Holocene Sediment Records From the Continental Shelf of Mac. Robertson Land, East Antarctica

Geochemical records are presented for five sediment cores from basins on the continental shelf of Mac. Robertson Land, East Antarctica. The cores contain 2-4 m thick sequences of hemipelagic, siliceous mud and ooze (SMO) deposited under seasonally open marine conditions. The inner and middle shelf SMO sequences are massive dark olive green material, whereas the outer shelf SMO sequences are dark olive material interspersed with light olive green layers similar to1-10 cm thick. The biogenic material is dominated by marine diatoms including Fragilariopsis curta, Fragilariopsis cylindrus, and Chaetoceros spp. in the dark-colored SMO and Corethron criophilum in the light-colored layers. Radiocarbon dates suggest that the cores provide continuous accumulation records extending from \u3c 1 kyr before present (B.P.) back as far as 4-15 kyr B.P., with estimated accumulation rates of 0.07-5 mm yr(-1). The three core records from the middle and outer shelf suggest six episodes of increased accumulation of biogenic material at 5.5 kyr B.P. tall three cores), 1, 2, and 6.2 kyr B.P. (two of the three cores), and 3.8 and 10.8 kyr B.P. tone core), most of which coincide with Corethron layers. We interpret these features as the result of enhanced diatom production over the outer shelf, possibly related to climatic warm periods. The absence of such features in the inner shelf core records is thought to reflect a relatively constant level of seasonal diatom production in adjacent waters maintained by a coastal polynya

(Table 2) Age determination of sediment cores from the continental shelf of Mac Roberston Land, East Antarctica

Geochemical records are presented for five sediment cores from basins on the continental shelf of Mac. Robertson Land, East Antarctica. The cores contain 2-4 m thick sequences of hemipelagic, siliceous mud and ooze (SMO) deposited under seasonally open marine conditions. The inner and middle shelf SMO sequences are massive dark olive green material, whereas the outer shelf SMO sequences are dark olive material interspersed with light olive green layers ~1-10 cm thick. The biogenic material is dominated by marine diatoms including Fragilariopsis curta, Fragilariopsis cylindrus, and Chaetoceros spp. in the dark-colored SMO and Corethron criophilum in the light-colored layers. Radiocarbon dates suggest that the cores provide continuous accumulation records extending from < 1 kyr before present (B.P.) back as far as 4-15 kyr B.P., with estimated accumulation rates of 0.07-5 mm/yr. The three core records from the middle and outer shelf suggest six episodes of increased accumulation of biogenic material at ~5.5 kyr B.P. (all three cores), 1, 2, and 6.2 kyr B.P. (two of the three cores), and 3.8 and 10.8 kyr B.P. (one core), most of which coincide with Corethron layers. We interpret these features as the result of enhanced diatom production over the outer shelf, possibly related to climatic warm periods. The absence of such features in the inner shelf core records is thought to reflect a relatively constant level of seasonal diatom production in adjacent waters maintained by a coastal polynya

Exercise reduces inflammatory cell production and cardiovascular inflammation via instruction of hematopoietic progenitor cells

A sedentary lifestyle, chronic inflammation and leukocytosis increase atherosclerosis; however, it remains unclear whether regular physical activity influences leukocyte production. Here we show that voluntary running decreases hematopoietic activity in mice. Exercise protects mice and humans with atherosclerosis from chronic leukocytosis but does not compromise emergency hematopoiesis in mice. Mechanistically, exercise diminishes leptin production in adipose tissue, augmenting quiescence-promoting hematopoietic niche factors in leptin-receptor-positive stromal bone marrow cells. Induced deletion of the leptin receptor in Prrx1-creERT2; Leprfl/fl mice reveals that leptin’s effect on bone marrow niche cells regulates hematopoietic stem and progenitor cell (HSPC) proliferation and leukocyte production, as well as cardiovascular inflammation and outcomes. Whereas running wheel withdrawal quickly reverses leptin levels, the impact of exercise on leukocyte production and on the HSPC epigenome and transcriptome persists for several weeks. Together, these data show that physical activity alters HSPCs via modulation of their niche, reducing hematopoietic output of inflammatory leukocytes

Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease

Abnormal hematopoiesis advances cardiovascular disease by generating excess inflammatory leukocytes that attack the arteries and the heart. The bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, but whether cardiovascular disease affects the hematopoietic organ's microvasculature is unknown. Here we show that hypertension, atherosclerosis and myocardial infarction (MI) instigate endothelial dysfunction, leakage, vascular fibrosis and angiogenesis in the bone marrow, altogether leading to overproduction of inflammatory myeloid cells and systemic leukocytosis. Limiting angiogenesis with endothelial deletion of Vegfr2 (encoding vascular endothelial growth factor (VEGF) receptor 2) curbed emergency hematopoiesis after MI. We noted that bone marrow endothelial cells assumed inflammatory transcriptional phenotypes in all examined stages of cardiovascular disease. Endothelial deletion of Il6 or Vcan (encoding versican), genes shown to be highly expressed in mice with atherosclerosis or MI, reduced hematopoiesis and systemic myeloid cell numbers in these conditions. Our findings establish that cardiovascular disease remodels the vascular bone marrow niche, stimulating hematopoiesis and production of inflammatory leukocytes

Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease

Abnormal hematopoiesis advances cardiovascular disease by generating excess inflammatory leukocytes that attack the arteries and the heart. The bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, but whether cardiovascular disease affects the hematopoietic organ's microvasculature is unknown. Here we show that hypertension, atherosclerosis and myocardial infarction (MI) instigate endothelial dysfunction, leakage, vascular fibrosis and angiogenesis in the bone marrow, altogether leading to overproduction of inflammatory myeloid cells and systemic leukocytosis. Limiting angiogenesis with endothelial deletion of Vegfr2 (encoding vascular endothelial growth factor (VEGF) receptor 2) curbed emergency hematopoiesis after MI. We noted that bone marrow endothelial cells assumed inflammatory transcriptional phenotypes in all examined stages of cardiovascular disease. Endothelial deletion of Il6 or Vcan (encoding versican), genes shown to be highly expressed in mice with atherosclerosis or MI, reduced hematopoiesis and systemic myeloid cell numbers in these conditions. Our findings establish that cardiovascular disease remodels the vascular bone marrow niche, stimulating hematopoiesis and production of inflammatory leukocytes