Objective To investigate cognitive strategies of emotion regulation in subjects with panic disorder (PD).Methods Subjects were 51 patients with PD and 54 healthy controls individually matched by age,sex and educational level.Cognitive Emotion Regulation Questionnaire (CERQ) were obtained from both panic and control group.Twenty-three panic disorder patients and 22 healthy controls completed a validated passive cognitive reappraisal task.Results (1) PD group scored significantly lower on the strategies of positive focus (4.4± 1.3 vs 5.4±1.3),positive reappraisal (4.9±2.0 vs 6.5±2.0) and putting into perspective (4.8±1.8 vs 6.2±1.9),and significantly higher on the strategies of catastrophizing (7.1 ±2.0 vs 4.5± 1.8) and rumination (6.8±2.2 vs 3.9± 1.9)than control group (P＜0.05).(2) In cognitive reappraisal task,significant picture type × group interactions were found in both valence and arousal 9-point scales (P＜0.05).Conclusion PD patients show obvious impairment of emotion regulation,and cognitive reappraisal defect may play an important role in it.

Objective To study the effect of Pleurotus eryngii polysaccharide on aging mice induced by D-galactose (D-gal). Methods 72 ICR mice were divided into high, moderate, and low dosages (of polysaccharide) groups, piracetam group, model group, and control group, 12 in each group. The model of aging mice was induced with D-gal. They were tested with Y-maze, and the contents of superoxide dismutase (SOD), malondialdehyde (MDA), lipofuscin and L-glutamate in cerebrum were determined 6 weeks after model. Results Compared with the model group, the achievement of Y-maze improved, the activities of SOD increased and the content of MDA and lipofuscin decreasd in high and moderate dosage groups (P<0.05), while the mass of brain and kidney increased and the L-glutamate decreased in the high dosage group (P<0.05). Conclusion Pleurotus eryngii polysaccharide can ameliorate aging of mice induced by D-gal.

Objective: To explore experience of wound treatment of extremely severe mass burn patients involved in August 2nd Kunshan factory aluminum dust explosion accident. Methods: On August 2nd, 2014, 98 extremely severe burn mass patients involved in August 2nd Kunshan factory aluminum dust explosion accident were admitted to 20 hospitals in China. The patients with complete medical record were enrolled in the study and divided into microskin graft group with 56 patients and Meek skin graft group with 42 patients. Split-thickness skin in area of residual skin were resected to repair wounds of patients in microskin graft group and Meek skin graft group by microskin grafting and Meek miniature skin grafting, respectively. The residual wound size on 28 days post injury and wound infection after skin grafting of patients in the two groups, and position of donor site of all patients were retrospectively analyzed. Data were processed with t test and chi-square test. Results: The size of residual wound of patients in Meek skin graft group on 28 days post injury was (59±13)% total body surface area (TBSA), which was obviously smaller than that in microskin graft group [(70±14)%TBSA, t=4.379, P<0.05]. Twenty-nine patients in microskin graft group and 11 patients in Meek skin graft group suffered from obvious wound infection after skin grafting. Wounds of patients in two groups were repaired with residual skin around wound in head, trunk, groin, armpit, and uncommon donor sites of scrotum (4 patients), vola (10 patients), and toe or finger web (8 patients). Conclusions Meek skin graft is the first choice for wound repair of extremely severe burn mass patients, with faster wound healing, less wound infection. Uncommon donor sites of scrotum, vola, and toe or finger web can also be used for wound repair in case of lack of skin.

Peripheral bacterial infections without impaired blood-brain barrier integrity have been attributed to the pathogenesis of Parkinson's disease (PD). Peripheral infection promotes innate immune training in microglia and exacerbates neuroinflammation. However, how changes in the peripheral environment mediate microglial training and exacerbation of infection-related PD is unknown. In this study, we demonstrate that GSDMD activation was enhanced in the spleen but not in the CNS of mice primed with low-dose LPS. GSDMD in peripheral myeloid cells promoted microglial immune training, thus exacerbating neuroinflammation and neurodegeneration during PD in an IL-1R-dependent manner. Furthermore, pharmacological inhibition of GSDMD alleviated the symptoms of PD in experimental PD models. Collectively, these findings demonstrate that GSDMD-induced pyroptosis in myeloid cells initiates neuroinflammation by regulating microglial training during infection-related PD. Based on these findings, GSDMD may serve as a therapeutic target for patients with PD.