Fueling of a marine-terrestrial ecosystem by a major seabird colony.

Seabirds redistribute nutrients between different ecosystem compartments and over vast geographical areas. This nutrient transfer may impact both local ecosystems on seabird breeding islands and regional biogeochemical cycling, but these processes are seldom considered in local conservation plans or biogeochemical models. The island of Stora Karlsö in the Baltic Sea hosts the largest concentration of piscivorous seabirds in the region, and also hosts a large colony of insectivorous House martins Delichon urbicum adjacent to the breeding seabirds. We show that a previously reported unusually high insectivore abundance was explained by large amounts of chironomids-highly enriched in δ15N-that feed on seabird residues as larvae along rocky shores to eventually emerge as flying adults. Benthic ammonium and phosphate fluxes were up to 163% and 153% higher close to the colony (1,300 m distance) than further away (2,700 m) and the estimated nutrient release from the seabirds at were in the same order of magnitude as the loads from the largest waste-water treatment plants in the region. The trophic cascade impacting insectivorous passerines and the substantial redistribution of nutrients suggest that seabird nutrient transfer should be increasingly considered in local conservation plans and regional nutrient cycling models.

Neurite Growth and Polarization on Vitronectin Substrate after in Vitro Trauma is not Enhanced after IGF Treatment.

Following traumatic brain injuries (TBI), insulin-like growth factor (IGF) is cortically widely upregulated. This upregulation has a potential role in the recovery of neuronal tissue, plasticity, and neurotrophic activity, though the molecular mechanisms involved in IGF regulation and the exact role of IGF after TBI remain unclear. Vitronectin (VN), an extracellular matrix (ECM) molecule, has recently been shown to be of importance for IGF-mediated cellular growth and migration. Since VN is downregulated after TBI, we hypothesized that insufficient VN levels after TBI impairs the potential beneficial activity of IGF. To test if vitronectin and IGF-1/IGFBP-2 could contribute to neurite growth, we cultured hippocampal neurons on ± vitronectin-coated coverslips and them treated with ± IGF-1/IGF binding protein 2 (IGFBP-2). Under same conditions, cell cultures were also subjected to in vitro trauma to investigate differences in the posttraumatic regenerative capacity with ± vitronectin-coated coverslips and with ± IGF-1/IGFBP-2 treatment. In both the control and trauma situations, hippocampal neurons showed a stronger growth pattern on vitronectin than on the control substrate. Surprisingly, the addition of IGF-1/IGFBP-2 showed a decrease in neurite growth. Since neurite growth was measured as the number of neurites per area, we hypothesized that IGF-1/IGFBP-2 contributes to the polarization of neurons and thus induced a less dense neurite network after IGF-1/IGFBP-2 treatment. This hypothesis could not be confirmed and we therefore conclude that vitronectin has a positive effect on neurite growth in vitro both under normal conditions and after trauma, but that addition of IGF-1/IGFBP-2 does not have a positive additive effect.

Low-frequency complex conductivity of sandy and clayey materials.

Low-frequency polarization of sands and sandstones seems to be dominated by the polarization of the Stern layer, the inner part of the electrical double layer coating the surface of the silica grains and clay particles. We investigate a simple model of Stern layer polarization combined with a simple complexation model of the surface of the grains immersed in a 1:1 electrolyte like NaCl. In isothermal conditions, the resulting model can be used to predict the complex conductivity of clayey materials as a function of the porosity, the cation exchange capacity of the clay fraction (alternatively the specific surface area of the material), and the salinity of the pore water. A new set of experimental data is presented. This dataset comprises low-frequency (1 mHz-45 kHz) complex conductivity measurements of saprolites and sandstones that are well characterized in terms of their petrophysical properties (porosity, permeability, specific surface area or CEC, and pore size). This dataset, together with incorporating additional data from the literature, is used to test the Stern layer polarization model. We find an excellent agreement between the predictions of this model and this experimental dataset indicating that the new model can be used to predict the complex conductivity of natural clayey materials and clay-free silica sands.

Bottom trawling resuspends sediment and releases bioavailable contaminants in a polluted fjord.

Sediments are sinks for contaminants in the world's oceans. At the same time, commercial bottom trawling is estimated to affect around 15 million km(2) of the world's seafloor every year. However, few studies have investigated whether this disturbance remobilises sediment-associated contaminants and, if so, whether these are bioavailable to aquatic organisms. This field study in a trawled contaminated Norwegian fjord showed that a single 1.8 km long trawl pass created a 3-5 million m(3) sediment plume containing around 9 t contaminated sediment; ie. 200 g dw m(-2) trawled, equivalent to c. 10% of the annual gross sedimentation rate. Substantial amounts of PCDD/Fs and non-ortho PCBs were released from the sediments, likely causing a semi-permanent contaminated sediment suspension in the bottom waters. PCDD/Fs from the sediments were also taken up by mussels which, during one month, accumulated them to levels above the EU maximum advised concentration for human consumption.

Semaphorin and neuropilin expression in motoneurons after intraspinal motoneuron axotomy.

We have examined mRNA and protein distribution for the axon guidance molecules semaphorin3A, 3F, 4F and semaphorin receptors neuropilin-1 and 2, 1-21 days after intramedullary axotomy of rat lumbar spinal cord motoneurons. We show that semaphorin3A mRNA and protein are up-regulated in the scar and in motoneurons from 3 days and upto 3 weeks after injury. Neuropilin-1 mRNA showed no changed expression in axotomized motoneurons. Semaphorin3F mRNA expression was found in ventral roots after ventral funiculus lesion (VFL) and neuropilin-2 mRNA was found in affected motoneurons from 1 day after injury throughout the examined period. Semaphorin4F mRNA was first found in motoneurons 3 weeks after lesion. These results suggest semaphorin/neuropilin involvement in the injury response of intramedullary axotomized motoneurons.

Cytokine inhibition of fibroblast-induced gel contraction is mediated by PGE(2) and NO acting through separate parallel pathways.

Contraction of three-dimensional collagen gels is a model of the contraction that characterizes normal healing and remodeling after injury. In the current study, we evaluated the hypothesis that a number of inflammatory factors, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and interferon (IFN)-gamma, modulate this process by induction of prostaglandin (PG) E(2) and nitric oxide (NO) production and that these secondary mediators function in an autocrine or paracrine manner to modulate contraction. Human fetal lung fibroblasts (HFL) were cultured in type I collagen gels and floated in medium containing TNF-alpha, IL-1 beta, or IFN-gamma alone or in combination (cytomix). All cytokines inhibited the contraction significantly. The potency order was IL-1 beta, TNF-alpha, IFN-gamma. The cytomix was no more potent than was IL-1 beta alone. PGE(2) production was increased by TNF-alpha (5.0 versus 0.16 ng/ml, P < 0.01), IL-1 beta (5.3 versus 0.16 ng/ml, P < 0.01), and cytomix (5.9 versus 0.16 ng/ml, P < 0.01), and was completely inhibited by indomethacin. Indomethacin (P < 0.05) and L-NG-monomethyl arginine citrate (L-NMMA) (P < 0.05) alone both partially attenuated the inhibition of contraction caused by cytokines alone or by cytomix. Indomethacin and L-NMMA together attenuated inhibition more than either alone (P < 0.05). Exogenous PGE(2) and exogenous NO donors (DETA nononate and 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium chloride) inhibited the contraction significantly. The protein kinase A inhibitor KT5270 and the protein kinase G inhibitor Rp-pCPT-cGMPS attenuated the inhibition induced by PGE(2) and NO, respectively. In summary, PGE(2) and NO appear to function in parallel as autocrine/paracrine mediators of cytokine-driven fibroblast inhibition of the contraction of collagen gels and may contribute to remodeling during repair and inflammation in lung disorders.

Induction of VEGF and VEGF receptors in the spinal cord after mechanical spinal injury and prostaglandin administration.

Vascular endothelial growth factor (VEGF) is an angiogenetic factor that promotes endothelial cell proliferation during development and after injury to various types of tissue, including the central nervous system (CNS). Using immunohistochemical and in situ hybridization methods we have here demonstrated that VEGF and its receptors Flk-1, Flt-1 and Neuropilin-1 mRNAs and proteins are induced after incisions in the rat spinal cord. The inducible enzyme for prostaglandin synthesis cyclooxygenase-2 (COX-2) is known to be upregulated after spinal injury, cerebral ischemia and to stimulate angiogenesis. To test the hypothesis that prostaglandins may be involved in the VEGF response after lesion we investigated whether intraspinal microinjections of prostaglandin F2alpha (PGF2alpha) alters VEGF expression in the spinal cord. Such treatment was followed by a strong upregulation of VEGF mRNA and protein in the injection area. Finally, by use of an in vitro model with cell cultures of meningeal fibroblast and astrocyte origin, resembling the lesion area cellular content after spinal cord injury but devoid of inflammatory cells, we showed that VEGF is expressed in this in vitro model cell system after treatment with PGF2alpha and prostaglandin E2 (PGE2). These data suggest that cells within a lesion area in the spinal cord are capable of expressing VEGF and its receptors in response to mechanical injury and that prostaglandins may induce VEGF expression in such cells, even in the absence of inflammatory cells.

Differential regulation of Ly49 expression on CD4+ and CD4-CD8- (double negative) NK1.1+ T cells.

The pan-NK cell marker NK1.1, present in some mouse strains, is also found on a subset of TCRalphabeta+ lymphocytes termed NKT cells. These cells are primarily CD4+ or CD4-CD8- (double negative, DN), and both NKT subpopulations contain cells reactive with the MHC class I-like molecule CD1d. Murine NK cells express clonally distributed inhibitory receptors of the Ly49 family that bind to different alleles of MHC class I molecules and transmit negative signals regulating NK cell function. Ly49 receptors are also found on TCRalphabeta+ NK1.1+ T cells. To investigate the potential role of inhibitory Ly49 markers in the regulation of NKT cells, we have done a thorough analysis of their expression on different NKT populations. The CD4+ and DN NK1.1+ T cell subsets have traditionally been dealt with as one NK1.1+ T cell population, but we found dramatic differences between these two NKT cell subsets. We demonstrate here expression of Ly49 receptors on DN, but not on CD4+, NK1.1+ T cells in spleen and liver. Absence of the specific MHC class I ligand in the host was associated with elevated levels of expression and, to a greater extent than has been found for NK cells, increased the frequencies of Ly49-positive cells within the DN subset, while CD4+ NK1.1+ cells remained negative. In the thymus and bone marrow both NK1.1+ T cell subsets contained high frequencies of Ly49-positive cells. Results from in vitro stimulation of DN NKT cells further suggest that activation and expansion of NKT cell subsets are regulated by the Ly49 receptors.

Endothelial cell-mediated type I collagen gel contraction is regulated by hemin.

The contraction of three-dimensional type I collagen gels is regarded as a model of contraction during wound healing and tissue remodeling. Because such a process could contribute to vessel narrowing, we hypothesized that endothelial cells may be able to mediate gel contraction. To demonstrate this, type I collagen was extracted from rat tail tendon and used to prepare collagen gels. Bovine arterial endothelial cells (BAECs) or human pulmonary artery endothelial cells (HPAECs) were then plated on the top of the gels in serum-free Ham's F-12 medium or 2% fetal calf serum-endothelium growth medium-2 (FCS-EGM2), respectively. After 48 hours of attachment, gels were released and floated in 0.2% FCS-Ham's F-12 medium (BAECs) or 2% FCS-EGM2 (HPAECs). Gel size was measured with an image analyzer daily for 5 consecutive days. Gels were then digested with collagenase to quantify DNA and hydroxyproline. BAECs contracted the gels in a time-dependent manner over the 5 days. Contraction was dependent on cell density (gel size was 100% of initial size after 5 days with no cells vs. 66.4%+/-0.5% with 0.9x10(4) cells/cm2 and 22.1%+/-0.3% with 7.5x10(4) cells/cm2) and was inversely related to collagen concentration (gel size was 22.3%+/-0.05%, 46.4%+/-0.9%, 72.3%+/-0.4%, and 87.4% +/-0.3% of initial size for gels prepared with 0.5 mg/mL, 0.75 mg/mL, 1 mg/mL, and 2 mg/mL of collagen, respectively). Hemin (a precursor for CO) and cytochalasin D inhibited collagen gel contraction mediated by both bovine and human endothelial cells without changing cell number or hydroxyproline content. In contrast, prostaglandin E2, an inhibitor, and transforming growth factor-beta1, a stimulator of fibroblast-mediated gel contraction, had no effect on endothelial cell-mediated contraction. These findings demonstrate that endothelial cells are able to contract native type I collagen gels and that this process can be modulated by exogenous mediators. Such a capability may cause remodeling of subjacent matrix of endothelial cells and may contribute to vessel narrowing.

CD1d-specific NK1.1+ T cells with a transgenic variant TCR.

The majority of T lymphocytes carrying the NK cell marker NK1.1 (NKT cells) depend on the CD1d molecule for their development and are distinguished by their potent capacity to rapidly secrete cytokines upon activation. A substantial fraction of NKT cells express a restricted TCR repertiore using an invariant TCR Valpha14-Jalpha281 rearrangement and a limited set of TCR Vbeta segments, implying recognition of a limited set of CD1d-associated ligands. A second group of CD1d-reactive T cells use diverse TCR potentially recognizing a larger diversity of ligands presented on CD1d. In TCR-transgenic mice carrying rearranged TCR genes from a CD1d-reactive T cell with the diverse type receptor (using Valpha3. 2/Vbeta9 rearrangements), the majority of T cells expressing the transgenic TCR had the typical phenotype of NKT cells. They expressed NK1.1, CD122, intermediate TCR levels, and markers indicating previous activation and were CD4/CD8 double negative or CD4+. Upon activation in vitro, the cells secreted large amounts of IL-4 and IFN-gamma, a characteristic of NKT cells. In mice lacking CD1d, TCR-transgenic cells with the NKT phenotype were absent. This demonstrates that a CD1d-reactive TCR of the "non-Valpha 14" diverse type can, in a ligand-dependent way, direct development of NK1.1+ T cells expressing expected functional and cell-surface phenotype characteristics.

[The bronchial epithelium--more than a mechanical protection. The role of bronchial epithelial cells in defective healing has been determined]. / Bronkepitelet--mer än ett mekaniskt skydd. Bronkepitelcellens roll vid defekt läkning har uppmärksammats.

The pulmonary epithelium forms a continuous lining to the airways and to the environment. In addition to its mechanical and transport functions, the epithelium may also contribute to host defence via interactions with other inflammatory cells and with its surrounding matrix. Moreover, the bronchial epithelium manifests ability to undergo repair after injury. However, this repair process may be impaired, resulting in fibrotic scarring and compromised physiological function. Thus, in all likelihood repair processes play a crucial part in such chronic airway diseases as asthma and chronic obstructive airway disease. The article consists in a brief review of pulmonary epithelial function with regard to host defence and to its involvement in repair processes.

Characterization of subpopulations of T-cell receptor intermediate (TCRint) T cells.

CD1-autoreactive T cells of two types have been demonstrated among T cells expressing the T-cell receptor (TCR) alphabeta at intermediate levels (TCRint cells). One type constitutes a major fraction of the natural killer (NK)1.1+ TCRint population in C57BL/6 (B6) mice and carries a restricted TCR composed of an alpha-chain with an invariant Valpha14-J281 rearrangement, and a beta-chain using Vbeta8. 2, 7 or 2. The second type utilises a variety of TCR and was derived from CD4+ cells in mice lacking MHC class II. To increase our understanding of the two different CD1-reactive subsets, we have investigated and compared the populations of origin: NK1.1+ and NK1. 1- TCRint subsets from MHC class II-deficient mice and CD4+NK1.1+ T cells from B6 mice. The three TCRint populations shared a phenotype indicating previous activation, and contained low frequencies of cells expressing NK receptors of the Ly49 family. In contrast to control CD4+ cells, the three TCRint subsets produced high amounts of interleukin (IL)-4 and interferon (IFN)-gamma after activation. Importantly, no IL-10 could be detected in either TCRint population, implying a distinct function for these cells, different from those of conventional CD8+ and CD4+ cells, including the typical T-helper 2 (Th2) cell. Analysis of TCR expression indicated that the proportion of cells using the semi-invariant Valpha14/Vbeta8.2-type TCR was lower in NK1.1+ cells from MHC class II-negative mice than in CD4+NK1.1+ B6 cells. Further, usage of the Valpha14-J281 rearrangement was also demonstrated among NK1.1- TCRint cells.

[Early diagnosis of parenchymal lung diseases is now possible. Reduced risk of fibrosis and irreversibly reduced lung function]. / Tidig diagnos nu möjlig vid lungparenkymsjukdomar. Minskar risken för fibros och irreversibel lungfunktionsnedsättning.

Although parenchymal, or interstitial lung diseases constitute a heterogeneous category, a common feature is the occurrence of an alveolar and interstitial inflammatory reaction. The alveolitis may regress, but may also heal with scarring and fibrosis, resulting in chronic impairment of lung function. Early diagnosis is important in order to identify patients at risk of lung function impairment. Diagnosis has been facilitated by the advent of sophisticated, particularly radiological and bronchoscopic methods in recent years, thus enabling intervention at an earlier stage in the disease course. The various diagnostic alternatives available for the investigation of parenchymal lung diseases are reviewed in the article.

Smoking alters the phenotype of macrophages in induced sputum.

To investigate the effect of chronic smoke exposure on pulmonary macrophages (PM), the expression of seven different surface and intracellular molecules of PM was studied in induced sputum (IS) samples from healthy volunteers--nine smokers and seven non-smokers. Sputum was induced by inhalation of nebulized saline (3.5% NaCl). Cell viability and total cell counts (TCC) were performed immediately. Cell differentials were determined on May-Grunwald Giemsa-stained cytospin preparations. The PM were immunologically characterized by use of the following monoclonal antibodies: RFD1, RFD7, CD11b, CD54, CD68, CD71 and HLA-DR. The stainings were performed with a three-step, indirect immuno-alkaline phosphate method. Viability and TCC did not differ between the groups. Smokers had a higher percentage of macrophages (P < 0.05) and a lower proportion of neutrophils (P < 0.05). The percentage of macrophages expressing RFD1, HLA-DR, CD71 (P < 0.01 for all) and CD54 (P < 0.05) was significantly lower in smokers, whereas the remaining markers were expressed equally in the two groups. The results indicate that smoking induces a decrease in the expression by PM of surface molecules known to be associated with the antigen-presenting function.

Differential inhibition of inflammatory cytokine release from cultured alveolar macrophages from smokers and non-smokers by NO2.

Human alveolar macrophages (AMs) obtained from smokers and non-smokers by bronchoalveolar lavage (BAL) were subjected to various concentrations of NO2 in an inverted monolayer exposure model. Culture supernatants were collected 4 h after the exposure and assayed for secreted TNF-alpha, IL-1 beta, IL-8 and MIP-1 alpha. The steady state levels of the mRNAs for these cytokines were also analysed in the cells. The adherence of BAL cells to plastic prior to exposure to the gas elevated the steady state mRNA levels of all four cytokines tested in smoker's cells and that of TNF-alpha and IL-1 beta, but not IL-8 (MIP-1 alpha not tested), in non-smoker's cells. Interestingly, adherent cells from non-smokers released circa 15-, 3-, 1.5- and 3-fold the amounts of IL-1 beta, IL-8, TNF-alpha and MIP-1 alpha, respectively, than smoker's cells during control incubation or exposure to air. A 20 min exposure to NO2 (5 or 20 p.p.m.) did not increase the secretion of any of the cytokines from either cell type. In contrast, NO2 caused a concentration-dependent inhibition of the secretion of all cytokines except IL-1 beta from smoker's cells. Additionally, NO2 greatly diminished the release of all cytokines in response to further treatment with lipopolysaccharide (LPS). In contrast, only the secretion of TNF-alpha from non-smoker's cells was inhibited by the gas in a concentration-dependent manner, whilst LPS-induced secretion of the cytokines was not affected by the gas. The steady state levels of the respective mRNAs for each of the cytokines were not significantly affected in smoker's cells by exposure to NO2, except for a negative, dose-dependent trend in the case of TNF-alpha. Nitrogen dioxide also failed to elevate the levels of the mRNAs in non-smoker's cells but, again, tended to diminish the levels, particularly of IL-1 beta mRNA. However, exposure to the gas inhibited LPS-induced accumulation of cytokine mRNAs in smoker's cells only. The data suggest that macrophage-derived cytokine mediators of the sepsis response may not play a role in the generation of NO2-induced inflammation in the human lung. Conversely, the gas seems to non-specifically inhibit the release and/or production of cytokines, particularly from smoker's cells, at the post-transcriptional level, and impairs the ability of the cells to increase the transcription and release of the cytokines in response to bacterial LPS. The fact that NO2 seriously impaired the already diminished capacity of smoker's cells to release several important pro-inflammatory cytokines, both under control conditions and in response to LPS, strongly suggest that the inhalation of NO2 in cigarette smoke may contribute to impairing host defence against infection in the lung.

Bronchoalveolar lavage findings in firefighters.

Firefighters are exposed to irritating, asphyxiating toxic gases and aerosols. Previous studies indicate that this may result in acute as well as chronic lung function impairment. It is well known that inhalation of organic material can cause alveolitis. The purpose of this study was to investigate whether firefighters repeatedly exposed to fire gases and other combustion products develop inflammatory changes in the lower airways and, if so, what subtype of cells and soluble components accumulate. Thirteen nonsmoking firefighters underwent bronchoalveolar lavage (BAL), and the results were compared to a reference group of 112 nonsmoking healthy volunteers. The firefighters showed lower recovery of instilled lavage fluid (61% vs 72%; P < 0.01) and an increase in the proportion of lymphocytes in that fluid (8.2% vs 5.7%; P < 0.05). Alveolar macrophage fluorescence, which is a sign of uptake of inhaled fluorescent material, rather than a reflection of the degree of inflammation, was increased in two firefighters. Further, the lavage fluid had higher concentrations of native fibronectin (34.6 vs 22.0 micrograms/L; P < 0.01) and hyaluronic acid (27.7 vs 10.0 micrograms/L; P < 0.05). This may indicate local cell activation, since the alveolar capillary membrane probably was intact, as indicated by an unaffected albumin concentration. The observed changes in the deep airways are probably caused by exposure to smoke. It cannot be concluded whether these changes are permanent or are part of a natural temporary defense mechanism.

The childbirth experience: a study of 295 new mothers.

BACKGROUND: The childbirth experience is multidimensional, and therefore difficult to describe and explain. Studies of it have produced inconsistent findings, and the phenomenon is often confused with satisfaction with the care provided. This study aimed to clarify different aspects of the birth experience, and to identify factors that could explain the variation in women's overall assessment of it. METHODS: All Swedish-speaking women in a large city who gave birth during a two-week period in 1994 were given a questionnaire one day after the birth, and 295 (91%) of the questionnaires were returned. Information about the labor process and medical interventions was collected from hospital records. RESULTS: Women usually experienced severe pain and various degrees of anxiety, and most were seized with panic for a short time or some part of their labor. Despite these negative feelings, most women felt greatly involved in the birth process, were satisfied with their own achievement, and thought they had coped better than expected. The overall experience was assessed as positive by 77 percent of women and negative by 10 percent. No statistical difference was observed between primiparas and multiparas in total birth experience, and few differences in the specific aspects of the birth. Of the 38 variables tested in regression analysis, the six that contributed to explaining women's overall birth experience were support from the midwife (sensitivity to needs), duration of labor, pain, expectations of the birth, involvement and participation in the birth process, and surgical procedures (emergency cesarean section, vacuum extraction, forceps, episiotomy). CONCLUSIONS: The study showed that negative and positive feelings can coexist, thus confirming the multidimensional character of the birth experience. Women's assessment of their childbirth is influenced by both physical and psychosocial factors, highlighting the importance of a comprehensive approach to care in labor.

Ornidazole: a new antiprotozoal compound for treatment of Trichomonas vaginalis infection.

A new anti-protozoal compound, ornidazole, a derivative of nitroimidazole, was given in a single 2 g dose to 20 women with Trichomonas vaginalis infection. All the women were cured, but they suffered some side-effects. Plasma levels of ornidazole reached a peak five to eight times higher than minimum inhibitory concentrations and exceeded this level for at least 36 hours. It is therefore possible that a smaller dose might have had an adequate trichomonicidal effect and fewer side-effects. Further studies are in progress.