Objective:To analyze the risk factors of postinflammatory hyperpigmentation (PIH) after laser in the treatment of acquired bilateral nevus of Ota-like macules (ABNOM).Methods:A retrospective study was conducted to follow up 120 patients with acquired bilateral nevus of Ota-like macules in the Department of Laser and Physiotherapy, Guangzhou Institute of Dermatology between January 2011 and December 2018, which accepted 1064-nm Q-switched neodymium: yttrium-aluminum-garnet laser treatment. The difference was analyzed between different age, sex, clinical classification, Fitzpatrick skin classification, ABNOM with melasma and postinflammatory pigmentation after laser treatment. Logistic regression was used to analyze the risk factors of postinflammatory hyperpigmentation after 1064-nm Q-switched neodymium: yttrium-aluminum-garnet laser treatment of acquired bilateral nevus of Ota-like macules.Results:Fifty-three ABNOM patients (44.17%) developed PIH after laser treatment. Univariate analysis showed that age, clinical classification, Fitzpatrick skin classification and the patients with both ABNOM and melasma all affected the occurrence of PIH after laser in the treatment of ABNOM, and the difference was statistically significant ( P<0.01). Logistic regression showed that older age, more severe clinical classification and the presence of ABNOM with melasma were the risk factors of PIH after treatment of ABNOM. Conclusions:ABNOM patients should be treated as early as possible. The risk of inducing PIH is great after laser treatment in patients with more severe clinical classification and patients with both ABNOM and melasma.

Objective To investigate the prevalence of musculoskeletal disorders (MSD) in dentists and to analyze the risk factors of MSD to provide suggestions for preventing and reducing MSD in dentists. Methods Through stratified cluster random sampling, 373 dentists were selected from one Hospital of Stomatolagy and five general hospitals among Three-A hospitals in Wuhan as the research objects. The prevalence of MSD was surveyed using the Nordic musculoskeletal disorders standard questionnaire (NMQ) and Numerical Rating Scale (NRS) of pain measurement, and the risk factors of MSD was analyzed with binary Logistic regression. Results The total MSD annual prevalence rate of dentists was 93.3%, with a prevalence rate in neck, shoulder and back, waist and wrist at 78.3%, 70.0%, 56.0% and 36.2% respectively. Through Binary Logistic regression analysis, it was found that the risk factors associated with neck MSD were work fatigue（χ²=24.00，P=0.000）, neck hunching（χ²=23.55，P=0.000）, and shoulder side lift（χ²=24.52，P=0.000）. The risk factors associated with MSD in shoulder and back were work fatigue（χ²=34.64，P=0.000）, neck twisting（χ²=21.68，P=0.000） and wrist bending（χ²=45.87，P=0.000）. The risk factors associated with waist MSD were age（χ²=29.83，P=0.000）, majors（χ²=16.68，P=0.028）, work fatigue（χ²=21.08，P=0.000）, waist bending（χ²=22.88，P=0.000）. The risk factors associated with wrist MSD were gender（χ²=4.17，P=0.041）, majors（χ²=23.47，P=0.001）, working years（χ²=11.63，P=0.009）, physical activities（χ²=9.14，P=0.028）, number of patient visits per day（χ²=18.41，P=0.000）, bending and twisting（χ²=24.12，P=0.000）, wrist twisting（χ²=34.41，P=0.000）, and prevalence of microscope using（χ²=12.09，P=0.020）, while physical exercise was a protective factor for wrist MSD.The differences of the above-mentioned risk factors were statistically significant (P<0.05). Conclusion The prevalence of MSD in dentists is relatively high, and hospital management should strengthen organizational training to help dentists to realize the importance of adopting correct operating posture, a 5-minute breaks during work, prevent MSD at an early stage.

Oligoasthenospermia is the primary cause of infertility. However, there are still enormous challenges in the screening of critical candidates and targets of oligoasthenospermia owing to its complex mechanism. In this study, stem cell factor (SCF), c-kit, and transient receptor potential vanilloid 1 (TRPV1) biosensors were successfully established and applied to studying apoptosis and autophagy mechanisms. Interestingly, the detection limit reached 2.787 × 10^-15 g/L, and the quantitative limit reached 1.0 × 10^-13 g/L. Furthermore, biosensors were used to investigate the interplay between autophagy and apoptosis. Schisandrin A is an excellent candidate to form a system with c-kit similar to SCF/c-kit with a detection constant (K_D) of 5.701 × 10^-11 mol/L, whereas it had no affinity for SCF. In addition, it also inhibited autophagy in oligoasthenospermia through antagonizing TRPV1 with a K_D of up to 4.181 × 10^-10 mol/L. In addition, in vivo and in vitro experiments were highly consistent with the biosensor. In summary, high-potency schisandrin A and two potential targets were identified, through which schisandrin A could reverse the apoptosis caused by excessive autophagy during oligoasthenospermia. Our study provides promising insights into the discovery of effective compounds and potential targets via a well-established in vitro-in vivo strategy.

The mechanisms underlying autophagic defects in nonalcoholic steatohepatitis (NASH) remain largely unknown. We aimed to elucidate the roles of hepatic cyclooxygenase 1 (COX1) in autophagy and the pathogenesis of diet-induced steatohepatitis in mice. Human nonalcoholic fatty liver disease (NAFLD) liver samples were used to examine the protein expression of COX1 and the level of autophagy. Cox1^Δhepa mice and their wildtype littermates were generated and fed with 3 different NASH models. We found that hepatic COX1 expression was increased in patients with NASH and diet-induced NASH mice models accompanied by impaired autophagy. COX1 was required for basal autophagy in hepatocytes and liver specific COX1 deletion exacerbated steatohepatitis by inhibiting autophagy. Mechanistically, COX1 directly interacted with WD repeat domain, phosphoinositide interacting 2 (WIPI2), which was crucial for autophagosome maturation. Adeno-associated virus (AAV)-mediated rescue of WIPI2 reversed the impaired autophagic flux and improved NASH phenotypes in Cox1^Δhepa mice, indicating that COX1 deletion-mediated steatohepatitis was partially dependent on WIPI2-mediated autophagy. In conclusion, we demonstrated a novel role of COX1 in hepatic autophagy that protected against NASH by interacting with WIPI2. Targeting the COX1-WIPI2 axis may be a novel therapeutic strategy for NASH.