Stakeholders are increasingly aware of the environmental and human rights issues related to highly conspicuous fashion merchandising. To mitigate the negative responses from environmentally conscious consumer groups, fashion merchandisers have sought to partner with non-governmental organizations (NGOs). While there is a growing body of literature on sustainability and social responsibility (SSR), the increasingly popular practice of fast-fashion industry partnering with NGOs has been neglected, and so far, remained under the radar. Such partnerships may be of success, but at the same time while promising on the surface, they can actually go awry, resulting in adverse outcomes for both parties. We build upon the loose-coupling theory to explain the relationships between fast-fashion multinational enterprises (MNEs) and NGOs. We discuss three causes (casual indeterminacy; fragmented external environment; discrete internal environment) and four key benefits (adaptability to environmental changes, flexibility, innovation, and firewalls for separate identity) for loosely-coupled partnerships. We then explore the dark side of such partnerships, identifying three challenges (power imbalance, mistrust and opportunism, and misaligning goals). Finally, we offer a set of propositions as a way of advancing our knowledge of partnerships in fashion merchandising industry.

De novo pyrimidine synthesis was studied in mouse liver, intestine, and kidney by intraperitoneal infusion of l5NH4C1 and analysis of "N incorporation into uracil nucleotide pools. When the dose of a 1-h infusion of "NH4C1 was increased from 50 pmol to 250 pmol the fraction of the total uracil nucleotide pool formed by de novo synthesis increased 4.0-fold in liver to 8.4% and 2.3-fold in intestine to 13.7%. The increase in intestine was independent of the increase in liver as evidenced by the lack of correlation between the increase observed in the intestine and liver of the same animal and the different distributions of label in the uracil ring nitrogens. A 2.4-fold increase in newly formed uracil nucleotides was observed in kidney when the infusion dose was raised from 150 pmol to 250 pmol. The increase in kidney was correlated with the increase in liver in the same animal and the distribution of label in the uracil ring nitrogens was similar to the distribution in liver. These results suggest that the increase in newly formed uracil nucleotides in intestine is due to increased de novo synthesis of pyrimidines in the intestine, while the increase in the kidney is due to increased salvage synthesis of uracil nucleotides from uridine synthesized in the liver and output to the circulation.In mammalian liver under normal physiological conditions the production of carbamoyl phosphate is thought to be rate-limiting for both the production of urea [1, 21 and the de novo synthesis of pyrimidines [3 -51. Carbamoyl phosphate for urea synthesis is formed by the mitochondrial enzyme carbamoyl phosphate synthase (CPS I). This enzyme uses ammonia for its substrate and is activated by N-acetyl-Lglutamate [6,7]. Carbamoyl phosphate for de novo pyrimidine synthesis is produced by the cytosolic enzyme, carbamoyl phosphate synthase I1 (CPS 11). CPS I1 is activated by 5'-phosphoribosyl diphosphate, inhibited by UTP and preferentially utilizes glutamine [3]. The intracellular separation of these enzymes serves to keep the two carbamoyl phosphate pools distinct and responsive to independent regulatory controls. However, in the presence of excess ammonium ions, the stimulation of CPS I increases mitochondrial carbamoyl phosphate levels to the point where mitochondrial carbamoyl phosphate can make substantial contributions to the cytosolic carbamoyl phosphate pool [8 -lo]. This provides a source

The initial rate of uptake of [3H]myo-inositol by L1210 murine leukaemia cells is directly proportional to the extracellular concentration and unaffected by several analogues of myo-inositol even at millimolar concentrations. Scyllitol, a geometric isomer of myo-inositol, partially inhibited the uptake of myo-inositol (40% at 0.1 mM). A portion of the uptake of myo-inositol was not inhibited even at 5 mM-scyllitol. At steady-state the intracellular concentration of [3H]myo-inositol is directly proportional to the extracellular concentration. Addition of myo-inositol to medium does not enhance the growth of L1210 cells; these cells can maintain an extracellular concentration of 20 microM-myo-inositol even when grown in myo-inositol-free medium. Synthesis of myo-inositol from glucose by L1210 cells was demonstrated by use of [13C]glucose and m.s. L1210 cells maintain myo-inositol pools by a combination of synthesis de novo and uptake of exogenous myo-inositol by either passive diffusion or a low affinity carrier.

We examine the 2022 JIBS Decade Award article by Ioannou and Serafeim (J Int Bus Stud 43(9):834–864, 2012) and review the literature since 2012 to clarify research developments in corporate social responsibility and corporate social performance (CSP) in the multinational enterprise, articulating key themes, findings and antecedents. We present a general framework that highlights unique traits and processes of CSP for MNEs. To advance scholarly progress, we delineate how new theoretical perspectives, such as organizational identity and strategic choice, can be blended with the IB literature to deepen theorization of the topic. We also discuss how new global dynamics, such as geopolitics, digitization, and activism, may shape CSP strategies and activities for MNEs and how future research can tackle these issues.