Suicide is a serious public health problem. In the international literature there is evidence to support the notion that certain temperaments and personality traits are often associated with suicidal behavior. In this study, 150 psychiatric inpatients were investigated using the TEMPS-A, the MMPI-2 and the Beck Hopelessness Scale (BHS) and evaluated for suicide risk through the critical items of the Mini International Neuropsychiatric Interview (MINI). Statistical analysis, including linear regression analysis and multiple regression analysis, showed that suicide risk contributed to the prediction of hopelessness. Among the temperaments, only the Hyperthymic temperament, as a protective factor, and the Dys/Cyc/Anx temperament contributed significantly to the prediction of hopelessness. Irritable temperament and Social Introversion were protective factors for suicidal risk. Hopelessness and depression were associated with higher suicidal behavior and ideation, but, unexpectedly, depression as measured by the MMPI did not contribute significant to the multiple regression.. The present study indicated that, although suicidal psychiatric patients have MMPI-2’s profiles in the pathologic range, they exhibit several differences from nonsuicidal patients. Patients at risk of suicide have specific temperaments as well as personality and defense mechanism profiles. They are more social introverted, depressed and psychasthenic, and use hysterical and schizoid mechanisms more often. Generalizability of the findings was limited by the small sample size, mix of BPD-I, BPD-II, MDD and psychotic disorder patients.

In around ≈25% of early-type galaxies (ETGs) UV emission from young stellar populations is present. Molecular gas reservoirs have been detected in these systems (e.g. Young et al. (2011), providing the fuel for this residual star-formation. The environment in which this molecular gas is found is quite different than that in spiral galaxies however, with harsher radiation fields, deeper potentials and high metallicity and alpha-element abundances. Here we report on one element of our multi-faceted programme to understand the similarities and differences between the gas reservoirs in spirals and ETGs. We use spatially resolved observations from the CARMA mm-wave interferometer to investigate the size of the molecular reservoirs in the the CO-rich ATLAS3D ETGs (survey described in Alatalo et al. 2012, submitted). We find that the molecular gas extent is smaller in absolute terms in ETGs than in late-type galaxies, but that the size distributions are similar once scaled by the galaxies optical/stellar characteristic scale-lengths (Fig 1, left). Amongst ETGs, we find that the extent of the molecular gas is independent of the kinematic misalignment, despite the many reasons why misaligned gas might have a smaller extent. The extent of the molecular gas does depend on environment, with Virgo cluster ETGs having less extended molecular gas reservoirs (Fig 1, right). Whatever the cause, this further emphases that cluster ETGs follow different evolutionary pathways from those in the field. Full details of this work will be presented in Davis et al. (2012), submitted.

Recently, massive early-type galaxies have shed their red-and-dead moniker, thanks to the discovery that many host residual star formation. As part of the ATLAS-3D project, we have conducted a complete, volume-limited survey of the molecular gas in 260 local early-type galaxies with the IRAM-30m telescope and the CARMA interferometer, in an attempt to understand the fuel powering this star formation. We find that around 22% of early-type galaxies in the local volume host molecular gas reservoirs. This detection rate is independent of galaxy luminosity and environment. Here we focus on how kinematic misalignment measurements and gas-to-dust ratios can be used to put constraints on the origin of the cold ISM in these systems. The origin of the cold ISM seems to depend strongly on environment, with misaligned, dust poor gas (indicative of externally acquired material) being common in the field but completely absent in rich groups and in the Virgo cluster. Very massive galaxies also appear to be devoid of accreted gas. This suggests that in the field mergers and/or cold gas accretion dominate the gas supply, while in clusters internal secular processes become more important. This implies that environment has a strong impact on the cold gas properties of ETGs.

Narrow-Line Seyfert 1 (NLS1) class of active galactic nuclei (AGNs) is generally radio-quiet, but a small percent of them are radio-loud. The recent discovery by Fermi/LAT of high-energy γ-ray emission from 4 NLS1s proved the existence of relativistic jets in these systems. It is therefore important to study this new class of γ-ray emitting AGNs. Here we report preliminary results about the observations of the July 2010 γ-ray outburst of PMN J0948+0022, when the source flux exceeded for the first time 10−6 ph cm−2 s−1 (E > 100 MeV).

Early-type galaxies (ETGs) satisfy a now classic scaling relation Re ∝ σ1.2eI−0.8e, the Fundamental Plane (FP; Djorgovski & Davis 1987; Dressler et al. 1987), between their size, stellar velocity dispersion and mean surface brightness. A significant effort has been devoted in the past twenty years to try to understand why the coefficients of the relation are not the ones predicted by the virial theorem Re ∝ σ2eI−1e.

Cell numbers in four organs of large, control and small mice were estimated by nuclear counts. Average cell mass was estimated from the cell number and the organ weight. The mice were from the selected Q-strain with six replicate lines in each size-group. The organs were lung, liver, spleen and kidney. At 6 weeks of age the large mice had more cells and larger cells than the controls in all organs; the small mice had fewer and smaller cells than the controls. The regression of log cell-number on log-organ weight provides a measure of how much, proportionately, cell number contributes to the differences in organ weight. In the lung and spleen, cell number contributed about 70% of the strain differences in organ weight, cell mass contributing about 30%; in the liver and kidney the relative contributions were about equal, at 50%.

Cell counts at different ages from 3 to 15 weeks showed that cell number and cell mass contributed to the increases of organ weights during growth in roughly the same proportions as stated above. From this it is concluded that the main effect of selection for body weight has been to speed up or slow down the normal processes of cellular growth.

Tabby males were irradiated with 500 r and mated to Bn Mobr♀♀. Daughters conceived during the first 3 weeks after irradiation were tested for the presence of sex-linked recessive mutations in their progeny, each daughter representing one irradiated gamete. One visible, but no lethal, was found in the Bn–Mobr segment among 154 tested gametes; one gamete was proved free of lethals or visibles in the Bn–Ta segment, and 21 gametes in the Ta–Mobr segment. Among the whole 176 tested gametes there was no indication of a lethal in the adjoining segments.

Puberty was studied in mice of the ninth selected generation of the Q-strain. There were 6 replicate lines selected for large body size (6-week weight), 6 replicates selected for small size and 6 replicate unselected controls. Female puberty was assessed by the opening of the vagina and male puberty by the first copulation plug. The sexes differed in the mean age at puberty, males being older by 13 days in the large, 4 days in the control and 8 days in the small lines. The sexes differed also in the way size affected puberty. In males the large and small lines reached puberty at the same age and both were older than the controls. In females the large lines on average were heavier and younger at puberty than the controls, and the small lines were lighter and older than the controls, though not significantly older. The replicates within each size-group, however, reached puberty at about the same weight, irrespective of their differences in growth rate. Thus, the differences of growth between the large, control and small groups affected both the weight and the age of females at puberty, but the differences of growth between the replicate lines within each size affected only the age at puberty. No explanation was found for this inconsistency between size-groups and replicates. Several lines of evidence led to the conclusion that in females puberty is partly or mainly weight-dependent, whereas in males it is almost wholly age-dependent.

1. A mild diabetes insipidus is associated with the oligosyndactyly caused by the dominant gene Os. No recombinants were observed between the diabetes and the oligosyndactyly so the diabetes is probably a pleiotropic effect of the Os gene.

2. There are one or more modifying genes which in combination with Os enhance the manifestation and cause a severe diabetes insipidus. This affects both sexes and becomes progressively worse in older animals, the average water intake reaching 50–60 ml. per 24 hours, or 1·7 times the body weight.

3. The modifying gene or genes, in the absence of the Os gene, themselves produce a mild diabetes insipidus, which becomes severe in some old females.

4. The severe diabetes insipidus associated with Os and the modifying genes together is probably renal in origin.

The gene (dw) causing hypopituitary dwarfism was transferred by repeated backcrosses into strains of mice differing genetically in growth-rate through previous selection. The dwarf mice lack growth hormone, and the purpose was to find out if the differences in growth-rate between the strains were in any part due to differences in their growth hormone status – amount of hormone or tissue sensitivity. In the absence of growth hormone, i.e. in the dwarfs, the strains still grew at different rates, proving that growth hormone status was not the only cause of their differences. The effect of substituting the dw gene was, however, greater in the large strain than in the unselected control, and less in the small strain than in the control. The growth differences between the strains were therefore in part due to growth hormone. Tissue sensitivity in the three strains was compared by their responses to graded doses of exogenous growth hormone. The large and control strains did not differ, but the small strain had a lower sensitivity. The results suggest that the increased growth-rate of the large strain is partly due to an increased amount, or activity, of its circulating growth hormone, while the reduced growth-rate of the small strain is in part due to a reduced sensitivity of its target organs to growth hormone.

1. A random bred population of mice was subjected to inbreeding and the changes of litter size, measured as the number of live young in first litters, were followed.

2. The mean litter size declined at a rate of 0·56 young per 10% increase of the inbreeding coefficient.

3. Selection for large litters within the lines during the inbreeding did not effectively reduce the rate of decline.

4. Out of twenty lines at the beginning of the inbreeding seventeen were lost by the time the inbreeding coefficient reached 76%. Two more were lost later and one survived indefinitely. The three lines that survived longest started at a level below the mean and did not decline in litter size. The one that survived indefinitely reached 99% inbreeding without dropping below the non-inbred control.

5. The three lines surviving at 81% inbreeding were crossed and the litters produced by the crossbred progeny were larger than the non-inbred control by about two young per litter. This gain from heterosis is attributable to selection among the lines on their performance as inbreds. A second and third cycle of inbreeding and crossing yielded no further progress, and the level of the first cross was never regained. This is attributable to the ineffectiveness of the selection applied and to the previous restrictions of the population size.

6. The behaviour of the lines in the inbreeding and crossing point to simple dominance rather than over-dominance at the loci causing variation of litter size.

7. This experiment suggests that, as a means of improvement of farm animals, cyclical inbreeding and crossing does not look very hopeful.

Aggregation chimaeras were made from embryos of strains of mice selected for large and small body size and of unselected controls. The strains were combined in pairs marked by albino coat colour and by allo-zyme variants at the Gpi-1 locus. The proportion of cells derived from each component was scored visually in the coat melanocytes and by electrophoresis in ten other organs or tissues (blood, liver, lung, spleen, spinal cord, brain, pituitary, kidney, adrenal and testis). The object was to find out how body weight is related to cell proportions in the body as a whole and in the separate organs. Individuals varied widely in their mean cell proportions but there were significant differences between organs within individuals. Body weight was linearly related to the mean cell proportions which accounted for most, or possibly all, of the chimaeric variance of body weight. No one of the organs studied could be identified as being solely responsible for growth control, or as having a predominant influence on growth. The weights of some organs were probably influenced to a small extent by their own cell proportions independently of the individual's mean, but the differences of body weight were too great to be accounted for by the summation of localized effects on organs. The mean cell proportion, averaged over individuals, was close to 50%, proving that there was no tendency for cells from the larger component to outgrow those from the smaller. It is concluded that growth control must be systemic, but it was not possible to decide whether the systemic effect comes from some particular organ not studied, or is in some undefined way the consequence of the cell proportions in the body as a whole. There was some evidence, though it was inconclusive, that chimaeras show ‘heterosis’ for body weight.

The sex-linked gene, brindled, in the mouse produces a coat-colour variegation in heterozygous females. There is much individual variation in the relative areas of mutant and wild-type colour, but it was not known if any of this variation was genetic. The main object, when the experiments were started, was to test the simple expectation of the Lyon hypothesis, that if X-inactivation is random the variegation should not be modifiable by selection. On the assumption that the variegation is due to X-chromosome inactivation, modification by selection would show that the inactivation process, or some property of the derived cell populations, is under genetic control. Heterozygous females were accordingly selected for the area of coat showing the mutant colour. Selection based on individual phenotypes was ineffective, but four cycles of reciprocal recurrent selection based on progeny-means produced a ‘High’ line with 64% mutant area and a ‘Low’ line with 30% mutant area, from a base population with 53% mutant area. Autosomal modifiers were not responsible for the response; the difference between the selected lines was entirely due to properties of the X chromosomes carrying the brindled gene. The changed properties of the X chromosomes were not restricted to the locus of brindled, but extended at least as far as the locus of tabby. The chromosomes carrying the wild-type allele of brindled were not altered by the selection, but normal X chromosomes from other strains affected the degree of variegation. It was concluded that the difference between the selected lines was due either to non-random inactivation or to somatic cell selection. It was not possible to distinguish between these two mechanisms. The results obtained in these experiments with a structurally normal X chromosome were in all essentials similar to those obtained by Cattanach with his X-autosome translocation.

The gene ‘sex-linked anaemia’ (sla) appeared first in the progeny of a daughter of a male that had been irradiated with 500 r. of X-rays. The daughter was born one month after the irradiation of her father. Mated to an unrelated wild-type male she produced sixteen sons of which six were anaemic. Her fertility was normal. Experience in subsequent matings showed the anaemia to be rather difficult to classify. In litters examined on the day of birth the anaemic young were usually clearly distinguishable by their pale colour. But in older litters, and even in a few at birth, the classification could not be made with confidence. The haematology of the anaemics is described by Grewal (1962).

Curly-whiskers (cw) is a recessive gene which was found in 1958 by Mr C. J. W. Smith of the Chester Beatty Research Institute, London. It arose in a subline of the CBA/Cbi inbred strain. The first mutant animals were one male and one female in a litter of five. The two mutants were mated together and a sib-mated subline was continued from them in which 500 mice were bred, all of which were curly-whiskered. This established the mutant to be fully penetrant. Curly-whiskers resembles the hair-waving genes in causing waving of the vibrissae, but it has no obvious waving effect on the hairs of the coat. The coat texture is, however, slightly abnormal and Mr Smith noted also that on the CBA background there was an appreciable darkening of the coat colour. Homozygotes (cw/cw) are easily classifiable soon after birth by the curled vibrissae. Heterozygotes (+/cw) often have slightly curled vibrissae, and the gene is therefore not fully recessive; but the distinction between +/cw and +/+ could not be relied on, and in the linkage tests cw was treated as a recessive gene.