Sonic diaspora, vibrations and rhythm: thinking through the sounding of the Jamaican dancehall session

The propagation of vibrations may provide a better way of understanding diasporic spread than the conventional focus on the circulation of products (Hall 1980, Appadurai 1986, 1996, Gilroy 1993a, Brah 1996). Jamaican sound systems operate as a broadcast medium and a source of CDs, DVDs and other commercial products (Henriques 2007a). But the dancehall sound system session also propagates a broad spectrum of frequencies diffused through a range of media and activities - described as “sounding” (following Small’s 1998 concept of “musicking”). These include the material vibrations of the signature low-pitched auditory frequencies of Reggae as a bass culture (Johnson 1980), at the loudness of “sonic dominance” (Henriques 2003). Secondly a session propagates the corporeal vibrations of rituals, dance routines and bass-line “riddims” (Veal 2007). Thirdly it propagates the ethereal vibrations (Henriques 2007b), “vibes” or atmosphere of the sexually charged popular subculture by which the crowd (audience) appreciate each dancehall session as part of the Dancehall scene (Cooper 2004). The paper concludes that thinking though vibrating frequencies makes it easier to appreciate how audiences with no direct or inherited connection with a particular music genre can be energetically infected and affected - to form a sonic diaspora

IGF2BP1/IMP1 Deletion Enhances a Facultative Stem Cell State via Regulation of MAP1LC3BSummary

Background & Aims: The intestinal epithelium interfaces with a diverse milieu of luminal contents while maintaining robust digestive and barrier functions. Facultative intestinal stem cells are cells that survive tissue injury and divide to re-establish the epithelium. Prior studies have shown autophagic state as functional marker of facultative intestinal stem cells, but regulatory mechanisms are not known. The current study evaluated a post-transcriptional regulation of autophagy as an important factor for facultative stem cell state and tissue regeneration. Methods: We evaluated stem cell composition, autophagic vesicle content, organoid formation, and in vivo regeneration in mice with intestinal epithelial deletion of the RNA binding protein IGF2 messenger RNA binding protein 1 (IMP1). The contribution of autophagy to resulting in vitro and in vivo phenotypes was evaluated via genetic inactivation of Atg7. Molecular analyses of IMP1 modulation of autophagy at the protein and transcript localization levels were performed using IMP1 mutant studies and single-molecule fluorescent in situ hybridization. Results: Epithelial Imp1 deletion reduced leucine rich repeat containing G protein coupled receptor 5 cell frequency but enhanced both organoid formation efficiency and in vivo regeneration after irradiation. We confirmed prior studies showing increased autophagy with IMP1 deletion. Deletion of Atg7 reversed the enhanced regeneration observed with Imp1 deletion. IMP1 deletion or mutation of IMP1 phosphorylation sites enhanced expression of essential autophagy protein microtubule-associated protein 1 light chain 3β. Furthermore, immunofluorescence imaging coupled with single-molecule fluorescent in situ hybridization showed IMP1 colocalization with MAP1LC3B transcripts at homeostasis. Stress induction led to decreased colocalization. Conclusions: Depletion of IMP1 enhances autophagy, which promotes intestinal regeneration via expansion of facultative intestinal stem cells

Activation of GPR44 decreases severity of myeloid leukemia via specific targeting of leukemia initiating stem cells

Summary: Relapse of acute myeloid leukemia (AML) remains a significant concern due to persistent leukemia-initiating stem cells (LICs) that are typically not targeted by most existing therapies. Using a murine AML model, human AML cell lines, and patient samples, we show that AML LICs are sensitive to endogenous and exogenous cyclopentenone prostaglandin-J (CyPG), Δ12-PGJ2, and 15d-PGJ2, which are increased upon dietary selenium supplementation via the cyclooxygenase-hematopoietic PGD synthase pathway. CyPGs are endogenous ligands for peroxisome proliferator-activated receptor gamma and GPR44 (CRTH2; PTGDR2). Deletion of GPR44 in a mouse model of AML exacerbated the disease suggesting that GPR44 activation mediates selenium-mediated apoptosis of LICs. Transcriptomic analysis of GPR44−/− LICs indicated that GPR44 activation by CyPGs suppressed KRAS-mediated MAPK and PI3K/AKT/mTOR signaling pathways, to enhance apoptosis. Our studies show the role of GPR44, providing mechanistic underpinnings of the chemopreventive and chemotherapeutic properties of selenium and CyPGs in AML