Although heme oxygenase-1 (HO-1) is part of an endogenous defense system implicated in the homeostatic response, its role in cell proliferation and tumor progression is still controversial. Endometrial hyperplasia (EH) is associated with high risk of endometrial cancer (EC). Therefore, we aimed to evaluate the effect of hemin, a HO-1 inducer, against EH. Thirty-two female rats (60–70 days old) were divided into 4 groups treated for 1 week: vehicle control group, hemin group (25 mg/kg; i.p. 3 times/week), estradiol valerate (EV) group (2 mg/kg per day, p.o.), and hemin plus EV group. Sera were obtained for reduced glutathione level. Uterine malondialdehyde, superoxide dismutase, total nitrite/nitrate, and interleukin-1β levels were estimated. HO-1 and p38 mitogen-activated protein kinase expressions were obtained in uterine tissue. Uterine histological and immunohistochemical assessment of iNOS and Ki67 were also done. Results demonstrated that upregulation of HO-1 expression in hemin plus EV rats led to amelioration of EH which was confirmed with histological examination. This was associated with significant decrease in oxidative stress parameters, p38 mitogen-activated protein kinase expression, and interleukin-1β level. Also, uterine iNOS and Ki67 expressions were markedly suppressed. In conclusion, upregulation of HO-1 expression via hemin has ameliorative effect against EH through its antioxidant, anti-inflammatory, and antiproliferative actions.
Background
There is paucity of literature on why and how patients are intubated, and by whom, in Irish Emergency Departments (EDs). The aim of this pilot study was to characterise emergency airway management (EAM) of critically unwell patients presenting to Irish EDs.
Methods
A multisite prospective pilot study was undertaken from February 10 to May 10, 2020. This project was facilitated through the Irish Trainee Emergency Research Network (ITERN). All patients over 16 years of age requiring EAM were included. Eleven EDs participated in the project. Data recorded included patients’ demographics, indication for intubation, technique of airway management, medications used to facilitate intubation, level of training and specialty of the intubating clinician, number of attempts, success/complications rates and variation across centres.
Results
Over a 3-month period, 118 patients underwent 131 intubation attempts across 11 EDs. The median age was 57 years (IQR: 40–70). Medical indications were reported in 83% of patients compared to 17% for trauma. Of the 118 patients intubated, Emergency Medicine (EM) doctors performed 54% of initial intubations, while anaesthesiology/intensive care medicine (ICM) doctors performed 46%. The majority (90%) of intubating clinicians were at registrar level. Emergency intubation check lists, video laryngoscopy and bougie were used in 55, 53 and 64% of first attempts, respectively. The first pass success rate was 89%. Intubation complications occurred in 19% of patients. EM doctors undertook a greater proportion of intubations in EDs with > 50,000 attendance (65%) compared to EDs with < 50,000 attendances (16%) (p < 0.000).
Conclusion
This is the first study to describe EAM in Irish EDs, and demonstrates comparable first pass success and complication rates to international studies. This study highlights the need for continuous EAM surveillance and could provide a vector for developing national standards for EAM and EAM training in Irish EDs.
In case of a life‐threatening, stressful event, the body prepares for an emergency. Indeed, the lung is unique in which alveolar cells are constantly exposed to physical and chemical stresses. This study aimed to study the impact of immobilization stress on the blood–air barrier and how it initiate and maintain an inflammatory response, plus determining the resolution of lung inflammation and repair. There was a significant increase in the plasma levels of stress markers “corticosterone and catecholamines” with a decrease in surfactant protein A (a lung‐injury marker). Chronic stress produced a significant increase in the pulmonary oxidative and inflammatory markers malondialdehyde, tumor necrosis factor α, and induced nitric oxide synthase when compared with that of acute stress. Both stresses provoked marked pulmonary morphological and ultrastructural changes with a significant increase in caspase‐3 immunoexpression. There was increasing evidence of lung’s capacity for repair. This process involved edema resolution, cell proliferation, and tissue remodeling in improving the lung‐injury, oxidative, and inflammatory markers.
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