A Psychological Exploration of Engagement in Geek Culture

Geek culture is a subculture of enthusiasts that is traditionally associated with obscure media (Japanese animation, science fiction, video games, etc.). However, geek culture is becoming increasingly mainstream; for example, in the past year alone, Dragon*Con, a major Geek convention in Atlanta, Georgia, attracted an attendance of over 57,000 members. The present article uses an individual differences approach to examine three theoretical accounts of geek culture. Seven studies (N = 2354) develop the Geek Culture Engagement Scale (GCES) to quantify geek engagement and assess its relationships to theoretically relevant personality and individual differences variables. These studies present evidence that individuals may engage in geek culture in order to maintain narcissistic self-views (the great fantasy migration hypothesis), to fulfill belongingness needs (the belongingness hypothesis), and to satisfy needs for creative expression (the need for engagement hypothesis). Geek engagement is found to be associated with elevated grandiose narcissism, extraversion, openness to experience, depression, and subjective well-being across multiple samples. These data lay the groundwork for further exploration of geek culture as well as provide a foundation for examining other forms of subculture participation.     

Does a long‐term shift in Wood Stork diet foreshadow adaptability to human‐induced rapid environmental change?

To preserve biodiversity, identifying at‐risk populations and developing conservation plans to mitigate the effects of human‐induced rapid environmental change (HIREC) are essential. Changes in diet, especially for food‐limited species, can aid in detecting populations being impacted by HIREC, and characterizing the quality, abundance, and temporal and spatial consistency of newly consumed food items may provide insight concerning the likelihood of a species persisting in a changing environment. We used Wood Storks (Mycteria americana) nesting in the Florida Everglades as a model system to study the possible effects of HIREC on a food‐limited population. We compared the diets of Wood Storks in 2013 and 2014 with those reported during the 1970s before major anthropogenic activities affected the Everglades system and prey availability. Wood Storks in our study consumed more large‐bodied sunfish species (Lepomis spp.), fewer native marsh fishes, and more non‐native fish species than during the 1970s. Large sunfish and non‐native fish are relatively rare in the drying pools of Everglades marshes where storks traditionally forage, suggesting that Wood Storks may be using novel foraging habitats such as created wetlands (i.e., canals and stormwater ponds). Although created wetlands have long hydroperiods conducive to maintaining large‐bodied fishes and could provide alternative foraging habitat when prey availability is reduced in natural marshes, additional studies are needed to determine the extent to which these wetlands are used by Wood Storks and, importantly, the quality of prey items potentially available to foraging Wood Storks in created wetlands.     

TWO BOTANISTS,A FINANCIAL CRISIS AND BRITAIN'S FIRST EMBASSY TO CHINA

This essay reveals a financial dimension to Captain John Blake and his son John Bradby Blake's involvement with China, namely, their participation in financing the Canton trade through predatory loans to Chinese Hong merchants. Widespread predatory lending in Canton led to a financial crisis during the late 1770s, which ruined several British and Chinese merchants. In an effort to recover the money they claimed was owed to them, many British traders, including John Blake, formed a lobby group in London and authorized Britain's first Ambassador to China to negotiate with the Emperor in Beijing on their behalf.     

Morphological and Gene Expression Changes in Cattle Embryos from Hatched Blastocyst to Early Gastrulation Stages after Transfer of In Vitro Produced Embryos

A detailed morphological staging system for cattle embryos at stages following blastocyst hatching and preceding gastrulation is presented here together with spatiotemporal mapping of gene expression for BMP4, BRACHYURY, CERBERUS1 (CER1), CRIPTO, EOMESODERMIN, FURIN and NODAL. Five stages are defined based on distinct developmental events. The first of these is the differentiation of the visceral hypoblast underlying the epiblast, from the parietal hypoblast underlying the mural trophoblast. The second concerns the formation of an asymmetrically positioned, morphologically recognisable region within the visceral hypoblast that is marked by the presence of CER1 and absence of BMP4 expression. We have termed this the anterior visceral hypoblast or AVH. Intra-epiblast cavity formation and the disappearance of the polar trophoblast overlying the epiblast (Rauber’s layer) have been mapped in relation to AVH formation. The third chronological event involves the transition of the epiblast into the embryonic ectoderm with concomitant onset of posterior NODAL, EOMES and BRACHYURY expression. Lastly, gastrulation commences as the posterior medial embryonic ectoderm layer thickens to form the primitive streak and cells ingress between the embryonic ectoderm and hypoblast. At this stage a novel domain of CER1 expression is seen whereas the AVH disappears. Comparison with the mouse reveals that while gene expression patterns at the onset of gastrulation are well conserved, asymmetry establishment, which relies on extraembryonic tissues such as the hypoblast and trophoblast, has diverged in terms of both gene expression and morphology.     

Cellular resistance to the antimelanoma immunotoxin ZME-gelonin and strategies to target resistant cells

 The development of cellular resistance to immunotoxins has been demonstrated in a variety of models and can involve a number of mechanisms. For the present study, an immunotoxin was utilized composed of an antimelanoma antibody ZME-018 recognizing a 240-kDa surface glycoprotein (gp 240) and the plant toxin gelonin. Human melanoma cells (A375-M) were grown in the presence of increasing amounts of ZME-gelonin and a clonal variant (A-375-ZR) was developed that was 100-fold resistant to ZME-gelonin compared to parental cells. Scatchard analysis showed that the A375-M parental cells had 260×10³ ZME-gelonin-binding sites/cell with relatively low affinity (5 nM). In contrast, resistant A375-ZR cells demonstrated a reduced number of low-affinity sites (160×10³/cell), but showed a small number (47×10³) of higher-affinity sites (0.8 nM). Internalization rates and degradation rates of ¹²⁵I-labeled ZME-gelonin were identical in both the parental and resistant cells. A375-ZR cells were found to be more resistant to vincristine and doxorubicin than were parental cells. Both cell lines were almost equally sensitive to native gelonin, 5-fluorouracil (5-FU), cisplatin, melphalan, carmustine, interferon γ (IFNγ) and IFNα. In addition, both cell lines were equally sensitive to another gelonin-antibody conjugate that binds to cell-surface, GD₂ (antibody 14G₂A). However, resistant cells were twice as sensitive to the cytotoxic effects of etoposide than were parental cells. Finally, a variety of agents were tested in combination with ZME-gelonin against A375-ZR cells in an attempt to identify agents to augment immunotoxin cytotoxic effects against resistant cells. The agents 5-FU, cisplatin, IFNγ, IFNα, and etoposide were the most effective in augmenting the cytotoxicity of ZME-gelonin against resistant cells. These studies suggest that development of resistance to one immunotoxin does not cause development of cross-resistance to other gelonin immunotoxins. Further, specific biological response modifiers and chemotherapeutic agents may be effective in augmenting the effectiveness of immunotoxins and specifically targeting or reducing the emergence of immunotoxin-resistant cells. Received: 15 March 1995 / Accepted: 28 November 1995     

MicroID2: A Novel Biotin Ligase Enables Rapid Proximity-Dependent Proteomics

Identifying protein–protein and other proximal interactions is central to dissecting signaling and regulatory processes in cells. BioID is a proximity-dependent biotinylation method that uses an “abortive” biotin ligase to detect proximal interactions in cells in a highly reproducible manner. Recent advancements in proximity-dependent biotinylation tools have improved efficiency and timing of labeling, allowing for measurement of interactions on a cellular timescale. However, issues of size, stability, and background labeling of these constructs persist. Here we modified the structure of BioID2, derived from Aquifex aeolicus BirA, to create a smaller, highly active, biotin ligase that we named MicroID2. Truncation of the C terrminus of BioID2 and addition of mutations to alleviate blockage of biotin/ATP binding at the active site of BioID2 resulted in a smaller and highly active construct with lower background labeling. Several additional point mutations improved the function of our modified MicroID2 construct compared with BioID2 and other biotin ligases, including TurboID and miniTurbo. MicroID2 is the smallest biotin ligase reported so far (180 amino acids [AAs] for MicroID2 versus 257 AAs for miniTurbo and 338 AAs for TurboID), yet it demonstrates only slightly less labeling activity than TurboID and outperforms miniTurbo. MicroID2 also had lower background labeling than TurboID. For experiments where precise temporal control of labeling is essential, we in addition developed a MicroID2 mutant, termed lbMicroID2 (low background MicroID2), that has lower labeling efficiency but significantly reduced biotin scavenging compared with BioID2. Finally, we demonstrate utility of MicroID2 in mass spectrometry experiments by localizing MicroID2 constructs to subcellular organelles and measuring proximal interactions.