PAHs in high Arctic copepods Calanus hyperboreus following exposure of residues from in situ burning of oil spill.

In situ burning of marine oil spills reduces the total amount of oil in the environment, but a negative side effect may be the generation of environmentally hazardous polycyclic aromatic hydrocarbons (PAHs) that may pose a risk for bioaccumulation, particularly in organisms having a high lipid content. In this study uptake of PAHs from oil and burn residue were examined in the high arctic copepod Calanus hyperboreus. A major part of the low ring number petrogenic PAHs in the oil was removed during burning and relative higher concentrations of pyrogenic high ring number PAHs was found in the burn residue. This suggests that burning markedly reduces the general PAH exposure load. Furthermore, the pyrogenic PAHs generated during the burn were not bioconcentrated to quantifiable levels in the copepods. We conclude that in situ burning can mitigate the potential risk of PAH uptake for copepods and other pelagic organisms in the marine environment as the pyrogenic PAHs only pose low risk for uptake from the water by the copepods and other pelagic organisms.

Acute oil exposure reduces physiological process rates in Arctic phyto- and zooplankton.

Arctic shipping and oil exploration are expected to increase, as sea ice extent is reduced. This enhances the risk for accidental oil spills throughout the Arctic, which emphasises the need to quantify potential consequences to the marine ecosystem and to evaluate risk and choose appropriate remediation methods. This study investigated the sensitivity of Arctic marine plankton to the water accommodated fraction (WAF) of heavy fuel oil. Arctic marine phytoplankton and copepods (Calanus finmarchicus) were exposed to three WAF concentrations corresponding to total hydrocarbon contents of 0.07 mg l-1, 0.28 mg l-1 and 0.55 mg l-1. Additionally, the potential phototoxic effects of exposing the WAF to sunlight, including the UV spectrum, were tested. The study determined sub-lethal effects of WAF exposure on rates of key ecosystem processes: primary production of phytoplankton and grazing (faecal pellet production) of copepods. Both phytoplankton and copepods responded negatively to WAF exposure. Biomass specific primary production was reduced by 6, 52 and 73% and faecal pellet production by 18, 51 and 86% with increasing WAF concentrations compared to controls. The phototoxic effect reduced primary production in the two highest WAF concentration treatments by 71 and 91%, respectively. This experiment contributes to the limited knowledge of acute sub-lethal effects of potential oil spills to the Arctic pelagic food web.

Bioaccumulation of oil compounds in the high-Arctic copepod Calanus hyperboreus.

Oil and gas exploration in the Arctic will increase the risk for accidental oil spills and thereby have a potential impact on the ecosystem and the organisms inhabiting these areas. Lipid rich copepods are an important food source for higher trophic levels in Arctic marine ecosystems. However, high lipid content and a slower metabolism increase the risk for bioaccumulation in Arctic species. Here we exposed three late development stages of the lipid rich high-Arctic copepod species Calanus hyperboreus to two different 14C-marked crude oil model compounds, the alkane dodecane (log Kow 6.10) and the polycyclic aromatic hydrocarbon (PAH) phenanthrene (log Kow 4.46) on a short-term scale of 4days. Exposure was followed by a depuration phase of 3days. We observed a difference in estimated bioaccumulation of the two model compounds between stages and found a slower depuration of dodecane than of phenanthrene in the two largest and most lipid rich stages. However, depuration of dodecane and phenanthrene was non-significant for all three stages. The results indicate that even short-term exposure may result in long-term bioaccumulation and internal exposure of oil compounds in the lipid rich high-Arctic copepods C. hyperboreus. Slow elimination and depuration of oil components indicate a risk for transfer of oil component up the food web to pelagic fish, seabirds and baleen whales.

Transient neuroprotection by SRY upregulation in dopamine cells following injury in males.

Emerging evidence suggest sex-specific regulation of dopamine neurons may underlie susceptibility of males to disorders such as Parkinson's disease (PD). In healthy male dopamine neurons, the Y-chromosome gene product, the sex-determining region on the Y chromosome (SRY) modulates dopamine biosynthesis and motor function. We investigated the regulation and function of SRY in a model of dopamine cell injury. Treatment with the dopaminergic toxin, 6-hydroxydopamine (6-OHDA), significantly elevated SRY mRNA expression (9-fold) in human male dopamine M17 cells. SRY up-regulation occurred via the p-quinone pathway, associated with a 3.5-fold increase in expression of GADD45γ, a DNA damage inducible factor gene and known SRY regulator. In turn, a signaling cascade involving GADD45γ/p38-MAPK/GATA activated the SRY promoter. Knockdown of SRY mRNA in 6-OHDA-treated M17 cells was deleterious, increasing levels of reactive oxygen species (ROS), pro-apoptotic marker PUMA mRNA, and cell injury (+25%, +32% and +34%, respectively). Conversely, ectopic over-expression of SRY in 6-OHDA-treated female SH-SY5Y cells was protective, decreasing ROS, PUMA, and cell injury (-40%, -46%, and -30%, respectively). However, the 6-OHDA-induced increase in SRY expression was diminished with higher concentrations of toxins or with chronic exposure to 6-OHDA. We conclude that SRY upregulation after dopamine cell injury is initially a protective response in males, but diminishes with gradual loss in dopamine cells. We speculate that dysregulation of SRY may contribute the susceptibility of males to PD.

Outcome and knee-related quality of life after anterior cruciate ligament reconstruction: a long-term follow-up.

The aim of the present investigation was to study patient-reported long-term outcome after anterior cruciate ligament (ACL) reconstruction. On an average 11.5 years after ACL reconstruction with bone-patellar tendon-bone (BPTB) autograft 56 patients were asked to answer four different questionnaires about their knee function and knee-related quality of life. Another aim was to study whether there were any correlations between clinical tests, commonly used for evaluating patients with ACL injuries, which were performed 2 years after ACL reconstruction, and patient-reported outcome in terms of knee function and knee-related quality of life on an average 9.5 years later. All patients who had unilateral BPTB ACL reconstructions were examined at 2 years and on an average 11.5 years after surgery. At 2 years one-leg hop test for distance, isokinetic muscle torque measurement, sagittal knee laxity, Lysholm knee scoring scale and Tegner activity scale were used for clinical evaluation. At the follow-up on an average 9.5 years later the patients were evaluated with knee injury osteoarthritis outcome score (KOOS), short form health survey (SF 36), Lysholm knee scoring scale and Tegner activity scale. The SF-36 showed that the patients had a similar health condition as an age- and gender-matched normal population in Sweden on an average 11.5 years after ACL reconstruction. There was no correlation between the results of one-leg hop test for distance, isokinetic muscle torque measurement, sagittal knee laxity evaluated 2 years after surgery and the result of KOOS (function in sport and recreation, knee-related quality of life) and SF-36 evaluated on an average 11.5 years after surgery. We also compared patients that 2 years after surgery demonstrated a side-to-side difference in anterior-posterior knee laxity of more than 3 mm with those with 3 mm or less and found no significant group differences in terms of knee function as determined with KOOS. We found no correlation between the results of KOOS and SF-36 at the long-term follow-up and the time between injury and surgery, age at surgery or gender, respectively. We conclude that there is no correlation between patient-reported knee function in sport and recreation and knee-related quality of life on an average 11.5 years after BPTP ACL reconstruction and the evaluation methods used 2 years after surgery.

Gene expression profiling from endomyocardial biopsy tissue allows distinction between subentities of dilated cardiomyopathy.

OBJECTIVE: Expression profile analysis using endomyocardial biopsy specimens from patients with cardiomyopathies promises to improve the differential diagnosis of heart failure. METHODS: In this study, left ventricular endomyocardial biopsy specimens were obtained from 50 patients and histopathologically classified according to the World Heart Federation Task Force criteria as having dilated cardiomyopathy (n = 17), inflammatory cardiomyopathy (n = 11), myocarditis (n = 15), or pericarditis (n = 7). Microarrays were performed by hybridization of synthesized complementary DNA against a Lab-Arraytor60-combi microarray (SIRS-Lab, Jena, Switzerland). Differentially expressed genes were clustered hierarchically according to their variation in hybridization signals. RESULTS: In samples from patients with dilated cardiomyopathy, two different types of gene expression profiles were distinguishable. One pattern was unique for dilated cardiomyopathy and inflammatory cardiomyopathy, respectively, and the other more closely resembled that seen in samples from inflammatory heart disease. Additionally, we confirmed the microarray data by showing that dilated cardiomyopathy is associated with a reduced myocardial toll-like receptor 9 expression that resulted from progressive loss of functional cardiomyocytes. Taken together, our data demonstrate the utility and validity of microarrays from endomyocardial biopsy specimens in detecting subentities of dilated cardiomyopathy that do not differ histopathologically, but transcriptionally, from each other. The gene expression profile observed in one subgroup of patients with dilated cardiomyopathy is indicative of ongoing immune activation, albeit infiltrating immunocompetent cells were not detected histopathologically. CONCLUSION: Thus, our transcriptional data indicate that dilated cardiomyopathy constitutes a heterogeneous disease with an broad overlap to inflammatory heart disease.

Transcription in response to physical stress--clues to the molecular mechanisms of exercise-induced asthma.

To clarify stress-induced immunological reactions and molecular events during exercise and the potential relevance to exercise-induced bronchoconstriction, transcriptional responses to standardized physical stress were determined. Six healthy, young volunteers underwent an endurance exercise of 90% of their individual anaerobic threshold for 90 min. Time-dependent alterations in the expression pattern of leukocytes from healthy, trained subjects were analyzed by DNA microarrays before and 2 h and 6 h after exercise. Starting out from a large collection of cDNA library clones comprising more than 70,000 human expressed sequence tags, we selected, designed, and immobilized oligonucleotide probes (60-70mers) for transcripts of 5000 stress- and inflammation-relevant genes. Exercise-induced stress provoked changes in the expression of 433 gene activities 2 h and/or 6 h after exercise, which could be grouped into six clusters. The most prominent feature was an enhanced transcription of two genes, coding for 5-lipoxygenase (ALOX5) and ALOX5-activating protein. Moreover, enhanced levels of leukotriene B4 (LTB4) and LTC4 (P<0.05) were detected in plasma after exercise. Our data demonstrate that exercise alters the activities of a distinct number of genes. In particular, they possibly provide novel insights into the molecular mechanisms of exercise-induced bronchoconstriction and suggest that enhanced transcription of ALOX5 and its activating protein together with a present predisposition of the subject critically contribute to exercise-induced asthma.