Estrogen regulation of cardiac cAMP-L-type Ca2+ channel pathway modulates sex differences in basal contraction and responses to ß2AR-mediated stress in left ventricular apical myocytes.

BACKGROUNDS/AIM: Male and female hearts have many structural and functional differences. Here, we investigated the role of estrogen (E2) in the mechanisms of sex differences in contraction through the cAMP-L-type Ca2+channel pathway in adult mice left ventricular (LV) apical myocytes at basal and stress state. METHODS: Isolated LV apical myocytes from male, female (Sham) and ovariectomised mice (OVX) were used to investigate contractility, Ca2+ transients and L-type Ca2+ channel (LTCC) function. The levels of ß2AR, intracellular cAMP, phosphodiesterase (PDE 3 and PDE 4), RyR2, PLB, SLN, and SERCA2a were compared among the experimental groups. RESULTS: We found that (1) intracellular cAMP, ICaL density, contraction and Ca2+ transient amplitudes were larger in Sham and OVX + E2 myocytes compared to male and OVX. (2) The mRNA expression of PDE 3 and 4 were lower in Sham and OVX + E2 groups compared with male and OVX groups. Treatment of myocytes with IBMX (100 µM) increased contraction and Ca2+ transient amplitude in both sexes and canceled differences between them. (3) ß2AR-mediated stress decreased cAMP concentration and peak contraction and Ca2+ transient amplitude only in male and OVX groups but not in Sham or OVX + E2 groups suggesting a cardioprotective role of E2 in female mice. (4) Pretreatment of OVX myocytes with GPR30 antagonist G15 (100 nM) abolished the effects of E2, but ERα and ERß antagonist ICI 182,780 (1 µM) did not. Moreover, activation of GPR30 with G1 (100 nM) replicated the effects of E2 on cAMP, contraction and Ca2+ transient amplitudes suggesting that the acute effects of E2 were mediated by GPR30 via non-genomic signaling. (5) mRNA expression of RyR2 was higher in myocytes from Sham than those of male while PLB and SLN were higher in male than Sham but no sex differences were observed in the mRNA of SERCA2a. CONCLUSION: Collectively, these results demonstrate that E2 modulates the expression of genes related to the cAMP-LTCC pathway and contributes to sex differences in cardiac contraction and responses to stress. We also show that estrogen confers cardioprotection against cardiac stress by non-genomic acute signaling via GPR30.

Analysis of frequent species and antibacterial resistance of pathogenic bacteria causing infections in burn patients in a hospital from 2012 to 2014 / 国际检验医学杂志

Objective To investigate the frequent species of pathogenic bacteria causing infections in burn patients and their re‐sistance to commonly used antibacterial agents ,so as to provide references for rational use of antibacterials in clinic .Methods The distribution and drug susceptibility of pathogenic bacteria isolated from secretions of wound surfaces of 140 cases of burn patients from January 2012 to December 2014 were retrospectively analyzed .Results A total of 152 strains of pathogenic bacteria were iso‐lated .The gram‐negative bacteria accounted for 59 .2% ,in which Pseudomonas aeruginosa ,Proteus mirabilis and Acinetobacter bau‐mannii were the most common isolates ;the gram‐positive bacteria accounted for 34 .2% ,in which Staphylococcus aures ,Staphylo‐coccus haemolyticus and Enterococcus faecalis were the most common isolates ;and fungi were accounted for 6 .6% .A majority of these isolates were multiple resistant to the antibacterial agents .Conclusion Culturing ,identifing and carring out drug‐sensitivity test of pathogenic bacteria isolated from burn patients could provide basis for rational application of antibacterial agents and effec‐tive control of infection .

A comment on "α-stability and α-synchronization for fractional-order neural networks".

In this paper, we point out that an inequality in the paper [J. Yu, C. Hu, H. Jiang, α-stability and α-synchronization for fractional-order neural networks, Neural Networks 35 (2012) 82-87] is not correct. The main theorems in this paper are not valid, since they are proved by this inequality.