Risk factors for brain injury in premature infants with twin-to-twin transfusion syndrome: a retrospective cohort study.

Background: Brain injury (BI) is prevalent in premature infants with twin-to-twin transfusion syndrome (TTTS), while risk factors of BI in these patients remains unknown. Our study aims to discern potential risk factors that contribute to BI in premature infants with TTTS. Methods: We conducted a retrospective cohort and analyzed clinical data of premature infants diagnosed with TTTS at the Northwest Women's and Children's Hospital between January 1, 2015 and January 1, 2020. Data included the infants' perinatal information, key postnatal examinations, laboratory tests, and treatments. Results: Of the 84 patients enrolled in the study, 22 (26.2%) were categorized in the BI group and 62 (73.8%) in the non-BI group, based on cranial imaging. No significant differences were found at baseline between the groups in relation to the proportion of males (40.9% vs. 35.5%, P=0.845), median gestational age (weeks) [31.9 (31.5, 33.4) vs. 34.2 (31.6, 35.4), P=0.061], average weight (g) (1,676.4±567.5 vs. 1,845.2±511.7, P=0.200), maternal age (years) [29.5 (26.0, 31.0) vs. 28.5 (27.8, 31.0), P=0.656], the proportion of in-vitro fertilization (9.1% vs. 16.1%, P=0.648), cesarean sections (86.4% vs. 93.5%, P=0.549) or TTTS donor infants (50.0% vs. 51.6%, P=0.897). Multivariate logistic regression analysis indicated that invasive mechanical ventilation [invasive mechanical ventilation (IMV); odds ratio (OR) =4.365; 95% confidence interval (CI): 1.066-17.870; P=0.040], [necrotizing enterocolitis (NEC); OR =8.632; 95% CI: 1.542-48.318; P=0.014], [single intrauterine fetal demise (sIUFD); OR =14.067; 95% CI: 1.298-224.421; P=0.031], and a 5-minute Apgar score <9 (OR =4.663; 95% CI: 1.015-21.419; P=0.048) were strongly associated with BI in TTTS premature infants. Conclusions: Our study identifies IMV, NEC, sIUFD, and a 5-minute Apgar score <9 as independent risk factors for BI in premature infants with TTTS.

Mechanism of Polygonum capitatum intervention in pulmonary fibrosis based on network pharmacology and molecular docking technology: A review.

Pulmonary fibrosis (PF) is a serious interstitial disease that includes diffuse collagen deposition of lung tissue. Polygonum capitatum Buch.-Ham. ex D. Don (THL) is a traditional vaccine that has antibacterial and anti-inflammatory effects. In this research, to investigate the mechanism of action of THL in the intervention of pulmonary fibrosis by network pharmacology and molecular docking related research methods, in order to provide a theoretical basis for expanding the scope of THL medication. A total of 49 active ingredients were analyzed and screened in Cephalus cephalusis, including 35 pulmonary fibrosis targets, and 10 key targets such as ALB, EGFR were screened after software analysis. The molecular docking results showed that there were 44 binding energies less than -3 kcal·mol-1 in the 60 docking results, indicating that most proteins had strong binding energies with compounds. The key targets of KEGG enrichment analysis were mainly enriched in 20 core action pathways, such as hemostasis-related pathway, regulation of kinase activity. This study shows that based on network pharmacology, the multicomponent-multitarget-multipathway effect of THL intervention in pulmonary fibrosis is discussed.

Sigma-1 Receptor Alleviates Airway Inflammation and Airway Remodeling Through AMPK/CXCR4 Signal Pathway.

Sigma non-opioid intracellular receptor 1 (Sigma-1R) has been proven to play a major role in inflammation and structural remodeling. However, its role in airway inflammation and airway remodeling remains unclear. The purpose of this study aimed to explore the role and mechanism of Sigma-1R in airway remodeling and epithelial-mesenchymal transition (EMT) process in vivo and in vitro. We observed the decrease of Sigma-1R in lung tissue of asthma model. In the mouse model of allergic airway inflammation (AAI), Sigma-1R agonist RPE-084 significantly relieved airway inflammation and airway remodeling, while Sigma-1R antagonist BD1047 (B8562) had opposite effects. Further research showed that RPE-084 treatment increased the expression of pAMPK and inhibited the expression of CXCR4. Furthermore, RPE-084 treatment suppressed the levels of IL-4, IL-5, and IL-13 in BALF. We found that RPE-084 or Sigma-1R overexpression vector treatment regulated cell cycle and inhibited cell proliferation, migration, and EMT process in TGF-ß1-induced 16HBE cells. Finally, we confirmed that AMP-activated protein kinase (AMPK) inhibitor compound C or CXCR4 agonist ATI-2341 both reversed the effects of Sigma-1R on TGF-ß1-induced 16 HBE cells. In a word, our research shows that Sigma-1R is helpful to improve airway remodeling of asthma, and emphasizes a new candidate molecular for asthma treatment.

A non-motorized spectro-goniometric system to measure the bi-directional reflectance spectra of particulate surfaces in the visible and near-infrared.

Reflectance spectroscopy is a powerful tool for remotely identifying the compositional and physical properties of surface materials. Due to the anisotropic scattering nature of most surfaces, the spectral features, including the absolute reflectance value, spectral slope, and band depth, are influenced by illumination and viewing configurations. Therefore, it is important to understand how spectral features vary with illumination and observation geometries for various particulate surfaces through laboratory measurements. Here, we describe a non-motorized spectro-goniometric system capable of measuring the bi-directional reflectance of particulate surfaces in the upper hemisphere in the wavelength range from 350 to 2150 nm. The incident and the viewing zenith angles can be varied from 0° to 55° and from 0° to 70°, respectively. The relative viewing azimuth angle can be varied from 0° to 360°. Measurements on Labsphere Spectralon agree well with measurements done with other instruments. We also present measurement results on two typical planetary analog materials, the JSC-1A Martian soil simulant and the JSC-1A lunar regolith simulant.

SOX18 enhances the proliferation and migration of airway smooth muscle cells induced by tumor necrosis factor-α via the regulation of Notch1 signaling.

Childhood asthma is a frequent chronic disease of pediatric populations. The excessive proliferation and migration of airway smooth muscle cells contribute to airway remodeling during asthma pathogenesis. Sex-determining region on the Y chromosome-related high mobility group box 18 (SOX18) has been reported to be over-expressed in asthma. However, whether SOX18 plays a role in modulating the airway remodeling of asthma is not fully understood. The purposes of this work were to assess the potential role of SOX18 in modulating airway remodeling using tumor necrosis factor-α (TNF-α)-stimulated airway smooth muscle cells in vitro. Our results showed that SOX18 expression was increased following TNF-α stimulation in airway smooth muscle cells. The silencing of SOX18 markedly prohibited the proliferation and migration of airway smooth muscle cells induced by TNF-α, whilst the over-expression of SOX18 produced the opposite effects. Further investigation revealed that SOX18 promoted the expression of Notch1, and enhanced the activation of Notch1 signaling in airway smooth muscle cells stimulated by TNF-α. The inhibition of Notch1 markedly diminished SOX18-over-expression-evoked promotion effects on TNF-α-induced proliferation and migration of airway smooth muscle cells. In addition, the reactivation of Notch1 signaling markedly reversed the SOX18-silencing-induced suppressive effect on the TNF-α-induced proliferation and the migration of airway smooth muscle cells. In summary, the findings of this work demonstrate that SOX18 regulates the proliferation and migration of airway smooth muscle cells induced by TNF-α via the modulation of Notch1 signaling. This study indicates a potential role for SOX18 in promoting airway remodeling during asthma pathogenesis.