Fandom

This entry presents an overview of the development and current state of fan studies, exploring the “reverse image” of media effects. The field of fan studies offers the ultimate rebuttal of the traditional media effects-model, by stressing the independence, agency and power of media consumers vis-à-vis media producers. After providing a short historiography of the discipline, this entry dives deeper into three themes that have been central to discussions within fan studies since its early beginnings: fan fiction, fan communities, and places of fandom

Description, Host-specificity, and Strain Selectivity of the Dinoflagellate Parasite Parvilucifera sinerae sp.nov. (Perkinsozoa)

17 pages, 7 figures, 2 tablesA new species of parasite, Parvilucifera sinerae sp. nov., isolated froma bloomof the toxic Dinoflagellate Alexandrium minutum in the harbor of Arenys de Mar (Mediterranean Sea, Spain), is described. This species is morphologically, behaviourally, and genetically (18S rDNA sequence) different from Parvilucifera infectans, until now the only species of the genus Parvilucifera to be genetically analyzed. Sequence análisis of the 18S ribosomal DNA supported P. Sinerae as a new species placed within the Perkinsozoa and close to P. infectans. Data on the seasonal occurrence of P. sinerae, its infective rates in natural and laboratory cultures, and intra-species strain-specific Resistance are presented. Life-cycle studies in field simples showed that the dinoflagellate resting zygote (restingcyst) was resistant to infection, but the mobile zygote (planozygote) orpelli clestage (temporary cyst) became infected. The effects of Light and salinity level son the growth of P. sinerae were examined, and the results showed that low salinity levels promote both sporangial germination and higher rates of infection. Our findings on this newly described parasite point to a complex host—parasite interaction and provide valuable information that leads to a reconsideration of the biological strategy to control dinoflagellate blooms by jeans of intentional parasitic infectionsThis research was funded by the EU Project SEED (GOCE-CT-2005-003875). R.I. Figueroa work is supported by a I3P contract and E. Garcés’ work is supported by a Ramon y Cajal grant, both from the Spanish Ministry of Education and SciencePeer reviewe

Surgical and Hardware-Related Adverse Events of Deep Brain Stimulation:A Ten-Year Single-Center Experience

INTRODUCTION: Although deep brain stimulation (DBS) is effective for treating a number of neurological and psychiatric indications, surgical and hardware-related adverse events (AEs) can occur that affect quality of life. This study aimed to give an overview of the nature and frequency of those AEs in our center and to describe the way they were managed. Furthermore, an attempt was made at identifying possible risk factors for AEs to inform possible future preventive measures. MATERIALS AND METHODS: Patients undergoing DBS-related procedures between January 2011 and July 2020 were retrospectively analyzed to inventory AEs. The mean follow-up time was 43 ± 31 months. Univariate logistic regression analysis was used to assess the predictive value of selected demographic and clinical variables. RESULTS: From January 2011 to July 2020, 508 DBS-related procedures were performed including 201 implantations of brain electrodes in 200 patients and 307 implantable pulse generator (IPG) replacements in 142 patients. Surgical or hardware-related AEs following initial implantation affected 40 of 200 patients (20%) and resolved without permanent sequelae in all instances. The most frequent AEs were surgical site infections (SSIs) (9.95%, 20/201) and wire tethering (2.49%, 5/201), followed by hardware failure (1.99%, 4/201), skin erosion (1.0%, 2/201), pain (0.5%, 1/201), lead migration (0.52%, 2/386 electrode sites), and hematoma (0.52%, 2/386 electrode sites). The overall rate of AEs for IPG replacement was 5.6% (17/305). No surgical, ie, staged or nonstaged, electrode fixation, or patient-related risk factors were identified for SSI or wire tethering. CONCLUSIONS: Major AEs including intracranial surgery-related AEs or AEs requiring surgical removal or revision of hardware are rare. In particular, aggressive treatment is required in SSIs involving multiple sites or when Staphylococcus aureus is identified. For future benchmarking, the development of a uniform reporting system for surgical and hardware-related AEs in DBS surgery would be useful

Loss of p53 triggers Wnt-dependent systemic inflammation to drive breast cancer metastasis

Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer

Loss of p53 triggers Wnt-dependent systemic inflammation to drive breast cancer metastasis

Cancer-associated systemic inflammation is strongly linked to poor disease outcome in patients with cancer1,2. For most human epithelial tumour types, high systemic neutrophil-to-lymphocyte ratios are associated with poor overall survival3, and experimental studies have demonstrated a causal relationship between neutrophils and metastasis4,5. However, the cancer-cell-intrinsic mechanisms that dictate the substantial heterogeneity in systemic neutrophilic inflammation between tumour-bearing hosts are largely unresolved. Here, using a panel of 16 distinct genetically engineered mouse models for breast cancer, we uncover a role for cancer-cell-intrinsic p53 as a key regulator of pro-metastatic neutrophils. Mechanistically, loss of p53 in cancer cells induced the secretion of WNT ligands that stimulate tumour-associated macrophages to produce IL-1β, thus driving systemic inflammation. Pharmacological and genetic blockade of WNT secretion in p53-null cancer cells reverses macrophage production of IL-1β and subsequent neutrophilic inflammation, resulting in reduced metastasis formation. Collectively, we demonstrate a mechanistic link between the loss of p53 in cancer cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression. These insights illustrate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic inflammation, and set the stage for personalized immune intervention strategies for patients with cancer

Prevalence of abnormal Alzheimer’s disease biomarkers in patients with subjective cognitive decline: cross-sectional comparison of three European memory clinic samples

Introduction: Subjective cognitive decline (SCD) in cognitively unimpaired older individuals has been recognized as an early clinical at-risk state for Alzheimer's disease (AD) dementia and as a target population for future dementia prevention trials. Currently, however, SCD is heterogeneously defined across studies, potentially leading to variations in the prevalence of AD pathology. Here, we compared the prevalence and identified common determinants of abnormal AD biomarkers in SCD across three European memory clinics participating in the European initiative on harmonization of SCD in preclinical AD (Euro-SCD). Methods: We included three memory clinic SCD samples with available cerebrospinal fluid (CSF) biomaterial (IDIBAPS, Barcelona, Spain, n = 44; Amsterdam Dementia Cohort (ADC), The Netherlands, n = 50; DELCODE multicenter study, Germany, n = 42). CSF biomarkers (amyloid beta (Aβ)42, tau, and phosphorylated tau (ptau181)) were centrally analyzed in Amsterdam using prespecified cutoffs to define prevalence of pathological biomarker concentrations. We used logistic regression analysis in the combined sample across the three centers to investigate center effects with regard to likelihood of biomarker abnormality while taking potential common predictors (e.g., age, sex, apolipoprotein E (APOE) status, subtle cognitive deficits, depressive symptoms) into account. Results: The prevalence of abnormal Aβ42, but not tau or ptau181, levels was different across centers (64% DELCODE, 57% IDIBAPS, 22% ADC; p < 0.001). Logistic regression analysis revealed that the likelihood of abnormal Aβ42 (and also abnormal tau or ptau181) levels was predicted by age and APOE status. For Aβ42 abnormality, we additionally observed a center effect, indicating between-center heterogeneity not explained by age, APOE, or the other included covariates. Conclusions: While heterogeneous frequency of abnormal Aβ42 was partly explained by between-sample differences in age range and APOE status, the additional observation of center effects indicates between-center heterogeneity that may be attributed to different recruitment procedures. These findings highlight the need for the development of harmonized recruitment protocols for SCD case definition in multinational studies to achieve similar enrichment rates of preclinical AD

Multi - Girl - Culture : An Ethnography of Doing Identity

In this highly readable book, Linda Duits investigates girl culture in the Dutch multicultural society. Her ethnographic account provides a thick description of life at school, still the most prominent setting foor todays youth. She followed young girls of diverse ethnic backgrounds in their transition from primary to secondary school, focusing on the ways they use the body, clothing and media in their performance of identity. Countering several media hypes, including the internet generation, the headscarf debate and the sexualisation of society, Duits shows how contemporary girl culture is a mundane culture that is reflexively negotiated in an everyday setting

Kiezen om normaal te zijn. Normen en waarden in multiculturele meisjescultuur

This article focuses on the norms that govern everyday girl culture. It investigates how young girls talk about social behaviour and appearance. Based on 1.5 years of ethnographic fieldwork, it reconstructs four interpretative repertoires through which girls reflect on themselves and others: the politically correct repertoire, and the repertoires of choice, authenticity and normalcy. The article argues that identity is reflexively constructed with others based on these norms.