bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Widespread Drought‐Induced Aspen Mortality on Understory Plants
Authors: Anderegg William R. L. , Anderegg Leander D. L. , Sherman Clare , Karp Daniel S. 
Published: August 2012

AbstractForest die‐off around the world is expected to increase in coming decades as temperature increases due to climate change. Forest die‐off will likely affect understory plant communities, which have substantial influence on regional biological diversity, ecosystem function, and land–atmosphere interactions, but how die‐off alters these plant communities is largely unknown. We examined changes in understory plant communities following a widespread, drought‐induced die‐off of trembling aspen (Populus tremuloides) in the western United States. We assessed shrub and herbaceous cover and volume in quadrats in 55 plots located across a wide range of levels of aspen mortality. We measured species richness and composition of herbaceous plant communities by recording species presence and absence in 12 sets of paired (1 healthy, 1 dying) aspen plots. Although understory composition in healthy and dying stands was heterogeneous across the landscape, shrub abundance, cover, and volume were higher and abundance of herbaceous species, cover, and volume were lower in dying aspen stands. Shrub cover and volume increased from 2009 to 2011 in dying stands, which suggests that shrub growth and expansion is ongoing. Species richness of herbs declined by 23% in dying stands. Composition of herbs differed significantly between dying and healthy stands. Richness of non‐native species did not differ between stand types. The understory community in dying aspen stands was not similar to other shrub‐dominated plant communities in the region and may constitute a novel community. Our results suggest that changes in understory plant communities as forests die off could be a significant indirect effect of climate change on biological diversity and forest communities.Efectos de la Mortalidad Extensiva de Álamos Inducida por Sequía sobre Plantas del Sotobosque
Albumin Limits Mesenteric Endothelial Dysfunction and Inflammatory Response in Cardiopulmonary Bypass
Authors: Doguet Fabien , Tamion Fabienne , Le Guillou Vincent , Bubenheim Michael , Thuillez Christian , Richard Vincent , Bessou Jean Paul 
Published: August 2012

AbstractThe aim of this study was to investigate the potential anti‐inflammatory and endothelial protective properties of albumin during cardiopulmonary bypass (CPB) in an experimental porcine model. Two groups underwent CPB for 90 min (n = 7 in each group), and a baseline (BL) control group did not undergo CPB (n = 7). Priming consisted of a gelatin solution (4% gelofusine, CPBG group) or colloid solution (5% albumin, CPBA group). Mesenteric arterial segments were isolated and exposed in vitro to phenylephrine (with or without nitric oxide synthase inhibition) to assess contractility, and exposed to acetylcholine and sodium nitroprusside to assess relaxation. Plasma tumor necrosis factor (TNF)‐α levels, intestinal and pulmonary TNF‐α and heme oxygenase (HO)‐1 mRNA expression, and organ injury were studied. Upon sacrifice, TNF‐α levels were significantly higher in the CPBG group than in the CPBA and BL groups. The contractile response was significantly higher in the CPBG group, whereas the response to acetylcholine was significantly lower in the CPBG group than in the other groups. HO‐1 mRNA expression was significantly higher in intestine samples in the CPBA group than in the CPBG and BL groups. HO‐1 mRNA expression was significantly higher in lung samples in the CPBA group than in the CPBG group. Leukocyte infiltration was significantly higher in intestine and lung samples in the CPBG group than in the CPBA and BL groups. Albumin priming reduced CPB‐induced mesenteric vascular dysfunction and prevented the development of a systemic inflammatory response by modeling HO‐1 expression in target organs.
Expression of the carcinoma markers: the sialylated Lewis A and X carbohydrate antigens in normal laryngeal surface epithelium and submucosal glands from old humans
Authors: Kirkeby Svend , Moe Dennis 
Published: August 2012

Aberrant surface expression of the carbohydrate ABH and Lewis antigens are often used as markers for the diagnosis of cancer, but while the distribution of these histo‐blood group antigens is relatively well‐described in tissues and organs from young and middle‐aged humans little is known of their expression in old age. The objective for this study was to estimate if the Lewis A and X antigens together with their sialylated modifications, are expressed in sections of normal laryngeal tissue from old humans. Antibodies directed against the tumor markers Sialyl Lewis A and Sialyl Lewis X showed positive reaction in the surface epithelia from normal larynx autopsies obtained from people aged 77–90 years. The sialylated and non‐sialylated Lewis A antigens were more frequently expressed in the pseudostratified epithelium than in squamous surface epithelium. Both the sialylated and the non‐sialylated carbohydrates were stained in the submucosal glands in all the autopsies. In conclusion, visualization of Lewis tumor markers in the larynx should be interpreted with great care, as they may be present in normal laryngeal epithelial cells from old humans.
Inflammation links excess fat to insulin resistance: the role of the interleukin‐1 family
Authors: Tack Cees J. , Stienstra Rinke , Joosten Leo A. B. , Netea Mihai G. 
Published: August 2012

SummaryA growing body of evidence suggests that cytokines of the interleukin‐1 (IL‐1) family, particularly IL‐1β but also IL‐1Ra and IL‐18, are involved in obesity‐associated inflammation. IL‐1β is produced via cleavage of pro‐IL‐1β by caspase‐1, which in turn is activated by a multiprotein complex called the inflammasome. The components of the NLRP3 inflammasome are involved in sensing obesity‐associated danger signals, both in mice and in human (obese) subjects, with caspase‐1 seemingly the most crucial regulator. Autophagy is upregulated in obesity and may function as a mechanism to control IL‐1β gene expression in adipose tissue to mitigate chronic inflammation. All these mechanisms are operative in human adipose tissue and appear to be more pronounced in human visceral compared to subcutaneous tissue. In animal studies, blocking caspase‐1 activity results in decreased weight gain, decreased inflammation, and improved insulin sensitivity. Human intervention studies with IL‐1Ra (anakinra) have reported beneficial effects in patients with diabetes, yet without significant changes in insulin sensitivity. Clearly, the IL‐1 family of cytokines, especially IL‐1β, plays an important role in obesity‐associated inflammation and insulin resistance and may represent a therapeutic target to reverse the detrimental metabolic consequences of obesity.
Programmed necrosis and autophagy in immune function
Authors: Lu Jennifer V. , Walsh Craig M. 
Published: August 2012

SummaryIt has long been known that apoptosis is vital to the generation and maintenance of proper adaptive immune function. An example is the essential requirement for apoptotic signaling during the generation of self‐tolerant lymphocytes: the apoptotic death of B and T cells with overt autoreactivity is essential to central tolerance. More recently, the contributions of additional processes including cellular autophagy and programmed necrosis have been implicated in controlling both innate and adaptive immune functions. Evidence has been provided to demonstrate that the death of cells following ligation of death receptors (DRs), a subfamily of cell surface molecules related to tumor necrosis factor receptor 1, is not exclusively the domain of caspase‐dependent apoptosis. In cells lacking the capacity to activate caspase‐8 following DR ligation, cell death instead occurs via programmed necrosis, or as it has been recently termed, ‘necroptosis’. This death process depends on RIP1 and RIP3, serine/threonine kinases that are recruited by DRs, and likely by other cellular signals including DNA damage and antigen receptor ligation. The generation of RIP1/RIP3 containing ‘necrosomes’ activates downstream necroptotic signaling that ultimately targets cellular energetic metabolism. Also related to cellular metabolic regulation, cellular autophagy has also been found to play unique and important roles in immunity. In this review, we describe the roles of necroptosis and autophagy in innate and adaptive immunity and speculate on the intriguing interplay between these two cellular processes.
Distinct metabolic programs in activated T cells: opportunities for selective immunomodulation
Authors: Wahl Daniel R. , Byersdorfer Craig A. , Ferrara James L. M. , Opipari Anthony W. , Glick Gary D. 
Published: August 2012

SummaryFor several decades, it has been known that T‐cell activation in vitro leads to increased glycolytic metabolism that fuels proliferation and effector function. Recently, this simple model has been complicated by the observation that different T‐cell subsets differentially regulate fundamental metabolic pathways under the control of distinct molecular regulators. Although the majority of these data have been generated in vitro, several recent studies have documented the metabolism of T cells activated in vivo. Here, we review the recent data surrounding the differential regulation of metabolism by distinct T‐cell subsets in vitro and in vivo and discuss how differential metabolic regulation might facilitate T‐cell function vis‐à‐vis proliferation, survival, and energy production. We further discuss the important therapeutic implications of differential metabolism across T‐cell subsets and review recent successes in exploiting lymphocyte metabolism to treat immune‐mediated diseases.
Metabolic switching and fuel choice during T‐cell differentiation and memory development
Authors: van der Windt Gerritje J. W. , Pearce Erika L. 
Published: August 2012

SummaryClearance or control of pathogens or tumors usually requires T‐cell‐mediated immunity. As such, understanding the mechanisms that govern the function, maintenance, and persistence of T cells will likely lead to new treatments for controlling disease. During an immune response, T‐cell development is marked by striking changes in metabolism. There is a growing appreciation that these metabolic changes underlie the capacity of T cells to perform particular functions, and this has led to a recent focus on the idea that the manipulation of cellular metabolism can be used to shape adaptive immune responses. Although interest in this area has grown in the last few years, a full understanding of the metabolic control of T‐cell functions, particularly during an immune response in vivo, is still lacking. In this review, we first provide a basic overview of metabolism in T cells, and then we focus on recent studies providing new or updated insights into the regulation of metabolic pathways and how they underpin T‐cell differentiation and memory T‐cell development.
At the crossroad of T cells, adipose tissue, and diabetes
Authors: Matarese Giuseppe , Procaccini Claudio , De Rosa Veronica 
Published: August 2012

SummaryThe study of how different intracellular metabolic signaling pathways impact the control of self‐immune tolerance and how metabolic dysregulation in overweight, obesity, and diabetes is able to alter self‐immune tolerance are topics of intensive investigation. Recent evidence suggests that metabolic and autoimmune diseases, both characterized by chronic inflammation and an altered self‐immune tolerance, are more common in affluent countries. The reasons for such phenomena are still not completely understood, but the ‘metabolic pressure’ induced by nutritional overload, typical of more developed countries, seems to play a role. In this context, the discovery of the adipose tissue‐derived hormone leptin has shed fundamental insights on how these processes might occur. We believe that there is a strong relationship among leptin, metabolic state, and immunological self‐tolerance. We hypothesize that the leptin‐induced metabolic pressure sets the basis for an exaggerated immuno‐inflammatory response to altered self or non‐self, leading to chronic inflammation, metabolic dysregulation, and autoimmunity in subjects with risk factors (i.e. genetic predisposition, environment, sex, infectious agents, etc). Capitalizing on our joint effort and trans‐disciplinary expertise in metabolism, self‐tolerance, and autoimmune diseases, this review highlights key questions on the basic mechanisms governing immune tolerance in the context of metabolic and autoimmune disease susceptibility.
Effects of electrical stimulation on periodontal tissue remodeling in rats
Authors: Tomofuji T. , Ekuni D. , Azuma T. , Irie K. , Endo Y. , Kasuyama K. , Nagayama M. , Morita M. 
Published: August 2012

Background and ObjectiveElectric current is used to promote wound healing. However, it is unclear whether electrical stimulation contributes to gingival tissue remodeling. This study examined the effects of electrical stimulation on gingival tissue remodeling in a rat periodontitis model.Material and MethodsMale Wistar rats (n = 28, 8 wks of age) were divided into four groups of seven rats each. The control group did not receive any treatment for 6 wks. In the other groups, periodontitis was ligature‐induced for 4 wks. After 4 wks, the rats with periodontitis were given daily electrical stimulation of 0, 50 or 100 μA for 2 wks.ResultsThe periodontitis group stimulated with 0 μA showed a higher density of polymorphonuclear leukocytes and a lower density of collagen in gingival tissue compared with the control group (p < 0.05). The two remaining groups treated with 50 or 100 μA of electrical stimulation exhibited a lower density of polymorphonuclear leukocytes (p < 0.05) and a higher density of collagen than the group stimulated with 0 μA (p < 0.05). They also showed higher expression of fibroblast growth factor‐2 than the group treated with 0 μA of electrical stimulation (p < 0.05).ConclusionElectric stimulation may offer a novel approach to promote gingival tissue remodeling in periodontal lesions.
Postnatal intestinal disturbances in small‐for‐gestational‐age premature infants after prenatal haemodynamic disturbances
Authors: Robel‐Tillig E , Vogtmann Chr , Faber R 
Published: August 2012

Robel‐Tillig E, Vogtmann C, Faber R. Postnatal intestinal disturbances in small‐for‐gestational‐age premature infants after prenatal haemodynamic disturbances. Acta Paediatr 2000; 89: 324‐30. Stockholm. ISSN 0803–5253Uteroplacental insufficiency leads to fetal growth retardation, which is a major cause of perinatal and postnatal morbidity. In the present study we investigated the relationship between prenatal haemodynamic disturbances and postnatal intestinal perfusion and gastrointestinal function in small‐for‐gestational‐age neonates. Prospectively, 114 preterm neonates with a birthweight below 1500 g were assigned to one of two groups according to their prenatal Doppler sonographic measurements: neonates with or without prenatal haemodynamic disturbances. We defined a pathological fetal perfusion by a pulsatility index of uterine arteries, umbilical artery and fetal thoracic aorta above the 90th percentile and by a pulsatility index of middle cerebral artery below the 10th percentile of a normal group. We compared the postnatal respiratory and intestinal adaptation in both groups as well as the blood flow velocity waveforms of the superior mesenteric artery in all neonates. Postnatally, all 36 neonates with prenatal haemodynamic disturbances were classified to be small for gestational age. Thirty‐one of these neonates developed abdominal problems with delayed meconium passage, abdominal distension, bilious vomiting and a delay in tolerating in enteral feeding within the first days of life. Six of them needed surgical intervention, but none of these infants revealed typical signs of necrotizing enterocolitis. In contrast, all neonates after normal prenatal perfusion were classified to be appropriate for gestational age. Only 19 of 78 neonates of this group showed signs of intestinal disturbances postnatally.By Doppler sonographic investigations we found significant lower systolic, mean and end‐diastolic flow velocities and higher pulsatility indices of the superior mesenteric artery in neonates with prenatal haemodynamic disturbances. This may occur as a result of postnatal persistent redistribution of regional blood flow and results in gastrointestinal problems and may adversely affect gut motility.
Early predictors of adverse outcome in term infants with post‐asphyxial hypoxic ischaemic encephalopathy
Authors: Toh VC 
Published: August 2012

Toh VC. Early predictors of adverse outcome in term infants with post‐asphyxial hypoxic ischaemic encephalopathy. Acta Pædiatr 2000; 89: 343‐7. Stockholm. ISSN 0803–5253Severe metabolic acidosis of base deficit ≥25 mEq/L was associated with a high risk of dying: PPV 77.8% and specificity 88.9%.A retrospective study of 35 term infants with post‐asphyxial hypoxic‐ischaemic encephalopathy (HIE) was conducted to identify early clinical predictors of either death or major motor disability at 18 mo of age. Twenty‐three had severe adverse outcome: 13 died and 10 had major neurological sequelae. The significant risk factors were a low 5 min Apgar score, use of adrenaline, low first arterial pH and high base deficit. A base deficit ≥20 mEq/L is a useful predictor of death or disability with a high positive predictive value (PPV) of 93.8%, followed by 93.3% and 84.2% for pH < 7.1 and 5 min Apgar score <4, respectively. The PPV of death or disability is enhanced in the model combining base deficit of ≥20 mEq/L and 5 min Apgar score of <4. This model has a sensitivity of 66.7% and specificity of 100%.
Identification of drought‐responsive genes by cDNA‐amplified fragment length polymorphism in maize
Authors: Liu L. , Hao Z. , Weng J. , Li M. , Zhang D. , Bai L. , Wang L. , Li X. , Zhang S. 
Published: August 2012

AbstractThe cDNA‐AFLP (amplified fragment length polymorphism) technique was performed to detect transcript‐derived fragments related to drought tolerance in maize inbred lines X178 and B73 to identify and understand drought‐responsive genes at the transcriptional level. By comparing the sequences of fragments differentially expressed between these lines under water‐stressed and well‐watered conditions, 72 drought‐responsive unique expressed sequence tags (ESTs) were identified with 41 primer combinations targeting PstI/MseI restriction sites. Most of the fragments isolated in these experiments were found to be associated with genes responsive to abiotic or biotic stresses. Subsequently, a putative R1‐type MYB transcription factor gene corresponding to ZmMYB‐R1 on bin 9.03 was obtained by in silico cloning by homology to EST sequence P36M87‐366, which matched one of the AFLPs identified in this study. The 1881 bp sequence encodes a protein of 626 amino acids that contains a single conserved MYB‐like DNA‐binding domain. Expression of green fluorescence protein fusions showed that ZmMYB‐R1 was localised in the cell nucleus. Quantitative real‐time polymerase chain reaction revealed that ZmMYB‐R1 was induced by drought, high salt, heat, cold and exogenous ABA in maize. The expression of ZmMYB‐R1 initially reaches its highest levels in leaves, then is subsequently also detected in stems and roots. This work revealed genes potentially responsible for drought tolerance in maize, and a new gene, ZmMYB‐R1, was shown to be associated with water stress.
Influence of small-scale inhomogeneities on the cosmological consistency tests
Authors: Busti V. C. , Lima J. A. S. 
Published: August 2012

Abstract
The current cosmological dark sector (dark matter plus dark energy) is challenging our comprehension about the physical processes taking place in the Universe. Recently, some authors tried to falsify the basic underlying assumptions of such dark matter–dark energy paradigm. In this Letter, we show that oversimplifications of the measurement process may produce false positives to any consistency test based on the globally homogeneous and isotropic Λ cold dark matter (ΛCDM) model and its expansion history based on distance measurements. In particular, when local inhomogeneity effects due to clumped matter or voids are taken into account, an apparent violation of the basic assumptions (‘Copernican Principle’) seems to be present. Conversely, the amplitude of the deviations also probes the degree of reliability underlying the phenomenological Dyer–Roeder procedure by confronting its predictions with the accuracy of the weak lensing approach. Finally, a new method is devised to reconstruct the effects of the inhomogeneities in a ΛCDM model, and some suggestions of how to distinguish between clumpiness (or void) effects from different cosmologies are discussed.
Evidence‐based practice for the busy nurse practitioner: Part two: Searching for the best evidence to clinical inquiries
Authors: Facchiano Lynda , Snyder Charlene Hoffman 
Published: August 2012

AbstractPurpose: The purpose of this four‐part evidence‐based practice (EBP) series is to enhance the nurse practitioner's (NP's) EBP skills by reviewing the process of developing a clinical question, searching for the best evidence, and critically appraising and applying the findings. Part two of the series focuses on how to search the published scientific literature for the most relevant studies that will answer a specific clinical question of importance to the NP.Data sources: Scientific literature review, gray searching, PubMed and other online literature databases and resources, and online EBP websites.Conclusions: Technology has allowed multiple healthcare resources to be available at one's fingertips enabling both NPs and their patients to find answers to clinical questions. EBP databases can be categorized as synthesized/filtered, unfiltered, and background information/expert opinion resources. Learning which database can best answer the clinical inquiry can streamline the search process.Implications for practice: For the busy NP, EBP has emerged as an important strategy to maintain valid, accurate, and relevant clinical knowledge. It is expected that this part of the series will enable NPs to identify appropriate databases to answer clinical inquires while refining their search strategy skills, which takes both time and practice.
Assessment of provider adherence to obesity treatment guidelines
Authors: Farran Nicole , Ellis Peggy , Lee Barron Mary 
Published: August 2012

AbstractPurposeDespite the presence of obesity treatment guidelines, healthcare providers often provide suboptimal weight management. The purpose of the quality improvement project was to systematically assess adherence with adult overweight/obesity guidelines in primary care to reduce patient risk.Data sourcesRetrospective analysis of 420 encounter notes from overweight and obese adult patients in three primary care clinics. Data were collected before and after a continuing education session for providers on guidelines for optimal management of obesity. Measures of completeness of quality indicators were abstracted from records.ConclusionsSignificant improvement in the completeness score and documentation of body mass index, height, diagnosis of overweight/obesity, and counseling for diet and physical activity were achieved.Implications for practiceThe proposed measures for systematically assessing the integration of obesity guidelines in primary care are feasible quality indicators and useful for evidence‐based decision making.