Viewers base estimates of face matching accuracy on their own familiarity: Explaining the photo-ID paradox.

Matching two different images of a face is a very easy task for familiar viewers, but much harder for unfamiliar viewers. Despite this, use of photo-ID is widespread, and people appear not to know how unreliable it is. We present a series of experiments investigating bias both when performing a matching task and when predicting other people's performance. Participants saw pairs of faces and were asked to make a same/different judgement, after which they were asked to predict how well other people, unfamiliar with these faces, would perform. In four experiments we show different groups of participants familiar and unfamiliar faces, manipulating this in different ways: celebrities in experiments 1-3 and personally familiar faces in experiment 4. The results consistently show that people match images of familiar faces more accurately than unfamiliar faces. However, people also reliably predict that the faces they themselves know will be more accurately matched by different viewers. This bias is discussed in the context of current theoretical debates about face recognition, and we suggest that it may underlie the continued use of photo-ID, despite the availability of evidence about its unreliability.

Shared decision-making at end-of-life is aided by graphical trending of illness severity.

The Rothman Index (RI) gives a visual picture of patient's condition and progress for the physician and family to view together. This case demonstrates how the RI graph facilitates physician-family communication. An 85-year-old man with normal pressure hydrocephalus and ventriculoperitoneal shunt presented with a subdural haematoma. He required a temporoparietal craniotomy and evacuation of left subdural haematoma, followed by care in an intensive inpatient rehabilitation unit. His course was complicated by aspiration pneumonia, dehydration, renal failure and phenytoin toxicity. During hospitalisation, the patient's RI graph was reviewed daily with his family. The RI provided an unambiguous visualisation of the trend of patient acuity, which depicted the patient's persistent decline in health, and made clear to the family the situation of the patient. This clarity was instrumental in prompting frank discussions of prognosis and consideration of comfort measures, resulting in timely transfer to hospice.

Measuring the modified early warning score and the Rothman index: advantages of utilizing the electronic medical record in an early warning system.

Early detection of an impending cardiac or pulmonary arrest is an important focus for hospitals trying to improve quality of care. Unfortunately, all current early warning systems suffer from high false-alarm rates. Most systems are based on the Modified Early Warning Score (MEWS); 4 of its 5 inputs are vital signs. The purpose of this study was to compare the accuracy of MEWS against the Rothman Index (RI), a patient acuity score based upon summation of excess risk functions that utilize additional data from the electronic medical record (EMR). MEWS and RI scores were computed retrospectively for 32,472 patient visits. Nursing assessments, a category of EMR inputs only used by the RI, showed sharp differences 24 hours before death. Receiver operating characteristic curves for 24-hour mortality demonstrated superior RI performance with c-statistics, 0.82 and 0.93, respectively. At the point where MEWS triggers an alarm, we identified the RI point corresponding to equal sensitivity and found the positive likelihood ratio (LR+) for MEWS was 7.8, and for the RI was 16.9 with false alarms reduced by 53%. At the RI point corresponding to equal LR+, the sensitivity for MEWS was 49% and 77% for RI, capturing 54% more of those patients who will die within 24 hours.

Clinical implications and validity of nursing assessments: a longitudinal measure of patient condition from analysis of the Electronic Medical Record.

OBJECTIVES: This study investigates risk of mortality associated with nurses' assessments of patients by physiological system. We hypothesise that nursing assessments of in-patients performed at entry correlate with in-hospital mortality, and those performed just before discharge correlate with postdischarge mortality. DESIGN: Cohort study of in-hospital and postdischarge mortality of patients over two 1-year periods. SETTING: An 805-bed community hospital in Sarasota, Florida, USA. SUBJECTS: 42 302 inpatients admitted for any reason, excluding obstetrics, paediatric and psychiatric patients. OUTCOME MEASURES: All-cause mortalities and mortality OR. RESULTS: Patients whose entry nursing assessments, other than pain, did not meet minimum standards had significantly higher in-hospital mortality than patients meeting minimums; and final nursing assessments before discharge had large OR for postdischarge mortality. In-hospital mortality OR were found to be: food, 7.0; neurological, 9.4; musculoskeletal, 6.9; safety, 5.6; psychosocial, 6.7; respiratory, 8.1; skin, 5.2; genitourinary, 3.0; gastrointestinal, 2.3; peripheral-vascular, 3.9; cardiac, 2.8; and pain, 1.1. CI at 95% are within ±20% of these values, with p<0.001 (except for pain). Similar results applied to postdischarge mortality. All results were comparable across the two 1-year periods, with 0.85 intraclass correlation coefficient. CONCLUSIONS: Nursing assessments are strongly correlated with in-hospital and postdischarge mortality. No multivariate analysis has yet been performed, and will be the subject of a future study, thus there may be confounding factors. Nonetheless, we conclude that these assessments are clinically meaningful and valid. Nursing assessment data, which are currently unused, may allow physicians to improve patient care. The mortality OR and the dynamic nature of nursing assessments suggest that nursing assessments are sensitive indicators of a patient's condition. While these conclusions must remain qualified, pending future multivariate analyses, nursing assessment data ought to be incorporated in risk-related health research, and changes in record-keeping software are needed to make this information more accessible.

Sociosexuality predicts women's preferences for symmetry in men's faces.

Although men displaying cues of good physical condition possess traits that are desirable in a mate (e.g., good health), these men are also more likely to possess antisocial characteristics that are undesirable in a long-term partner (e.g., aggression and tendency to infidelity). How women resolve this trade-off between the costs and benefits associated with choosing a mate in good physical condition may lead to strategic variation in women's mate preferences. Because the costs of choosing a mate with antisocial personality characteristics are greater in long- than short-term relationships, women's sociosexuality (i.e., the extent to which they are interested in uncommitted sexual relationships) may predict individual differences in their mate preferences. Here we investigated variation in 99 heterosexual women's preferences for facial symmetry, a characteristic that is thought to be an important cue of physical condition. Symmetry preferences were assessed using pairs of symmetrized and original (i.e., relatively asymmetric) versions of 10 male and 10 female faces. Analyses showed that women's sociosexuality, and their sociosexual attitude in particular, predicted their preferences for symmetry in men's, but not women's, faces; women who reported being more interested in short-term, uncommitted relationships demonstrated stronger attraction to symmetric men. Our findings present new evidence for potentially adaptive variation in women's symmetry preferences that is consistent with trade-off theories of attraction.

Opposite-sex siblings decrease attraction, but not prosocial attributions, to self-resembling opposite-sex faces.

Contextual cues of genetic relatedness to familiar individuals, such as cosocialization and maternal-perinatal association, modulate prosocial and inbreeding-avoidance behaviors toward specific potential siblings. These findings have been interpreted as evidence that contextual cues of kinship indirectly influence social behavior by affecting the perceived probability of genetic relatedness to familiar individuals. Here, we test a more general alternative model in which contextual cues of kinship can influence the kin-recognition system more directly, changing how the mechanisms that regulate social behavior respond to cues of kinship, even in unfamiliar individuals for whom contextual cues of kinship are absent. We show that having opposite-sex siblings influences inbreeding-relevant perceptions of facial resemblance but not prosocial perceptions. Women with brothers were less attracted to self-resembling, unfamiliar male faces than were women without brothers, and both groups found self-resemblance to be equally trustworthy for the same faces. Further analyses suggest that this effect is driven by younger, rather than older, brothers, consistent with the proposal that only younger siblings exhibit the strong kinship cue of maternal-perinatal association. Our findings provide evidence that experience with opposite-sex siblings can directly influence inbreeding-avoidance mechanisms and demonstrate a striking functional dissociation between the mechanisms that regulate inbreeding and the mechanisms that regulate prosocial behavior toward kin.

Variation in perceptions of physical dominance and trustworthiness predicts individual differences in the effect of relationship context on women's preferences for masculine pitch in men's voices.

Several studies have found that women tend to demonstrate stronger preferences for masculine men as short-term partners than as long-term partners, though there is considerable variation among women in the magnitude of this effect. One possible source of this variation is individual differences in the extent to which women perceive masculine men to possess antisocial traits that are less costly in short-term relationships than in long-term relationships. Consistent with this proposal, here we show that the extent to which women report stronger preferences for men with low (i.e., masculine) voice pitch as short-term partners than as long-term partners is associated with the extent to which they attribute physical dominance and low trustworthiness to these masculine voices. Thus, our findings suggest that variation in the extent to which women attribute negative personality characteristics to masculine men predicts individual differences in the magnitude of the effect of relationship context on women's masculinity preferences, highlighting the importance of perceived personality attributions for individual differences in women's judgments of men's vocal attractiveness and, potentially, their mate preferences.

Are attractive men's faces masculine or feminine? The importance of controlling confounds in face stimuli.

Women's preferences for male masculinity are highly variable. Although many researchers explain this variability as reflecting systematic individual differences in how women resolve the tradeoff between the costs and benefits of choosing a masculine partner, others suggest that methodological differences between studies are responsible. A recent study found general femininity preferences for judgments of faces that were manipulated in sexual dimorphism of shape but general masculinity preferences for judgments of faces that were based on perceived masculinity. Using the original stimuli, we replicated these previous results but found equivalent general femininity preferences for both types of faces when nonface confounds in the stimuli (e.g. hairstyle) were eliminated through masking. We conclude that care must be taken to control potential confounds in stimuli and that the influence of nonface cues on preferences for facial masculinity deserves further study.

Kin recognition signals in adult faces.

Maloney and Dal Martello [Maloney, L.T., Dal Martello, M.F. (2006). Kin recognition and the perceived facial similarity of children. Journal of Vision, 6(10), 1047-1056. http://www.journalofvision.org/6/10/4/] reported that similarity ratings of pairs of related and unrelated children were almost perfect predictors of the probability that those children were judged as being siblings by a second group of observers. Surprisingly, similarity ratings were poor predictors of whether a pair was same-sex or opposite-sex, suggesting that people ignore cues that are uninformative about kinship when making similarity judgments of faces. Using adult sibling faces, we find that similarity ratings for same-sex pairs were significantly higher than for opposite-sex pairs, suggesting that similarity judgments of adult faces are not entirely synonymous with kinship judgments.

Men report stronger attraction to femininity in women's faces when their testosterone levels are high.

Many studies have shown that women's judgments of men's attractiveness are affected by changes in levels of sex hormones. However, no studies have tested for associations between changes in levels of sex hormones and men's judgments of women's attractiveness. To investigate this issue, we compared men's attractiveness judgments of feminized and masculinized women's and men's faces in test sessions where salivary testosterone was high and test sessions where salivary testosterone was relatively low. Men reported stronger attraction to femininity in women's faces in test sessions where salivary testosterone was high than in test sessions where salivary testosterone was low. This effect was found to be specific to judgments of opposite-sex faces. The strength of men's reported attraction to femininity in men's faces did not differ between high and low testosterone test sessions, suggesting that the effect of testosterone that we observed for judgments of women's faces was not due to a general response bias. Collectively, these findings suggest that changes in testosterone levels contribute to the strength of men's reported attraction to femininity in women's faces and complement previous findings showing that testosterone modulates men's interest in sexual stimuli.

Point-of-care controls for nosocomial legionellosis combined with chlorine dioxide potable water decontamination: a two-year survey at a Welsh teaching hospital.

This study reports a two-year programme of attempted eradication of Legionella colonization in the potable water supply of a 1000-bed tertiary care teaching hospital in Wales. There was a simultaneous, point-of-care, sterile-water-only policy for all intensive care units (ICU) and bone marrow and renal transplant units in order to prevent acquisition of nosocomial Legionnaires' disease. The programme was initiated following a case of nosocomial pneumonia caused by Legionella pneumophila serogroup 1-Bellingham-like genotype A on the cardiac ICU. The case occurred 14 days after mitral and aortic valve replacement surgery. Clinical and epidemiological investigations implicated aspiration of hospital potable water as the mechanism of infection. Despite interventions with chlorine dioxide costing over 25000 UK pounds per annum, Legionella has remained persistently present in significant numbers (up to 20000 colony forming units/L) and with little reduction in the number of positive sites. Two further cases of nosocomial disease occurred over the following two-year period; in one case, aspiration of tap water was implicated again, and in the other case, instillation of contaminated water into the right main bronchus via a misplaced nasogastric tube was implicated. These cases arose because of inadvertent non-compliance with the sterile-water-only policy in high-risk locations. Enhanced clinical surveillance over the same two-year period detected no other cases of nosocomial disease. This study suggests that attempts at eradication of Legionella spp. from complex water systems may not be a cost-effective measure for prevention of nosocomial infections, and to the best of our knowledge is the first study from the UK to suggest that the introduction of a sterile-water-only policy for ICUs and other high-risk units may be a more cost-effective approach.

Regulation of PDGF production and ERK activation by estrogen is associated with TSC2 gene expression.

Mechanisms that regulate the growth response to estrogen (17beta-estradiol, E2) are poorly understood. Recently, loss of function of the tuberous sclerosis complex 2 (TSC2) gene has been associated with E2-related conditions that are characterized by benign cellular proliferation. We examined the growth response to E2 in vascular smooth muscle cells (VSMCs) that possess wild-type TSC2 and compared them with ELT-3 smooth muscle cells that do not express TSC2. In TSC2-expressing VSMCs, growth inhibition in response to E2 was associated with downregulation of platelet-derived growth factor (PDGF), PDGF receptor (PDGFR), and limited activation of extracellular signal-regulated kinase (ERK). In contrast, the growth-promoting effect of E2 in TSC2-null ELT-3 cells was associated with induction of PDGF, robust phosphorylation of PDGFR, and sustained activation of ERK. Furthermore, in ELT-3 cells, cellular growth and ERK activation by E2 were inhibited by the PDGFR inhibitor tyrphostin AG 17 and by PDGF-neutralizing antibody. These results demonstrate that autocrine production of PDGF and augmentation of the ERK pathway leads to estrogen-induced cellular proliferation in TSC2-null cells, a pathway that was downregulated in cells that express TSC2. Understanding the mechanisms that regulate the diverse responses to the steroid hormone estrogen could lead to novel approaches to the treatment of estrogen-related diseases that are characterized by aberrant cell proliferation.

Synthesis and cytotoxic activity of 7-oxo-7H-dibenz[f,ij]isoquinoline and 7-oxo-7H-benzo[e]perimidine derivatives.

A series of 7-oxo-7H-dibenz[f,ij]isoquinoline and 7-oxo-7H-benzo[e]perimidines bearing cationic side chains were prepared from aminoanthraquinones. The perimidines were prepared from 1-aminoanthraquinone by initial condensation with urea or dimethylacetamide. A series of 2-, 4-, 8-, and 11-carboxy derivatives of the dibenzisoquinolines were prepared from aminoanthraquinonecarboxylic acids. The cationic derivatives were prepared from these via amide, amine, or methylene linkers to study the effects of side chain positioning on biological activity. Within the series of carboxamide-linked compounds, the order of increasing cytotoxicity was 8- < 4- < 2- < 11-. The 2- and 4-carboxamides showed substantial growth delays against in vivo subcutaneous colon 38 tumors in mice, but the 11-carboxamide had curative activity in this refractory model and is being investigated further.

Dicationic bis(9-methylphenazine-1-carboxamides): relationships between biological activity and linker chain structure for a series of potent topoisomerase targeted anticancer drugs.

Bis(9-methylphenazine-1-carboxamides) joined by a variety of dicationic (CH(2))(n)()NR(CH(2))(m)NR(CH(2))(n) linkers of varying length (carboxamide N-N distances from 11.0 to 18.4 A) and rigidity were prepared by reaction of 9-methylphenazine-1-carboxylic acid imidazolide with the appropriate polyamines. The compounds were evaluated for growth inhibitory properties in P388 leukemia, Lewis lung carcinoma, and wild-type (JL(C)) and mutant (JL(A) and JL(D)) forms of human Jurkat leukemia with low levels of topoisomerase II (topo II). The compounds all had IC(50) ratios of <1 in the resistant Jurkat lines, consistent with topo II inhibition not being the primary mechanism of action. Analogues joined by an (CH(2))(2)NR(CH(2))(2)NR(CH(2))(2) linker were extremely potent cytotoxins, with selectivity toward the human cell lines, but absolute potencies declined sharply from R = H through R = Me to R = Pr and Bu. In contrast, (CH(2))(2)NR(CH(2))(3)NR(CH(2))(2) compounds showed reverse effects, with the R = Me analogue being more potent than the R = H one as well as being the most potent in the series [IC(50) in JL(C) cells 0.08 nM; superior to that for the clinical bis(naphthalimide) LU 79553]. Overall, the IC(50)s of analogues with linker chains (CH(2))(n)NH(CH(2))(m)NH(CH(2))(n) were inversely proportional to linker length. Constraining the rigidity of the linker chain by incorporating a piperazine ring did not decrease potency significantly. A representative compound bound tightly to DNA with high selectivity for GC sites, compatible with recent work suggesting that compounds of this type place their side chains in the major groove, making specific contacts with guanine bases. Representative compounds were susceptible to transport mediated resistance, being much less effective in cells that overexpressed P-glycoprotein. Overall the results suggest these compounds have a similar mode of action, mediated primarily by poisoning of topo I (possibly with some involvement of topo II). The bis(9-methylphenazine-1-carboxamides) show very high in vitro growth inhibitory potencies compared to their monomeric analogues. Two compounds showed in vivo activity in murine colon 38 syngeneic and HT29 human colon tumor xenograft models using intraperitoneal dosing.

Positioning of the carboxamide side chain in 11-oxo-11H-indeno[1,2-b]quinolinecarboxamide anticancer agents: effects on cytotoxicity.

A series of 11-oxo-11H-indeno[1,2-b]quinolines bearing a carboxamide-linked cationic side chain at various positions on the chromophore was studied to determine structure-activity relationships between cytotoxicity and the position of the side chain. The compounds were prepared by Pfitzinger synthesis from an appropriate isatin and 1-indanone, followed by various oxidative steps, to generate the required carboxylic acids. The 4- and 6-carboxamides (with the side chain on a terminal ring, off the short axis of the chromophore) were effective cytotoxins. The dimeric 4- and 6-linked analogues were considerably more cytotoxic than the parent monomers, but had broadly similar activities. In contrast, analogues with side chains at the 8-position (on a terminal ring but off the long axis of the chromophore) or 10-position (off the short axis of the chromophore but in a central ring) were drastically less effective. The 4,10- and 6,10-biscarboxamides had activities between those of the corresponding parent monocarboxamides. The first of these showed good activity against advanced subcutaneous colon 38 tumours in mice.

Topoisomerase I/II selectivity among derivatives of N-[2-(dimethylamino)ethyl]acridine-4-carboxamide (DACA).

DACA (N-[2-(dimethylamino)ethyl]acridine-4-carboxamide dihydrochloride) has high experimental antitumor activity and has completed phase I/II clinical trials. It targets both topoisomerase (topo) I and II, but the roles of each of these enzymes in the antitumour action of DACA are not known. We have used a series of DACA analogues (mainly monosubstituted halogen derivatives) to relate in vitro and in vivo biological activity. We measured topo II selectivity by comparing the inhibition of Jurkat human leukaemia cell lines with high and low topo II content. We determined survival curves following exposure of H460 human lung carcinoma cells for 1 h. We used plasmid DNA to compare the effects of DACA analogues on isolated topo I and II, measuring in particular the inhibition of topo I- and II-mediated DNA relaxation. The results indicate that 5-halogen substituted derivatives are the most active in clonogenic cytotoxicity assays and that this activity is related to their selective activity towards Jurkat cells with high topo II activity. In isolated topo assays, 5-halogen substituted derivatives were also the most potent and in each case the concentration required for inhibition of topo II relaxation was greater than that for inhibition of topo I relaxation. The drug concentration providing efficient cytotoxicity corresponded to that which suppressed the activity of topo I but not of topo II. We hypothesize that DACA analogues act both in vitro and in vivo to simultaneously poison topo II and inhibit topo I catalytic activity, and that this combination contributes to the high antitumour activity of DACA analogues.

Synthesis of substituted indeno[1,2-b]quinoline-6-carboxamides, [1]benzothieno[3,2-b]quinoline-4-carboxamides and 10H-quindoline-4-carboxamides: evaluation of structure-activity relationships for cytotoxicity.

New substituted indeno[1,2-b]quinoline-6-carboxamides, [1]benzothieno[3,2-b]quinoline-4-carboxamides and 10H-quindoline-4-carboxamides were prepared from methyl 2-amino-3-formylbenzoate by a new Friedlander synthesis. Evaluation of these carboxamides for cytotoxicity in a panel of cell lines showed that small lipophilic substituents in the non-carboxamide ring, in a pseudo-peri position to the side chain, significantly increased cytotoxic potency while retaining a pattern of cytotoxicity consistent with a non-topo II mode of action. The methyl-substituted indeno[1,2-b]quinoline-6-carboxamide demonstrated substantial effectiveness (20-day growth delays) in a sub-cutaneous colon 38 in vivo tumor model. This is comparable to that reported for the dual topo I/II inhibitor DACA that is in clinical trial.

Synthesis and antitumor activity of some indeno[1,2-b]quinoline-based bis carboxamides.

A series of bis(11-oxo-11H-indeno[1,2-b]quinoline-6-carboxamides) linked through the 6-carboxamides were prepared by coupling the requisite acid imidazolides with various diamines. Compounds with mono-cationic linker chains were more potent cytotoxins than the corresponding monomer in a panel of rodent and human cell lines, while those with the dicationic linker chains (CH2)2NR(CH2)2NR(CH2)2 and (CH2)2NR(CH2)3NR(CH2)2 showed extraordinarily high potencies (for example, IC50s of 0.18-1.4 nM against human Jurkat leukemia; up to 1000-fold more potent than the parent monomer). As seen previously in the monomeric series, small, lipophilic 4-substituents significantly increased potency in cell culture. The dimeric compounds were all slightly to significantly more potent in the mutant JL(A) and JL(D) cell lines that under-express topo II, suggesting that this enzyme is not their primary target. An 11-imino-linked dimer was much less active, and an asymmetric indeno[1,2-b]quinoline-6-carboxamide/naphthalimide dimer was less active than the comparable symmetric bis(indeno[1,2-b]quinoline-6-carboxamide). Selected analogues were active against sub-cutaneously implanted colon 38 tumors in mice, giving growth delays comparable to that of the clinical topo I inhibitor irinotecan at up to 10-fold lower doses. These compounds form an interesting new class of putative topo I inhibitors.

Transforming growth factor-beta 1-induced activation of the ERK pathway/activator protein-1 in human lung fibroblasts requires the autocrine induction of basic fibroblast growth factor.

Transforming growth factor-beta (TGF-beta) is involved in multiple processes including cell growth and differentiation. In particular, TGF-beta has been implicated in the pathogenesis of fibrotic lung diseases. In this study, we examined regulation of the mitogen-activated protein kinase pathway by TGF-beta1 in primary human lung fibroblasts. TGF-beta1 treatment resulted in extracellular signal-regulated kinase (ERK) pathway activation in a delayed manner, with maximal activity at 16 h. ERK activation occurred concomitantly with the induction of activator protein-1 (AP-1) binding, a nuclear factor required for activation of multiple genes involved in fibrosis. AP-1 binding was dependent on ERK activation, since the MEK-1 (mitogen-activated protein kinase kinase) inhibitor PD98059 inhibited TGF-beta1-induced binding. Induction of the receptor tyrosine kinase-linked growth factor, basic fibroblast growth factor (bFGF) protein expression temporally paralleled the activation of ERK/AP-1. Induction of AP-1 by TGF-beta1-conditioned medium was observed at 2 h, similar to AP-1 induction in response to exogenous bFGF. Dependence of ERK/AP-1 activation on bFGF induction was demonstrated by inhibition of TGF-beta1-induced ERK/AP-1 activation when conditioned medium from TGF-beta1-treated cells was incubated with bFGF-neutralizing antibody. Together, these results demonstrate that TGF-beta1 regulates the autocrine induction of bFGF, resulting in activation of the ERK mitogen-activated protein kinase pathway and induction of AP-1 binding.