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Only a minority of the buildings illustrated in the Tribune's \"hidden treasures\" series actually had any true architectural distinction.

Recently every syndicated political columnist in the country has had something to say about the 5 percent or so of our young men who have failed to register for the country's nonexistent draft.

The world, as people are so fond of saying, keeps getting smaller. And they probably started saying it the first time a horse got hitched to something with wheels. Nowadays we can get on a plane in New York and end up in London seven hours later.

The world, as people are so fond of saying, keeps getting smaller. And they probably started saying it the first time a horse got hitched to something with wheels. Nowadays we can get on a plane in New York and end up in London seven hours later.

Now, a quibble. The Tribune, like many news organizations, doesn't seem able to get the association's name right. You might want to make a note in your stylebook that the official name is The International Association of Lions Clubs (note the plural), or Lions Clubs International. Technically it is the Lions club that is the member of the association. So instead of Lions Club International Foundation, it should be Lions Clubs.

Whether schizophrenia and bipolar disorder are the clinical outcomes of discrete or shared causative processes is much debated in psychiatry. We aimed to assess genetic and environmental contributions to liability for schizophrenia, bipolar disorder, and their comorbidity. We linked the multi-generation register, which contains information about all children and their parents in Sweden, and the hospital discharge register, which includes all public psychiatric inpatient admissions in Sweden. We identified 9 009 202 unique individuals in more than 2 million nuclear families between 1973 and 2004. Risks for schizophrenia, bipolar disorder, and their comorbidity were assessed for biological and adoptive parents, offspring, full-siblings and half-siblings of probands with one of the diseases. We used a multivariate generalised linear mixed model for analysis of genetic and environmental contributions to liability for schizophrenia, bipolar disorder, and the comorbidity. First-degree relatives of probands with either schizophrenia (n=35 985) or bipolar disorder (n=40 487) were at increased risk of these disorders. Half-siblings had a significantly increased risk (schizophrenia: relative risk [RR] 3·6, 95% CI 2·3–5·5 for maternal half-siblings, and 2·7, 1·9–3·8 for paternal half-siblings; bipolar disorder: 4·5, 2·7–7·4 for maternal half-siblings, and 2·4, 1·4–4·1 for paternal half-siblings), but substantially lower than that of the full-siblings (schizophrenia: 9·0, 8·5–11·6; bipolar disorder: 7·9, 7·1–8·8). When relatives of probands with bipolar disorder were analysed, increased risks for schizophrenia existed for all relationships, including adopted children to biological parents with bipolar disorder. Heritability for schizophrenia and bipolar disorder was 64% and 59%, respectively. Shared environmental effects were small but substantial (schizophrenia: 4·5%, 4·4%–7·4%; bipolar disorder: 3·4%, 2·3%–6·2%) for both disorders. The comorbidity between disorders was mainly (63%) due to additive genetic effects common to both disorders. Similar to molecular genetic studies, we showed evidence that schizophrenia and bipolar disorder partly share a common genetic cause. These results challenge the current nosological dichotomy between schizophrenia and bipolar disorder, and are consistent with a reappraisal of these disorders as distinct diagnostic entities. Swedish Council for Working Life and Social Research, and the Swedish Research Council.

Intelligence is highly heritable 1 and a major determinant of human health and well-being 2 . Recent genome-wide meta-analyses have identified 24 genomic loci linked to variation in intelligence 3 – 7 , but much about its genetic underpinnings remains to be discovered. Here, we present a large-scale genetic association study of intelligence ( n  = 269,867), identifying 205 associated genomic loci (190 new) and 1,016 genes (939 new) via positional mapping, expression quantitative trait locus (eQTL) mapping, chromatin interaction mapping, and gene-based association analysis. We find enrichment of genetic effects in conserved and coding regions and associations with 146 nonsynonymous exonic variants. Associated genes are strongly expressed in the brain, specifically in striatal medium spiny neurons and hippocampal pyramidal neurons. Gene set analyses implicate pathways related to nervous system development and synaptic structure. We confirm previous strong genetic correlations with multiple health-related outcomes, and Mendelian randomization analysis results suggest protective effects of intelligence for Alzheimer’s disease and ADHD and bidirectional causation with pleiotropic effects for schizophrenia. These results are a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders. Meta-analysis of genome-wide association studies for cognitive ability identifies 190 new loci and implicates 939 new genes related to neurogenesis, neuron differentiation and synaptic structure.