Heavy metals are often found in soil and can contaminate drinking water, posing a serious threat to human health. Molecular pathways and curation therapies for mitigating heavy metal toxicity have been studied for a long time. Recent studies on oxidative stress and aging have shown that the molecular foundation of cellular damage caused by heavy metals, namely, apoptosis, endoplasmic reticulum stress, and mitochondrial stress, share the same pathways as those involved in cellular senescence and aging. In recent aging studies, many types of heavy metal exposures have been used in both cellular and animal aging models. Chelation therapy is a traditional treatment for heavy metal toxicity. However, recently, various antioxidants have been found to be effective in treating heavy metal-induced damage, shifting the research focus to investigating the interplay between antioxidants and heavy metals. In this review, we introduce the molecular basis of heavy metal-induced cellular damage and its relationship with aging, summarize its clinical implications, and discuss antioxidants and other agents with protective effects against heavy metal damage.

We aimed to investigate whether the degree of hearing loss with GJB2 mutations could be predicted by distinguishing between truncating and non-truncating mutations and whether the genotype could predict the hearing loss level. Additionally, we examined the progression of hearing loss in individuals monitored for over 2 years for an average of 6.9 years. The proportion of truncating mutations was higher in patients with profound and severe hearing loss, but it was not accurate enough to predict the degree of hearing loss. Via genotype analysis, mutations of the p.Arg143Trp variants were associated with profound hearing loss, while mutations of the p.Leu79Cysfs*3 allele exhibited a wide range of hearing loss, suggesting that specific genotypes can predict the hearing loss level. Notably, there were only three cases of progression in four ears, all of which involved the p.Leu79Cysfs*3 mutation. Over the long-term follow-up, 4000 Hz was significant, and there was a trend of progression at 250 Hz, suggesting that close monitoring at these frequencies during follow-up may be crucial to confirm progression. The progression of hearing loss was observed in moderate or severe hearing loss cases at the time of the initial diagnosis, emphasizing that children with this level of hearing loss need regular follow-ups.

Artificial Intelligence (AI) is a concept whose goal is to imitate human intellectual activity in computers. It emerged in the 1950s and has gone through three booms. We are in the third boom, and it will continue. Medical applications of AI include diagnosing otitis media from images of the eardrum, often outperforming human doctors. Temporal bone CT and MRI analyses also benefit from AI, with segmentation accuracy improved in anatomically significant structures or diagnostic accuracy improved in conditions such as otosclerosis and vestibular schwannoma. In treatment, AI predicts hearing outcomes for sudden sensorineural hearing loss and post-operative hearing outcomes for patients who have undergone tympanoplasty. AI helps patients with hearing aids hear in challenging situations, such as in noisy environments or when multiple people are speaking. It also provides fitting information to help improve hearing with hearing aids. AI also improves cochlear implant mapping and outcome prediction, even in cases of cochlear malformation. Future trends include generative AI, such as ChatGPT, which can provide medical advice and information, although its reliability and application in clinical settings requires further investigation.

Patients with m.3243A>G mutation of mitochondrial DNA develop bilaterally symmetric sensorineural hearing loss. However, it is unclear how fast their hearing loss progresses over time, and whether they experience rapid progression of hearing loss. In the present study, we conducted a long-term hearing evaluation in patients with MELAS or MIDD who harbored the m.3243A>G mutation of mitochondrial DNA. A retrospective chart review was performed on 15 patients with this mutation who underwent pure-tone audiometry at least once a year for more than two years. The mean follow-up period was 12.8 years. The mean progression rate of hearing loss was 5.5 dB per year. Hearing loss progressed rapidly to be profoundly deaf in seven patients during the observation period. Heteroplasmy and age-corrected heteroplasmy levels correlated with the age of onset of hearing loss. These results indicate that patients with m.3243A>G mutation have a gradual progression of hearing loss in the early stages and rapid decline in hearing to be profoundly deaf in approximately half of the patients. Although it is possible to predict the age of onset of hearing loss from heteroplasmy and age-corrected heteroplasmy levels, it is difficult to predict whether and when the rapid hearing loss will occur.

Single-sided deafness (SSD) significantly restricts social participation in hearing/speaking cultures due to the person’s difficulty hearing conversations on their deaf side. Although hearing aids for SSD are effective in social situations, the acceptance rate remains low at 4%. To address this problem, we designed and developed a bone conduction-based device to be worn with eyeglasses, involving 53 individuals with SSD including two authors. We conducted a four-week diary study comparing our proposed device with traditional Contralateral Routing of Signals (CROS) hearing aids and explored the factors that might affect the acceptance rate of assistive devices for SSD. The findings indicated that our design was more acceptable for users with SSD due to its effectiveness, social acceptability, and the ability for wearers to use other devices simultaneously, such as earbuds. Based on our results, we discuss implications for designing wearable assistive devices to promote greater acceptance among the target population.