Becoming-Amazon: Femininity, Embodiment, and Sexuality in a Photographic and Digital Breast Cancer Project.

In recent decades, digital and photographic life narratives by women living with breast cancer and mastectomy have gained public visibility. This article examines how a documentary and fashion photography project in contemporary Berlin rethinks normative concepts of femininity, embodiment, and sexuality through the performance of the breast cancer patient as Amazon warrior. Based on feminist theory, disability studies, media studies, and in particular Gilles Deleuze's concept of becoming, I coin the term "becoming-Amazon" for the process of relational subjectivity formation that the project opens up. Uta Melle's project shifts notions of post-mastectomy bodies as unfeminine, incomplete, or asexual and envisions and celebrates a multiplicity of relational femininities, embodiments, and erotic zones with difference. By combining digital cancer activism and an aesthetics and politics of visibility, difference, and intercorporeality, Melle's project intervenes in contemporary cancer discourse and unsettles what has been considered as redemptive cancer culture.

Writing autohistoria-teoría: agency and illness in German life narratives by Evelyne Leandro and Mely Kiyak.

Health concerns by migrants have been neglected in the German healthcare system, and they are impacted by discriminating discourses of othering. By analysing two autobiographical illness narratives by immigrants in contemporary Germany, this article exposes limitations in existing discourses of migration health and argues for more relational and affirmative theories of illness and care. Evelyn Leandro's diary The Living Death: The Struggle with a Long-Forgotten Illness (2017) describes her own drawn-out therapy against leprosy as a Brazilian in Berlin. In Mr Kiyak Thought That the Best Part of His Life Will Start Now (2013), the Turkish-German journalist Mely Kiyak narrates her father's experience with advanced lung cancer in a German hospital. Drawing on medical anthropology, postcolonial theory and material (eco)feminism, I argue that these narratives establish migrant health and agency in transnational assemblages that include chemotherapy, lungs and skin, family networks, healthcare providers, food cultures and health policies. These assemblages of illness are connected with the narratives' hybrid and relational aesthetics and politics: similar to Gloria Anzaldúa's practice of autohistoria-teoría, I show how Kiyak's and Leandro's life writing combines personal and communal storytelling with critical theorising to include diverse voices, languages, histories and identities. By transgressing identities of self and other, German and foreign, patient and physician, human and non-human, the narratives inspire a greater sense of the extent to which (all) bodies, histories, cultures, technology and medicine are entangled in a dense network of relations. This article envisions a relational and hybrid ontology and aesthetics of migration health and thereby intervenes into the growing field of transcultural medicine and medical humanities.

Protective effect of an elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin oligodendroglial glycoprotein.

BACKGROUND: The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-ß treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with Th17 cells is exacerbated by IFN-ß, in contrast to disease induced with Th1 where treatment attenuated symptoms. OBJECTIVE: This study demonstrates the similarities between NMO and Th17 EAE and how neutrophils mediate pathology in Th17 disease. METHODS: Levels of blood biomarkers in NMO were assessed by Luminex and ELISA. Effects of IFN-ß on neutrophils were assessed by culture assays and immunofluorescence. EAE was induced by transfer of myelin-specific Th1 or Th17 cells and treated with Sivelestat sodium hydrate, a neutrophil elastase inhibitor. RESULTS: We show Th17 cytokines, granulocyte chemokines, type 1 interferon and neutrophil elastase are elevated in patients with definitive NMO. In culture, we find that IFN-ß stimulates neutrophils to release neutrophil elastase. In Th17 EAE, we demonstrate neutrophilic infiltration in the optic nerve and spinal cord which was not present in Th1 EAE. Blockade of neutrophil elastase with Sivelestat had efficacy in Th17 EAE but not Th1 EAE. CONCLUSIONS: The similarities between Th17 EAE and NMO indicate that this model represents several aspects of NMO. Neutrophils are critical in the pathologies of both Th17-EAE and NMO, and therefore blockade of neutrophil elastase is a promising target in treating NMO.

Attention Network Test reveals alerting network dysfunction in multiple sclerosis.

Attention is one of the cognitive domains typically affected in multiple sclerosis. The Attention Network Test was developed to measure the function of the three distinct attentional networks, alerting, orienting, and executive control. The Attention Network Test has been performed in various neuropsychiatric conditions, but not in multiple sclerosis. Our objective was to investigate functions of attentional networks in multiple sclerosis by means of the Attention Network Test. Patients with relapsing-remitting multiple sclerosis (n = 57) and healthy controls (n = 57) matched for age, sex, and education performed the Attention Network Test. Significant differences between patients and controls were detected in the alerting network (p = 0.003), in contrast to the orienting (p = 0.696) and the conflict (p = 0.114) network of visual attention. Mean reaction time in the Attention Network Test was significantly longer in multiple sclerosis patients than in controls (p = 0.032), Multiple sclerosis patients benefited less from alerting cues for conflict resolution compared with healthy controls. The Attention Network Test revealed specific alterations of the attention network in multiple sclerosis patients which were not explained by an overall cognitive slowing.

Reversal of paralysis and reduced inflammation from peripheral administration of ß-amyloid in TH1 and TH17 versions of experimental autoimmune encephalomyelitis.

ß-Amyloid 42 (Aß42) and ß-amyloid 40 (Aß40), major components of senile plaque deposits in Alzheimer's disease, are considered neurotoxic and proinflammatory. In multiple sclerosis, Aß42 is up-regulated in brain lesions and damaged axons. We found, unexpectedly, that treatment with either Aß42 or Aß40 peptides reduced motor paralysis and brain inflammation in four different models of experimental autoimmune encephalomyelitis (EAE) with attenuation of motor paralysis, reduction of inflammatory lesions in the central nervous system (CNS), and suppression of lymphocyte activation. Aß42 and Aß40 treatments were effective in reducing ongoing paralysis induced with adoptive transfer of either autoreactive T helper 1 (T(H)1) or T(H)17 cells. High-dimensional 14-parameter flow cytometry of peripheral immune cell populations after in vivo Aß42 and Aß40 treatment revealed substantial modulations in the percentage of lymphoid and myeloid subsets during EAE. Major proinflammatory cytokines and chemokines were reduced in the blood after Aß peptide treatment. Protection conferred by Aß treatment did not require its delivery to the brain: Adoptive transfer with lymphocytes from donors treated with Aß42 attenuated EAE in wild-type recipient mice, and Aß deposition in the brain was not detected in treated EAE mice by immunohistochemical analysis. In contrast to the improvement in EAE with Aß treatment, EAE was worse in mice with genetic deletion of the amyloid precursor protein. Therefore, in the absence of Aß, there is exacerbated clinical EAE disease progression. Because Aß42 and Aß40 ameliorate experimental autoimmune inflammation targeting the CNS, we might now consider its potential anti-inflammatory role in other neuropathological conditions.

Neuroprotective effect of combination therapy of glatiramer acetate and epigallocatechin-3-gallate in neuroinflammation.

Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central nervous system. However, studies of MS and the animal model, experimental autoimmune encephalomyelitis (EAE), indicate that neuronal pathology is the principle cause of clinical disability. Thus, there is need to develop new therapeutic strategies that not only address immunomodulation but also neuroprotection. Here we show that the combination therapy of Glatiramer acetate (GA), an immunomodulatory MS therapeutic, and the neuroprotectant epigallocatechin-3-gallate (EGCG), the main phenol in green tea, have synergistic protective effects in vitro and in the EAE model. EGCG and GA together led to increased protection from glutamate- and TRAIL-induced neuronal cell death in vitro. EGCG combined with GA induced regeneration of hippocampal axons in an outgrowth assay. The combined application of EGCG and GA did not result in unexpected adverse events in vivo. Neuroprotective and neuroregenerative effects could be translated in the in vivo model, where combination treatment with EGCG and GA significantly delayed disease onset, strongly reduced clinical severity, even after onset of symptoms and reduced inflammatory infiltrates. These results illustrate the promise of combining neuroprotective and anti-inflammatory treatments and strengthen the prospects of EGCG as an adjunct therapy for neuroinflammatory and neurodegenerative diseases.

Patterns of retinal nerve fiber layer loss in multiple sclerosis patients with or without optic neuritis and glaucoma patients.

OBJECTIVE: Optical coherence tomography (OCT) has gained increasing attention in multiple sclerosis (MS) research and has been suggested as outcome measure for neuroprotective therapies. However, to date it is not clear whether patterns of retinal nerve fiber layer thickness (RNFLT) loss are different in MS compared to other diseases such as glaucoma and data on RNFLT loss in MS patients with or without optic neuritis (ON/NON) have remained inconsistent or even contradictory. METHODS: In this large cross-sectional study we analyzed the patterns of axonal loss of retinal ganglion cells in MS eyes (n=262) with and without history of ON (MS/ON: 73 eyes; MS/NON: 189 eyes) and patients eyes with glaucomatous optic disc atrophy (GA: n=22; 39 eyes) in comparison to healthy control eyes (HC: n=406 eyes). RESULTS: We found that significant average and quadrant RNFLT loss is detectable by OCT in both MS and GA patients compared to healthy controls (p<0.01). The age- and gender adjusted average and quadrant RNFLT did not differ significantly between MS and GA patients (p>0.05). Average (p<0.0001) and quadrant (p<0.05) RNFL thinning is significantly more severe in MS/ON versus MS/NON eyes, and the extent of RNFL thinning varies across quadrants in MS/ON eyes with the highest degree of RNFLT loss in the temporal quadrant (p<0.001). CONCLUSION: RNFLT reduction across all four quadrants in MS patients as a whole as well as in MS/NON eyes argues for a diffuse neurodegenerative process. Superimposed inflammatory attacks to the optic nerve may cause additional axonal damage with a temporal preponderance. Future studies are necessary to further evaluate the capacity of OCT to depict disease specific damage patterns.