Acute lung injury (ALI) is a severe inflammatory lung disease with a rapid onset. The anti‑inflammatory functions of microRNA‑93 (miRNA/miR‑93) have been described in various types of tissue injury and disease. However, the biological role of miR‑93 and its molecular mechanisms underlying the initiation and progression of ALI have not yet been reported, at least to the best of our knowledge. The present study aimed to investigate the regulatory effects exerted by miR‑93 in ALI. Using an in vivo murine model of ALI induced by lipopolysaccharide (LPS), miR‑93 expression was found to be downregulated in the lung tissues and bronchoalveolar lavage fluid (BALF) compared with the control group. Following agomiR‑93 injection, it was observed that agomiR‑93 attenuated lung injury, as evidenced by decreased lung permeability, a reduced lung wet/dry weight ratio and an increased survival rate of the mice. Concomitantly, agomiR‑93 significantly reduced LPS‑induced the interleukin (IL)‑6, IL‑1β, and tumor necrosis factor (TNF)‑α levels in BALF. Of note, Toll‑like receptor 4 (TLR4), an upstream regulator of the nuclear factor (NF)‑κB signaling pathway, was directly suppressed by miR‑93 in RAW 264.7 cells. Importantly, agomiR‑93 induced a significant suppression of the TLR4/myeloid differentiation primary response 88 (MyD88)/NF‑κB signaling pathway, as demonstrated by the downregulation of MyD88, and the phosphorylation of IκB‑α and p65 in the lung tissues of mice with ALI. Taken together, the findings of the present study indicate that miR‑93 attenutes LPS‑induced lung injury by regulating the TLR4/MyD88/NF‑κB signaling pathway, suggesting that miR‑93 may prove to be a potential therapeutic target for ALI.

Premature rupture of membranes (PROM) is a common pregnancy complication that frequently results in maternal and perinatal morbidity. The present methods for diagnosing PROM do not satisfy clinical requirements. The present study aimed to examine the proteome profile of amniotic fluid (AF) and maternal plasma, screen unique proteins in AF, and evaluate their diagnostic value for diagnosing PROM. The proteome profiles of AF and maternal plasma were examined via liquid chromatography coupled with tandem mass spectrometry‑based proteomic techniques. The protein expression levels of diagnostic candidates in AF, maternal plasma and vaginal fluid were determined by ELISA analysis and Magnetic Luminex® screening assays. The diagnostic value of potential biomarkers was evaluated using receiver operating characteristic curves. A lateral flow assay was developed based on colloidal gold immunochromatography technology. The present study identified 540 unique proteins in AF, 12 of which were chosen for further detection. The present results demonstrated that expression levels of pulmonary surfactant‑associated protein B, BPI fold‑containing family A member 1, zymogen granule protein 16 homolog B, EGF‑containing fibulin‑like extracellular matrix protein 1, keratin, type II cytoskeletal 4, keratin, type I cytoskeletal 19, placental protein 14 (PP14), insulin‑like growth factor‑binding protein 2, mesothelin and serpin family B member 3 were significantly higher in AF compared with in maternal plasma (P<0.01). Furthermore, PP14 was observed to have excellent diagnostic accuracy for preterm PROM (PPROM), with a respective sensitivity and specificity of 100 and 87.5% when the cutoff value was 0.008 µg/ml. The PP14‑based lateral flow assay demonstrated a visual detection threshold of 0.008 µg/ml. The results from the present study suggested that PP14 may be a novel potential biomarker for PPROM, and may be developed into a lateral flow assay for bedside application to rapidly diagnose PPROM.

Tumor necrosis factor (TNF) is an immunomodulatory cytokine that plays an important role in many inflammatory and autoimmune diseases. We investigated the correlation between single-nucleotide polymorphisms of the TNF gene [i.e., TNF-α (−308), TNF-α (−857), TNF-α (−863), TNF-α (−1031), and TNF-β (+252)] and dilated cardiomyopathy (DCM). A total of 110 DCM patients and 110 control subjects were genotyped using polymerase chain reaction–restriction fragment length polymorphism and DNA-sequencing assay. GA/AA genotypes of TNF-α (−308) were significantly associated with increased risk of DCM compared with GG genotype (odds ratio [OR] = 1.92; 95% confidence intervals [CI], 1.05–3.52). Similarly, GA/AA of TNF-β (+252) was significantly associated with increased risk of DCM compared with GG genotype (OR = 1.97; 95% CI, 1.14–3.38). Additionally, A allele of TNF-α (−308) and TNF-β (+252) was associated with a 1.76-fold increased risk of DCM compared with G allele (OR = 1.76; 95% CI, 1.05–2.95 and OR = 1.79; 95% CI, 1.22–2.63, respectively). However, no association between DCM and TNF-α (−857), TNF-α (−1031), and TNF-α (−863) was observed. TNF gene polymorphisms may be associated with risk of DCM.