Observation of Curative Effect of Lung Recruitment in Patients with Acute Respiratory Distress Syndrome after Cardiopulmonary Bypass Surgery.

Recruitment maneuver (RM) has become a routine supplementary maneuver for clinical rescue of severe ARDS with low tidal volume/pressure-limited mechanical ventilation. Recruitment of patients with ARDS mechanical ventilation can improve the lung compliance, promote the opening of collapsed alveoli, improve the ratio of ventilation to blood flow, reduce dead space, reduce shunt flow, and improve oxygenation function. In this paper, the patients were divided into lung recruitment group and conventional treatment group by the random number permutation table method. When the patient's percutaneous oxygen saturation is less than or equal to 88%, the partial pressure of oxygen in the arterial blood gas is less than or equal to 55 mmHg, or the ventilator tube is disconnected during sputum suction or other accidents, a CPAP × 60 - second lung recruitment maneuver is required. Then adjust the ventilator parameters in the same way. In the process of lung recruitment, the changes in invasive continuous arterial blood pressure will also be observed. If the blood pressure dropped to ≤90/60 mmHg, one recruitment maneuver was terminated in advance. And both groups of patients used the Dräger- or PB840-imported multifunctional ventilator. The treatment of primary disease and predisposing factors, fluid management strategies, antibiotics and glucocorticoids, nutrition, and metabolic support in the two groups of patients in the study were the same. The PaO2/FiO2 value improved by 51% 10 minutes after recruitment, and the median increased from 111 (IQR, 73-265) before recruitment to 170 (IQR, 102-340) (P < 0.01), the improvement of PaO2/FiO2 at 4 hours after recruitment and 12 hours after recruitment was 78% (P < 0.05) and 39% (P < 0.01), respectively, and the median PaO2/FiO2 at 4 hours after recruitment was 198 (IQR, 116-256). The median PaO2/FiO2 became 155 (IQR, 127-235) 12 hours after recruitment. Recruitment can reduce the accumulation of neutrophils in lung tissue, reduce the release of inflammatory factors, reduce pulmonary edema, and reduce pathological damage.

KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis.

Histone modifier lysine-specific demethylase 2B (KDM2B) has been previously reported to activate the inflammatory response by transcription initiation of the IL-6 gene. However, the effects of KDM2B on the inflammatory response during myocardial ischemia-reperfusion (I/R) injury and corresponding mechanisms remain poorly understood. The present study aimed to investigate the role and mechanism of KDM2B in myocardial I/R injury. Therefore, a myocardial I/R injury model was established in rats through coronary artery ligation. Adeno-associated virus-encoding KDM2B and small interfering RNA-KDM2B were designed to determine the effects of KDM2B on myocardial I/R injury using H&E staining and a TUNEL assay in the myocardial tissues. Reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expression levels of KDM2B, toll-like receptor 4 (TLR4), NF-κB p65 and NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3). ELISA was used to detect the levels of TNF-α, IL-6 and IL-1ß in the peripheral blood samples. Pathological analysis demonstrated that the cells in the model group were disordered, with a large area of necrosis and neutrophil infiltration. Knocking down KDM2B expression significantly upregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB p65 and the ratio of phosphorylated (p)-p65 to p65. KDM2B knockdown also significantly increased the levels of IL-1ß, IL-6 and TNF-α in the peripheral blood, which aggravated myocardial injury and promoted the apoptosis of myocardial cells. However, overexpression of KDM2B downregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB P65, the ratio of p-p65 to p65 whilst reducing the levels of IL-1ß, IL-6 and TNF-α in the peripheral blood, which markedly improved myocardial injury and significantly inhibited the apoptosis of cells in myocardial tissue. In conclusion, the results indicated that overexpression of KDM2B may prevent myocardial I/R injury in rats by reducing the inflammatory response through regulation of the TLR4/NF-κB p65 axis.

Bi-allelic mutations in DNAH7 cause asthenozoospermia by impairing the integrality of axoneme structure.

Asthenozoospermia is the most common cause of male infertility. Dynein protein arms play a crucial role in the motility of both the cilia and flagella, and defects in these proteins generally impair the axoneme structure and cause primary ciliary dyskinesia. But relatively little is known about the influence of dynein protein arm defects on sperm flagella function. Here, we recruited 85 infertile patients with idiopathic asthenozoospermia and identified bi-allelic mutations in DNAH7 (NM_018897.3) from three patients using whole-exome sequencing. These variants are rare, highly pathogenic, and very conserved. The spermatozoa from the patients with DNAH7 bi-allelic mutations showed specific losses in the inner dynein arms. The expression of DNAH7 in the spermatozoa from the DNAH7-defective patients was significantly decreased, but these patients were able to have their children via intra-cytoplasmic sperm injection treatment. Our study is the first to demonstrate that bi-allelic mutations in DNAH7 may impair the integrality of axoneme structure, affect sperm motility, and cause asthenozoospermia in humans. These findings may extend the spectrum of etiological genes and provide new clues for the diagnosis and treatment of patients with asthenozoospermia.