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Background The care of wounds is an ongoing issue for Indigenous people worldwide, yet culturally safe Indigenous wound care training programs for rural and remote Australian Aboriginal Health Workers are largely unavailable. The higher prevalence of chronic disease, lower socioeconomic status and poorer access to services experienced by Aboriginal and Torres Strait Islanders compared to non-Indigenous people, leads to a greater incidence of chronic wounds in Aboriginal and Torres Strait Islander people. Identifying the barriers and enablers for delivering wound care will establish areas of need for facilitating the development of a specific wound care program for Aboriginal Health Workers and Aboriginal Health Practitioners. This paper reports the first phase of a larger project directly aligned to the Indigenous Australians’ Health Program’s objective of supporting the delivery and access to high quality, culturally appropriate health care and services to Aboriginal and Torres Strait Islander Australians. This study aimed to examine experiences of Aboriginal Health Workers, Aboriginal Health Practitioners, and nurses for managing chronic wounds within rural and remote Aboriginal Medical Services in Queensland, Australia. Methods Yarning facilitated by two Aboriginal researchers among Aboriginal Health Workers, Aboriginal Health Practitioners, and nurses currently employed within four Aboriginal Medical Services located in rural and remote areas of Queensland, Australia. Results Two themes were developed through rigorous data analysis of yarning information and responses: participants’ experiences of managing wounds and barriers and enablers to effective wound care. Conclusions This study contributes an insight into the experiences of Aboriginal Health Workers on the current barriers and enablers to timely treatment of chronic wounds. Results from this study indicate a significant barrier to obtaining timely and effective wound care in regional and remote settings is access to an appropriately skilled, culturally competent, and resourced health work force. A lack of education and professional development for Aboriginal Health Workers can compromise their ability to maximise patient outcomes and delay wound healing. Findings have informed the development of an evidence based, culturally competent open access chronic wound care education program for Aboriginal Health Workers.

High‐intensity exercise hyperpnea places substantial demands upon the respiratory muscles, but whether this causes respiratory muscle damage is unknown. We investigated respiratory muscle damage following volitional hyperpnea (equivalent to 85% of participants maximum minute ventilation produced during a maximal incremental cycling test) using a skeletal muscle damage biomarker panel. Eight healthy men (33 + 2 years) underwent 10‐min trials of volitional hyperpnea and rest (control) two weeks apart. Serum was collected before and at 1, 24, and 48 h after both volitional hyperpnea and control trials. Creatine kinase muscle‐type (CKM), fast skeletal troponin I (sTnI) and slow sTnI were measured using enzyme‐linked immunosorbent assay. Two‐way analysis of variance revealed time × trial interaction effects for slow sTnI (p = 0.018), but not for CKM (p = 0.072) and fast sTnI (p = 0.140). Slow sTnI was significantly higher at +24 h post volitional hyperpnea (p < 0.001) as compared to the same time point of the control trial. These results indicate that high‐intensity exercise hyperpnea may induce a small amount of respiratory muscle damage as evidenced by the increases in slow sTnI. Future studies including more time points, different respiratory muscle exercise protocols, and examining the differences between sexes could provide additional insights into the utility of blood biomarkers for identifying respiratory muscle damage. Biomarkers of respiratory muscle damage following volitional hyperpnea.

Cellulose nanocrystals (CNCs), derived from renewable cellulose sources, have emerged as a versatile class of nanomaterial with exceptional mechanical strength, tuneable surface chemistry and inherent biocompatibility. In the scenario of contemporary commercial hydrogel products, which are expensive and rely on synthetic materials, the sustainable origin and unique physicochemical properties have positioned CNCs as promising sustainable functional building blocks for next-generation hydrogels in biomedical applications. Over the past decade, CNC-based hydrogels have gained momentum as soft biomaterials capable of interacting with diverse tissue types, predominantly demonstrated through in vitro cell line studies. This review critically examines the current landscape of research on biomedical applications of CNC-based hydrogels, focusing on their biomedical utility across 22 systematically screened studies. It revealed applications spanning around bone and cartilage tissue engineering, wound healing, medical implants and sensors, and drug delivery. We highlight the predominance of microcrystalline cellulose as the CNC source and sulfuric acid hydrolysis as the preferred extraction method, with several studies incorporating surface modifications to enhance functionality. Despite growing interest, there remains a lack of data for transitioning towards human clinical studies and commercialisation. Hence, this review highlights the pressing need for scalable, sustainable, and affordable CNC-based hydrogel systems that can democratise access to advanced biomedical technologies.

Hydrogel-based products are used in many areas of biomedicine and healthcare. Recently, the incorporation of cellulose nanocrystals (CNC), a renewable and functional nanomaterial, into hydrogels has enhanced their functionality, particularly by imparting mechanical strength and structural integrity. This scoping review aims to appraise the types of biomedical models and assays that have been utilised to investigate the effects of CNC incorporation into hydrogels in tissue engineering, wound healing, medical implantation and drug delivery applications, and reports on the rationale for including these models and assays. A structured literature search was undertaken in major scientific databases (PubMed Central, PubMed, BioMed Central, ScienceDirect, Wiley and EBSCOhost), focusing on identifying primary research published between 2016 and 2024. From this process, fifteen studies providing biomedical analyses met the inclusion criteria. Most of these investigations employed in vitro cell-line models (n = 12), with a smaller number utilising in vivo experimental systems (n = 5). Across the included studies, CNC incorporation typically yielded measurable performance gains: reported compressive or storage modulus improvements of 20–40% over hydrogel-only controls, consistently high cell viability (>85%) across multiple human and murine cell types for up to 21 days, and sustained drug release profiles (days–weeks) in stent and antitumour contexts. Where quantified, functional outcomes in vivo included preserved graft volume (autologous fat grafts) and reduced intimal hyperplasia signals in vascular graft models. Critical gaps included heterogeneous CNC sources and surface chemistries, inconsistent reporting of CNC concentration and hydrogel formulation parameters, the limited duration and scope of biocompatibility testing, and minimal alignment with standard evaluation protocols, constraining reproducibility and cross-study comparability. To date, there are no human clinical trials of CNC-hydrogels. Translational readiness will require standardised ISO-compliant biocompatibility evaluations. Large-animal studies under relevant mechanical and physiological conditions, and rigorous long-term degradation and immunogenicity assessments to de-risk progression to human trials. We recommend standardised CNC sources and surface functionalisation reporting, concentration (wt%) ranges, hydrogel rheological characterisation (G′, G″, swelling), and consistent biological endpoints (viability, differentiation, inflammation panels) to enable robust meta-analyses and translational benchmarking. Distinct from prior nanocellulose reviews that emphasise material synthesis and properties, this analysis centres on the biomedical models and assays applied to CNC-incorporated hydrogels, identifying the methodological convergence and divergence that directly impact translational pathways.

Background: COVID-19 patients experience respiratory muscle damage, leading to reduced respiratory function and functional capacity often requiring mechanical ventilation which further increases susceptibility to muscle weakness. Inspiratory muscle training (IMT) may help mitigate this damage and improve respiratory function and functional capacity. Methods: We studied the effects of IMT on muscle damage biomarkers, respiratory function, and functional capacity in COVID-19 recovered young adults, successfully weaned from mechanical ventilation. Participants were randomly allocated to either an IMT (n = 11) or control (CON; n = 11) intervention for 4 weeks. The IMT group performed 30 dynamic inspiratory efforts twice daily, at 50% of their maximal inspiratory mouth pressure (PMmax) while the CON group performed 60 inspiratory efforts at 10% of pMmax daily. Serum was collected at baseline, week two, and week four to measure creatine kinase muscle-type (CKM), fast skeletal troponin-I (sTnI) and slow sTnI. Results: Time × group interaction effects were observed for CKM and slow sTnI, but not for fast sTnI. Both were lower at two and 4 weeks for the IMT compared to the CON group, respectively. Time × group interaction effects were observed for forced expiratory volume in 1s, forced vital capacity, PMmax and right- and left-hand grip strength. These were higher for the IMT compared to the CON group. Conclusion: Four weeks of IMT decreased muscle damage biomarkers and increased respiratory function and grip strength in recovered COVID-19 patients after weaning from mechanical ventilation.

Recent evidence suggests that numerous long non-coding RNAs (lncRNAs) are dysregulated in cancer, and have critical roles in tumour development and progression. The present study investigated the ghrelin receptor antisense lncRNA growth hormone secretagogue receptor opposite strand (GHSROS) in breast cancer. Reverse transcription-quantitative polymerase chain reaction revealed that GHSROS expression was significantly upregulated in breast tumour tissues compared with normal breast tissue. Induced overexpression of GHSROS in the MDA-MB-231 breast cancer cell line significantly increased cell migration in vitro, without affecting cell proliferation, a finding similar to our previous study on lung cancer cell lines. Microarray analysis revealed a significant repression of a small cluster of major histocompatibility class II genes and enrichment of immune response pathways; this phenomenon may allow tumour cells to better evade the immune system. Ectopic overexpression of GHSROS in the MDA-MB-231 cell line significantly increased orthotopic xenograft growth in mice, suggesting that in vitro culture does not fully capture the function of this lncRNA. This study demonstrated that GHSROS may serve a relevant role in breast cancer. Further studies are warranted to explore the function and therapeutic potential of this lncRNA in breast cancer progression.

Breast cancer is the most diagnosed cancer globally. While the breast cancer prevalence continues to rise, so too do patient survival rates, thus resulting in a large survivor population. Up to 75% of this population report experiencing cancer-related cognitive impairment during their cancer journey, thus reducing their quality of survivorship. This review systematically evaluates the effect of physical activity and exercise training on cerebrovascular function and cognition in breast cancer survivors. Cross-sectional, intervention or observational studies that examined the effect of acute or chronic exercise training or physical activity levels on cerebrovascular function and cognition in female breast cancer survivors were searched for systematically. The 11 included studies were tabulated and described narratively. The included studies primarily focused on aerobic exercise training, while only four studies investigated the effect of resistance exercise training or concurrent training on cerebrovascular function and/or cognition in breast cancer survivors. Collectively, these studies provide preliminary evidence supporting the positive effect of exercise training on cerebrovascular function and cognition in breast cancer survivors, irrespective of their age, stage of breast cancer and treatment regimen. However, more research is required to comprehensively evaluate the effect of exercise training on cerebrovascular function and cognition in breast cancer survivors and the mechanisms leading to these potential improvements.

The peptide hormone ghrelin is a potent orexigen produced predominantly in the stomach. It has a number of other biological actions, including roles in appetite stimulation, energy balance, the stimulation of growth hormone release and the regulation of cell proliferation. Recently, several ghrelin gene splice variants have been described. Here, we attempted to identify conserved alternative splicing of the ghrelin gene by cross-species sequence comparisons. We identified a novel human exon 2-deleted variant and provide preliminary evidence that this splice variant and in1-ghrelin encode a C-terminally truncated form of the ghrelin peptide, termed minighrelin. These variants are expressed in humans and mice, demonstrating conservation of alternative splicing spanning 90 million years. Minighrelin appears to have similar actions to full-length ghrelin, as treatment with exogenous minighrelin peptide stimulates appetite and feeding in mice. Forced expression of the exon 2-deleted preproghrelin variant mirrors the effect of the canonical preproghrelin, stimulating cell proliferation and migration in the PC3 prostate cancer cell line. This is the first study to characterise an exon 2-deleted preproghrelin variant and to demonstrate sequence conservation of ghrelin gene-derived splice variants that encode a truncated ghrelin peptide. This adds further impetus for studies into the alternative splicing of the ghrelin gene and the function of novel ghrelin peptides in vertebrates.

Ghrelin is a 28 amino acid peptide hormone that is expressed in the stomach and a range of peripheral tissues, where it frequently acts as an autocrine/paracrine growth factor. Ghrelin is modified by a unique acylation required for it to activate its cognate receptor, the growth hormone secretagogue receptor (GHSR), which mediates many of the actions of ghrelin. Recently, the enzyme responsible for adding the fatty acid residue (octanoyl/acyl group) to the third amino acid of ghrelin, GOAT (ghrelin O-acyltransferase), was identified. We used cell culture, quantitative real-time reverse transcription (RT)-PCR and immunohistochemistry to demonstrate the expression of GOAT in prostate cancer cell lines and tissues from patients. Real-time RT-PCR was used to demonstrate the expression of prohormone convertase (PC)1/3, PC2 and furin in prostate cancer cell lines. Prostate-derived cell lines were treated with ghrelin and desacyl ghrelin and the effect on GOAT expression was measured using quantitative RT-PCR. We have demonstrated that GOAT mRNA and protein are expressed in the normal prostate and human prostate cancer tissue samples. The RWPE-1 and RWPE-2 normal prostate-derived cell lines and the LNCaP, DU145, and PC3 prostate cancer cell lines express GOAT and at least one other enzyme that is necessary to produce mature, acylated ghrelin from proghrelin (PC1/3, PC2 or furin). Finally, ghrelin, but not desacyl ghrelin (unacylated ghrelin), can directly regulate the expression of GOAT in the RWPE-1 normal prostate derived cell line and the PC3 prostate cancer cell line. Ghrelin treatment (100nM) for 6 hours significantly decreased GOAT mRNA expression two-fold (P < 0.05) in the PC3 prostate cancer cell line, however, ghrelin did not regulate GOAT expression in the DU145 and LNCaP prostate cancer cell lines. This study demonstrates that GOAT is expressed in prostate cancer specimens and cell lines. Ghrelin regulates GOAT expression, however, this is likely to be cell-type specific. The expression of GOAT in prostate cancer supports the hypothesis that the ghrelin axis has autocrine/paracrine roles. We propose that the RWPE-1 prostate cell line and the PC3 prostate cancer cell line may be useful for investigating GOAT regulation and function.

The molecular mechanisms involved in non-small cell lung cancer tumourigenesis are largely unknown; however, recent studies have suggested that long non-coding RNAs (lncRNAs) are likely to play a role. In this study, we used public databases to identify an mRNA-like, candidate long non-coding RNA, GHSROS (GHSR opposite strand), transcribed from the antisense strand of the ghrelin receptor gene, growth hormone secretagogue receptor (GHSR). Quantitative real-time RT-PCR revealed higher expression of GHSROS in lung cancer tissue compared to adjacent, nontumour lung tissue. In common with many long non-coding RNAs, GHSROS is 5′ capped and 3′ polyadenylated (mRNA-like), lacks an extensive open reading frame and harbours a transposable element. Engineered overexpression of GHSROS stimulated cell migration in the A549 and NCI-H1299 non-small cell lung cancer cell lines, but suppressed cell migration in the Beas-2B normal lung-derived bronchoepithelial cell line. This suggests that GHSROS function may be dependent on the oncogenic context. The identification of GHSROS, which is expressed in lung cancer and stimulates cell migration in lung cancer cell lines, contributes to the growing number of non-coding RNAs that play a role in the regulation of tumourigenesis and metastatic cancer progression.