Spatial analytical methods for deriving a historical map of physiological equivalent temperature of Hong Kong

Lai P-C, Choi CCY, Wong PPY, et al. Spatial analytical methods for deriving a historical map of physiological equivalent temperature of Hong Kong. Building and Environment. 2015;99:22-28

Macrophages exert homeostatic actions in pregnancy to protect against preterm birth and fetal inflammatory injury

Macrophages are commonly thought to contribute to the pathophysiology of preterm labor by amplifying inflammation — but a protective role has not previously been considered to our knowledge. We hypothesized that given their antiinflammatory capability in early pregnancy, macrophages exert essential roles in maintenance of late gestation and that insufficient macrophages may predispose individuals to spontaneous preterm labor and adverse neonatal outcomes. Here, we showed that women with spontaneous preterm birth had reduced CD209⁺CD206⁺ expression in alternatively activated CD45⁺CD14⁺ICAM3⁻ macrophages and increased TNF expression in proinflammatory CD45⁺CD14⁺CD80⁺HLA-DR⁺ macrophages in the uterine decidua at the materno-fetal interface. In Cd11b(DTR/DTR) mice, depletion of maternal CD11b⁺ myeloid cells caused preterm birth, neonatal death, and postnatal growth impairment, accompanied by uterine cytokine and leukocyte changes indicative of a proinflammatory response, while adoptive transfer of WT macrophages prevented preterm birth and partially rescued neonatal loss. In a model of intra-amniotic inflammation–induced preterm birth, macrophages polarized in vitro to an M2 phenotype showed superior capacity over nonpolarized macrophages to reduce uterine and fetal inflammation, prevent preterm birth, and improve neonatal survival. We conclude that macrophages exert a critical homeostatic regulatory role in late gestation and are implicated as a determinant of susceptibility to spontaneous preterm birth and fetal inflammatory injury.Nardhy Gomez-Lopez, Valeria Garcia-Flores, Peck Yin Chin, Holly M. Groome, Melanie T. Bijland, Kerrilyn R. Diener, Roberto Romero, and Sarah A. Robertso

Regulatory T cells are paramount effectors in progesterone regulation of embryo implantation and fetal growth

Published: June 8, 2023Progesterone (P4) is essential for embryo implantation, but the extent to which the pro-gestational effects of P4 depend on the maternal immune compartment is unknown. Here, we investigate whether regulatory T cells (Treg cells) act to mediate luteal phase P4 effects on uterine receptivity in mice. P4 antagonist RU486 administered to mice on days 0.5 and 2.5 post coitum (dpc) to model luteal phase P4 deficiency caused fewer CD4+Foxp3+ Treg cells and impaired Treg functional competence, along with dysfunctional uterine vascular remodeling and perturbed placental development in mid-gestation. These effects were linked with fetal loss and fetal growth restriction, accompanied by a Th1/CD8-skewed T cell profile. Adoptive transfer at implantation of Treg cells - but not T conventional (Tconv) cells - alleviated fetal loss and fetal growth restriction by mitigating adverse effects of reduced P4 signaling on uterine blood vessel remodeling and placental structure, and restoring maternal T cell imbalance. These findings demonstrate an essential role for Treg cells in mediating P4 effects at implantation, and indicate that Treg cells are a sensitive and critical effector mechanism through which P4 drives uterine receptivity to support robust placental development and fetal growth.Ella S. Green, Lachlan M. Moldenhauer, Holly M. Groome, David J. Sharkey, Peck Y. Chin, Alison S. Care, Rebecca L. Robker, Shaun R. McColl, and Sarah A., Robertso

CoOOH nanosheets on cobalt substrate as a non-enzymatic glucose sensor

10.1016/j.elecom.2012.04.012Electrochemistry Communications201128-132ECCM

CoOOH nanosheet electrodes: Simple fabrication for sensitive electrochemical sensing of hydrogen peroxide and hydrazine

10.1016/j.bios.2012.07.061Biosensors and Bioelectronics391255-260BBIO

Co/Al layered double hydroxides nanostructures: A binderless electrode for electrochemical capacitor

10.1016/j.elecom.2014.03.001Electrochemistry Communications439-12ECCM

Insight into the strong inhibitory action of salt on activity of neocarzinostatin

Enediyne anticancer drugs belong to one of the most potent category in inducing DNA damage. We report 85 +/- 5% inhibition on activity of neocarzinostatin by salt. As high sodium ion concentration is a known tumor cell feature, we explored the dynamic mechanism of inhibition. Using various analytical tools, we examined parameters involved in the four consecutive steps of the drug action, namely, drug releasing from carrier protein, drug-DNA binding, drug activating, and DNA damaging. Neither protein stability, nor drug release rate, was altered by salt. The salt inhibition level was similar in between the protein-bound and unbound enediyne chromophore. Salt did not quench the thiol-induced drug activation. The inhibition was independent of DNA lesion types and irrelevant with thiol structures. Collectively, no salt interaction was found in the releasing, activating, and DNA damaging step of the drug action. However, binding with DNA decreased linearly with salt and corresponded well with the salt-induced inhibition on the drug activity. Salt interference on the affinity of DNA binding was the main and sole cause of the severe salt inhibition. The inhibition factor should be carefully considered for all agents with similar DNA binding mode. (C) 2010 Elsevier Ltd. All rights reserved

Toll-like receptor-4 antagonist (+)-naloxone confers sexually dimorphic protection from inflammation-induced fetal programming in mice

Inflammation elicited by infection or non-infectious insults during gestation induces pro-inflammatory cytokines that can shift the trajectory of development to alter offspring phenotype, promote adiposity and increase susceptibility to metabolic disease in later life. Here we utilize mice to investigate the utility of a small molecule TLR4 antagonist (+)-naloxone, the non-opioid isomer of the opioid receptor antagonist (-)-naloxone, for mitigating altered fetal metabolic programming induced by a modest systemic inflammatory challenge in late gestation. In adult progeny exposed to LPS challenge in utero, male but not female offspring exhibited elevated adipose tissue, reduced muscle mass and elevated plasma leptin at 20 weeks of age. Effects were largely reversed by co-administration of (+)-naloxone following LPS. When given alone without LPS, (+)-naloxone elicited accelerated post-weaning growth and elevated muscle and fat mass in adult male but not female offspring. LPS induced expression of inflammatory cytokines Il1a, Il1b, Il6, Tnf and Il10 in fetal brain, placental and uterine tissues, and (+)-naloxone suppressed LPS-induced cytokine expression. Fetal sex-specific regulation of cytokine expression was evident, with higher Il1a, Il1b, Il6 and Il10 induced by LPS in tissues associated with male fetuses, and greater suppression by (+)-naloxone of Il6 in females. These data demonstrate that modulating TLR4 signaling with (+)-naloxone provides protection from inflammatory diversion of fetal developmental programming in utero, associated with attenuation of gestational tissue cytokine expression in a fetal sex-specific manner. The results suggest that pharmacologic interventions targeting TLR4 warrant evaluation for attenuating developmental programming effects of fetal exposure to maternal inflammatory mediators.Peck Yin Chin, Camilla Dorian, David J. Sharkey, Mark R. Hutchinson, Kenner C. Rice, Lachlan M. Moldenhauer, and Sarah A. Robertso