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1
Mantovani, Andrea, and Giordano Mion. "Advertising and endogenous exit in a differentiated duopoly." Recherches économiques de Louvain 72, no. 1 (2006): 19–47. http://dx.doi.org/10.1017/s0770451800007168.
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SummaryIn this paper we consider a two-stage duopoly game where firms first decide whether to invest in advertising and then compete in prices. Advertising has two effects: a market enlargement for both firms and a predatory gain for the investing firm only.Both symmetric and asymmetric equilibria may arise. The two most interesting cases are a coordination game where both firms investing and non-investing are equilibria, and a chicken game where only one firm invests while the other is possibly driven (endogenously) out of the market. Our results suggest that product differentiation has an ambiguous impact on investment in advertising and that strong product substitutabihty may induce a coordination problem.
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Mantovani, Andrea, and Giordano Mion. "Advertising and endogenous exit in a differentiated duopoly." Recherches économiques de Louvain 72, no. 1 (2006): 19. http://dx.doi.org/10.3917/rel.721.0019.
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Lavrutich, Maria N. "Capacity choice under uncertainty in a duopoly with endogenous exit." European Journal of Operational Research 258, no. 3 (2017): 1033–53. http://dx.doi.org/10.1016/j.ejor.2016.09.048.
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Chang, Myong-Hun. "Entry, Exit, and the Endogenous Market Structure in Technologically Turbulent Industries." Eastern Economic Journal 37, no. 1 (2010): 51–84. http://dx.doi.org/10.1057/eej.2010.55.
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Bayer, Christian. "Investment timing and predatory behavior in a duopoly with endogenous exit." Journal of Economic Dynamics and Control 31, no. 9 (2007): 3069–109. http://dx.doi.org/10.1016/j.jedc.2006.10.006.
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Wang, Z. M., H. Yang, and D. M. Livingston. "Endogenous E2F-1 promotes timely G0 exit of resting mouse embryo fibroblasts." Proceedings of the National Academy of Sciences 95, no. 26 (1998): 15583–86. http://dx.doi.org/10.1073/pnas.95.26.15583.
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Cont, Rama, and Lakshithe Wagalath. "RUNNING FOR THE EXIT: DISTRESSED SELLING AND ENDOGENOUS CORRELATION IN FINANCIAL MARKETS." Mathematical Finance 23, no. 4 (2012): 718–41. http://dx.doi.org/10.1111/j.1467-9965.2011.00510.x.
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Lys, Thomas Z., and Jayanthi Sunder. "Endogenous entry/exit as an alternative explanation for the disciplining role of independent analysts." Journal of Accounting and Economics 45, no. 2-3 (2008): 317–23. http://dx.doi.org/10.1016/j.jacceco.2008.02.001.
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Thiel, Jurre H. "Adviser Compensation, Endogenous Entry, and the Advice Gap." American Economic Journal: Microeconomics 14, no. 3 (2022): 76–130. http://dx.doi.org/10.1257/mic.20200074.
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To prevent biased advice, regulators increasingly ban commission payments to financial advisers. Such bans are associated with “advice gaps,” meaning that advice becomes less accessible. To understand the trade-off between the quality and accessibility of advice, this paper develops a model of price competition in advice markets with endogenous entry of advisers. While commission bans increase consumer surplus in the short run, they hurt the profitability of advisers. In the long run, advisers exit the market, advice becomes inaccessible, and consumer surplus decreases. These results imply that accounting for the endogeneity of market structure is important when regulating advice. (JEL D82, J33, L51, L84, L88, M52)
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Saito, Yuta. "A Note on Time Inconsistency and Endogenous Exits from a Currency Union." Games 13, no. 2 (2022): 21. http://dx.doi.org/10.3390/g13020021.
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This paper investigates the effects of members’ exits from a currency union on the credibility of the common currency. In our currency union model, the inflation rate of the common currency is determined by majority voting among N member countries that are heterogeneous with respect to their output shocks. Once an inflation rate of the common currency has been selected, each member decides whether to remain in the currency union or not. If a member decides to exit, it has to pay a fixed social cost and individually chooses the inflation rate of its currency. Unlike previous research on this topic, we focus on the possibility of achieving an optimal outcome, which generates no inflation bias, when more than one member is expected to leave the currency union. We show that the optimal outcome can only be achieved if no members leave the currency union.
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Yao, Haixiang, Yongzeng Lai, and Zhifeng Hao. "Uncertain exit time multi-period mean–variance portfolio selection with endogenous liabilities and Markov jumps." Automatica 49, no. 11 (2013): 3258–69. http://dx.doi.org/10.1016/j.automatica.2013.08.023.
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Geiger, Donald R., Jerome C. Servaites, and Mark A. Fuchs. "Role of starch in carbon translocation and partitioning at the plant level." Functional Plant Biology 27, no. 6 (2000): 571. http://dx.doi.org/10.1071/pp99128.
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Endogenous regulation of translocation and of carbon partitioning, major factors for integrating plant function, depend on diurnal regulation of starch synthesis and mobilization. Regulated diurnal cycling of transitory starch provides a steady carbon supply to sink growth and avoids potentially adverse high sugar levels. Carbon availability from starch affects development and alters carbon availability with respect to nitrogen. Along with sugar sensing, the level and turnover of starch are involved in endogenous regulation in response to carbohydrate status. Despite their key roles in plant metabolism, mechanisms for endogenous regulation of starch synthesis and degradation are not well characterized. Time course studies with labeled carbon reveal endogenous diurnal regulation of starch metabolism, by which sucrose synthesis from starch and newly-fixed carbon are mutually regulated in support of translocation at night, under low light, and during periods of water stress. Even under steady irradiance, which supports photosynthesis at midday levels, starch synthesis begins gradually and slows under an end-of-day circadian regulation that anticipates the dark period. Studies with Arabidopsis mutants identified two requisite components of starch mobilization, endoamylase, and glucose transport across the chloroplast inner envelope. Time course studies of carbohydrate levels and labeling studies of plant-level carbon metabolism in mutant plants with impaired ability to mobilize starch identified steps in starch mobilization that support diurnal regulation of translocation. Endogenously regulated exit of glucose across the chloroplast membrane appears to regulate starch mobilization.
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Castle, Anna M., Amy Y. Huang, and J. David Castle. "Passive Sorting in Maturing Granules of AtT-20 Cells: The Entry and Exit of Salivary Amylase and Proline-rich Protein." Journal of Cell Biology 138, no. 1 (1997): 45–54. http://dx.doi.org/10.1083/jcb.138.1.45.
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Previous studies have suggested that salivary amylase and proline-rich protein are sorted differently when expressed in AtT-20 cells (Castle, A.M., L.E. Stahl, and J.D. Castle. 1992. J. Biol. Chem. 267:13093– 13100; Colomer, V., K. Lal, T.C. Hoops, and M.J. Rindler. 1994.EMBO (Eur. Mol. Biol. Organ.) J. 13:3711– 3719). We now show that both exocrine proteins behave similarly and enter the regulated secretory pathway as judged by immunolocalization and secretagogue- dependent stimulation of secretion. Analysis of stimulated secretion of newly synthesized proline-rich protein, amylase, and endogenous hormones indicates that the exogenous proteins enter the granule pool with about the same efficiency as the endogenous hormones. However, in contrast to the endogenous hormones, proline-rich protein and amylase are progressively removed from the granule pool during the process of granule maturation such that only small portions remain in mature granules where they colocalize with the stored hormones. The exogenous proteins that are not stored are recovered from the incubation medium and are presumed to have undergone constitutive-like secretion. These results point to a level of sorting for regulated secretion after entry of proteins into forming granules and indicate that retention is essential for efficient storage. Consequently, the critical role of putative sorting receptors for regulated secretion may be in retention rather than in granule entry.
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Wollmann, Thomas G. "Trucks without Bailouts: Equilibrium Product Characteristics for Commercial Vehicles." American Economic Review 108, no. 6 (2018): 1364–406. http://dx.doi.org/10.1257/aer.20160863.
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The entry and exit of products, rather than firms, serve as the main equilibrating force in many markets, so accurately predicting changes from a merger or bankruptcy should incorporate this behavior. This paper estimates a structural model of the US commercial vehicle market and demonstrates the importance of allowing for endogenous product offerings in the context of the $85 billion automotive industry bailout in 2009. Under alternate policies that facilitate an acquisition or liquidation of GM and Chrysler, product entry and exit moderate markup increases and output decreases by up to three-quarters. (JEL D22, G33, G34, H81, L13, L62)
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Hayashi, Fumio, and Junko Koeda. "Exiting from quantitative easing." Quantitative Economics 10, no. 3 (2019): 1069–107. http://dx.doi.org/10.3982/qe1058.
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We propose an empirical framework for analyzing the macroeconomic effects of quantitative easing (QE) and apply it to Japan. The framework is a regime‐switching structural vector autoregression in which the monetary policy regime, chosen by the central bank responding to economic conditions, is endogenous and observable. QE is modeled as one of the regimes. The model incorporates an exit condition for terminating QE. We find that higher reserves at the effective lower bound raise inflation and output, and that terminating QE may be contractionary or expansionary, depending on the state of the economy at the point of exit.
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Dorey, Peter. "Towards Exit from the EU: The Conservative Party’s Increasing Euroscepticism since the 1980s." Politics and Governance 5, no. 2 (2017): 27–40. http://dx.doi.org/10.17645/pag.v5i2.873.
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Since the 1980s, Britain’s Conservative Party has become increasingly critical of the European Union, and of the country’s membership of it. So contentious and controversial has this issue become that it was a significant factor in the downfall of three consecutive Conservative Prime Ministers, all of whom found it increasingly difficult to manage their Party in Parliament, and thereby maintain any semblance of Party unity. Initially, during the 1980s and 1990s, the intra-Party divisions were between Europhiles (pro-Europeans) and Eurosceptics, but this demarcation was subsequently superseded by a division between soft Eurosceptics and hard Eurosceptics. The development and deepening of these intra-Party divisions are attributable to a plethora of endogenous and exogenous factors, the combined and cumulative effect of which ultimately led to the ‘Brexit’ vote in the June 2016 referendum.
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Chiroli, Elena, Roberta Fraschini, Alessia Beretta, Mariagrazia Tonelli, Giovanna Lucchini, and Simonetta Piatti. "Budding yeast PAK kinases regulate mitotic exit by two different mechanisms." Journal of Cell Biology 160, no. 6 (2003): 857–74. http://dx.doi.org/10.1083/jcb.200209097.
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We report the characterization of the dominant-negative CLA4t allele of the budding yeast CLA4 gene, encoding a member of the p21-activated kinase (PAK) family of protein kinases, which, together with its homologue STE20, plays an essential role in promoting budding and cytokinesis. Overproduction of the Cla4t protein likely inhibits both endogenous Cla4 and Ste20 and causes a delay in the onset of anaphase that correlates with inactivation of Cdc20/anaphase-promoting complex (APC)–dependent proteolysis of both the cyclinB Clb2 and securin. Although the precise mechanism of APC inhibition by Cla4t remains to be elucidated, our results suggest that Cla4 and Ste20 may regulate the first wave of cyclinB proteolysis mediated by Cdc20/APC, which has been shown to be crucial for activation of the mitotic exit network (MEN). We show that the Cdk1-inhibitory kinase Swe1 is required for the Cla4t-dependent delay in cell cycle progression, suggesting that it might be required to prevent full Cdc20/APC and MEN activation. In addition, inhibition of PAK kinases by Cla4t prevents mitotic exit also by a Swe1-independent mechanism impinging directly on the MEN activator Tem1.
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Igami, Mitsuru, and Kosuke Uetake. "Mergers, Innovation, and Entry-Exit Dynamics: Consolidation of the Hard Disk Drive Industry, 1996–2016." Review of Economic Studies 87, no. 6 (2019): 2672–702. http://dx.doi.org/10.1093/restud/rdz044.
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Abstract How far should an industry be allowed to consolidate when competition and innovation are endogenous? We develop a stochastically alternating-move game of dynamic oligopoly and estimate it using data from the hard disk drive industry, in which a dozen global players consolidated into only three in the last 20 years. We find plateau-shaped equilibrium relationships between competition and innovation, with heterogeneity across time and productivity. Our counterfactual simulations suggest the current rule-of-thumb policy, which stops mergers when three or fewer firms exist, strikes approximately the right balance between pro-competitive effects and value-destruction side effects in this dynamic welfare trade-off.
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Durceylan, Esra. "Tax efficiency in a model of endogenous markups." SERIEs 10, no. 3-4 (2019): 401–18. http://dx.doi.org/10.1007/s13209-019-00209-w.
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Abstract Efficiency comparison of ad valorem and unit taxes has been traditionally based on consumer welfare. However, if the tax instrument also affects the distribution of firms over their productivities, the policy maker may be concerned about the implications on aggregate productivity as well. This paper makes an efficiency comparison of ad valorem and unit taxes by allowing the distribution of firms to respond to changes in policy. First, I make an efficiency comparison in a model with monopolistically competitive firms that are homogenous with respect to their productivity levels. Consumer preferences exhibit love for variety and allow firms to adjust their markups. I find that ad valorem tax is more efficient. Allowing for firm heterogeneity overturns this result at high revenue requirements. As the tax rate increases, ad valorem tax causes excessive exit of firms which makes the market more competitive. Hence, few surviving firms price lower by decreasing their markups. Lower prices decrease the tax revenue collected. As a result under ad valorem tax regime, higher consumer surplus is dominated by lower tax revenue. On the other hand, production is concentrated among relatively more productive firms. Thus, aggregate productivity is higher under ad valorem tax regime.
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Acemoglu, Daron, Ufuk Akcigit, Harun Alp, Nicholas Bloom, and William Kerr. "Innovation, Reallocation, and Growth." American Economic Review 108, no. 11 (2018): 3450–91. http://dx.doi.org/10.1257/aer.20130470.
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We build a model of firm-level innovation, productivity growth, and reallocation featuring endogenous entry and exit. A new and central economic force is the selection between high- and low-type firms, which differ in terms of their innovative capacity. We estimate the parameters of the model using US Census microdata on firm-level output, R&D, and patenting. The model provides a good fit to the dynamics of firm entry and exit, output, and R&D. Taxing the continued operation of incumbents can lead to sizable gains (of the order of 1.4 percent improvement in welfare) by encouraging exit of less productive firms and freeing up skilled labor to be used for R&D by high-type incumbents. Subsidies to the R&D of incumbents do not achieve this objective because they encourage the survival and expansion of low-type firms. (JEL D21, D24, H25, L52, O31, O34)
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Moon, Soojae. "Endogenous Tradability, International Relative Prices, and the International Transmission of Business Cycles." Research in Applied Economics 11, no. 3 (2019): 111. http://dx.doi.org/10.5296/rae.v11i3.15272.
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This paper propose a two-country, dynamic, stochastic, general equilibrium (DSGE) model with endogenous tradability, product differentiation, variously determined physical capital, and an elastic labor supply to explore the propagation of business cycles across countries. The model successfully addresses international relative price dynamics (its appreciation with positive home productivity shock, called the ‘Harrod-Balassa-Samuelson Effect’) through the entry of producers and their cut-off productivities of exporting. The use of endogenous physical capital in the model induces a more realistic framework since the simulated model is compared to the U.S. investment data that covers spending on capital equipment, structures and inventories for producers’ entry and exit dynamics. Building the model with endogenous capital and elastic labor supply weakens the volatility of investment compared to conventional international real business cycle (IRBC) models. The model also accounts for several features of the data, such as the volatility of aggregate variables and their correlations with GDP.
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Li, Binghui, Nan Jia, Reuben Kapur, and Kristin T. Chun. "Cul4A targets p27 for degradation and regulates proliferation, cell cycle exit, and differentiation during erythropoiesis." Blood 107, no. 11 (2006): 4291–99. http://dx.doi.org/10.1182/blood-2005-08-3349.
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AbstractAs erythroid progenitors differentiate into precursors and finally mature red blood cells, lineage-specific genes are induced, and proliferation declines until cell cycle exit. Cul4A encodes a core subunit of a ubiquitin ligase that targets proteins for ubiquitin-mediated degradation, and Cul4A-haploinsufficient mice display hematopoietic dysregulation with fewer multipotential and erythroid-committed progenitors. In this study, stress induced by 5-fluorouracil or phenylhydrazine revealed a delay in the recovery of erythroid progenitors, early precursors, and normal hematocrits in Cul4A+/– mice. Conversely, overexpression of Cul4A in a growth factor-dependent, proerythroblast cell line increased proliferation and the proportion of cells in S phase. When these proerythroblasts were induced to terminally differentiate, endogenous Cul4A protein expression declined 3.6-fold. Its enforced expression interfered with erythrocyte maturation and cell cycle exit and, instead, promoted proliferation. Furthermore, p27 normally accumulates during erythroid terminal differentiation, but Cul4A-enforced expression destabilized p27 and attenuated its accumulation. Cul4A and p27 proteins coimmunoprecipitate, indicating that a Cul4A ubiquitin ligase targets p27 for degradation. These findings indicate that a Cul4A ubiquitin ligase positively regulates proliferation by targeting p27 for degradation and that Cul4A down-regulation during terminal erythroid differentiation allows p27 to accumulate and signal cell cycle exit.
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Li, Yan, and Kiwon Song. "The N-Terminal Domain of Bfa1 Coordinates Mitotic Exit Independent of GAP Activity in Saccharomyces cerevisiae." Cells 11, no. 14 (2022): 2179. http://dx.doi.org/10.3390/cells11142179.
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The spindle position checkpoint (SPOC) of budding yeast delays mitotic exit in response to misaligned spindles to ensure cell survival and the maintenance of genomic stability. The GTPase-activating protein (GAP) complex Bfa1–Bub2, a key SPOC component, inhibits the GTPase Tem1 to induce mitotic arrest in response to DNA and spindle damage, as well as spindle misorientation. However, previous results strongly suggest that Bfa1 exerts a GAP-independent function in blocking mitotic exit in response to misaligned spindles. Thus, the molecular mechanism by which Bfa1 controls mitotic exit in response to misaligned spindles remains unclear. Here, we observed that overexpression of the N-terminal domain of Bfa1 (Bfa1-D16), which lacks GAP activity and cannot localize to the spindle pole body (SPB), induced cell cycle arrest along with hyper-elongation of astral microtubules (aMTs) as Bfa1 overexpression in Δbub2. We found that Δbub2 cells overexpressing Bfa1 or Bfa1-D16 inhibited activation of Mob1, which is responsible for mitotic exit. In anaphase-arrested cells, Bfa1-D16 overexpression inhibited Tem1 binding to the SPB as well as Bfa1 overexpression. Additionally, endogenous levels of Bfa1-D16 showed minor SPOC activity that was not regulated by Kin4. These results suggested that Bfa1-D16 may block mitotic exit through inhibiting Tem1 activity outside of SPBs. Alternatively, Bfa1-D16 dispersed out of SPBs may block Tem1 binding to SPBs by physically interacting with Tem1 as previously reported. Moreover, we observed hyper-elongated aMTs in tem1-3, cdc15-2, and dbf2-2 mutants that induce anaphase arrest and cannot undergo mitotic exit at restrictive temperatures, suggesting that aMT dynamics are closely related to the regulation of mitotic exit. Altogether, these observations suggest that Bfa1 can control the SPOC independent of its GAP activity and SPB localization.
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Shad, Muhammad Riaz, and Sajid Iqbal. "FROM INTERVENTION TO EXIT: AN ANALYSIS OF POST-9/11 US STRATEGIES IN AFGHANISTAN." Margalla Papers 25, no. 2 (2021): 23–34. http://dx.doi.org/10.54690/margallapapers.25.2.70.
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Following the US exit from Afghanistan, the debate revolves around why US intervention in Afghanistan, the longest and one of the most expensive in its history, has failed in defeating the Taliban and realising a durable state-building. The debate considers endogenous factors that explore US and Taliban strategies and exogenous factors that underline the role of regional and extra-regional actors in determining the outcome of the Afghan conflict. This paper, therefore, focuses on faults and inconsistencies within and across US strategies in Afghanistan, i.e., the use of military force, political settlement, and state-building. It also examines US strategies vis-à-vis conflict in Afghanistan under four US administrations – from Bush to Biden – to ascertain why these strategies proved ineffective. These strategies have been analysed by following the conceptual framework of Game Theory. The paper argues that US strategies for entering Afghanistan were detached from the ground realities, which was the critical factor for its failure to achieve the desired outcome of the conflict. Bibliography Entry Shad, Muhammad Riaz, Sajid Iqbal. 2021. "From Intervention to Exit: An Analysis of Post-9/11 US Strategies in Afghanistan." Margalla Papers 25 (2): 23-34.
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Shad, Muhammad Riaz, and Sajid Iqbal. "FROM INTERVENTION TO EXIT: AN ANALYSIS OF POST-9/11 US STRATEGIES IN AFGHANISTAN." Margalla Papers 25, no. 2 (2021): 23–34. http://dx.doi.org/10.54690/margallapapers.25.2.70.
Texte intégralRésumé :
Following the US exit from Afghanistan, the debate revolves around why US intervention in Afghanistan, the longest and one of the most expensive in its history, has failed in defeating the Taliban and realising a durable state-building. The debate considers endogenous factors that explore US and Taliban strategies and exogenous factors that underline the role of regional and extra-regional actors in determining the outcome of the Afghan conflict. This paper, therefore, focuses on faults and inconsistencies within and across US strategies in Afghanistan, i.e., the use of military force, political settlement, and state-building. It also examines US strategies vis-à-vis conflict in Afghanistan under four US administrations – from Bush to Biden – to ascertain why these strategies proved ineffective. These strategies have been analysed by following the conceptual framework of Game Theory. The paper argues that US strategies for entering Afghanistan were detached from the ground realities, which was the critical factor for its failure to achieve the desired outcome of the conflict. Bibliography Entry Shad, Muhammad Riaz, Sajid Iqbal. 2021. "From Intervention to Exit: An Analysis of Post-9/11 US Strategies in Afghanistan." Margalla Papers 25 (2): 23-34.
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Arnaud, Frederick, Pablo R. Murcia, and Massimo Palmarini. "Mechanisms of Late Restriction Induced by an Endogenous Retrovirus." Journal of Virology 81, no. 20 (2007): 11441–51. http://dx.doi.org/10.1128/jvi.01214-07.
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ABSTRACT The host has developed during evolution a variety of “restriction factors” to fight retroviral infections. We investigated the mechanisms of a unique viral block acting at late stages of the retrovirus replication cycle. The sheep genome is colonized by several copies of endogenous retroviruses, known as enJSRVs, which are highly related to the oncogenic jaagsiekte sheep retrovirus (JSRV). enJS56A1, one of the enJSRV proviruses, can act as a restriction factor by blocking viral particles release of the exogenous JSRV. We show that in the absence of enJS56A1 expression, the JSRV Gag (the retroviral internal structural polyprotein) targets initially the pericentriolar region, in a dynein and microtubule-dependent fashion, and then colocalizes with the recycling endosomes. Indeed, by inhibiting the endocytosis and trafficking of recycling endosomes we hampered JSRV exit from the cell. Using a variety of approaches, we show that enJS56A1 and JSRV Gag interact soon after synthesis and before pericentriolar/recycling endosome targeting of the latter. The transdominant enJS56A1 induces intracellular Gag accumulation in microaggregates that colocalize with the aggresome marker GFP-250 but develop into bona fide aggresomes only when the proteasomal machinery is inhibited. The data argue that dominant-negative proteins can modify the overall structure of Gag multimers/viral particles hampering the interaction of the latter with the cellular trafficking machinery.
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Galvanovskis, Juris, Matthias Braun та Patrik Rorsman. "Exocytosis from pancreatic β-cells: mathematical modelling of the exit of low-molecular-weight granule content". Interface Focus 1, № 1 (2010): 143–52. http://dx.doi.org/10.1098/rsfs.2010.0006.
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Pancreatic β-cells use Ca 2+ -dependent exocytosis of large dense core vesicles to release insulin. Exocytosis in β-cells has been studied biochemically, biophysically and optically. We have previously developed a biophysical method to monitor release of endogenous intragranular constituents that are co-released with insulin. This technique involves the expression of ionotropic membrane receptors in the β-cell plasma membrane and enables measurements of exocytosis of individual vesicles with sub-millisecond resolution. Like carbon fibre amperometry, this method allows fine details of the release process, like the expansion of the fusion pore (the narrow connection between the granule lumen and the extracellular space), to be monitored. Here, we discuss experimental data obtained with this method within the framework of a simple mathematical model that describes the release of low-molecular constituents during exocytosis of the insulin granules. Our findings suggest that the fusion pore functions as a molecular sieve, allowing differential release of low- and high-molecular-weight granule constituents.
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Callahan, K. M., J. F. Rowell, M. J. Soloski, C. E. Machamer, and R. F. Siliciano. "HIV-1 envelope protein is expressed on the surface of infected cells before its processing and presentation to class II-restricted T lymphocytes." Journal of Immunology 151, no. 6 (1993): 2928–42. http://dx.doi.org/10.4049/jimmunol.151.6.2928.
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Abstract T lymphocytes are activated upon binding of their Ag receptors to a complex of Ag-derived peptides and MHC class I or class II molecules expressed on the surface of APC. It is now well established that APC degrade exogenous Ag in acidic endosomal compartments, and that Ag fragments bind to class II molecules moving through these compartments on their way to the surface of the APC. Although peptides derived from some endogenous Ag can also bind to class II molecules and subsequently be recognized by class II-restricted T cells, the intracellular trafficking pathways that enable endogenous proteins to be processed for association with class II molecules remain controversial. We have analyzed the mechanism by which the envelope (env) protein of the HIV-1 is processed in infected cells for recognition by class II-restricted T cells. A large number of env-specific class II-restricted human CTL clones were shown to lyse B-lymphoblastoid cell lines expressing the env. A novel dilutional assay proved that A novel dilutional assay proved that recognition of endogenous env protein was not a consequence of release and re-uptake of the env protein and subsequent processing by the standard class II-restricted pathway. Processing of endogenous env protein required that the protein be co-translationally translocated into the endoplasmic reticulum (ER) and then exit the ER, since the class II-restricted CTL did not recognize env protein localized to the cytosol or retained in the ER of target cells. Under these conditions, however, class I-restricted recognition was readily demonstrated. Finally, class II-restricted recognition was strikingly dependent upon the steady state level of surface env protein, since extracellular reagents that removed intact env protein from the surface of target cells inhibited recognition. This inhibition operated at the Ag-processing level rather than at the level of subsequent Ag recognition. These results provide the first direct evidence that endogenously synthesized membrane proteins enter the class II-restricted Ag-processing pathway after expression on the cell surface in an intact form.
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Chun, Kristin T., Nan Jia, Yahaira M. Naaldjik, Reuben Kapur, and Binghui Li. "CUL-4A Targets p27 for Degradation and Regulates Proliferation, Cell Cycle Exit, and Differentiation during Erythropoiesis." Blood 106, no. 11 (2005): 1358. http://dx.doi.org/10.1182/blood.v106.11.1358.1358.
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Abstract As erythroid progenitors differentiate into precursors and finally mature red blood cells, they induce the expression of lineage-specific genes, and their proliferation declines until cell cycle exit. CUL-4A encodes a core subunit of a ubiquitin ligase that targets proteins for ubiquitin-mediated degradation, and CUL-4A haploinsufficient mice display hematopoietic dysregulation with fewer multipotential and erythroid committed progenitors (3-fold and 5-fold, respectively). In this study, stress induced by 5-fluorouracil or phenylhydrazine reveals a delay in the ability of CUL-4A +/− mice to recover erythroid progenitors and precursors and to reestablish normal hematocrits. Conversely, over-expression of CUL-4A in a growth factor-dependent, proerythroblast cell line increases proliferation 34% (tritiated thymidine incorporation) and the proportion of cells in S-phase 5%. When these cells are induced to terminally differentiate, endogenous CUL-4A protein expression declines 3.6-fold. Its enforced expression interferes with erythrocyte maturation (beta-globin induction) and cell cycle exit, and instead promotes proliferation. Furthermore, p27 accumulates during erythroid terminal differentiation, but CUL-4A enforced expression increases p27 protein turnover nearly 7-fold and attenuates its accumulation. CUL-4A and p27 proteins co-immunoprecipitate, indicating that a Cul-4A ubiquitin ligase targets p27 for degradation. These findings suggest that a Cul-4A ubiquitin ligase positively regulates proliferation by targeting p27 for degradation and that CUL-4A down-regulation during erythroid terminal differentiation allows p27 to accumulate and signal cell cycle exit.
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Flatt, Patricia M., Luo Jia Tang, Caroline D. Scatena, Suzanne T. Szak, and Jennifer A. Pietenpol. "p53 Regulation of G2 Checkpoint Is Retinoblastoma Protein Dependent." Molecular and Cellular Biology 20, no. 12 (2000): 4210–23. http://dx.doi.org/10.1128/mcb.20.12.4210-4223.2000.
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ABSTRACT In the present study, we investigated the role of p53 in G2 checkpoint function by determining the mechanism by which p53 prevents premature exit from G2 arrest after genotoxic stress. Using three cell model systems, each isogenic, we showed that either ectopic or endogenous p53 sustained a G2arrest activated by ionizing radiation or adriamycin. The mechanism was p21 and retinoblastoma protein (pRB) dependent and involved an initial inhibition of cyclin B1-Cdc2 activity and a secondary decrease in cyclin B1 and Cdc2 levels. Abrogation of p21 or pRB function in cells containing wild-type p53 blocked the down-regulation of cyclin B1 and Cdc2 expression and led to an accelerated exit from G2after genotoxic stress. Thus, similar to what occurs in p21 and p53 deficiency, pRB loss can uncouple S phase and mitosis after genotoxic stress in tumor cells. These results indicate that similar molecular mechanisms are required for p53 regulation of G1 and G2 checkpoints.
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Natarajan, Rajalaxmi, and Adam D. Linstedt. "A Cyclingcis-Golgi Protein Mediates Endosome-to-Golgi Traffic." Molecular Biology of the Cell 15, no. 11 (2004): 4798–806. http://dx.doi.org/10.1091/mbc.e04-05-0366.
Texte intégralRésumé :
Toxins can invade cells by using a direct endosome-to-Golgi endocytic pathway that bypasses late endosomes/prelysosomes. This is also a route used by endogenous proteins, including GPP130, which is an integral membrane protein retrieved via the bypass pathway from endosomes to its steady-state location in the cis-Golgi. An RNA interference-based test revealed that GPP130 was required for efficient exit of Shiga toxin B-fragment from endosomes en route to the Golgi apparatus. Furthermore, two proteins whose Golgi targeting depends on endosome-to-Golgi retrieval in the bypass pathway accumulated in early/recycling endosomes in the absence of GPP130. GPP130 activity seemed specific to bypass pathway trafficking because the targeting of other tested proteins, including those retrieved to the Golgi via the more conventional late endosome route, was unaltered. Thus, a distally cycling Golgi protein mediates exit from endosomes and thereby underlies Shiga toxin invasion and retrieval-based targeting of other cycling Golgi proteins.
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Okamuro, Hiroyuki, Yasushi Hara, and Yunosuke Iwaki. "Impact of Consumer Awareness and Behavior on Business Exits in the Hospitality, Tourism, Entertainment, and Culture Industries under the COVID-19 Pandemic." Administrative Sciences 12, no. 4 (2022): 169. http://dx.doi.org/10.3390/admsci12040169.
Texte intégralRésumé :
Empirical studies on small business survival and exits focus on endogenous firms and top manager characteristics, whereas few studies consider exogenous demand shocks and local consumer awareness and behavior, which are especially important for local hospitality industries. Therefore, this study addresses this research gap by targeting the COVID-19 pandemic and anti-contagion policies as a local demand shock for service industries. We empirically investigate the causal effects of changing local consumer awareness and behavior under COVID-19 on business exits at the prefecture-industry level. Based on a panel fixed-effect estimation using a longitudinal dataset of 32 service industries in 47 prefectures over 10 months in Japan, we demonstrate that an increase in consumers’ risk aversion and sympathy for self-restraint from going out, and a decrease in going out with family members, significantly increase the exit ratio in specific service industries in the same prefecture. Moreover, we find that these effects vary by consumer type depending on factors such as gender, age, income level, and household structure.
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Wong, Christopher, and Richard Roy. "AMPK Regulates Developmental Plasticity through an Endogenous Small RNA Pathway in Caenorhabditis elegans." International Journal of Molecular Sciences 21, no. 6 (2020): 2238. http://dx.doi.org/10.3390/ijms21062238.
Texte intégralRésumé :
Caenorhabditis elegans larvae can undergo developmental arrest upon entry into the dauer stage in response to suboptimal growth conditions. Dauer larvae can exit this stage in replete conditions with no reproductive consequence. During this diapause stage, the metabolic regulator AMP-activated protein kinase (AMPK) ensures that the germ line becomes quiescent to maintain germ cell integrity. Animals that lack all AMPK signalling undergo germline hyperplasia upon entering dauer, while those that recover from this stage become sterile. Neuronal AMPK expression in otherwise AMPK-deficient animals is sufficient for germline quiescence and germ cell integrity and its effects are likely mediated through an endogenous small RNA pathway. Upon impairing small RNA biosynthesis, the post-dauer fertility is restored in AMPK mutants. These data suggest that AMPK may function in neurons to relay a message through small RNAs to the germ cells to alter their quiescence in the dauer stage, thus challenging the permeability of the Weismann barrier.
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Song, Sukgil, and Kyung S. Lee. "A Novel Function of Saccharomyces cerevisiae CDC5 in Cytokinesis." Journal of Cell Biology 152, no. 3 (2001): 451–70. http://dx.doi.org/10.1083/jcb.152.3.451.
Texte intégralRésumé :
Coordination of mitotic exit with timely initiation of cytokinesis is critical to ensure completion of mitotic events before cell division. The Saccharomyces cerevisiae polo kinase Cdc5 functions in a pathway leading to the degradation of mitotic cyclin Clb2, thereby permitting mitotic exit. Here we provide evidence that Cdc5 also plays a role in regulating cytokinesis and that an intact polo-box, a conserved motif in the noncatalytic COOH-terminal domain of Cdc5, is required for this event. Depletion of Cdc5 function leads to an arrest in cytokinesis. Overexpression of the COOH-terminal domain of Cdc5 (cdc5ΔN), but not the corresponding polo-box mutant, resulted in connected cells. These cells shared cytoplasms with incomplete septa, and possessed aberrant septin ring structures. Provision of additional copies of endogenous CDC5 remedied this phenotype, suggesting a dominant-negative inhibition of cytokinesis. The polo-box–dependent interactions between Cdc5 and septins (Cdc11 and Cdc12) and genetic interactions between the dominant-negative cdc5ΔN and Cyk2/Hof1 or Myo1 suggest that direct interactions between cdc5ΔN and septins resulted in inhibition of Cyk2/Hof1- and Myo1-mediated cytokinetic pathways. Thus, we propose that Cdc5 may coordinate mitotic exit with cytokinesis by participating in both anaphase promoting complex activation and a polo-box–dependent cytokinetic pathway.
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Lu, Zhuomei, Donald Joseph, Elisabeth Bugnard, Kristien J. M. Zaal, and Evelyn Ralston. "Golgi Complex Reorganization during Muscle Differentiation: Visualization in Living Cells and Mechanism." Molecular Biology of the Cell 12, no. 4 (2001): 795–808. http://dx.doi.org/10.1091/mbc.12.4.795.
Texte intégralRésumé :
During skeletal muscle differentiation, the Golgi complex (GC) undergoes a dramatic reorganization. We have now visualized the differentiation and fusion of living myoblasts of the mouse muscle cell line C2, permanently expressing a mannosidase-green fluorescent protein (GFP) construct. These experiments reveal that the reorganization of the GC is progressive (1–2 h) and is completed before the cells start fusing. Fluorescence recovery after photobleaching (FRAP), immunofluorescence, and immunogold electron microscopy demonstrate that the GC is fragmented into elements localized near the endoplasmic reticulum (ER) exit sites. FRAP analysis and the ER relocation of endogenous GC proteins by phospholipase A2 inhibitors demonstrate that Golgi-ER cycling of resident GC proteins takes place in both myoblasts and myotubes. All results support a model in which the GC reorganization in muscle reflects changes in the Golgi-ER cycling. The mechanism is similar to that leading to the dispersal of the GC caused, in all mammalian cells, by microtubule-disrupting drugs. We propose that the trigger for the dispersal results, in muscle, from combined changes in microtubule nucleation and ER exit site localization, which place the ER exit sites near microtubule minus ends. Thus, changes in GC organization that initially appear specific to muscle cells, in fact use pathways common to all mammalian cells.
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Kops, Geert J. P. L., Rene H. Medema, Janet Glassford, et al. "Control of Cell Cycle Exit and Entry by Protein Kinase B-Regulated Forkhead Transcription Factors." Molecular and Cellular Biology 22, no. 7 (2002): 2025–36. http://dx.doi.org/10.1128/mcb.22.7.2025-2036.2002.
Texte intégralRésumé :
ABSTRACT AFX-like Forkhead transcription factors, which are controlled by phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling, are involved in regulating cell cycle progression and cell death. Both cell cycle arrest and induction of apoptosis are mediated in part by transcriptional regulation of p27kip1. Here we show that the Forkheads AFX (FOXO4) and FKHR-L1 (FOXO3a) also directly control transcription of the retinoblastoma-like p130 protein and cause upregulation of p130 protein expression. Detailed analysis of p130 regulation demonstrates that following Forkhead-induced cell cycle arrest, cells enter G0 and become quiescent. This is shown by a change in phosphorylation of p130 to G0-specific forms and increased p130/E2F-4 complex formation. Most importantly, long-term Forkhead activation causes a sustained but reversible inhibition of proliferation without a marked increase in apoptosis. As for the activity of the Forkheads, we also show that protein levels of p130 are controlled by endogenous PI3K/PKB signaling upon cell cycle reentry. Surprisingly, not only nontransformed cells, but also cancer cells such as human colon carcinoma cells, are forced into quiescence by Forkhead activation. We therefore propose that Forkhead inactivation by PKB signaling in quiescent cells is a crucial step in cell cycle reentry and contributes to the processes of transformation and regeneration.
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Héron-Milhavet, Lisa, Celine Franckhauser, Vanessa Rana, et al. "Only Akt1 Is Required for Proliferation, while Akt2 Promotes Cell Cycle Exit through p21 Binding." Molecular and Cellular Biology 26, no. 22 (2006): 8267–80. http://dx.doi.org/10.1128/mcb.00201-06.
Texte intégralRésumé :
ABSTRACT Protein kinase B (PKB/Akt) is an important modulator of insulin signaling, cell proliferation, and survival. Using small interfering RNA duplexes in nontransformed mammalian cells, we show that only Akt1 is essential for cell proliferation, while Akt2 promotes cell cycle exit. Silencing Akt1 resulted in decreased cyclin A levels and inhibition of S-phase entry, effects not seen with Akt2 knockdown and specifically rescued by microinjection of Akt1, not Akt2. In differentiating myoblasts, Akt2 knockout prevented myoblasts from exiting the cell cycle and showed sustained cyclin A expression. In contrast, overexpression of Akt2 reduced cyclin A and hindered cell cycle progression in M-G1 with increased nuclear p21. p21 is a major target in the differential effects of Akt isoforms, with endogenous Akt2 and not Akt1 binding p21 in the nucleus and increasing its level. Accordingly, Akt2 knockdown cells, and not Akt1 knockdown cells, showed reduced levels of p21. A specific Akt2/p21 interaction can be reproduced in vitro, and the Akt2 binding site on p21 is similar to that in cyclin A spanning T145 to T155, since (i) prior incubation with cyclin A prevents Akt2 binding, (ii) T145 phosphorylation on p21 by Akt1 prevents Akt2 binding, and (iii) binding Akt2 prevents phosphorylation of p21 by Akt1. These data show that specific interaction of the Akt2 isoform with p21 is key to its negative effect on normal cell cycle progression.
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Irwin, Douglas A. "Did Late-Nineteenth-Century U.S. Tariffs Promote Infant Industries? Evidence from the Tinplate Industry." Journal of Economic History 60, no. 2 (2000): 335–60. http://dx.doi.org/10.1017/s0022050700025122.
Texte intégralRésumé :
Did late-nineteenth-century U.S. tariffs promote infant industries? After earlier failures, the tinplate industry became established and flourished after receiving protection with the 1890 McKinley tariff. Treating producers' entry and exit decisions as endogenous, a probability model is estimated to determine the conditions under which domestic tinplate production will occur. Counterfactual simulations indicate that, without the McKinley duties, domestic tinplate production would have arisen about a decade later as U.S. iron and steel input prices converged with those in Britain. Although the traiff accelerated the industry's development, welfare calculations suggest that protection does not pass a cost-benefit test.
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Paris, Maryline, Wen-Horng Wang, Min-Hwa Shin, David S. Franklin, and Ourania M. Andrisani. "Homeodomain Transcription Factor Phox2a, via Cyclic AMP-Mediated Activation, Induces p27Kip1 Transcription, Coordinating Neural Progenitor Cell Cycle Exit and Differentiation." Molecular and Cellular Biology 26, no. 23 (2006): 8826–39. http://dx.doi.org/10.1128/mcb.00575-06.
Texte intégralRésumé :
ABSTRACT Mechanisms coordinating neural progenitor cell cycle exit and differentiation are incompletely understood. The cyclin-dependent kinase inhibitor p27Kip1 is transcriptionally induced, switching specific neural progenitors from proliferation to differentiation. However, neuronal differentiation-specific transcription factors mediating p27Kip1 transcription have not been identified. We demonstrate the homeodomain transcription factor Phox2a, required for central nervous system (CNS)- and neural crest (NC)-derived noradrenergic neuron differentiation, coordinates cell cycle exit and differentiation by inducing p27Kip1 transcription. Phox2a transcription and activation in the CNS-derived CAD cell line and primary NC cells is mediated by combined cyclic AMP (cAMP) and bone morphogenetic protein 2 (BMP2) signaling. In the CAD cellular model, cAMP and BMP2 signaling initially induces proliferation of the undifferentiated precursors, followed by p27Kip1 transcription, G1 arrest, and neuronal differentiation. Small interfering RNA silencing of either Phox2a or p27Kip1 suppresses p27Kip1 transcription and neuronal differentiation, suggesting a causal link between p27Kip1 expression and differentiation. Conversely, ectopic Phox2a expression via the Tet-off expression system promotes accelerated CAD cell neuronal differentiation and p27Kip1 transcription only in the presence of cAMP signaling. Importantly, endogenous or ectopically expressed Phox2a activated by cAMP signaling binds homeodomain cis-acting elements of the p27Kip1 promoter in vivo and mediates p27Kip1-luciferase expression in CAD and NC cells. We conclude that developmental cues of cAMP signaling causally link Phox2a activation with p27Kip1 transcription, thereby coordinating neural progenitor cell cycle exit and differentiation.
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Munarriz, Eliana, Daniela Barcaroli, Anastasis Stephanou, et al. "PIAS-1 Is a Checkpoint Regulator Which Affects Exit from G1 and G2 by Sumoylation of p73." Molecular and Cellular Biology 24, no. 24 (2004): 10593–610. http://dx.doi.org/10.1128/mcb.24.24.10593-10610.2004.
Texte intégralRésumé :
ABSTRACT p73 is a recently described member of the p53 family, and, like p53, it undergoes a number of posttranslational modifications. Here we show, by yeast two-hybrid screening, pull-down assays, and coimmunoprecipitation, that p73α, -β, and -γ bind to the protein inhibitor of activated STAT-1 (PIAS-1) and that this binding stabilizes p73. PIAS-1 also sumoylates p73α, although not the C-terminally truncated isoforms p73β and -γ, and this requires the RING finger domain of PIAS-1. The ΔNp73α isoform can also bind, and be sumoylated by, PIAS-1. PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix. PIAS-1 is expressed predominantly during S phase, and PIAS-1 overexpression reduces p73-mediated transcription of p21, with a reduction of cells in G1 and cell cycle reentry. Inhibition of endogenous PIAS-1 by RNA interference reduces the proportion of cells in S phase and induces G2 arrest. These data suggest that PIAS-1, acting partly through binding and sumoylation of p73, is an important component of the cell cycle machinery.
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van Zon, Wouter, Janneke Ogink, Bas ter Riet, René H. Medema, Hein te Riele, and Rob M. F. Wolthuis. "The APC/C recruits cyclin B1–Cdk1–Cks in prometaphase before D box recognition to control mitotic exit." Journal of Cell Biology 190, no. 4 (2010): 587–602. http://dx.doi.org/10.1083/jcb.200912084.
Texte intégralRésumé :
The ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated at prometaphase by mitotic phosphorylation and binding of its activator, Cdc20. This initiates cyclin A degradation, whereas cyclin B1 is stabilized by the spindle checkpoint. Upon checkpoint release, the RXXL destruction box (D box) was proposed to direct cyclin B1 to core APC/C or Cdc20. In this study, we report that endogenous cyclin B1–Cdk1 is recruited to checkpoint-inhibited, phosphorylated APC/C in prometaphase independently of Cdc20 or the cyclin B1 D box. Like cyclin A, cyclin B1 binds the APC/C by the Cdk cofactor Cks and the APC3 subunit. Prior binding to APC/CCdc20 makes cyclin B1 a better APC/C substrate in metaphase, driving mitotic exit and cytokinesis. We conclude that in prometaphase, the phosphorylated APC/C can recruit both cyclin A and cyclin B1 in a Cks-dependent manner. This suggests that the spindle checkpoint blocks D box recognition of APC/C-bound cyclin B1, whereas distinctive complexes between the N terminus of cyclin A and Cdc20 evade checkpoint control.
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JESO, Bruno DI, Luca ULIANICH, Francesco PACIFICO, et al. "Folding of thyroglobulin in the calnexin/calreticulin pathway and its alteration by loss of Ca2+ from the endoplasmic reticulum." Biochemical Journal 370, no. 2 (2003): 449–58. http://dx.doi.org/10.1042/bj20021257.
Texte intégralRésumé :
During its initial folding in the endoplasmic reticulum (ER), newly synthesized thyroglobulin (Tg) is known to interact with calnexin and other ER molecular chaperones, but its interaction with calreticulin has not been examined previously. In the present study, we have investigated the interactions of endogenous Tg with calreticulin and with several other ER chaperones. We find that, in FRTL-5 and PC-Cl3 cells, calnexin and calreticulin interact with newly synthesized Tg in a carbohydrate-dependent manner, with largely overlapping kinetics that are concomitant with the maturation of Tg intrachain disulphide bonds, preceding Tg dimerization and exit from the ER. Calreticulin co-precipitates more newly synthesized Tg than does calnexin; however, using two different experimental approaches, calnexin and calreticulin were found in ternary complexes with Tg, making this the first endogenous protein reported in ternary complexes with calnexin and calreticulin in the ER of live cells. Depletion of Ca2+ from the ER elicited by thapsigargin (a specific inhibitor of ER Ca2+-ATPases) results in retention of Tg in this organelle. Interestingly, thapsigargin treatment induces the premature exit of Tg from the calnexin/calreticulin cycle, while stabilizing and prolonging interactions of Tg with BiP (immunoglobulin heavy chain binding protein) and GRP94 (glucose-regulated protein 94), two chaperones whose binding is not carbohydrate-dependent. Our results suggest that calnexin and calreticulin, acting in ternary complexes with a large glycoprotein substrate such as Tg, might be engaged in the folding of distinct domains, and indicate that lumenal Ca2+ strongly influences the folding of exportable glycoproteins, in part by regulating the balance of substrate binding to different molecular chaperone systems within the ER.
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Warenius, Hilmar, Tracy Gorman, Matthew Jones, et al. "168 Post-radiation exit from G2 is related to endogenous RAF-1 protein levels in human cells expressing wild-type p53." International Journal of Radiation Oncology*Biology*Physics 36, no. 1 (1996): 242. http://dx.doi.org/10.1016/s0360-3016(97)85508-3.
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Roberts, James W., and Andrew Sweeting. "Bailouts and the Preservation of Competition: The Case of the Federal Timber Contract Payment Modification Act." American Economic Journal: Microeconomics 8, no. 3 (2016): 257–88. http://dx.doi.org/10.1257/mic.20150070.
Texte intégralRésumé :
We estimate the value of competition in United States Forest Service (USFS) timber auctions, in the context of the Reagan administration's bailout of firms that faced substantial losses on existing contracts. We use a model with endogenous entry by asymmetric firms, allowing survivors to respond to the exit of bailed-out firms by entering more auctions and for these marginal entrants to have lower values than firms that would choose to enter in any event, a selective entry effect. Observed asymmetries and selective entry contribute to us finding that the bailout may have increased USFS revenues in subsequent auctions quite substantially. (JEL D44, H81, H82, L73, Q23)
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Pinkovetskaia, Iuliia S. "ASSESSMENT OF REASONS FOR THE TERMINATION ACTIVITY OF ENTREPRENEURS IN MODERN ECONOMIES." Herald of Omsk University. Series: Economics 18, no. 1 (2020): 24–31. http://dx.doi.org/10.24147/1812-3988.2020.18(1).24-31.
Texte intégralRésumé :
Every entrepreneur sooner or later ceases their activities. At the same time, little
 attention is paid to this stage of the life cycle of entrepreneurs in scientific research. Proper
 understanding of the reasons for the exit of entrepreneurs from business is necessary for the
 further development of the business sector. Therefore, the analysis of features of termination
 of business activity in national economies is relevant at the present stage of research. Purpose of the study is to assess the reasons for the exit of entrepreneurs from their own business. The study used information from the 2018 global entrepreneurship monitor for 48 countries. We have studied and analyzed the reasons for the termination of entrepreneurial activity,
 proposed a classification of these reasons, assessed the levels of exit from their own business
 for different groups of reasons in all the countries considered. This estimate was based on the
 construction of economic-mathematical models. Models are functions of the density of the
 normal distribution. Based on the results of the computational experiment, the average values
 of indicators were determined and the countries characterized by high and low levels of termination of their activities by entrepreneurs were identified. It is proved that in most countries the
 termination of business activity is caused by endogenous reasons associated with problems in
 the organization and management of production, insufficient financial resources, low qualification of employees and management. Personal reasons also play a significant role in the exit of
 entrepreneurs. The impact of exogenous causes and the desire to convert the created business into cash is much lower. The obtained research results can be used in further studies, in
 the educational process of higher education in universities, as well as by public authorities
 associated with the regulation of entrepreneurial activity.
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Opp, Christian C. "Venture Capital and the Macroeconomy." Review of Financial Studies 32, no. 11 (2019): 4387–446. http://dx.doi.org/10.1093/rfs/hhz031.
Texte intégralRésumé :
Abstract I develop a model of venture capital (VC) intermediation that quantitatively explains central empirical facts about VC activity and can evaluate its macroeconomic relevance. The impact of VC-backed innovations is significantly larger than suggested by observed aggregate venture exit valuations, even after accounting for large exposures to systematic and uninsurable idiosyncratic risks. The risk properties of venture capital play a quantitatively important role in both explaining empirical regularities and shaping the value of ventures’ contributions to economic growth. The model is analytically tractable and yields exact solutions, despite the presence of matching frictions, imperfect risk sharing, and endogenous growth. Received January 16, 2018; editorial decision November 7, 2018 by Editor Stijn Van Nieuwerburgh.
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Beck, Olof, Anna-Carin Olin, and Ekaterina Mirgorodskaya. "Potential of Mass Spectrometry in Developing Clinical Laboratory Biomarkers of Nonvolatiles in Exhaled Breath." Clinical Chemistry 62, no. 1 (2016): 84–91. http://dx.doi.org/10.1373/clinchem.2015.239285.
Texte intégralRésumé :
Abstract BACKGROUND Exhaled breath contains nonvolatile substances that are part of aerosol particles of submicrometer size. These particles are formed and exhaled as a result of normal breathing and contain material from distal airways of the respiratory system. Exhaled breath can be used to monitor biomarkers of both endogenous and exogenous origin and constitutes an attractive specimen for medical investigations. CONTENT This review summarizes the present status regarding potential biomarkers of nonvolatile compounds in exhaled breath. The field of exhaled breath condensate is briefly reviewed, together with more recent work on more selective collection procedures for exhaled particles. The relation of these particles to the surfactant in the terminal parts of the respiratory system is described. The literature on potential endogenous low molecular weight compounds as well as protein biomarkers is reviewed. The possibility to measure exposure to therapeutic and abused drugs is demonstrated. Finally, the potential future role and importance of mass spectrometry is discussed. SUMMARY Nonvolatile compounds exit the lung as aerosol particles that can be sampled easily and selectively. The clinical applications of potential biomarkers in exhaled breath comprise diagnosis of disease, monitoring of disease progress, monitoring of drug therapy, and toxicological investigations.
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Manral, Lalit. "An evolutionary theory of demand-side determinants of strategy dynamics." Management Research Review 41, no. 3 (2018): 314–44. http://dx.doi.org/10.1108/mrr-08-2017-0249.
Texte intégralRésumé :
Purpose This paper aims to explain how the dynamic demand environment influences strategic firm behavior along an industry’s evolutionary path. A conceptual gap concerning the influence of demand-side environmental factors (vis-à-vis changes in technology and policy) on firms’ strategic choices motivates the theory developed herein. The paper’s contribution to the literature on “evolutionary perspective in strategy” also addresses an important gap in the emerging literature on “strategy dynamics”. Design/methodology/approach The conceptual framework in this paper features a dynamic demand environment that provides the structural context for firms’ strategic choices. It conceptualizes demand-side competence as a mediating firm-specific construct to explain the endogenous relationship between the characteristics of the demand environment and firms’ path dependent demand-side investments. Findings A review of the literature on evolutionary perspective in strategy reveals an important conceptual gap concerning the structural determinants of dynamic firm behavior. There is no explanation of the endogenous relationship between dynamic demand structure, firms’ dynamic demand-side competence, and temporally heterogeneous strategic choices. Originality/value The demand-side explanation of how idiosyncratic firm behavior is endogenously determined, with both structural characteristics (demand structure) and firm competences (demand-side competence), addresses an important conceptual gap. The novelty of the theory developed herein lies in its explication of the effect of dynamic demand environment on the evolution of idiosyncratic strategic firm behavior – entry, investment and exit – along the evolutionary path of an industry. The theory developed herein not only explains the effect of both determinants of idiosyncratic strategic firm behavior – the external industry environment (dynamic market structure) and internal firm environment (dynamic firm competences) – but also explains how the determinants evolve along the industry’s lifecycle.
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Perillo, Nancy L., Christel H. Uittenbogaart, Julie T. Nguyen, and Linda G. Baum. "Galectin-1, an Endogenous Lectin Produced by Thymic Epithelial Cells, Induces Apoptosis of Human Thymocytes." Journal of Experimental Medicine 185, no. 10 (1997): 1851–58. http://dx.doi.org/10.1084/jem.185.10.1851.
Texte intégralRésumé :
Galectin-1, a β-galactoside binding protein, is produced by thymic epithelial cells and binds to human thymocytes. We have previously reported that galectin-1 induces the apoptosis of activated T lymphocytes. Because the majority of thymocytes die via apoptosis while still within the thymus, we tested whether galectin-1 could induce the apoptosis of these cells. We now report that in vitro exposure to galectin-1 induced apoptosis of two subsets of CD4lo CD8lo thymocytes. The phenotypes of susceptible thymocytes were consistent with that of both negatively selected and nonselected cells. Galectin-1–induced apoptosis was enhanced by preexposure of thymocytes to antibody to CD3, suggesting that galectin-1 may be a participant in T-cell– receptor mediated apoptosis. In contrast, pretreatment of thymocytes with dexamethasone had no effect on galectin-1 susceptibility. We noted that 71% of the cells undergoing apoptosis after galectin-1 treatment had a DNA content greater than 2N, indicating that proliferating thymocytes were most sensitive to galectin-1. We propose that galectin-1 plays a role in the apoptosis of both negatively selected and nonselected thymocytes, and that the susceptibility of thymocytes to galectin-1 is regulated, in part, by entry or exit from the cell cycle.
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Zeng, Zheng. "CREDIT FRICTIONS AND FIRM DYNAMICS." Macroeconomic Dynamics 17, no. 7 (2012): 1467–95. http://dx.doi.org/10.1017/s1365100512000193.
Texte intégralRésumé :
In this paper I develop a dynamic stochastic general equilibrium model of credit frictions in which the production technology provides a U-shaped average cost curve, enabling endogenous solutions for firm size and quantity. Firms weigh the present value of future net revenues against the opportunity cost of staying in business in their entry or exit decisions. I find that credit frictions increase variable investment costs and result in a larger firm size and a smaller number of firms in the steady state. As the economy deviates from the steady state, however, the presence of credit frictions increases fluctuation in the number of firms, raising market entry during an economic upturn and market exit during a downturn. Also, I find that allowing free entry mitigates some of the effects of credit frictions due to macroeconomic fluctuations. In addition to the homogeneous-firm model, I examine the model when firms have heterogeneous access to credit and find that different credit access gives rise to different firm sizes in the steady state. Firms with easier access to credit become larger than those with less access to credit. Heterogeneous credit access also means that these two types of firms will respond differently to a common technology shock.