MPTCP has been proposed recently as a mechanism for supporting transparently multiple connections to the application layer. It is under discussion at the IETF. We show, however, that the current MPTCP suffers from two problems: (P1) Upgrading some TCP users to MPTCP can reduce the throughput of others without any benefit to the upgraded users, which is a symptom of not being Paretooptimal; and (P2) MPTCP users could be excessively aggressive towards TCP users. We attribute these problems to the linked-increases algorithm (LIA) of MPTCP and, more specifically, to an excessive amount of traffic transmitted over congested paths.The design of LIA forces a tradeoff between optimal resource pooling and responsiveness. We revisit the problem and show that it is possible to provide these two properties simultaneously. We implement the resulting algorithm, called opportunistic linked increases algorithm (OLIA), in the Linux kernel, and we study its performance over our testbed, by simulations and by theoretical analysis. We prove that OLIA is Pareto-optimal and satisfies the design goals of MPTCP. Hence it can avoid the problems P1 and P2. Our measurements and simulations indicate that MPTCP with OLIA is as responsive and non-flappy as MPTCP with LIA, and that it solves problems P1 and P2.

Various physiologically relevant processes are regulated by the interaction of the receptor tyrosine kinase (c-Kit) and its ligand stem cell factor (SCF), with SCF known to be the most important growth factor for mast cells (MCs). In spite of their traditional role in allergic disorders and innate immunity, MCs have lately emerged as versatile modulators of a variety of physiologic and pathologic processes. Here we show that MCs are critical for pregnancy success. Uterine MCs presented a unique phenotype, accumulated during receptivity and expanded upon pregnancy establishment. KitW-sh/W-sh mice, whose MC deficiency is based on restricted c-Kit gene expression, exhibited severely impaired implantation, which could be completely rescued by systemic or local transfer of wild-type bone marrow-derived MCs. Transferred wild-type MCs favored normal implantation, induced optimal spiral artery remodeling and promoted the expression of MC proteases, transforming growth factor-β and connective tissue growth factor. MCs contributed to trophoblast survival, placentation and fetal growth through secretion of the glycan-binding protein galectin-1. Our data unveil unrecognized roles for MCs at the fetomaternal interface with critical implications in reproductive medicine.

Abstract-We describe the real-time monitoring infrastructure of the smart-grid pilot on the EPFL campus. We experimentally validate the concept of a real-time state-estimation for a 20 kV active distribution network. We designed and put into operation the whole infrastructure composed by the following main elements: (1) dedicated PMUs connected on the medium-voltage side of the network secondary substations by means of specific current/voltage transducers; (2) a dedicated communication network engineered to support stringent time limits and (3) an innovative state estimation process for real-time monitoring that incorporates phasor-data concentration and state estimation processes. Special care was taken to make the whole chain resilient to cyber-attacks, equipment failures and power outages. The achieved latency is within 65ms. The refresh rate of the estimated state is 20ms. The real-time visualization of the state estimator output is made publicly available, as well as the historical data (PMU measurements and estimated states). To the best of our knowledge, the work presented here is the first operational system that provides low-latency real-time stateestimation by using PMU measurements of a real active distribution network.

Abstract-This paper aims to assess the performance of linear state estimation (SE) processes of power systems relying on synchrophasor measurements. The performance assessment is conducted with respect to two different families of SE algorithms, i.e., static ones represented by weighted least squares (WLS) and recursive ones represented by Kalman filter (KF). To this end, this paper firstly recalls the analytical formulation of linear WLS state estimator (LWLS-SE) and Discrete KF state estimator (DKF-SE). We formally quantify the differences in the performance of the two algorithms. The validation of this result, together with the comprehensive performance evaluation of the considered state estimators, is carried out using two case studies, representing distribution (IEEE 123-bus test feeder) and transmission (IEEE 39-bus test system) networks. As a further contribution, this paper validates the correctness of the most common process model adopted in DKF-SE of power systems. Index Terms-Discrete Kalman filter (KF), linear state estimation (LSE), performance evaluation, phasor measurement unit (PMU), weighted least squares (WLS).

Vascular endothelium is a key regulator of homeostasis. In physiological conditions it mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. However, endothelial dysfunction caused by physical injury of the vascular wall, for example during balloon angioplasty, acute or chronic inflammation, such as in atherothrombosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites. At the same time, the dysfunction promotes thrombin generation, fibrin deposition, and coagulation. The serine protease thrombin plays a pivotal role in the coagulation cascade. However, thrombin is not only the key effector of coagulation cascade; it also plays a significant role in inflammatory diseases. It shows an array of effects on endothelial cells, vascular smooth muscle cells, monocytes, and platelets, all of which participate in the vascular pathophysiology such as atherothrombosis. Therefore, thrombin can be considered as an important modulatory molecule of vascular homeostasis. This review summarizes the existing evidence on the role of thrombin in vascular inflammation.

Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.

T-helper (Th) cell differentiation drives specialized gene programs that dictate effector T cell function at sites of infection. Here, we have shown Th cell differentiation also imposes discrete motility gene programs that shape Th1 and Th2 cell navigation of the inflamed dermis. Th1 cells scanned a smaller tissue area in a G protein-coupled receptor (GPCR) and chemokine-dependent fashion, while Th2 cells scanned a larger tissue area independent of GPCR signals. Differential chemokine reliance for interstitial migration was linked to STAT6 transcription-factordependent programming of integrin a V b 3 expression: Th2 cell differentiation led to high a V b 3 expression relative to Th1 cells. Th1 and Th2 cell modes of motility could be switched simply by manipulating the amount of a V b 3 on the cell surface. Deviating motility modes from those established during differentiation impaired effector function. Thus, programmed expression of a V b 3 tunes effector T cell reliance on environmental cues for optimal exploration of inflamed tissues.

Lysophosphatidic acid (LPA) and the LPA-generating enzyme autotaxin (ATX) have been implicated in lymphocyte trafficking and the regulation of lymphocyte entry into lymph nodes. High local concentrations of LPA are thought to be present in lymph node high endothelial venules, suggesting a direct influence of LPA on cell migration. However, little is known about the mechanism of action of LPA, and more work is needed to define the expression and function of the six known G protein-coupled receptors (LPA 1–6) in T cells. We studied the effects of 18∶1 and 16∶0 LPA on naïve CD4+ T cell migration and show that LPA induces CD4+ T cell chemorepulsion in a Transwell system, and also improves the quality of non-directed migration on ICAM-1 and CCL21 coated plates. Using intravital two-photon microscopy, lpa2−/− CD4+ T cells display a striking defect in early migratory behavior at HEVs and in lymph nodes. However, later homeostatic recirculation and LPA-directed migration in vitro were unaffected by loss of lpa2. Taken together, these data highlight a previously unsuspected and non-redundant role for LPA2 in intranodal T cell motility, and suggest that specific functions of LPA may be manipulated by targeting T cell LPA receptors.