In medical adverse events, medical workers involved tend to become the second victims due to physical and mental injuries, next to the patient in question and his/her family. This article introduced second victim from the following perspectives of such victims: current situation and causes, traumatic experience, natural recovery process and supportive actions taken. These authors provided hospital management with suggestions on how to effective support such victims, in an effort to draw attention of the society to physical and mental health of the medical staff, and minimize injuries so incurred to such victims.

Objective To explore the relationship among depression,anxiety and social support in elderly patients in community outpatient clinic. Methods A total of 551 elderly outpatients from two com-munity health service centers of Hongkou District in Shanghai were evaluated with patient health question-naire-9 (PHQ-9),generalized anxiety disorder-7 (GAD-7),perceived social support scale( PSSS) for de-pression,anxiety,physical health and social support. Results The prevalence rates of depression and anxiety were 26. 1% and 17. 2%,respectively. The scores of PHQ-9 and GAD-7 were 2. 0(4. 0) and 1. 0(2. 0). There were statistically significant differences in the scores of family support,friend support,other support and social support among the elderly patients with different degrees of depression or anxiety (P<0. 01). Fam-ily support(B=-0. 196) and friend support(B=-0. 171) were protective factors of depression in elderly pa-tients in community outpatient clinic. Age,family support and friend support were protective factors of anxiety in elderly patients,while gender and fluctuation of physical diseases were protective factors of anxiety(P<0. 05). Con-clusions The depression and anxiety is intimately related to social support in elderly outpatients. Appropriate measures should be taken to optimize social support,mitigate bad mood negative improve their quality of life.

Objective: To investigate the specificity of endogenous metabolic profile in plasma of patients with occupational acute methyl acetate poisoning using non-targeted metabolomics. Methods: A total of six patients with occupational acute methyl acetate poisoning were selected as the poisoning group, while 10 healthy workers without occupational exposure history of chemical hazards in the same industry were selected as the control group using the judgment sampling method. Metabolites in patient plasma of the two groups were detected using ultra-high performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry, and non-targeted metabolomics analysis was performed. Principal component analysis and partial least squares discriminant analysis were used to identify differential metabolites and analyze their metabolic pathways. Results: There were significant differences in metabolite profiles in patient plasma between poisoning group and control group. A total of 195 differentially expressed metabolites were screened in plasma of patients in poisoning group, including 119 upregulated and 76 downregulated metabolites. Lipid substances (lipids and lipid-like molecules) accounted for the highest proportion (21.5%). The differential metabolites of poisoning group were related to folate biosynthesis, amino acid metabolism, pyrimidine metabolism, sphingolipid biosynthesis and other metabolic pathways in plasma compared with the control group (all P<0.05). Conclusion: Occupational acute methyl acetate poisoning affects metabolism of the body. The folic acid biosynthesis, amino acid and lipid metabolism and other pathways may be involved in the occurrence and development of poisoning.

The anterior disc displacement (ADD) leads to temporomandibular joint osteoarthritis (TMJOA) and mandibular growth retardation in adolescents. To investigate the potential functional role of fibrocartilage stem cells (FCSCs) during the process, a surgical ADD-TMJOA mouse model was established. From 1 week after model generation, ADD mice exhibited aggravated mandibular growth retardation with osteoarthritis (OA)-like joint cartilage degeneration, manifesting with impaired chondrogenic differentiation and loss of subchondral bone homeostasis. Lineage tracing using Gli1-CreER⁺; Tm^fl/-mice and Sox9-CreER⁺;Tm^fl/-mice showed that ADD interfered with the chondrogenic capacity of Gli1⁺ FCSCs as well as osteogenic differentiation of Sox9⁺ lineage, mainly in the middle zone of TMJ cartilage. Then, a surgically induced disc reposition (DR) mouse model was generated. The inhibited FCSCs capacity was significantly alleviated by DR treatment in ADD mice. And both the ADD mice and adolescent ADD patients had significantly relieved OA phenotype and improved condylar growth after DR treatment. In conclusion, ADD-TMJOA leads to impaired chondrogenic progenitor capacity and osteogenesis differentiation of FCSCs lineage, resulting in cartilage degeneration and loss of subchondral bone homeostasis, finally causing TMJ growth retardation. DR at an early stage could significantly alleviate cartilage degeneration and restore TMJ cartilage growth potential.
Animals ; Mice ; Osteogenesis ; Zinc Finger Protein GLI1 ; Fibrocartilage ; Temporomandibular Joint ; Disease Models, Animal ; Osteoarthritis ; Stem Cells ; Growth Disorders