Thoracic trauma is responsible for approximately 25% of trauma deaths, and rib fractures are present in as many as 40-80% of patients, and intensive care and/or ventilator support are frequently required for these patients. To identify their risk factors would improve treatment strategies for these patients. Between March 2005 and December 2013, consecutive patients with blunt thoracic trauma, who were admitted to the Department of Thoracic Surgery at Tungs' Taichung Metro Harbor Hospital (Taichung, Taiwan), were reviewed in this retrospective cohort study with the approval of the Institutional Review Board. The duration of hospital stay, ventilator support, injury severity score (ISS), type of injury, associated injuries, treatments, and mortality were analyzed statistically. A total of 1621 thoracic trauma patients were included in this study, with a male majority and an age range of 18-95 years (mean age, 51.2 years). Approximately 11.7% of these patients had an ISS ≥ 16 and a mortality rate of 6.9%. Among them, 78.5% had rib fractures; 31.8%, traumatic hemothorax; 15.6%, pneumothorax; 9.6%, hemopneumothorax; and 4.6%, lung contusion. The most common associated injury was extremity fracture, followed by head injury and clavicle fracture. Surgery on the extremities (20.6% of patients) and chest tube placement (22.7% of patients) were the most common treatments. The number of rib fractures was associated with prolonged hospital and intensive care unit (ICU) stays (≥7 days), an ISS ≥ 16, and pulmonary complications of hemothorax, pneumothorax, and hemopneumothorax, but not with mechanical ventilator use. Furthermore, old age was significantly associated with rib fractures in patients with thoracic trauma. The severity of traumatic rib fractures was identified in this study. Therefore, a trauma team needs better preparation to provide effective treatment strategies when encountering thoracic trauma patients, especially patients who are older and have rib fractures.

Umbilical cord-derived mesenchymal stromal cells (UCMSCs) have potential applications in regenerative medicine. UCMSCs have been demonstrated to repair tissue damage in many inflammatory and degenerative diseases. We have previously shown that UCMSC exosomes reduce nerve injury-induced pain in rats. In this study, we characterized UCMSC exosomes using RNA sequencing and proteomic analyses and investigated their protective effects on cisplatin-induced hearing loss in mice. Two independent experiments were designed to investigate the protective effects on cisplatin-induced hearing loss in mice: (i) chronic intraperitoneal cisplatin administration (4 mg/kg) once per day for 5 consecutive days and intraperitoneal UCMSC exosome (1.2 μg/μL) injection at the same time point; and (ii) UCMSC exosome (1.2 μg/μL) injection through a round window niche 3 days after chronic cisplatin administration. Our data suggest that UCMSC exosomes exert protective effects in vivo. The post-traumatic administration of UCMSC exosomes significantly improved hearing loss and rescued the loss of cochlear hair cells in mice receiving chronic cisplatin injection. Neuropathological gene panel analyses further revealed the UCMSC exosomes treatment led to beneficial changes in the expression levels of many genes in the cochlear tissues of cisplatin-injected mice. In conclusion, UCMSC exosomes exerted protective effects in treating ototoxicity-induced hearing loss by promoting tissue remodeling and repair.

Whether exposure to air pollution is associated with developing sensorineural hearing loss (SHL) remains controversial. Using data from the National Health Insurance Research Database, we recruited a total of 75,767 subjects aged older than 20 years with no history of SHL from 1998 to 2010, and they were followed up until SHL was observed, they withdrew from the National Health Insurance program, or the study ended. The subjects were evenly exposed to low-level, mid-level, and high-level carbon monoxide (CO) and nitrogen dioxide (NO₂). The incidence rate ratio of SHL for patients exposed to high-level CO was 1.24 (95% confidence interval (CI) = 1.14–1.36). The NO₂ pollutants increased the incidence rate ratios of SHL in mid-level NO₂ and high-level NO₂ exposures by 1.10 (95% CI = 1.10–1.32) and 1.36 (95% CI = 1.24–1.49) times, respectively. The adjusted hazard ratio (adj. HR) of SHL in patients exposed to high-level CO was 1.45 (95% CI = 1.31–1.59), relative to that of patients exposed to low-level CO. Compared to patients exposed to low-level NO₂, patients exposed to mid-level NO₂ (adj. HR = 1.40, 95% CI = 1.27–1.54) and high-level NO₂ (adj. HR = 1.63, 95% CI = 1.48–1.81) had a higher risk of developing SHL. The increased risk of SHL following the increased concentrations of air pollutants (CO and NO₂) was statistically significant in this study. In conclusion, the subjects’ exposure to air pollution exhibited a significantly higher risk of developing SHL in Taiwan.

Mitochondrial DNA (mtDNA) copy number correlates with tumor pathology in some cancers. To investigate mtDNA copy number in head and neck cancer (HNC). mtDNA copy number was determined and compared between HNC patients and malignancy-free controls. The mtDNA copy number was significantly higher in HNC patients, increased with cancer progression and correlated negatively with patient survival. mtDNA copy number appears to be associated with HNC stage and survival, but confirmation requires similar studies in larger cohorts. Studies to establish the nature of the relationship between mtDNA copy number and HNC are warranted.

Lung cancer is the leading cause of cancer deaths among Taiwanese women. Human papillomavirus (HPV) has been detected in lung cancer tissues. The aim of this study was to investigate the association between HPV infection and lung cancer among the Taiwanese women. The analytical data were collected from the longitudinal health insurance databases (LHID 2005 and 2010) of the National Health Insurance Research Database (NHIRD). The study participants were 30 years and older and included 24,162 individuals who were identified with HPV infection from 2001 to 2004 and 1,026,986 uninfected individuals. Lung cancer incidence among infected and uninfected individuals was compared using the univariate and multivariate regression models. Among the total participants, 24,162 individuals were diagnosed with HPV. After adjusting for age, gender, low income, residential area, and comorbidity, the risk of lung cancer was higher in women (hazard ratio [HR] 1.263, 95% CI 1.015-1.571), while all cancer risks were high in both men and women with corresponding hazard ratios (HR) of 1.161 (95% CI 1.083-1.245) and HR 1.240 (95% CI 1.154-1.331), respectively. This study showed a significant increase in lung cancer risk among Taiwanese women who were exposed to HPV infection.

Background: The association between exposure to air pollution and sudden sensorineural hearing loss (SSNHL) has not been extensively discussed in the literature. Therefore, we conducted this nationwide study to evaluate the risk of SSNHL in Taiwanese residents with exposure to air pollution.Methods: We enrolled subjects aged older than 20 years with no history of SSNHL from 1998 to 2010, and followed up until developing SSNHL, withdrawn from the National Health Insurance program, and the end of the database (2011/12/31). The air quality data are managed by Taiwan Environmental Protection Administration. The annual concentrations of PM_2.5, SO₂, CO, NO, and NO₂from 1998 to 2010 were classified into the three levels according to tertiles. We calculated the annual average of pollutants from baseline until the end of the study, and classified into tertiles. The adjusted hazard ratio (aHR) was estimated by using the multivariate Cox proportional hazard model.Results: When considered continuous air pollutants concentration, subjects who exposed with higher concentration of CO (aHR = 2.16, 95% CI 1.50–3.11), NO (aHR = 1.02, 95% CI 1.01–1.03), and NO₂(aHR = 1.02, 95% CI 1.01–1.04) developing significant higher risk of SSNHL. When classified air pollutants concentration into low, moderate and high level by tertiles, and selected low level as reference, patients exposed with moderate (aHR = 1.56, 95% CI 1.20–2.04) or high level (aHR = 1.33, 95% CI 1.01–1.75) of PM_2.5showed significant higher risk of developing SSNHL.Conclusion: This study indicated an increased risk of SSNHL in residents with long-term exposure to air pollution. Nevertheless, further experimental, and clinical studies are needed to validate the study findings.