Using trade policy to achieve foreign policy objectives, such as stable international relations, has a long history, from Kant to the founders of the GATT. Punishing enemies and rewarding ‘friends’ by granting or withholding market access is also not new, and sanctions or blockades are a venerable form of trade policy used as foreign policy. A more recent form is influencing the domestic policy of another country with non-commercial provisions in trade agreements. All these tools are based on linkage, on the assumption that a desired outcome can be achieved by interventions that would increase or decrease trade. The latest instance is so-called ‘friend-shoring’, which would in principle isolate enemies, although it will be difficult in practice and risks undermining multilateralism. The cost of these interventions is susceptible to economic analysis, even if the conclusion is that it is worth paying. Influenced by Alan Winters who referred to national security as a motivation for agriculture protection as a ‘so-called non-economic objective’ or SNO, I argue that using a trade policy tool for a foreign policy purpose as if there is no cost is a SNO job, an attempt to justify an intervention aimed at one objective by framing it as being valuable for another.

Increased production has been the major goal of animal breeding for many decades, and the correlated side-effects have grown to become a major issue in animal welfare. In this paper, the main genetic mechanisms in which such side-effects may occur are reviewed with examples from our own research in chickens. Pleiotropy, linkage and regulatory pathways are the most important means by which a number of traits may be affected simultaneously by the same selection pressure. Pleiotropy can be exemplified by the gene PMEL17 which causes a lack of black pigmentation in chickens and, simultaneously, predisposes them to become the victims of feather pecking. Linkage is a probable reason why a limited region on chicken chromosome 1 affects many different traits, such as growth, reproduction and fear-related behaviour. Gene regulation is affected by stress, and may cause modifications in behaviour and phenotype which are transferred from parents to offspring by means of epigenetic modifications. Insights into phenomena, such as these, may increase our understanding not only of how artificial selection works, but also evolution at large.

Geometric vertex decomposition and liaison are two frameworks that have been used to produce similar results about similar families of algebraic varieties. In this paper, we establish an explicit connection between these approaches. In particular, we show that each geometrically vertex decomposable ideal is linked by a sequence of elementary G-biliaisons of height $1$ to an ideal of indeterminates and, conversely, that every G-biliaison of a certain type gives rise to a geometric vertex decomposition. As a consequence, we can immediately conclude that several well-known families of ideals are glicci, including Schubert determinantal ideals, defining ideals of varieties of complexes and defining ideals of graded lower bound cluster algebras.

Blood cell concentrations for most cell types are highly heritable. Data from Nick Martin’s twin registry provided much of the data for the early heritability and linkage studies of blood cell related traits and have contributed significantly to more recent genomewide association studies that have successfully identified individual genetic loci.

The classical twin design relies on a number of strong number of assumptions in order to yield unbiased estimates of heritability. This includes the equal environments assumption — that monozygotic and dizygotic twins experience similar degrees of environmental similarity — an assumption that is likely to be violated in practice for many traits of interest. An alternative method of estimating heritability that does not suffer from many of these limitations is to model trait similarity between sibling pairs as a function of their empirical genome-wide identity by descent sharing, estimated from genetic markers. In this review, I recount the story behind Nick Martin’s and my development of this method, our first attempts at applying it in a human population and more recent studies using the original and related methods to estimate trait heritability.

Family, adoption and twin studies show that genetics influences suicidal behavior, but does not indicate specific susceptibility variants. Stress response is thought to be mediated by the corticotrophin-releasing hormone (CRH), which is known to be a regulator of the hypothalamic–pituitary–adrenal pathway (HPA). Alterations in HPA system have been related to impulsivity, aggression and suicidal behaviour, that are common features in Bipolar Disorder (BD). CRH is a hypothalamic factor that stimulates the pituitary gland. Two CRH receptors are known, CRHR1 and CRHR2. To search for markers conferring genetic susceptibility to suicide, we typed three polymorphisms of the CRHR2 gene, CRHR2(CA), CRHR2(GT), and CRHR2(GAT), in 312 families where at least one subject had DSM-IV bipolar disorder. Family based association analyses in the suicide attempters using FBAT yielded no difference in the distribution of the alleles for all three markers. HBAT analysis for quantitative measures on suicide-related traits showed association between haplotype 5-2-3 and higher severity. The current results show that haplotype variation at the CRHR2 locus is associated with suicidal behaviour. This is to our knowledge the first investigation on suicidal behavior and genetic variation at the CRHR2 locus, an important regulator of the HPA axis.

Animal models are often used for preclinical research on the neurobiology of psychiatric disorders. Whereas many are employed to screen new therapeutic agents, few of them are used to study the genetic bases of psychiatric diseases, probably because of the complex genetic determinism underlying quantitative behavioral traits such as mood, personality or intelligence. The present article presents a short review introducing an analysis model using mi the marker strains model. Using this model it is possible both to display genetic determinism data and to locate some of the chromosomal fragments involved in the regulation of anxiogenic processes. At present it cannot accurately determine the position of one or more genes, but it does provide a valuable means of ‘scanning’ the genome for an approximation. Through genetic analysis, using the model, an attempt will be made to identify autosomal fragments which may be involved in two behavioural traits: anxiety and chemical-induced seizures. In this paper, after reviewing theoretical aspects of looking for genes involved in behaviour, we will successively introduce studies in genetic topics in psychiatric human studies as well as appropriated behavioural animal studies. Then we will present a genetic model in mice which allows us to locate chromosomal fragments associated with a behavioural trait: multiple marker strains.

Kochia [Bassia scoparia (L.) A. J. Scott] is one of the most troublesome weeds throughout the North American Great Plains. Herbicides such as glyphosate and dicamba have been used widely to control B. scoparia for decades. However, many B. scoparia populations have evolved resistance to these herbicides due to selection. Especially, dicamba-resistant B. scoparia populations are often also found to be glyphosate-resistant. The objective of this research was to determine whether these two herbicide resistances are linked in B. scoparia. Reciprocal crosses were performed between glyphosate- and dicamba-resistant (GDR) and glyphosate- and dicamba-susceptible (GDS) B. scoparia to produce F1 and F2 progeny. Two F1 and seven F2 progeny families were screened with various doses of dicamba or glyphosate. All the F1 progeny survived both dicamba and glyphosate treatments. Chi-square analyses of F2 progeny suggest (1) glyphosate and dicamba resistances in B. scoparia are inherited via single, dominant nuclear genes; and (2) glyphosate- and dicamba-resistant genes are not linked. Thus, the dicamba and glyphosate resistances appear to have evolved independently due to intense selection but do not seem to spread together.

It is generally expected that, in the case of multiple herbicide resistance, different resistance mechanisms within a weed will follow Mendel’s law of independent assortment. Research was conducted to investigate anecdotal observations suggesting that target site–based resistances to inhibitors of acetolactate synthase (ALS) and protoporphyrinogen oxidase (PPO) did not follow independent assortment in common waterhemp. Cosegregation of the two resistances was observed in backcross lines (population sensitive to both herbicides as recurrent parent). Specifically, whereas 52% of backcross plants were resistant to a PPO inhibitor, this percentage increased to 92% when the backcross plants were preselected for resistance to an ALS inhibitor. Molecular marker analysis confirmed that the corresponding genes (ALS and PPX2) were genetically linked. When data from all plants analyzed were pooled, the genetic distance between the two genes was calculated to be 7.5 cM. The two genes were found to be about 195 kb apart in the recently published grain amaranth genome, explaining the observed genetic linkage. There is likely enough recombination that occurs between the linked genes to prevent the linkage from having significant implications in terms of resistance evolution. Nevertheless, documentation of the happenstance linkage between target-site genes for resistance to ALS and PPO inhibitors in waterhemp is a reminder that one should not assume distinct resistance mechanism will independently assort.

Most forms of behaviour whether normal or abnormal, show a tendency to run in families. However, these can range from symptoms of dementia and movement disorder caused by the comparatively rare autosomal dominant Huntington's disease to common everyday aspects of behaviour such as religious persuasion or career choice. Normal behaviours and most common disorders do not show simple mendelian inheritance but instead have more complex patterns of transmission involving either major genes with incomplete penetrance, multiple genes of small effect, or a combination of the two. In addition, common complex phenotypes usually involve the combination of genetic and environmental factors. Therefore once family studies have shown that a disorder or trait is familial the next stage is to perform twin studies and, if possible adoption studies to investigate whether this results from shared genes, shared environment or a combination of the two.

We propose a strategy to attack the problems of orbit determination arising from the large number of short arcs. The method uses a solution of the linkage problem depending on the first integrals of the Keplerian motion.

In the past, there have been many epidemiological and genetic studies of mood disorders, schizophrenia, and alcohol dependence, and in this study, the human serotonin 2A receptor (5-HTR2A) polymorphism was examined in 80 patients with mood disorders, 50 patients with schizophrenia and 41 patients with alcohol dependence. 5-HTR is related to affectivity, regulation, and pharmacologic effects of antidepressant, anti-anxiety and antipsychotic medications. The polymorphism in 5-HTR2A (102T/C, −1438 A/G) was identified by the polymerase chain reaction (PCR), followed by restriction fragment length polymorphism (RFLP). The results suggest that 5-HTR2A (102T/C, −1438G/A) polymorphism might not be associated with susceptibility to schizophrenia or mood disorders, and it might not be a risk factor contributing to alcohol dependency. We found that the 102T/C polymorphism was in linkage disequilibrium with the −1438G/A polymorphism in psychosis (mood disorder, schizophrenia, and alcohol dependence) and in health controls. Further studies are needed to determine whether or not the novel serotonin receptor (5-HTR) polymorphism reflects the pathogenesis of schizophrenia, mood disorders, and alcohol dependence.

Ten-valent pneumococcal conjugate vaccine (PCV10) was recently introduced into the Brazilian Immunization Programme. Secondary data are used as a measurement of community-acquired pneumonia (CAP) burden, but their completeness and reliability need to be ascertained. We performed probabilistic linkage between hospital primary data from active prospective population-based surveillance (APS) and hospital secondary data from the Hospital Information System administrative database of the National Unified Health System (SIH-SUS). Children aged 2–23 months hospitalized during January–December 2012 were identified. Incidence rates of hospitalized CAP were estimated. Agreement of case identification was measured by kappa index. A total of 1639 (26%) CAP cases were identified in APS and 1714 (35%) in SIH-SUS. Of these 3353 records, 1127 CAP cases were present in both databases. Kappa on CAP case identification was 0·72 (95% confidence interval 0·69–0·75). CAP hospitalization incidence using administrative (5285/100 000) and hospital (5054/100 000) primary data were similar (P = 0·184). Our findings suggest that administrative databases of hospitalizations are reliable sources to assess PCV10 impact in time-series analyses.

A central problem in liaison theory is to decide whether every arithmetically Cohen–Macaulay subscheme of projective $n$-space can be linked by a finite number of arithmetically Gorenstein schemes to a complete intersection. We show that this can indeed be achieved if the given scheme is also generically Gorenstein and we allow the links to take place in an $(n+ 1)$-dimensional projective space. For example, this result applies to all reduced arithmetically Cohen–Macaulay subschemes. We also show that every union of fat points in projective 3-space can be linked in the same space to a union of simple points in finitely many steps, and hence to a complete intersection in projective 4-space.

Background: We performed a genome-wide scan in a homogeneous Arab population to identify genomic regions linked to blood pressure (BP) and its intermediate phenotypes during mental and physical stress tests. Methods: The Oman Family Study subjects (N = 1277) were recruited from five extended families of ~10 generations. Hemodynamic phenotypes were computed from beat-to-beat BP, electrocardiography and impedance cardiography. Multi-point linkage was performed for resting, mental (word conflict test, WCT) and cold pressor (CPT) stress and their reactivity scores (s), using variance components decomposition-based methods implemented in SOLAR. Results: Genome-wide scans for BP phenotypes identified quantitative trait loci (QTLs) with significant evidence of linkage on chromosomes 1 and 12 for WCT-linked cardiac output (LOD = 3.1) and systolic BP (LOD = 3.5). Evidence for suggestive linkage for WCT was found on chromosomes 3, 17 and 1 for heart rate (LOD = 2.3), DBP (LOD = 2.4) and left ventricular ejection time (LVET), respectively. For △WCT, suggestive QTLs were detected for CO on chr11 (LOD = 2.5), LVET on chr3 (LOD = 2.0) and EDI on chr9 (LOD = 2.1). For CPT, suggestive QTLs for HR and LVET shared the same region on chr22 (LOD 2.3 and 2.8, respectively) and on chr9 (LOD = 2.3) for SBP, chr7 (LOD = 2.4) for SV and chr19 (LOD = 2.6) for CO. For △CPT, CO and TPR top signals were detected on chr15 and 10 (LOD; 2.40, 2.08) respectively. Conclusion: Mental stress revealed the largest number of significant and suggestive loci for normal BP reported to date. The study of BP and its intermediate phenotypes under mental and physical stress may help reveal the genes involved in the pathogenesis of essential hypertension.