Improving confidence set estimation when parameters are weakly identified

We consider inference in weakly identified moment condition models when additional partially identifying moment inequality constraints are available. We detail the limiting distribution of the estimation criterion function and consequently propose a confidence set estimator for the true parameter.National Science Foundation of China (Grant ID: 71301026)This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.spl.2016.06.01

Bombesin receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Mammalian bombesin (Bn) receptors comprise 3 subtypes: BB1, BB2, BB3 (nomenclature recommended by the NC-IUPHAR Subcommittee on bombesin receptors, [109]). BB1 and BB2 are activated by the endogenous ligands gastrin-releasing peptide (GRP), neuromedin B (NMB) and GRP-(18-27). bombesin is a tetradecapeptide, originally derived from amphibians. The three Bn receptor subtypes couple primarily to the Gq/11 and G12/13 family of G proteins [109]. Each of these receptors is widely distributed in the CNS and peripheral tissues [73, 109, 236, 265, 226, 348]. Activation of BB1 and BB2 receptors causes a wide range of physiological/pathophysiogical actions, including the stimulation of normal and neoplastic tissue growth, smooth-muscle contraction, feeding behavior, secretion and many central nervous system effects including regulation of circadian rhythm and mediation of pruritus [112, 113, 109, 115, 116, 155, 189, 236]. A physiological role for the BB3 receptor has yet to be fully defined although recently studies suggest an important role in glucose and insulin regulation, metabolic homeostasis, feeding, regulation of body temperature, obesity, diabetes mellitus and growth of normal/neoplastic tissues [73, 157, 203, 332]

Bombesin receptors in GtoPdb v.2021.2

Mammalian bombesin (Bn) receptors comprise 3 subtypes: BB1, BB2, BB3 (nomenclature recommended by the NC-IUPHAR Subcommittee on bombesin receptors, [115]). BB1 and BB2 are activated by the endogenous ligands neuromedin B (NMB), gastrin-releasing peptide (GRP), and GRP-(18-27). bombesin is a tetra-decapeptide, originally derived from amphibians. The three Bn receptor subtypes couple primarily to the Gq/11 and G12/13 family of G proteins [115]. Each of these receptors is widely distributed in the CNS and peripheral tissues [78, 115, 249, 278, 237, 362]. Activation of BB1 and BB2 receptors causes a wide range of physiological/pathophysiogical actions, including the stimulation of normal and neoplastic tissue growth, smooth-muscle contraction, gastrointestinal motility, feeding behavior, secretion and many central nervous system effects including regulation of circadian rhythm, body temperature control, sighing and mediation of pruritus [149, 202, 244, 115, 196, 249, 306, 68, 34, 332]. A physiological role for the BB3 receptor has yet to be fully defined although recently studies suggest an important role in glucose and insulin regulation, metabolic homeostasis, feeding, regulation of body temperature, obesity, diabetes mellitus and growth of normal/neoplastic tissues [148, 78, 162, 214, 346, 200]. Bn receptors are one of the most frequently overexpressed receptors in cancers and are receiving increased attention for their roles in tumor growth, as well as for tumour imaging and for receptor targeted cytotoxicity [202, 276, 8, 161]

Bombesin receptors in GtoPdb v.2023.1

Mammalian bombesin (Bn) receptors comprise 3 subtypes: BB1, BB2, BB3 (nomenclature recommended by the NC-IUPHAR Subcommittee on bombesin receptors, [117, 4]). BB1 and BB2 are activated by the endogenous ligands neuromedin B (NMB), gastrin-releasing peptide (GRP), and GRP-(18-27). bombesin is a tetra-decapeptide, originally derived from amphibians and structurally closely related to GRP. The three Bn receptor subtypes couple primarily to the Gq/11 and G12/13 family of G proteins [117]. Each of these receptors is widely distributed in the CNS and peripheral tissues [80, 117, 261, 290, 248, 375, 114, 164, 165]. Activation of BB1 and BB2 receptors causes a wide range of physiological/pathophysiogical actions, including the stimulation of normal and neoplastic tissue growth, smooth-muscle contraction, respiration, gastrointestinal motility, feeding behavior, secretion and many central nervous system effects including regulation of circadian rhythm, body temperature control, sighing, behavioral disorders and mediation of pruritus [153, 211, 255, 117, 205, 261, 318, 70, 35, 345, 212, 36]. BB3 is an orphan receptor, although some propose it is constitutively active [330]. BB3 receptor knockout studies show it has important roles in glucose and insulin regulation, metabolic homeostasis, feeding, regulation of body temperature, obesity, diabetes mellitus and growth of normal/neoplastic tissues [152, 80, 168, 224, 359, 209]. Bn receptors are one of the most frequently overexpressed receptors in cancers and are receiving increased attention for their roles in tumor growth, as well as for tumour imaging and for receptor-targeted cytotoxicity [211, 288, 9, 167, 171, 172, 135, 202]. Bn receptors are also receiving attention because they are one of the primary neurotransmitters for pruritus [36, 127, 35, 318]

Dynamics of value-tracking in financial markets

The effciency of a modern economy depends on value-tracking: that market prices of key assets broadly track some underlying value. This can be expected if a suffcient weight of market participants are valuation- based traders, buying and selling an asset when its price is, respectively, below and above their well-informed private valuations. Such tracking will never be perfect, and we propose a natural unit of tracking error, the 'deciblack' . We then use a simple discrete-time model to show how large tracking errors can arise if enough market participants are not valuation-based traders, regardless of how much information the valuation-based traders have. Similarly to Lux [17] and others who study subtly different models, we find a threshold above which value-tracking breaks down without any changes in the underlying value of the asset. We propose an estimator of the tracking error and establish its statistical properties. Because financial markets are increasingly dominated by non-valuation-based traders, assessing how much valuation-based investing is required for reasonable value tracking is of urgent practical interest

A rock-surface microweathering index from Schmidt hammer R-values and its preliminary application to some common rock types in southern Norway

An index of the degree of rock-surface microweathering based on Schmidt hammer R-values is developed for use in the field without laboratory testing. A series of indices - I2 to In, where n is the number of successive blows with the hammer - is first proposed based on the assumption that the R-values derived from successive impacts on the same spot on a weathered rock surface converge on the value characteristic of an unweathered surface of the same lithology. Of these indices, the I5 index, which measures the difference between the mean R-value derived from first and fifth impacts as a proportion of the mean R-value from the fifth impact, is regarded as optimal: use of fewer impacts (e.g. in an I2 index) underestimates the degree of weathering whereas use of more impacts (e.g. in an I10 index) makes little difference and is therefore inefficient and may also induce an artificial weakening of the rock. Field tests of these indices on weathered glacially-scoured bedrock outcrops of nine common metamorphic and igneous rock types from southern Norway show, however, that even after ten impacts, successive R-values fail to approach the values characteristic of unweathered rock surfaces (e.g. bedrock from glacier forelands and road cuttings). An improved *I5 index is therefore preferred, in which the estimated true R-value of an unweathered rock surface is substituted. Weathered rock surfaces exposed to the atmosphere for ~10,000 years in southern Norway exhibit *I5 indices of 36-57%, values that reflect a similarly high degree of weathering irrespective of the rock type

Class A Orphans in GtoPdb v.2023.1

Table 1 lists a number of putative GPCRs identified by NC-IUPHAR [161], for which preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. These GPCRs have recently been reviewed in detail [121]. The GPCRs in Table 1 are all Class A, rhodopsin-like GPCRs. Class A orphan GPCRs not listed in Table 1 are putative GPCRs with as-yet unidentified endogenous ligands.Table 1: Class A orphan GPCRs with putative endogenous ligands GPR3GPR4GPR6GPR12GPR15GPR17GPR20 GPR22GPR26GPR31GPR34GPR35GPR37GPR39 GPR50GPR63GPR65GPR68GPR75GPR84GPR87 GPR88GPR132GPR149GPR161GPR183LGR4LGR5 LGR6MAS1MRGPRDMRGPRX1MRGPRX2P2RY10TAAR2 In addition the orphan receptors GPR18, GPR55 and GPR119 which are reported to respond to endogenous agents analogous to the endogenous cannabinoid ligands have been grouped together (GPR18, GPR55 and GPR119)

Class A Orphans (version 2020.5) in the IUPHAR/BPS Guide to Pharmacology Database

Table 1 lists a number of putative GPCRs identified by NC-IUPHAR [194], for which preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. These GPCRs have recently been reviewed in detail [150]. The GPCRs in Table 1 are all Class A, rhodopsin-like GPCRs. Class A orphan GPCRs not listed in Table 1 are putative GPCRs with as-yet unidentified endogenous ligands.Table 1: Class A orphan GPCRs with putative endogenous ligands GPR3 GPR4 GPR6 GPR12 GPR15 GPR17 GPR20 GPR22 GPR26 GPR31 GPR34 GPR35 GPR37 GPR39 GPR50 GPR63 GRP65 GPR68 GPR75 GPR84 GPR87 GPR88 GPR132 GPR149 GPR161 GPR183 LGR4 LGR5 LGR6 MAS1 MRGPRD MRGPRX1 MRGPRX2 P2RY10 TAAR2 In addition the orphan receptors GPR18, GPR55 and GPR119 which are reported to respond to endogenous agents analogous to the endogenous cannabinoid ligands have been grouped together (GPR18, GPR55 and GPR119)

Class A Orphans in GtoPdb v.2022.3

Table 1 lists a number of putative GPCRs identified by NC-IUPHAR [161], for which preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. These GPCRs have recently been reviewed in detail [121]. The GPCRs in Table 1 are all Class A, rhodopsin-like GPCRs. Class A orphan GPCRs not listed in Table 1 are putative GPCRs with as-yet unidentified endogenous ligands.Table 1: Class A orphan GPCRs with putative endogenous ligands GPR3GPR4GPR6GPR12GPR15GPR17GPR20 GPR22GPR26GPR31GPR34GPR35GPR37GPR39 GPR50GPR63GPR65GPR68GPR75GPR84GPR87 GPR88GPR132GPR149GPR161GPR183LGR4LGR5 LGR6MAS1MRGPRDMRGPRX1MRGPRX2P2RY10TAAR2 In addition the orphan receptors GPR18, GPR55 and GPR119 which are reported to respond to endogenous agents analogous to the endogenous cannabinoid ligands have been grouped together (GPR18, GPR55 and GPR119)