Objective To quantify fetal cardiovascular parameters with Spatio-Temporal Image Correlation (STIC) and Virtual Organ Computed-aided AnaLysis (VOCAL™) utilizing the sub-feature: “Contour Finder: Trace”. Study Design A cross-sectional study was designed consisting of patients with normal pregnancies between 19 and 40 weeks of gestation. After STIC datasets were acquired, analysis was performed offline (4DView) and the following cardiovascular parameters were evaluated: ventricular volume in end systole and end diastole, stroke volume, cardiac output, and ejection fraction. To account for fetal size, cardiac output was also expressed as a function of head circumference, abdominal circumference, or femoral diaphysis length. Regression models were fitted for each cardiovascular parameter to assess the effect of gestational age and paired comparisons were made between the left and right ventricles. Results 1) Two hundred and seventeen patients were retrospectively identified, of whom 184 had adequate STIC datasets (85% acceptance); 2) ventricular volume, stroke volume, cardiac output, and adjusted cardiac output increased with gestational age; whereas, the ejection fraction decreased as gestation advanced; 3) the right ventricle was larger than the left in both systole (Right: 0.50 ml, IQR: 0.2 – 0.9; vs. Left: 0.27 ml, IQR: 0.1 – 0.5; p<0.001) and diastole (Right: 1.20 ml, IQR: 0.7 – 2.2; vs. Left: 1.03 ml, IQR: 0.5 – 1.7; p<0.001); 4) there were no differences between the left and right ventricle with respect to stroke volume, cardiac output, or adjusted cardiac output; and 5) the left ventricular ejection fraction was greater than the right (Left: 72.2%, IQR: 64 – 78; vs. Right: 62.4%, IQR: 56 – 69; p<0.001). Conclusion Fetal echocardiography, utilizing STIC and VOCAL™ with the sub-feature: “Contour Finder: Trace”, allows assessment of fetal cardiovascular parameters. Normal fetal cardiovascular physiology is characterized by ventricular volumes that are larger on the right and ejection fractions that are greater for the left ventricle resulting in similar left and right ventricular stroke volume and cardiac output.

Zinc is an essential trace element that plays a vital role in maintaining many biological processes and cellular homeostasis. Dysfunctional zinc signaling is associated with a number of chronic disease states including cancer, cardiovascular disease, Alzheimer's disease, and diabetes. Cellular homeostasis requires mechanisms that tightly control the uptake, storage, and distribution of zinc. This is achieved through the coordinated actions of zinc transporters and metallothioneins. Evidence on the role of these proteins in type 2 diabetes mellitus (T2DM) is now emerging. Zinc plays a key role in the synthesis, secretion and action of insulin in both physiological and pathophysiological states. Moreover, recent studies highlight zinc's dynamic role as a “cellular second messenger” in the control of insulin signaling and glucose homeostasis. This suggests that zinc plays an unidentified role as a novel second messenger that augments insulin activity. This previously unexplored concept would raise a whole new area of research into the pathophysiology of insulin resistance and introduce a new class of drug target with utility for diabetes pharmacotherapy.

COPD and lung cancer are major lung diseases affecting millions worldwide. Both diseases have links to cigarette smoking, and exert a considerable societal burden. People suffering from COPD are at a higher risk of developing lung cancer than those without COPD and are more susceptible to poor outcomes after diagnosis and treatment. Lung cancer and COPD are closely associated, possibly sharing common traits such as an underlying genetic predisposition, epithelial and endothelial cell plasticity, dysfunctional inflammatory mechanisms including the deposition of excessive extracellular matrix, angiogenesis, susceptibility to DNA damage and cellular mutagenesis. In fact, COPD could be the driving factor for lung cancer, providing a conducive environment that propagates its evolution. In the early stages of smoking, body defences provide a combative immune/oxidative response and DNA repair mechanisms are likely to subdue these changes to a certain extent; however, in patients with COPD with lung cancer the consequences could be devastating, potentially contributing to slower post-operative recovery after lung resection and increased resistance to radiotherapy and chemotherapy. Vital to the development of new-targeted therapies is an in-depth understanding of various molecular mechanisms that are associated with both pathologies. In this comprehensive review, we shall provide a detailed overview of possible underlying factors that link COPD and lung cancer and current therapeutic advances from both human and pre-clinical animal models that can effectively mitigate this unholy relationship. Running head-COPD and lung cancer: understanding and treatments

Dysfunctional zinc signaling is implicated in disease processes including cardiovascular disease, Alzheimer's disease and diabetes. Of the twenty-four mammalian zinc transporters, ZIP7 has been identified as an important mediator of the ‘zinc wave’ and in cellular signaling. Utilizing siRNA targeting Zip7 mRNA we have identified that Zip7 regulates glucose metabolism in skeletal muscle cells. An siRNA targeting Zip7 mRNA down regulated Zip7 mRNA 4.6-fold (p = 0.0006) when compared to a scramble control. This was concomitant with a reduction in the expression of genes involved in glucose metabolism including Agl, Dlst, Galm, Gbe1, Idh3g, Pck2, Pgam2, Pgm2, Phkb, Pygm, Tpi1, Gusb and Glut4. Glut4 protein expression was also reduced and insulin-stimulated glycogen synthesis was decreased. This was associated with a reduction in the mRNA expression of Insr, Irs1 and Irs2, and the phosphorylation of Akt. These studies provide a novel role for Zip7 in glucose metabolism in skeletal muscle and highlight the importance of this transporter in contributing to glycaemic control in this tissue.

Both glucose and lactate are nutrients of the ovine fetus. Each may be used by the fetus as a fuel for oxidation or as a source of carbon for energy storage and net tissue accretion.The present report describes the oxidation rates of glucose and lactate in vivo for the fetal lamb over a relatively short time period. The fraction of fetal glucose or lactate oxidized was defined as the ratio of 14C02 excretion across the umbilical circulation to the net entry of [14C]glucose or [14C]lactate into fetal tissues. The fraction of glucose oxidized over a 3-hr study averaged 6 1.296, accounting for 2.55 mgmin-I kg-' of glucose oxidized and for 2896 of the simultaneous net oxygen uptake. The fraction of lactate oxidized averaged 71.596, accounting for 4.12 mg min-I kg-' of lactate oxidized. Oxidation fractions and rates for both glucose and lactate increased with their concentrations in fetal blood suggesting sparing of other fuels for oxidation at higher glucose and lactate concentrations. 553