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Analyzing the U.S. Drone Program’s Deployment of Armed Unmanned Aerial Vehicles (UAVs) for Targeted Killings Outside of National Boundaries
Get PDFFollowing the 9/11 attacks, U.S. counterterrorism efforts have gradually shifted focus from Afghanistan to regions like Pakistan, Yemen, and Somalia. The deployment of armed drones in these areas to target al-Qaeda members and their affiliates has sparked a contentious international law debate. While the U.S. drone policy claims adherence to international targeting rules, the reality of operations in remote locations has led to numerous civilian casualties. With a rising toll of civilian deaths, challenges in distinguishing between combatants and non-combatants, and concerns about accountability in drone operations, it seems that the approach taken by U.S. policymakers may have misconstrued existing laws governing hostilities. The policy lacks clarity on the applicable legal framework and necessary constraints to prevent potential misuse of drone technology, fostering a perception that the U.S. administration consistently employs armed drones without transparency or accountability.
Despite extensive literature on the 9/11 attacks and scholarly discussions on U.S. drone use, the alignment between rules governing targeting under international humanitarian law and the practical implementation of drone operations by the U.S. remains an area with limited examination in international law. Consequently, given issues related to civilian casualties, collateral damage, and potential violations of humanitarian law principles, it becomes crucial to evaluate whether U.S. targeting practices violate the law of armed conflict
Galanin receptors in GtoPdb v.2025.1
Get PDFGalanin receptors (provisional nomenclature as recommended by NC-IUPHAR [57]) are activated by the endogenous peptides galanin and galanin-like peptide. Human galanin is a 30 amino-acid non-amidated peptide [52]; in other species, it is 29 amino acids long and C-terminally amidated. Amino acids 1-14 of galanin are highly conserved in mammals, birds, reptiles, amphibia and fish. Shorter peptide species (e.g. human galanin-1-19 [21] and porcine galanin-5-29 [170]) and N-terminally extended forms (e.g. N-terminally seven and nine residue elongated forms of porcine galanin [22, 170]) have been reported. More recently, the newly-identified peptide, spexin (SPX), has been reported to activate human GAL2 and GAL3 (but not GAL1) receptors in heterologous expression systems; and to alter GAL2/3 receptor-related behaviours in animals [89]
Eicosanoid turnover in GtoPdb v.2025.1
Get PDFEicosanoids are 20-carbon fatty acids, where the usual focus is the polyunsaturated analogue arachidonic acid and its metabolites. Arachidonic acid is thought primarily to derive from phospholipase A2 action on membrane phosphatidylcholine, and may be re-cycled to form phospholipid through conjugation with coenzyme A and subsequently glycerol derivatives. Oxidative metabolism of arachidonic acid is conducted through three major enzymatic routes: cyclooxygenases; lipoxygenases and cytochrome P450-like epoxygenases, particularly CYP2J2. Isoprostanes are structural analogues of the prostanoids (hence the nomenclature D-, E-, F-isoprostanes and isothromboxanes), which are produced in the presence of elevated free radicals in a non-enzymatic manner, leading to suggestions for their use as biomarkers of oxidative stress. Molecular targets for their action have yet to be defined
Recast(e)ing Medicine in India: Contested Hierarchies of Expertise in Digital Primary Care
No full textIn this article, I examine a public-private partnership project in West Bengal, India, that trains and deploys people from marginalised castes as digital health workers in rural areas. Although digital technologies offer new opportunities for access to the medical sector, caste hierarchies inherent to the field persist, reinforcing and perpetuating caste-based inequities. This is evident in the division of labour, shaped by caste dynamics and justified through the distinction between professional knowledge and technical skill. The widely-used metaphors of the doctor—and by extension the software—as the mind, and the health workers as foot soldiers, rely on and further entrench long-standing hierarchies of expertise where privileged castes do knowledge work while marginalised castes literally do the footwork. Nevertheless, health workers actively challenge these hierarchies and foreground their creative contributions. While caste lives on in projects of ‘empowerment’, particularly through the limited and limiting imaginations of health workers’ structural position, health workers find ways to visibilise and value their labour and expertise. I argue that their assertions and aspirations may open up new possibilities for thinking about ‘empowerment’. Overall, recast(e)ing medicine implies that caste in the health sector is being simultaneously perpetuated and reimagined in ambivalent and partly contradictory ways
Doing Health in the Clinical Research Centre: Care Work in Choreographies of Data Production
No full textHealth examinations are an essential part of cohort studies: questionnaires are filled in, biological samples drawn, bodies weighed and measured, their capacities and functions tested. Drawing on an ethnography of these clinical encounters, in the context of a population-based environmental health cohort in Switzerland, I describe the choreography of data production and how it blurs the boundary between healthcare and scientific research. In contrast to the notion of clinical labour, which describes logics of objectification and extraction, this Field Note paints a more nuanced and sensitive picture, in which care work performed by nurses, the active role played by participants, and the materialities around them, come together and move apart. These fragile choreographies point to the importance of care work as a form of expertise necessary for data production.
Enforcing Restrictive Measures Against Russia Through Criminal Law: A Truly Effectiveness-Enhancing Choice?
Get PDFAdhesion Class GPCRs in GtoPdb v.2025.3
Get PDFAdhesion GPCRs are structurally identified on the basis of a large extracellular region, similar to the Class B GPCR, but which is linked to the 7TM region by a GPCR autoproteolysis-inducing (GAIN) domain [15] containing a GPCR proteolysis site (GPS). The N-terminal extracellular region often shares structural homology with adhesive domains (e.g. cadherins, immunolobulin, lectins) facilitating inter- and matricellular interactions and leading to the term adhesion GPCR [120, 468]. Several receptors have been suggested to function as mechanosensors [355, 322, 442, 49, 327]. Cryo-EM structures of the 7-transmembrane domain of several adhesion GPCRs have been determined recently [326, 31, 450, 241, 334, 336, 490, 327]. The nomenclature of these receptors was revised in 2015 as recommended by NC-IUPHAR and the Adhesion GPCR Consortium [145]
GABAB receptors in GtoPdb v.2025.3
Get PDFFunctional GABAB receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on GABAB receptors [11, 74]) are formed from the heterodimerization of two similar 7TM subunits termed GABAB1 and GABAB2 [11, 73, 29, 74, 90]. GABAB receptors are widespread in the CNS and regulate both pre- and postsynaptic activity. The GABAB1 subunit, when expressed alone, binds both antagonists and agonists, but the affinity of the latter is generally 10-100-fold less than for the native receptor. Co-expression of GABAB1 and GABAB2 subunits allows transport of GABAB1 to the cell surface and generates a functional receptor that can couple to signal transduction pathways such as high-voltage-activated Ca2+ channels (Cav2.1, Cav2.2), or inwardly rectifying potassium channels (Kir3) [12, 11, 5]. The GABAB1 subunit harbours the GABA (orthosteric)-binding site within an extracellular domain (ECD) venus flytrap module (VTM), whereas the GABAB2 subunit mediates G protein-coupled signalling [11, 73, 42, 41]. The cryo-electron microscopy structures of the human full-length GABAB1-GABAB2 heterodimer have been solved in the inactive apo state, two intermediate agonist-bound forms and an active state in which the heterodimer is bound to an agonist and a positive allosteric modulator [84]. Phospholipids bound within the central cavity of the transmembrane domains stabilize the inactive state. The positive allosteric modulator binds to the transmembrane interface and stabilizes the active state. Recent evidence indicates that higher order assemblies of GABAB receptors comprising dimers of heterodimers occur in recombinant expression systems and in vivo, and that such complexes exhibit negative functional cooperativity between heterodimers [72, 23]. Adding further complexity, KCTD (potassium channel tetramerization proteins) 8, 12, 12b and 16 associate as tetramers with the carboxy terminus of the GABAB2 subunit to impart altered signalling kinetics and agonist potency to the receptor complex [89, 3, 82] and are reviewed by [75]. The molecular complexity of GABAB receptors is further increased through association with trafficking and effector proteins [83] and reviewed by [71]. The predominant GABAB1a and GABAB1b isoforms, which are most prevalent in neonatal and adult brain tissue respectively, differ in their ECD sequences as a result of the use of alternative transcription initiation sites. GABAB1a-containing heterodimers localise to distal axons and mediate inhibition of glutamate release in the CA3-CA1 terminals, and GABA release onto the layer 5 pyramidal neurons, whereas GABAB1b-containing receptors occur within dendritic spines and mediate slow postsynaptic inhibition [77, 94]. Amyloid precursor protein (APP) and soluble APP (sAPP) bind to the N- terminal sushi domain of the GABAB1a isoform to regulate axonal trafficking of GABAB receptors and release of neurotransmitters [79]. AJAP1 (Q9UKB5) is a dendritic protein that trans-synaptically recruits GABAB1a-containing receptors to presynaptic sites [31]. Missense variants in GABABR and AJAP1 genes as well as autoantibodies link receptor dysfunction to neurodevelopmental disorders and epileptic encephalopathies [17, 31, 57]