Empirical Models of Manufacturer-Retailer Interaction: A Review and Agenda for Future Research

The nature of the interaction between manufacturers and retailers has received a great deal of empirical attention in the last 15 years. One major line of empirical research examines the balance of power between them and ranges from reduced form models quantifying aggregate profit and other related trends for manufacturers and retailers to structural models that test alternative forms of manufacturer-retailer pricing interaction. A second line of research addresses the sources of leverage for each party, e.g., trade promotions and their pass-through, customer information from loyalty programs, manufacturer advertising, productassortment in general, and private label assortment in particular. The purpose of this article is to synthesize what has been learnt about the nature of the interaction between manufacturers and retailers and the effectiveness of each party’s sources of leverage and to highlight gaps in our knowledge that future research should attempt to fill

Thirteen Independent Genetic Loci Associated with Preserved Processing Speed in a Study of Cognitive Resilience in 330,097 Individuals in the UK Biobank

Cognitive resilience is the ability to withstand the negative effects of stress on cognitive functioning and is important for maintaining quality of life while aging. The UK Biobank does not have measurements of the same cognitive phenotype at distal time points. Therefore, we used education years (EY) as a proxy phenotype for past cognitive performance and current cognitive performance was based on processing speed. This represented an average time span of 40 years between past and current cognitive performance in 330,097 individuals. A confounding factor was that EY is highly polygenic and masked the genetics of resilience. To overcome this, we employed Genomics Structural Equation Modelling (GenomicSEM) to perform a genome-wide association study (GWAS)-by-subtraction using two GWAS, one GWAS of EY and resilience and a second GWAS of EY but not resilience, to generate a GWAS of Resilience. Using independent discovery and replication samples, we found 13 independent genetic loci for Resilience. Functional analyses showed enrichment in several brain regions and specific cell types. Gene-set analyses implicated the biological process “neuron differentiation”, the cellular component “synaptic part” and the “WNT signalosome”. Mendelian randomisation analysis showed a causative effect of white matter volume on cognitive resilience. These results may contribute to the neurobiological understanding of resilience

Polyoxygenated Cyclohexenes and Other Constituents of <i>Cleistochlamys kirkii</i> Leaves

Thirteen new metabolites, including the polyoxygenated cyclohexene derivatives cleistodiendiol (<b>1</b>), cleistodienol B (<b>3</b>), cleistenechlorohydrins A (<b>4</b>) and B (<b>5</b>), cleistenediols A–F (<b>6</b>–<b>11</b>), cleistenonal (<b>12</b>), and the butenolide cleistanolate (<b>13</b>), 2,5-dihydroxybenzyl benzoate (cleistophenolide, <b>14</b>), and eight known compounds (<b>2</b>, <b>15</b>–<b>21</b>) were isolated from a MeOH extract of the leaves of <i>Cleistochlamys kirkii</i>. The purified metabolites were identified by NMR spectroscopic and mass spectrometric analyses, whereas the absolute configurations of compounds <b>1</b>, <b>17</b>, and <b>19</b> were established by single-crystal X-ray diffraction. The configuration of the exocyclic double bond of compound <b>2</b> was revised based on comparison of its NMR spectroscopic features and optical rotation to those of <b>1</b>, for which the configuration was determined by X-ray diffraction. Observation of the co-occurrence of cyclohexenoids and heptenolides in <i>C. kirkii</i> is of biogenetic and chemotaxonomic significance. Some of the isolated compounds showed activity against <i>Plasmodium falciparum</i> (3D7, Dd2), with IC₅₀ values of 0.2–40 μM, and against HEK293 mammalian cells (IC₅₀ 2.7–3.6 μM). While the crude extract was inactive at 100 μg/mL against the MDA-MB-231 triple-negative breast cancer cell line, some of its isolated constituents demonstrated cytotoxic activity with IC₅₀ values ranging from 0.03–8.2 μM. Compound <b>1</b> showed the most potent antiplasmodial (IC₅₀ 0.2 μM) and cytotoxic (IC₅₀ 0.03 μM, MDA-MB-231 cell line) activities. None of the compounds investigated exhibited translational inhibitory activity in vitro at 20 μM

Polyoxygenated Cyclohexenes and Other Constituents of <i>Cleistochlamys kirkii</i> Leaves

Thirteen new metabolites, including the polyoxygenated cyclohexene derivatives cleistodiendiol (<b>1</b>), cleistodienol B (<b>3</b>), cleistenechlorohydrins A (<b>4</b>) and B (<b>5</b>), cleistenediols A–F (<b>6</b>–<b>11</b>), cleistenonal (<b>12</b>), and the butenolide cleistanolate (<b>13</b>), 2,5-dihydroxybenzyl benzoate (cleistophenolide, <b>14</b>), and eight known compounds (<b>2</b>, <b>15</b>–<b>21</b>) were isolated from a MeOH extract of the leaves of <i>Cleistochlamys kirkii</i>. The purified metabolites were identified by NMR spectroscopic and mass spectrometric analyses, whereas the absolute configurations of compounds <b>1</b>, <b>17</b>, and <b>19</b> were established by single-crystal X-ray diffraction. The configuration of the exocyclic double bond of compound <b>2</b> was revised based on comparison of its NMR spectroscopic features and optical rotation to those of <b>1</b>, for which the configuration was determined by X-ray diffraction. Observation of the co-occurrence of cyclohexenoids and heptenolides in <i>C. kirkii</i> is of biogenetic and chemotaxonomic significance. Some of the isolated compounds showed activity against <i>Plasmodium falciparum</i> (3D7, Dd2), with IC₅₀ values of 0.2–40 μM, and against HEK293 mammalian cells (IC₅₀ 2.7–3.6 μM). While the crude extract was inactive at 100 μg/mL against the MDA-MB-231 triple-negative breast cancer cell line, some of its isolated constituents demonstrated cytotoxic activity with IC₅₀ values ranging from 0.03–8.2 μM. Compound <b>1</b> showed the most potent antiplasmodial (IC₅₀ 0.2 μM) and cytotoxic (IC₅₀ 0.03 μM, MDA-MB-231 cell line) activities. None of the compounds investigated exhibited translational inhibitory activity in vitro at 20 μM

Polyoxygenated Cyclohexenes and Other Constituents of <i>Cleistochlamys kirkii</i> Leaves

Thirteen new metabolites, including the polyoxygenated cyclohexene derivatives cleistodiendiol (<b>1</b>), cleistodienol B (<b>3</b>), cleistenechlorohydrins A (<b>4</b>) and B (<b>5</b>), cleistenediols A–F (<b>6</b>–<b>11</b>), cleistenonal (<b>12</b>), and the butenolide cleistanolate (<b>13</b>), 2,5-dihydroxybenzyl benzoate (cleistophenolide, <b>14</b>), and eight known compounds (<b>2</b>, <b>15</b>–<b>21</b>) were isolated from a MeOH extract of the leaves of <i>Cleistochlamys kirkii</i>. The purified metabolites were identified by NMR spectroscopic and mass spectrometric analyses, whereas the absolute configurations of compounds <b>1</b>, <b>17</b>, and <b>19</b> were established by single-crystal X-ray diffraction. The configuration of the exocyclic double bond of compound <b>2</b> was revised based on comparison of its NMR spectroscopic features and optical rotation to those of <b>1</b>, for which the configuration was determined by X-ray diffraction. Observation of the co-occurrence of cyclohexenoids and heptenolides in <i>C. kirkii</i> is of biogenetic and chemotaxonomic significance. Some of the isolated compounds showed activity against <i>Plasmodium falciparum</i> (3D7, Dd2), with IC₅₀ values of 0.2–40 μM, and against HEK293 mammalian cells (IC₅₀ 2.7–3.6 μM). While the crude extract was inactive at 100 μg/mL against the MDA-MB-231 triple-negative breast cancer cell line, some of its isolated constituents demonstrated cytotoxic activity with IC₅₀ values ranging from 0.03–8.2 μM. Compound <b>1</b> showed the most potent antiplasmodial (IC₅₀ 0.2 μM) and cytotoxic (IC₅₀ 0.03 μM, MDA-MB-231 cell line) activities. None of the compounds investigated exhibited translational inhibitory activity in vitro at 20 μM

Polyoxygenated Cyclohexenes and Other Constituents of <i>Cleistochlamys kirkii</i> Leaves

Thirteen new metabolites, including the polyoxygenated cyclohexene derivatives cleistodiendiol (<b>1</b>), cleistodienol B (<b>3</b>), cleistenechlorohydrins A (<b>4</b>) and B (<b>5</b>), cleistenediols A–F (<b>6</b>–<b>11</b>), cleistenonal (<b>12</b>), and the butenolide cleistanolate (<b>13</b>), 2,5-dihydroxybenzyl benzoate (cleistophenolide, <b>14</b>), and eight known compounds (<b>2</b>, <b>15</b>–<b>21</b>) were isolated from a MeOH extract of the leaves of <i>Cleistochlamys kirkii</i>. The purified metabolites were identified by NMR spectroscopic and mass spectrometric analyses, whereas the absolute configurations of compounds <b>1</b>, <b>17</b>, and <b>19</b> were established by single-crystal X-ray diffraction. The configuration of the exocyclic double bond of compound <b>2</b> was revised based on comparison of its NMR spectroscopic features and optical rotation to those of <b>1</b>, for which the configuration was determined by X-ray diffraction. Observation of the co-occurrence of cyclohexenoids and heptenolides in <i>C. kirkii</i> is of biogenetic and chemotaxonomic significance. Some of the isolated compounds showed activity against <i>Plasmodium falciparum</i> (3D7, Dd2), with IC₅₀ values of 0.2–40 μM, and against HEK293 mammalian cells (IC₅₀ 2.7–3.6 μM). While the crude extract was inactive at 100 μg/mL against the MDA-MB-231 triple-negative breast cancer cell line, some of its isolated constituents demonstrated cytotoxic activity with IC₅₀ values ranging from 0.03–8.2 μM. Compound <b>1</b> showed the most potent antiplasmodial (IC₅₀ 0.2 μM) and cytotoxic (IC₅₀ 0.03 μM, MDA-MB-231 cell line) activities. None of the compounds investigated exhibited translational inhibitory activity in vitro at 20 μM

Formation and functions of the corneocyte lipid envelope (CLE)

Corneocytes in mammalian stratum corneum are surrounded by a monolayer of covalently bound ω-OH-ceramides that form the corneocyte (-bound) lipid envelope (CLE). We review here the structure, composition, and possible functions of this structure, with insights provided by inherited and acquired disorders of lipid metabolism