Understanding changes in pathogen and pneumonia prevalence among pediatric pneumonia patients is important for the prevention of infectious diseases. We retrospectively analyzed data of children younger than 18 years diagnosed with pneumonia at 117 Emergency Departments in Korea between 2007 and 2014. Over the study period, 329,380 pediatric cases of pneumonia were identified. The most frequent age group was 1-3 years old (48.6%) and the next was less than 12 months of age (17.4%). Based on International Classification of Diseases, 10th revision diagnostic codes, confirmed cases of viral pneumonia comprised 8.4% of all cases, pneumonia due to Mycoplasma pneumoniae comprised 3.8% and confirmed cases of bacterial pneumonia 1.3%. The prevalence of confirmed bacterial pneumonia decreased from 3.07% in 2007 and 4.01% in 2008 to 0.65% in 2014. The yearly rate of pneumococcal pneumonia also decreased from 0.47% in 2007 to 0.08% in 2014. A periodic prevalence of M. pneumoniae pneumonia (MP) was identified. The increased number of patients with pneumonia, bacterial pneumonia, pleural effusion, and empyema in 2011 and 2013-2014 resulted from an MP epidemic. We provide evidence that the frequency of confirmed cases of bacterial pneumonia and pneumococcal pneumonia has declined from 2007 to 2014, which can simultaneously reflect the effectiveness of the pneumococcal conjugate vaccine.
Cyclosporine A (CsA) is effective in treating moderate-to-severe atopic dermatitis (AD). This systematic review and meta-analysis aimed to summarize the effectiveness and safety of low-dose (<4 mg/kg) versus high-dose (≥4 mg/kg) CsA and other systemic immunomodulatory agents in patients with AD. Five randomized controlled trials met the inclusion criteria. The meta-analysis included 159 patients with moderate-to-severe AD who were randomized to receive low-dose CsA, and 165 patients randomized to receive high-dose CsA and other systemic immunomodulatory agents. We found that low-dose CsA was not inferior to high-dose CsA and other systemic immunomodulatory agents in reducing AD symptoms [standard mean difference (SMD) −1.62, 95% confidence interval (CI) −6.47; 3.23]. High-dose CsA and other systemic immunomodulatory agents showed a significantly lower incidence of adverse events [incidence rate ratio (IRR) 0.72, 95% CI 0.56; 0.93], however, after sensitivity analysis, there was no difference between the two groups except for one study (IRR 0.76, 95% CI 0.54; 1.07). Regarding serious adverse events requiring discontinuation of treatment, we observed no significant differences between low-dose CsA and other systemic immunomodulatory agents (IRR 1.83, 95% CI 0.62; 5.41). Our study may justify the use of low-dose CsA rather than high-dose CsA and other systemic immunomodulatory agents in moderate-to-severe AD.
RT is commonly used to treat malignant tumors. However, tumor regrowth is a major limitation to RT as an antitumor treatment. In the present study, we investigated the tumor-promoting effects of high-dose (or ablative) RT treatments on tumor-bearing mice. We focused on the role of macrophages that interact with IR-CCs in the TME, which cause tumor regrowth. We observed that CT26(H-2d) tumor growth was enhanced by i.v. injection of IR-CT26 cells compared with NR control CT26 cells. The levels of iNOS gene expression and NO production from RAW264.7 macrophages (H-2d) in response to the interaction with IR-CT26 cells were higher than with NR-CT26 cells. When CT26 tumor-bearing mice were treated i.v. with L-NMMA, a NOS inhibitor, the reduction in in vivo tumor growth was higher in the IR-CT26-injected group compared with the NR-CT26-injected control group. In vivo CT26 tumor growth was decreased after transplanting PEM extracted from L-NMMA-treated, tumor-bearing mice. Although iNOS activity was reduced by inhibiting TLR1 expression with TLR1-siRNA, it was enhanced by TLR1 overexpression. Transcriptional activation and protein expression levels of iNOS were also decreased in the presence of TLR1-siRNA but increased as a result of TLR1 overexpression. These results demonstrate that postradiotherapeutic tumor regrowth may be caused by interaction of IR-CCs with macrophages that induce TLR1-mediated iNOS expression and NO production. Our data suggest that iNOS in macrophages could be a useful target to regulate postradiotherapeutic responses in hosts and subsequently limit tumor regrowth.
1 January 2020 in Clinical and Experimental Vaccine Research