Initial respiratory support modality and outcome in preterm infants with less than 32 weeks of gestation in China: A multicentre retrospective cohort study.

BACKGROUND: For initial respiratory management, continuous positive airway pressure (CPAP) is increasingly used for preterm infants, especially for gestational age less than 32 weeks. However, neonatologists are concerned about the potential risks of CPAP support failure. OBJECTIVES: To examine the association between different initial respiratory support modalities and the outcomes of preterm infants at <32 weeks of gestation across multiple neonatal intensive care units (NICU) in China. METHODS: This study was carried out over a period of 12 months in 2018. Unadjusted relative risks (RR) for demographic and clinical characteristics were calculated for CPAP failure and CPAP success in the total cohort using log-linear model based on generalised estimating equations for clustered observations. RESULTS: Among 1560 preterm infants delivered at <32 weeks, the incidence of CPAP failure was 10.3%. After adjustment for demographic and clinical factors, the relative risk of mortality (RR 7.54, 95% CI 5.56, 10.44), pneumothorax (RR 9.85, 95% CI 2.89, 61.53), pulmonary haemorrhage (RR 7.78, 95% CI 4.51, 14.64) and BPD (RR 3.65, 95% CI 3.65, 4.51) were considerably higher for infants in the CPAP failure group than those in the CPAP-S group. However, the risk of poor outcomes in CPAP failure infants was similar to that of those in the initial mechanical ventilation (MV) group. CONCLUSIONS: Continuous positive airway pressure failure was associated with an increased risk of mortality and major morbidities, including BPD, pulmonary haemorrhage and pneumothorax, and was comparable to the risk associated with initial MV.

[The bio-effects of high single-dose radiation on xenografts of Lewis lung carcinoma].

OBJECTIVE: To investigate the bio-effects of high single-dose radiation on xenografts of Lewis lung carcinoma. METHODS: Female 8-week-old C57 mice bearing 4-6 mm diameter Lewis lung carcinoma tumors in the hind legs were divided into 3 groups, control group (0 Gy), high single-dose group (12 Gy/one fraction/day) and routine radiation group (22 Gy/11 fraction/15 d). The mean biological effective dose (BED) of both radiation groups was 26.4 Gy. Changes in hypoxia, DNA damage and cell cycle of the tumor cells at 1, 3, 8, 15 and 21 d after first irradiation was assessed by immunofluorescence and flow-cytometry and the tumor growth curve was also made. RESULTS: Compared to the fractionated treatment, the tumor growth was delayed after single dose irradiation. The percent of hypoxic cells after single dose radiation was lower than fractioned irradiation at 3, 8, 15 d after first radiation. The foci of gamma-H2AX showed that the single dose caused heavier DNA damages than fractioned irradiation at 1, 3 d after first radiation. The decline of G0/G1 percentage and increase of G2/M percentage of cells was found in both radiation schedules, but the G2/M percentage after single dose radiation was higher. CONCLUSION: In the C57 mice bearing Lewis lung carcinoma, the high single-dose regimen inhibits the tumor growth more than fractioned irradiation. We hypothesized that conversion of high single-dose to BED using the LQ formalism under estimated the in vivo effect of hypofractionated radiation.

Analysis of Risk Factors for Intraoperative Bleeding in the Surgical Treatment of Cesarean Scar Pregnancy and Development of Predictive Models.

Objective: The objective of this study was to investigate the risk factors associated with cesarean scar pregnancy (CSP) and to develop a model for predicting intraoperative bleeding risk. Methods: We retrospectively analyzed the clinical data of 208 patients with CSP who were admitted to the People's Hospital of Leshan between January 2018 and December 2022. Based on whether intraoperative bleeding was ≥ 200 mL, we categorized them into two groups for comparative analysis: the excessive bleeding group (n = 27) and the control group (n = 181). Identifying relevant factors, we constructed a prediction model and created a nomogram. Results: We observed that there were significant differences between the two groups in several parameters. These included the time of menstrual cessation (P = 0.002), maximum diameter of the gestational sac (P < 0.001), thickness of the myometrium at the uterine scar (P = 0.001), pre-treatment blood HCG levels (P = 0.016), and the grade of blood flow signals (P < 0.001). We consolidated the above data and constructed a clinical prediction model. The model exhibited favorable results in terms of predictive efficacy, discriminative ability (C-index = 0.894, specificity = 0.834, sensitivity = 0.852), calibration precision (mean absolute error = 0.018), and clinical decision-making utility, indicating its effectiveness. Conclusion: The clinical prediction model related to the risk of hemorrhage that we developed in this experiment can assist in the development of appropriate interventions and effectively improve patient prognosis.

Repeated oral administration of oleanolic acid produces cholestatic liver injury in mice.

Oleanolic acid (OA) is a triterpenoid and a fantastic molecule with many beneficial effects. However, high-doses and long-term use can produce adverse effects. This study aimed to characterize the hepatotoxic potential of OA. Mice were given OA at doses of 100-3,000 µmol/kg (45-1,350 mg/kg), po for 10 days, and the hepatotoxicity was determined by serum biochemistry, histopathology, and toxicity-related gene expression via real-time RT-PCR. Animal body weight loss was evident at OA doses of 1,000 µmol/kg and above. Serum alanine aminotransferase activities were increased in a dose-dependent manner, indicative of hepatotoxicity. Serum total bilirubin concentrations were increased, indicative of cholestasis. OA administration produced dose-dependent pathological lesions to the liver, including inflammation, hepatocellular apoptosis, necrosis, and feathery degeneration indicative of cholestasis. These lesions were evident at OA doses of 500 µmol/kg and above. Real-time RT-PCR revealed that OA produced dose-dependent increases in acute phase proteins (MT-1, Ho-1, Nrf2 and Nqo1), decreases in bile acid synthesis genes (Cyp7a1 and Cyp8b1), and decreases in liver bile acid transporters (Ntcp, Bsep, Oatp1a1, Oatp1b2, and Ostß). Thus, the clinical use of OA and OA-type triterpenoids should balance the beneficial effects and toxicity potentials.

AflatoxinB1 (AFB1 ) and its toxic effect on the broilers intestine: A review.

Aflatoxin B1 (AFB1 ) is the predominant mycotoxin that originated toxicity in broilers through oxidative damage, intestinal barrier dysfunction, reduced immune system and dysfunction of microorganisms and enzymes in target organs. The intestine is the first AFB1 target organ destroyed after the bird's body is induced. This review summarises the current knowledge of the negative results of AFB1 -induced intestinal damage on broiler production. It was conducted in accordance with the relevant studies in the cited literatures being retrieved from PubMed, Google Scholar, Science Direct and Web of Science. First, AFB1 can change the intestinal barrier function by destroying the intestinal architecture, tissue and cell integrity of the gut epithelium. Second, AFB1 can damage the immune barrier function of the gastrointestinal mucosa. Third, the microbiota of birds interacts closely with the ingested aflatoxin. Finally, because broilers are tremendously sensitive to AFB1 contamination, the poisonous and noxious effects of this mycotoxin in the broiler industry cause millions of dollars in losses every year. This review briefly discussed that the AFB1 , which affects the intestines of broiler chickens, was reduced the immune apparatus, antioxidant protection system, gastric system, and broiler production status and its impact on human health. Therefore, this review will improve our perception of the important intestine in a bird's health and the adverse effect of AFB1 .

[Metabolomics research on focal cerebral ischemia reperfusion injury in rats' brain treated by musk combined with borneol].

OBJECTIVE: To study the metabolomics of focal cerebral ischemia reperfusion injury in rats' brain treated by musk combined with borneol. METHODS: Amino acids, fatty acids, organic acids, glucose,and sterols were transferred to ethers or esters which were heat stable and evaporated easily. The chromatographic conditions were optimized to analyze the endogenous metabolites from serum of the rats. RESULTS: The metabolic fingerprints of the endogenous metabolites were obtained by the optimum method. Twenty-nine chromatographic peaks in the metabolic fingerprints were identified by mass data and standard references. And the difference between normal, model rats, and model rats treated by musk with borneol was analyzed by the Principal Component Analysis (PCA). CONCLUSION: The metabolic fingerprints based on the derivation reaction combined with GC-MS could analyze the endogenous metabolites; The variation between different groups was related to the quantity of the biomarkers which could be in accordance with focal cerebral ischemia reperfusion injury.

Pharmacologic Effect of Miao Medicine Illicium simonsii Maxim. on Collagen-Induced Arthritis in Rats.

OBJECTIVES: To study the pharmacologic effect and mechanism of action of Miao medicine Illicium simonsii Maxim. (ISM) in treating rheumatoid arthritis. METHODS: Sixty rats were randomly divided to six groups: normal control (normal), collagen-induced arthritis (CIA) model (model), CIA + tripterygium glycosides (TG), CIA + ISM high dose oral (ISM-H), CIA + ISM low-dose oral (ISM-L), and CIA + ISM topical application (ISM-T). The treatment doses were selected based on published reports and folk medicine practice. The outcome measurements included paw swelling, joint pathology, organ index, blood count, T helper 17 (Th17) cell count, and interleukin-6 (IL-6) level. RESULTS: Compared to the CIA model group, all treatment groups showed a significant reduction in paw swelling, blood vessel pathology, Th17 cell count, and IL-6 levels (p < 0.05 or p < 0.01). All treatment groups showed alleviated foot swelling and lower total number of white blood cells, and these effects were observed earlier with oral ISM than topical ISM. The effect of ISM was weaker than that of TG. In addition, less organ damage was observed with topical ISM than oral ISM but better than TG. CONCLUSIONS: These results suggest that, by downregulating Th17 cells, ISM inhibits the production of Il-6, thereby alleviating the proliferation of endothelial and rheumatoid-like cells and leukocytosis in CIA rats, ultimately eliminating foot swelling.

Oeanolic acid protects against the hepatotoxicity of D-galactosame plus endotoxin in mice.

Oleanolic acid (OA) is a triterpenoid contained in many herbal medicines. The aim of this study was to investigate the protective effect of OA against D-galactosame plus lipopolysaccharides (D-GalN/LPS)-induced acute liver injury and the underling mechanisms. Mice were randomly divided into normal control with vehicles only (corn oil), D-GalN/LPS only (700mg/10µg/kg, ip), OA-po (200µmol/kg in corn oil, po) plus D-GalN/LPS, and OA-sc (50µmol/kg in 2% tween 80, sc) plus D-GalN/LPS groups. OA pretreatment was conducted twice daily for 4 consecutive days. Hepatotoxicity was evaluated by histopathology, serum enzyme activity, hepatic lipid peroxidation and GSH levels. To reveal the possible mechanisms of the protection, mRNA and protein expressions of toxicity-relevant genes and proteins were examined by real-time RT-PCR and western-blot analysis. Both OA-po and OA-sc at therapeutic doses successfully protected liver injury induced by D-GalN/LPS, as evidenced by reduced serum enzyme activities, prevented liver hemorrhage, massive necrosis, and reduced degenerative lesions. OA increased hepatic GSH contents and decreased lipid peroxidation (MDA) levels. Furthermore, OA significantly inhibited the mRNA expression of the tumor necrosis factor-α (TNF-α) and ER responsive gene Gadd45. D-GalN/LPS-induced activation of p-JNK and NF-κB p65, and protein overexpression of caspase-3, caspase-8, and COX2 were significantly suppressed by OA. These results clearly demonstrated OA-po is effective as OA-sc in protecting against D-GalN/LPS-induced liver injury, and the protection mechanisms are related to reduction of oxidative damage, suppression of TNFα-triggered signaling through the NF-kB and JNK pathways, thus reducing apoptosis and hepatocellular death.

Ablative hypofractionated radiotherapy normalizes tumor vasculature in lewis lung carcinoma mice model.

Ablative hypofractionated radiotherapy (HFRT) significantly improves the overall survival of inoperable non-small cell lung cancer (NSCLC) patients compared with conventional radiation therapy. However, the radiobiological mechanisms of ablative HFRT remain largely unknown. The purpose of this study was to investigate the dynamic changes of tumor vessels and perfusion during and after ablative hypofractionated radiotherapy. Lewis lung carcinoma-bearing mice were treated with sham (control) and ablative hypofractionated radiotherapy of 12 Gy in 1 fraction (12 Gy/1F) and 36 Gy in 3 fractions (36 Gy/3F). Tumor microvessel density (MVD), morphology and function were examined at different times after irradiation. The results showed that, compared to the controls the MVD and hypoxia in ablative HFRT groups decreased, which were accompanied by an increase in the number of pericytes and their coverage of vessels. Functional tests revealed that tumor hypoxia and perfusion were improved, especially in the 36 Gy/3F group. Our results revealed that ablative hypofractionated radiotherapy not only repressed MVD and hypoxia, but also increased the vascular perfusion and the number of pericyte-covered vessels, suggesting that ablative HFRT normalized the tumor vasculature.