bluuebunny/crossref_metadata_2025 huggingface dataset:
Human Bocavirus: Passenger or Pathogen in Acute Respiratory Tract Infections?
Authors: Schildgen Oliver , Müller Andreas , Allander Tobias , Mackay Ian M. , Völz Sebastian , Kupfer Bernd , Simon Arne
Published: April 2008

Human bocavirus (HBoV) is a newly identified virus tentatively assigned to the family
Parvoviridae
, subfamily
Parvovirinae
, genus
Bocavirus
. HBoV was first described in 2005 and has since been detected in respiratory tract secretions worldwide. Herein we review the literature on HBoV and discuss the biology and potential clinical impact of this virus. Most studies have been PCR based and performed on patients with acute respiratory symptoms, from whom HBoV was detected in 2 to 19% of the samples. HBoV-positive samples have been derived mainly from infants and young children. HBoV DNA has also been detected in the blood of patients with respiratory tract infection and in fecal samples of patients with diarrhea with or without concomitant respiratory symptoms. A characteristic feature of HBoV studies is the high frequency of coinciding detections, or codetections, with other viruses. Available data nevertheless indicate a statistical association between HBoV and acute respiratory tract disease. We present a model incorporating these somewhat contradictory findings and suggest that primary HBoV infection causes respiratory tract symptoms which can be followed by prolonged low-level virus shedding in the respiratory tract. Detection of the virus in this phase will be facilitated by other infections, either simply via increased sample cell count or via reactivation of HBoV, leading to an increased detection frequency of HBoV during other virus infections. We conclude that the majority of available HBoV studies are limited by the sole use of PCR diagnostics on respiratory tract secretions, addressing virus prevalence but not disease association. The ability to detect primary infection through the development of improved diagnostic methods will be of great importance for future studies seeking to assign a role for HBoV in causing respiratory illnesses.
Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects
Authors: Rock R. Bryan , Olin Michael , Baker Cristina A. , Molitor Thomas W. , Peterson Phillip K.
Published: April 2008

Tuberculosis of the central nervous system (CNS) is a highly devastating form of tuberculosis, which, even in the setting of appropriate antitubercular therapy, leads to unacceptable levels of morbidity and mortality. Despite the development of promising molecular diagnostic techniques, diagnosis of CNS tuberculosis relies largely on microbiological methods that are insensitive, and as such, CNS tuberculosis remains a formidable diagnostic challenge. Insights into the basic neuropathogenesis of Mycobacterium tuberculosis and the development of an appropriate animal model are desperately needed. The optimal regimen and length of treatment are largely unknown, and with the rising incidence of multidrug-resistant strains of M. tuberculosis, the development of well-tolerated and effective antibiotics remains a continued need. While the most widely used vaccine in the world largely targets this manifestation of tuberculosis, the BCG vaccine has not fulfilled the promise of eliminating CNS tuberculosis. We put forth this review to highlight the current understanding of the neuropathogenesis of M. tuberculosis, to discuss certain epidemiological, clinical, diagnostic, and therapeutic aspects of CNS tuberculosis, and also to underscore the many unmet needs in this important field.
Respiratory Viruses Other than Influenza Virus: Impact and Therapeutic Advances
Authors: Nichols W. Garrett , Peck Campbell Angela J. , Boeckh Michael
Published: April 2008

Though several antivirals have been developed and marketed to treat influenza virus infections, the development of antiviral agents with clinical activity against other respiratory viruses has been more problematic. Here we review the epidemiology of respiratory viral infections in immunocompetent and immunocompromised hosts, examine the evidence surrounding the currently available antivirals for respiratory viral infections other than influenza, highlight those that are in the pipeline, and discuss the hurdles for development of such agents.
Clinical and ultrasonographic correlation between scapular dyskinesia and subacromial space measurement among junior elite tennis players
Authors: Silva R T , Hartmann L G , Laurino C F de Souza , Biló J P Rocha
Published: April 2008

Objectives

In this study, the hypothesis that tennis players with scapular dyskinesia present a smaller subacromial space than non-athletes was investigated. Additionally, the correlation between the size of the subacromial space and abnormalities in scapular movement during arm abduction was studied.

Design

Cross-sectional study.

Participants

A total of 53 elite tennis players and 20 control participants were enrolled in the study. Participation was restricted to elite-level, junior tennis players who had no current shoulder pain or history of shoulder injuries.

Intervention

Each individual was examined for scapular dyskinesia by a single physician and by ultrasound, with the results analysed in a blind fashion by a single radiologist.

Results

43.4% of the tennis players and 20% of control participants presented with scapular dyskinesia. Of the 106 shoulders evaluated, 39.6% of tennis players and 10% of control participants presented with scapular dyskinesia in the clinical examination (p = 0.005). Ultrasonographic measurements demonstrated that tennis players presented statistically smaller subacromial spaces compared with control participants (p<0.001). A decrease in the subacromial space was observed in tennis players when the shoulder was raised from 0° to 60° of abduction; however, dyskinesia-afflicted athletes demonstrated a significantly greater decrease following this movement (19.3 vs 13.8 mm, p = 0.002).

Conclusions

The results of this study demonstrated that tennis players with scapular dyskinesia present a smaller subacromial space than control participants. Furthermore, when the shoulder was analysed dynamically, moving from neutral abduction to 60° of elevation, the tennis players with scapular dyskinesia presented a greater reduction in the subacromial space compared with unaffected athletes.
Gene regulation by mechanotransduction in fibroblasts
Authors: Chiquet Matthias , Tunç-Civelek Vildan , Sarasa-Renedo Ana
Published: April 2008

Mechanical forces are important for connective tissue homeostasis. How do fibroblasts sense mechanical stress and how do they translate this information into an adaptive remodeling of the extracellular matrix (ECM)? Tenascin-C is rapidly induced in vivo by loading muscles and in vitro by stretching fibroblasts. Regulation of tenascin-C expression by mechanical signals occurs at the transcriptional level. Integrin receptors physically link the ECM to the cytoskeleton and act as force transducers: intracellular signals are triggered when integrins engage with ECM, and later when forces are applied. We found that cyclic strain does not induce tenascin-C messenger ribonucleic acid (mRNA) in fibroblasts lacking the β1-integrin chain. An important link in integrin-dependent mechanotransduction is the small guanosine 5′-triphosphatase. RhoA and its target kinase, ROCK. In fibroblasts, cyclic strain activates RhoA and thereby induces ROCK-dependent actin assembly. Interestingly, tenascin-C mRNA induction by cyclic strain was suppressed by relaxing the cytoskeleton with a ROCK inhibitor or by actin depolymerization. Conversely, chemical activators of RhoA enhanced the effect of strain both on actin dynamics and on tenascin-C expression. Thus, RhoA/ROCK-controlled actin dynamics are required for the induction of specific ECM genes by mechanical stress. These findings have implications for the understanding of regeneration and for tissue engineering.
Mechanisms of calcium-induced mitochondrial biogenesis and GLUT4 synthesis
Authors: Wright David C.
Published: April 2008

Regularly performed aerobic exercise leads to increases in skeletal muscle mitochondria and glucose transporter 4 (GLUT4) protein content, resulting in an enhanced capacity to oxidize substrates and improvements in insulin- and contraction-mediated glucose uptake. Although the specific mechanisms governing these adaptive responses have not been fully elucidated, accumulating evidence suggests that the increase in cytosolic Ca2+that occurs with each wave of sacrolemmal depolarization is a key component of these processes. Treating L6 muscle cells with agents that increase Ca2+without causing reductions in ~P or the activation of 5′-AMP-activated protein kinase leads to increases in GLUT4 and mitochondrial protein contents. This effect is likely controlled through calcium/calmodulin-dependent protein kinase (CaMK), since KN93, a specific CaMK inhibitor, blocks these adaptive responses. Recent findings provide evidence that the activation of p38 mitogen-activated protein kinase (MAPK) is involved in the pathway through which Ca2+/CaMK mediates mitochondrial and GLUT4 biogenesis. p38 MAPK initiates GLUT4 and mitochondrial biogenesis through the activation      of transcription factors and transcriptional coactivators such as myocyte enhancer factor 2 (MEF2) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α). Subsequent increases in the content of these proteins further enhance Ca2+-induced GLUT4 and mitochondrial biogenesis. Since decreases in mitochondrial and GLUT4 contents are associated with skeletal muscle insulin resistance, an understanding of the mechanisms by which these processes can be normalized will aid in the prevention and treatment of type 2 diabetes.
The energetic implications of uncoupling protein-3 in skeletal muscle
Authors: Costford Sheila R. , Seifert Erin L. , Bézaire Véronic , F. Gerrits Martin , Bevilacqua Lisa , Gowing Adrienne , Harper Mary-Ellen
Published: April 2008

Despite almost a decade of research since the identification of uncoupling protein-3 (UCP3), the molecular mechanisms and physiological functions of this mitochondrial anion carrier protein are not well understood. Because of its highly selective expression in skeletal muscle and the existence of mitochondrial proton leak in this tissue, early reports proposed that UCP3 caused a basal proton leak and increased thermogenesis. However, gene expression data and results from knockout and overexpression studies indicated that UCP3 does not cause basal proton leak or physiological thermogenesis. UCP3 expression is associated with increases in circulating fatty acids and in fatty acid oxidation (FAO) in muscle. Fatty acids are also well recognized as activators of the prototypic UCP1 in brown adipose tissue. This has led to hypotheses implicating UCP3 in mitochondrial fatty acid translocation. The corresponding hypothesized physiological roles include facilitated FAO and protection from the lipotoxic effects of fatty acids. Recent in vitro studies of physiological increases in UCP3 in muscle cells demonstrate increased FAO, and decreased reactive oxygen species (ROS) production. Detailed mechanistic studies indicate that ROS or lipid by-products of ROS can activate a UCP3-mediated proton leak, which in turn acts in a negative feedback loop to mitigate ROS production. Altogether, UCP3 appears to play roles in muscle FAO and mitigated ROS production. Future studies will need to elucidate the molecular mechanisms underlying increased FAO, as well as the physiological relevance of ROS-activated proton leak.
Cortisol and GH: odd and controversial ideas
Authors: Duclos Martine , Guinot Michel , Le Bouc Yves
Published: April 2008

Activation of the hypothalamo–pituitary–adrenal (HPA) axis and of the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis represents a physiological response to the energetic, metabolic, vascular, and sometimes neurophysiologic or psychological needs of exercise. Long-lasting increased and (or) decreased secretion of cortisol (the end-product of the HPA axis) or of GH is detrimental to health. This suggests that the activity of these hormonal axes is finely tuned toward homeostasia, tolerating limited prolonged homeostatic disruption. However, the relationships between exercise training and cortisol and GH secretion are full of odd and controversial ideas. In this review, the relationships between HPA axis adaptation to exercise training or disadaptation with overtraining will be discussed, with an emphasis on the limitation on the current measures used to profile hormonal activity. Knowledge of these relationships between cortisol and GH responses to exercise is an important tool to fight against doping with glucocorticoids and GH, and their health-damaging consequences.
Role of AMPK in skeletal muscle gene adaptation in relation to exercise
Authors: Jørgensen Sebastian B. , Jensen Thomas E. , Richter Erik A.
Published: April 2008

The 5′-AMP-activated protein kinase (AMPK) functions as an intracellular fuel sensor that affects metabolism and gene expression. AMPK is activated in skeletal muscle in response to exercise and is therefore believed to be an important signalling molecule in regulating adaptation of skeletal muscle to exercise training. This review first focuses on mechanisms regulating AMPK activity during muscle contraction. We then discuss the role of AMPK in regulating expression of genes encoding various enzymes in muscle in the basal state and in relation to exercise training. Although decreased AMPK activity in muscle causes reduced protein expression of mitochondrial enzymes in the basal state, AMPK does not appear to be indispensable for exercise-training induced increase in mitochondrial enzyme expression.
Exercise and MEF2–HDAC interactions
Authors: McGee Sean L.
Published: April 2008

Exercise increases the metabolic capacity of skeletal muscle, which improves whole-body energy homeostasis and contributes to the positive health benefits of exercise. This is, in part, mediated by increases in the expression of a number of metabolic enzymes, regulated largely at the level of transcription. At a molecular level, many of these genes are regulated by the class II histone deacetylase (HDAC) family of transcriptional repressors, in particular HDAC5, through their interaction with myocyte enhancer factor 2 transcription factors. HDAC5 kinases, including 5′-AMP-activated protein kinase and protein kinase D, appear to regulate skeletal muscle metabolic gene transcription by inactivating HDAC5 and inducing HDAC5 nuclear export. These mechanisms appear to participate in exercise-induced gene expression and could be important for skeletal muscle adaptations to exercise.
Skeletal muscle adaptation to fatty acid depends on coordinated actions of the PPARs and PGC1α: implications for metabolic disease
Authors: Muoio Deborah M. , Koves Timothy R.
Published: April 2008

Dyslipidemia and intramuscular accumulation of fatty acid metabolites are increasingly recognized as core features of obesity and type 2 diabetes. Emerging evidence suggests that normal physiological adaptations to a heavy lipid load depend on the coordinated actions of broad transcriptional regulators such as the peroxisome proliferator activated receptors (PPARs) and PPARγ coactivator 1α (PGC1α). The application of transcriptomics and targeted metabolic profiling tools based on mass spectrometry has led to our finding that lipid-induced insulin resistance is a condition in which upregulation of PPAR-targeted genes and high rates of β-oxidation are not supported by a commensurate upregulation of tricarboxylic acid (TCA) cycle activity. In contrast, exercise training enhances mitochondrial performance, favoring tighter coupling between β-oxidation and the TCA cycle, and concomitantly restores insulin sensitivity in animals fed a chronic high-fat diet. The exercise-activated transcriptional coactivator, PGC1α, plays a key role in coordinating metabolic flux through these 2 intersecting metabolic pathways, and its suppression by overfeeding may contribute to diet-induced mitochondrial dysfunction. Our emerging model predicts that muscle insulin resistance arises from a mitochondrial disconnect between β-oxidation and TCA cycle activity. Understanding of this “disconnect” and its molecular basis may lead to new therapeutic approaches to combatting metabolic disease.
Protein-mediated fatty acid uptake: regulation by contraction, AMP-activated protein kinase, and endocrine signals
Authors: Nickerson James G. , Momken Iman , Benton Carley R. , Lally James , Holloway Graham P. , Han Xiao-Xia , Glatz Jan F.C. , Chabowski Adrian , Luiken Joost J.F.P. , Bonen Arend
Published: April 2008

Fatty acid transport into heart and skeletal muscle occurs largely through a highly regulated protein-mediated mechanism involving a number of fatty acid transporters. Chronically altered muscle activity (chronic muscle stimulation, denervation) alters fatty acid transport by altering the expression of fatty acid transporters and (or) their subcellular location. Chronic exposure to leptin downregulates while insulin upregulates fatty acid transport by altering concomitantly the expression of fatty acid transporters. Fatty acid transport can also be regulated within minutes, by muscle contraction, AMP-activated protein kinase activation, leptin, and insulin, through induction of the translocation of fatty acid translocase (FAT)/CD36 from its intracellular depot to the plasma membrane. In insulin-resistant muscle, a permanent relocation of FAT/CD36 to the sarcolemma appears to account for the excess accretion of intracellular lipids that interfere with insulin signaling. Recent work has also shown that FAT/ CD36, but not plasma membrane associated fatty acid binding protein, is involved, along with carnitine palmitoyltransferase, in regulating mitochondrial fatty acid oxidation. Finally, studies in FAT/CD36 null mice indicate that this transporter has a key role in regulating fatty acid metabolism in muscle.
Molecular mechanisms of life- and health-span extension: role of calorie restriction and exercise intervention
Authors: Carter Christy S. , Hofer Tim , Seo Arnold Y. , Leeuwenburgh Christian
Published: April 2008

The aging process results in a gradual and progressive structural deterioration of biomolecular and cellular compartments and is associated with many pathological conditions, including cardiovascular disease, stroke, Alzheimer’s disease, osteoporosis, sarcopenia, and liver dysfunction. Concomitantly, each of these conditions is associated with progressive functional decline, loss of independence, and ultimately disability. Because disabled individuals require care in outpatient or home care settings, and in light of the social, emotional, and fiscal burden associated with caring for an ever-increasing elderly population, research in geriatric medicine has recently focused on the biological mechanisms that are involved in the progression towards functional decline and disability to better design treatment and intervention strategies. Although not completely understood, the mechanisms underlying the aging process may partly involve inflammatory processes, oxidative damage, mitochondrial dysfunction, and apoptotic tissue degeneration. These hypotheses are based on epidemiological evidence and data from animal models of aging, as well as interventional studies. Findings from these studies have identified possible strategies to decrease the incidence of age-related diseases and delay the aging process. For example, lifelong exercise is known to extend mean life-span, whereas calorie restriction (CR) increases both mean and maximum life-span in a variety of species. Optimal application of these intervention strategies in the elderly may positively affect health-related outcomes and possibly longevity. Therefore, the scope of this article is to (i) provide an interpretation of various theories of aging from a “health-span” perspective; (ii) describe interventional testing in animals (CR and exercise); and (iii) provide a translational interpretation of these data.
Hormetic effects of regular exercise in aging: correlation with oxidative stress
Authors: Goto Sataro , Naito Hisashi , Kaneko Takao , Chung Hae Young , Radák Zsolt
Published: April 2008

To explore mechanisms of the beneficial consequences of regular exercise, we studied the effects of regular swimming and treadmill exercise on oxidative stress in the brain and liver of rats. Protein carbonyl was significantly reduced and the activity of proteasome was upregulated in the brain extracts of young and middle-aged animals after 9 weeks of swimming training. Furthermore, their cognitive functions were significantly improved. In separate experiments, the activation of transcription nuclear factor κB was attenuated in the liver of old rats after 8 weeks of regular treadmill exercise and the DNA binding activity of glucocorticoid receptor reduced with age was restored, suggesting that inflammatory reactions are alleviated by the regimen. This was accompanied by upregulation of the glutathione level and reduced reactive oxygen species generation. Similar training reduced the 8-oxodeoxyguanosine content in the nuclear and mitochondrial DNA of the liver of old rats. Thus, these findings, together with reports of other investigators, suggest that moderate regular exercise attenuates oxidative stress. The mild oxidative stress possibly elicited by regular exercise appears to manifest a hormesis-like effect in nonmuscular tissues, constituting beneficial mechanisms of exercise by adaptively upregulating various antioxidant mechanisms, including antioxidative and repair–degradation enzymes for damaged molecules. Importantly, the adaptation induced by regular exercise was effective even if initiated late in life.
Role of nuclear factor κB and mitogen-activated protein kinase signaling in exercise-induced antioxidant enzyme adaptation
Authors: Ji Li Li , Gomez-Cabrera Maria-Carmen , Vina Jose
Published: April 2008

Activation of nuclear factor (NF) κB and mitogen-activated protein kinase (MAPK) pathways in skeletal muscle has been shown to enhance the gene expression of several enzymes that play an important role in maintaining oxidant–antioxidant homeostasis, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). While an acute bout of exercise activates NFκB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression. Thus, ROS generation during exercise may have duel effects: the infliction of oxidative stress and damage, and the stimulation of adaptive responses favoring long-term protection. This scenario explains why animals and humans involved in exercise training have demonstrated increased resistance to oxidative damage under a wide range of physiological and pathological stresses.
Regulation of Na+–K+ homeostasis and excitability in contracting muscles: implications for fatigue
Authors: Nielsen Ole Bækgaard , de Paoli Frank Vincenzo
Published: April 2008

The performance of skeletal muscles depends on their ability to initiate and propagate action potentials along their outer membranes in response to motor signals from the central nervous system. This excitability of muscle fibres is related to the function of Na+ and K+ and Cl– channels and to steep chemical gradients for the ions across the cell membranes, i.e., the sarcolemma and T-tubular membranes. At rest, the chemical gradients for Na+ and K+ are maintained within close limits by the action of the Na+–K+ pump. During contractile activity, however, the muscles lose K+, which causes an increase in the concentration of K+ in the extracellular compartments of the body, the magnitude of which depends on the intensity of the exercise and the size of the muscle groups involved. Since the ensuing reduction in the chemical K+ gradient can have adverse effects on muscle excitability, it has repeatedly been suggested that, during intense exercise, the loss of K+ from muscle fibres can contribute to the complex set of mechanisms that leads to the development of muscle fatigue. In this review, aspects of the regulation of Na+–K+ homeostasis and excitability in contracting muscles is discussed within this context, together with the implications for the contractile function of skeletal muscles.
Non-obese patients with type 2 diabetes and prediabetic subjects: distinct phenotypes requiring special diabetes treatment and (or) prevention?
Authors: Vaag Allan , Lund Søren S.
Published: April 2008

A major reason for the increased incidence of type 2 diabetes mellitus (T2DM) across the world is the so-called obesity epidemic, which occurs both in developed and developing countries. However, a large proportion of patients with T2DM in European and, in particular, Asian countries are non-obese. The non-obese T2DM phenotype is characterized by disproportionally reduced insulin secretion and less insulin resistance, as compared with obese patients with T2DM. Importantly, non-obese patients with T2DM have a similar increased risk of cardiovascular disease as obese T2DM patients. The risk of T2DM in non-obese patients is influenced by genetics as well as factors operating in utero indicated by low birth weight. Furthermore, this phenotype is slightly more prevalent among patients with latent autoimmune diabetes in adults, characterized by positive anti-GAD antibodies. The recently identified TCF7L2 gene polymorphism resulting in low insulin secretion influences the risk of T2DM in both obese and non-obese subjects, but is relatively more prevalent among non-obese patients with T2DM. Furthermore, the Pro12Ala polymorphism of the PPARγ gene influencing insulin action increases the risk of T2DM in non-obese subjects. Despite a “normal” body mass index, non-obese patients with T2DM are generally characterized by a higher degree of both abdominal and total fat masses (adiposity). Prevention of T2DM with lifestyle intervention is at least as effective in non-obese as in obese prediabetic subjects, and recent data suggest that metformin treatment targeting insulin resistance and non-glycemic cardiovascular disease risk factors is as beneficial in non-obese as in obese patients with T2DM. Nevertheless, non-obese patients with T2DM may progress to insulin treatment more rapidly as compared with obese patients with T2DM.
Effects of physical training on endothelial function and limb blood flow in type 2 diabetes
Authors: Sonne Mette Paulli , Scheede-Bergdahl Celena , Olsen David Benee , Lise Højbjerre  , Alibegovic Amra , Nielsen Ninna Bo , Stallknecht Bente , Helge Jørn Wulff , Vaag Allan , Dela Flemming
Published: April 2008

The term “endothelial dysfunction” refers to the inability or attenuated effect of the endothelial cells in participating in the relaxation of the adjacent smooth muscle, thus causing less vasodilation. Although endothelial dysfunction is often seen in patients with type 2 diabetes, it does not necessarily follow that insulin resistance and (or) hyperglycemia is causing the inability to respond properly to vasodilatory stimuli. Rather, this could be related to the impact of concomitant cardiovascular risk factors that are almost invariably present in patients with type 2 diabetes. The impact of physical training — or the opposite, inactivity — on endothelial function is not fully elucidated. Some studies have shown positive effects of physical training, whereas others have not. In general, physical training can improve endothelial function when this is impaired. However, physical training does not seem to have any effect on endothelial function when this is normal.
Stresses induced by alkali–silica reactivity in prototypes of reinforced concrete columns incorporating various types of reactive aggregates
Authors: Smaoui N. , Bissonnette B. , Bérubé M. A. , Fournier B.
Published: April 2008

Prototypes of columns were cast with different percentages of rebars and stirrups and various alkali–silica reactive aggregates. The deformations of concrete were measured along the three directions using surface metal studs and internal vibrating wire gauges. The deformations of steel were measured using fiber-optic gauges and short rods welded to rebars and stirrups. Along each direction, the deformations of concrete and steel were quite similar up to 0.08% longitudinal expansion, beyond which the rebars were generally showing less (longitudinal) expansion than concrete. The rebars reduced the longitudinal expansion; the higher the percentage of longitudinal steel, the higher this reduction. On the other hand, the expansion increased in the other two transverse directions to give comparable volumetric expansions for all specimens of the same mixture, with or without relatively spaced-out stirrups. The transverse expansion perpendicular to the casting plane was always higher than the transverse expansion parallel to this plane. The rebars were tensioned up to 280 MPa. The concrete was prestressed parallel to the rebars, up to 3.3 MPa. For their part, the stirrups were highly stressed in tension and flexure, and usually reached plastification.
Dynamic complex modulus predictions of hot-mix asphalt using a micromechanical-based finite element model
Authors: You Zhanping , Dai Qingli
Published: April 2008

A micromechanical-based finite element (FE) model was used to predict the dynamic complex modulus ( E*) of the hot-mix asphalt (HMA). The microstructure of HMA was captured with a high resolution scanner. Two material phases (aggregates and sand mastic) of HMA were modelled with finite elements. The sand mastic herein was composed of fines and asphalt binder with some fine aggregates. The dynamic complex modulus of the sand mastic under different temperatures and loading frequencies was measured in an experimental program. The corresponding principles were applied to bridge the elastic simulation and viscoelastic behavior with the input of the viscoelastic mastic properties. The input parameters in the FE model include the dynamic complex modulus of the sand mastic, the elastic modulus of the aggregates, and the microstructure of the HMA. The E* values of the HMA were measured and used to compare the E* predicted from the FE model. It is found that the FE approach used in this paper has the ability to predict HMA dynamic modulus across a range of temperatures and loading frequencies. The FE prediction of the E* was compared with a recently developed discrete element modelling approach and found the E* prediction from these two approaches to be very similar.
Implementation of subsurface utility engineering in Ontario: cases and a cost model
Authors: Osman Hesham , El-Diraby Tamer
Published: April 2008

This paper investigates a relatively new engineering service that is being introduced in Ontario: subsurface utility engineering (SUE). This service combines civil engineering, surveying, geophysics, and nondestructive excavation for the accurate mapping of underground utilities. This paper presents the results of a one-year study that investigated the use of SUE on large infrastructure projects in Ontario. The study involved performing a detailed cost analysis of nine successful SUE projects, four of which are presented in this paper. Potential cost savings were estimated for each case study and all indicated that SUE has a positive return on investment. In addition, two industry-wide surveys were conducted to investigate the effects of inaccurate utility information on projects. Results indicate that inaccurate utility information has a significant impact on project cost, schedule, and damage to existing utilities. Using the results of the case study analysis and the survey, a generic cost model for SUE was developed that relates project specific characteristics to costs that could be incurred because of inaccurate utility information. This investigation provides valuable insight to the application of a relatively new process in Canada following successful results in the United States.
Repair of steel structures by bonded carbon fibre reinforced polymer patching: experimental and numerical study of carbon fibre reinforced polymer – steel double-lap joints under tensile loading
Authors: Lam Angus C.C. , Cheng J.J. Roger , Yam Michael C.H. , Kennedy Gaylene D.
Published: April 2008

The behavior of carbon fibre reinforced polymer (CFRP) composite bonded to a steel plate double-lap joint was investigated experimentally. A total of 19 specimens were tested with the major test parameters being the bonded lap length, LL, and the axial adherend stiffness ratio, ETR. Five of the 19 specimens were prepared using CFRP sheets, and the rest using CFRP plates. Two CFRP plate specimens were prepared with a tapered lap joint, and their results were compared with those of counterpart specimens prepared without tapered lap joints. In general, the behavior of specimens made from either CFRP sheets or CFRP plates were similar. The joint's axial load carrying capacity increased with increasing LLup to a certain limit, when the joint's load carrying capacity could no longer be increased by increasing LL. However, experimental results showed that a larger failure deformation could be achieved by increasing LLpast this limit. Specimens that had the same inner adherend thickness but higher axial adherend stiffness ratios showed higher axial load carrying capacities. Test results also showed that the strengths of tapered lap joints were almost the same as those of nontapered lap joints with the same LL. Nonlinear finite element analysis was carried out to study the stress–strain behavior of the adherend and the adhesive of the double-lap joint. Using finite element analysis results in an analytical solution obtained from the literature, predictions of the joint's maximum axial strength and minimum required LLwere made. This analytical solution provided good predictions when compared with test results, producing test to predicted ratios from 0.88 to 1.14.
Assessment of ductility demand and reliability of bilinear single-degree-of-freedom systems under earthquake loading
Authors: Hong H. P. , Hong P.
Published: April 2008

Probabilistic assessments of the ductility demand and reliability analysis were carried out for hysteretic bilinear single-degree-of-freedom (SDOF) systems. The assessment considered a set of strong ground motion records, and focused on evaluating the mean and coefficient of variation of the ductility demand for a given normalized yield strength. Results indicated that the ductility demand could be modeled as a Frechet (extreme value type II) variate. Based on the obtained results, empirical equations were provided to predict the mean ductility demand for hysteretic bilinear SDOF systems considering different natural vibration periods, damping ratios, and post-yield stiffness to initial stiffness ratios. Numerical results showed that the coefficient of variation of the ductility demand can go as high as one, depending on the characteristics of the structure. Also, a simple approach was given to estimate the probabilities of incipient damage and incipient collapse using the developed probabilistic characterization of the ductility demand. This approach, which could be suitable for design code calibration analysis, is illustrated numerically in this study.
From cytogenetics to next-generation sequencing technologies: advances in the detection of genome rearrangements in tumorsThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB — Systems and Chemical Biology, and has undergone the Journal's usual peer review process.
Authors: Morozova Olena , Marra Marco A.
Published: April 2008

Genome rearrangements have long been recognized as hallmarks of human tumors and have been used to diagnose cancer. Techniques used to detect genome rearrangements have evolved from microscopic examinations of chromosomes to the more recent microarray-based approaches. The availability of next-generation sequencing technologies may provide a means for scrutinizing entire cancer genomes and transcriptomes at unparalleled resolution. Here we review the methods that have been used to detect genome rearrangements and discuss the scope and limitations of each approach. We end with a discussion of the potential that next-generation sequencing technologies may offer to the field.
Steps towards a repertoire of comprehensive maps of human protein interaction networks: the Human Proteotheque Initiative (HuPI)This paper is one of a selection of papers published in this Special Issue, entitled CSBMCB — Systems and Chemical Biology, and has undergone the Journal's usual peer review process.
Authors: Coulombe Benoit , Blanchette Mathieu , Jeronimo Célia
Published: April 2008

Defining human protein interaction networks has become essential to develop an overall, systems-based understanding of the molecular events that sustain cell growth in normal and disease conditions. To characterize protein interaction networks from human cells, we have undertaken the development of a systematic, unbiased technology pipeline that couples experimental and computational approaches. This discovery engine is central to the Human Proteotheque Initiative (HuPI), a multidisciplinary project aimed at building a repertoire of comprehensive maps of human protein interaction networks, the Human Proteotheque. The information contained in the Proteotheque is made publicly available through an interactive web site that can be consulted to visualize some of the fundamental molecular connections formed in human cells and to determine putative functions of previously uncharacterized proteins based on guilt by association. The process governing the evolution of HuPI towards becoming a repository of accurate and complete protein interaction maps is described.
Riboswitches that sense S-adenosylmethionine and S-adenosylhomocysteineThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB — Systems and Chemical Biology, and has undergone the Journal's usual peer review process.
Authors: Wang Joy Xin , Breaker Ronald R.
Published: April 2008

Numerous riboswitches have been discovered that specifically recognize metabolites and modulate gene expression. Each riboswitch class is defined either by the consensus sequence and structural features of its metabolite-binding aptamer domain, or by the distinct metabolite that the aptamer recognizes. Several distinct classes of riboswitches that respond to S-adenosylmethionine (SAM or AdoMet) have been discovered. Representatives of these classes have been shown to strongly discriminate against S-adenosylhomocystenine (SAH or AdoHcy), which is the metabolic byproduct produced when SAM is used as a cofactor for methylation reactions. However, a distinct class of riboswitches that selectively binds SAH, and strongly discriminates against SAM, also has been discovered. Herein we compare the features of SAM and SAH riboswitches, which help showcase the enormous structural diversity that RNA can harness to form precision genetic switches for compounds that are critical for fundamental metabolic processes.
Virulence potential and genetic diversity ofAeromonas caviae,Aeromonas veronii, andAeromonas hydrophilaclinical isolates from Mexico and Spain: a comparative study
Authors: Aguilera-Arreola Ma. Guadalupe , Hernández-Rodríguez César , Zúñiga Gerardo , Figueras María José , Garduño Rafael A. , Castro-Escarpulli Graciela
Published: April 2008

A comparative study of 109 Aeromonas clinical isolates belonging to the 3 species most frequently isolated from patients with diarrhea in Mexico and Spain was performed to investigate the distribution of 3 prominent toxin genes and the gene encoding flagellin of lateral flagella; 4 well-established virulence factors in the genus Aeromonas. The aerolysin–hemolysin toxin genes were the most prevalent, being present in 89% of the total isolates. The ast toxin gene was conspicuously absent from the Aeromonas caviae and Aeromonas veronii groups but was present in 91% of the Aeromonas hydrophila isolates. Both the alt toxin gene and the lafA flagellin gene also had a low incidence in A. caviae and A. veronii. Differences in the prevalence of alt and lafA were observed between isolates from Mexico and Spain, confirming genus heterogeneity according to geographic location. Carriage of multiple toxin genes was primarily restricted to A. hydrophila isolates, suggesting that A. caviae and A. veronii isolates circulating in Mexico and Spain possess a limited array of virulence genes. Enterobacterial repetitive intergenetic consensus – polymerase chain reaction showed that the Aeromonas populations sampled lack dominant clones and were genetically heterogeneous, with A. caviae being the most diverse species. Further surveys of virulence determinants in genetically heterogeneous populations of Aeromonas isolates circulating worldwide are required to enhance the understanding of their capacity to cause disease.
Analysis and comparison of nonlinear tree height prediction strategies for Douglas-fir forests
Authors: Temesgen H. , Monleon V. J. , Hann D. W.
Published: April 2008

Using an extensive Douglas-fir data set from southwest Oregon, we examined the (1) performance and suitability of selected prediction strategies, (2) contribution of relative position and stand-density measures in improving tree height (h) prediction values, and (3) effect of different subsampling designs to fill in missing h values in a new stand using a regional nonlinear model. Nonlinear mixed-effects models (NMEM) substantially improved the accuracy and precision of height prediction over the conventional nonlinear fixed-effects model (NFEM) that assumes the observations are independent, particularly when a few trees are subsampled for height. The predictive performance of a correction factor on a NFEM with relative position and stand-density measures was comparable to that of a NMEM when four or more trees were subsampled for height. When two or more heights were randomly subsampled, the NMEM efficiently explained the differences in the height–diameter relationship because of the variations in relative position of trees and stand density without having to incorporate them into the model. When only one height was subsampled, selecting the largest diameter tree in the stand would result in a lower predicted root mean square error (RMSE) than randomly selecting the height, regardless of the model form or fitting strategy used.
Sudden and sustained response of Acacia koa crop trees to crown release in stagnant stands
Authors: Baker Patrick J. , Robinson Andrew P. , Ewel John J.
Published: April 2008

We examined the growth response of Acacia koa Gray (koa) in dense (10 000 trees/ha), ~25-year-old, second-growth stands on Hawai‘i to crown release (thinning) and grass control. Koa diameter increment increased within 2 months of thinning across the range of residual densities (200–900 trees/ha). After 3 years, diameter increment in the most intense thinning treatment was 180% greater than in the control treatment (1.4 vs. 0.5 cm/year); in the least intense thinning treatment diameter increment was 100% greater than the control (1.0 vs. 0.5 cm/year). Koa’s growth response was independent of all measures of tree size (diameter at breast height, height, and leaf area) across the range of tree sizes sampled. A grass control treatment to determine if reduced competition for soil water would improve koa growth showed no improvement in growth response. Koa phyllode δ13C values, which represent an integrated measure of tree water status, showed no evidence of tree water stress (mean δ13C = –28.3‰) and were not significantly different between the grass removal and control treatments. These results demonstrate that koa is capable of responding quickly and positively to crown release despite years of suppressed growth and suggest that landowners interested in managing koa forests may have considerable flexibility in the timing and application of thinning treatments to koa stands.
Somatic embryogenesis in Greek fir
Authors: Krajňáková Jana , Gömöry Dušan , Häggman Hely
Published: April 2008

To induce somatic embryogenesis of Greek fir, Abies cephalonica Loud., the influence of different cultivation media, sampling dates, and cold treatment storage were examined. The initiation frequencies ranged from 1% to 25%. The sampling date had a significant effect on the initiation of embryogenic cultures and a high frequency was observed within a 5 week window. The effect of cone storage, composition of initiation media, and the medium by storage interaction also remained nonsignificant after 3 and 10 months of proliferation growth. At the maturation phase, the highest tested concentrations of abscisic acid (ABA), 16 and 32 µmol/L, increased both the capability of embryogenic cell masses (ECMs) to produce embryos and the mean number of embryos. Of the two tested carbohydrates, maltose-containing media produced more embryos altogether (1943, on the average of 22.3 embryos per gram fresh mass) and 76% of the ECMs were able to produce embryos when compared with the corresponding values (152, on the average 3.0 embryos per gram fresh mass) and 15.3%, respectively, on sucrose-containing medium. However, 93.5% of embryos on maltose-containing medium died during the germination phase, whereas the corresponding percentage on sucrose-containing medium was 78.2%.
An examination of species-specific growing space utilization
Authors: Lhotka John M. , Loewenstein Edward F.
Published: April 2008

A comparison is made among the size–density relationships of sugar maple ( Acer saccharum Marsh.), European beech ( Fagus sylvatica L.), Norway spruce ( Picea abies (L.) Karst), lodgepole pine ( Pinus contorta Dougl. ex Loud. var. latifolia Engelm.), eastern white pine ( Pinus strobus L.), Scots pine ( Pinus sylvestris L.), loblolly pine ( Pinus taeda L.), and Douglas-fir ( Pseudotsuga menziesii (Mirb.) Franco var. menziesii ). Species-specific minimum density of full site occupancy (NMCA) and average maximum density (NAMax) equations were developed using forest inventory data and existing models. NMCA and NAMax estimates were used to compare species growing space utilization over a range of stand diameters (12–50 cm). Results suggest growing space utilization varies among the evaluated species and that species differences may change over the diameter range evaluated. Analysis also highlights that a growing space usage gradient is present across species. One end of the gradient is occupied by species that maintain higher densities at small sizes and exhibit greater rates of density decline as mean diameter increases. In contrast, other species maintain lower densities at small diameter, but have lesser rates of density reduction as diameter increases. Finally, results highlight the importance of using species-specific models when quantifying size–density relationships and developing stand-density management regimes.
Large-scale spatial patterns of forest structural diversity
Authors: McRoberts Ronald E. , Winter Susanne , Chirici Gherardo , Hauk Elmar , Pelz Dieter R. , Moser W. Keith , Hatfield Mark A.
Published: April 2008

Forest structural diversity was estimated for an ecological province in the north-central region of the United States of America using data for nearly 350 000 trees observed on >12 000 forest inventory plots. Each plot was 672 m2 in area, and the sampling intensity was approximately 1 plot/2400 ha. Two indices were used for each of two commonly and accurately measured inventory variables: species count and the Shannon index for tree species and standard deviation and the Shannon index for tree diameter. The primary results of the study were fourfold: (i) ranges of spatial correlation for diversity indices were small, on the order of 5–10 km, (ii) high proportions of provincewide diversity were realized for circular areas with radii as small as 15 km, (iii) diversity for both species and diameter exhibited strong northwest to southeast spatial patterns, and (iv) plot-level α diameter diversity was highly correlated with mean plot-level tree diameter.