Aspiration Pneumonia Caused by Prevotella Causing Prothorax after Pulmonary Puncture: a Case Report.

BACKGROUND: Aspiration pneumonia in patients in immunocompetent populations is rare, and secondary pyothorax due to puncture operations during treatment has been reported rarely. METHODS: We report a confirmed case of aspiration pneumonia caused by Prevotella. The pathogen was detected and confirmed using percutaneous lung puncture and high-throughput next-generation sequencing (NGS). RESULTS: The patient developed secondary pyothorax, severe rash, and exacerbation of symptoms following the lung puncture. Finally, after adjusting the antibiotic regimen and performing chest drainage and washout, the patient's lesions were absorbed, symptoms improved, and the rash disappeared. CONCLUSIONS: Prevotella aspiration pneumonia can occur in immunocompetent individuals, and invasive bronchoscopic alveolar lavage may be considered as an option to reduce the risk of infectious organism translocation.

let-7b-5p suppresses the proliferation and migration of pulmonary artery smooth muscle cells via down-regulating IGF1.

OBJECTIVES: Some previous studies indicated that the excessive proliferation and migration of Pulmonary Artery Smooth Muscle Cells (PASMCs) could be observed in pulmonary artery intima after Pulmonary Embolism (PE) occurred. In addition, recent studies identified some miRNAs that are differentially expressed in the blood of PE patients, which might be used as a diagnostic biomarker for PE, including let-7a-5p, let-7b-5p, and miR-150-5p. Hence, the authors sought to explore the effects of let-7b-5p in PASMC proliferation and migration and the corresponding regulatory mechanism. METHODS: Platelet-Derived Growth Factor (PDGF) was utilized to induce the hyper-proliferation model in PASMCs. The mRNA and protein expression levels were detected by RT-qPCR and western blot, respectively. The proliferation of PASMCs was evaluated by the detection of PCNA expression, as well as CCK-8 and Edu assays. Wound healing and Transwell assays were exploited to assess the migration ability of PASMCs. The targets of let-7b-5p were predicted based on two bioinformatics online tools. Dual-luciferase and Ago2 pull-down assays were applied to confirm the interaction between let-7b-5p and IGF1. RESULTS: 40 ng/mL PDGF was selected as the optimal concentration to induce PASMCs. let-7b-5p mimics suppressed the proliferation and migration of PDGF-induced PASMCs, while let-7b-5p inhibitor led to the opposite result. In further mechanism exploration, IGF1 was predicted and confirmed as the direct target gene of let-7b-5p. The promotion role of IGF1 overexpression on the proliferation and migration of PDGF-induced PASMCs was dramatically countered by let-7b-5p mimics. CONCLUSION: let-7b-5p prohibits the proliferation and migration of PDGF-induced PASMCs by modulating IGF1.

let-7b-5p suppresses the proliferation and migration of pulmonary artery smooth muscle cells via down-regulating IGF1

Abstract Objectives Some previous studies indicated that the excessive proliferation and migration of Pulmonary Artery Smooth Muscle Cells (PASMCs) could be observed in pulmonary artery intima after Pulmonary Embolism (PE) occurred. In addition, recent studies identified some miRNAs that are differentially expressed in the blood of PE patients, which might be used as a diagnostic biomarker for PE, including let-7a-5p, let-7b-5p, and miR-150-5p. Hence, the authors sought to explore the effects of let-7b-5p in PASMC proliferation and migration and the corresponding regulatory mechanism. Methods Platelet-Derived Growth Factor (PDGF) was utilized to induce the hyper-proliferation model in PASMCs. The mRNA and protein expression levels were detected by RT-qPCR and western blot, respectively. The proliferation of PASMCs was evaluated by the detection of PCNA expression, as well as CCK-8 and Edu assays. Wound healing and Transwell assays were exploited to assess the migration ability of PASMCs. The targets of let-7b-5p were predicted based on two bioinformatics online tools. Dual-luciferase and Ago2 pull-down assays were applied to confirm the interaction between let-7b-5p and IGF1. Results 40 ng/mL PDGF was selected as the optimal concentration to induce PASMCs. let-7b-5p mimics suppressed the proliferation and migration of PDGF-induced PASMCs, while let-7b-5p inhibitor led to the opposite result. In further mechanism exploration, IGF1 was predicted and confirmed as the direct target gene of let-7b-5p. The promotion role of IGF1 overexpression on the proliferation and migration of PDGF-induced PASMCs was dramatically countered by let-7b-5p mimics. Conclusion let-7b-5p prohibits the proliferation and migration of PDGF-induced PASMCs by modulating IGF1.

An Updated Understanding of the Current Emerging Respiratory Infection: COVID-19.

According to the World Health Organization (WHO), the COVID-19 pandemic has been declared as a priority disease. Some patients with COVID-19 had symptoms of multiple organ failure and death. The published articles on COVID-19 infection were reviewed. The origin of SARS-CoV-2 is still not completely established. Person-to-person transmission via droplets, probable aerosols, or close contact is considered as the main mode of transmission. With increased mortality due to SARS-CoV-2, valuable clinical indicators or treatments should be further identified and summarized. CT scanning plays an important role in the diagnosis and evaluation of COVID-19 in asymptomatic patients or those with initially negative RT-PCR results. No specific antiviral therapy is recommended, except the main supportive treatments, and effective measures should be taken into consideration to protect important organs and prevent the development of acute respiratory distress syndrome (ARDS) in patients with severe infection.

Antiplatelet Therapy for Critically Ill Patients: A Pairwise and Bayesian Network Meta-Analysis.

Antiplatelet therapy is an attractive treatment option for critically ill patients. However, more evidence on the benefit of this therapy is required. We searched the PubMed and Embase databases from their inception to June 2017 for randomized controlled trials and observational studies that assess the effect of antiplatelet therapy in critically ill patients. Antiplatelet therapy resulted in significant decreases in hospital mortality (risk ratio [RR] 0.81, 95% confidence interval [CI], 0.68-0.97; P = 0. 025), intensive care unit (ICU) mortality (RR 0.78, 95% CI, 0.63-0.97; P = 0. 027), incidence of respiratory distress syndrome or acute lung injury (RR 0.73, 95% CI, 0.58-0.91; P = 0.006), and incidence of sepsis (RR 0.81, 95% CI, 0.68-0.97; P = 0.021). A predefined subgroup analysis according to patient type suggested that hospital mortality and ICU mortality benefits were seen only in septic patients (RR 0.71, 95% CI, 0.58-0.86; P < 0.0001) and (RR 0.65, 95% CI, 0.49-0.86; P = 0.002). By network meta-analysis, the predictive interval plot showed that patients treated with aspirin and clopidogrel had lower risk of hospital mortality as compared with control group. The assessment of rank probabilities using SUCRA plots indicated that aspirin presented the greatest likelihood of having lowest hospital mortality rate. The results of this meta-analysis suggest that antiplatelet therapy is useful for the treatment in critically ill patients, and this is primarily due to an effect on septic patients. Network meta-analysis shows that the probability of being the best antiplatelet therapy for critically ill patients was aspirin.

MnSOD Val16Ala polymorphism and prostate cancer susceptibility: a meta-analysis involving 8,962 subjects.

PURPOSE: Published data on the association between manganese superoxide dismutase (MnSOD) Val(16)Ala polymorphism and prostate cancer (PCA) risk are inconclusive. To derive a more precise estimate of the association between them, a meta-analysis was performed. METHODS: PubMed and Embase were searched. All eligible studies were retrieved. The pooled odds ratio (OR) with 95% confidence interval (CI) for PCA risk associated with Val/Ala versus Val/Val, Ala/Ala versus Val/Val, dominant model (Ala/Ala + Val/Ala vs. Val/Val), and recessive model (Ala/Ala vs. Val/Ala + Val/Val) were estimated, respectively. RESULTS: A total of 12 studies including 8,962 subjects were involved in this meta-analysis. Overall, the meta-analysis indicated that significantly elevated cancer risk was associated with Ala variant genotype when all the eligible studies were pooled into the meta-analysis (for Val/Ala vs. Val/Val: OR = 1.11, 95% CI = 1.00-1.24; for Ala/Ala vs. Val/Val: OR = 1.22, 95% CI = 1.00-1.49; for dominant model: OR = 1.14, 95% CI = 1.03-1.26). In the subgroup analysis by ethnicity, statistically significant increased risks were found among Caucasians with Ala allele (for Val/Ala vs. Val/Val: OR = 1.12, 95% CI = 1.00-1.25; for dominant model: OR = 1.14, 95% CI = 1.02-1.26). However, no significant associations were found in Africans. CONCLUSIONS: This meta-analysis suggests that the Ala allele of the MnSOD gene was a low-penetrance susceptible gene in PCA development, especially in Caucasians.

KRAS mutations and resistance to EGFR-TKIs treatment in patients with non-small cell lung cancer: a meta-analysis of 22 studies.

Epidemiologic studies have evaluated the association between KRAS mutations and resistance to the treatment of epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs) in patients with non-small cell lung cancer (NSCLC). However, results were inconclusive. To derive a more precise estimation of the relationship, we performed this meta-analysis. Systematic computerized searches of the PubMed and Medline databases (up to Jun 30, 2009) were performed. A total of 22 studies were included in the final meta-analysis, consisting of 1470 NSCLC patients, of whom 231 had KRAS mutations (16%). Current or former smokers had a higher frequency of KRAS mutations than never smokers (25% versus 6%; OR=4.36; P<0.01). Mutations were more common among adenocarcinoma than other histologies (26% versus 16%; OR=1.98; P<0.01). The objective response rate (ORR) of NSCLC patients with mutant KRAS was 3% (6/210), whereas the ORR of NSCLC patients with wild-type KRAS was 26% (287/1125). The overall pooled RR for ORR was 0.29 (95% CI: 0.18-0.47; P<0.01). Subgroup analyses were conducted on the basis of ethnicity and study treatment, all the results were not materially altered and did not draw different conclusions, indicating that our results were robust. In summary, this meta-analysis suggests that KRAS mutations may represent negative predictive biomarkers for tumor response in NSCLC patients treated with EGFR-TKIs. However, due to a mutually exclusive relationship between KRAS and EGFR mutation and no difference in survival between KRAS mutant/EGFR wild-type and KRAS wild-type/EGFR wild-type NSCLC, the clinical usefulness of KRAS mutation as a selection marker for EGFR-TKIs sensitivity in NSCLC is limited.