The Physical Inactivity Matrix: Lessons from the classification of physical inactivity interventions

Physical inactivity (PI), a leading modifiable cause of disease and injury, is endemic in industrialised nations. Although considerable research has been undertaken in this field, we lack a system to synthesise the research literature to inform policy and identify research needs. The aims of this study were to (1) develop a system to classify physical inactivity intervention studies, (2) examine the distribution of PI interventions published in the peer-reviewed health literature using the system, and (3) consider implications for future research. We developed the Physical Inactivity Matrix (PIM), with 12 intervention points, created by the intersection of two dimensions: the intervention target (individual, physical environment and social/cultural environment) and the activity focus (transport, work/school, leisure and consumer). A formal search of the health research literature identified 529 eligible studies and each was classified into one of the 12 cells of the PIM. Most studies were categorised as: individual-leisure (68%), individual-work/school (12%) or social/cultural environment-leisure (13%). Only 4% targeted the physical environment. The findings of this initial application of the PIM support the call for greater investment in policies, interventions and research that focus on the relationship between the environment and PI, and transportation in particular. There would be merit in establishing the inter-rater reliability of the PIM and applying it to a wider variety of studies, including those published in the transportation and urban planning literatures. The PIM could be a useful tool for monitoring trends in research directions and funding levels over time and across countries.     

Morphometric analysis of the great vessels in early fetal life

Pathological examination of the heart and great vessels wasperformed in 61 specimens obtained after surgical terminationof pregnancy for psychosocial indications at 9–18 weeksof gestation. The aorta and pulmonary trunk were identifiedand external diameters were measured at the level of, and distalto the aortic valve and pulmonary valve, the level of the aorticisthmus and thoracic aorta, and the proximal and distal ductusarteriosus. All eight vessel diameters increased linearly withgestational age and the ratio of the diameter of the aorticisthmus to that of the aortic valve or the distal ductus arteriosusalso increased with gestation. Early pregnancy is characterizedby rapid growth of the fetal head and this may well be the consequenceof a preferential distribution of left ventricular output infavour of the head due to relative narrowing of the aortic isthmusat this gestation.     

Fetal heart rate and umbilico-placental Doppler flow velocity waveforms in early pregnancies with a chromosomal abnormality and/or an increased nuchal translucency thickness

Fetal heart rate, umbilical artery pulsatility index, end-diastolicflow,nuchal translucency thickness and placental thickness were recordedin 250 women with a viable singleton pregnancy undergoing chorionicvillous sampling for fetal karyotyping at 11–14 weeksof gestation. The fetal karyotype was normal in 210 cases andabnormal in 40, including 21 with trisomy 21, 13 with trisomy18, three with triploidy, two with monosomy X and one with trisomy13. A total of 52 fetuses with a normal karyotype had a nuchaltranslucency 3 mm and were considered separately. There wasa stable and significant increase in the mean fetal heart ratein trisomy 21 pregnancies compared to controls. No significantdifference was found for the other variables between the groups.In chromosomally normal fetuses with an increased nuchal thickness,the development of fetal heart rate and compliance of the umbilico-placentalcirculation were within the normal ranges. Some fetuses withtrisomy 18 or triploidy had an increased resistance to bloodflow in the umbilical artery, which was probably due to abnormalplacental development.     

Placental expression of interferon-gamma (IFN-gamma) and its receptor IFN-gamma R2 fail to switch from early hypoxic to late normotensive development in preeclampsia

The inability of the mother to switch from T helper cell type 1 (Th1) to Th2 cytokine profiles at the fetal-maternal interface has been proposed as one of the primary causes of miscarriage, intrauterine growth restriction (IUGR), and preeclampsia (PE). The Th1 [interferon-gamma (IFN-gamma), TNF-alpha, and IL-12] and Th2 (IL-4 and IL-10) cytokines have opposite effects on human pregnancy. Leukemia inhibitory factor (LIF) promotes embryo implantation and sustains pregnancy, whereas IFN-gamma and TNF-alpha are detrimental to pregnancy. Both IFN-gamma and LIF are produced by maternal cells and tissues at the fetal-maternal interface, whereas the IFN-gamma receptors (IFN-gamma R1 and IFN-gamma R2) and LIF receptor are abundantly expressed on the surface of placental trophoblasts. The effect of IFN-gamma on T lymphocyte activation is influenced by the relative membrane density of its two receptors, particularly IFN-gamma R2. In this study we report that in PE (25-40 wk gestation) and PE complicated by IUGR, IFN-gamma R2 protein expression is severely down-regulated and is similar to that observed in early placenta (7-10 wk gestation) developing under low O(2) tension. IFN-gamma production was found to be inversely related to the IFN-gamma R2 protein expression, and LIF receptor protein expression in PE mimicked that in early placental development. These results show that in PE, placental trophoblasts fail to establish an early to late switch with respect to IFN-gamma and IFN-gamma R2 expression. This supports the hypothesis that trophoblasts control the polarization of maternal immune effectors and cytokine profiles at the fetal-maternal interface that could be subject to oxidative stress in PE.     

Use of alcohol intoxication codes for serious non-fatal hospitalised injury

Aim

To determine the extent to which ICD-10 alcohol intoxication codes are used for serious hospitalised injury and the distribution of these codes according to gender, age, injury mechanism and intent, severity of injury, and whether the patient was treated in an Intensive Care Unit.

Design

Cross-sectional study.

Setting

New Zealand.

Participants

All injury hospital discharges in 2010 that met specified severity criteria.

Measurements

Cases which had a measurement of BAC (Y90) coded, or only a subjective assessment of alcohol intoxication (F10.0).

Findings

2.5% had a blood alcohol recorded (Y90) and a further 3% were coded as being intoxicated but there was no blood alcohol code. All factors investigated were shown to be independently associated with the assignation of codes. Notable findings were the elevated odds of an alcohol code for males, assault and the more severe injuries.

Conclusions

Assessment of alcohol intoxication among seriously injured persons appears to be very uncommon. The development of a standardised instrument for clinical judgement of intoxication would be highly desirable.     

Sulfated Progesterone Metabolites That Enhance Insulin Secretion via TRPM3 Are Reduced in Serum From Women With Gestational Diabetes Mellitus

Serum progesterone sulfates were evaluated in the etiology of gestational diabetes mellitus (GDM). Serum progesterone sulfates were measured using ultra-performance liquid chromatography–tandem mass spectrometry in four patient cohorts: 1) the Hyperglycemia and Adverse Pregnancy Outcomes study; 2) London-based women of mixed ancestry and 3) U.K.-based women of European ancestry with or without GDM; and 4) 11–13 weeks pregnant women with BMI ≤25 or BMI ≥35 kg/m² with subsequent uncomplicated pregnancies or GDM. Glucose-stimulated insulin secretion (GSIS) was evaluated in response to progesterone sulfates in mouse islets and human islets. Calcium fluorescence was measured in HEK293 cells expressing transient receptor potential cation channel subfamily M member 3 (TRPM3). Computer modeling using Molecular Operating Environment generated three-dimensional structures of TRPM3. Epiallopregnanolone sulfate (PM5S) concentrations were reduced in GDM (P < 0.05), in women with higher fasting plasma glucose (P < 0.010), and in early pregnancy samples from women who subsequently developed GDM with BMI ≥35 kg/m² (P < 0.05). In islets, 50 µmol/L PM5S increased GSIS by at least twofold (P < 0.001); isosakuranetin (TRPM3 inhibitor) abolished this effect. PM5S increased calcium influx in TRPM3-expressing HEK293 cells. Computer modeling and docking showed identical positioning of PM5S to the natural ligand in TRPM3. PM5S increases GSIS and is reduced in GDM serum. The activation of GSIS by PM5S is mediated by TRPM3 in both mouse and human islets.