Anti-Oppression and Academia: Applying critical methodologies to study identity and student experiences in university settings

With increasing frequency we hear calls from activists and academics alike to tackle the structural roots of the current global social-ecological crisis. For those of us situated within academia, this provides an opportunity to critically examine how underlying processes related to the roots of this crisis manifest in and are perpetuated by our own institutions, and how to make academic programs within the ‘pipeline’ into environmental work more attractive and accessible to diverse voices. Traditional academic research often reinforces negative power structures, and so it is necessary to explore anti-oppressive research methodologies to tackle these structural roots. Thus, this thesis examines how identity shapes student experiences, including our own, in the context of Lund University’s master’s program in Human Ecology - Culture, Power and Sustainability (CPS), with an eye to the development of an activist-academic research collective. Via a methodological and epistemological foundation rooted in feminist theory, critical race theory, anti-oppression, queer methodologies, and participatory action research, we conducted 17 open-ended interviews and two focus groups with current and former CPS students while emphasizing ongoing consent, collaborative participation, and constant methodological self-reflection. Our results reveal a number of themes in student experiences that we connect to broader phenomena. We identify perceived institutional mis/mal-recognition of CPS due to the program’s critiques of the status quo and leftist environmentalist perspectives, but increased positive recognition of activist/leftist/politicized identities within our program’s community. Interpersonal dynamics in the classroom tended to reproduce broader power structures (such as sexism, racism, classism and ableism), which some respondents attributed to the unstructured nature of class discussion. There is a strong desire amongst respondents to engage with non-university communities and for opportunities for environmental justice-oriented practical research. We conclude by identifying potential focuses for an activist-academic research collective and recommendations for the Lund Human Ecology division with relevance for academic institutions in general. The thesis also includes considerable methodological reflections - relevant for anyone interested in conducting anti-oppressive research within their own community

Delayed wound repair in sepsis is associated with reduced local pro-inflammatory cytokine expression

Sepsis is one of the main causes for morbidity and mortality in hospitalized patients. Moreover, sepsis associated complications involving impaired wound healing are common. Septic patients often require surgical interventions that in-turn may lead to further complications caused by impaired wound healing. We established a mouse model to the study delayed wound healing during sepsis distant to the septic focus point. For this reason cecal ligation and puncture (CLP) was combined with the creation of a superficial wound on the mouse ear. Control animals received the same procedure without CPL. Epithelialization was measured every second day by direct microscopic visualization up to complete closure of the wound. As interplay of TNF-α, TGF-β, matrix metalloproteinases (MMP), and tissue inhibitors of metalloproteinases (TIMP) is important in wound healing in general, TNF-α, TGF-β, MMP7, and TIMP1 were assessed immunohistochemical in samples of wounded ears harvested on days 2, 6, 10 and 16 after wounding. After induction of sepsis, animals showed a significant delay in wound epithelialization from day 2 to 12 compared to control animals. Complete wound healing was attained after mean 12.2± standard deviation (SD) 3.0 days in septic animals compared to 8.7± SD 1.7 days in the control group. Septic animals showed a significant reduction in local pro-inflammatory cytokine level of TNF-α on day 2 and day 6 as well as a reduced expression of TGF-β on day 2 in wounds. A significant lower expression of MMP7 as well as TIMP1 was also observed on day 2 after wounding. The induction of sepsis impairs wound healing distant to the septic focus point. We could demonstrate that expression of important cytokines for wound repair is deregulated after induction of sepsis. Thus restoring normal cytokine response locally in wounds could be a good strategy to enhance wound repair in sepsis

The Microvascular System of the Striate and Extrastriate Visual Cortex of the Macaque

In functional neuroimaging, neurovascular coupling is used to generate maps of hemodynamic changes that are assumed to be surrogates of regional neural activation. The aim of this study was to characterize the microvascular system of the primate cortex as a basis for understanding the constraints imposed on a region's hemodynamic response by the vascular architecture, density, as well as area- and layer-specific variations. In the macaque visual cortex, an array of anatomical techniques has been applied, including corrosion casts, immunohistochemistry, and cytochrome oxidase (COX) staining. Detailed measurements of regional vascular length density, volume fraction, and surface density revealed a similar vascularization in different visual areas. Whereas the lower cortical layers showed a positive correlation between the vascular and cell density, this relationship was very weak in the upper layers. Synapse density values taken from the literature also displayed a very moderate correlation with the vascular density. However, the vascular density was strongly correlated with the steady-state metabolic demand as measured by COX activity. This observation suggests that although the number of neurons and synapses determines an upper bound on an area's integrative capacity, its vascularization reflects the neural activity of those subpopulations that represent a "default” mode of brain steady stat

Dynamics of refugee settlements and energy provision: the case of forest stocks in Zambia

Purpose – This article aims to investigate the impact of (1) the establishment of a refugee settlement, (2) the energy demand of a host and refugee population, (3) the residence time of refugees and (4) interventions in the energy sector on sustainable utilization of the forest. Design/methodology/approach – Refugee movements from the Democratic Republic of Congo and settlement construction in a Zambian host society provide the setting. An agent-based model is developed. It uses survey data from 277 Zambian households, geographic information system coordinates and supplementary data inputs. Findings – The future forest stock remains up to 30 years without an influx of refugees. Refugee developments completely deplete the forest over time. The settlement construction severely impacts the forest, while refugees' energy needs seem less significant. Compared with the repatriation of refugees, permanent integration has no influential impact on forest resources. Interventions in the energy sector through alternative sources slow down deforestation. Once a camp is constructed, tree cutting by hosts causes forest covers to decline even if alternative energy is provided. Practical implications – The analysis is useful for comparable host–refugee settings and United Nations High Commissioner for Refugees interventions in settlement situations. Forest and energy sector interventions should involve host and refugee stakeholders. Originality/value – This article adds value through an agent-based model in the Zambian deforestation–refugee context. The study has a pilot character within the United Nation's Comprehensive Refugee Response Framework. It fills a gap in long-term assessments of refugee presence in local host communities

Hemipiperazines as peptide-derived molecular photoswitches with low-nanomolar cytotoxicity

The development of photochromic systems is an important and growing area of research, in particular for bioactive molecular photoswitches. Here, the authors report on photopharmacological antimitotic agents, operational under visible light, based on a peptide-derived hemipiperazine photochrome. Molecular photoswitches transform light energy into reversible structural changes. Their combination with known pharmacophores often allows for photomodulation of the biological activity. The effort to apply such compounds in photopharmacology as light-activated pro-drugs is, however, hampered by serious activity reduction upon pharmacophore modifications, or limited biostability. Here we report that a potent antimitotic agent plinabulin and its derivatives demonstrate up to 56-fold reversible activity photomodulation. Alternatively, irreversible photoactivation with cyan light can enhance the cytotoxicity up to three orders of magnitude-all without compromising the original activity level, as the original pharmacophore structure is unchanged. This occurs due to the presence of a peptide-derived photoswitchable motif hemipiperazine inside the plinabulin scaffold. Furthermore, we systematically describe photochromism of these thermally stable and biocompatible hemipiperazines, as well as a photoswitchable fluorophore derived from plinabulin. The latter may further expand the applicability of hemipiperazine photochromism towards super-resolution microscopy.Peer reviewe

Hemipiperazines as peptide-derived molecular photoswitches with low-nanomolar cytotoxicity

The development of photochromic systems is an important and growing area of research, in particular for bioactive molecular photoswitches. Here, the authors report on photopharmacological antimitotic agents, operational under visible light, based on a peptide-derived hemipiperazine photochrome. Molecular photoswitches transform light energy into reversible structural changes. Their combination with known pharmacophores often allows for photomodulation of the biological activity. The effort to apply such compounds in photopharmacology as light-activated pro-drugs is, however, hampered by serious activity reduction upon pharmacophore modifications, or limited biostability. Here we report that a potent antimitotic agent plinabulin and its derivatives demonstrate up to 56-fold reversible activity photomodulation. Alternatively, irreversible photoactivation with cyan light can enhance the cytotoxicity up to three orders of magnitude-all without compromising the original activity level, as the original pharmacophore structure is unchanged. This occurs due to the presence of a peptide-derived photoswitchable motif hemipiperazine inside the plinabulin scaffold. Furthermore, we systematically describe photochromism of these thermally stable and biocompatible hemipiperazines, as well as a photoswitchable fluorophore derived from plinabulin. The latter may further expand the applicability of hemipiperazine photochromism towards super-resolution microscopy.Peer reviewe

Liquid spherical shells are a non-equilibrium steady state of active droplets

Liquid-liquid phase separation yields spherical droplets that eventually coarsen to one large, stable droplet governed by the principle of minimal free energy. In chemically fueled phase separation, the formation of phase-separating molecules is coupled to a fuel-driven, non-equilibrium reaction cycle. It thus yields dissipative structures sustained by a continuous fuel conversion. Such dissipative structures are ubiquitous in biology but are poorly understood as they are governed by non-equilibrium thermodynamics. Here, we bridge the gap between passive, close-to-equilibrium, and active, dissipative structures with chemically fueled phase separation. We observe that spherical, active droplets can undergo a morphological transition into a liquid, spherical shell. We demonstrate that the mechanism is related to gradients of short-lived droplet material. We characterize how far out of equilibrium the spherical shell state is and the chemical power necessary to sustain it. Our work suggests alternative avenues for assembling complex stable morphologies, which might already be exploited to form membraneless organelles by cells

Acute mental stress drives vascular inflammation and promotes plaque destabilization in mouse atherosclerosis

Publisher Copyright: © 2021 The Author(s). Published by Oxford University Press on behalf of the European Society of Cardiology.Aims: Mental stress substantially contributes to the initiation and progression of human disease, including cardiovascular conditions. We aim to investigate the underlying mechanisms of these contributions since they remain largely unclear. Methods and results: Here, we show in humans and mice that leucocytes deplete rapidly from the blood after a single episode of acute mental stress. Using cell-tracking experiments in animal models of acute mental stress, we found that stress exposure leads to prompt uptake of inflammatory leucocytes from the blood to distinct tissues including heart, lung, skin, and, if present, atherosclerotic plaques. Mechanistically, we found that acute stress enhances leucocyte influx into mouse atherosclerotic plaques by modulating endothelial cells. Specifically, acute stress increases adhesion molecule expression and chemokine release through locally derived norepinephrine. Either chemical or surgical disruption of norepinephrine signalling diminished stress-induced leucocyte migration into mouse atherosclerotic plaques. Conclusion: Our data show that acute mental stress rapidly amplifies inflammatory leucocyte expansion inside mouse atherosclerotic lesions and promotes plaque vulnerability.publishersversionPeer reviewe