bluuebunny/crossref_metadata_2025 huggingface dataset:
Sexual differences in food re‐caching by New Zealand robins Petroica australis
Authors: Burns K. C. , Van Horik Jayden
Published: March 2007

We presented monogamous pairs of New Zealand robins Petroica australis with a superabundant supply of artificial prey and then observed birds re‐cache previously hoarded prey. Males and females frequently relocated and redistributed previously hoarded prey. Both sexes also re‐cached prey that was originally hoarded by their mate. However, re‐caching rates of retrieved and pilfered prey differed between sexes. Female‐made caches were re‐cached at the same rate by both females and pilfering males, while male‐made caches were re‐cached more frequently by pilfering females. The re‐caching of previously hoarded prey is consistent with the hypothesis that re‐caching reduces theft. However, re‐caching pilfered prey suggests that it might also play a role in cache theft strategies. Higher rates of re‐caching by pilfering females cannot be explained by current hypotheses used to account avian re‐caching behaviours. We suggest two new hypotheses, sexual dimorphism in spatial memory and indirect mate provisioning, which may help to explain the evolution of re‐caching in New Zealand robins.
Involvement of l‐glutamate and ATP in the neurotransmission of the sympathoexcitatory component of the chemoreflex in the commissural nucleus tractus solitarii of awake rats and in the working heart–brainstem preparation
Authors: Braga Valdir A. , Soriano Renato N. , Braccialli Alex L. , De Paula Patrícia M. , Bonagamba Leni G. H. , Paton Julian F. R. , Machado Benedito H.
Published: March 2007

Peripheral chemoreflex activation with potassium cyanide (KCN) in awake rats or in the working heart–brainstem preparation (WHBP) produces: (a) a sympathoexcitatory/pressor response; (b) bradycardia; and (c) an increase in the frequency of breathing. Our main aim was to evaluate neurotransmitters involved in mediating the sympathoexcitatory component of the chemoreflex within the nucleus tractus solitarii (NTS). In previous studies in conscious rats, the reflex bradycardia, but not the pressor response, was reduced by antagonism of either ionotropic glutamate or purinergic P2 receptors within the NTS. In the present study we evaluated a possible dual role of both P2 and NMDA receptors in the NTS for processing the sympathoexcitatory component (pressor response) of the chemoreflex in awake rats as well as in the WHBP. Simultaneous blockade of ionotropic glutamate receptors and P2 receptors by sequential microinjections of kynurenic acid (KYN, 2 nmol (50 nl)−1) and pyridoxalphosphate‐6‐azophenyl‐2′,4′‐disulphonate (PPADS, 0.25 nmol (50 nl)−1) into the commissural NTS in awake rats produced a significant reduction in both the pressor (+38 ± 3 versus+8 ± 3 mmHg) and bradycardic responses (−172 ± 18 versus−16 ± 13 beats min−1; n= 13), but no significant changes in the tachypnoea measured using plethysmography (270 ± 30 versus 240 ± 21 cycles min−1, n= 7) following chemoreflex activation in awake rats. Control microinjections of saline produced no significant changes in these reflex responses. In WHBP, microinjection of KYN (2 nmol (20 nl)−1) and PPADS (1.6 nmol (20 nl)−1) into the commissural NTS attenuated significantly both the increase in thoracic sympathetic activity (+52 ± 2%versus+17 ± 1%) and the bradycardic response (−151 ± 17 versus−21 ± 3 beats min−1) but produced no significant changes in the increase of the frequency of phrenic nerve discharge (+0.24 ± 0.02 versus+0.20 ± 0.02 Hz). The data indicate that combined microinjections of PPADS and KYN into the commissural NTS in both awake rats and the WHBP are required to produce a significant reduction in the sympathoexcitatory response (pressor response) to peripheral chemoreflex activation. We conclude that glutamatergic and purinergic mechanisms are part of the complex neurotransmission system of the sympathoexcitatory component of the chemoreflex at the level of the commissural NTS.
Dopamine D1 receptor activation regulates sodium channel‐dependent EPSP amplification in rat prefrontal cortex pyramidal neurons
Authors: Rotaru Diana C. , Lewis David A. , Gonzalez‐Burgos Guillermo
Published: March 2007

Dopamine (DA) effects on prefrontal cortex (PFC) neurons are essential for the cognitive functions mediated by this cortical area. However, the cellular mechanisms of DA neuromodulation in neocortex are not well understood. We characterized the effects of D1‐type DA receptor (D1R) activation on the amplification (increase in duration and area) of excitatory postsynaptic potentials (EPSPs) at depolarized potentials, in layer 5 pyramidal neurons from rat PFC. Simulated EPSPs (sEPSPs) were elicited by current injection, to determine the effects of D1R activation independent of modulation of transmitter release or glutamate receptor currents. Application of the D1R agonist SKF81297 attenuated sEPSP amplification at depolarized potentials in a concentration‐dependent manner. The SKF81297 effects were inhibited by the D1R antagonist SCH23390. The voltage‐gated Na+ channel blocker tetrodotoxin (TTX) abolished the effects of SKF81297 on sEPSP amplification, suggesting that Na+ currents are necessary for the D1R effect. Furthermore, blockade of 4‐AP‐ and TEA‐sensitive K+ channels in the presence of TTX significantly increased EPSP amplification, arguing against the possibility that SKF81297 up‐regulates currents that attenuate sEPSP amplification. SKF81297 application attenuated the subthreshold response to injection of depolarizing current ramps, in a manner consistent with a decrease in the persistent Na+ current. In addition, D1R activation decreased the effectiveness of temporal EPSP summation during 20 Hz sEPSP trains, selectively at depolarized membrane potentials. Therefore, the effects of D1R activation on Na+ channel‐dependent EPSP amplification may regulate the impact of coincidence detection versus temporal integration mechanisms in PFC pyramidal neurons.
Cell‐type specific interaction of endothelin and the nitric oxide system: pattern of prepro‐ET‐1 expression in kidneys ofl‐NAME treated prepro‐ET‐1 promoter‐lacZ‐transgenic mice
Authors: Slowinski Torsten , Kalk Philipp , Christian Maren , Schmager Fred , Relle Katharina , Godes Michael , Funke‐Kaiser Heiko , Neumayer Hans‐H. , Bauer Christian , Theuring Franz , Hocher Berthold
Published: March 2007

Nitric oxide (NO) and endothelin‐1 (ET‐1) are known to play a major role in renal and vascular pathophysiology and exhibit a close interaction with ET‐1, stimulating NO production; NO in turn inhibits ET‐1 expression. Our objectives were (1) to establish a novel transgenic mouse model facilitating ET‐1 expression assessmentin vivo, (2) to validate this model by assessing prepro‐ET‐1 promoter activity in mice embryos by means of our novel model and comparing expression sites to well‐established data on ET‐1 in fetal development and (3) to investigate renal ET–NO interaction by assessing prepro‐ET‐1 promoter activity in different structures of the renal cortex in the setting of blocked NO synthases vial‐NAME administration. We established transgenic mice carrying alacZreporter gene under control of the human prepro‐ET‐1 gene promoter sequence (8 kb of 5′ sequences). Bluo‐Gal staining of tissue sections revealed intracellular blue particles as indicators of prepro‐ET‐1 promoter activity. In mouse embryos, we detected high prepro‐ET‐1 promoter activity in the craniofacial region, as well as in bone and cartilage consistent with the literature. In order to investigate the interaction of ET‐1 and NO in the kidneyin vivo, transgenic mice at the age of 3–4 months were treated with a single dose of the NO synthase inhibitorl‐NAME (25 mg (kg bw)−1i.p.) 12 h before kidney removal. Bluo‐Gal staining of kidney sections revealed intracellular blue particles as indicators of prepro‐ET‐1 promoter activity in tubular and vascular endothelium and glomerular cells. Particle count was closely correlated to kidney tissue ET‐1 content (R= 0.918,P< 0.001). Comparison of counts revealed an increase by 135 ± 53% inl‐NAME treated (n= 12) compared to non‐treated mice (n= 10,P= 0.001). Cell‐type specific evaluation revealed an increase of 136 ± 51% in tubular (P= 0.001) and 105 ± 41% in glomerular cells (P= 0.046), but no significant increase in vascular endothelium. In conclusion, our study revealed a close interaction of renal endothelin and the NO system in a cell‐type specific manner. Our new transgenic model provides a unique opportunity to analyse regulation of the ET system on a cellular levelin vivo.
Regulation of M(Kv7.2/7.3) channels in neurons by PIP2and products of PIP2hydrolysis: significance for receptor‐mediated inhibition
Authors: Brown David A. , Hughes Simon A. , Marsh Stephen J. , Tinker Andrew
Published: March 2007

M‐channels are voltage‐gated K+ channels that regulate the excitability of many neurons. They are composed of Kv7 (KCNQ) family subunits, usually Kv7.2 + Kv7.3. Native M‐channels and expressed Kv7.2 + 7.3 channels are inhibited by stimulating Gq/11‐coupled receptors – prototypically the M1 muscarinic acetylcholine receptor (M1‐mAChR). The channels require membrane phosphatidylinositol‐4,5‐bisphosphate (PIP2) to open and the effects of mAChR stimulation result primarily from the reduction in membrane PIP2levels following Gq/phospholipase C‐catalysed PIP2hydrolysis. However, in sympathetic neurons, M‐current inhibition by bradykinin appears to be mediated through the release and action of intracellular Ca2+ by inositol‐1,4,5‐trisphosphate (IP3), a product of PIP2hydrolysis, rather than by PIP2depletion. We have therefore compared the effects of bradykinin and oxotremorine‐M (a muscarinic agonist) on membrane PIP2in sympathetic neurons using a fluorescently tagged mutated C‐domain of the PIP2binding probe, ‘tubby’. In concentrations producing equal M‐current inhibition, bradykinin produced about one‐quarter of the reduction in PIP2produced by oxotremorine‐M, but equal reduction when PIP2synthesis was blocked with wortmannin. Likewise, wortmannin restored bradykinin‐induced M‐current inhibition when Ca2+ release was prevented with thapsigargin. Thus, inhibition by bradykinin can use product (IP3/Ca2+)‐dependent or substrate (PIP2) dependent mechanisms, depending on Ca2+ availability and PIP2synthesis rates.
Modulation of TRPs by PIPs
Authors: Voets Thomas , Nilius Bernd
Published: March 2007

The TRP superfamily of cation channels encompasses 28 mammalian members related to the product of the Drosophila trp (transient receptor potential) gene. TRP channels have a widespread distribution in many cell types and organs and gate in response to a broad variety of physical and chemical stimuli; as such, they can be considered as ubiquitous cellular sensors. Several recent studies reported modulation of different TRP channels by phosphoinositides, in particular by phosphatidylinositol 4,5‐bisphosphate (PIP2). In most cases, PIP2 promotes TRP channel activation. Here we provide a brief overview of current insights and controversies about the mechanisms and structural determinants of PIP2–TRP channel interactions, and zoom in on the regulation of the Ca2+‐ and voltage‐gated TRPM4 by phosphoinositides.
Where does all the PIP2 come from?
Authors: Loew Leslie M.
Published: March 2007

Despite its very low concentration in the plasma membrane, PIP2 is the precursor for the important second messenger InsP3 and, independently, is a key modulator of membrane signalling molecules such as ion channels. However, it has been difficult to determine the spatial and temporal characteristics of PIP2 and InsP3 during a cell signalling event. Our laboratory used bradykinin stimulation of N1E‐115 neuroblastoma cells to infer the InsP3 dynamics from calcium imaging studies, biochemical analysis and InsP3 uncaging. We have used computational modelling with Virtual Cell to help analyse and interpret experimental data on the details of the calcium release process as well as to build a comprehensive image‐based model of agonist‐induced calcium release in a neuronal cell. These data provided a constraint for the further investigation of how low levels of cellular PIP2 could provide sufficient InsP3 for calcium release. Using biochemical assays, quantitative imaging of GFP‐based probe translocation and computational analysis, it was shown that PIP2 synthesis is stimulated concomitant with its hydrolysis. This mechanism should be important not just for consideration of PIP2 as a precursor of InsP3, but for any pathway that can be directly or indirectly modulated by PIP2.
Attitudes towards clinical research among cancer trial participants and non-participants: an interview study using a Grounded Theory approach: Table 1
Authors: Madsen S M , Holm S , Riis P
Published: March 2007

The attitudes of women patients with cancer were explored when they were invited to participate in one of three randomised trials that included chemotherapy at two university centres and a satellite centre. Fourteen patients participating in and 15 patients declining trials were interviewed. Analysis was based on the constant comparative method. Most patients voiced positive attitudes towards clinical research, believing that trials are necessary for further medical development, and most spontaneously argued that participation is a moral obligation. Most trial decliners, however, described a radical change in focus as they faced the actual personal choice. Almost no one got an impression of clinical equipoise between treatments in the trials, and most patients expressed discomfort with randomisation. A patient’s choice to participate was mainly determined by whether the primary focus was on treatment effect or on adverse effects. Both knowledge about and feelings towards trials originated mostly from the media, although paradoxically the media were largely seen as untrustworthy. Mistrust was shown towards the pharmaceutical industry, and although most patients originally trusted that doctors primarily pursued the interest of patients, they did not trust the adequacy of doctors or industry in maintaining self-regulation. Thus, public control measures were judged to be essential.
A “Queen of Hearts” trial of organ markets: why Scheper-Hughes’s objections to markets in human organs fail
Authors: Taylor J S
Published: March 2007

Nancy Scheper-Hughes is one of the most prominent critics of markets in human organs. Unfortunately, Scheper-Hughes rejects the view that markets should be used to solve the current (and chronic) shortage of transplant organs without engaging with the arguments in favour of them. Scheper-Hughes’s rejection of such markets is of especial concern, given her influence over their future, for she holds, among other positions, the status of an adviser to the World Health Organization (Geneva) on issues related to global transplantation. Given her influence, it is important that Scheper-Hughes’s moral condemnation of markets in human organs be subject to critical assessment. Such critical assessment, however, has not generally been forthcoming. A careful examination of Scheper-Hughes’s anti-market stance shows that it is based on serious mischaracterisations of both the pro-market position and the medical and economic realities that underlie it. In this paper, the author will expose and correct these mischaracterisations and, in so doing, show that her objections to markets in human organs are unfounded.
Proportional ethical review and the identification of ethical issues
Authors: Hunter D
Published: March 2007

Presently, there is a movement in the UK research governance framework towards what is referred to as proportional ethical review. Proportional ethical review is the notion that the level of ethical review and scrutiny given to a research project ought to reflect the level of ethical risk represented by that project. Relatively innocuous research should receive relatively minimal review and relatively risky research should receive intense scrutiny. Although conceptually attractive, the notion of proportional review depends on the possibility of effectively identifying the risks and ethical issues posed by an application with some process other than a full review by a properly constituted research ethics committee. In this paper, it is argued that this cannot be achieved and that the only appropriate means of identifying risks and ethical issues is consideration by a full committee. This implies that the suggested changes to the National Health Service research ethics system presently being consulted on should be strenuously resisted.
The concept of brain death did not evolve to benefit organ transplants: Table 1
Authors: Machado Calixto , Kerein Julius , Ferrer Yazmina , Portela Liana , de la C García Maria , Manero José M
Published: March 2007

Although it is commonly believed that the concept of brain death (BD) was developed to benefit organ transplants, it evolved independently. Transplantation owed its development to advances in surgery and immunosuppressive treatment; BD owed its origin to the development of intensive care. The first autotransplant was achieved in the early 1900s, when studies of increased intracranial pressure causing respiratory arrest with preserved heartbeat were reported. Between 1902 and 1950, the BD concept was supported by the discovery of EEG, Crile’s definition of death, the use of EEG to demonstrate abolition of brain potentials after ischaemia, and Crafoord’s statement that death was due to cessation of blood flow. Transplantation saw the first xenotransplant in humans and the first unsuccessful kidney transplant from a cadaver. In the 1950s, circulatory arrest in coma was identified by angiography, and the death of the nervous system and coma dépassé were described. Murray performed the first successful kidney transplant. In the 1960s, the BD concept and organ transplants were instantly linked when the first kidney transplant using a brain-dead donor was performed; Schwab proposed to use EEG in BD; the Harvard Committee report and the Sydney Declaration appeared; the first successful kidney, lung and pancreas transplants using cadaveric (not brain-dead) donors were achieved; Barnard performed the first human heart transplant. This historical review demonstrates that the BD concept and organ transplantation arose separately and advanced in parallel, and only began to progress together in the late 1960s. Therefore, the BD concept did not evolve to benefit transplantation.
Withholding and withdrawing life support in critical care settings: ethical issues concerning consent
Authors: Gedge E , Giacomini M , Cook D
Published: March 2007

The right to refuse medical intervention is well established, but it remains unclear how best to respect and exercise this right in life support. Contemporary ethical guidelines for critical care give ambiguous advice, largely because they focus on the moral equivalence of withdrawing and withholding care without confronting the very real differences regarding who is aware and informed of intervention options and how patient values are communicated and enacted. In withholding care, doctors typically withhold information about interventions judged too futile to offer. They thus retain greater decision-making burden (and power) and face weaker obligations to secure consent from patients or proxies. In withdrawing care, there is a clearer imperative for the doctor to include patients (or proxies) in decisions, share information and secure consent, even when continued life support is deemed futile. How decisions to withhold and withdraw life support differ ethically in their implications for positive versus negative interpretations of patient autonomy, imperatives for consent, definitions of futility and the subjective evaluation of (and submission to) benefits and burdens of life support in critical care settings are explored. Professional reflection is required to respond to trends favouring a more positive interpretation of patient autonomy in the context of life support decisions in critical care. Both the bioethics and critical care communities should investigate the possibilities and limits of growing pressure for doctors to disclose their reasoning or seek patient consent when decisions to withhold life support are made.
Effect of smoking regulations in local restaurants on smokers’ anti-smoking attitudes and quitting behaviours
Authors: Albers Alison B , Siegel Michael , Cheng Debbie M , Biener Lois , Rigotti Nancy A
Published: March 2007

Objective:To examine the effect of smoking regulations in local restaurants on anti-smoking attitudes and quitting behaviours among adult smokers.

Design:Hierarchical linear modelling (HLM) was used to assess the relationship between baseline strength of town-level restaurant smoking regulation and follow-up (1) perceptions of the social acceptability of smoking and (2) quitting behaviours.

Setting:Each of the 351 Massachusetts towns was classified as having strong (complete smoking ban) or weak (all other and no smoking restrictions) restaurant smoking regulations.

Subjects:1712 adult smokers of Massachusetts aged ⩾18 years at baseline who were interviewed via random-digit-dial telephone survey in 2001–2 and followed up 2 years later.

Main outcome measures:Perceived social acceptability of smoking in restaurants and bars, and making a quit attempt and quitting smoking.

Results:Among adult smokers who had made a quit attempt at baseline, living in a town with a strong regulation was associated with a threefold increase in the odds of making a quit attempt at follow-up (OR = 3.12; 95% CI 1.51 to 6.44). Regulation was found to have no effect on cessation at follow-up. A notable, although marginal, effect of regulation was observed for perceiving smoking in bars as socially unacceptable only among smokers who reported at baseline that smoking in bars was socially unacceptable.

Conclusions:Although local restaurant smoking regulations did not increase smoking cessation rates, they did increase the likelihood of making a quit attempt among smokers who had previously tried to quit, and seem to reinforce anti-social smoking norms among smokers who already viewed smoking in bars as socially unacceptable.
Does smoking increase sick leave? Evidence using register data on Swedish workers
Authors: Lundborg Petter
Published: March 2007

Objective:To examine the effect of smoking on sick leave.

Methods:Nationally representative data on 14 272 workers aged 16–65 years from the 1988–91 waves of the Swedish Survey of Living Conditions were used for the analyses. The data are linked to register-based data, on the annual number of absences due to sickness, from the National Board of Social Insurance. As outcome variable, the annual number of days of sick leave was used. This outcome was analysed as a function of smoking status and an extensive number of control variables, including occupational risk factors, work characteristics and health status.

Results:Smoking was found to increase the annual number of days of absence by 10.7 compared with never smoking. Controlling for risk factors at work, and thereby accounting for some of the selection of smokers into riskier jobs, reduced the effect to 9.7 days, corresponding to 38% of all annual absences due to sickness. Moreover, controlling for health status further reduced the effect of smoking to 7.7 days. The effect of smoking on sick leave was similar for men and women.

Conclusions:Smoking showed a large positive effect on the annual number of sick leaves. Hence, the results suggest that the gains to preventing and/or reducing smoking, in terms of reduced production losses, may be large. However, since the large effect of smoking persists when controlling for a range of health factors and occupational factors, the results also suggest that much of the higher number of absences among smokers may be explained by factors other than reduced health. The estimates should be viewed as upper bounds of the effect of smoking on sick leave, since smoking is potentially an endogenous variable.
Nicotine pharmacokinetics and subjective effects of three potential reduced exposure products, moist snuff and nicotine lozenge
Authors: Kotlyar Michael , Mendoza-Baumgart M Irene , Li Zhong-ze , Pentel Paul R , Barnett Brianne C , Feuer Rachel M , Smith Erin A , Hatsukami Dorothy K
Published: March 2007

Objective:To compare nicotine pharmacokinetics and subjective effects of three new smokeless tobacco potential reduced exposure products (PREPs; Ariva, Revel and Stonewall) with moist snuff (Copenhagen) and medicinal nicotine (Commit lozenge).

Methods:10 subjects completed a randomised, within-subject, crossover study. Subjects used one product for 30 min at each of the five laboratory sessions. Maximal nicotine concentration (Cmax) was determined and area under the concentration time curve (AUC) was calculated for a 90-min period (during use and 60 min after use). Nicotine craving, withdrawal symptoms and ratings of product effects and liking were measured during product use.

Results:Nicotine AUC and Cmaxwere higher for Copenhagen than for any other product (p<0.002) and higher for Commit than for either Ariva or Revel (p<0.001). Cmaxfor Commit was also higher than for Stonewall (p = 0.03). Craving was lowest during use of Copenhagen (p<0.03). Craving during use of Stonewall, Ariva and Commit was lower than during use of Revel (p<0.05). Withdrawal symptom score during use of Copenhagen was lower than during use of Revel (p = 0.009). Copenhagen scores were higher (p<0.005) than all other products in several measures of drug effects and liking (feel good effects, satisfaction, liking and desire for product, and strength of product).

Conclusion:The new smokeless tobacco PREPs result in lower nicotine concentrations and equivalent or lower reductions in subjective measures compared with medicinal nicotine. Since health effects of PREPs are largely unknown, medicinal nicotine should be preferentially encouraged for smokers or smokeless tobacco users wishing to switch to lower-risk products.
THE RADIATIVE LEPTON FLAVOR VIOLATING DECAYS IN THE SPLIT FERMION SCENARIO IN THE TWO-HIGGS DOUBLET MODEL
Authors: ILTAN E. O.
Published: March 2007

We study the branching ratios of the lepton flavor violating processes μ→eγ, τ→eγ and τ→μγ in the split fermion scenario, in the framework of the two-Higgs doublet model. We observe that the branching ratios are relatively more sensitive to the compactification scale and the Gaussian widths of the leptons in the extra dimensions, for two extra dimensions and especially for the τ→μγ decay.
PROPER CURVATURE COLLINEATIONS IN KANTOWSKI–SACHS AND BIANCHI TYPE III SPACETIMES
Authors: SHABBIR GHULAM , BAKAR MEHMOOD ABU
Published: March 2007

A study of Kantowski–Sachs and Bianchi type III spacetimes according to their proper curvature collineations is given by using the rank of the 6×6 Riemann matrix and direct integration techniques. It is shown that when the above spacetimes admit proper curvature collineations, they form an infinite dimensional vector space.
THE HADRONIC LIGHT-BY-LIGHT CONTRIBUTION TO THE MUON ANOMALOUS MAGNETIC MOMENT: WHERE DO WE STAND?
Authors: BIJNENS JOHAN , PRADES JOAQUIM
Published: March 2007

We review the status of the hadronic light-by-light contribution to the muon anomalous magnetic moment and critically compare recent calculations. We also study in detail which momentum regions the π0 exchange main contribution originates. We also argue that [Formula: see text] encompasses the present understanding of this contribution and comment on some directions to improve on that.
FIVE-DIMENSIONAL DUST COLLAPSE WITH COSMOLOGICAL CONSTANT
Authors: GHOSH S. G. , DESHKAR D. W. , SASTE N. N.
Published: March 2007

We study the five-dimensional spherical collapse of an inhomogeneous dust in the presence of a positive cosmological constant. The general interior solutions, in the closed form, of the Einstein field equations, i.e. the 5D Tolman–Bondi–de Sitter, is obtained which in turn is matched to the exterior 5D Schwarzschild–de Sitter. It turns out that the collapse proceeds in the same way as in the Minkowski background, i.e. the strong curvature naked singularities form and thus violate the cosmic censorship conjecture. A brief discussion on the causal structure singularities and horizons is also given.
A REGULARIZED SOLUTION OF THE LINEARIZED EINSTEIN EQUATIONS
Authors: FEOLI A.
Published: March 2007

Given a suitable energy density distribution, we find a solution of the linearized field equations of General Relativity that has some properties required by Einstein to be interpreted as a classical model of an extended elementary particle. It is spherically symmetric, free from singularities, smoothly connected with the outside linearized Schwarzschild solution and leads to a sort of "gravitational asymptotic freedom" in the limit r → 0. The case of a strong gravitational field is also studied with a numerical approach and the smooth behavior of the solution does not change.
ABSORPTION CROSS-SECTION OF A SCHWARZSCHILD–DE SITTER BLACK HOLE
Authors: SINI R. , KURIAKOSE V. C.
Published: March 2007

The Hawking temperature corresponding to the black hole horizon of Schwarzschild–de Sitter (SdS) black hole was found using WKB approximation and the effect of reflection of waves from the quantum horizon. The absorption cross-section σ abs when SdS black hole is placed in a Klein-Gordon field is calculated and is found to be inversely proportional to the Hawking temperature.
VARYING SPEED OF LIGHT, MODIFIED CHAPLYGIN GAS AND ACCELERATING UNIVERSE
Authors: SINGHA ANUP KUMAR , DEBNATH UJJAL
Published: March 2007

In this paper, we have considered a model of modified Chaplygin gas in VSL theory with variable gravitational constant G. We have shown that the evolution of the universe starts from radiation era to phantom model. The whole evolution of the universe has been shown diagramatically by using statefinder parameters.
ON THE SUPERSTRING BLACK HOLE
Authors: POLLOCK M. D.
Published: March 2007

The effective Lagrangian for the heterotic superstring theory of Gross et al. contains higher-derivative gravitational terms [Formula: see text], n ≥ 2, which become important at large curvatures. This leads to a natural realization of the limiting-curvature hypothesis of Frolov et al., which was formulated to describe the interior of black holes. Assuming a purely geometrical, four-dimensional Schwarzschild black hole, for which all matter fields are zero, this interior consists of two regions: a shell of effective energy-density ρ immediately beyond the event horizon at r+ = 2M, due to the back reaction of the [Formula: see text] on the Schwarzschild metric, extending inward to a transition radius r0 ≈ M⅓, where the shell signature (- + - -) reverts to the exterior Lorentzian form (+ - - -), and an innermost core tending asymptotically to anti-de Sitter space as r → 0. The total mass-energy content of the hole M can be expressed in terms of the effective energy–momentum tensor Sij as the Nordström mass [Formula: see text], since the space–time is static and free of physical singularities. The conjecture that ρ N (r) is positive in the shell, which is necessary for the contribution to M N to be positive, is shown to be true for the term [Formula: see text], due to the unrenormalized [Formula: see text]. The corresponding "potential" energy–momentum tensor calculated in the Schwarzschild background is isotropic in the region r0 ≪ r ≪ r+, where [Formula: see text], while the dominant "kinetic" contribution is [Formula: see text], so that [Formula: see text].
HGF ameliorates a high-fat diet-induced fatty liver
Authors: Kosone Takashi , Takagi Hitoshi , Horiguchi Norio , Ariyama Yasuyo , Otsuka Toshiyuki , Sohara Naondo , Kakizaki Satoru , Sato Ken , Mori Masatomo
Published: March 2007

Hepatocyte growth factor (HGF) has various effects especially on epithelial cells. However, the precise role of HGF on lipogenesis is still not fully understood. A high-fat diet was administered to HGF transgenic mice and wild-type control mice in vivo. Furthermore, recombinant human HGF (rhHGF) was administered to HepG2 cell line in vitro. We performed an analysis regarding the factors relating to lipid metabolism. An overexpression of HGF dramatically ameliorates a high-fat diet-induced fatty liver. HGF transgenic mice showed an apparently reduced lipid accumulation in the liver. The activation of microsomal triglyceride transfer protein (MTP) and apolipoprotein B (ApoB) accompanying higher triglyceride levels in the serum were found in HGF transgenic mice on a normal diet. Interestingly, this upregulation of the MTP activation became more apparent in the high-fat diet. In addition, the administration of rhHGF stimulated MTP and ApoB expression while reducing reduced the intracellular lipid content in HepG2 cell line. However, this induction of MTP and ApoB by HGF was clearly inhibited by PD98059 (MAPK inhibitor). In conclusion, the data presented in this study indicated that HGF ameliorates a high-fat diet-induced fatty liver via the activation of MTP and ApoB.
GERD is associated with shortened telomeres in the squamous epithelium of the distal esophagus
Authors: Souza Rhonda F. , Lunsford Tisha , Ramirez Ruben D. , Zhang Xi , Lee Edward L. , Shen Yuenan , Owen Charles , Shay Jerry W. , Morales Carmela , Spechler Stuart Jon
Published: March 2007

Telomeres are repetitive DNA sequences located at the ends of chromosomes. Telomeres are shortened by repeated cell divisions and by oxidative DNA damage, and cells with critically shortened telomeres cannot divide. We hypothesized that chronic gastroesophageal reflux disease (GERD)-induced injury of the esophageal squamous epithelium results in progressive telomeric shortening that eventually might interfere with mucosal healing. To address our hypothesis, we compared telomere length and telomerase activity in biopsy specimens of esophageal squamous epithelium from GERD patients and control patients. Endoscopic biopsies were taken from the esophageal squamous epithelium of 38 patients with GERD [10 long-segment Barrett's esophagus (LSBE), 15 short-segment (SSBE), 13 GERD without Barrett's esophagus] and 16 control patients without GERD. Telomere length was assessed using the terminal restriction fragment assay, and telomerase activity was studied by the PCR-based telomeric repeat amplification protocol assay. Patients with GERD had significantly shorter telomeres in the distal esophagus than controls [8.3 ± 0.5 vs. 10.9 ± 1.5 (SE) Kbp, P = 0.043]. Among the patients with GERD, telomere length in the distal esophagus did not differ significantly in those with and without Barrett's esophagus (LSBE 7.9 ± 0.8, SSBE 8.6 ± 0.9, GERD without BE 8.7 ± 1.0 Kbp). No significant differences in telomerase activity in the distal esophagus were noted between patients with GERD and controls (4.0 ± 0.39 vs. 5.2 ± 0.53 RIUs). Telomeres in the squamous epithelium of the distal esophagus of patients who have GERD, with and without Barrett's esophagus, are significantly shorter than those of patients without GERD despite similar levels of telomerase activity.
Enteroendocrine cells express functional Toll-like receptors
Authors: Bogunovic Milena , Davé Shaival H. , Tilstra Jeremy S. , Chang Diane T. W. , Harpaz Noam , Xiong Huabao , Mayer Lloyd F. , Plevy Scott E.
Published: March 2007

Intestinal epithelial cells (IECs) provide a physical and immunological barrier against enteric microbial flora. Toll-like receptors (TLRs), through interactions with conserved microbial patterns, activate inflammatory gene expression in cells of the innate immune system. Previous studies of the expression and function of TLRs in IECs have reported varying results. Therefore, TLR expression was characterized in human and murine intestinal sections, and TLR function was tested in an IEC line. TLR1, TLR2, and TLR4 are coexpressed on a subpopulation of human and murine IECs that reside predominantly in the intestinal crypt and belong to the enteroendocrine lineage. An enteroendocrine cell (EEC) line demonstrated a similar expression pattern of TLRs as primary cells. The murine EEC line STC-1 was activated with specific TLR ligands: LPS or synthetic bacterial lipoprotein. In STC-1 cells stimulated with bacterial ligands, NF-κB and MAPK activation was demonstrated. Furthermore, the expression of TNF and macrophage inhibitory protein-2 were induced. Additionally, bacterial ligands induced the expression of the anti-inflammatory gene transforming growth factor-β. LPS triggered a calcium flux in STC-1 cells, resulting in a rapid increase in CCK secretion. Finally, conditioned media from STC-1 cells inhibited the production of nitric oxide and IL-12 p40 by activated macrophages. In conclusion, human and murine IECs that express TLRs belong to the enteroendocrine lineage. Using a murine EEC model, a broad range of functional effects of TLR activation was demonstrated. This study suggests a potential role for EECs in innate immune responses.
Retention of lung distension information in pump cell spike trains
Authors: Marchenko Vitaliy , Rogers Robert F.
Published: March 2007

Respiratory control requires feedback signals from the viscera, including mechanoreceptors and chemoreceptors. We previously showed that typical pulmonary stretch receptor (PSR) spike trains provide the central nervous system with ∼31% of the theoretical maximum information regarding the amplitude of lung distension. However, it is unknown whether the spatiotemporal convergence of many PSR inputs onto second-order neurons (e.g., pump cells) results in more, or less, information about the stimulus carried by second-order cell spike trains. We recorded pump cell activity in adult, anesthetized, paralyzed, artificially ventilated rabbits during continuous manipulation of ventilator rate and volume to test the hypothesis that less information is carried by spike trains of individual pump cells than PSRs. Using previously developed analytic methods, we quantified the information carried by the pump cell spike trains and compared it with the same values derived from PSR data. Our results provide evidence that rejects our hypothesis: pump cells as a group did not carry significantly less information about the lung distension stimulus than PSRs, although that trend was implied by the data. By comparing the response variances with the theoretical minimum, we discovered that the trend toward information loss depends on response strength, with higher mean responses associated with larger response variances in pump cells than in PSRs. Thus spatiotemporal integration may result in information loss within certain analytic/stimulus parameters, but this is counterbalanced by the consistency of pump cell responses during brief integration times and/or low stimulus amplitudes, resulting in retention of total information.
Mechanical basis for lingual deformation during the propulsive phase of swallowing as determined by phase-contrast magnetic resonance imaging
Authors: Felton Samuel M. , Gaige Terry A. , Reese Timothy G. , Wedeen Van J. , Gilbert Richard J.
Published: March 2007

The tongue is an intricately configured muscular organ that undergoes a series of rapid shape changes intended to first configure and then transport the bolus from the oral cavity to the pharynx during swallowing. To assess the complex array of mechanical events occurring during the propulsive phase of swallowing, we employed tongue pressure-gated phase-contrast MRI to represent the tissue's local strain rate vectors. Validation of the capacity of phase-contrast MRI to represent local compressive and expansive strain rate was obtained by assessing deformation patterns induced by a synchronized mechanical plunger apparatus in a gelatinous material phantom. Physiological strain rate data were acquired in the sagittal and coronal orientations at 0, 200, 400, and 600 ms relative to the gating pulse during 2.5-ml water bolus swallows. This method demonstrated that the propulsive phase of swallowing is associated with a precisely organized series of compressive and expansive strain rate events. At the initiation of propulsion, bolus position resulted from obliquely aligned compressive and expansive strain, vertically aligned compressive strain and orthogonal expansion, and compressive strain aligned obliquely to the styloid process. Bolus reconfiguration and translocation resulted from a combination of compressive strain occurring in the middle and posterior tongue aligned obliquely between the anterior-inferior and the posterior-superior regions with commensurate orthogonal expansion, along with bidirectional contraction in the distribution of the transversus and verticalis muscle fibers. These data support the concept that propulsive lingual deformation is due to complex muscular interactions involving both extrinsic and intrinsic muscles.
Inactivity, exercise training and detraining, and plasma lipoproteins. STRRIDE: a randomized, controlled study of exercise intensity and amount
Authors: Slentz Cris A. , Houmard Joseph A. , Johnson Johanna L. , Bateman Lori A. , Tanner Charles J. , McCartney Jennifer S. , Duscha Brian D. , Kraus William E.
Published: March 2007

Exercise has beneficial effects on lipoproteins. Little is known about how long the effects persist with detraining or whether the duration of benefit is effected by training intensity or amount. Sedentary, overweight subjects ( n = 240) were randomized to 6-mo control or one of three exercise groups: 1) high-amount/vigorous-intensity exercise; 2) low-amount/vigorous-intensity exercise; or 3) low-amount/moderate-intensity exercise. Training consisted of a gradual increase in amount of exercise followed by 6 mo of exercise at the prescribed level. Exercise included treadmill, elliptical trainer, and stationary bicycle. The number of minutes necessary to expend the prescribed kilocalories per week (14 kcal·kg body wt−1·wk−1for both low-amount groups; 23 kcal·kg body wt−1·wk−1for high-amount group) was calculated for each subject. Average adherence was 83–92% for the three groups; minutes per week were 207, 125, and 203 and sessions per week were 3.6, 2.9, and 3.5 for high-amount/vigorous-intensity, low-amount/vigorous intensity, and low-amount/moderate-intensity groups, respectively. Plasma was obtained at baseline, 24 h, 5 days, and 15 days after exercise cessation. Continued inactivity resulted in significant increases in low-density lipoprotein (LDL) particle number, small dense LDL, and LDL-cholesterol. A modest amount of exercise training prevented this deterioration. Moderate-intensity but not vigorous-intensity exercise resulted in a sustained reduction in very-low-density lipoprotein (VLDL)-triglycerides over 15 days of detraining ( P < 0.05). The high-amount group had significant improvements in high-density lipoprotein (HDL)-cholesterol, HDL particle size, and large HDL levels that were sustained for 15 days after exercise stopped. In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism.
Relationship between Sexual Satiety and Brain Androgen Receptors
Authors: Romano-Torres Mónica , Phillips-Farfán Bryan V. , Chavira Roberto , Rodríguez-Manzo Gabriela , Fernández-Guasti Alonso
Published: March 2007

Recently we showed that 24 h after copulation to satiety, there is a reduction in androgen receptor density (ARd) in the medial preoptic area (MPOA) and in the ventromedial hypothalamic nucleus (VMH), but not in the bed nucleus of the stria terminalis (BST). The present study was designed to analyze whether the ARd changes in these and other brain areas, such as the medial amygdala (MeA) and lateral septum, ventral part (LSV), were associated with changes in sexual behavior following sexual satiety. Males rats were sacrificed 48 h, 72 h or 7 days after sexual satiety (4 h ad libitum copulation) to determine ARd by immunocytochemistry; additionally, testosterone serum levels were measured in independent groups sacrificed at the same intervals. In another experiment, males were tested for recovery of sexual behavior 48 h, 72 h or 7 days after sexual satiety. The results showed that 48 h after sexual satiety 30% of the males displayed a single ejaculation and the remaining 70% showed a complete inhibition of sexual behavior. This reduction in sexual behavior was accompanied by an ARd decrease exclusively in the MPOA-medial part (MPOM). Seventy-two hours after sexual satiety there was a recovery of sexual activity accompanied by an increase in ARd to control levels in the MPOM and an overexpression of ARd in the LSV, BST, VMH and MeA. Serum testosterone levels were unmodified during the post-satiety period. The results are discussed on the basis of the similarities and discrepancies between ARd in specific brain areas and male sexual behavior.
Analysis of Risk Factors for Urinary Incontinence after Radical Prostatectomy
Authors: Majoros Attila , Bach Dietmar , Keszthelyi Attila , Hamvas Antal , Mayer Peter , Riesz Peter , Seidl Evelyn , Romics Imre
Published: March 2007

Introduction: Our aim was to identify the independent risk factors associated with urinary incontinence after radical retropubic prostatectomy (RRP). Materials and Methods: Using univariate and multivariate analyses, we examined several pre- and perioperative factors. One hundred and sixty-six patients were divided into three groups: patients who were immediately continent after catheter removal (group I), patients who became continent later (group II) and incontinent patients (group III). Results: There were 34 patients (20.5%) in group I, 111 (66.9%) in group II, and 21 (12.6%) in group III. The multivariate analysis between the continent and incontinent patients proved that the postoperatively measured total length of the posterior urethra (strongly associated with length of the sphincter, length of the urethral stump and the presence of anastomotic stricture) was the independent risk factor for permanent incontinence or delayed continence following RRP. The age of patients per se represented a risk factor only for delayed continence, but not for permanent incontinence. Conclusions: Postoperatively measured shorter posterior urethral length results in an increased risk of urinary incontinence and delays continence after RRP. It seems that older age only delays reaching continence.
Is There an Impact of Postoperative Urethral and Periurethral Anatomical Features in Post-Radical Retropubic Prostatectomy Incontinence?
Authors: Kordan Y. , Alkibay T. , Sozen S. , Bozkurt Y. , Acar C. , Talu T. , Bozkirli I.
Published: March 2007

Objectives: To determine the anatomical changes in urethral and periurethral tissues after radical retropubic prostatectomy (RRP) by magnetic resonance imaging (MRI) and correlate these changes to continence. Materials and Methods: 14 patients with grade 2–5 incontinence and 16 continent (grade 1) patients who had undergone non-nerve-sparing RRP for clinically localized prostatic carcinoma were evaluated. The sphincteric urethral length, transverse and craniocaudal diameters of both levator ani muscles and the volume of periurethral fibrosis were determined by abdominopelvic MRI. Continent (group 1) and incontinent (group 2) groups were compared in terms of sphincteric urethral length, transverse and craniocaudal diameters of levator ani muscles, volume of periurethral fibrosis, prostate volume, age and pathological stage. Results: Among all the evaluated parameters, a statistically significant correlation was found only between the volume of periurethral fibrosis and the number of postoperative operations for urethral strictures in the incontinent group (p = 0.013, r = 0.859). Conclusions: Our results suggest that the postoperative sphincteric urethral length is not the sole factor in regaining continence after RRP as mentioned in the literature.