian species) for six dispersal categories: wind, unassisted, water, ant, vertebrate‐ingestion and vertebrate‐attachment dispersal mechanisms. We validated our models on the dispersal mechanisms of 50 Australian, 30 Californian, 30 Swiss plant species and a global compilation of 70 species. 3. Growth form, seed mass and vegetation type were the main predictor variables. Our models predicted dispersal mechanisms for Australian and Californian plant species equally well (c. 70% correct) and to a lesser extent for the Swiss flora (c. 50% correct). Our models predicted observed dispersal mechanisms (c. 50% correct) equally well to inferred dispersal mechanisms (based on seed morphology). 4. Synthesis. Our approach of using easily obtainable traits for predicting dispersal mechanisms of species allows dispersal information to be predicted for species where little is known. From here, the application of realistic dispersal curves to the predicted dispersal mechanisms will further understanding on the dispersal capabilities of species.
Subtelomeric rearrangements and copy number variations in people with intellectual disabilities
Authors: Christofolini D. M. , De Paula Ramos M. A. , Kulikowski L. D. , Da Silva Bellucco F. T. , Belangero S. I. N. , Brunoni D. , Melaragno M. I. 
Published: August 2010

AbstractBackground  The most prevalent type of structural variation in the human genome is represented by copy number variations that can affect transcription levels, sequence, structure and function of genes.Method  In the present study, we used the multiplex ligation‐dependent probe amplification (MLPA) technique and quantitative PCR for the detection of copy number variation in 132 intellectually disabled male patients with normal karyotypes and negative fragile‐X‐testing.Results  Ten of these patients (7.6%) showed copy number variation in the subtelomeric regions, including deletions and duplications.Discussion  Duplications of the SECTM1 gene, located at 17q25.3, and of the FLJ22115 gene, located at 20p13, could be associated with phenotype alterations. This study highlights the relevance in the aetiology of intellectual disability of subtelomeric rearrangements that can be screened by MLPA and other molecular techniques.