Gender equality related to gender differences in life expectancy across the globe gender equality and life expectancy

Life expectancy (LE) depends on the wider determinants of health, many of which have gendered effects worldwide. Therefore, this study aimed to investigate whether gender equality was associated with LE for women and men and the gender gap in LE across the globe. Gender equality in 156 countries was estimated using a modified global gender gap index (mGGGI), based on the index developed by the World Economic Forum between 2010 and 2021. Linear regression was used to investigate the association between the mGGGI and its economic, political, and education subindices and the gender gap in LE and women and men's LE. Overall, the mGGGI increased from 58% in 2010 to 62% in 2021. Globally, changes in the mGGGI and its economic and political subindexes were not associated with changes in the gender gap in LE or with LE for women and men between 2010 and 2020. Improvements in gender equality in education were associated with a longer LE for women and men and widening of the gender gap in LE. In 2021, each 10% increase in the mGGGI was associated with a 4.3-month increase in women's LE and a 3.5-month increase in men's LE, and thus with an 8-month wider gender gap. However, the direction and magnitude of these associations varied between regions. Each 10% increase in the mGGGI was associated with a 6-month narrower gender gap in high-income countries, and a 13- and 16-month wider gender gap in South and Southeast Asia and Oceania, and in Sub-Saharan Africa, respectively. Globally, greater gender equality is associated with longer LE for both women and men and a widening of the gender gap in LE. The variation in this association across world regions suggests that gender equality may change as countries progress towards socioeconomic development and gender equality

Real-time all-optical ultrasound imaging of a dynamic heart valve phantom

All-optical ultrasound imaging, in which ultrasound is generated and received using light, is well-suited to minimally invasive surgical procedures. Here we present a device that can provide real-time M-mode ultrasound images, and demonstrate its use imaging a dynamic heart valve phantom. This device, comprising two optical fibres, one with a graphene-polydimethylsiloxane composite coating for ultrasound generation, and a second with a concave Fabry-Perot cavity for ultrasound reception, had a diameter of 30 MHz) that enabled imaging with high axial resolution ( 2 cm). M-mode imaging with an A-line rate of 100 Hz was demonstrated on a heart valve phantom with realistic mitral valve motion. This work demonstrates the potential for all-optical ultrasound imaging to be used for guidance of intracardiac interventions

Long-term change in respiratory function following spinal cord injury.

STUDY DESIGN: Retrospective study. OBJECTIVES: To model the effect of time since injury on longitudinal respiratory function measures in spinal cord injured-individuals and to investigate the effect of patient characteristics. SETTING: A total of 173 people who sustained a spinal cord injury between 1966 and April 2013 and who had previously participated in research or who underwent clinically indicated outpatient respiratory function tests at the Austin Hospital in Melbourne, Australia, were included in the study. At least two measurements over time were available for analysis in 59 patients. METHODS: Longitudinal data analysis was performed using generalised linear regression models to determine changes in respiratory function following spinal cord injury from immediately post injury to many years later. Secondly, we explored whether injury severity, age, gender and body mass index (BMI) at injury altered the time-dependent change in respiratory function. RESULTS: The generalised linear regression model showed no significant change (P=0.276) in respiratory function measured in (forced) vital capacity ((F)VC) after the spinal cord injury. However, significant (P30 kg m(-2).Spinal Cord advance online publication, 12 January 2016; doi:10.1038/sc.2015.233

Associations of Hemostatic Variables with Cardiovascular Disease and Total Mortality: The Glasgow MONICA Study

The associations of plasma levels of hemostatic factors, other than fibrinogen, with risks of cardiovascular disease (CVD) and all-cause mortality are not well defined. In two phases of the Glasgow MONICA study, we assayed coagulation factors (VII, VIII, IX, and von Willebrand factor), coagulation inhibitors (antithrombin, protein C, protein S), coagulation activation markers (prothrombin fragment 1þ2, thrombin–antithrombin complexes, D-dimer), and the fibrinolytic factors, tissue plasminogen activator (t-PA) antigen and plasminogen activator inhibitor type 1. Over 15 to 20 years, we followed up between 382 and 1,123 men and women aged 30 to 74 years, without baseline CVD, for risks of CVD and mortality. Age- and sex-adjusted hazard ratios (HRs) for CVD (top third vs bottom third) were significant only for factor VIII (1.30; 95% confidence interval [CI], 1.06–1.58) and factor IX (1.18; 95% CI, 1.01–1.39); these HRs were attenuated by further adjustment for CVD risk factors: 1.17 (95% CI, 0.94–1.46) and 1.07 (95% CI, 0.92–1.25), respectively. In contrast, factor VIII (HR, 1.63; 95% CI, 1.35–1.96), D-dimer (HR, 2.34; 95% CI, 1.26–4.35), and t-PA (HR, 2.81; 95% CI, 1.43–5.54) were strongly associated with mortality after full risk factor adjustment. Further studies, including meta-analyses, are required to assess the associations of these hemostatic factors with the risks of stroke and heart disease and causes of mortality

Changing the Landscape? Women in academic leadership in Australia.

This paper analyses interviews with 41 men and women in senior academic leadership roles in five Australian universities. It explores whether management cultures change when women hold power. It contrasts interviewees' conceptions of the role gender has played in career success with notions which posit a gender-neutral organization. It probes the impact of the differentially constructed careers of men and women for appointment to senior positions. It identifies factors that sustain women, specifically collegiality, support from senior colleague and a critical mass of other women in power. Finally, in considering the unwillingness of some women to apply for further promotions, it suggests women are still positioned as outsiders to university management, although there is evidence that this is changing

The impact of delirium on the prediction of in-hospital mortality in intensive care patients

Introduction: predictive models, such as acute physiology and chronic health evaluation II (APACHE-II), are widely used in intensive care units (ICUs) to estimate mortality. Although the presence of delirium is associated with a higher mortality in ICU patients, delirium is not part of the APACHE-II model. The aim of the current study was to evaluate whether delirium, present within 24 hours after ICU admission, improves the predictive value of the APACHE-II score.Methods: in a prospective cohort study 2116 adult patients admitted between February 2008 and February 2009 were screened for delirium with the confusion assessment method-ICU (CAM-ICU). Exclusion criteria were sustained coma and unable to understand Dutch. Logistic regression analysis was used to estimate the predicted probabilities in the model with and without delirium. Calibration plots and the Hosmer-Lemeshow test (HL-test) were used to assess calibration. The discriminatory power of the models was analyzed by the area under the receiver operating characteristics curve (AUC) and AUCs were compared using the Z-test.Results: 1740 patients met the inclusion criteria, of which 332 (19%) were delirious at the time of ICU admission or within 24 hours after admission. Delirium was associated with in-hospital mortality in unadjusted models, odds ratio (OR): 3.22 (95% confidence interval [CI]: 2.23 - 4.66). The OR between the APACHE-II and in-hospital mortality was 1.15 (95% CI 1.12 - 1.19) per point. The predictive accuracy of the APACHE-II did not improve after adding delirium, both in the total group as well as in the subgroup without cardiac surgery patients. The AUC of the APACHE model without delirium was 0.77 (0.73 - 0.81) and 0.78 (0.74 - 0.82) when delirium was added to the model. The z-value was 0.92 indicating no improvement in discriminative power, and the HL-test and calibration plots indicated no improvement in calibration.Conclusions: although delirium is a significant predictor of mortality in ICU patients, adding delirium as an additional variable to the APACHE-II model does not result in an improvement in its predictive estimate

Translational outcomes in a full gene deletion of ubiquitin protein ligase E3A rat model of Angelman syndrome.

Angelman syndrome (AS) is a rare neurodevelopmental disorder characterized by developmental delay, impaired communication, motor deficits and ataxia, intellectual disabilities, microcephaly, and seizures. The genetic cause of AS is the loss of expression of UBE3A (ubiquitin protein ligase E6-AP) in the brain, typically due to a deletion of the maternal 15q11-q13 region. Previous studies have been performed using a mouse model with a deletion of a single exon of Ube3a. Since three splice variants of Ube3a exist, this has led to a lack of consistent reports and the theory that perhaps not all mouse studies were assessing the effects of an absence of all functional UBE3A. Herein, we report the generation and functional characterization of a novel model of Angelman syndrome by deleting the entire Ube3a gene in the rat. We validated that this resulted in the first comprehensive gene deletion rodent model. Ultrasonic vocalizations from newborn Ube3am-/p+ were reduced in the maternal inherited deletion group with no observable change in the Ube3am+/p- paternal transmission cohort. We also discovered Ube3am-/p+ exhibited delayed reflex development, motor deficits in rearing and fine motor skills, aberrant social communication, and impaired touchscreen learning and memory in young adults. These behavioral deficits were large in effect size and easily apparent in the larger rodent species. Low social communication was detected using a playback task that is unique to rats. Structural imaging illustrated decreased brain volume in Ube3am-/p+ and a variety of intriguing neuroanatomical phenotypes while Ube3am+/p- did not exhibit altered neuroanatomy. Our report identifies, for the first time, unique AS relevant functional phenotypes and anatomical markers as preclinical outcomes to test various strategies for gene and molecular therapies in AS

High dietary fat consumption impairs axonal mitochondrial function in vivo

Peripheral neuropathy (PN) is the most common complication of prediabetes and diabetes. PN causes severe morbidity for Type 2 diabetes (T2D) and prediabetes patients, including limb pain followed by numbness resulting from peripheral nerve damage. PN in T2D and prediabetes is associated with dyslipidemia and elevated circulating lipids; however, the molecular mechanisms underlying PN development in prediabetes and T2D are unknown. Peripheral nerve sensory neurons rely on axonal mitochondria to provide energy for nerve impulse conduction under homeostatic conditions. Models of dyslipidemia in vitro demonstrate mitochondrial dysfunction in sensory neurons exposed to elevated levels of exogenous fatty acids. Herein, we evaluated the effect of dyslipidemia on mitochondrial function and dynamics in sensory axons of the saphenous nerve of a male high-fat diet (HFD)-fed murine model of prediabetes to identify mitochondrial alterations that correlate with PN pathogenesis in vivo. We found that the HFD decreased mitochondrial membrane potential (MMP) in axonal mitochondria and reduced the ability of sensory neurons to conduct at physiological frequencies. Unlike mitochondria in control axons, which dissipated their MMP in response to increased impulse frequency (from 1 to 50 Hz), HFD mitochondria dissipated less MMP in response to axonal energy demand, suggesting a lack of reserve capacity. The HFD also decreased sensory axonal Ca^{2+} levels and increased mitochondrial lengthening and expression of PGC1α, a master regulator of mitochondrial biogenesis. Together, these results suggest that mitochondrial dysfunction underlies an imbalance of axonal energy and Ca^{2+} levels and impairs impulse conduction within the saphenous nerve in prediabetic PN