Clinical Outcome of Deep Vein Thrombosis Is Related to Thrombophilic Risk Factors.

Deep vein thrombosis (DVT) and the associated possible complication of pulmonary artery embolism (LAE) represent a recognized reason for significant perioperative morbidity and mortality. There is a risk of pulmonary artery embolism through embolization. The aim of the study was to investigate the influence of various risk factors on the clinical outcome of the therapy, particularly regarding whether maintenance therapy offers a benefit in terms of the frequency of bleeding and thrombotic events. 80 patients were included, some of them retrospectively from July 2018. The observational period was set to 12 months after the DVT event. In the present sample with n = 80, with 57.5% men and 42.5% women (after 12 months of observation: n = 78), a success rate of the therapies administered of 89.7% was recorded. Only 8.9% showed partial recanalization. 3.8% of the patients had a relapse (also beyond the localization of the leg and pelvic veins) and 8.8% had a residual thrombus during the first 12 months of observation. In this study, BARC (Bleeding Academic Research Consortium) and HAS-BLED (Hypertension, Abnormal renal and liver function, Stroke, Bleeding, Labile INR, Elderly, Drugs or alcohol) scores for identifying the risk of bleeding and Wells scores for assessing the risk of having a thrombosis were used. The Villalta score tested in this study showed significant correlations with residual thrombus (P < .001), recurrence within 12 months (P < .001), and the risk of bleeding (P < .001) and is capable to provide an assessment of the variables mentioned not only at the possible end of therapy but also at the start of anticoagulant therapy.

The serotonin transporter expression in Drosophila melanogaster.

The serotonin transporter is an important regulator of serotonergic signaling. In order to analyze where the Drosophila melanogaster ortholog of the mammalian serotonin transporter (dSERT) is expressed in the nervous system, a dSERT antibody serum was used. Ectopic expression studies and loss of function analysis revealed that the dSERT antibody serum specifically recognizes dSERT. It was shown that in the embryonic nervous system dSERT is expressed in a subset of Engrailed-positive neurons. In the larval brain, dSERT is exclusively expressed in serotonergic neurons, all of which express dSERT. dSERT-positive neurons surround almost all brain neuropiles. In the mushroom body of the adult brain, extrinsic serotonergic neurons expressing dSERT engulf the mushroom body lobes. These neurons show regional differences in dSERT and serotonin expression. At the presynaptic terminals, serotonin release is sterically linked to serotonin reuptake. In contrast to this, there are other areas in serotonergic neurons where dSERT expression and/or function are uncoupled from synaptic neurotransmitter recycling and serotonin release. The localization pattern of dSERT can be employed to further understanding and analysis of serotonergic networks.

Thrombin stimulation of p38 MAP kinase in human platelets is mediated by ADP and thromboxane A2 and inhibited by cGMP/cGMP-dependent protein kinase.

p38 MAP kinase in human platelets is activated by platelet agonists including thrombin, thromboxane A2 (TxA2), ADP, and others. However, both upstream mechanisms of p38 MAP kinase activation, and their downstream sequelae, are presently controversial and essentially unclear. Certain studies report sequential activation of cGMP-dependent protein kinase (PKG) and p38/ERK pathways by platelet agonists, leading to integrin activation and secretion, whereas others establish an essential role of Src/ERK-mediated TxA2 generation for fibrinogen receptor activation in human platelets. Here, we show that ADP secreted from platelet-dense granules, and subsequent activation of P2Y12 receptors, as well as TxA2 release are important upstream mediators of p38 MAP kinase activation by thrombin. However, p38 MAP kinase activation did not significantly contribute to calcium mobilization, P-selectin expression, alphaIIbbeta3 integrin activation, and aggregation of human platelets in response to thrombin. Finally, PKG activation did not stimulate, but rather inhibited, p38 MAP kinase in human platelets.