Ocean-atmosphere interactions on decadal timescales

In this thesis, different processes that might contribute to the generation of decadal climate variability were investigated using general circulation models (GCMs) of the atmosphere and the ocean. First, the sensitivity of the atmospheric circulation to decadal changes in the underlying sea surface temperatures (SSTs) was esti- mated from an ensemble of six integrations of the Hadley Centre atmospheric GCM HadAMl, all forced by observed SSTs and sea-ice extents for the period 1949-93. Using a novel approach to estimate the 'true' SST-forced atmospheric response in the presence of spatially correlated internal atmospheric variability, the decadal at- mospheric variability was studied over the North Atlantic and North Pacific regions. After filtering out the atmospheric circulation changes associated with the El Niño - Southern Oscillation (ENSO) phenomenon, the dominant mode of forced variability over the North Atlantic exhibits a meridional dipole in the mean sea level pressure (MSLP) field and is related to a tripole in the anomalous North Atlantic SSTs. Over large parts of the North Atlantic region, however, the atmospheric response is not consistent enough to provide feedbacks to the underlying ocean that could cause self-sustained decadal oscillations. Over the North Pacific the atmospheric response is dominated by ENSO. In addition to the ENSO-related response an independent decadal atmospheric signal was detected. It consistently involves iarge-scaie wind stress curl anomalies over the North Pacific region. The effect of such wind stress curl anomalies on the ocean was studied in the second part of this thesis using the Hamburg Ocean Primitive Equation model (HOPE). It is shown how the adjust- ment of the North Pacific gyre circulation to large-scale wind stress curl anomalies determines the decadal timescale and how it may be exploited for predictions of decadal upper-ocean temperature changes in the central North Pacific. The HOPE model was also used to investigate a mechanism for the generation of decadal cli- mate variability in the tropical Pacific which relies on subduction of midlatitudinal North Pacific SST anomalies and their equatorward propagation within the oceanic thermocline. It is demonstrated that such a mechanism is unlikely to cause decadal climate variability in the tropical Pacific

Neural Networks for Encoding Dynamic Security-Constrained Optimal Power Flow to Mixed-Integer Linear Programs

This paper introduces a framework to capture previously intractable optimization constraints and transform them to a mixed-integer linear program, through the use of neural networks. We encode the feasible space of optimization problems characterized by both tractable and intractable constraints, e.g. differential equations, to a neural network. Leveraging an exact mixed-integer reformulation of neural networks, we solve mixed-integer linear programs that accurately approximate solutions to the originally intractable non-linear optimization problem. We apply our methods to the AC optimal power flow problem (AC-OPF), where directly including dynamic security constraints renders the AC-OPF intractable. Our proposed approach has the potential to be significantly more scalable than traditional approaches. We demonstrate our approach for power system operation considering N-1 security and small-signal stability, showing how it can efficiently obtain cost-optimal solutions which at the same time satisfy both static and dynamic security constraints

POMK regulates dystroglycan function via LARGE-mediated elongation of matriglycan

Matriglycan [-GlcA-β1,3-Xyl-α1,3-]n serves as a scaffold in many tissues for extracellular matrix proteins containing laminin-G domains including laminin, agrin, and perlecan. Like-acetylglucosaminyltransferase-1 (LARGE1) synthesizes and extends matriglycan on α-dystroglycan (α-DG) during skeletal muscle differentiation and regeneration; however, the mechanisms which regulate matriglycan elongation are unknown. Here, we show that Protein O-Mannose Kinase (POMK), which phosphorylates mannose of core M3 (GalNac-β1,3-GlcNac-β1,4-Man) preceding matriglycan synthesis, is required for LARGE1-mediated generation of full-length matriglycan on α-DG (~150 kDa). In the absence of Pomk in mouse skeletal muscle, LARGE1 synthesizes a very short matriglycan resulting in a ~90 kDa α-DG which binds laminin but cannot prevent eccentric contraction-induced force loss or muscle pathology. Solution NMR spectroscopy studies demonstrate that LARGE1 directly interacts with core M3 and binds preferentially to the phosphorylated form. Collectively, our study demonstrates that phosphorylation of core M3 by POMK enables LARGE1 to elongate matriglycan on α-DG, thereby preventing muscular dystrophy