Matrix metalloproteinase-9 (MMP-9) belongs to the MMP family and has been widely investigated. Excessive MMP-9 expression can enhance extracellular matrix degradation and promote plaque instability. Studies have demonstrated that MMP-9 levels are higher in vulnerable plaques than in stable plaques. Additionally, several human studies have demonstrated that MMP-9 may be a predictor of atherosclerotic plaque instability and a risk factor for future adverse cardiovascular and cerebrovascular events. MMP-9 deficiency or blocking MMP-9 expression can inhibit plaque inflammation and prevent atherosclerotic plaque instability. All of these results suggest that MMP-9 may be a useful predictive biomarker for vulnerable atherosclerotic plaques, as well as a therapeutic target for preventing atherosclerotic plaque instability. In this review, we describe the structure, function, and regulation of MMP-9. We also discuss the role of MMP-9 in predicting and preventing atherosclerotic plaque instability.

Neutrophil extracellular traps (NETs) are characterized as extracellular DNA fibers comprised of histone and cytoplasmic granule proteins. NETs were first described as a form of innate response against pathogen invasion, which can capture pathogens, degrade bacterial toxic factors, and kill bacteria. Additionally, NETs also provide a scaffold for protein and cell binding. Protein binding to NETs further activate the coagulation system which participates in thrombosis. In addition, NETs also can damage the tissues due to the proteins they carry. Many studies have suggested that the excessive formation of NETs may contribute to a range of diseases, including thrombosis, atherosclerosis, autoimmune diseases, and sepsis. In this review, we describe the structure and components of NETs, models of NET formation, and detection methods. We also discuss the molecular mechanism of NET formation and their disease relevance. Modulation of NET formation may provide a new route for the prevention and treatment of releated human diseases.

Purpose: The prognostic nutritional index (PNI) is a common indicator of nutritional and inflammatory status and is associated with various diseases such as cancer, cardiovascular diseases and infectious diseases. However, to date, no study has concentrated on the role of PNI in assessing and predicting the presence and severity of neonatal sepsis. Therefore, the present study aimed to explore the association of the PNI with the presence and severity of neonatal sepsis. Materials and Methods: A total of 1196 neonates with suspected sepsis were enrolled in this study and their complete clinical and laboratory data were collected. PNI was calculated as serum albumin (g/L) + 5 × total lymphocyte count (10⁹/L). Multivariate logistic regression analysis was performed to identify the risk factors for the presence and severity of neonatal sepsis. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the predictive value of PNI. All statistical analyses were performed using the statistical package SPSS 24.0. Results: PNI was lower in neonates with sepsis and decreased significantly with the severity of sepsis. The correlation analysis demonstrated that the PNI was negatively correlated with the levels of the inflammatory marker procalcitonin (PCT) and C-reactive protein (CRP), and the length of hospital stay. Multivariate logistic regression analysis revealed that the PNI was independently and inversely associated with the presence and severity of neonatal sepsis. The area under the ROC curve of the PNI was 0.64 (95% confidence interval (CI): 0.61– 0.67, P < 0.001) for severe sepsis and 0.69 (95% CI: 0.60– 0.78, P < 0.001) for septic shock. In addition, our data revealed that PNI was also independently correlated with the length of hospital stay. Conclusion: PNI is an independent predictor for the presence and severity of neonatal sepsis.

The purpose of this study is to review the molecular characteristics, the diagnosis, and treatment of the widespread infection of macrolide-resistant Mycoplasma pneumoniae (M. pneumoniae; MRMP) in children, thus providing a better knowledge of this infection and presenting the associated problems. Single point mutations in the V region of the 23S rRNA gene of M. pneumoniae genome are associated with macrolide resistance. P1–1, MLVA4-5-7-2, and ST3 are usually the predominated genetic types in the M. pneumoniae epidemics. The short-term two times serological IgM (or together with IgG) test in the acute stage can be used for confirmation. Combined serological testing and PCR might be a more prudent method to reduce macrolide consumption and antibiotic selective pressure in a clinical setting. Molecular methods for the detection of single-nucleotide mutations in the V region of the 23S rRNA gene can be used for the diagnosis of MRMP. The routine use of macrolide for the treatment of macrolide-sensitive Mycoplasma pneumoniae (MSMP) infections can get good effect, but the effects are limited for severe MRMP infections. Additional corticosteroids may be required for the treatment of severe MRMP infections in children in China during the era of MRMP.

Pneumonia is a serious and common infectious disease in children. If not treated in time, it may develop into severe pneumonia. Severe pneumonia in children is mainly characterized by hypoxia and acidosis, often accompanied by various complications such as sepsis and multiple organ dysfunction. Severe pneumonia has a rapid onset and progression, and a high mortality rate. Biomarkers assist clinicians in the early diagnosis and treatment of patients by quickly and accurately identifying their conditions and prognostic risks. In this study, common clinical and novel biomarkers of severe pneumonia in children were reviewed, and the application value of biomarkers related to the severity and prognosis of severe pneumonia in children was evaluated to provide help for early identification and precise intervention by clinicians.