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In this study, we quantify the impacts of shipping pollution on air quality and shortwave radiative effect in northern Norway, using WRF-Chem simulations combined with high resolution, real-time STEAM2 shipping emissions. STEAM2 emissions are evaluated using airborne measurements from the ACCESS campaign, which was conducted in summer 2012, in two ways. First, emissions of NOx and SO2 are derived for specific ships from in-situ measurements in ship plumes and FLEXPART-WRF plume dispersion modeling, and these values are compared to STEAM2 emissions for the same ships. Second, regional WRF-Chem runs with and without ship emissions are performed at two different resolutions, 3km x 3km and 15km x 15km, and evaluated against measurements along flight tracks and average campaign profiles in the marine boundary layer and lower troposphere. These comparisons show that differences between STEAM2 emissions and calculated emissions can be quite large (-57 to + 148%) for individual ships, but that WRF-Chem simulations using STEAM2 emissions reproduce well the average NOx, SO2 and O3 measured during ACCESS flights. The same WRF-Chem simulations show that the magnitude of NOx and O3 production from ship emissions at the surface is not very sensitive (< 5%) to the horizontal grid resolution (15 or 3 km), while surface PM10 enhancements due to ships are moderately sensitive (15%) to resolution. The 15 km resolution WRF-Chem simulations are used to estimate the local and regional impacts of shipping pollution in northern Norway. Our results indicate that ship emissions are an important local source of pollution, enhancing 15 day averaged surface concentrations of NOx (~ +80%), O3 (~ +5%), black carbon (~ +40%) and PM2.5 (~ +10%) along the Norwegian coast. Over the same period ship emissions in northern Norway have a shortwave (direct + semi-direct + indirect) radiative effect of -9.3mW m-2 at the global scale. [ABSTRACT FROM AUTHOR]

Ozone pollution transported to the Arctic is a significant concern because of the rapid, enhanced warming in high northern latitudes, which is caused, in part, by short-lived climate forcers, such as ozone. Long-range transport of pollution contributes to background and episodic ozone levels in the Arctic. However, the extent to which plumes are photochemically active during transport, particularly during the summer, is still uncertain. In this study, regional chemical transport model simulations are used to examine photochemical production of ozone in air masses originating from boreal fire and anthropogenic emissions over North America and during their transport toward the Arctic during early July 2008. Model results are evaluated using POLARCAT aircraft data collected over boreal fire source regions in Canada (ARCTAS-B) and several days downwind over Greenland (POLARCAT-France and POLARCAT-GRACE) during the study period. Model results are generally in good agreement with the observations, except for certain trace gas species over boreal fire regions, in some cases indicating that the fire emissions are too low. Anthropogenic and biomass burning pollution (BB) from North America was rapidly uplifted during transport east and north to Greenland where pollution plumes were observed in the mid- and upper-troposphere during POLARCAT. A model sensitivity study shows that CO levels are in better agreement with POLARCAT measurements (fresh and aged fire plumes) upon doubling CO emissions from fires. Analysis of model results, using ΔO3/Δ CO enhancement ratios, shows that pollution plumes formed ozone during transport towards the Arctic. Fresh anthropogenic plumes have average ΔO3/Δ CO enhancement ratios of 0.28 increasing to 0.99 for aged anthropogenic plumes, indicating additional ozone production during aging. Fresh fire plumes are only slightly enhanced in ozone (ΔO3/ΔCO =0.11), but form ozone downwind with ΔO3/Δ CO of 0.50 for aged BB plumes. We estimate that aged anthropogenic and BB pollution together made an important contribution to ozone levels with an average contribution for latitudes > 55° N of up to 6.5ppbv (18%) from anthropogenic pollution and 3 ppbv (5.2 %) from fire pollution in the model domain in summer 2008. [ABSTRACT FROM AUTHOR]

Arctic warming leading to reduced summertime sea-ice is likely to lead to increased local shipping especially along the Northeast Passage near the northern coasts of Norway and Russia, which are shorter than the traditional southerly routes. Here, the regional chemistry-transport model WRF-Chem is used to examine the effects of shipping emissions on levels of air pollutants and deposition fluxes over the Barents Sea both for present-day and future conditions, based on a high growth scenario. Present-day shipping emissions are found to have already substantial effects on ozone concentrations, but limited effects on sulphate and nitrate aerosols. Predicted future changes in ozone are also important, particularly in regions with low nitrogen oxide concentrations, and results are sensitive to the way in which diversion shipping is distributed due to non-linear effects on photochemical ozone production. Whilst modest future increases in sulphate and nitrate aerosols are predicted, large enhancements in dry deposition of sulphur dioxide and wet deposition of nitrogen compounds to the Barents Sea are predicted. Such levels of future nitrogen deposition would represent a significant atmospheric source of oceanic nitrogen affecting sensitive marine ecosystems., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Elevated concentrations of atmospheric bromine are known to cause ozone depletion in the Arctic, which is most frequently observed during springtime. We implement a detailed description of bromine and chlorine chemistry within the WRF-Chem 4.1.1 model, and two different descriptions of Arctic bromine activation: (1) heterogeneous chemistry on surface snow on sea ice, triggered by ozone deposition to snow (Toyota et al., 2011 https://doi.org/10.5194/acp-11-3949-2011), and (2) heterogeneous reactions on sea salt aerosols emitted through the sublimation of lofted blowing snow (Yang et al., 2008, https://doi.org/10.1029/2008gl034536). In both mechanisms, bromine activation is sustained by heterogeneous reactions on aerosols and surface snow. Simulations for spring 2012 covering the entire Arctic reproduce frequent and widespread ozone depletion events, and comparisons with observations of ozone show that these developments significantly improve model predictions during the Arctic spring. Simulations show that ozone depletion events can be initiated by both surface snow on sea ice, or by aerosols that originate from blowing snow. On a regional scale, in spring 2012, snow on sea ice dominates halogen activation and ozone depletion at the surface. During this period, blowing snow is a major source of Arctic sea salt aerosols but only triggers a few depletion events., (© 2021. The Authors. Journal of Advances in Modeling Earth Systems published by Wiley Periodicals LLC on behalf of American Geophysical Union.)

Local emissions of Arctic air pollutants and their impacts on climate, ecosystems and health are poorly understood. Future increases due to Arctic warming or economic drivers may put additional pressures on the fragile Arctic environment already affected by mid-latitude air pollution. Aircraft data were collected, for the first time, downwind of shipping and petroleum extraction facilities in the European Arctic. Data analysis reveals discrepancies compared to commonly used emission inventories, highlighting missing emissions (e.g. drilling rigs) and the intermittent nature of certain emissions (e.g. flaring, shipping). Present-day shipping/petroleum extraction emissions already appear to be impacting pollutant (ozone, aerosols) levels along the Norwegian coast and are estimated to cool and warm the Arctic climate, respectively. Future increases in shipping may lead to short-term (long-term) warming (cooling) due to reduced sulphur (CO 2 ) emissions, and be detrimental to regional air quality (ozone). Further quantification of local Arctic emission impacts is needed.

The detection of hypoxia by the carotid bodies elicits a ventilatory response of utmost importance for tolerance to high altitude. Germline mutations in three genes encoding subunit B, C and D of succinate dehydrogenase (SDHB, SDHC and SDHD) have been associated with paragangliomas of the carotid body. We hypothesized that SDH dysfunction within the carotid body could result in low chemoresponsiveness and intolerance to high altitude. The frequency of polymorphisms of SDHs, hypoxia-inducible factor type 1 (HIF1alpha) and angiotensin converting enzyme (ACE) genes was compared between 40 subjects with intolerance to high altitude and a low hypoxic ventilatory response at exercise (HVRe < or = 0.5 ml min(-1) kg(-1); HVR- group) and 41 subjects without intolerance to high altitude and a high HVRe (> or = 0.80 ml min(-1) kg(-1); HVR+). We found no significant association between low or high HVRe and (1) the allele frequencies for nine single nucleotide polymorphisms (SNPs) in the SDHD and SDHB genes, (2) the ACE insertion/deletion polymorphism and (3) four SNPs in the HIF1alpha gene. However, a marginal significant association was found between the synonymous polymorphism c.18A>C of the SDHB gene and chemoresponsiveness: 8/40 (20%) in the HVR- group and 3/41 (7%) in the HVR+ group (p = 0.12). A principal component analysis showed that no subject carrying the 18C allele had both high ventilatory and cardiac response to hypoxia. In conclusion, no clear association was found between gene variants involved in oxygen sensing and chemoresponsiveness, although some mutations in the SDHB and SDHD genes deserve further investigations in a larger population.

We report the natural history of 17 brain lymphomas (11 primary, 6 disseminated) from a post-mortem series of 130 patients with AIDS. Primary lymphomas appeared lately in the course of AIDS. They were often associated with a severe T-cell immunodepression and with more frequent opportunistic disorders than disseminated lymphomas. Associated Kaposi's sarcomas were surprisingly frequent. All patients presented with neurological manifestations. Heterogeneous features were seen at CT examination. The CSF was abnormal in 12/13 cases, with an increase of protein contents and secretion of immunoglobulins; it contained activated lymphocytes in 5/6 cases of disseminated lymphomas, and malignant cells in only one case. Cellular density never exceeded 8/mm3 for primary lymphomas, and the lymphocytes were considered normal. The pre-mortem diagnosis of cerebral lymphomas was made in five patients, with a time lapse of 1 to 7 months between the first neurological symptoms and death, and of 5 to 30 days between the diagnosis and death. Cerebral biopsy was diagnostic in 4 cases of primary cerebral lymphomas. In only 1/6 patients with disseminated lymphomas, the diagnosis had been made when the patient was still alive, based on CSF and bone marrow lymphomatous infiltrations. The diagnosis of cerebral lymphoma (7 primary, 5 disseminated) was post-mortem in 12 cases. It was made only at microscopic examination in 2/12 cases of primary lymphomas. The histopathological study frequently showed a multicentric involvement, and always an immunoblastic cell type with plasmablastic differentiation and frequent medium size cells. Marked gliosis and significant necrosis were often observed. Neuropathological lesions associated with HIV-1 infection (toxoplasmosis, CMV and HIV-1 encephalitis) were seen in 8 cases with primary lymphomas.

We investigated 49 acquired immunodeficiency syndrome-related lymphomas (ARLs) for Epstein-Barr virus (EBV) by Southern blotting and in situ hybridization and, in positive cases, used cryostat immunohistology to compare EBV-latent gene expression (EBV encoded small RNA-1 [EBER-1], EBV nuclear antigen-2 [EBNA-2], latent membrane protein-1 [LMP-1] and host cell immunophenotype (CD11a, CD18, CD54, CD58, CD21, CD23, CD30, CD39, CDw70, immunoglobulin) patterns with those reported in other EBV infections. EBV+ immunoblast-rich/large cell ARLs (n = 22) showed three patterns of latency: broad (EBER+EBNA-2+/LMP-1+; n = 9), reminiscent of a lymphoblastoid cell line phenotype; restricted (EBER+/EBNA-2-/LMP-1-; n = 6), similar to endemic Burkitt's lymphoma; and intermediate (EBER+/EBNA-2-/LMP-1+; n = 7), a pattern rarely described in vitro but seen in certain EBV-related malignancies. EBNA-2 expression was associated with extranodal lymphomas. EBV+ Burkitt-type ARLs (n = 11) usually showed the restricted latency pattern (n = 8), but some expressed the intermediate form (n = 3). Adhesion (CD54, CD58) and activation (CD30, CD39, CDw70) molecule expression varied with morphology (immunoblast-rich/large cell versus Burkitt-type), but was not independently correlated with EBV-positivity. CD30 and LMP-1 expression were associated. ARLs show heterogeneity regarding both the presence of EBV and latency pattern. Comparison of these phenotypically distinct lymphoma groups with known forms of EBV infection provides clues to their possible pathogenesis.

A 58 year old man was admitted with a pseudo-coronary pain. Cardiological investigations (ECG, chest X-ray, enzymes) were normal. Pain however was exacerbated by movement, coughing and pressure over T4 to T10 vertebrae. On the 4th day, the patient developed a weakness of the right lower limb which worsened 15 days later. On examination there were in the right lower limb a combination of central (Babinski sign) and peripheral signs (diminished deep reflexes, loss of sensation to all modalities ipsilateral to the paralysis). Metrizamide myelography was within normal limits. Spinal angiography revealed a dural arteriovenous fistula draining into spinal veins, at the level of T5. Following the removal of the fistula, the pain disappeared and the other symptoms and signs improved.

Bilateral hypothenar muscular spasm ("dimpling") was discovered in a 62 year-old man. The spasms consisted of recurrent arrhythmic contractions of the palmaris brevis muscle. E.M.G. showed no signs of denervation but the contractions could be stopped by infiltration of the ulnar nerve by xylocaine. Apparently, this syndrome has previously been reported in only two cases. Its clinical and electromyographic characteristics are similar to hemifacial spasm. Compression of the ulnar nerve after its division at the wrist could be a cause.