bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modelled photosynthesis predicts woody plant richness at three geographic scales across the north‐western United States
Authors: Swenson Jennifer J. , Waring Richard H. 
Published: July 2006

ABSTRACTAim We analyse regional patterns of woody plant species richness collected from field data in relation to modelled gross photosynthesis, Pg, compare the performance of Pgin relation to other productivity surrogates, and examine the effect of increasing scale on the productivity–richness relationship.Location The forested areas in the north‐western states of Oregon, Washington, Idaho, and Montana, USA.Methods Data on shrub and tree species richness were assembled from federal vegetation surveys and compared with modelled growing season gross photosynthesis, Pg(the sum of above‐ and below‐ground production plus autotrophic respiration) and two measures of spatial heterogeneity. We analysed the productivity–richness relationship at different scales by changing the focus size through spatial aggregation of field plots using 100 and 1000 km2windows covering the study area. Regression residuals were plotted spatially. Using the best available tree data set (Continuous Vegetation Survey: CVS), we compared different productivity indices, such as actual evapotranspiration and average temperature, in their ability to predict patterns of tree species richness.Results The highest species richness (species/unit area) occurred at intermediate levels of productivity. After accounting for variable sampling intensity, the richness–productivity relationship improved as more field plots were aggregated. At coarser levels of aggregation, modelled productivity accounted for 57–71% of the variation in richness patterns for shrubs and trees (CVS data set). Measures of spatial heterogeneity accounted for more variation in richness patterns aggregated by 100 km2windows than aggregation by 1000 km2windows. Pgwas a better predictor of tree richness in Oregon and Washington (CVS data set) than any surrogate productivity index.Main conclusions Pgwas observed to be a strong unimodal predictor of both tree (CVS) and shrub (FIA) richness when field data were aggregated. For the tree data set examined, seasonally integrated estimates of photosynthesis (Pg) predicted tree richness patterns better than climatic indices did.
Beyond Rapoport's rule: evaluating range size patterns of New World birds in a two‐dimensional framework
Authors: Hawkins Bradford A. , Felizola Diniz‐Filho José Alexandre 
Published: July 2006

ABSTRACTAim  To evaluate Rapoport's rule for New World birds in two‐dimensional geographical space. We specifically test for a topography × climate interaction that predicts little difference in range sizes between lowlands and mountains in cold climates, whereas in the tropics, montane species have narrow ranges and lowland species have broad ranges.Location  The western hemisphere.Methods  We used digitized range maps of breeding birds to generate mean range sizes in grids of 27.5 × 27.5 km and 110 × 110 km across North and South America. We examined the geographical pattern with respect to range in elevation, mean temperature in the coldest month, their interaction, biome size and continental width, using model II analysis of variance, multiple regression and simple correlation.Results  In northern latitudes species have broad ranges in both mountainous and flat areas. However, range sizes in the mountains and lowlands diverge southwards, with the most extreme differences in the tropics. Further, there are minimal differences in range sizes across latitudes in lowlands. The smallest mean ranges occur in the tropical Andes. Mean range sizes in north‐central Canada, Central America and Argentina/Chile are also small, reflecting the narrowing of the continents in these areas. The best regression model explained 51% of the variation in mean range size.Main conclusions  The two‐dimensional range size pattern indicates that neither winter temperature nor annual variability in temperature strongly influences the distribution of range sizes directly; rather, climate influences bird range sizes indirectly via effects on habitat size. Also, macroclimate interacts with topographic relief across latitudes, generating sharp mesoscale habitat gradients in tropical mountains but not in high latitude mountains or in lowlands at any latitude. Birds respond to these habitat gradients, resulting in ‘latitudinal’ range size gradients in topographically complex landscapes but not in simple landscapes.
How much may I eat? Calorie estimates based upon energy expenditure prediction equations
Authors: Heymsfield S. B. , Harp J. B. , Rowell P. N. , Nguyen A. M. , Pietrobelli A. 
Published: July 2006

SummaryHow much may I eat? Most healthcare workers, when asked this question, have insufficient knowledge to educate their patients on a healthy energy intake level. In this review we examine the available methods for estimating adult energy requirements with a focus on the newly developed National Academy of Sciences/Institute of Medicine (NAS/IOM) doubly‐labelled water total energy expenditure (TEE) prediction equations. An overview is first provided of the traditional factorial method of estimating energy requirements. We then extend this overview by exploring the development of the NAS/IOM TEE prediction models and their role in estimating energy requirments as a function of sex, age, weight, height and physical activity level. The NAS/IOM prediction models were developed for evaluating group energy requirements, although the formulas can be applied in individual ‘example’ patients for educational purposes. Potential limitations and interpretation issues of both the factorial and NAS/IOM methods are examined. This information should provide healthcare professionals with the tools and understanding to appropriately answer the question, ‘How much may I eat?’
Community‐onset methicillin‐resistant Staphylococcus aureus in an urban HIV clinic
Authors: Skiest D , Brown K , Hester J , Moore T , Crosby C , Mussa HR , Hoffman‐Roberts H , Cooper T 
Published: July 2006

ObjectivesTo determine the proportion of skin/soft tissue infections (SSTIs) and to determine risks for MRSA infection caused by methicillin‐resistant Staphylococcus aureus (MRSA) in HIV‐infected out‐patients.MethodsWe conducted a prospective study of SSTIs in HIV‐infected out‐patients. A questionnaire was used to record MRSA risk factors and treatment. In vitro testing for antibiotic susceptibility, inducible clindamycin resistance, panton‐valentine leucocidin (PVL) toxin, and the staphylococcal chromosomal cassette mec (SCCmec) type was performed using standardized methods. Treatment outcomes included resolution of primary site of infection, nonresolution of infection and reinfection and were confirmed at clinic visit and/or telephone follow‐up.ResultsForty‐one of 44 patients had an SSTI caused by MRSA. African‐Americans comprised 21 of 41 MRSA patients. The median CD4 count of MRSA patients was 411 cells/μL. Four patients required hospitalization and three patients had secondary bacteraemia. Twenty‐one of 41 MRSA patients had healthcare‐associated (HCA) MRSA risk factors including a history of prior MRSA infection (n=9) and hospitalization within 6 months (n=11). Other prevalent MRSA risk factors included receipt of systemic antibiotics within 6 months (n=21) and previous incarceration (n=19). Twenty‐two patients had a significant non‐HIV‐related comorbid illness. The majority of isolates were susceptible to trimethoprim‐sulfamethoxazole, tetracycline, and clindamycin. Inducible clindamycin resistance was detected in 0 of 16 erythromycin‐resistant, clindamycin‐susceptible MRSA isolates. Twenty‐one of 24 isolates tested positive for SCCmec type IV. Twenty‐four of 24 isolates tested positive for the PVL gene. Antibiotic treatment was discordant (bacteria nonsusceptible to antibiotic used) in eight MRSA patients. The primary SSTI resolved in 37 of 40 MRSA patients. Recurrence of infection at a site other than the primary site was relatively common (11 patients).ConclusionsWe found a high rate of MRSA causing SSTI in community‐dwelling patients. The majority of isolates were positive for PVL and SCCmec IV, which is typical of community‐associated MRSA isolates causing SSTIs in the general population. Inducible clindamycin resistance was not detected. Most patients had MRSA risk factors. The initial site of infection resolved in most cases but subsequent MRSA infection was relatively common.
Abnormal glucose metabolism among older men with or at risk of HIV infection
Authors: Howard AA , Floris‐Moore M , Lo Y , Arnsten JH , Fleischer N , Klein RS 
Published: July 2006

ObjectivesTo determine factors associated with diabetes, insulin resistance, and abnormal glucose tolerance in older men with or at risk of HIV infection.MethodsDiabetes was assessed by self‐report in 643 men ≥49 years old with or at risk of HIV infection. In a subset of 216 men without previously diagnosed diabetes [including 90 HIV‐uninfected men, 28 HIV‐infected, antiretroviral‐naive men, 28 HIV‐infected men taking non‐protease inhibitor (PI)‐containing highly active antiretroviral therapy (HAART), and 70 HIV‐infected men taking PI‐containing HAART], an oral glucose tolerance test with insulin levels was performed. HIV serology, CD4 cell count, weight, height and waist circumference were measured. Antiretroviral use, drug use, family history of diabetes, physical activity and sociodemographic data were obtained using standardized interviews.ResultsOf 643 participants, 116 (18%) had previously diagnosed diabetes. With the oral glucose tolerance test, 15 of 216 men (7%) were found to have undiagnosed diabetes and 40 (18%) impaired glucose tolerance. Factors independently associated with previously diagnosed diabetes included use of non‐PI‐containing HAART, methadone treatment, positive CAGE test for alcoholism, obesity and family history of diabetes. Factors independently associated with greater insulin resistance included waist circumference and heroin use. Factors independently associated with abnormal glucose tolerance (impaired glucose tolerance or diabetes) included age ≥55 years and Hispanic ethnicity.ConclusionsHIV‐infected men with diabetes risk factors should undergo screening for diabetes regardless of HAART use. Interventions targeting modifiable risk factors, including overweight and physical inactivity, are warranted. The potential impact of opiate and alcohol abuse on glucose metabolism should be recognized in clinical care, and addressed in future research studies of HIV‐infected persons.
A randomized, open‐label study to compare the effects of two different doses of recombinant human growth hormone on fat reduction and fasting metabolic parameters in HIV‐1‐infected patients with lipodystrophy
Authors: Bickel M , Zangos S , Jacobi V , Lutz T , Knecht G , Goebel F , Staszewski S , Klauke S 
Published: July 2006

BackgroundSeveral studies have shown beneficial effects of recombinant human growth hormone (r‐hGH) in reducing visceral adipose tissue (VAT) in HIV‐1‐infected patients with lipodystrophy.MethodsPatients were randomized to r‐hGH 4 mg daily (group A) or three times per week (group B) over 12 weeks, followed by a 2 mg daily maintenance dose for 12 weeks. Magnetic resonance imaging (MRI) scans were performed to assess body composition.ResultsA total of 26 subjects were included in the study. VAT was reduced overall by 35.1 cm2 (29.5%) at week 12 and by 49 cm2 (39.9%) at week 24, respectively, compared with baseline (P<0.001 for both comparisons). By week 12, VAT was reduced by 27 and 29% (A vs B; P=0.47) while facial fat was reduced by 3.3 and 2.6 cm2 in groups A and B, respectively (P=0.96). Over 24 weeks, VAT was reduced by 42 and 38% (P=0.35) and facial fat by 3.2 and 2.4 cm2 in groups A and B, respectively (P=0.91), compared with baseline. There was a greater increase in high‐density lipoprotein (HDL) in group A than in group B (4.9 vs 2.4 mg/dL in week 12 and 7.1 vs −0.4 mg/dL in week 24; P=0.03). Fasting insulin levels increased, whereas glucose and insulin measured in oral glucose tolerance tests remained unchanged. Drug‐related side effects were transient and reversible, but more common in group A (67%) than in group B (29%).ConclusionsThis study confirms reports that r‐hGH effectively reduces VAT, with a relatively small reduction of facial and limb fat.
Prevalence of risk factors for cardiovascular disease in HIV‐infected patients over time: the Swiss HIV Cohort Study
Authors: Glass TR , Ungsedhapand C , Wolbers M , Weber R , Vernazza PL , Rickenbach M , Furrer H , Bernasconi E , Cavassini M , Hirschel B , Battegay M , Bucher HC ,   the Swiss HIV Cohort Study
Published: July 2006

ObjectiveMetabolic changes caused by antiretroviral therapy (ART) may increase the risk of coronary heart disease (CHD). We evaluated changes in the prevalence of cardiovascular risk factors (CVRFs) and 10‐year risk of CHD in a large cohort of HIV‐infected individuals.MethodsAll individuals from the Swiss HIV Cohort Study (SHCS) who completed at least one CVRF questionnaire and for whom laboratory data were available for the period February 2000 to February 2006 were included in the analysis. The presence of a risk factor was determined using cut‐offs based on the guidelines of the National Cholesterol Education Program (NCEP ATP III), the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7), the American Diabetes Association, and the Swiss Society for Cardiology.ResultsOverall, 8033 individuals completed at least one CVRF questionnaire. The most common CVRFs in the first completed questionnaire were smoking (57.0%), low high‐density lipoprotein (HDL) cholesterol (37.2%), high triglycerides (35.7%), and high blood pressure (26.1%). In total, 2.7 and 13.8% of patients were categorized as being at high (>20%) and moderate (10–20%) 10‐year risk for CHD, respectively. Over 6 years the percentage of smokers decreased from 61.4 to 47.6% and the percentage of individuals with total cholesterol >6.2 mmol/L decreased from 21.1 to 12.3%. The prevalence of CVRFs and CHD risk was higher in patients currently on ART than in either pretreated or ART‐naive patients.ConclusionDuring the 6‐year observation period, the prevalence of CVRFs remains high in the SHCS. Time trends indicate a decrease in the percentage of smokers and individuals with high cholesterol.
Return Dynamics in Bosnia1and Croatia: A Comparative Analysis
Authors: Harvey Joanna 
Published: July 2006

ABSTRACTMore than ten years after the end of the conflicts in Bosnia and Croatia, this paper examines the process of return of the displaced to their homes, offering a comparison of factors affecting the process in the two countries. The first section sketches the nature and modality of obstruction to minority return in places of origin, describing some of the ways in which politicized obstruction has interacted with other conditions in return locations. The second section looks at the impact on the return process of conditions in places of refuge, examining how particular circumstances of their displacement have differently affected questions of mobilization and representation among displaced communities. In particular, some observations are made about the relationships between the displaced communities and the authorities in the various places of refuge, and about the effect that these relationships have had on the approach taken to the question of return by the different communities. In the final section a comparison is made of the nature of international intervention to support minority returns in the two countries, arguing that considerably more resources, attention, and diplomatic pressure were focused on the question of minority return to Bosnia than to Croatia. Some possible explanations for this include the burden on third countries of large numbers of Bosnian refugees, the perceived peace‐building imperative behind minority returns in Bosnia, and the attempt to redress the highly visible failures of the international community in preventing ethnic cleansing there. These factors are absent in the Croatian context, and it is argued that the corresponding lack of attention to minority return there demonstrates an inconsistency behind the moral claim made by international actors in upholding the right to return. The paper concludes by commenting on the effect of the combination of these factors on individual displaced persons and refugees, and on the parallels that can be drawn with other situations of forced migration, specifically Kosovo (Republic of Serbia).3Current opportunities to redress some of the inconsistencies in approach and outstanding obstacles to return are highlighted.
Changes in cerebral membrane lipid composition and fluidity during thioacetamide‐induced hepatic encephalopathy
Authors: Swapna I. , SathyaSaiKumar K. V. , Murthy Ch. R. K. , Dutta‐Gupta A. , Senthilkumaran B. 
Published: July 2006

AbstractLipids are an essential structural and functional component of cellular membranes. Changes in membrane lipid composition are known to affect the activities of many membrane‐associated enzymes, endocytosis, exocytosis, membrane fusion and neurotransmitter uptake, and have been implicated in the pathophysiology of many neurodegenerative disorders. In the present study, we investigated changes in the lipid composition of membranes isolated from the cerebral cortex of rats treated with thioacetamide (TAA), a hepatotoxin that induces fulminant hepatic failure (FHF) and thereon hepatic encephalopathy (HE). HE refers to acute neuropsychiatric changes accompanying FHF. The estimation of membrane phospholipids, cholesterol and fatty acid content in cerebral cortex membranes from TAA‐treated rats revealed a decrease in cholesterol, phosphatidylserine, sphingomyelin, a monounsaturated fatty acid, namely oleic acid, and the polyunsaturated fatty acids γ‐linolenic acid, decosa hexanoic acid and arachidonic acid compared with controls. Assessment of membrane fluidity with pyrene, 1,6‐diphenyl‐1,3,5‐hexatriene and 1‐[4‐(trimethylammonio)phenyl]‐6‐phenyl‐1,3,5‐hexatriene revealed a decrease in the annular membrane fluidity, whereas the global fluidity was unaffected. The level of the thiobarbituric acid reactive species marker for lipid peroxidation also increased in membranes from TAA‐treated rats, thereby indicating the prevalence of oxidative stress. Results from the present study demonstrate gross alterations in cerebral cortical membrane lipid composition and fluidity during TAA‐induced HE, and their possible implications in the pathogenesis of this condition are also discussed.
Interleukin‐1β induces the expression of aquaporin‐4 through a nuclear factor‐κB pathway in rat astrocytes
Authors: Ito Hiroaki , Yamamoto Naoki , Arima Hajime , Hirate Hiroyuki , Morishima Tetsuro , Umenishi Fuminori , Tada Toyohiro , Asai Kiyofumi , Katsuya Hirotada , Sobue Kazuya 
Published: July 2006

AbstractInterleukin (IL)‐1β is known to play a role in the formation of brain edema after various types of injury. Aquaporin (AQP)4 is also reported to be involved in the progression of brain edema. We tested the hypothesis that AQP4 is induced in response to IL‐1β. We found that expression of AQP4 mRNA and protein was significantly up‐regulated by IL‐1β in cultured rat astrocytes, and that intracerebroventricular administration of IL‐1β increased the expression of AQP4 protein in rat brain. The effects of IL‐1β on induction of AQP4 were concentration and time dependent. The effects of IL‐1β on AQP4 were mediated through IL‐1β receptors because they were abolished by co‐incubation with IL‐1 receptor antagonist. It appeared that IL‐1β increased the level of AQP4 mRNA without involvement of de novo protein synthesis because cycloheximide, a protein synthesis inhibitor, did not inhibit the effects of IL‐1β. Inhibition of the nuclear factor‐κB (NF‐κB) pathway blocked the induction of AQP4 by IL‐1β in a concentration‐dependent manner. These findings show that IL‐1β induces expression of AQP4 through a NF‐κB pathway without involvement of de novo protein synthesis in rat astrocytes.
Reduced expression of neuropeptide genes in a genome‐wide screen of a secretion‐deficient mouse
Authors: Bouwman J. , Spijker S. , Schut D. , Wächtler B. , Ylstra B. , Smit A. B. , Verhage M. 
Published: July 2006

AbstractActivity‐dependent changes in synapses rely on functional changes in resident proteins and on gene expression. We addressed the relationship between synapse activity and the expression of synaptic genes by comparing RNA levels in the neocortex of normal mice versus secretion‐deficient and therefore synaptically silent munc18‐1 (mammalian homologue of Caenorhabditis elegans uncoordinated locomotion‐18) null mutants, using microarray expression analysis, real‐time quantitative PCR and northern blotting. We hypothesized that genes under the control of synaptic activity would be differentially expressed between mutants and controls. We found that few synaptic genes were differentially expressed. However, most neuropeptide genes with detectable expression on the microarray were differentially expressed, being expressed 3–20‐fold higher in control cortex. Several other secreted proteins were also differentially expressed, but genes encoding their receptors and many other synaptic components were not. Differential expression was confirmed by real‐time quantitative PCR analysis. In situ hybridization indicated that the difference in neuropeptide expression was uniform and not due to the loss of specific cells in the mutant. In primary sensory neurons, which do not depend on synaptic activity for their input, the differential expression of neuropeptides was not observed. These data argue against a general relationship between the activity of synapses and the expression of their resident proteins, but suggest a link between secretion and the expression of genes encoding the secreted products.
JAK2 and STAT3 activation contributes to neuronal damage following transient focal cerebral ischemia
Authors: Satriotomo Irawan , Bowen Kellie K. , Vemuganti Raghu 
Published: July 2006

AbstractIncreased levels of interleukin‐6 (IL‐6) play a role in post‐ischemic cerebral inflammation. IL‐6 binding to its receptors induces phosphorylation of the receptor associated janus kinases (JAKs), and the down‐stream signal transducer and activator of transcription (STAT) family of transcription factors, which amplify the IL‐6 signal transduction. We evaluated the functional significance of JAK2 and STAT3 activation in focal ischemia‐induced neuronal damage. Transient middle cerebral artery occlusion in adult rats led to increased JAK2 and STAT3 phosphorylation in the ipsilateral cortex and striatum after 6–72 h of reperfusion. Fluorescent immunohistochemistry with cell specific markers (NeuN for neurons, glial fibrillary acidic protein for reactive astrocytes and ED1/OX42 for activated macrophages/microglia) showed that both pJAK2 and pSTAT3 staining is predominantly localized in the macrophages/microglia in the post‐ischemic brain. Intracerebroventricular infusion of rats with AG490 (a JAK2 phosphorylation inhibitor) prevented the post‐ischemic JAK2 and STAT3 phosphorylation and significantly decreased the infarct volume, number of apoptotic cells and neurological deficits, compared to vehicle control. Furthermore, intracerebral injection of siRNA specific for STAT3 led to curtailed STAT3 mRNA expression and phosphorylation, decreased infarct volume, fewer apoptotic cells and improved neurological function following transient middle cerebral artery occlusion. These studies show that JAK2‐STAT3 activation plays a role in post‐ischemic brain damage.