University of Queensland

About: University of Queensland is a education organization based out in Brisbane, Queensland, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 51138 authors who have published 155721 publications receiving 5717659 citations. The organization is also known as: UQ & The University of Queensland.

High-intensity interval training in patients with lifestyle-induced cardiometabolic disease: a systematic review and meta-analysis

Abstract: Background/Aim Cardiorespiratory fitness (CRF) is a strong determinant of morbidity and mortality. In athletes and the general population, it is established that high-intensity interval training (HIIT) is superior to moderate-intensity continuous training (MICT) in improving CRF. This is a systematic review and metaanalysis to quantify the efficacy and safety of HIIT compared to MICT in individuals with chronic cardiometabolic lifestyle diseases. Methods The included studies were required to have a population sample of chronic disease, where poor lifestyle is considered as a main contributor to the disease. The procedural quality of the studies was assessed by use of a modified Physiotherapy Evidence Base Database (PEDro) scale. A meta-analysis compared the mean difference (MD) of preintervention versus postintervention CRF (VO2peak) between HIIT and MICT. Results 10 studies with 273 patients were included in the meta-analysis. Participants had coronary artery disease, heart failure, hypertension, metabolic syndrome and obesity. There was a significantly higher increase in the VO2peak after HIIT compared to MICT (MD 3.03 mL/kg/ min, 95% CI 2.00 to 4.07), equivalent to 9.1%. Conclusions HIIT significantly increases CRF by almost double that of MICT in patients with lifestyle-induced chronic diseases.

DNA methylation age of blood predicts all-cause mortality in later life.

Abstract: Background: DNA methylation levels change with age. Recent studies have identified biomarkers of chronological age based on DNA methylation levels. It is not yet known whether DNA methylation age captures aspects of biological age. Results: Here we test whether differences between people’s chronological ages and estimated ages, DNA methylation age, predict all-cause mortality in later life. The difference between DNA methylation age and chronological age (Δage) was calculated in four longitudinal cohorts of older people. Meta-analysis of proportional hazards models from the four cohorts was used to determine the association between Δage and mortality. A 5-year higher Δage is associated with a 21% higher mortality risk, adjusting for age and sex. After further adjustments for childhood IQ, education, social class, hypertension, diabetes, cardiovascular disease, and APOE e4 status, there is a 16% increased mortality risk for those with a 5-year higher Δage. A pedigree-based heritability analysis of Δage was conducted in a separate cohort. The heritability of Δage was 0.43. Conclusions: DNA methylation-derived measures of accelerated aging are heritable traits that predict mortality independently of health status, lifestyle factors, and known genetic factors.

Biochar reduces the bioavailability and phytotoxicity of heavy metals

Abstract: Biochar has attracted research interest due to its ability to increase the soil carbon pool and improve crop productivity. The objective of this study was to evaluate the metal immobilizing impact of chicken manure- and green waste-derived biochars, and their effectiveness in promoting plant growth. The immobilization and phytoavailability of Cd, Cu and Pb was examined using naturally contaminated shooting range and spiked soils. Biochar samples prepared from chicken manure and green waste were used as soil amendments. Application of biochar significantly reduced NH4NO3 extractable Cd, Cu and Pb concentrations of soils, indicating the immobilization of these metals. Chicken manure-derived biochar increased plant dry biomass by 353 and 572% for shoot and root, respectively with 1% of biochar addition. This might be attributed to reduced toxicity of metals and increased availability of nutrients such as P and K. Both biochars significantly reduced Cd, Cu and Pb accumulation by Indian mustard (Brassica juncea), and the reduction increased with increasing amount of biochar application except Cu concentration. Metal sequential fractionation data indicated that biochar treatments substantially modified the partitioning of Cd, Cu and Pb from the easily exchangeable phase to less bioavailable organic bound fraction. The results clearly showed that biochar application was effective in metal immobilization, thereby reducing the bioavailability and phytotoxicity of heavy metals.

Microenvironment-induced PTEN loss by exosomal microRNA primes brain metastasis outgrowth

Abstract: The development of life-threatening cancer metastases at distant organs requires disseminated tumour cells' adaptation to, and co-evolution with, the drastically different microenvironments of metastatic sites. Cancer cells of common origin manifest distinct gene expression patterns after metastasizing to different organs. Clearly, the dynamic interaction between metastatic tumour cells and extrinsic signals at individual metastatic organ sites critically effects the subsequent metastatic outgrowth. Yet, it is unclear when and how disseminated tumour cells acquire the essential traits from the microenvironment of metastatic organs that prime their subsequent outgrowth. Here we show that both human and mouse tumour cells with normal expression of PTEN, an important tumour suppressor, lose PTEN expression after dissemination to the brain, but not to other organs. The PTEN level in PTEN-loss brain metastatic tumour cells is restored after leaving the brain microenvironment. This brain microenvironment-dependent, reversible PTEN messenger RNA and protein downregulation is epigenetically regulated by microRNAs from brain astrocytes. Mechanistically, astrocyte-derived exosomes mediate an intercellular transfer of PTEN-targeting microRNAs to metastatic tumour cells, while astrocyte-specific depletion of PTEN-targeting microRNAs or blockade of astrocyte exosome secretion rescues the PTEN loss and suppresses brain metastasis in vivo. Furthermore, this adaptive PTEN loss in brain metastatic tumour cells leads to an increased secretion of the chemokine CCL2, which recruits IBA1-expressing myeloid cells that reciprocally enhance the outgrowth of brain metastatic tumour cells via enhanced proliferation and reduced apoptosis. Our findings demonstrate a remarkable plasticity of PTEN expression in metastatic tumour cells in response to different organ microenvironments, underpinning an essential role of co-evolution between the metastatic cells and their microenvironment during the adaptive metastatic outgrowth. Our findings signify the dynamic and reciprocal cross-talk between tumour cells and the metastatic niche; importantly, they provide new opportunities for effective anti-metastasis therapies, especially of consequence for brain metastasis patients.