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Low-cost Particulate Matter (PM) sensors offer an excellent opportunity to improve our knowledge about this type of pollution. Their size and cost, which support multi-node network deployment, along with their temporal resolution, enable them to report fine spatio-temporal resolution for a given area. These sensors have known issues across performance metrics. Generally, the literature focuses on the PM mass concentration reported by these sensors, but some models of sensors also report Particle Number Concentrations (PNCs) segregated into different PM size ranges. In this study, eight units each of Alphasense OPC-R1, Plantower PMS5003 and Sensirion SPS30 have been exposed, under controlled conditions, to short-lived peaks of PM generated using two different combustion sources of PM, exposing the sensors’ to different particle size distributions to quantify and better understand the low-cost sensors performance across a range of relevant environmental ranges. The PNCs reported by the sensors were analysed to characterise sensor-reported particle size distribution, to determine whether sensor-reported PNCs can follow the transient variations of PM observed by the reference instruments and to determine the relative impact of different variables on the performances of the sensors. This study shows that the Alphasense OPC-R1 reported at least five size ranges independently from each other, that the Sensirion SPS30 reported two size ranges independently from each other and that all the size ranges reported by the Plantower PMS5003 were not independent of each other. It demonstrates that all sensors tested here could track the fine temporal variation of PNCs, that the Alphasense OPC-R1 could closely follow the variations of size distribution between the two sources of PM, and it shows that particle size distribution and composition are more impactful on sensor measurements than relative humidity.

Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long-term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group-based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person-years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person-years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00-1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08-2.09) for ≥60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87-1.00) was also observed. HRs of 1.48 (95% CI: 1.10-1.99) for noncardia and 0.51 (95% CI: 0.26-1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (Phomogeneity = .02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences.

Background: Neisseria gonorrhoeae, the bacterium that causes gonococcal disease, is primarily a sexually transmitted infection. The best available data indicate both increasing gonococcal disease rates, and antimicrobial resistance. Whilst the increases in rates and resistances appear unrelated, the key concerns from a global health perspective are a lack of understanding of the mechanisms that drive the emergence and establishment of resistance in populations. Over time, it has become apparent that travel associated resistant gonococcal infections support the idea that potential reservoirs of resistant strains particularly in South East Asia. The recent emergence of multi and extensively drug resistant infections associated with travel in this region have escalated concerns. In the absence of a vaccine, disease control relies upon primary prevention strategies, effective treatment for patients and their partners as well as an understandings of disease dynamics. Antimicrobial resistance in Neisseria gonorrhoeae threatens effective treatment strategies with current empiric therapy with ceftriaxone currently compromised and no available next antibiotic option. Recent advancements in genomic technologies with higher discriminatory capabilities, combined with clinical and epidemiological data, have enabled deeper investigations into the emergence, evolution and spread of antimicrobial resistant strains at the: local, national and international level.In this study the complete archive of Neisseria gonorrhoeae isolates from 10 year period 1991-1999, when ciprofloxacin resistance emerged and became established in New South Wales, Australia, were subjected to genomic analysis to understand the factors and drivers of establishment of resistance in this population.Methods: The index, and all subsequent clinical isolates (n=325) were genotyped using a previously described method. Region of acquisition data, where available, were used to determine whether cases were travel asso

Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long-term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group-based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person-years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person-years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00-1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08-2.09) for >= 60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87-1.00) was also observed. HRs of 1.48 (95% CI: 1.10-1.99) for noncardia and 0.51 (95% CI: 0.26-1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (P-homogeneity = .02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences.

Globally, gastric cancer (GC) is the fifth most common malignancy. As a multifactorial disease, Helicobacter pylori infection and host genetics are crucial for GC development. Autophagy, the protective mechanism that is triggered upon pathogen invasion, is regulated by the Human Immunity-related GTPase M (IRGM) protein. The current study aimed to determine the association between IRGM polymorphisms and the risk of GC in three ethnically diverse populations through a case-control study, and to determine the functional relevance of IRGM rs4958847 by in vitro studies.The case-control study cohort comprised 1246 subjects from high-risk ethnic Chinese (N=304) and Colombian (N=587) populations, and one low-risk Australian population (N=304). IRGM polymorphisms (rs4958847 and rs13361189) were genotyped by MADLI-TOF mass spectrometry. Using CRISPR/Cas9, a knock-in (IRGM rs4958847) gastric epithelial cell line (AGS) was generated. Infection assays were conducted, and gene and protein expression levels of pro-inflammatory cytokine (IL8) and important autophagic regulators (IRGM, MAP1LC3B and SQSTM1) were analysed. Our analyses suggest that the IRGM rs4958847 A allele increased GC risk in Chinese (A>G, OR:0.28, p-value:0.01) and Colombians (G>A, OR:2.63, p-value:0.15) but decreased the risk in Australians (G>A, OR:0.17, p-value:0.09). The IRGM rs13361189 C allele appeared to increase GC risk in both ethnic Chinese (OR:1.37, p-value:0.08) and Colombian (OR:1.51, p-value:0.08) populations. A synergistic relationship was established between the selected polymorphisms and infection with H. pylori in ethnic Chinese and Australians. The presence of IRGM rs4958847 and rs13361189 in H. pylori-infected individuals increased GC risk by 2.5-fold, and 16-fold, respectively. Upon infection, expression levels of IL8 were downregulated in edited cells (GG) as compared with wild-type cells (AG) (Fold change:0.42, p-value:0.10); a result corroborated at the protein level (p-value:<0.01). Impor