Hyperbaric oxygen (HBO) is widely applied to treat several hypoxia-related diseases. Previous studies have focused on the immediate effect of HBO-exposure induced oxidative stress on the lungs, but knowledge regarding the chronic effects from repetitive HBO exposure is limited, especially at the gene expression level. We found that repetitive HBO exposure did not alter the morphology of murine lungs. However, by deconvolution of RNA-seq from those mice lungs using CIBERSORTx and the expression profile matrices of 8 mesenchymal cell subtypes obtained from bleomycin-treated mouse lungs, we identify several mesenchymal cell subtype changes. These include increases in Col13a1 matrix fibroblasts, mesenchymal progenitors and mesothelial cell populations and decreases in lipofibroblasts, endothelial and Pdgfrb high cell populations. Our data suggest that repetitive HBO exposure may affect biological processes in the lungs such as response to wounding, extracellular matrix, vasculature development and immune response.

ObjectivesThe influence of commercial helium–oxygen saturation diving on divers’ gut microbiotas was assessed to provide dietary suggestion.MethodsFaecal samples of 47 divers working offshore were collected before (T1), during (T2) and after (T3) saturation diving. Their living and excursion depths were 55–134 metres underwater with a saturation duration of 12–31 days and PaO2 of 38–65 kPa. The faecal samples were examined through 16S ribosomal DNA amplicon sequencing based on the Illumina sequencing platform to analyse changes in the bacteria composition in the divers’ guts.ResultsAlthough the α and β diversity of the gut microbiota did not change significantly, we found that living in a hyperbaric environment of helium–oxygen saturation decreased the abundance of the genus Bifidobacterium, an obligate anaerobe, from 2.43%±3.83% at T1 to 0.79%±1.23% at T2 and 0.59%±0.79% at T3. Additionally, the abundance of some short-chain fatty acid (SCFA)-producing bacteria, such as Fusicatenibacter, Faecalibacterium, rectale group and Anaerostipes, showed a decreased trend in the order of before, during and after diving. On the contrary, the abundance of species, such as Lactococcus garvieae, Actinomyces odontolyticus, Peptoclostridium difficile, Butyricimonas virosa, Streptococcus mutans, Porphyromonas asaccharolytica and A. graevenitzii, showed an increasing trend, but most of them were pathogens.ConclusionsOccupational exposure to high pressure in a helium–oxygen saturation environment decreased the abundance of Bifidobacterium and some SCFA-producing bacteria, and increased the risk of pathogenic bacterial infection. Supplementation of the diver diet with probiotics or prebiotics during saturation diving might prevent these undesirable changes.

The prevalence of pulmonary fibrosis is increasing with an aging population and its burden is likely to increase following COVID-19, with large financial and medical implications. As approved therapies in pulmonary fibrosis only slow disease progression, there is a significant unmet medical need. Hyperbaric oxygen (HBO) is the inhaling of pure oxygen, under the pressure of greater than one atmosphere absolute, and it has been reported to improve pulmonary function in patients with pulmonary fibrosis. Our recent study suggested that repetitive HBO exposure may affect biological processes in mice lungs such as response to wounding and extracellular matrix. To extend these findings, a bleomycin-induced pulmonary fibrosis mouse model was used to evaluate the effect of repetitive HBO exposure on pulmonary fibrosis. Building on our previous findings, we provide evidence that HBO exposure attenuates bleomycin-induced pulmonary fibrosis in mice. In vitro, HBO exposure could reverse, at least partially, transforming growth factor (TGF)-β–induced fibroblast activation, and this effect may be mediated by downregulating TGF-β–induced expression of hypoxia inducible factor (HIF)-1α. These findings support HBO as a potentially life-changing therapy for patients with pulmonary fibrosis, although further research is needed to fully evaluate this.

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Familial hypercholesterolemia (FH) is one of the most common inherited metabolic disorders characterized by elevated low-density lipid cholesterol (LDL-C) levels that lead to coronary artery disease at an early age and a low occurrence of cerebrovascular disease. Low-density lipoprotein receptor (LDLR) gene mutation is the most common cause of FH. Here, we report a case of a 47-year-old woman who had multiple carotid artery stenosis and brain ischemic foci, an elevated level of LDL-C, underwent eyelid xanthoma excision, and a family history of hyperlipidemia. Thereafter, she was diagnosed with FH according to the Dutch Lipid Clinical Network criteria and whole genome sequencing revealed compound heterozygous LDLR mutations. However, she denied a history of coronary heart disease (CAD). The patient underwent stenting of the right subclavicular artery and right internal carotid artery in our hospital.Lipid-lowering drugs were also administered to prevent stroke recurrence. During a 3-year follow-up, the blood lipid level of the patient reduced, and the condition of intracranial and extracranial vascular stenosis improved. Furthermore, a cascade screening was performed in her pedigree, and 7/9 family members were found to have elevated LDL-C, 6/7 were found to carry one of the two LDLR variants detected in the proband, and in 4/6, the carotid intima-media thickness was ≥1 mm, which was predicted as a high risk factor of cerebrovascular disease. Her relatives with high risks of cardiovascular or cerebrovascular diseases have been under lipid monitoring and management of risk factors since then. To date, no cardiovascular or cerebrovascular event has been reported. In conclusion, this case reminds us to consider FH screening in early-onset stroke or transient ischemic attack patients with elevated LDL-C level. Our report also demonstrates the beneficial role of genetic testing and cascade screening in the relatives of FH patients.