Decadal-scale thermohaline variability in the Atlantic sector of the Southern Ocean

An enhanced Altimetry Gravest Empirical Mode (AGEM), including both adiabatic and diabatic trends, is developed for the Antarctic Circumpolar Current (ACC) south of Africa using updated hydrographic CTD sections, Argo data, and satellite altimetry. This AGEM has improved accuracy compared to traditional climatologies and other proxy methods. The AGEM for the Atlantic Southern Ocean offers an ideal technique to investigate the thermohaline variability over the past two decades in a key region for water mass exchanges and transformation. In order to assess and attribute changes in the hydrography of the region, we separate the changes into adiabatic and diabatic components. Integrated over the upper 2000 dbar of the ACC south of Africa, results show mean adiabatic changes of 0.16 ± 0.11°C decade−1 and 0.006 ± 0.014 decade−1, and diabatic differences of −0.044 ± 0.13°C decade−1 and −0.01 ± 0.017 decade−1 for temperature and salinity, respectively. The trends of the resultant AGEM, that include both adiabatic and diabatic variability (termed AD-AGEM), show a significant increase in the heat content of the upper 2000 dbar of the ACC with a mean warming of 0.12 ± 0.087°C decade−1. This study focuses on the Antarctic Intermediate Water (AAIW) mass where negative diabatic trends dominate positive adiabatic differences in the Subantarctic Zone (SAZ), with results indicating a cooling (−0.17°C decade−1) and freshening (−0.032 decade−1) of AAIW in this area, whereas south of the SAZ positive adiabatic and diabatic trends together create a cumulative warming (0.31°C decade−1) and salinification (0.014 decade−1) of AAIW

Modeling interannual dense shelf water export in the region of the Mertz Glacier Tongue (1992-2007)

1] Ocean observations around the Australian-Antarctic basin show the importance of coastal latent heat polynyas near the Mertz Glacier Tongue (MGT) to the formation of Dense Shelf Water (DSW) and associated Antarctic Bottom Water (AABW). Here, we use a regional ocean/ice shelf model to investigate the interannual variability of the export of DSW from the Adélie (west of the MGT) and the Mertz (east of the MGT) depressions from 1992 to 2007. The variability in the model is driven by changes in observed surface heat and salt fluxes. The model simulates an annual mean export of DSW through the Adélie sill of about 0.07 ± 0.06 Sv. From 1992 to 1998, the export of DSW through the Adélie (Mertz) sills peaked at 0.14 Sv (0.29 Sv) during July to November. During periods of mean to strong polynya activity (defined by the surface ocean heat loss), DSW formed in the Adélie depression can spread into the Mertz depression via the cavity under the MGT. An additional simulation, where ocean/ice shelf thermodynamics have been disabled, highlights the fact that models without ocean/ice shelf interaction processes will significantly overestimate rates of DSW export. The melt rates of the MGT are 1.2 ± 0.4 m yr−1 during periods of average to strong polynya activity and can increase to 3.8 ± 1.5 m/yr during periods of sustained weak polynya activity, due to the increased presence of relatively warmer water interacting with the base of the ice shelf. The increased melting of the MGT during a weak polynya state can cause further freshening of the DSW and ultimately limits the production of AABW

OCP acquires FTTH player

PURPOSE OF REVIEW: In this review, we highlight the most important cellular and molecular mechanisms that contribute to cardiac inflammation and fibrosis. We also discuss the interplay between inflammation and fibrosis in various precursors of heart failure (HF) and how such mechanisms can contribute to myocardial tissue remodelling and development of HF. RECENT FINDINGS: Recently, many research articles attempt to elucidate different aspects of the interplay between inflammation and fibrosis. Cardiac inflammation and fibrosis are major pathophysiological mechanisms operating in the failing heart, regardless of HF aetiology. Currently, novel therapeutic options are available or are being developed to treat HF and these are discussed in this review. A progressive disease needs an aggressive management; however, existing therapies against HF are insufficient. There is a dynamic interplay between inflammation and fibrosis in various precursors of HF such as myocardial infarction (MI), myocarditis and hypertension, and also in HF itself. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the inflammatory and fibrotic pathways are essential, and specific drugs that target these pathways need to be evaluated

The role of immune checkpoints in cardiovascular disease

Immune checkpoint inhibitors (ICI) are monoclonal antibodies which bind to immune checkpoints (IC) and their ligands to prevent inhibition of T-cell activation by tumor cells. Currently, multiple ICI are approved targeting Cytotoxic T-lymphocyte antigen 4 (CTLA-4), Programmed Death Protein 1 (PD-1) and its ligand PD-L1, and Lymphocyte-activation gene 3 (LAG-3). This therapy has provided potent anti-tumor effects and improved prognosis for many cancer patients. However, due to systemic effects, patients can develop immune related adverse events (irAE), including possible life threatening cardiovascular irAE, like atherosclerosis, myocarditis and cardiomyopathy. Inhibition of vascular IC is associated with increased atherosclerotic burden and plaque instability. IC protect against atherosclerosis by inhibiting T-cell activity and cytokine production, promoting regulatory T-cell differentiation and inducing T-cell exhaustion. In addition, PD-L1 on endothelial cells might promote plaque stability by reducing apoptosis and increasing expression of tight junction molecules. In the heart, IC downregulate the immune response to protect against cardiac injury by reducing T-cell activity and migration. Here, inhibition of IC could induce life-threatening T-cell-mediated-myocarditis. One proposed purpose behind lymphocyte infiltration is reaction to cardiac antigens, caused by decreased self-tolerance, and thereby increased autoimmunity because of IC inhibition. In addition, there are several reports of ICI-mediated cardiomyopathy with immunoglobulin G expression on cardiomyocytes, indicating an autoimmune response. IC are mostly known due to their cardiotoxicity. However, t his review compiles current knowledge on mechanisms behind IC function in cardiovascular disease with the aim of providing an overview of possible therapeutic targets in prevention or treatment of cardiovascular irAEs