The coronavirus disease (COVID-19) pandemic has resulted in an increasing population that is experiencing a wide range of long-lasting symptoms after recovery from the acute infection. Long COVID refers to this specific condition and is associated with diverse symptoms, such as fatigue, myalgias, dyspnea, headache, cognitive impairment, neurodegenerative symptoms, anxiety, depression, and a sense of despair. The potential of hyperbaric oxygen therapy (HBOT) to improve chronic fatigue, cognitive impairments, and neurological disorders has been established; therefore, the use of HBOT to treat long COVID has also been studied. We conducted a literature search between 1 January 2019 and 30 October 2023, focusing on the clinical efficacy and utility of HBOT for treating long COVID and found ten clinical studies that fit the review topic, including one case report, five one-group pretest-posttest design studies, one safety report from a randomized controlled trial (RCT), and three complete reports of RCTs. Most studies found that HBOT can improve quality of life, fatigue, cognition, neuropsychiatric symptoms, and cardiopulmonary function. Although HBOT has shown some benefits for long COVID symptoms, further rigorous large-scale RCTs are required to establish precise indications, protocols, and post-treatment evaluations.

A rotator cuff tear is a prevalent ailment affecting the shoulder joint. The clinical efficacy of combined therapy remains uncertain for partial rotator cuff tears. In this study, we integrated extracorporeal shockwave therapy (ESWT) with platelet-rich plasma (PRP) injection, juxtaposed with PRP in isolation. Both cohorts exhibited significant improvements in visual analogue scale (VAS), Constant–Murley score (CMS), degrees of forward flexion, abduction, internal rotation, and external rotation, and the sum of range of motion (SROM) over the six-month assessment period. The application of ESWT in conjunction with PRP exhibited notable additional enhancements in both forward flexion (p = 0.033) and abduction (p = 0.015) after one month. Furthermore, a substantial augmentation in the range of shoulder motion (SROM) (p < 0.001) was observed after six months. We employed isobaric tag for relative and absolute quantitation (iTRAQ) to analyze the differential plasma protein expression in serum samples procured from the two groups after one month. The concentrations of S100A8 (p = 0.042) and S100A9 (p = 0.034), known to modulate local inflammation, were both lower in the ESWT + PRP cohort. These findings not only underscore the advantages of combined therapy but also illuminate the associated molecular changes.

Non-traumatic osteonecrosis of the femoral head (ONFH) is a multifactorial disorder in which genetic susceptibility is thought to play an important role, yet the contribution of many candidate genes remains unclear. The catenin beta-1 (CTNNB1) gene encodes β-catenin, a key regulator of the Wnt/β-catenin signaling pathway involved in bone homeostasis and vascular regulation, and may therefore influence susceptibility to non-traumatic ONFH. In this case–control study, genotype data from China Medical University Hospital were analyzed to evaluate the association between CTNNB1 polymorphisms and the risk of ONFH. A total of 609 patients with ONFH and 2436 age- and sex-matched controls were included. Fourteen CTNNB1 single-nucleotide polymorphisms (SNPs) with a minor allele frequency greater than 5% were selected and analyzed using logistic regression under multiple genetic models, with Hardy–Weinberg equilibrium assessed in controls. Two SNPs, rs3774370 and rs11564478, showed significant differences in allele frequencies between cases and controls, with lower minor allele frequencies observed in the ONFH group. Both variants were associated with a reduced risk of ONFH, and these associations remained significant under dominant genetic models. These findings suggest that specific CTNNB1 polymorphisms may confer a protective effect against non-traumatic ONFH and provide further insight into the genetic architecture of this disease.

Background and Objectives: Non-traumatic osteonecrosis of the femoral head (ONFH) is a multifactorial disorder influenced by both environmental and genetic factors. The nuclear receptor subfamily 3 group C member 1 (NR3C1) gene encodes the glucocorticoid receptor, which plays a key role in bone metabolism, vascular regulation, and stress response. This study aimed to investigate the association between NR3C1 polymorphisms and susceptibility to ONFH, with particular emphasis on age-related genetic effects. Materials and Methods: A hospital-based case–control study was conducted using genotyping data from the Taiwan Biobank version 2 (TWBv2) custom array. A total of 609 patients with ONFH and 2436 age- and sex-matched controls were included. Forty-nine single-nucleotide polymorphisms (SNPs) within or near the NR3C1 gene with a minor allele frequency greater than 5% were analyzed. Logistic regression models were applied to estimate odds ratios (ORs) and 95% confidence intervals (CIs) under multiple genetic inheritance models. Age-stratified analyses were also performed. Results: Among the analyzed SNPs, rs28593206 and rs315199 demonstrated nominally significant differences in allele distributions between cases and controls (p = 0.024 and p = 0.009, respectively), with minor alleles showing nominal associations with increased odds of ONFH. Additional exploratory analyses under different genetic models identified several SNPs with nominal associations with ONFH susceptibility, while rs7709864 showed a possible nominal protective association. In age-stratified analyses, several SNPs showed nominal associations with ONFH risk among individuals older than 40 years, whereas no nominally significant associations were observed in younger individuals. Conclusions: This exploratory study suggests that NR3C1 polymorphisms may be nominally associated with susceptibility to ONFH, particularly among individuals older than 40 years. However, because no formal correction for multiple comparisons was performed and detailed etiological data were unavailable, these findings should be interpreted cautiously and regarded as hypothesis-generating rather than clinically applicable evidence. Further studies incorporating larger cohorts, etiological stratification, multiple-testing correction, replication analyses, and functional validation are required to confirm these observations and clarify the underlying biological mechanisms.