Direct Foreign Investment in the Caribbean: A Legal and Policy Analysis

The purpose of this Article is to delineate the central issues facing countries which seek to encourage direct foreign investment in their local economies, and to suggest which approaches to these issues appear most likely to facilitate the attraction of foreign capital, technology and expertise, while preserving local control over the potentially detrimental effects of such investment

Direct Foreign Investment in the Caribbean: A Legal and Policy Analysis

The purpose of this Article is to delineate the central issues facing countries which seek to encourage direct foreign investment in their local economies, and to suggest which approaches to these issues appear most likely to facilitate the attraction of foreign capital, technology and expertise, while preserving local control over the potentially detrimental effects of such investment

DEVELOPMENT AND DESIGN OF ANTISURGE AND PERFORMANCE CONTROL SYSTEMS FOR CENTRIFUGAL COMPRESSORS

TutorialThe development and design of control systems for centrifugal and axial compressors is discussed and explanations given to bring together features of control systems on varying machine designs. Potential problems resulting from such differences will be addressed and resolutions offered

Krox-20 inhibits Jun-NH2-terminal kinase/c-Jun to control Schwann cell proliferation and death

The transcription factor Krox-20 controls Schwann cell myelination. Schwann cells in Krox-20 null mice fail to myelinate, and unlike myelinating Schwann cells, continue to proliferate and are susceptible to death. We find that enforced Krox-20 expression in Schwann cells cell-autonomously inactivates the proliferative response of Schwann cells to the major axonal mitogen β–neuregulin-1 and the death response to TGFβ or serum deprivation. Even in 3T3 fibroblasts, Krox-20 not only blocks proliferation and death but also activates the myelin genes periaxin and protein zero, showing properties in common with master regulatory genes in other cell types. Significantly, a major function of Krox-20 is to suppress the c-Jun NH2-terminal protein kinase (JNK)–c-Jun pathway, activation of which is required for both proliferation and death. Thus, Krox-20 can coordinately control suppression of mitogenic and death responses. Krox-20 also up-regulates the scaffold protein JNK-interacting protein 1 (JIP-1). We propose this as a possible component of the mechanism by which Krox-20 regulates JNK activity during Schwann cell development

Development and Design of Antisurge and Performance Control System for Centrifugal Compressor

TutorialThe development and design of control systems for centrifugal and axial compressors is discussed and explanations given to bring together features of control systems on varying machine designs. Potential problems resulting from such differences will be addressed and resolutions offered

DEVELOPMENT AND DESIGN OF ANTISURGE AND PERFORMANCE CONTROL SYSTEMS FOR CENTRIFUGAL COMPRESSORS

TutorialThe development and design of control systems for centrifugal and axial compressors is discussed and explanations given to bring together features of control systems on varying machine designs. Potential problems resulting from such differences will be addressed and resolutions offered

Deep Learning Mixture-of-Experts Approach for Cytotoxic Edema Assessment in Infants and Children

This paper presents a deep learning framework for image classification aimed at increasing predictive performance for Cytotoxic Edema (CE) diagnosis in infants and children. The proposed framework includes two 3D network architectures optimized to learn from two types of clinical MRI data , a trace Diffusion Weighted Image (DWI) and the calculated Apparent Diffusion Coefficient map (ADC). This work proposes a robust and novel solution based on volumetric analysis of 3D images (using pixels from time slices) and 3D convolutional neural network (CNN) models. While simple in architecture, the proposed framework shows significant quantitative results on the domain problem. We use a dataset curated from a Childrens Hospital Colorado (CHCO) patient registry to report a predictive performance F1 score of 0.91 at distinguishing CE patients from children with severe neurologic injury without CE. In addition, we perform analysis of our systems output to determine the association of CE with Abusive Head Trauma (AHT) , a type of traumatic brain injury (TBI) associated with abuse , and overall functional outcome and in hospital mortality of infants and young children. We used two clinical variables, AHT diagnosis and Functional Status Scale (FSS) score, to arrive at the conclusion that CE is highly correlated with overall outcome and that further study is needed to determine whether CE is a biomarker of AHT. With that, this paper introduces a simple yet powerful deep learning based solution for automated CE classification. This solution also enables an indepth analysis of progression of CE and its correlation to AHT and overall neurologic outcome, which in turn has the potential to empower experts to diagnose and mitigate AHT during early stages of a childs life.Comment: 7 figure

c-Jun is a negative regulator of myelination

Schwann cell myelination depends on Krox-20/Egr2 and other promyelin transcription factors that are activated by axonal signals and control the generation of myelin-forming cells. Myelin-forming cells remain remarkably plastic and can revert to the immature phenotype, a process which is seen in injured nerves and demyelinating neuropathies. We report that c-Jun is an important regulator of this plasticity. At physiological levels, c-Jun inhibits myelin gene activation by Krox-20 or cyclic adenosine monophosphate. c-Jun also drives myelinating cells back to the immature state in transected nerves in vivo. Enforced c-Jun expression inhibits myelination in cocultures. Furthermore, c-Jun and Krox-20 show a cross-antagonistic functional relationship. c-Jun therefore negatively regulates the myelinating Schwann cell phenotype, representing a signal that functionally stands in opposition to the promyelin transcription factors. Negative regulation of myelination is likely to have significant implications for three areas of Schwann cell biology: the molecular analysis of plasticity, demyelinating pathologies, and the response of peripheral nerves to injury

Pathogenic variants in SQOR encoding sulfide:quinone oxidoreductase are a potentially treatable cause of Leigh disease

Hydrogen sulfide, a signaling molecule formed mainly from cysteine, is catabolized by sulfide:quinone oxidoreductase (gene SQOR). Toxic hydrogen sulfide exposure inhibits complex IV. We describe children of two families with pathogenic variants in SQOR. Exome sequencing identified variants; SQOR enzyme activity was measured spectrophotometrically, protein levels evaluated by western blotting, and mitochondrial function was assayed. In family A, following a brief illness, a 4- year- old girl presented comatose with lactic acidosis and multiorgan failure. After stabilization, she remained comatose, hypotonic, had neurostorming episodes, elevated lactate, and Leigh- like lesions on brain imaging. She died shortly after. Her 8- year- old sister presented with a rapidly fatal episode of coma with lactic acidosis, and lesions in the basal ganglia and left cortex. Muscle and liver tissue had isolated decreased complex IV activity, but normal complex IV protein levels and complex formation. Both patients were homozygous for c.637G- >- A, which we identified as a founder mutation in the Lehrerleut Hutterite with a carrier frequency of 1 in 13. The resulting p.Glu213Lys change disrupts hydrogen bonding with neighboring residues, resulting in severely reduced SQOR protein and enzyme activity, whereas sulfide generating enzyme levels were unchanged. In family B, a boy had episodes of encephalopathy and basal ganglia lesions. He was homozygous for c.446delT and had severely reduced fibroblast SQOR enzyme activity and protein levels. SQOR dysfunction can result in hydrogen sulfide accumulation, which, consistent with its known toxicity, inhibits complex IV resulting in energy failure. In conclusion, SQOR deficiency represents a new, potentially treatable, cause of Leigh disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162807/2/jimd12232.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162807/1/jimd12232_am.pd