Epidemiological studies have indicated increased risk for breast cancer within 10 years of childbirth. Acute inflammation during mammary involution has been suggested to promote this parity-associated breast cancer. We report here that estrogen exacerbates mammary inflammation during involution. Microarray analysis shows that estrogen induces an extensive proinflammatory gene signature in the involuting mammary tissue. This is associated with estrogen-induced neutrophil infiltration. Furthermore, estrogen induces the expression of protumoral cytokines/chemokines, COX-2 and tissue-remodeling enzymes in isolated mammary neutrophils and systemic neutrophil depletion abolished estrogen-induced expression of these genes in mammary tissue. More interestingly, neutrophil depletion diminished estrogen-induced growth of ERα-negative mammary tumor 4T1 in Balb/c mice. These findings highlight a novel aspect of estrogen action that reprograms the activity of neutrophils to create a pro-tumoral microenvironment during mammary involution. This effect on the microenvironment would conceivably aggravate its known neoplastic effect on mammary epithelial cells.

There is strong evidence that the pro-inflammatory microenvironment during post-partum mammary involution promotes parity-associated breast cancer. Estrogen exposure during mammary involution drives tumour growth through neutrophils' activity. However, how estrogen and neutrophils influence mammary involution are unknown. Combined analysis of transcriptomic, protein, and immunohistochemical data in BALB/c mice showed that estrogen promotes involution by exacerbating inflammation, cell death and adipocytes repopulation. Remarkably, 88% of estrogen-regulated genes in mammary tissue were mediated through neutrophils, which were recruited through estrogen-induced CXCR2 signalling in an autocrine fashion. While neutrophils mediate estrogen-induced inflammation and adipocytes repopulation, estrogen-induced mammary cell death was via lysosome-mediated programmed cell death through upregulation of cathepsin B, Tnf and Bid in a neutrophil-independent manner. Notably, these multifaceted effects of estrogen are mostly mediated by ERα and unique to the phase of mammary involution. These findings are important for the development of intervention strategies for parity-associated breast cancer.

In 2016, Singapore introduced the release of male Wolbachia-Aedes mosquitoes to complement vector control efforts and suppress Aedes aegypti mosquitoes in selected study sites. With ongoing expansion of Project Wolbachia–Singapore to cover larger areas, a household-based survey was conducted between July 2019 to February 2020 in two Project Wolbachia study sites using a structured questionnaire, to evaluate current sentiments and assess the need for enhanced public messaging and engagement. The association of factors that influence awareness, attitudes, and knowledge towards the use of Wolbachia-Aedes technology was analysed using Pearson’s Chi-square test and binary logistic regression. Of 500 respondents, 74.8% were aware of Project Wolbachia–Singapore. Comparatively, the level of knowledge on Wolbachia-Aedes technology was lower, suggesting knowledge gaps that require enhanced communication and messaging to address misinformation. Longer exposure to the project predicted greater awareness, whereas higher education levels predicted higher knowledge levels. Younger age groups and higher education levels were associated with high acceptance towards the project. High levels of trust and acceptance towards the project were also observed across the population. The public’s positive perception of the project is a testament to the effective public communication undertaken to date and will facilitate programme expansion.

Air traffic forecasting is important as it helps stakeholders to plan their budgets and facilities. Thus, three most commonly used forecasting models were compared to see which model suited the air passenger traffic the best. General forecasting equations were also created to forecast the passenger traffic. The equations could forecast around 6.0% growth from 2015 onwards. Another study sought to provide an initial work for determining a theoretical airspace load with relevant calculations. The air traffic was simulated to investigate the current airspace load. Logical and reasonable results were obtained from the modelling and simulations. The current utilization percentages for airspace load per hour and the static airspace load in the interested airspace were found to be 6.64% and 11.21% respectively. Our research also studied how ADS-B would affect the time taken for aircraft to travel. 6000 flights departing from and landing at the airport were studied. New flight plans were simulated with improved flight paths due to the implementation of ADS-B, and flight times of all studied flights could be improved.

21There is strong evidence that the pro-inflammatory microenvironment during post-partum 22 mammary involution promotes parity-associated breast cancer. Estrogen exposure during 23 mammary involution drives tumour growth through the activity of neutrophils. However, how 24 estrogen and neutrophils influence mammary involution are unknown. Combined analysis of 25 transcriptomic, protein, and immunohistochemical data in Balb/c mice with and without 26 neutrophil depletion showed that estrogen promotes involution by exacerbating inflammation, 27 cell death and adipocytes repopulation through neutrophil-dependent and neutrophil-28 independent mechanisms. Remarkably, 88% of estrogen-regulated genes in mammary tissue 29 were mediated through neutrophils, which were recruited through estrogen-induced CXCL2-30 CXCR2 signalling. While neutrophils mediate estrogen-induced inflammation and adipocytes 31 repopulation, estrogen-induced mammary cell death was mediated by neutrophils-independent 32 upsurges of cathepsins and their lysosomal leakages that are critical for lysosome-mediated 33 cell death. Notably, these multifaceted effects of estrogen are unique to the phase of mammary 34 involution. These findings are important for the development of intervention strategies for 35 parity-associated breast cancer. 36 37There is strong evidence that the mammary microenvironment during the post-partum 38 mammary involution promotes mammary tumour progression. High levels of tissue fibrillar 39 collagen and elevated expression of cyclooxygenase-2 (COX-2) in the mammary gland have 40 been shown to drive tumour growth and lymph angiogenesis [1,2]. Wound healing-like tissue 41 environment associated with mammary involution is also known to promote tumour 42 development and dissemination [3]. Estrogen has been shown to stimulate the growth of 43 estrogen receptor-negative mammary tumours during mammary involution and estrogen-44 stimulated neutrophil activity plays a crucial role in fostering the pro-tumoral 45 microenvironment [4]. This suggests that estrogen exposure during post-weaning mammary 46 involution is a risk factor for parity-associated breast cancer. However, the functional roles of 47 estrogen and neutrophils in mammary biology during involution have been little studied to date. 48 Post-weaning mammary involution is a process for the lactating mammary gland to 49 return to the pre-pregnancy state. The distinctive features of mammary involution include 50 massive cell death of the secretory mammary alveoli, acute inflammation, extracellular matrix 51 remodelling and adipocyte repopulation. Involution is commonly divided into two phases. In 52 mice, the first phase is the reversible phase whereby the reintroduction of the pups within 48h 53 can re-initiate lactation [5,6]. It is typified by a decrease in milk protein synthesis and increased 54 mammary cell death resulting in the appearance of shed, dying cells within the lumen of the 55 distended alveoli [7,8]. Inflammation also occurs in the first phase with the infiltrati...