A number of scholars reported that reproductive factors play a significant role in thyroid cancer and the correlation between the two may affect the diagnosis and treatment of thyroid carcinoma during pregnancy. To determine whether pregnancy reproductive factors affect thyroid carcinoma, we conducted a meta-analysis of studies that investigated the association between pregnancy factors and thyroid carcinoma. PubMed, OVID and the Cochrane Library were searched from their inception to April 1st, 2013. The searched publications mainly investigated reproductive factors and the morbidity or prognosis of female thyroid carcinoma. The studies were filtered by predetermined standards and the quality of the included studies was evaluated by the Newcastle-Ottawa scale inventory. Two researchers independently extracted information on first author, year of publication, study design (case-control or prospective cohort), compared populations, inclusion and exclusion criteria and total sample size. Other researchers assessed the studies for publication bias and performed statistical analyses. Discrepancies were resolved by consensus. A total of 21 studies were selected for the meta-analysis, including 406,329 cases in total. Compared to the control group, the risk of thyroid carcinoma in women with a history of pregnancy was not significantly discrepant, [odds ratio (OR)=1.00, 95% confidence interval (CI): 0.91-1.11]. However, the risk of thyroid carcinoma in women with a history of ≥ 3 pregnancies was significantly increased (OR=1.39, 95% CI: 1.21-1.59). Furthermore, an interval of ≤ 5 years since the last pregnancy was closely associated with thyroid carcinoma (OR=1.53, 95% CI: 1.29-1.81). The patients developed thyroid carcinoma during pregnancy did not exhibit an increased risk of lymphatic metastasis (OR=0.94, 95% CI: 0.53-1.67); the risk of distant metastasis also did not increase significantly (OR=1.03, 95% CI: 0.86-1.24). Therefore, multiple pregnancies and a ≤ 5-year interval between pregnancies were identified as high-risk factors for thyroid carcinoma, whereas thyroid carcinoma during pregnancy was not associated with a significant risk of lymphatic and distant metastasis.

ObjectivesThe objective of the study was to identify the acute high-intensity recreational noise-induced effects on auditory function, especially the cochlear synaptopathy-related audiological metrics, in humans with normal hearing.MethodsThis prospective cohort study enrolled 32 young adults (14 males and 18 females); the mean age was 24.1 ± 2.4 years (ranging from 20 to 29). All participants with normal hearing (audiometric thresholds ≤25 dB HL at frequencies of 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz for both ears) had already decided to participate in the outdoor music festival. Participants were asked to measure the noise exposure dose and complete auditory examinations, including the air-conduction pure-tone audiometry (PTA), distortion product otoacoustic emission (DPOAE), contralateral suppression (CS) on transient evoked otoacoustic emission (TEOAE), auditory brainstem response (ABR) test and Mandarin Hearing in Noise Test (MHINT), at baseline and 1 day and 14 days after music festival noise exposure.ResultsThe mean time of attending the music festival was 7.34 ± 0.63 h (ranging from 6.4 to 9.5), the mean time-weighted average (TWA) of noise exposure dose was 93.2 ± 2.39 dB(A) (ranging from 87.9 to 97.7). At neither 1 day nor 14 days post exposure, there were no statistically significant effects on PTA thresholds, DPOAE amplitudes, CS on TEOAEs, or MHINT signal-to-noise ratios (SNRs) of acute outdoor music festival noise exposure, regardless of sex. While the ABR wave I amplitudes significantly decreased at 1 day after exposure and recovered at 14 days after exposure, the exposed/unexposed ABR wave I amplitude ratio was significantly correlated with MHINT SNR change at 1 day after exposure, although it was not correlated with the noise exposure dose.ConclusionIn young adults with normal hearing, we found the self-compared decrement of ABR wave I amplitudes at 1 day post acute recreational noise exposure at high intensity, which also contributes to the change in speech perceptual ability in noisy backgrounds. This study indicated that auditory electrophysiological metric changes might be a more sensitive and efficient indicator of noise-induced cochlear synaptic dysfunction in humans. More attention should be paid to the recreational noise-induced cochlear synaptopathy and auditory perceptual disorder.

It is widely accepted that even a single acute noise exposure at moderate intensity that induces temporary threshold shift (TTS) can result in permanent loss of ribbon synapses between inner hair cells and afferents. However, effects of repeated or chronic noise exposures on the cochlear synapses especially medial olivocochlear (MOC) efferent synapses remain elusive. Based on a weeklong repeated exposure model of bandwidth noise over 2-20 kHz for 2 hours at seven intensities (88 to 106 dB SPL with 3 dB increment per gradient) on C57BL/6J mice, we attempted to explore the dose-response mechanism of prolonged noise-induced audiological dysfunction and cochlear synaptic degeneration. In our results, mice repeatedly exposed to relatively low-intensity noise (88, 91, and 94 dB SPL) showed few changes on auditory brainstem response (ABR), ribbon synapses, or MOC efferent synapses. Notably, repeated moderate-intensity noise exposures (97 and 100 dB SPL) not only caused hearing threshold shifts and the inner hair cell ribbon synaptopathy but also impaired MOC efferent synapses, which might contribute to complex patterns of damages on cochlear function and morphology. However, repeated high-intensity (103 and 106 dB SPL) noise exposures induced PTSs mainly accompanied by damages on cochlear amplifier function of outer hair cells and the inner hair cell ribbon synaptopathy, rather than the MOC efferent synaptic degeneration. Moreover, we observed a frequency-dependent vulnerability of the repeated acoustic trauma-induced cochlear synaptic degeneration. This study provides a sight into the hypothesis that noise-induced cochlear synaptic degeneration involves both afferent (ribbon synapses) and efferent (MOC terminals) pathology. The pattern of dose-dependent pathological changes induced by repeated noise exposure at various intensities provides a possible explanation for the complicated cochlear synaptic degeneration in humans. The underlying mechanisms remain to be studied in the future.

Background: The definition of notched audiogram for noise-induced hearing loss (NIHL) is presently based on clinical experience, but audiometric phenotypes of NIHL are highly heterogeneous. The data-driven clustering of subtypes could provide refined characteristics of NIHL, and help identify individuals with typical NIHL at diagnosis.Methods: This cross-sectional study initially recruited 12,218 occupational noise-exposed employees aged 18–60 years from two factories of a shipyard in Eastern China. Of these, 10,307 subjects with no history of otological injurie or disease, family history of hearing loss, or history of ototoxic drug use were eventually enrolled. All these subjects completed health behavior questionnaires, cumulative noise exposure (CNE) measurement, and pure-tone audiometry. We did data-driven cluster analysis (k-means clustering) in subjects with hearing loss audiograms (n = 6,599) consist of two independent datasets (n = 4,461 and n = 2,138). Multinomial logistic regression was performed to analyze the relevant characteristics of subjects with different audiometric phenotypes compared to those subjects with normal hearing audiograms (n = 3,708).Results: A total of 10,307 subjects (9,165 males [88.9%], mean age 34.5 [8.8] years, mean CNE 91.2 [22.7] dB[A]) were included, 3,708 (36.0%) of them had completely normal hearing, the other 6,599 (64.0%) with hearing loss audiograms were clustered into four audiometric phenotypes, which were replicable in two distinct datasets. We named the four clusters as the 4–6 kHz sharp-notched, 4–6 kHz flat-notched, 3–8 kHz notched, and 1–8 kHz notched audiogram. Among them, except for the 4–6 kHz flat-notched audiogram which was not significantly related to NIHL, the other three phenotypes with different relevant characteristics were strongly associated with noise exposure. In particular, the 4–6 kHz sharp-notched audiogram might be a typical subtype of NIHL.Conclusions: By data-driven cluster analysis of the large-scale noise-exposed population, we identified three audiometric phenotypes associated with distinct NIHL subtypes. Data-driven sub-stratification of audiograms might eventually contribute to the precise diagnosis and treatment of NIHL.