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    “I Ran to the Comments”: Social Media Culture, Hate-Speech, and Hyperreality

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    While social media has allowed our world to become more interconnected and informed on global issues than ever. It has also aroused much criticism in the way it facilitates unrestricted hate-speech and violent rhetoric, especially towards historically oppressed groups. While the abundance of hate-speech online may be credited to the facelessness facilitated by internet profiles that negates accountability, this essay argues that there is a more cognitive and deeper explanation for how people are able to engage so violently with one another online. It will explain this through the framework of Baudrillard’s “Simulacra and Simulation”, elaborating that this discourse on social media exists within a hyperreality in which people are trained to jump to comment in a discriminatory way as soon as they witness the existence of a represents historical traits of otherness. The essay situates this idea of otherness in literature concerning the social architecture of gender, race and sexuality. Due to this process of reproduction of information, people are able to comment so aggressively as they are not witnessing another human being but instead, through the hyperreality they are only witnessing an image of a historically category of other, and thus they do not authentically engage with what they see but instead play into the simulation

    Meta-skills: exciting opportunity or neo-liberal retread?

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    The term Meta-skills has become prominent in education in the last decade and, in Scotland, has increasingly been seen at the forefront of policy agendas. Based on the idea of Metacognition, and so claiming to derive from evidence of Psychology and Cognitive Science, the Meta-skills concept seems to offer an exciting and quintessentially 21st century opportunity.  Or does it? Is the idea coherent and evidence-based? Indeed, is it new or merely a rebranding of those key/core/transferable/soft skills that have been contested since the 1980s?  Does it represent a further neo-liberal strategy to vocationalise education, prioritising making learners ‘ready for the market’? This paper asks what are Meta-skills and what do they have to offer (or threaten) to those working in adult education

    Transient Receptor Potential channels (TRP) in GtoPdb v.2025.1

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    The TRP superfamily of channels (nomenclature as agreed by NC-IUPHAR [177, 1080]), whose founder member is the Drosophila Trp channel, exists in mammals as six families; TRPC, TRPM, TRPV, TRPA, TRPP and TRPML based on amino acid homologies. TRP subunits contain six putative TM domains and assemble as homo- or hetero-tetramers to form cation selective channels with diverse modes of activation and varied permeation properties (reviewed by [734]). Established, or potential, physiological functions of the individual members of the TRP families are discussed in detail in the recommended reviews and in a number of books [404, 690, 1163, 258]. The established, or potential, involvement of TRP channels in disease [1134] is reviewed in [452, 689], [692] and [468], together with a special edition of Biochemica et Biophysica Acta on the subject [689]. Additional disease related reviews, for pain [637], stroke [1143], sensation and inflammation [994], itch [130], and airway disease [313, 1058], are available. The pharmacology of most TRP channels has been advanced in recent years. Broad spectrum agents are listed in the tables along with more selective, or recently recognised, ligands that are flagged by the inclusion of a primary reference. See Rubaiy (2019) for a review of pharmacological tools for TRPC1/C4/C5 channels [810]. Most TRP channels are regulated by phosphoinostides such as PtIns(4,5)P2 although the effects reported are often complex, occasionally contradictory, and likely to be dependent upon experimental conditions, such as intracellular ATP levels (reviewed by [1015, 693, 806]). Such regulation is generally not included in the tables.When thermosensitivity is mentioned, it refers specifically to a high Q10 of gating, often in the range of 10-30, but does not necessarily imply that the channel\u27s function is to act as a \u27hot\u27 or \u27cold\u27 sensor. In general, the search for TRP activators has led to many claims for temperature sensing, mechanosensation, and lipid sensing. All proteins are of course sensitive to energies of binding, mechanical force, and temperature, but the issue is whether the proposed input is within a physiologically relevant range resulting in a response. TRPA (ankyrin) familyTRPA1 is the sole mammalian member of this group (reviewed by [295]). TRPA1 activation of sensory neurons contribute to nociception [417, 895, 606]. Pungent chemicals such as mustard oil (AITC), allicin, and cinnamaldehyde activate TRPA1 by modification of free thiol groups of cysteine side chains, especially those located in its amino terminus [579, 60, 368, 581]. Alkenals with α, β-unsaturated bonds, such as propenal (acrolein), butenal (crotylaldehyde), and 2-pentenal can react with free thiols via Michael addition and can activate TRPA1. However, potency appears to weaken as carbon chain length increases [26, 60]. Covalent modification leads to sustained activation of TRPA1. Chemicals including carvacrol, menthol, and local anesthetics reversibly activate TRPA1 by non-covalent binding [428, 515, 1089, 1088]. TRPA1 is not mechanosensitive under physiological conditions, but can be activated by cold temperatures [429, 213]. The electron cryo-EM structure of TRPA1 [745] indicates that it is a 6-TM homotetramer. Each subunit of the channel contains two short ‘pore helices’ pointing into the ion selectivity filter, which is big enough to allow permeation of partially hydrated Ca2+ ions. TRPC (canonical) familyMembers of the TRPC subfamily (reviewed by [286, 783, 18, 4, 94, 450, 744, 70]) fall into the subgroups outlined below. TRPC2 is a pseudogene in humans. It is generally accepted that all TRPC channels are activated downstream of Gq/11-coupled receptors, or receptor tyrosine kinases (reviewed by [770, 959, 1080]). A comprehensive listing of G-protein coupled receptors that activate TRPC channels is given in [4]. Hetero-oligomeric complexes of TRPC channels and their association with proteins to form signalling complexes are detailed in [18] and [451]. TRPC channels have frequently been proposed to act as store-operated channels (SOCs) (or compenents of mulimeric complexes that form SOCs), activated by depletion of intracellular calcium stores (reviewed by [746, 18, 775, 825, 1129, 157, 730, 64, 158]). However, the weight of the evidence is that they are not directly gated by conventional store-operated mechanisms, as established for Stim-gated Orai channels. TRPC channels are not mechanically gated in physiologically relevant ranges of force. All members of the TRPC family are blocked by 2-APB and SKF96365 [350, 349]. Activation of TRPC channels by lipids is discussed by [70]. Important progress has been recently made in TRPC pharmacology [810, 623, 440, 102, 856, 192, 293]. TRPC channels regulate a variety of physiological functions and are implicated in many human diseases [298, 71, 890, 1038, 1032, 154, 103, 565, 918, 412]. TRPC1/C4/C5 subgroup TRPC1 alone may not form a functional ion channel [230]. The structures of the apo and antagonist-bound states of TRPC1/TRPC4 heteromeric channels have been resolved by cryo-EM [1070]. TRPC4/C5 may be distinguished from other TRP channels by their potentiation by micromolar concentrations of La3+. TRPC2 is a pseudogene in humans, but in other mammals appears to be an ion channel localized to microvilli of the vomeronasal organ. It is required for normal sexual behavior in response to pheromones in mice. It may also function in the main olfactory epithelia in mice [1122, 727, 728, 1123, 543, 1176, 1117].TRPC3/C6/C7 subgroup All members are activated by diacylglycerol independent of protein kinase C stimulation [350].TRPM (melastatin) familyMembers of the TRPM subfamily (reviewed by [277, 349, 746, 1159]) fall into the five subgroups outlined below. TRPM1/M3 subgroupIn darkness, glutamate released by the photoreceptors and ON-bipolar cells binds to the metabotropic glutamate receptor 6 , leading to activation of Go . This results in the closure of TRPM1. When the photoreceptors are stimulated by light, glutamate release is reduced, and TRPM1 channels are more active, resulting in cell membrane depolarization. Human TRPM1 mutations are associated with congenital stationary night blindness (CSNB), whose patients lack rod function. TRPM1 is also found melanocytes. Isoforms of TRPM1 may present in melanocytes, melanoma, brain, and retina. In melanoma cells, TRPM1 is prevalent in highly dynamic intracellular vesicular structures [401, 712]. TRPM3 (reviewed by [718]) exists as multiple splice variants which differ significantly in their biophysical properties. TRPM3 is expressed in somatosensory neurons and may be important in development of heat hyperalgesia during inflammation (see review [947]). TRPM3 is frequently coexpressed with TRPA1 and TRPV1 in these neurons. TRPM3 is expressed in pancreatic beta cells as well as brain, pituitary gland, eye, kidney, and adipose tissue [717, 946]. TRPM3 may contribute to the detection of noxious heat [1024]. TRPM2TRPM2 is activated under conditions of oxidative stress (respiratory burst of phagocytic cells). The direct activators are calcium, adenosine diphosphate ribose (ADPR) [976] and cyclic ADPR (cADPR) [1126]. As for many ion channels, PI(4,5)P2 must also be present [1117]. Numerous splice variants of TRPM2 exist which differ in their activation mechanisms [240]. Recent studies have reported structures of human (hs) TRPM2, which demonstrate two ADPR binding sites in hsTRPM2, one in the N-terminal MHR1/2 domain and the other in the C-terminal NUDT9-H domain. In addition, one Ca2+ binding site in the intracellular S2-S3 loop is revealed and proposed to mediate Ca2+ binding that induces conformational changes leading the ADPR-bound closed channel to open [390, 1034]. Meanwhile, a quadruple-residue motif (979FGQI982) was identified as the ion selectivity filter and a gate to control ion permeation in hsTRPM2 [1128]. TRPM2 is involved in warmth sensation [853], and contributes to several diseases [76]. TRPM2 interacts with extra synaptic NMDA receptors (NMDAR) and enhances NMDAR activity in ischemic stroke [1172]. Activation of TRPM2 in macrophages promotes atherosclerosis [1173, 1155]. Moreover, silica nanoparticles induce lung inflammation in mice via ROS/PARP/TRPM2 signaling-mediated lysosome impairment and autophagy dysfunction [1035]. Recent studies have designed various compounds for their potential to selectively inhibit the TRPM2 channel, including ACA derivatives A23, and 2,3-dihydroquinazolin-4(1H)-one derivatives [1145, 1147]. TRPM4/5 subgroupTRPM4 and TRPM5 have the distinction within all TRP channels of being impermeable to Ca2+ [1080]. A splice variant of TRPM4 (i.e.TRPM4b) and TRPM5 are molecular candidates for endogenous calcium-activated cation (CAN) channels [330]. TRPM4 is active in the late phase of repolarization of the cardiac ventricular action potential. TRPM4 deletion or knockout enhances beta adrenergic-mediated inotropy [597]. Mutations are associated with conduction defects [407, 597, 884]. TRPM4 has been shown to be an important regulator of Ca2+ entry in to mast cells [999] and dendritic cell migration [52]. TRPM5 in taste receptor cells of the tongue appears essential for the transduction of sweet, amino acid and bitter stimuli [541] TRPM5 contributes to the slow afterdepolarization of layer 5 neurons in mouse prefrontal cortex [517]. Both TRPM4 and TRPM5 are required transduction of taste stimuli [247]. TRPM6/7 subgroupTRPM6 and 7 combine channel and enzymatic activities (‘chanzymes’) [173]. These channels have the unusual property of permeation by divalent (Ca2+, Mg2+, Zn2+) and monovalent cations, high single channel conductances, but overall extremely small inward conductance when expressed to the plasma membrane. They are inhibited by internal Mg2+ at ~0.6 mM, around the free level of Mg2+ in cells. Whether they contribute to Mg2+ homeostasis is a contentious issue. PIP2 is required for TRPM6 and TRPM7 activation [815, 1085]. When either gene is deleted in mice, the result is embryonic lethality [416, 1073]. The C-terminal kinase region of TRPM6 and TRPM7 is cleaved under unknown stimuli, and the kinase phosphorylates nuclear histones [483, 484]. TRPM7 is responsible for oxidant- induced Zn2+ release from intracellular vesicles [3] and contributes to intestinal mineral absorption essential for postnatal survival [626]. The putative metal transporter proteins CNNM1-4 interact with TRPM7 and regulate TRPM7 channel activity [40, 471]. TRPM8Is a channel activated by cooling and pharmacological agents evoking a ‘cool’ sensation and participates in the thermosensation of cold temperatures [63, 179, 225] reviewed by [1017, 566, 461, 653]. Direct chemical agonists include menthol and icilin[1094]. Besides, linalool can promote ERK phosphorylation in human dermal microvascular endothelial cells, down-regulate intracellular ATP levels, and activate TRPM8 [68]. Recent studies have found that TRPM8 has typical S4-S5 connectomes with clear selective filters and exowell rings [516], and have identified cryo-electron microscopy structures of mouse TRPM8 in closed, intermediate, and open states along the ligand- and PIP2-dependent gated pathways [1119]. Moreover, the last 36 amino acids at the carboxyl terminal of TRPM8 are key protein sequences for TRPM8\u27s temperature-sensitive function [195]. TRPM8 deficiency reduced the expression of S100A9 and increased the expression of HNF4α in the liver of mice, which reduced inflammation and fibrosis progression in mice with liver fibrosis, and helped to alleviate the symptoms of bile duct disease [560]. Channel deficiency also shortens the time of hypersensitivity reactions in migraine mouse models by promoting the recovery of normal sensitivity [12]. A cyclic peptide DeC‐1.2 was designed to inhibit ligand activation of TRPM8 but not cold activation, which can eliminate the side effects of cold dysalgesia in oxaliplatin-treated mice without changing body temperature [9]. Analysis of clinical data shows that TRPM8-specific blockers WS12 can reduce tumor growth in colorectal cancer xenografted mice by reducing transcription and activation of Wnt signaling regulators and β-catenin and its target oncogenes, such as C-Myc and Cyclin D1 [736]. TRPML (mucolipin) familyThe TRPML family [787, 1140, 780, 1092, 191] consists of three mammalian members (TRPML1-3). TRPML channels are probably restricted to intracellular vesicles and mutations in the gene (MCOLN1) encoding TRPML1 (mucolipin-1) cause the neurodegenerative disorder mucolipidosis type IV (MLIV) in man. TRPML1 is a cation selective ion channel that is important for sorting/transport of endosomes in the late endocytotic pathway and specifically, fission from late endosome-lysosome hybrid vesicles and lysosomal exocytosis [827]. TRPML2 and TRPML3 show increased channel activity in low luminal sodium and/or increased luminal pH, and are activated by similar small molecules [322, 147, 882]. A naturally occurring gain of function mutation in TRPML3 (i.e. A419P) results in the varitint waddler (Va) mouse phenotype (reviewed by [787, 694]). TRPP (polycystin) familyThe TRPP family (reviewed by [217, 215, 303, 1068, 377]) or PKD2 family is comprised of PKD2 (PC2), PKD2L1 (PC2L1), PKD2L2 (PC2L2), which have been renamed TRPP1, TRPP2 and TRPP3, respectively [1080]. It should also be noted that the nomenclature of PC2 was TRPP2 in old literature. However, PC2 has been uniformed to be called TRPP2 [348]. PKD2 family channels are clearly distinct from the PKD1 family, whose function is unknown. PKD1 and PKD2 form a hetero-oligomeric complex with a 1:3 ratio. [910]. Although still being sorted out, TRPP family members appear to be 6TM spanning nonselective cation channels. TRPV (vanilloid) familyMembers of the TRPV family (reviewed by [1001]) can broadly be divided into the non-selective cation channels, TRPV1-4 and the more calcium selective channels TRPV5 and TRPV6. TRPV1-V4 subfamilyTRPV1 is involved in the development of thermal hyperalgesia following inflammation and may contribute to the detection of noxius heat (reviewed by [767, 887, 927]). Numerous splice variants of TRPV1 have been described, some of which modulate the activity of TRPV1, or act in a dominant negative manner when co-expressed with TRPV1 [849]. The pharmacology of TRPV1 channels is discussed in detail in [332] and [1022]. TRPV2 is probably not a thermosensor in man [740], but has recently been implicated in innate immunity [551]. Functional TRPV2 expression is described in placental trophoblast cells of mouse [205]. TRPV3 and TRPV4 are both thermosensitive. There are claims that TRPV4 is also mechanosensitive, but this has not been established to be within a physiological range in a native environment [127, 534]. TRPV5/V6 subfamily TRPV5 and TRPV6 are highly expressed in placenta, bone, and kidney. Under physiological conditions, TRPV5 and TRPV6 are calcium selective channels involved in the absorption and reabsorption of calcium across intestinal and kidney tubule epithelia (reviewed by [1064, 206, 655, 272]).TRPV6 is reported to play a key role in calcium transport in the mouse placenta [1063]

    SLC8 family of sodium/calcium exchangers in GtoPdb v.2025.1

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    The sodium/calcium exchangers (NCX) use the extracellular sodium concentration to facilitate the extrusion of calcium out of the cell. Alongside the plasma membrane Ca2+-ATPase (PMCA) and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), as well as the sodium/potassium/calcium exchangers (NKCX, SLC24 family), NCX allow recovery of intracellular calcium back to basal levels after cellular stimulation. When intracellular sodium ion levels rise, for example, following depolarisation, these transporters can operate in the reverse direction to allow calcium influx and sodium efflux, as an electrogenic mechanism. Structural modelling suggests the presence of 9 TM segments, with a large intracellular loop between the fifth and sixth TM segments [1]

    Pattern recognition receptors in GtoPdb v.2025.1

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    Pattern Recognition Receptors (PRRs, [118]) (nomenclature as agreed by NC-IUPHAR sub-committee on Pattern Recognition Receptors, [21]) participate in the innate immune response to microbial agents, the stimulation of which leads to activation of intracellular enzymes and regulation of gene transcription. PRRs express multiple leucine-rich regions to bind a range of microbially-derived ligands, termed PAMPs or pathogen-associated molecular patterns or endogenous ligands, termed DAMPS or damage-associated molecular patterns. These include peptides, carbohydrates, peptidoglycans, lipoproteins, lipopolysaccharides, and nucleic acids. PRRs include both cell-surface and intracellular proteins. PRRs may be divided into signalling-associated members, identified here, and endocytic members, the function of which appears to be to recognise particular microbial motifs for subsequent cell attachment, internalisation and destruction. Some are involved in inflammasome formation, and modulation of IL-1β cleavage and secretion, and others in the initiation of the type I interferon response. PRRs included in the Guide To PHARMACOLOGY are:Catalytic PRRs (see links below this overview)Toll-like receptors (TLRs)Nucleotide-binding oligomerization domain, leucine-rich repeat containing receptors (NLRs, also known as NOD (Nucleotide oligomerisation domain)-like receptors)RIG-I-like receptors (RLRs)Caspase 4 and caspase 5 Non-catalytic PRRsAbsent in melanoma (AIM)-like receptors (ALRs)C-type lectin-like receptors (CLRs)Other pattern recognition receptorsAdvanced glycosylation end-product specific receptor (RAGE

    ​​Data on the Mind:​ How the Data on the Use of Force in Psychiatry Interacts with Professional Judgment

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    Psychiatric clinicians and managers increasingly use data to monitor the use of force on psychiatric patients. In this study, we describe how Danish authorities simultaneously emphasise a need for close data monitoring and tell a story of failure: rather than reducing force, they claim that data monitoring of mechanical restraint has simply replaced this type of force with other types. We show here how the official narrative of failure is based on highly selective data practices. It inadequately conveys the efforts of the psychiatric staff, with potentially negative implications for the development of clinical judgment. While the authorities and many clinicians support continued data monitoring, we argue a need to rethink the role of data in relation to force and to better appreciate how data practices affect understandings of expertise. We base our analysis on policy papers and official reports on monitoring practices in Denmark, secondary analysis of data from these monitoring practices, as well as observations from and qualitative interviews with clinical managers, administrators and clinicians. By engaging these policies and practices, we point to a need for a new form of anthropological engagement with the data politics currently shaping psychiatric expertise.

    ​​MedTech in Tanzania:​ Reflecting and Making Judgments

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    Studying cutting-edge technologies in the domains of medicine built by Tanzanian experts operating on the margins of global techno-science has often led me to fall into a Manichean outlook. That is, seeing these processes in which technologies are built from rather than merely for the country, as either dispiriting evidence for another technological fix or as an encouraging sign pointing towards the building of new sovereign techno-science futures. Given our own expertise as social scientists, we are expected not to succumb to such binary reasoning and develop more sophisticated approaches. In this Position Piece, I propose that given the doggedness of such binaries that I suggest we might all be liable of falling into, we should work hard to develop a curiosity and reflectiveness about our own judgements and the process of making them.

    From ‘Freedom After Speech’ to ‘Freedom of Speech’: How Does a Spoiled Child Undermine Democracy on a Global Scale

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    In the aftermath of October 7, the world has intensified its focus on Israel\u27s genocidal policies in Palestine. With this issue gaining urgency, legal experts, scholars, and academics are rightly scrutinising whether Israel can be held accountable for war crimes, crimes against humanity, and genocide in international courts. However, the implications of this matter are far more overarching. In this paper, I will examine the impact of the unconditional support that Israel receives—particularly from Western countries, led by the United States— on democracy and the fundamental principle of freedom of speech. In this context, I will argue that the IHRA\u27s definition of anti-Semitism and its so-called illustrative examples are wielded like a Sword of Damocles over those who criticise Israeli governments, demonstrating how this corrupted version of anti-Semitism poses a threat as dangerous as bullets. By analysing real-world cases, I will explore how the concept of Chosen Trauma, introduced by political psychologist Vamik Volkan, is manipulated by Israeli government officials to exploit the Holocaust—one of the greatest tragedies in history—for political purposes. Finally, using real-world examples, I will reveal how specific forms of freedom of speech, such as media and academic freedom, are undermined through censorship, self-censorship, intimidation, and coercion. In an environment where even writing about such a topic is challenging, the aim of this study remains modest: to stand against pressures and threats with the most valuable weapon we possess in the 21st century—freedom of speech—and to encourage colleagues who share similar concerns to do the same

    Thinking Through Voice with a Somali (Love Doctor) Poet

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    During research on love songs and political poetry in Somaliland, one of my closest interlocutors has been a poet named Weedhsame who describes his work as arising from a duty to ‘give voice to the voiceless’. Collaborating with a musician and singer to ‘give voice’ to otherwise mute love-sufferers, Weedhsame is revered as a ‘love doctor’ whose words provide therapeutic relief to his ‘patients’. His political maanso poems also powerfully ‘give voice’—sonically and textually—to the otherwise inaudible concerns of marginalised communities. My conversations with Weedhsame have provided me with a compelling emic perspective on what it means to ‘give voice’ to others, and the intimately social work of vocal mediation. They have also challenged me to think about my own anthropological voicing practices. In this reflection, I use my conversations with Weedhsame to consider the politics and practices of ‘giving voice’ in Somaliland, in matters of love and politics, before turning these lessons back on my own practice. I focus especially on what these practices might mean for how anthropologists gather, assemble and sound the stories and ‘voices’ of others in our work

    Reckless Local and Ill-Fated Stranger: Reimagining Vietnamese National Sentiment during COVID-19

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    Since the beginning of the COVID-19 pandemic in Vietnam, the media has meticulously covered disease prevention and reported on infection cases. This article will explore the current and shifting gender relations of Vietnam’s state and societal expectations by comparing Patient 17, a female Vietnamese citizen, and Patient 91, a British male pilot. While Patient 91 has received sympathy and international acclaim, Patient 17 has been heavily criticised and shunned from Vietnamese society. Through these case studies, I seek to understand how individual patient cases reflect the nuances of nationalism in Vietnam and how online citizens interpret the quintessential traits of Vietnamese character. Drawing on media analyses from an online news outlet, I delve into themes of media representation, gender, class, and race. By exploring how media coverage and online commentators shape perceptions of these patients, I aim to shed light on how patient stories can transcend individual experiences and become emblematic of broader societal ideals

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