While kidney stone disease is common and ureteroscopy (URS) is perceived as minimally invasive, there is mortality associated with treatment.
 
  The aim of this review was to ascertain the number of mortalities from URS for stone disease over the past three decades, identify relevant patient risk factors and predictors of mortality, and summarise the key recommendations so that similar instances can be avoided, and lessons can be learnt.
 
  A systematic literature search was conducted following Cochrane and Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) methodology for English-language article reporting on data from 1990 to December 2020. Data collated from each study included patient and stone characteristics, number of mortalities, and cause of death.
 
  Fifteen studies met our inclusion criteria and revealed a total of 72 mortalities from ten countries. The age range of reported patients varied from 21 to 89 yr, with over 60% being above 65 yr of age and 97% with some comorbiditd ways to minimise this. Evidence shows that although reported mortality remains low, there seems to be an increase in mortality in the past decade and urologists must remain vigilant of this.
 We reviewed the risk factors associated with postureteroscopy mortality and ways to minimise this. Evidence shows that although reported mortality remains low, there seems to be an increase in mortality in the past decade and urologists must remain vigilant of this.Congenital heart disease (CHD) represents a large clinical burden, representing the most common cause of birth defect-related death in the newborn. The mainstay of treatment for CHD remains palliative surgery using prosthetic vascular grafts and valves. These devices have limited effectiveness in pediatric patients due to thrombosis, infection, limited endothelialization, and a lack of growth potential. Tissue engineering has shown promise in providing new solutions for pediatric CHD patients through the development of tissue engineered vascular grafts, heart patches, and heart valves. In this review, we examine the current surgical treatments for congenital heart disease and the research being conducted to create tissue engineered products for these patients. While much research remains to be done before tissue engineering becomes a mainstay of clinical treatment for CHD patients, developments have been progressing rapidly towards translation of tissue engineering devices to the clinic.For more than 200 years, pure oxygen was given ad libitum to newborn infants requiring resuscitation. Due to oxidative stress and injury concerns, a paradigm shift towards using "less" oxygen, including air (21% oxygen) instead of pure (100%) oxygen, occurred about twenty years ago. A decade later, clinicians were advised to adjust fractional inspired oxygen (FiO2) to target oxygen saturations (SpO2) that were derived from spontaneously breathing, healthy, mature infants. Whether these recommendations are achievable, beneficial, harmful or redundant is uncertain. The underlying pathology leading to resuscitation varies between infants and may considerably alter an infant's response to supplemental oxygen. In this review, we summarize available evidence for the use of SpO2 monitoring at delivery for newborn infants, elucidate existing knowledge and service gaps, and suggest future research recommendations that will lead to the safest clinical strategies for this standard and important practice.Despite important advances in neonatal care, rates of bronchopulmonary dysplasia (BPD) have remained persistently high. Numerous drugs and ventilator strategies are used for the prevention and treatment of BPD. Some, such as exogenous surfactant, volume targeted ventilation, caffeine, and non-invasive respiratory support, are associated with modest but important reductions in rates of BPD and long-term respiratory morbidities. Many other therapies, such as corticosteroids, diuretics, nitric oxide, bronchodilators and anti-reflux medications, are widely used despite conflicting, limited or no evidence of efficacy and safety. This paper examines the range of therapies used for the prevention or treatment of BPD. They are classified into those supported by evidence of effectiveness, and those which are widely used despite limited evidence or unclear risk to benefit ratios. Finally, the paper explores emerging therapies and approaches which aim to prevent or reduce BPD and long-term respiratory morbidity.Methionine sulfoxide reductase A (MsrA) is a widely expressed antioxidant enzyme that counteracts oxidative protein damage and contributes to protein regulation by reversing oxidation of protein methionine residues. In retinal pigment epithelial (RPE) cells in culture, MsrA overexpression increases phagocytic capacity by supporting mitochondrial ATP production. Here, we show elevated retinal protein carbonylation indicative of oxidation, decreased RPE mitochondrial membrane potential, and attenuated RPE phagocytosis in msra-/- mice. Moreover, electroretinogram recordings reveal decreased light responses specifically of cone photoreceptors despite normal expression and localization of cone opsins. Impairment in msra-/- cone-driven responses is similar from 6 weeks to 13 months of age. These functional changes match dramatic decreases in lectin-labeled cone sheaths and reduction in cone arrestin in msra-/- mice. Strikingly, cone defects in light response and in lectin-labeled cone sheath are completely prevented by dark rearing. Together, our data show that msra-/- mice provide a novel small animal model of preventable cone-specific photoreceptor dysfunction that may have future utility in analysis of cone dystrophy disease mechanisms and testing therapeutic approaches aiming to alleviate cone defects.miR-101-3p may play a therapeutic role in various tumours.  https://www.selleckchem.com/products/monomethyl-auristatin-e-mmae.html  However, its anti-tumour mechanism remains unclear, and a definitive strategy to treat tumour cells in vivo is lacking. The objective of this study was to investigate the inhibitory mechanism of miR-101-3p on tumour cells and to develop relevant nanomedicines for in vivo therapy. The expression levels of miR-101-3p and its target protein TBLR1 in tumour tissues and cells were detected, and their relationship with ferroptosis was clarified. Furthermore, the efficacy of nanocarriers in achieving in vivo therapeutic gene delivery was evaluated. Nanomedicine was further developed, with the anti-proliferative in vivo therapeutic effect validated using a subcutaneous xenograft cancer model. The expression level of miR-101-3p negatively correlated with clinical tumour size and TNM stage. miR-101-3p restores ferroptosis in tumour cells by directly targeting TBLR1, which in turn promotes apoptosis and inhibits proliferation. We developed nanomedicine that can deliver miR-101-3p to tumour cells in vivo to achieve ferroptosis recovery, as well as to inhibit in vivo tumour proliferation.