Genesis of the Antarctic Slope Current in West Antarctica

The stability of the West Antarctic Ice Sheet (WAIS) depends on ocean heat transport toward its base and remains a source of uncertainty in sea level rise prediction. The Antarctic Slope Current (ASC), a major boundary current of the ocean's global circulation, serves as a dynamic gateway for heat transport toward Antarctica. Here, we use observations collected from the Bellingshausen Sea to propose a mechanistic explanation for the initiation of the westward‐flowing ASC. Waters modified throughout the Bellingshausen Sea by ocean‐sea‐ice and ocean‐ice‐shelf interactions are exported to the continental slope in a narrow, topographically steered western boundary current. This focused outflow produces a localized front at the shelf break that supports the emerging ASC. This mechanism emphasizes the importance of buoyancy forcing, integrated over the continental shelf, as opposed to local wind forcing, in the generation mechanism and suggests the potential for remote control of melt rates of WAIS' largest ice shelves

Bone mass and microarchitecture of irradiated and bone marrow-transplanted mice: influences of the donor strain

Summary Total body irradiation and bone marrow transplantation induced dramatic trabecular bone loss and cortical thickening in mice. Transplanted cells were engrafted in bone marrow, along trabeculae, and in periosteal and endosteal envelopes. None of the osteocytes were of donor origin. Bone microarchitecture of transplanted mice changed to tend toward the donor phenotype. Introduction Osteopenia and osteoporosis are complications of bone marrow transplants (BMT) attributed to related chemotherapy. However, the specific influence of total body irradiation (TBI) is unknown. Methods We investigated the effects of TBI and BMT on bone mass and microarchitecture by micro-CT. Eighteen C57Bl/6 (B6) mice receiving lethal TBI had a BMT with marrow cells from green fluorescent protein--transgenic-C57Bl/6 (GFP) mice. Transplanted (TGFPB6), B6, and GFP mice were euthanized 1, 3, and 6 months after BMT or at a related age. Results TGFPB6 presented a dramatic bone loss compared with B6 and did not restore their trabecular bone mass over time, despite a cortical thickening 6 months after BMT. Serum testosterone levels were not significantly reduced after BMT. During aging, GFP mice have less trabeculae, thicker cortices, but a narrower femoral shaft than B6 mice. From 3 months after BMT, cortical characteristics of TGFPB6 mice differed statistically from B6 mice and were identical to those of GFP mice. GFP+ cells were located along trabecular surfaces and in periosteal and endosteal envelopes, but none of the osteocytes expressed GFP. Conclusion Our findings suggest that engrafted cells did not restore the irradiation-induced trabecular bone loss, but reconstituted a marrow microenvironment and bone remodeling similar to those of the donor. The effects of irradiation and graft on bone remodeling differed between cortical and trabecular bone

Understanding brain dysfunction in sepsis

Sepsis often is characterized by an acute brain dysfunction, which is associated with increased morbidity and mortality. Its pathophysiology is highly complex, resulting from both inflammatory and noninflammatory processes, which may induce significant alterations in vulnerable areas of the brain. Important mechanisms include excessive microglial activation, impaired cerebral perfusion, blood–brain-barrier dysfunction, and altered neurotransmission. Systemic insults, such as prolonged inflammation, severe hypoxemia, and persistent hyperglycemia also may contribute to aggravate sepsis-induced brain dysfunction or injury. The diagnosis of brain dysfunction in sepsis relies essentially on neurological examination and neurological tests, such as EEG and neuroimaging. A brain MRI should be considered in case of persistent brain dysfunction after control of sepsis and exclusion of major confounding factors. Recent MRI studies suggest that septic shock can be associated with acute cerebrovascular lesions and white matter abnormalities. Currently, the management of brain dysfunction mainly consists of control of sepsis and prevention of all aggravating factors, including metabolic disturbances, drug overdoses, anticholinergic medications, withdrawal syndromes, and Wernicke’s encephalopathy. Modulation of microglial activation, prevention of blood–brain-barrier alterations, and use of antioxidants represent relevant therapeutic targets that may impact significantly on neurologic outcomes. In the future, investigations in patients with sepsis should be undertaken to reduce the duration of brain dysfunction and to study the impact of this reduction on important health outcomes, including functional and cognitive status in survivors

International Health Regulations—What Gets Measured Gets Done

Focus on goals and metrics for 4 core capacities illustrates 1 approach to implementing IHR

From coordination to stochastic models of QoS

Reo is a channel-based coordination model whose operational semantics is given by Constraint Automata (CA). Quantitative Constraint Automat

Elastic properties of grafted microtubules

We use single-particle tracking to study the elastic properties of single microtubules grafted to a substrate. Thermal fluctuations of the free microtubule's end are recorded, in order to measure position distribution functions from which we calculate the persistence length of microtubules with contour lengths between 2.6 and 48 micrometers. We find the persistence length to vary by more than a factor of 20 over the total range of contour lengths. Our results support the hypothesis that shearing between protofilaments contributes significantly to the mechanics of microtubules.Comment: 9 pages, 3 figure

Translational evidence for two distinct patterns of neuroaxonal injury in sepsis: a longitudinal, prospective translational study

Background Brain homeostasis deteriorates in sepsis, giving rise to a mostly reversible sepsis-associated encephalopathy (SAE). Some survivors experience chronic cognitive dysfunction thought to be caused by permanent brain injury. In this study, we investigated neuroaxonal pathology in sepsis. Methods We conducted a longitudinal, prospective translational study involving (1) experimental sepsis in an animal model; (2) postmortem studies of brain from patients with sepsis; and (3) a prospective, longitudinal human sepsis cohort study at university laboratory and intensive care units (ICUs). Thirteen ICU patients with septic shock, five ICU patients who died as a result of sepsis, fourteen fluid-resuscitated Wistar rats with fecal peritonitis, eleven sham-operated rats, and three human and four rat control subjects were included. Immunohistologic and protein biomarker analysis were performed on rat brain tissue at baseline and 24, 48, and 72 h after sepsis induction and in sham-treated rats. Immunohistochemistry was performed on human brain tissue from sepsis nonsurvivors and in control patients without sepsis. The clinical diagnostics of SAE comprised longitudinal clinical data collection and magnetic resonance imaging (MRI) and electroencephalographic assessments. Statistical analyses were performed using SAS software (version 9.4; SAS Institute, Inc., Cary, NC, USA). Because of non-Gaussian distribution, the nonparametric Wilcoxon test general linear models and the Spearman correlation coefficient were used. Results In postmortem rat and human brain samples, neurofilament phosphoform, β-amyloid precursor protein, β-tubulin, and H&E stains distinguished scattered ischemic lesions from diffuse neuroaxonal injury in septic animals, which were absent in controls. These two patterns of neuroaxonal damage were consistently found in septic but not control human postmortem brains. In experimental sepsis, the time from sepsis onset correlated with tissue neurofilament levels (R = 0.53, p = 0.045) but not glial fibrillary acidic protein. Of 13 patients with sepsis who had clinical features of SAE, MRI detected diffuse axonal injury in 9 and ischemia in 3 patients. Conclusions Ischemic and diffuse neuroaxonal injury to the brain in experimental sepsis, human postmortem brains, and in vivo MRI suggest these two distinct lesion types to be relevant. Future studies should be focused on body fluid biomarkers to detect and monitor brain injury in sepsis. The relationship of neurofilament levels with time from sepsis onset may be of prognostic value

The Antarctic Coastal Current in the Bellingshausen Sea

The ice shelves of the West Antarctic Ice Sheet experience basal melting induced by underlying warm, salty Circumpolar Deep Water. Basal meltwater, along with runoff from ice sheets, supplies fresh buoyant water to a circulation feature near the coast, the Antarctic Coastal Current (AACC). The formation, structure, and coherence of the AACC has been well documented along the West Antarctic Peninsula (WAP). Observations from instrumented seals collected in the Bellingshausen Sea offer extensive hydrographic coverage throughout the year, providing evidence of the continuation of the westward flowing AACC from the WAP towards the Amundsen Sea. The observations reported here demonstrate that the coastal boundary current enters the eastern Bellingshausen Sea from the WAP and flows westward along the face of multiple ice shelves, including the westernmost Abbot Ice Shelf. The presence of the AACC in the western Bellingshausen Sea has implications for the export of water properties into the eastern Amundsen Sea, which we suggest may occur through multiple pathways, either along the coast or along the continental shelf break. The temperature, salinity, and density structure of the current indicates an increase in baroclinic transport as the AACC flows from the east to the west, and as it entrains meltwater from the ice shelves in the Bellingshausen Sea. The AACC acts as a mechanism to transport meltwater out of the Bellingshausen Sea and into the Amundsen and Ross seas, with the potential to impact, respectively, basal melt rates and bottom water formation in these regions

Ice‐shelf meltwater overturning in the Bellingshausen Sea

Hydrographic data are analyzed for the broad continental shelf of the Bellingshausen Sea, which is host to a number of rapidly‐thinning ice shelves. The flow of warm Circumpolar Deep Water (CDW) onto the continental shelf is observed in the two major glacially‐carved troughs, the Belgica and Latady troughs. Using ship‐based measurements of potential temperature, salinity and dissolved oxygen, collected across several coast‐to‐coast transects over the Bellingshausen shelf in 2007, the velocity and circulation patterns are inferred based on geostrophic balance and further constrained by the tracer and mass budgets. Meltwater was observed at the surface and at intermediate depth toward the western side of the continental shelf, collocated with inferred outflows. The maximum conversion rate from the dense CDW to lighter water masses by mixing with glacial meltwater is estimated to be 0.37±0.1 Sv in both depth and potential density spaces. This diapycnal overturning is comparable to previous estimates made in the neighboring Amundsen Sea, highlighting the overlooked importance of water mass modification and meltwater production associated with glacial melting in the Bellingshausen Sea