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Sediment cores from Kløverbladvatna, a threshold lake in Wahlenbergfjorden, Nordaustlandet, Svalbard were used to reconstruct Holocene glacier fluctuations. Meltwater from Etonbreen spills over a threshold to the lake, only when the glacier is significantly larger than at present. Lithological logging, loss-on-ignition, ITRAX scanning and radiocarbon dating of the cores show that Kløverbladvatna became isolated from Wahlenbergfjorden c. 5.4 cal. kyr BP due to glacioisostatic rebound. During the Late Holocene, laminated clayey gyttja from lacustrine organic production and surface runoff from the catchment accumulated in the lake. The lacustrine sedimentary record suggests that meltwater only spilled over the threshold at the peak of the surge of Etonbreen in AD 1938. Hence, we suggest that this was the largest extent of Etonbreen in the (mid-late) Holocene. In Palanderbukta, a tributary fjord to Wahlenbergfjorden, raised beaches were surveyed and organic material collected to determine the age of the beaches and reconstruct postglacial relative sea level change. The age of the postglacial raised beaches ranges from 10.7 cal. kyr BP at 50 m a.s.l. to 3.13 cal. kyr BP at 2 m a.s.l. The reconstructed postglacial relative sea level curve adds valuable spatial and chronological data to the relative sea level record of Nordaustlandet.

Background and Aims: The pronounced neutrophilia observed in patients with coronavirus disease 2019 (COVID-19) infections suggests a role for these leukocytes in the pathology of the disease. Monocyte and neutrophil expression of CD64 and CD11b have been reported as early biomarkers to detect infections. The aim of this study was to study the expression of receptors for IgG (CD64) and adhesion molecules (CD11b, CD15s, CD65, CD162, CD66b) on neutrophils and monocytes in patients with severe COVID-19 after admission to an intensive care unit (ICU). Methods: The expression of receptors was analyzed using flow cytometry. EDTA blood from 23 patients with confirmed COVID-19 infection was sampled within 48 h of admission to the ICU. Leukocytes were labeled with antibodies to CD11b, CD15s, CD65s, CD162, CD64, and CD66b. Expression of receptors was reported as mean fluorescence intensity (MFI) or the percentage of cells expressing receptors. Results: Results are presented as comparison of COVID-19 patients with the healthy group and the receptor expression as MFI. Neutrophil receptors CD64 (2.5 versus 0.5) and CD66b (44.5 versus 34) were increased and CD15 decreased (21.6 versus 28.3) when CD65 (6.6 versus 4.4), CD162 (21.3 versus 21.1) and CD11b (10.5 versus 12) were in the same range. Monocytes receptors CD64 (30.5 versus 16.6), CD11b (18.7 versus 9.8), and CD162 (38.6 versus 36.5) were increased and CD15 decreased (10.3 versus 17.9); CD65 were in the same range (2.3 versus 1.96). Conclusion: Monocytes and neutrophils are activated during severe COVID-19 infection as shown by strong upregulation of CD64. High monocyte and neutrophil CD64 can be an indicator of a severe form of COVID19. The adhesion molecules (CD11b, CD162, CD65, and CD15) are not upregulated on otherwise activated neutrophils, which might lead to relative impairment of tissue migration. Low adhesion profile of neutrophils suggests immune dysfunction of neutrophils. Monocytes maintain upregulation of some adhesion molecules (CD11b, CD162) suggesting the persistence of an increased ability to migrate into tissues, even during a severe stage of COVID-19. Future research should focus on CD64 and CD11b kinetics in the context of prognosis.

Introduction Rheumatoid arthritis (RA) patients with autoantibodies against collagen type II (CII) are characterized by acute RA onset with elevated inflammatory measures and early joint erosions as well as increased production of tumor necrosis factor-α (ΤΝF-α) by peripheral blood mononuclear cells (PBMC) stimulated by anti-CII immune complexes (IC) in vitro . Polymorphonuclear granulocytes (PMN) are abundant in RA synovial fluids, where they might interact directly with anti-CII IC in the articular cartilage, but no studies have investigated PMN responses towards anti-CII IC. The aim was to investigate whether PMN react towards anti-CII IC, and to what extent such reactivity might relate to the clinical acute onset RA phenotype associated with elevated levels of anti-CII. Methods PMN and PBMC isolated from healthy donors were stimulated with IC made with a set of 72 baseline patient sera (24 anti-CII positive, 48 anti-CII negative) chosen from a clinically well-characterized RA cohort with two-year radiological follow-up with Larsen scoring. PMN expression of cluster of differentiation (CD)11b, CD66b, CD16 and CD32 was measured by flow cytometry, whereas PMN production of myeloperoxidase (MPO) and interleukin (IL)-17, and PBMC production of ΤΝF-α was measured with enzyme linked immunosorbent assay. Results PMN expression of CD11b, CD66b and MPO, and PBMC production of ΤΝF-α were upregulated whereas PMN expression of CD16 and CD32 were downregulated by anti-CII IC. CD16, CD66b, and MPO production correlated to serum anti-CII levels (Spearman’s ρ = 0.315, 0.675 and 0.253, respectively). CD16 was associated with early joint erosions ( P  = 0.024, 0.034, 0.046 at baseline, one and two years) and CD66b was associated with changes in joint erosions ( P  = 0.017 and 0.016, at one and two years compared to baseline, respectively). CD66b was associated with baseline C-reactive protein and PBMC production of ΤΝF-α was associated with baseline erythrocyte sedimentation rate, in accordance with our earlier findings. No clinical associations were observed for MPO or IL-17. Conclusion PMN responses against anti-CII IC are more closely associated with early joint erosions than are PBMC cytokine responses. PMN reactivity against anti-CII IC may contribute to joint destruction in newly diagnosed RA patients with high levels of anti-CII.

Background: A prerequisite for an effective innate immunity is the migrative ability of neutrophils to respond to inflammatory and infectious agents such as the intermediate interleukin (IL)-8 and the end-target formyl-methionyl-leucyl-phenylalanine (fMLP) chemoattractants. The aim was to study the chemotactic capacity of neutrophils from newborn infants and adults in response to IL-8 and the bacterial peptide fMLP. Methods: In the under-agarose cell migration assay, isolated leukocytes from healthy adults and from cord blood of healthy term newborn infants were studied with dose responses towards IL-8 and fMLP. The same number of leukocytes (1 × 10 5 cells), with the same distribution of neutrophils and monocytes, were analyzed in neonates and adults. Chemotaxis was distinguished from randomly migrating neutrophils, and the neutrophil pattern of migration, i.e. the migration distance and the number of migrating neutrophils per distance, was evaluated. Results: In comparison to adults, fewer neutrophils from newborn infants migrated towards IL-8 and for a shorter distance (P < .01, respectively). The number of neutrophils migrating to different gradients of fMLP, the distance they migrated, and the correlation between the number and the distance were the same for neonates and adults. Random migration did not differ in any instance. Conclusion: Chemotaxis of neutrophils from newborn infants was as co-ordinated as neutrophils from adults in response to fMLP, whereas the response to IL-8 was reduced. The differential response of neutrophils from neonates to intermediate and end-target chemoattractants could indicate a reduced infectious response.

Background The Eosinophil Cationic Protein (ECP) is a potent multifunctional protein. Three common polymorphisms are present in the ECP gene, which determine the function and production of the protein. The aim was to study the relationship of these ECP gene polymorphisms to signs and symptoms of allergy and asthma in a community based cohort (The European Community Respiratory Health Survey (ECRHS)). Methods Swedish and Estonian subjects (n = 757) were selected from the larger cohort of the ECRHS II study cohort. The prevalence of the gene polymorphisms ECP434(G>C) (rs2073342), ECP562(G>C) (rs2233860) and ECP c.-38(A>C) (rs2233859) were analysed by DNA sequencing and/or real-time PCR and related to questionnaire-based information of allergy, asthma, smoking habits and to lung functions. Results Genotype prevalence showed both ethnic and gender differences. Close associations were found between the ECP434(G>C) and ECP562(G>C) genotypes and smoking habits, lung function and expression of allergic symptoms. Non-allergic asthma was associated with an increased prevalence of the ECP434GG genotype. The ECP c.-38(A>C) genotypes were independently associated to the subject being atopic. Conclusion Our results show associations of symptoms of allergy and asthma to ECP-genotypes, but also to smoking habits. ECP may be involved in impairment of lung functions in disease. Gender, ethnicity and smoking habits are major confounders in the evaluations of genetic associations to allergy and asthma.

Most small land-terminating glaciers in Svalbard have experienced large recession since the Little Ice Age (LIA) and today are thin, cold, and largely inactive. This likely contrasts to their LIA conditions, but the observational record from that time is sparse. We investigate the evolution of five small glaciers in central Nordenskiöld Land, Svalbard, from the LIA to 2019. Photogrammetric reconstructions and ground penetrating radar are used to reconstruct their geometric changes since 1936, and historical observation, photographs, and geomorphological mapping extend this history to before the 1900s. Our results show that from 1936 to 2019, the study glaciers on average lost 49.6% of their area and 77.4% ± 7.7% of their volume, with the greatest volume loss at Scott Turnerbreen of 91% ± 5%. Four out of these five glaciers strongly indicate a history of surge-like advances near the end of the LIA within one or two decades, and the rate of subsequent mass loss seems connected to their previous dynamics. This apparent switch to high activity during a period of rapid climatic change, could have implications for our understanding of past and future glacier evolution; climate change and highly dynamic glacier responses may be more connected than previously thought.

Background: Studies using rush immunotherapy (RIT) have shown that rapid protection can be achieved using protocols allowing a fast increment of allergen dose. We examined the early effects of RIT on basophil numbers and expression of CD203c, production of interleukin (IL)-4 and IL-13 and histamine release by basophils in the peripheral blood of patients treated with immunotherapy and controls. Methods: Twelve patients treated with RIT and 4 untreated controls were included in the study. Any adverse events were evaluated during the incremental phase of RIT. Mononuclear cells were isolated before the start of RIT and 3 days, 1 week, 4 weeks and 3 months after the beginning of the treatment. Histamine release upon allergen stimulation, expression of CD203c and allergen-induced production of IL-4 and IL-13 by basophils were examined. Results: Significant decreases in blood basophil count (p = 0.02) were observed early in the treatment, returning to baseline values 1 week after the start of RIT. Similarly, histamine release decreased at day 3 (p = 0.02), but returned to pretreatment levels after 1 week. Also, the percentage of IL-4+ and IL-13+ basophils and levels of CD203c expression were markedly reduced early in the treatment. IL-4 and IL-13 production correlated with histamine release and CD203c expression. Histamine release and production of IL-4 and IL-13 by basophils before the treatment correlated with the severity of adverse events during the incremental phase of RIT. Conclusion: We report the decrease in blood basophil numbers, their lower activation status and the reduced production of IL-4 and IL-13 early in the course of RIT. This early suppression of basophil activation could be one mechanism behind the protective effect of RIT.

We report on 10 Be and optically stimulated luminescence ages from moraines and glaciolacustrine sediments on eastern Jameson Land, East Greenland. Sampled landforms and sediment are associated with advances of outlet glaciers from the local Liverpool Land ice cap situated in the coastal Scoresby Sund region. Previous studies have tentatively correlated these advances with the Milne Land Stade moraines, which are prominent moraine sets deposited by mountain glaciers in the inner Scoresby Sund region. Recent constraints on the formation of the outer and inner of these moraines have suggested two advances of local glaciers, one prior to or during the Younger Dryas and another during the Preboreal. In this paper, we test the correlation of the Liverpool Land glacial advance with the Milne Land Stade. Our results show that outlet glaciers from the Liverpool Land ice cap reached ice-marginal positions marked by moraines in east-facing valleys on Jameson Land sometime during late glacial-early Holocene time (ca. 13-11 Kya). This confirms the correlation of these moraines with the Milne Land Stade moraines described elsewhere in the Scoresby Sund region.

Earlier work in northeast Greenland has suggested a limited advance of the Greenland Ice Sheet during the Last Glacial Maximum (LGM). However, this concept has recently been challenged by marine geological studies, indicating grounded ice on the continental shelf at this time. New Be-10-ages from the Store Koldewey island, northeast Greenland, suggest that unscoured mountain plateaus at the outer coast were covered at least partly by cold-based ice during the LGM. It is, however, still inconclusive whether this ice was dynamically connected to the Greenland Ice Sheet or not. Regardless of the LGM ice sheet extent, the Be-10 results from Store Koldewey add to a growing body of evidence suggesting considerable antiquity of crystalline unscoured terrain near present and Pleistocene ice sheet margins.

Background: Albumin is known to induce chemokinesis and facilitate chemotaxis of human granulocytes in the Boyden chamber assay, but its mechanisms of action remain obscure. We have previously found that IL-2 inhibits albumin-stimulated eosinophil migration. The aim of this study was to identify the mechanisms behind the effects of albumin and IL-2 on the migration of human eosinophils. Methods: Purified eosinophils were preincubated with inhibitors of signal transduction molecules before incubation with or without albumin and IL-2. The migration assay was performed in a 48-well microchemotaxis chamber. The effect of albumin and IL-2 on cell size and on the surface expression of adhesion molecules was studied with flow cytometry. Results: Albumin-stimulated migration was inhibited by the PI3-kinase inhibitors wortmannin and LY-294002, but not by the PKC inhibitor RO-31-8220. IL-2 had no effect after preincubation with wortmannin or LY-294002. In contrast, the inhibitory effect of IL-2 remained after preincubation with RO-31-8220. Albumin increased the cell size as measured by forward scatter, and the expression of CD49d and CD49f decreased after incubation with albumin. IL-2 affected neither the expression of adhesion molecules nor the forward scatter. Conclusions: The stimulation of eosinophil migration by albumin is mediated by PI3-kinase, and the increase in cell size caused by albumin indicates activation of the cells. Decreased expression of CD49d and CD49f by albumin may diminish the adhesiveness of the cells, which in turn may facilitate migration. These are novel findings that indicate an active role for albumin in eosinophil migration.