Sensitivity to cuteness in baby faces is not influenced by pregnancy

BackgroundThe ability to discriminate cuteness may aid caregivers in prioritising care to the neediest child. This biologically important ability has been indirectly linked to higher levels of female reproductive hormones via studies of hormonal contraception and menopausal status. Pregnancy provides an opportunity to further investigate the role of reproductive hormones in cuteness discrimination since it is a time of substantial natural hormonal fluctuation.MethodsPregnant (n=23) and matched non-pregnant women (n=11) were assessed four times over 8 months (at 20 weeks of gestation, 32 weeks of gestation, 2 weeks postpartum, 12 weeks postpartum). At each visit, cuteness sensitivity, cuteness intensity ratings, and basic visuospatial perception were assessed. Cuteness sensitivity was assessed by presenting two versions of the same face side by side, with one subtly altered by graphics software to be more or less cute than the other; women were asked to select the cuter face. Cuteness intensity was rated on a seven-point Likert scale. Results were analysed with repeated measures ANOVA.FindingsThere was no difference between pregnant/postpartum mothers and control women in cuteness sensitivity, cuteness intensity ratings, or basic visuospatial perception. There was no change in these abilities across time.InterpretationThis result is not what we hypothesised. It seems that the link between female reproductive hormones and cuteness sensitivity is more indirect and complex than initially thought. Possibly female reproductive hormones other than those elevated in pregnancy are important in determining cuteness sensitivity.FundingWellcome Trust.     

The Prevalence of Mutations in KCNQ1, KCNH2, and SCN5A in an Unselected National Cohort of Young Sudden Unexplained Death Cases

Introduction: Sudden unexplained death account for one‐third of all sudden natural deaths in the young (1–35 years). Hitherto, the prevalence of genopositive cases has primarily been based on deceased persons referred for postmortem genetic testing. These deaths potentially may represent the worst of cases, thus possibly overestimating the prevalence of potentially disease causing mutations in the 3 major long‐QT syndrome (LQTS) genes in the general population. We therefore wanted to investigate the prevalence of mutations in an unselected population of sudden unexplained deaths in a nationwide setting. Methods: DNA for genetic testing was available for 44 cases of sudden unexplained death in Denmark in the period 2000–2006 (equaling 33% of all cases of sudden unexplained death in the age group). KCNQ1, KCNH2, and SCN5A were sequenced and in vitro electrophysiological studies were performed on novel mutations. Results: In total, 5 of 44 cases (11%) carried a mutation in 1 of the 3 genes corresponding to 11% of all investigated cases (R190W KCNQ1, F29L KCNH2 (2 cases), P297S KCNH2 and P1177L SCN5A). P1177L SCN5A has not been reported before. In vitro electrophysiological studies of P1177L SCN5A revealed an increased sustained current suggesting a LQTS phenotype. Conclusion: In a nationwide setting, the genetic investigation of an unselected population of sudden unexplained death cases aged 1–35 years finds a lower than expected number of mutations compared to referred populations previously reported. We therefore conclude that the prevalence of mutations in the 3 major LQTS associated genes may not be as abundant as previously estimated. (J Cardiovasc Electrophysiol, Vol. 23 pp. 1092‐1098, October 2012)     

Effect of interleukin-5 exposure during in vitro eosinophilopiesis on MAC-1 adhesion molecule expression and function on cultured human eosinophils

We examined the selective effects of interleukin (IL-5) in regulating the maturational expression of surface adhesion molecules on human eosinophils and adhesion to endothelial cells during eosinophiiopolesis in vitro. Expression of the beta 2 integrins (CD11/CD18) and the beta 1 integrin, VLA-4 (CD49d/ CD29), was assessed during development in culture with IL-3, IL-5, and granulocyte-macrophage colony stimulating factor in cultures of human umbilical cord blood-derived eosinophil (CDE) precursor cells. Expression of both CD11b and CD18 subunits of Mac-1 was lower on CDE which were continuously (= chronically) exposed to IL-5 than on CDE which were cultured without IL-5 for the final week of culture. CD11b expression on cells grown without IL-5 was 71.3 +/- 5.92 (mean specific fluorescence value [MSF] as measured by flow cytometry) versus 52.5 +/- 4.48 MSF for Mac-1 alpha (CD11b) on CDE grown in the continued presence of 2 x 10 - 11 mol/L IL-5 (P < .01). Although expression of VLA-4 decreased as CDE matured, expression of CD29 and CD49d were similar regardless of cytokine exposure for the final week of culture. For eosinophils cultured without IL-5, acute stimulation with 10 - 8 mol/L IL-5 increased CD11b surface expression and increased the number of cells adhering to unstimulated human umbilical vein endothelial cells (HUVEC) from 4,570 +/- 780 cells (9.14 +/- 1.56% adhesion) to 8,385 +/- 515 cells (16.8 +/- 1.03% adhesion) (P < .01). Basal adhesion to unstimulated HUVEC of CDE cultured continuously with IL-5 was comparable (8.62 +/- 1.12% adhesion; P = NS), but neither CD11b expression (50.3 +/- 11.8 MSF; P = NS v control) nor adhesion to HUVEC (6.77 +/- 1.35%; P = NS) was enhanced in these eosinophils after acute stimulation with IL-5. Blockade of adhesion to IL-1-stimulated HUVEC caused by the anti-CD49d monoclonal antibody (MoAb), HP2/1, was comparable for cells cultured with IL-5 and without IL-5. However, the anti-CD18 MoAb, R15.7, caused 47.6 +/- 5.08% inhibition of adhesion of eosinophils cultured without IL-5 and only 25.8 +/- 5.20% for cells cultured continuously with IL-5 (P < .01), and failed to block significantly the adhesion of only the latter cells to IL-4-stimulated HUVEC. Our data show that continuous, chronic exposure to low concentrations of IL-5 causes decreased expression of Mac-1 and refractoriness to acute stimulation with IL-5 of adhesion to HUVEC. These data further demonstrate that CDE maturing in the continued presence of IL-5 adhere to HUVEC predominantly through VLA-4 ligation.     

Mortality related to after-hours discharge from intensive care in Australia and New Zealand, 2005–2012

Introduction

After-hours discharge from the intensive care unit (ICU) is associated with adverse patient outcomes including increased ICU readmissions and mortality. Since Australian and New Zealand data were last published, overall ICU patient mortality has decreased; however it is unknown whether changes in discharge practices have contributed to these improved outcomes. Our aim was to examine trends over time in discharge timing and the contemporary associations with mortality and ICU readmission.

Methods

Retrospective cohort study using data from the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS APD) for patients admitted to Australian and New Zealand ICUs between January 2005 and December 2012. Data collected included patient characteristics, time of ICU discharge, hospital mortality and ICU readmissions.

Results

Between 1 January 2005 and 31 December 2012, there were 710,535 patients available for analysis, of whom 109,384 (15.4 %) were discharged after-hours (1800–0600 hours). There were no changes in timing of ICU discharge over the 8 years of the study. Patients discharged after-hours had a higher hospital mortality (6.4 versus 3.6 %; P < 0.001) and more ICU readmissions (5.1 versus 4.5 %; P < 0.001) than patients discharged in-hours. Although post-ICU mortality for all patients declined during the study period, the risk associated with after-hours discharge remained elevated throughout (odds ratio 1.34, 95 % confidence intervals 1.30–1.38).

Conclusions

After-hours discharge remains an important independent predictor of hospital mortality and readmission to ICU. Despite widespread dissemination this evidence has not translated into fewer after-hours discharges or reduction in risk in Australian and New Zealand hospitals.     

Metformin treatment may be associated with decreased levels of NT-proBNP in patients with type 2 diabetes

PurposeIndividuals with type 2 diabetes (T2DM) are at increased risk of cardiovascular disease, including heart failure (HF). In patients with T2DM elevated serum concentrations of the N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) correlate with cardiovascular morbidity and mortality. We aimed to identify predictors of increased serum NT-proBNP levels in patients with T2DM.MethodsThe study included 185 patients with T2DM treated with either oral antidiabetic agents (49.7%) or insulin (17.8%), or both (32.5%). We divided the patients into two groups: with high (>200 pg/mL) and low (≤200 pg/mL) NT-proBNP concentrations.ResultsWe found differences between the patients with high and low NT-proBNP levels including age, prevalence of dyslipidemia and HF, history of previous myocardial infarction (MI), heart rate, hemoglobin level, platelet count, creatinine, urea and uric acid concentrations, use of beta-blockers, loop diuretics, metformin and insulin. In a multivariate analysis metformin was a negative predictor of increased NT-proBNP concentration. Age, history of HF and decreased estimated glomerular filtration rate (eGFR) were positive predictors. We found no correlation between NT-proBNP serum concentration and insulin treatment or history of coronary artery disease or MI.ConclusionMetformin correlates with lower concentrations of NT-proBNP in patients with T2DM.     

A study to the fibroblast—populated collagen lattices

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复方硫酸氢黄连素灌肠液的抗菌活性研究

目的观察复方硫酸氢黄连素灌肠液比单方黄连素制剂抗菌活性是否有所增加.方法采用琼脂平板稀释法和平皿法,并以志贺氏痢疾杆菌感染小鼠为动物模型,测定复方硫酸氢黄连素灌肠液的体内、体外抗菌活性.结果复方制剂比单方制剂的MIC和MBC分别降低1～125倍和1～15倍,抑菌环增大,敏感性增强,体内感染细菌小鼠死亡率降低.结论复方硫酸氢黄连素灌肠液对常见细菌感染比单方黄连素制剂具有较强的抗感染作用.