Objective To investigate the changes of hippocampal neurogenesis and cognitive dysfunction induced by cranial radiation therapy.Methods C57BL/6J mice aged 10 d were subjected to 10 Gy whole brain irradiation with 6 MV X-rays to develop irradiation-induced brain injury model.Morris water maze was designed to estimate spatial learning and memory.At different time post irradiation,brain tissue was removed to stain with hematoxylin-eosin for the pathological results.DCX and PCNA immunohistochemical staining was used to mark the level of neurogenesis in the hippocampus,and ED1immunohistochemical staining to mark the activation of microglia.The TUNEL assay was used to assess the apoptotic neuron death in situ in the hippocampus.Real-time PCR was supplied to inspect the expression of TNF-α and IL-1 β mRNA.Enzyme Linked Immunosorbent Assay (ELISA) was tested for the concentration of TNF-αt in the plasma.Results Pathological studies demonstrated that radiation could induce interstitial edema,inflammatory cell infiltration,cell degeneration,necrosis,apoptosis in the acute phase,edema subsiding,reduction of inflammatory cells,and cytothesis in the dentate gyrus of the hippocampus.IHC studies revealed that,at different time post irradiation,the number of DCX-positive cells and PCNA-positive cells decreased (F =4.9-12.5,5.2-15.7,P ＜ 0.05) but ED1-positive cells increased significantly (F =20.8,P ＜ 0.05).TUNEL-positive cells began to appear in the dentate gyrus of hippocampus 6 h post-irradiation,and its number reached to the highest level at 48 h post-irradiation (F =15.1,P ＜ 0.05).The formation of γ-H2AX foci got at the top 0.5 h post-irradiation (F =18.4,P ＜0.05) and then decreased.After irradiation,the expressions of TNF-α and IL-1β mRNA in the the irradiated group was higher than those of the control group (t =16.3,12.7,P ＜ 0.05).The concentration of TNF-α in the plasma of the irradiated group was higer than that in the control group 3 h post-irradiation,and maximized at 1 week post-irradiation (F =10.5,P ＜ 0.05).Morris water maze tests showed that the latency had no significant differences between the irradiated group and the control group at 1,2,3 d postirradiation,but the latency in the irradiated group was longer than that in the control group with a significant differences at 4,5,6 d post-irradiation (F =7.01,8.17,4.22,P ＜ 0.05).Conclusions Irradiation-induced cognitive dysfunction may be caused by microglial activation and suppression in hippocampal neurogenesis following cranial radiation therapy.

To report a case of nonbullous neutrophilic lupus erythematosus. A 57-year-old male patient presented with recurrent erythematous pruritic papules and plaques on the trunk and extremities for over 10 years. Skin examination revealed scattered urticaria-like papules and plaques on the trunk and limbs, with thin scales on the edge of some lesions. Laboratory tests showed positive antinuclear antibodies at a titer of 1∶320 (granular type), anti-Sj?gren syndrome A (SSA) antibodies (++), anti-SSB antibodies (+++), anti-Ro-52 antibodies (+++), and anti-neutrophil cytoplasmic antibodies at a level of 369.09 RU/ml (reference range: 0 - 20 RU/ml). Histopathological analysis of the skin lesions on the back revealed epidermal hyperkeratosis in a basket-like shape, liquefaction degeneration of basal cells, infiltration of numerous neutrophils in the superficial dermis with karyorrhexis, perivascular infiltration of lymphocytes in the superficial and middle dermis, and extensive extracellular mucin deposition throughout the dermis. Finally, the patient was diagnosed with nonbullous neutrophilic lupus erythematosus.

OBJECTIVE To investigate the treatment plan for az treonam-resistant metallo- β-lactamase（MBL）-producing Enterobacteriaceae infection in pediatric solid organ transplant recipients. METHODS The clinical data of aztreonam-resistant MBL-producing Klebsiella pneumoniae caused intra-abdominal infection of an infant after liver transplantation were retrospectively analyzed. Abdominal infection occurred after operation. The pathogenic bacterium was MBL-producing K. pneumoniae . The drug sensitivity results showed that the infant was resistant to aztreonam. Based on the results of sensitivity test ，polymyxin B combined with tigecycline were selected as initial regimen. The treatment effect was poor ，with recurrent disease and shock spots. The clinical pharmacist assisted the clinician to formulate treatment regimen of ceftazidime avibactam 0.5 g，q8 h combined with aztreonam 0.18 g，q6 h. Relevant domestic and foreign literature were reviewed ，and the treatment plan of MBL-producing Enterobacteriaceae infection after solid organ transplantation was summarized. RESULTS & CONCLUSIONS The infant was finally cured and discharged with ceftazidime avibatan combined and aztreonam. Several foreign literature reported that ceftazidime avibactam combined with aztreonam could effectively treat the infection caused by aztreonam-resistant MBL-producing Enterobacteriaceae infection in patients with organ transplantation. It is expected to be an effective treatment for aztreonam-resistant MBL-producing Enterobacteriaceae infection in pediatric solid organ transplant recipients.