bluuebunny/crossref_metadata_2025_split huggingface dataset:
Life history of a small form of the plethodontid salamander Desmognathus quadramaculatus
Authors: Beachy Christopher , Bruce Richard 
Published: March 2003

AbstractWe sampled Desmognathus quadramaculatus, one of the largest species of plethodontid salamanders in eastern North America, from a population exhibiting extremely small adult body sizes in the Bald Mountains of North Carolina (USA). In order to test the hypothesis that miniaturization in desmognathine salamanders is due to early metamorphosis and maturation, we estimated ages and sizes at metamorphosis and maturation. Analysis of size-frequency distributions suggests that most larvae metamorphose after 24 months, with the remainder metamorphosing after 36. The minimum age of sexually mature individuals in the summer months is estimated to be 4 years in males and 5 years in females; some may mature 1 year earlier. This is earlier than other reliable estimates of age at maturation in D. quadramaculatus, and appears to account for the small size of the species at this locality. Larval and juvenile growth rates are within the range of growth rates of other populations. As in other populations of D. quadramaculatus, males are smaller than females at maturation, but grow to larger sizes. Estimates of clutch sizes based on dissection of gravid females are relatively low. The other species of salamanders in this community do not appear to be miniaturized.
Intrapopulation variation in life history traits of Boa constrictor occidentalis in Argentina
Authors: Sironi Mariano , Chiaraviglio Margarita , Lucino Sergio , Bertona Miguel 
Published: March 2003

AbstractWe provide data on intrapopulation variation of life history traits of Boa constrictor occidentalis in the District of Pocho, Córdoba, Argentina. A total of 153 individuals were captured. The distribution of individuals among four size classes differed significantly among the five years of study. The proportion of mature individuals did not differ between sexes but it showed variation among years. Females were longer and heavier than males. The mean litter size of the species was 24 and there was a linear relationship between litter size and maternal snout-vent length. Most boas were captured during the dry season. There were no significant sex differences in the time of capture and air temperature in either the wet or the dry seasons. However, we found significant differences in the time of capture and air temperature between the seasons. The long-term monitoring of wild populations should be a priority for the development of conservation and management plans for this boid.
NF-κB-dependent lymphocyte hyperadhesiveness to synovial fibroblasts by hypoxia and reoxygenation: potential role in rheumatoid arthritis
Authors: Han Myung-Kwan , Kim Jong-Suk , Park Byung-Hyun , Kim Jung-Ryul , Hwang Byung-Yun , Lee Hak-Yong , Song Eun-Kyung , Yoo Wan-Hee 
Published: March 2003

Abstract
Hypoxia/reoxygenation has been incriminated as a major factor in the pathogenesis of ischemia/reperfusion injury in various ischemic diseases such as rheumatoid arthritis (RA). In this study, we have investigated the effect of hypoxia/reoxygenation on the expression of intercellular adhesion molecule-1 (ICAM-1) in synovial fibroblasts and adherence of lymphocytes to synovial fibroblasts. Hypoxia/reoxygenation strongly activated nuclear factor-κB (NF-κB) in synovial fibroblasts to the levels produced by phorbol 12-myristate 13-acetate and caused lymphocyte hyperadhesiveness to synovial fibroblasts as well as up-regulation of ICAM-1, both of which were completely blocked by a NF-κB antagonist (pyrrolidine dithiocarbamate). These results indicate that hypoxia/reoxygenation has a major role in sequestration of inflammatory cells to synovium mediated by the activation of NF-κB. Our data suggest that hypoxia/reoxygenation could be an important target for the development of new, therapeutic strategies in RA.
Creating conditions similar to those that occur during exposure of cells to microgravity induces apoptosis in human lymphocytes by 5-lipoxygenase-mediated mitochondrial uncoupling and cytochrome c release
Authors: Maccarrone Mauro , Battista Natalia , Meloni Mariantonia , Bari Monica , Galleri Grazia , Pippia Proto , Cogoli Augusto , Finazzi-Agrò Alessandro 
Published: March 2003

Abstract
Creating conditions similar to those that occur during exposure of cells to microgravity induced a sixfold increase of apoptotic bodies and DNA fragments in human lymphocytes, paralleled by an early (within 2 h) fourfold increase in 5-lipoxygenase (5-LOX) activity and a fivefold decrease in mitochondrial membrane potential and increase in cytochrome c release (within 4 and 8 h, respectively). Similar membrane potential and cytochrome c release were observed in isolated mitochondria treated with physiological amounts of 5-LOX and were enhanced by creating conditions similar to those that occur during exposure of cells to microgravity. 5-LOX inhibitors, 5,8,11,14-eicosatetraynoic acid and caffeic acid, completely prevented apoptosis, whereas the phospholipase A2 inhibitor methyl-arachidonoyl fluorophosphonate and the 5-LOX activating protein inhibitor MK886 reduced it to 65–70%. The intracellular calcium chelator EGTA-acetoxymethylester reduced 5-LOX activity and apoptosis to 30–40% of controls, whereas the p38 mitogen-activated protein kinase inhibitor SB203580 was ineffective. The caspase-3 and caspase-9 inhibitors Z-Asp(OCH3)-Glu(OCH3)-Val-Asp(OCH3)-fluoromethylketone (FMK) and Z-Leu-Glu(OCH3)-His-Asp(OCH3)-FMK reduced apoptotic bodies to 25–30% of the control cells. Finally, creating conditions similar to those that occur during exposure of cells to microgravity did not induce apoptosis in human lymphoma U937 cells, which did not express an active 5-LOX.
Arachidonic acid activates phospholipase D in human neutrophils; essential role of endogenous leukotriene B4 and inhibition by adenosine A2A receptor engagement
Authors: Grenier Sonya , Flamand Nicolas , Pelletier Julie , Naccache Paul H , Borgeat Pierre , Bourgoin Sylvain G 
Published: March 2003

Abstract
We report in human neutrophils (PMN) that phospholipase D (PLD) was stimulated by micromolar concentrations of arachidonic acid (AA) and nanomolar concentrations of leukotriene B4 (LTB4), and eicosapentaenoic acid was inactive. The stimulatory effect of AA occurred only when adenosine was eliminated from PMN suspensions or when PMN were incubated with adenosine A2A receptor antagonists. The mechanism of AA-induced PLD activation was investigated. The results show that AA- and LTB4-induced PLD activation were inhibited by the LTB4 receptor 1 (BLTR1) antagonist CP 105,696, whereas the LTA4 hydrolase inhibitor SC57461A and the LT biosynthesis inhibitor MK-0591 inhibited AA- but not LTB4-mediated PLD activation. The AA-induced ARF1 and RhoA translocation to PMN membranes was inhibited by CP 105,696 and SC57461A. These results provide evidence of a requirement for an autocrine-stimulatory loop involving LTB4 and BLTR1 in the translocation of small GTPases to membranes and the activation of PMN PLD by AA.
Differential sensitivity of human monocytes and macrophages to ANP: a role of intracellular pH on reactive oxygen species production through the phospholipase involvement
Authors: Baldini P M , De Vito P , Martino A , Fraziano M , Grimaldi C , Luly P , Zalfa F , Colizzi V 
Published: March 2003

AbstractAtrial natriuretic peptide (ANP), a cardiovascular hormone, elicits different biological actions in the immune system. The aim of the present work was to study the effect of ANP on the intracellular pH (pHi) of human monocytes and macrophages and to investigate whether pHi changes could play a role on phospholipase activities and reactive oxygen species (ROS) production. Human macrophages isolated by peripheral blood mononuclear cells and THP-1 monocytes, which were shown to express all three natriuretic peptide receptors (NPR-A, NPR-B, and NPR-C), were treated with physiological concentrations of ANP. A significant decrease of pHi was observed in ANP-treated macrophages with respect to untreated cells; this effect was paralleled by enhanced phospholipase activity and ROS production. Moreover, all assessed ANP effects seem to be mediated by the NPR-C. In contrast, no significant effect on pHi was observed in THP-1 monocytes treated with ANP. Treatment of macrophages or THP-1 monocytes with 5-(N-ethyl-N-isopropyl)amiloride, a specific Na+/H+ antiport inhibitor, decreases pHi in macrophages and monocytes. Our results indicate that only macrophages respond to ANP in terms of pHi and ROS production, through diacylglycerol and phosphatidic acid involvement, pointing to ANP as a new modulator of ROS production in macrophages.
Accelerated wound closure in neutrophil-depleted mice
Authors: Dovi Julia V , He Li-Ke , DiPietro Luisa A 
Published: March 2003

Abstract
The infiltration of neutrophils into injured tissue is known to protect wounds from invading pathogens. However, more recent studies suggest that neutrophils might inhibit the wound repair process. To investigate the role of neutrophils in wounds, mice were neutrophil-depleted by injection with rabbit anti-mouse neutrophil serum. Remarkably, epidermal healing, measured by wound closure, proceeded significantly faster in neutropenic than control mice (77.7+14.2% vs. 41.2+0.9%, P&lt;0.02 at day 2). Dermal healing was not affected by neutrophil depletion, as neither collagen deposition nor wound-breaking strength was significantly different between neutropenic and control mice. As the delayed repair of diabetic individuals exhibits robust inflammation, the effect of neutrophil depletion on diabetic wound healing was investigated. Similar to the observations in wild-type mice, wound closure was accelerated by nearly 50% in neutropenic, diabetic mice. The results suggest that although neutrophils may provide protection against infection, they may retard wound closure.
Peritoneal dialysis solutions inhibit the differentiation and maturation of human monocyte-derived dendritic cells: effect of lactate and glucose-degradation products
Authors: Puig-Kröger Amaya , Muñiz-Pello Oscar , Selgas Rafael , Criado Gabriel , Bajo M-Auxiliadora , Sánchez-Tomero Jose A , Alvarez Vicente , del Peso Gloria , Sánchez-Mateos Paloma , Holmes Clifford , Faict Dirk , López-Cabrera Manuel , Madrenas Joaquín , Corbí Angel L 
Published: March 2003

Abstract
Peritoneal dialysis (PD) is a well-established therapy for end-stage renal failure, but its efficiency is limited by recurrent peritonitis. As PD solutions impair local inflammatory responses within the peritoneal cavity, we have analyzed their influence on the in vitro maturation of human monocyte-derived dendritic cells (MDDC). Evaluation of MDDC maturation parameters [expression of adhesion and costimulatory molecules, receptor-mediated endocytosis, allogeneic T cell activation, production of tumor necrosis factor α, interleukin (IL)-6 and IL-12 p70, and nuclear factor (NF)-κB activation] revealed that currently used PD solutions differentially inhibit the lipopolysaccharide (LPS)-induced maturation of MDDC, an inhibition that correlated with their ability to impair the LPS-stimulated NF-κB activation. Evaluation of PD components revealed that sodium lactate and glucose-degradation products impaired the acquisition of maturation parameters and NF-κB activation in a dose-dependent manner. Moreover, PD solutions impaired monocyte-MDDC differentiation, inhibiting the acquisition of DC markers such as CD1a and DC-specific intercellular adhesion molecule-3 grabbing nonintegrin (CD209). These findings have important implications for the initiation of immune responses under high lactate conditions, such as those occurring within tumor tissues or after macrophage activation.
Indirect capture augments leukocyte accumulation on P-selectin in flowing whole blood
Authors: St. Hill Catherine A , Alexander Shelia R , Walcheck Bruce 
Published: March 2003

Abstract
Leukocytes are captured directly by E- and P-selectin on activated endothelium and by indirect means, which includes attached leukocytes capturing free-flowing leukocytes. However, controversy exists as to whether the latter mechanism occurs in the presence of red blood cells. We analyzed leukocyte capture mechanisms on P-selectin under circulatory hydrodynamics using whole blood. The selective disruption of leukocyte–leukocyte interactions with an L-selectin monoclonal antibody reduced leukocyte accumulation by &gt;50% under various stringencies (substrate concentrations and shear stresses). In addition, a direct analysis of leukocyte capture events revealed that 69% were indirect. Our data indicate that in the presence of red blood cells, P-selectin-attached leukocytes, individually and as a monolayer, augment leukocyte accumulation by indirect capture. This mechanism may contribute to increasing the density of leukocytes on discrete areas of activated endothelial cells at sites of inflammation. These findings are significant since L-selectin accounts for the majority of the leukocyte rolling flux in small venules at diverse inflammatory settings. Yet, the primary mechanism by which L-selectin mediates leukocyte accumulation remains unresolved.
Concurrent evolution and resolution in an acute inflammatory model of rat carrageenin-induced pleurisy
Authors: Murai Naoki , Nagai Kiyohito , Fujisawa Hideyuki , Hatanaka Ko , Kawamura Michiko , Harada Yoshiteru 
Published: March 2003

Abstract
Granulocyte apoptosis and subsequent clearance by phagocytes are critical for the resolution of inflammation. However, no studies have addressed how the resolution proceeds in the inflammatory site. We studied the time course of neutrophil apoptosis and the following ingestion by mononuclear leukocytes in rat carrageenin-induced pleurisy, detecting DNA fragmentation by the deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) method, by acridine orange staining, and from the DNA ladder pattern on electrophoresis. Neutrophil accumulation started 3–5 h after carrageenin injection and then maintained a plateau until 24 h. Neutrophils decreased steeply between days 1 and 3. Mononuclear leukocytes started to accumulate at 5 h and reached a peak at day 2. TUNEL-positive bodies and acridine orange-positive bodies first became detectable in the cytoplasm of the mononuclear leukocytes from 24 h and 9 h, respectively. Both methods indicated that mononuclear leukocytes containing fragmented DNA increased rapidly on days 1 and 2 and reached a peak at day 3. The characteristic ladder pattern of neutrophil DNA was observed from 5 h. Tumor necrosis factor α was detectable on the start, and the levels of interleukin-10 and transforming growth factor-β1 rose together with signs of neutrophil apoptosis and the following ingestion by mononuclear leukocytes. These results indicate that neutrophils start to undergo apoptosis just after the beginning of their accumulation in the inflammation site. Thus, evolution and resolution processes may proceed concurrently in acute inflammation.
Fever-like thermal conditions regulate the activation of maturing dendritic cells
Authors: Tournier Jean-Nicolas , Hellmann Anne Quesnel , Lesca Gaëtan , Jouan Alain , Drouet Emmanuel , Mathieu Jacques 
Published: March 2003

Abstract
Fever is one of the most frequent clinical signs encountered in pathology, especially with respect to infectious diseases. It is currently thought that the role of fever on immunity is limited to activation of innate immunity; however, its relevance to activation of adaptive immunity remains unclear. Dendritic cells (DCs) that behave as sentinels of the immune system provide an important bridge between innate and adaptive immunity. To highlight the role of fever on adaptive immunity, we exposed murine bone marrow-derived lipopolysaccharide (LPS)- or live bacteria-maturing DCs over a 3-h period to 37°C or to fever-like thermal conditions (39°C or 40°C). At these three temperatures, we measured the kinetics of cytokine production and the ability of DCs to induce an allogeneic mixed lymphocyte reaction. Our results show that short exposure of DCs to temperatures of 39°C or 40°C differentially increased the secretion of interleukin (IL)-12p70 and decreased the secretion of IL-10 and tumor necrosis factor α by maturing DCs. These fever-like conditions induced a regulation of cytokine production at the single-cell level. In addition, short-term exposed LPS-maturing DCs to 39°C induced a stronger reaction with allogeneic CD4+ T cells than maturing DCs incubated at 37°C. These results provide evidence that temperature regulates cytokine secretion and DC functions, both of which are of particular importance in bacterial diseases.
A PI-3 kinase-dependent, Stat1-independent signaling pathway regulates interferon-stimulated monocyte adhesion
Authors: Navarro Angels , Anand-Apte Bela , Tanabe Yoshinari , Feldman Gerald , Larner Andrew C 
Published: March 2003

Abstract
Type I interferon (IFN)-α/β and type II IFN-γ induce the expression of early response genes through activation of the Janus tyrosine kinase/signal transducer and activator of transcription (Stat) pathway. Although IFNs regulate a variety of other signaling cascades, little is known about how they contribute to the biological activities of these cytokines. In this study, we demonstrate that IFN-β or IFN-γ induces the phosphorylation of the serine/threonine kinase Akt in primary human peripheral blood monocytes. Abrogation of the IFN-stimulated Akt activation by phosphatidylinositol-3 kinase (PI-3K) inhibitors prevents IFN-induced adhesion in these cells, and IFN activation of the Stat1-dependent guanylate-binding protein (GBP) gene is not affected. Importantly, Stat1-deficient bone marrow macrophages displayed a similar level of IFN-γ-stimulated adhesion compared with macrophages derived from wild-type littermates. These findings demonstrate for the first time that IFN stimulation of a PI-3K signaling cascade modulates the ability of these cytokines to regulate monocyte adhesion, and this process does not require the expression of Stat1, a primary mediator of IFN-γ signaling.
National Inventory of Hospital Trauma Centers
Authors: MacKenzie Ellen J. , Hoyt David B. , Sacra John C. , Jurkovich Gregory J. , Carlini Anthony R. , Teitelbaum Sandra D. , Teter Harry 
Published: March 2003

ContextTrauma centers benefit thousands of injured individuals every day and play a critical role in responding to disasters. The last full accounting of the number and distribution of trauma centers identified 471 trauma centers in the United States in 1991.ObjectiveTo determine the number and configuration of trauma centers and identify gaps in coverage.Design, Setting, and SubjectsInterviews with trauma center directors (September 2001 to April 2002), data from the American Hospital Association's Annual Survey of Hospitals (2000), and the US Health Resources Administration's Area Resource File (2001) were used to determine characteristics of trauma center hospitals and the geographic areas they serve in all 50 states and in the District of Columbia. Characteristics of trauma centers were examined by level of care and compared with nontrauma centers. Hospitals are designated or certified as trauma centers by a state or regional authority or verified as trauma centers by the American College of Surgeons Committee on Trauma. Trauma centers that treat only children (n = 31) were excluded.Main Outcome MeasureTotal number of trauma centers and number of trauma centers per million population.ResultsIn 2002, there were 1154 trauma centers in the United States, including 190 level I centers and 263 level II centers. Several states have categorized every hospital with an emergency department at some level of trauma care while others have designated a limited number of level I and level II centers only. The number of level I and II centers per million population ranges from 0.19 to 7.8 by state. When compared with nontrauma center hospitals, trauma centers are larger, more likely to be teaching hospitals, and more likely to offer specialized services.ConclusionsAlthough the availability of trauma centers has improved, challenges remain to ensure the optimal number, distribution, and configuration of trauma centers. These challenges must be addressed, especially in light of the recent emphasis on hospital preparedness and homeland security.
Plastic energy dissipation and its role on heating/melting of single‐component polymers and multi‐component polymer blends
Authors: Qian Bainian , Todd David B. , Gogos Costas G. 
Published: March 2003

AbstractPlastic energy dissipation (PED) of polymer particulates is, essentially, the energy dissipated during large and repeated plastic deformations of compacted polymer particulates while still in the solid state. PED is higher or much higher than VED, the viscous energy dissipation source of polymeric melts, because the stresses necessary to plastically deform viscoelastic polymer solids are orders of magnitude higher than the stresses needed to support viscous flow. In the last few years our group has demonstrated experimentally the dominant role which PED plays in the heating/melting of solid polymer (compacted) particulate beds in compounding processing equipment, such as twin‐screw extruders and counterrotating continuous mixers/melters, in which the deformation of solid polymers is mandatory. We have also developed simple empirical methods of predicting the total axial distance needed for melting a given polymer in specific processing/compounding machines and processing. conditions, as well as the melting rates, all based on the mechanical energy dissipated during solid particulate compression. This work explores the more complex issue of how the PED behavior of single‐component polymers may affect the PED (and the heating/melting) behavior of multi‐component polymer blends. © 2003 Wiley Periodicals, Inc. Adv Polym Techn 22: 85–95, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/adv.10039
Synergistic effects of carbon fillers on shielding effectiveness in conductive nylon 6,6‐ and polycarbonate‐based resins
Authors: Krueger Quinton J. , King Julia A. 
Published: March 2003

AbstractElectrically conductive resins can be made by adding electrically conductive fillers to typically insulating polymers. Resins with an electrical resistivity of approximately 100 Ω cm or less can be used for electromagnetic and radio frequency interference shielding applications. This research focused on performing compounding runs followed by injection molding and shielding effectiveness (SE) testing of carbon filled nylon 6,6‐ and polycarbonate‐based resins. The three carbon fillers investigated included an electrically conductive carbon black, synthetic graphite particles, and a milled pitch‐based carbon fiber. For each polymer, conductive resins were produced and tested that contained varying amounts of these single carbon fillers. In addition, combinations of fillers were investigated by conducting a full 23 factorial design and a complete replicate in each polymer. The objective of this study was to determine the effects and interactions of each filler on the SE properties of the conductive resins. Carbon black caused the largest increase in SE. Also, each single filler and each two filler interaction caused a statistically significant increase in SE. © 2003 Wiley Periodicals, Inc. Adv Polym Techn 22: 96–111, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/adv.10040