The relationship between population growth and precipitation change in some regions across Vietnam: implications for urbanization effect.

According to a review of numerous publications and scientific reports, the effects of urbanization on urban climate are of greatest concern. This study aims to evaluate the impact of urbanization focusing on population growth on precipitation trends in 11 provinces across Vietnam during the period 2008-2018 by identifying the relationship between population growth and precipitation change. Regression analysis is used to determine the trends of precipitation and population growth. Precipitation maps and graphs show the overall precipitation trends, changes, and patterns in past decades. Overall, population growth tends to correlate with precipitation change trends. Furthermore, the type of region groups (countryside region, small city, or medium city) also plays a crucial role in determining the magnitude of the change in precipitation trends for each region. This further lends credibility to the notion that urbanization contributes to changes in precipitation trends.

The stalk domain and the glycosylation status of the activating natural killer cell receptor NKp30 are important for ligand binding.

The natural cytotoxicity receptors are a unique set of activating proteins expressed mainly on the surface of natural killer (NK) cells. The human natural cytotoxicity receptor family comprises the three type I membrane proteins NKp30, NKp44, and NKp46. Especially NKp30 is critical for the cytotoxicity of NK cells against different targets including tumor, virus-infected, and immature dendritic cells. Although the crystal structure of NKp30 was recently solved (Li, Y., Wang, Q., and Mariuzza, R. A. (2011) J. Exp. Med. 208, 703-714; Joyce, M. G., Tran, P., Zhuravleva, M. A., Jaw, J., Colonna, M., and Sun, P. D. (2011) Proc. Natl. Acad. Sci. U.S.A. 108, 6223-6228), a key question, how NKp30 recognizes several non-related ligands, remains unclear. Therefore, we investigated the parameters that impact ligand recognition of NKp30. Based on various NKp30-hIgG1-Fc fusion proteins, which were optimized for minimal background binding to cellular Fcγ receptors, we identified the flexible stalk region of NKp30 as an important but so far neglected module for ligand recognition and related signaling of the corresponding full-length receptor proteins. Moreover, we found that the ectodomain of NKp30 is N-linked glycosylated at three different sites. Mutational analyses revealed differential binding affinities and signaling capacities of mono-, di-, or triglycosylated NKp30, suggesting that the degree of glycosylation could provide a switch to modulate the ligand binding properties of NKp30 and NK cell cytotoxicity.

Catalysis leads to posttranslational inactivation of the type 1 deiodinase and alters its conformation.

Previously, it was shown that the type 1 deiodinase (D1) is subject to substrate-dependent inactivation that is blocked by pretreatment with the inhibitor of D1 catalysis, propylthiouracil (PTU). Using HepG2 cells with endogenous D1 activity, we found that while considerable D1-mediated catalysis of reverse tri-iodothyronine (rT(3)) is observed in intact cells, there was a significant loss of D1 activity in sonicates assayed from the same cells in parallel. This rT(3)-mediated loss of D1 activity occurs despite no change in D1 mRNA levels and is blocked by PTU treatment, suggesting a requirement for catalysis. Endogenous D1 activity in sonicates was inactivated in a dose-dependent manner in HepG2 cells, with a ∼50% decrease after 10 nM rT(3) treatment. Inactivation of D1 was rapid, occurring after only half an hour of rT(3) treatment. D1 expressed in HEK293 cells was inactivated by rT(3) in a similar manner. (75)Se labeling of the D1 selenoprotein indicated that after 4 h rT(3)-mediated inactivation of D1 occurs without a corresponding decrease in D1 protein levels, though rT(3) treatment causes a loss of D1 protein after 8-24 h. Bioluminescence resonance energy transfer studies indicate that rT(3) exposure increases energy transfer between the D1 homodimer subunits, and this was lost when the active site of D1 was mutated to alanine, suggesting that a post-catalytic structural change in the D1 homodimer could cause enzyme inactivation. Thus, both D1 and type 2 deiodinase are subject to catalysis-induced loss of activity although their inactivation occurs via very different mechanisms.

Dexamethasone effects on group B streptococcal infection in newborn rats.

BACKGROUND: We previously published that human neutrophil-mediated bacterial killing of group B Streptococcus (GBS) in vitro was dependent on the timing and concentration of dexamethasone exposure. HYPOTHESIS: Dexamethasone treatment would affect neutrophil mediated killing of GBS in an animal model. METHODS: Wistar rat pups were randomly allocated to receive placebo or dexamethasone before, early or late after GBS infection. Suckling rats were infected with 104 or 105 colony-forming units of GBS or nothing. Pups were followed for survival, quantitative bacteremia, growth and neutrophil-mediated bacterial killing. Neutrophils for bacterial killing were obtained via cardiac puncture before infection. Statistics included chi square for survival, Mann-Whitney U test for bacteremia, analysis of variance for growth and paired Student's t test for bacterial killing analyses. RESULTS: Dexamethasone treatment before invasive GBS infection decreases quantitative bacteremia, improves survival and improves neonatal neutrophil-mediated bacterial killing in suckling rats, whereas dexamethasone treatment after infection increases bacteremia and decreases survival. Regardless of timing of dexamethasone treatment, before or after invasive GBS infection, growth was significantly impaired in all suckling rats receiving dexamethasone compared with controls. CONCLUSION: Treatment with dexamethasone before invasive GBS infection improves survival and decreases bacteremia in suckling rats; this appears in part to be mediated by improved neonatal neutrophil-mediated bacterial killing. We speculate that this improvement in outcome may be a result of improved number or function of neutrophil cell surface receptors.