Macrophages are a subset of mononuclear phagocytes of the innate immune system with high plasticity and heterogeneity. At the maternal–fetal interface, macrophages are present in all stages of pregnancy and involved in a variety of activities, including regulation of immune cell activities, decidualization, placental cell invasion, angiogenesis, parturition, and postpartum uterine involution. The activation state and function of uterine–placental macrophages are largely dependent on the local tissue microenvironment. However, disruption of the uterine microenvironment can have profound effects on macrophage activity and subsequently impact pregnancy outcome. Thus, appropriately and timely regulated macrophage polarization has been considered a key determinant of successful pregnancy. Targeting macrophage polarization might be an efficient strategy for maintaining maternal–fetal immune homeostasis and a normal pregnancy. Here, we will review the latest findings regarding the modulators regulating macrophage polarization in healthy pregnancies and pregnancy complications, which might provide a basis for macrophage-centered therapeutic strategies.

Postsynaptic density protein-95 (PSD-95) localizes AMPA-type glutamate receptors (AMPARs) to postsynaptic sites of glutamatergic synapses. Its postsynaptic displacement is necessary for loss of AMPARs during homeostatic scaling down of synapses. Here, we demonstrate that upon Ca influx, Ca/calmodulin (Ca/CaM) binding to the N-terminus of PSD-95 mediates postsynaptic loss of PSD-95 and AMPARs during homeostatic scaling down. Our NMR structural analysis identified E17 within the PSD-95 N-terminus as important for binding to Ca/CaM by interacting with R126 on CaM. Mutating E17 to R prevented homeostatic scaling down in primary hippocampal neurons, which is rescued via charge inversion by ectopic expression of CaM, as determined by analysis of miniature excitatory postsynaptic currents. Accordingly, increased binding of Ca/CaM to PSD-95 induced by a chronic increase in Ca influx is a critical molecular event in homeostatic downscaling of glutamatergic synaptic transmission.

Pseudomonas aeruginosa is an opportunistic bacterial pathogen and a primary cause of nosocomial infection in humans. The rate of antibiotic resistance in P. aeruginosa is increasing worldwide leading to an unmet need for discovery of new chemical compounds distinctly different from present antimicrobials. Protein synthesis is an essential metabolic process and a validated target for the development of new antibiotics. Initiation factor 1 from P. aeruginosa (Pa-IF1) is the smallest of the three initiation factors that act to establish the 30S initiation complex during initiation of protein biosynthesis. Here we report the characterization and solution NMR structure of Pa-IF1. Pa-IF1 consists of a five-stranded b-sheet with an unusual extended b-strand at the C-terminus and one short a-helix arranged in the sequential order b1-b2-b3-a1-b4-b5. The structure adopts a typical b-barrel fold and contains an oligomer-binding motif. A cluster of basic residues (K39, R41, K42, K64, R66, R70, and R72) located on the surface of strands b4 and b5 near the short a-helix may compose the binding interface with the 30S subunit.

Summary Short sleep duration has been found recently to be a predictor of proteinuria. However, population‐based investigations addressing the association between self‐reported sleep duration and glomerular filtration rate (GFR) among hypertensive patients are lacking. We therefore sought to investigate the extent to which self‐reported sleep duration might be associated with reduced GFR in a large hypertensive population in rural northeast China. A total of 5555 hypertensive participants, aged ≥35 years, in rural areas of Liaoning Province, China, were screened between January 2012 and August 2013, using a stratified, cluster multi‐stage sampling scheme. Anthropometric measurements, self‐reported sleep duration, blood biochemical indexes and other health‐related variables were collected by medically trained personnel. Reduced GFR was defined as the estimated GFR (eGFR) < 60 mL min−1 1.73 m2. On average, participants slept for 6.9 ± 1.6 h per night. Mean self‐reported sleep duration decreased with eGFR (P < 0.001). For both genders, a lower prevalence of reduced GFR was observed among participants who slept ≤6 h per night in total. In the multivariable regression model, after adjustments for age, gender, ethnicity, lifestyle factors, clinical correlates, depressive symptoms and general quality of life, participants who slept for 6 h or less per night were associated with a higher risk of reduced GFR [odds ratio (OR: 1.70, 95% confidence interval (CI): 1.05–2.73] compared with the reference group (self‐reported sleep duration >7 and ≤8 h day−1). We concluded that short self‐reported sleep duration (≤6 h per night) was related significantly to an increased risk of reduced GFR in a hypertensive population. This novel risk factor should be taken into consideration during daily management of hypertension to prevent chronic kidney disease.

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