Persistent infections caused by the superbug

and its resistance to multiple antimicrobial agents are huge threats to patients with cystic fibrosis as well as those with compromised immune systems. Multidrug-resistant

has posed a major challenge to conventional antibiotics and therapeutic approaches, which show limited efficacy and cause serious side effects. The public demand for new antibiotics is enormous; yet, drug development pipelines have started to run dry with limited targets available for inventing new antibacterial drugs. Consequently, it is important to uncover potential therapeutic targets.

The authors review the current state of drug development strategies that are promising in terms of the development of novel and potent drugs to treat

infection.

The prevention of

infection is increasingly challenging. Furthermore, targeting key virulence regulators has great potential for developing novel anti-

drugs. Additional promising strategies include bacteriophage therapy, immunotherapies, and antimicrobial peptides. Additionally, the authors believe that in the coming years, the overall network of molecular regulatory mechanism of

virulence will be fully elucidated, which will provide more novel and promising drug targets for treating

infections.

The prevention of P. aeruginosa infection is increasingly challenging. Furthermore, targeting key virulence regulators has great potential for developing novel anti-P. aeruginosa drugs. Additional promising strategies include bacteriophage therapy, immunotherapies, and antimicrobial peptides. Additionally, the authors believe that in the coming years, the overall network of molecular regulatory mechanism of P. aeruginosa virulence will be fully elucidated, which will provide more novel and promising drug targets for treating P. aeruginosa infections.

Takotsubo syndrome (TTS) and its differentiation from anterior wall ST-elevation myocardial infarction on electrocardiography (ECG) has been a debate.

Six studies comparing ECG changes in TTS and AW-STEMI were identified. The primary endpoint was reciprocal changes, presence of Q-waves, and QT-interval. An unadjusted odds ratio (OR) with a 95% confidence interval (CI) was calculated using Review Manager (RevMan) 5.3.

Six studies consisting of 1090 patients (TTS=220, AW-STEMI=870) were included. Reciprocal changes on ECG were less commonly associated with TTS than AW STEMI with OR of 0.05 and 95%CI- 0.02-0.11 (P-<0.00001). Q-wave presence on ECG was comparable between the groups with OR-0.68, 95%CI-0.08-5.63 (p-0.72). QT interval on ECG was comparable between the two groups with OR-1.09, 95%CI-0.63-1.54 (p-<0.00001). There was minimal publication bias among the studies.

AW STEMI is associated with reciprocal changes. Q-waves and QT interval has no differentiating significance between AW STEMI and TTS.

AW STEMI is associated with reciprocal changes. Q-waves and QT interval has no differentiating significance between AW STEMI and TTS.Exposure to fine particulate matter (PM2.5) is closely linked with cardiovascular diseases. However, the underlying mechanism of PM2.5 on cardiac function remains unknown. Phenylbutyrate This study was aimed to investigate the role of microRNA-205 (miR-205) on PM2.5-induced myocardial inflammation and cardiac dysfunction. PM2.5 increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), following by decreased cell viability and antioxidant enzymes, resulting in apoptosis of cardiomyocytes (AC16). The histopathological and ultrastructural analysis demonstrated that PM2.5 caused myocardial damage via interstitial edema, inflammatory cell infiltration, and myocardial fiber destruction. PM2.5 enhanced the release of inflammatory factors in AC16 cells and heart tissue. Microarray analysis and dual-luciferase reporter gene assays demonstrated that PM2.5-induced down-regulation of miR-205 regulated interleukin 1 receptor-associated kinase 2 (IRAK2), which further activated the TNF receptor-associated factor 6 (TRAF6)/nuclear transcription factor-κB (NF-κB) signaling pathway in vivo. Moreover, the chemical mimics of miR-205 markedly inhibited the IRAK2/TRAF6/NF-κB signaling pathway, whereas the chemical inhibitors of miR-205 amplified PM2.5-induced activation of the IRAK2 signaling pathway in vitro. In summary, our results found that PM2.5 could trigger myocardial toxicity via miR-205 negative regulating the IRAK2/TRAF6/NF-κB signaling pathway. Our study suggests that miR-205 could be a promising target molecule for mitigating the hazardous effects of PM2.5 on the cardiovascular system.

To assess the acute response of cardiac autonomic modulation (ACAM) during and after a session of virtual reality-based therapy (VRBT) compared to a session of conventional cardiovascular rehabilitation (CR) and to evaluate the effects of 12weeks of training on this response.

We assessed 28 volunteers (63.4±12.5years). The ACAM was judged by linear indexes of heart rate variability (HRV) in VRBT and CR sessions. Later, patients completed 12weeks of VRBT+CR and the assessment was repeated at the 12

week.

Throughout the 1

VRBT session vagal withdrawal occurred (RMSSD/HFnu); sympathetic nervous system stimulation (LFnu) and progressive decrease of global HRV (SDNN). During the recovery, the SDNN, HFnu, and LFnu improved from the 5

minute on both therapies. After 12weeks, the LFnu, HFnu, and the LF/HF-ratio revealed no significant changes in Ex3-Ex4 equated to Rep during VRBT. In recovery, the HFnu and LFnu improved before the 5

minute on both therapies.

ACAM during and after the VRBT was comparable to CR, yet, the extents were greater in the VRBT. After 12weeks of VRBT training, the subjects adapted to the exercises from the 15

minute and exhibited faster recovery of HFnu and LFnu indexes compared to the 1

week.

ACAM during and after the VRBT was comparable to CR, yet, the extents were greater in the VRBT. After 12 weeks of VRBT training, the subjects adapted to the exercises from the 15thminute and exhibited faster recovery of HFnu and LFnu indexes compared to the 1st week.