Passport to neoliberal normality? A critical exploration of COVID-19 vaccine passports.

Throughout the COVID-19 pandemic governments across the world including in France, Canada, Lithuania, Austria, Italy, and Ireland imposed ‘vaccine passports’ on the premise that they would curtail transmission of the virus, reduce COVID-19 related mortalities, and enable society to return to neoliberal normality. However, vaccine passports raise several important and troubling issues that have not been given sufficient attention within the social sciences. Therefore, this article offers a critique of vaccine passports. It is structured into three key themes: (a) scientifically and ethically problematic, (b) the death of the social and the ‘Other’, and (c) digital surveillance and freedom. The article begins by exploring how vaccine passports make little scientific sense and further entrench some unvaccinated peoples’ sense of political and medical mistrust. It then discusses how they amplify social divisions, creating the unvaccinated Other in society and intensifying the neoliberal shift towards a post-social, contactless world. The paper closes with an outline of how vaccine passports were cast as enabling a return to neoliberal normality and freedom, hinging upon an assumption of harmlessness while cementing the negative ideology of capitalist realism

Passport to Neoliberal Normality? A Critical Exploration of COVID-19 Vaccine Passports

Throughout the COVID-19 pandemic governments across the world including in France, Canada, Lithuania, Austria, Italy, and Ireland imposed ‘vaccine passports’ on the premise that they would curtail transmission of the virus, reduce COVID-19 related mortalities, and enable society to return to neoliberal normality. However, vaccine passports raise several issues that have not been given sufficient attention within the social sciences. Vaccine passports should be of criminological and zemiological concern because of their harmful consequences upon social relations, surveillance implications, as well as how they aid a return to neoliberal normality with all its criminogenic implications from corporate boardrooms to zones of permanent recession. Therefore, this article offers a critique of vaccine passports. It is structured into three key themes: (a) scientifically and ethically problematic, (b) the death of the social and the ‘Other’, and (c) digital surveillance and freedom. The paper begins by exploring how vaccine passports make little scientific sense and further entrench some unvaccinated peoples’ sense of political and medical mistrust. It then discusses how they amplify social divisions, creating the unvaccinated Other in society and intensifying the neoliberal shift towards a post-social, contactless world. The article closes with an outline of how vaccine passports were cast as enabling a return to neoliberalism and freedom, hinging upon an assumption of harmlessness while cementing the negative ideology of capitalist realism

Evaluation of Pharmaceutical Compounding Training in the Australian Undergraduate Pharmacy Curricula

Introduction: In recent decades the role of the Australian community pharmacist hasevolved to focus primarily on pharmaceutical care provision. Despite this, compounding remainsan important product service offered by pharmacists. The aim of this study was to qualitativelydescribe the current integration of training in compounding within Bachelor of Pharmacy courses inAustralia. Methods: The Australian Health Practitioner Regulatory Agency website was searchedto identify eligible university courses. Subsequently, the educational providers’ homepages wereconsulted, and Bachelor of Pharmacy handbooks and curricula perused. All relevant informationregarding training in compounding was extracted. Results: In total, 16 Bachelor of Pharmacy courseswere identified. All of these contain compounding training in their curricula, including laboratoryclasses. Most curricula have units specifically dedicated to compounding and drug formulation.Three universities offer a curriculum which is organ-systems based, and include compoundingrelevant to the individual organ systems. Discussion and Conclusions: In Australia, the training incompounding is well integrated into pharmacy curriculum and is more emphasised than in manyother developed countries. This is congruent with the International Pharmaceutical Federation’sneeds-based approach to local pharmacy education. In Australia there is a need for pharmacists toroutinely dispense simple compounded products. Further research is required to evaluate Australianpharmacy graduates’ compounding abilities and how best to promote the achievement of the requiredknowledge and skills to enable simple compounding

Mitogen-activated protein kinase phosphatase-2 deletion impairs synaptic plasticity and hippocampal-dependent memory

Mitogen-activated protein kinases (MAPKs) regulate brain function and their dysfunction is implicated in a number of brain disorders, including Alzheimer’s disease. Thus there is great interest in understanding the signalling systems that control MAPK function. One family of proteins that contribute to this process, the mitogen-activated protein kinase phosphatases (MKPs), directly inactivate MAPKs through dephosphorylation. Recent studies have identified novel functions of MKPs in development, the immune system and cancer. However, a significant gap in our knowledge remains in relation to their role in brain functioning. Here, using transgenic mice where the Dusp4 gene encoding MKP-2 has been knocked out (MKP-2-/- mice), we show that long-term potentiation (LTP) is impaired in MKP-2-/- mice compared to MKP-2+/+ controls whereas neuronal excitability, evoked synaptic transmission and paired-pulse facilitation remain unaltered. Furthermore, spontaneous excitatory postsynaptic currents (sEPSC) frequency was increased in acute slices and primary hippocampal cultures prepared from MKP-2-/- mice with no effect on EPSC amplitude observed. An increase in synapse number was evident in primary hippocampal cultures which may account for the increase in spontaneous EPSC frequency. In addition no change in ERK activity was detected in both brain tissue and primary hippocampal cultures, suggesting that the effects of MKP-2 deletion were MAPK independent. Consistent with these alterations in hippocampal function, MKP-2-/- mice show deficits in spatial reference and working memory when investigated using the Morris water maze. These data show that MKP-2 plays a role in regulating hippocampal function and that this effect may be independent of MAPK signalling

The human insulin receptor mRNA contains a functional internal ribosome entry segment.

Regulation of mRNA translation is an important mechanism determining the level of expression of proteins in eukaryotic cells. Translation is most commonly initiated by cap-dependent scanning, but many eukaryotic mRNAs contain internal ribosome entry segments (IRESs), providing an alternative means of initiation capable of independent regulation. Here, we show by using dicistronic luciferase reporter vectors that the 5'-UTR of the mRNA encoding human insulin receptor (hIR) contains a functional IRES. RNAi-mediated knockdown showed that the protein PTB was required for maximum IRES activity. Electrophoretic mobility shift assays confirmed that PTB1, PTB2 and nPTB, but not unr or PTB4, bound to hIR mRNA, and deletion mapping implicated a CCU motif 448 nt upstream of the initiator AUG in PTB binding. The IR-IRES was functional in a number of cell lines, and most active in cells of neuronal origin, as assessed by luciferase reporter assays. The IRES was more active in confluent than sub-confluent cells, but activity did not change during differentiation of 3T3-L1 fibroblasts to adipocytes. IRES activity was stimulated by insulin in sub-confluent cells. The IRES may function to maintain expression of IR protein in tissues such as the brain where mRNA translation by cap-dependent scanning is less effective

Anti-CD52 antibody treatment in murine experimental autoimmune encephalomyelitis induces dynamic and differential modulation of innate immune cells in peripheral immune and central nervous systems

Anti-CD52 antibody (anti-CD52-Ab) leads to a rapid depletion of T and B cells, followed by reconstitution of immune cells with tolerogenic characteristics. However, very little is known about its effect on innate immune cells. In this study, experimental autoimmune encephalomyelitis mice were administered murine anti-CD52-Ab to investigate its effect on dendritic cells and monocytes/macrophages in the periphery lymphoid organs and the central nervous system (CNS). Our data show that blood and splenic innate immune cells exhibited significantly increased expression of MHC-II and costimulatory molecules, which was associated with increased capacity of activating antigen-specific T cells, at first day but not three weeks after five daily treatment with anti-CD52-Ab in comparison with controls. In contrast to the periphery, microglia and infiltrating macrophages in the CNS exhibited reduced expression levels of MHC-II and costimulatory molecules after antibody treatment at both time-points investigated when compared to controls. Furthermore, the transit response of peripheral innate immune cells to anti-CD52-Ab treatment was also observed in the lymphocyte-deficient SCID mice, suggesting the changes are not a direct consequence of the mass depletion of lymphocytes in the periphery. Our study demonstrates a dynamic and tissue-specific modulation of the innate immune cells in their phenotype and function following the antibody treatment. The findings of differential modulation of the microglia and infiltrating macrophages in the CNS in comparison with the innate immune cells in the peripheral organs support the CNS-specific beneficial effect of alemtuzumab treatment on inhibiting neuroinflammation in multiple sclerosis patients

Phosphorylation of eIF4GII and 4E-BP1 in response to nocodazole treatment: a reappraisal of translation initiation during mitosis

Translation mechanisms at different stages of the cell cycle have been studied for many years, resulting in the dogma that translation rates are slowed during mitosis, with cap-independent translation mechanisms favored to give expression of key regulatory proteins. However, such cell culture studies involve synchronization using harsh methods, which may in themselves stress cells and affect protein synthesis rates. One such commonly used chemical is the microtubule de-polymerization agent, nocodazole, which arrests cells in mitosis and has been used to demonstrate that translation rates are strongly reduced (down to 30% of that of asynchronous cells). Using synchronized HeLa cells released from a double thymidine block (G 1/S boundary) or the Cdk1 inhibitor, RO3306 (G 2/M boundary), we have systematically re-addressed this dogma. Using FACS analysis and pulse labeling of proteins with labeled methionine, we now show that translation rates do not slow as cells enter mitosis. This study is complemented by studies employing confocal microscopy, which show enrichment of translation initiation factors at the microtubule organizing centers, mitotic spindle, and midbody structure during the final steps of cytokinesis, suggesting that translation is maintained during mitosis. Furthermore, we show that inhibition of translation in response to extended times of exposure to nocodazole reflects increased eIF2α phosphorylation, disaggregation of polysomes, and hyperphosphorylation of selected initiation factors, including novel Cdk1-dependent N-terminal phosphorylation of eIF4GII. Our work suggests that effects on translation in nocodazole-arrested cells might be related to those of the treatment used to synchronize cells rather than cell cycle status