Spatial and Temporal Dynamics of Chemical and Microbial Contamination in Nonurban Floodwaters.

During major flood events, waterborne contaminants are relatively poorly characterized. This is due to logistical difficulties associated with obtaining water samples in potentially dangerous flood conditions. Herein, we report analyses of water samples from a large, flooded landscape in Victoria, Australia, during a major flood event.

Mortality burden attributable to exceptional PM air pollution events in Australian cities: A health impact assessment.

Background: People living in Australian cities face increased mortality risks from exposure to extreme air pollution events due to bushfires and dust storms. However, the burden of mortality attributable to exceptional PM levels has not been well characterised. We assessed the burden of mortality due to PM pollution events in Australian capital cities between 2001 and 2020.

Biomimetic Dp44mT-nanoparticles selectively induce apoptosis in Cu-loaded glioblastoma resulting in potent growth inhibition.

Selective targeting of elevated copper (Cu) in cancer cells by chelators to induce tumor-toxic reactive oxygen species (ROS) may be a promising approach in the treatment of glioblastoma multiforme (GBM). Previously, the Cu chelator di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone (Dp44mT) attracted much interest due to its potent anti-tumor activity mediated by the formation of a highly redox-active Cu-Dp44mT complex. However, its translational potential was limited by the development of toxicity in murine models of cancer reflecting poor selectivity.

Avoidable Mortality Attributable to Anthropogenic Fine Particulate Matter (PM) in Australia.

Ambient fine particulate matter <2.5 µm (PM) air pollution increases premature mortality globally. Some PM is natural, but anthropogenic PM is comparatively avoidable.

A statistical downscaling approach for generating high spatial resolution health risk maps: a case study of road noise and ischemic heart disease mortality in Melbourne, Australia.

Introduction: Road traffic noise increases the risk of mortality from ischemic heart disease (IHD). Because noise is highly localized, high resolution maps of exposures and health outcomes are key to urban planning interventions that are informed by health risks. In Australia, publicly accessible IHD deaths data are only available at the coarse spatial aggregation level of local government area (LGA), in which about 130,000 people reside.

Hypoxia inhibits hepcidin expression in HuH7 hepatoma cells via decreased SMAD4 signaling.

Hepcidin negatively regulates systemic iron homeostasis in response to inflammation and elevated serum iron. Conversely, hepcidin expression is diminished in response to hypoxia, oxidative stress, and increased erythropoietic demand, though the molecular intermediates involved are incompletely understood. To address this, we have investigated hypoxic hepcidin regulation in HuH7 hepatoma cells either cultured alone or cocultured with activated THP-1 macrophages.

Erythropoietin regulates intestinal iron absorption in a rat model of chronic renal failure.

Erythropoietin is produced by the kidney and stimulates erythropoiesis; however, in chronic renal disease its levels are reduced and patients develop anemia that is treatable with iron and recombinant hormone. The mechanism by which erythropoietin improves iron homeostasis is still unclear, but it may involve suppression of the iron regulatory peptide hepcidin and/or a direct effect on intestinal iron absorption. To investigate these possibilities, we used the well-established 5/6th nephrectomy rat model of chronic renal failure with or without human recombinant erythropoietin treatment.

Hepcidin decreases iron transporter expression in vivo in mouse duodenum and spleen and in vitro in THP-1 macrophages and intestinal Caco-2 cells.

Hepcidin is thought to control iron metabolism by interacting with the iron efflux transporter ferroportin. In macrophages, there is compelling evidence that hepcidin directly regulates ferroportin protein expression. However, the effects of hepcidin on intestinal ferroportin levels are less conclusive.

Activated macrophages induce hepcidin expression in HuH7 hepatoma cells.

Background: Hepcidin is an iron regulatory peptide produced by the liver in response to inflammation and elevated systemic iron. Recent studies suggest that circulating monocytes and resident liver macrophages--Küpffer cells--may influence both basal and inflammatory expression of hepcidin.

Design And Methods: We used an in vitro co-culture model to investigate hepatocyte hepcidin regulation in the presence of activated THP1 macrophages.

Single frequency bioelectrical impedance is a poor method for determining fat mass in moderately obese women.

Background: The primary aim of weight loss intervention in obesity is the loss of fat mass (FM). Hence, determinations of changes in FM and fat free mass (FFM) during weight loss are of clinical value. The authors compared the clinical utility of SkinFold Thickness (SKF), tetrapolar bioelectrical impedance analysis (BIA) and a body mass index (BMI) based calculation, in determining changes in percentage of fat mass (delta%FM).

Systematic review of medium-term weight loss after bariatric operations.

Background: Although bariatric surgery is known to be effective in the short term, the durability of that effect has not been convincingly demonstrated over the medium term (> 3 years) and the long term (> 10 years). The authors studied the durability of weight loss after bariatric surgery based on a systematic review of the published literature.

Methods: All reports published up to September, 2005 were included if they were full papers in refereed journals published in English, of outcomes after Roux-en-Y gastric bypass (RYGBP), and its hybrid procedures of banded bypass (Banded RYGBP) and longlimb bypass (LL-RYGBP), biliopancreatic diversion with or without duodenal switch (BPD+/-DS) or laparoscopic adjustable gastric banding (LAGB).

Potent antitumor activity of novel iron chelators derived from di-2-pyridylketone isonicotinoyl hydrazone involves fenton-derived free radical generation.

Purpose: The development of novel and potent iron chelators as clinically useful antitumor agents is an area of active interest. Antiproliferative activity of chelators often relates to iron deprivation or stimulation of iron-dependent free radical damage. Recently, we showed that novel iron chelators of the di-2-pyridylketone isonicotinoyl hydrazone (PKIH) class have potent and selective antineoplastic activity (E.

Cytotoxic iron chelators: characterization of the structure, solution chemistry and redox activity of ligands and iron complexes of the di-2-pyridyl ketone isonicotinoyl hydrazone (HPKIH) analogues.

Di-2-pyridyl ketone isonicotinoyl hydrazone (HPKIH) and a range of its analogues comprise a series of monobasic acids that are capable of binding iron (Fe) as tridentate ( N, N, O) ligands. Recently, we have shown that these chelators are highly cytotoxic, but show selective activity against cancer cells. Particularly interesting was the fact that cytotoxicity of theHPKIH analogues is maintained even after complexation with Fe.

Iron chelators for the treatment of iron overload disease: relationship between structure, redox activity, and toxicity.

The success of the iron (Fe) chelator desferrioxamine (DFO) in the treatment of beta-thalassemia is limited by its lack of bioavailability. The design and characterization of synthetic alternatives to DFO has attracted much scientific interest and has led to the discovery of orally active chelators that can remove pathological Fe deposits. However, chelators that access intracellular Fe pools can be toxic by either inhibiting Fe-containing enzymes or promoting Fe-mediated free radical damage.

Interactions of the pyridine-2-carboxaldehyde isonicotinoyl hydrazone class of chelators with iron and DNA: implications for toxicity in the treatment of iron overload disease.

Iron chelation therapy for the management of iron-overload disease is dominated by desferrioxamine (DFO). However, treatment using DFO is very arduous. Recently, novel Fe chelators of the pyridine-2-carboxaldehyde isonicotinoyl hydrazone (PCIH) class have shown high chelation efficacy and the potential to replace DFO.

Examination of the antiproliferative activity of iron chelators: multiple cellular targets and the different mechanism of action of triapine compared with desferrioxamine and the potent pyridoxal isonicotinoyl hydrazone analogue 311.

Purpose: Tumors are sensitive to iron (Fe) chelation therapy with the clinically used chelator desferrioxamine (DFO). Recently, the potent inhibitor of ribonucleotide reductase, Triapine, has entered clinical trials as an anticancer agent. This compound is a potential Fe chelator, but despite this, no investigations have examined its effect on cellular Fe metabolism.