The prevalence of overweight and obesity has been increasing globally and has become a significant public health concern in Australia in the two past decades. This study explores the most recent national prevalence and trends of adult overweight and obesity in Australia. It will also investigate geographic remoteness as a potential risk factor for an individual being overweight or obese in adulthood. A retrospective longitudinal study that utilised 14 successive waves (wave 6 through 19) of a nationally representative linked individual-level survey. Data was obtained from the Household, Income and Labour Dynamics in Australia survey. The data on 199,675 observations from 26,713 individuals aged ≥ 15 years over the period 2006 to 2019 was analysed. Random-effects logit model was employed to estimate the association between geographic remoteness and the risk of excessive weight gain. The results reveal that the prevalence of overweight, obesity and combined overweight and obesity among Australian adults in 2019 were 34%, 26% and 60%, respectively. The analysis shows that the prevalence of overweight and obesity varies by geographic remoteness. Adults from regional city urban (OR 1.53, 95% CI 1.16-2.03) and rural areas (OR 1.32, 95% CI 1.18-1.47) were more likely to be obese compared with their counterparts from major city urban areas. The results also show that adults living in major city urban areas, regional city urban areas, and regional city rural areas in Australia were 1.53 (OR 1.53, 95% CI 1.16-2.03), 1.32 (OR 1.32, 95% CI 1.18-1.47), and 1.18 (OR 1.18, 95% CI 1.08-1.29) times more likely to be overweight compared with their counterparts from major city urban areas in Australia. Substantial geographic variation in the prevalence of overweight and obesity exists among Australian adults and appears to be increasing. Public health measures should focus on contextual obesogenic factors and behavioural characteristics to curb the rising prevalence of adult obesity.Streptomyces are one of the most important industrial microorganisms for the production of proteins and small-molecule drugs. Previously reported flow cytometry-based screening methods can only screen spores or protoplasts released from mycelium, which do not represent the filamentous stationary phase Streptomyces used in industrial cultivation. https://www.selleckchem.com/products/ucl-tro-1938.html Here we show a droplet-based microfluidic platform to facilitate more relevant, reliable and rapid screening of Streptomyces mycelium, and achieved an enrichment ratio of up to 334.2. Using this platform, we rapidly characterized a series of native and heterologous constitutive promoters in Streptomyces lividans 66 in droplets, and efficiently screened out a set of engineered promoter variants with desired strengths from two synthetic promoter libraries. We also successfully screened out several hyperproducers of cellulases from a random S. lividans 66 mutant library, which had 69.2-111.4% greater cellulase production than the wild type. Our method provides a fast, simple, and powerful solution for the industrial engineering and screening of Streptomyces in more industry-relevant conditions.Mammary serine protease inhibitor (maspin) is a tumor suppressor gene that is downregulated during carcinogenesis and breast cancer progression. While the nuclear localization of maspin is essential for tumor suppression, we previously reported that the cytoplasmic localization of maspin was significantly correlated with poor prognosis in breast cancer patients. To understand the mechanisms that underlie oncogenic role of cytoplasmic maspin, we studied its biological function in breast cancer cell lines. Subcellular localization of maspin in MDA-MB-231 breast cancer cells was mainly detected in the cytoplasm, whereas in MCF10A mammary epithelial cells, maspin was present in both cytoplasm and nucleus. In MDA-MB-231 cells, maspin overexpression promoted cell proliferation and cell invasion, whereas maspin downregulation resulted in the opposite effect. Further, we observed that SRGN protein levels were increased in MDA-MB-231 cells stably overexpressing maspin. Finally, maspin overexpression in MDA-MB-231 cells resulted in the N-cadherin and epithelial mesenchymal transition (EMT)-related transcription factors upregulation, and TGFβ signaling pathway activation. These results suggested that cytoplasmic maspin enhances the invasive and metastatic potential in breast cancer cells with aggressive phenotype by inducing EMT via SRGN/TGFβ axis. This study demonstrated a novel biological function of cytoplasmic maspin in progression of breast cancer cells with an aggressive phenotype.Injury/dysfunction of the endothelium of pulmonary arteries contributes to hypoxia-induced pulmonary hypertension (HPH). We investigated whether C1q/tumor necrosis factor-related protein-9 (CTRP9), a newly identified cardiovascular agent, has protective roles in the development of HPH. HPH was induced in adult male rats by chronic hypobaric hypoxia. CTRP9 overexpression by adeno-associated virus (AAV)-CTRP9 transfection attenuated the increases in right ventricular systolic pressure, right ventricular hypertrophy index, and pulmonary arterial remodeling of rats under hypoxia. Importantly, CTRP9 overexpression improved endothelium-dependent vasodilation in pulmonary arterioles in HPH rats. CTRP9 overexpression enhanced expression of phosphorylated 5'-adenosine monophosphate-activated protein kinase (p-AMPK) and phosphorylated endothelial nitric oxide synthase (p-eNOS), and reduced phosphorylated extracellular signal-regulated protein kinase (p-ERK1/2) expression in pulmonary microvascular endothelial cells (PMVECs) of HPH rats. In cultured PMVECs, CTRP9 not only preserved the decrease of AMPK and eNOS phosphorylation level and nitric oxide (NO) production induced by hypoxia, but also blocked the increase in hypoxia-induced ERK1/2 phosphorylation level and endothelin (ET)-1 production. Furthermore, the effects of CTRP9 were interrupted by inhibitors or knockdown of AMPK. CTRP9 enhances NO production and reduces ET-1 production by regulating AMPK activation. CTRP9 could be a target for HPH.