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Treatment options for viral lung infections are currently limited. We aimed to explore the safety and efficacy of inhaled ethanol in an influenza-infection mouse model.
Mucopolysaccharidosis type IIIA (MPS IIIA) is characterized by neurological and skeletal pathologies caused by reduced activity of the lysosomal hydrolase, sulfamidase, and the subsequent primary accumulation of undegraded heparan sulfate (HS). Respiratory pathology is considered secondary in MPS IIIA and the mechanisms are not well understood.
Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids
Alcohol pharmacotherapies pose unknown teratogenic risks in pregnancy and are therefore recommended to be avoided. This limits treatment options for pregnant individuals with alcohol use disorders (AUD). The information on the safety of these medications during pregnancy is uncertain, prompting a scoping review. The objective of this review was to investigate available information on the safety of alcohol pharmacotherapies in pregnancy.
The complex arborization of the feto-placental vasculature is crucial for optimal fetal nutrition, waste exchange and ultimately, development. Ethical and experimental limitations constrain research into the human placenta, hence experimental animal models such as mice and rats, are crucial to understand placental function. It is unclear how well the mouse and rat feto-placental vascular structure emulates human. Moreover, the implications of differences in vascular structure, especially in arborization, for placental function remain unclear.
Emerging data suggest that air pollution is a persistent source of neuroinflammation, reactive oxygen species, and neuropathology that contributes to central nervous system disorders. Previous research using animal models has shown that exposure to diesel exhaust causes considerable disruption of the blood-brain barrier, leading to marked neuroinflammation.
This study aimed to investigate acamprosate and naltrexone dispensing patterns in Australia.
Citation: Wang KCW, Elliot JG, Saglani S, et al. The airway smooth muscle layer is structurally abnormal in low birth weight infants: implications
Airway-associated adipose tissue increases with body mass index and is a local source of pro-inflammatory adipokines that may contribute to airway pathology in asthma co-existing with obesity. Genetic susceptibility to airway adiposity was considered in the present study through kisspeptin/kisspeptin receptor signalling, known to modulate systemic adiposity and potentially drive airway remodelling.
Adverse prenatal conditions can induce intrauterine growth restriction and increase the risk of adulthood metabolic disease. Mechanisms underlying developmentally programmed metabolic disease remain unclear but may involve disrupted postnatal circadian rhythms and kisspeptin signalling.