Biological wastewater treatment (BWT) is currently the most widely applied approach for treating wastewater. The performance of BWT systems depends on the complex microbial communities they support. Although bacteriophages (phages), which are the viruses that infect prokaryotes, are recognized as the most abundant life entities, understanding of their ecological roles in BWT systems remains limited. Here, we review recent progress in phage-associated researches in BWT systems, including the interactions between phage and host, polyvalent phages, the influence of phage activity on BWT performance, and the potential applications of phage-based control for sludge bulking/foaming and pathogens. The challenges and perspectives of phage ecology are also outlined, which are expected to provide implications for future research and applications.Key points• Phage-host interactions in BWT systems are summarized• Impacts of phage activities on BWT performance• Potential applications of phages in BWT systems.We have constructed an Escherichia coli-based platform producing (S)-reticuline, an important intermediate of benzylisoquinoline alkaloids (BIAs), using up to 14 genes. (S)-reticuline was produced from a simple carbon source such as glucose and glycerol via L-DOPA, which is synthesized by hydroxylation of L-tyrosine, one of the rate-limiting steps of the reaction. There are three kinds of enzymes catalyzing tyrosine hydroxylation tyrosinase (TYR), tyrosine hydroxylase (TH), and 4-hydroxyphenylacetate 3-monooxygenase (HpaBC). Here, to further improve (S)-reticuline production, we chose eight from these three kinds of tyrosine hydroxylation enzymes (two TYRs, four THs, and two HpaBCs) derived from various organisms, and examined which enzyme was optimal for (S)-reticuline production in E. coli. TH from Drosophila melanogaster was the most suitable for (S)-reticuline production under the experimental conditions tested. We improved the productivity by genome integration of a gene set for L-tyrosine overproduction in E. coli. • New insights were provided on constructing an alkaloid production system with multi-step reactions in E. coli.We investigated the ability of triticale uptake of Mercury (Hg), clarified whether triticale root uptake of Hg2+ via Zinc (Zn2+) transports, using hydroponic experiments. At 25℃, when Hg exposure in solution was lower than 20 μM, Hg concentration in the roots can be better described by a hyperbolic function, which shows a saturable characteristic. Under ice-cold ( less then  2℃) conditions, a nonsaturable (linear) component was found. Low exposure of Zn2+ (0-1 μM) inhibited plant Hg uptake when Hg exposure in the solution ranged from 1 to 10 μM, it showed an antagonistic effect of Zn on plant uptake of Hg. When Hg exposure was 20 μM, it revealed a synergistic effect of Zn on plant uptake of Hg, Hg in the root increased at the Zn (1 μM) exposure in the solution. Our results will deepen the understanding of Hg transfer in the soil-plant system. Schizophrenia is associated with increased premature mortality and physical morbidity. This study aimed to examine prevalence of pre-existing chronic physical diseases, and association between physical multimorbidity burden and mortality rates among patients with newly diagnosed schizophrenia. This population-based cohort study investigated patients with first-recorded diagnosis of schizophrenia between January 2006 and December 2016, using territory-wide medical-record database of public healthcare service in Hong Kong. Physical morbidities were measured by Charlson Comorbidity Index (CCI), taking into consideration both number and severity of physical diseases, and were grouped into nine broad disease categories for analyses. Physical multimorbidity burden was stratified into three levels according to CCI of 0, 1 or ≥ 2. Cox proportional hazards regression models were used to examine associations of physical multimorbidity with mortality rates. Of the 13,945 patients, 8.6% (n = 1207) had pre-existing mature mortality compared to those without physical morbidity. Physical multimorbidity confers incremental impact on excess mortality. Early detection and intervention of physical morbidity in the initial phase of schizophrenia is necessary to reduce avoidable mortality.The liver hormone hepcidin regulates systemic iron homeostasis. Hepcidin is also expressed by the kidney, but exclusively in distal nephron segments. Several studies suggest hepcidin protects against kidney damage involving Fe2+ overload. The nephrotoxic non-essential metal ion Cd2+ can displace Fe2+ from cellular biomolecules, causing oxidative stress and cell death. The role of hepcidin in Fe2+ and Cd2+ toxicity was assessed in mouse renal cortical [mCCD(cl.1)] and inner medullary [mIMCD3] collecting duct cell lines. Cells were exposed to equipotent Cd2+ (0.5-5 μmol/l) and/or Fe2+ (50-100 μmol/l) for 4-24 h. Hepcidin (Hamp1) was transiently silenced by RNAi or overexpressed by plasmid transfection. Hepcidin or catalase expression were evaluated by RT-PCR, qPCR, immunoblotting or immunofluorescence microscopy, and cell fate by MTT, apoptosis and necrosis assays. Reactive oxygen species (ROS) were detected using CellROX™ Green and catalase activity by fluorometry. Hepcidin upregulation protected against Fe2+-induced mIMCD3 cell death by increasing catalase activity and reducing ROS, but exacerbated Cd2+-induced catalase dysfunction, increasing ROS and cell death. https://www.selleckchem.com/products/ccs-1477-cbp-in-1-.html Opposite effects were observed with Hamp1 siRNA. Similar to Hamp1 silencing, increased intracellular Fe2+ prevented Cd2+ damage, ROS formation and catalase disruption whereas chelation of intracellular Fe2+ with desferrioxamine augmented Cd2+ damage, corresponding to hepcidin upregulation. Comparable effects were observed in mCCD(cl.1) cells, indicating equivalent functions of renal hepcidin in different collecting duct segments. In conclusion, hepcidin likely binds Fe2+, but not Cd2+. Because Fe2+ and Cd2+ compete for functional binding sites in proteins, hepcidin affects their free metal ion pools and differentially impacts downstream processes and cell fate.