Challenging the production function approach to assess the developmental effects of FDI

From a theoretical point of view, it is traditionally assumed that foreign firms possess a centrally accumulated firm-specific technological advantage over domestic firms (see, for example, Findlay, 1978; Dunning, 1979). Given a sufficient level of absorptive capacity and human capital, domestic firms in host economies are able to benefit from various externalities stimulated by the presence of foreign firms

The WISDOM of power spectra: how the galactic gravitational potential impacts a galaxy?s central gas reservoir in simulations and observations

Observations indicate that the central gas discs are smoother in early-type galaxies than their late-type counterparts, while recent simulations predict that the dynamical suppression of star formation in spheroid-dominated galaxies is preceded by the suppression of fragmentation of their interstellar media. The mass surface density power spectrum is a powerful tool to constrain the degree of structure within a gas reservoir. Specifically here, we focus on the power spectrum slope and aim to constrain whether the shear induced by a dominant spheroidal potential can induce sufficient turbulence to suppress fragmentation, resulting in the smooth central gas discs observed. We compute surface density power spectra for the nuclear gas reservoirs of fourteen simulated isolated galaxies and twelve galaxies observed as part of the mm-Wave Interferometric Survey of Dark Object Masses (WISDOM) project. Both simulated and observed galaxies range from disc-dominated galaxies to spheroids, with central stellar mass surface densities, a measure of bulge dominance, varying by more than an order of magnitude. For the simulations, the power spectra steepen with increasing central stellar mass surface density, thereby clearly linking the suppression of fragmentation to the shear-driven turbulence induced by the spheroid. The WISDOM observations show a different (but potentially consistent) picture: while there is no correlation between the power spectrum slopes and the central stellar mass surface densities, the slopes scatter around a value of 2.6. This is similar to the behaviour of the slopes of the simulated galaxies with high central stellar mass surface densities, and could indicate that high shear eventually drives incompressible turbulence

Star Formation Laws and Efficiencies across 80 Nearby Galaxies

We measure empirical relationships between the local star formation rate (SFR) and properties of the star-forming molecular gas on 1.5 kpc scales across 80 nearby galaxies. These relationships, commonly referred to as "star formation laws," aim at predicting the local SFR surface density from various combinations of molecular gas surface density, galactic orbital time, molecular cloud free-fall time, and the interstellar medium dynamical equilibrium pressure. Leveraging a multiwavelength database built for the PHANGS survey, we measure these quantities consistently across all galaxies and quantify systematic uncertainties stemming from choices of SFR calibrations and the CO-to-H$_2$ conversion factors. The star formation laws we examine show 0.3-0.4 dex of intrinsic scatter, among which the molecular Kennicutt-Schmidt relation shows a $\sim$10% larger scatter than the other three. The slope of this relation ranges $\beta\approx0.9{-}1.2$, implying that the molecular gas depletion time remains roughly constant across the environments probed in our sample. The other relations have shallower slopes ($\beta\approx0.6{-}1.0$), suggesting that the star formation efficiency (SFE) per orbital time, the SFE per free-fall time, and the pressure-to-SFR surface density ratio (i.e., the feedback yield) may vary systematically with local molecular gas and SFR surface densities. Last but not least, the shapes of the star formation laws depend sensitively on methodological choices. Different choices of SFR calibrations can introduce systematic uncertainties of at least 10-15% in the star formation law slopes and 0.15-0.25 dex in their normalization, while the CO-to-H$_2$ conversion factors can additionally produce uncertainties of 20-25% for the slope and 0.10-0.20 dex for the normalization.Comment: 10 pages main text + 2 appendices. ApJL in press. Data products available at https://www.canfar.net/storage/list/phangs/RELEASES/Sun_etal_2023 . Slides summarizing key results can be found at https://www.dropbox.com/s/5gsegexeo9n0t05/Sun_et_PHANGS_2023.pptx?dl=

Corporealities of violence in Southern and Eastern Africa

no abstract availabl

Characterization of the Endothelial Cell Cytoskeleton following HLA Class I Ligation

Vascular endothelial cells (ECs) are a target of antibody-mediated allograft rejection. In vitro, when the HLA class I molecules on the surface of ECs are ligated by anti-HLA class I antibodies, cell proliferation and survival pathways are activated and this is thought to contribute to the development of antibody-mediated rejection. Crosslinking of HLA class I molecules by anti-HLA antibodies also triggers reorganization of the cytoskeleton, which induces the formation of F-actin stress fibers. HLA class I induced stress fiber formation is not well understood.The present study examines the protein composition of the cytoskeleton fraction of ECs treated with HLA class I antibodies and compares it to other agonists known to induce alterations of the cytoskeleton in endothelial cells. Analysis by tandem mass spectrometry revealed unique cytoskeleton proteomes for each treatment group. Using annotation tools a candidate list was created that revealed 12 proteins, which were unique to the HLA class I stimulated group. Eleven of the candidate proteins were phosphoproteins and exploration of their predicted kinases provided clues as to how these proteins may contribute to the understanding of HLA class I induced antibody-mediated rejection. Three of the candidates, eukaryotic initiation factor 4A1 (eIF4A1), Tropomyosin alpha 4-chain (TPM4) and DDX3X, were further characterized by Western blot and found to be associated with the cytoskeleton. Confocal microscopy analysis showed that class I ligation stimulated increased eIF4A1 co-localization with F-actin and paxillin.Colocalization of eIF4A1 with F-actin and paxillin following HLA class I ligation suggests that this candidate protein could be a target for understanding the mechanism(s) of class I mediated antibody-mediated rejection. This proteomic approach for analyzing the cytoskeleton of ECs can be applied to other agonists and various cells types as a method for uncovering novel regulators of cytoskeleton changes

ER Stress Negatively Modulates the Expression of the miR-199a/214 Cluster to Regulates Tumor Survival and Progression in Human Hepatocellular Cancer

Background: Recent studies have emphasized causative links between microRNAs (miRNAs) deregulation and tumor development. In hepatocellular carcinoma (HCC), more and more miRNAs were identified as diagnostic and prognostic cancer biomarkers, as well as additional therapeutic tools. This study aimed to investigate the functional significance and regulatory mechanism of the miR-199a2/214 cluster in HCC progression. Methods and Findings: In this study, we showed that miR-214, as well as miR-199a-3p and miR-199a-5p levels were significantly reduced in the majority of examined 23 HCC tissues and HepG2 and SMMC-7721 cell lines, compared with their nontumor counterparts. To further explore the role of miR-214 in hepatocarcinogenesis, we disclosed that the ER stressinduced pro-survival factor XBP-1 is a target of miR-214 by using western blot assay and luciferase reporter assay. Reexpression of miR-214 in HCC cell lines (HepG2 and SMMC-7721) inhibited proliferation and induced apoptosis. Furthermore, ectopic expression of miR-214 dramatically suppressed the ability of HCC cells to form colonies in vitro and to develop tumors in a subcutaneous xenotransplantation model of the BALB/c athymic nude mice. Moreover, reintroduction of XBP-1s attenuated miR-214-mediated suppression of HCC cells proliferation, colony and tumor formation. To further understand the mechanism of the miR-199a/214 cluster down-expression in HCC, we found that thapsigargin (TG) and tunicamycin (TM) or hypoxia-induced unfolded protein response (UPR) suppresses the expression of the miR-199a/21