Objective To evaluate the role of hippocampal histone acetylation in isoflurane-induced amnestic effect in mice.Methods Fifty-four male C57BL/6J mice,aged 8 weeks,weighing 18-22 g,were randomly divided into 3 groups (n =18 each) using a random number table:control group (group C),isoflurane group (group ISO) and histone deacetylase inhibitor sodium butyrate group (group SB).Group C inhaled 35％ oxygen for 30 ain,and ISO and SB groups inhaled the mixture of 35 ％ oxygen and 0.4％ isoflurane for 30 min,and then the animals underwent contextual fear conditioning training.After the end of training,normal saline 6 ml/kg was intraperitoneally injected in C and ISO groups,while in group SB,sodium butyrate 1.2 g/kg was intraperitoneally injected.One hour after the end of training,3 mice were sacrificed randomly in each group and their hippocampi were immediately removed for determination of the expression of acetylated histone-H3 (Ac-H3) and Ac-H4 by Western blot.Twenty-four hours after the end of training,contextual fear conditioning test and open field test were conducted.The freezing time,total distance and time of staying at the central zone were recorded.Results Compared with group C,Ac-H3 and Ac-H4 expression was significantly down-regulated,and the percentage of freezing time during testing was decreased in group ISO (P ＜ 0.05).Compared with group ISO,Ac-H3 and Ac-H4 expression was significantly up-regulated,and the percentage of freezing time during testing was increased in group SB (P ＜ 0.05).There was no significant difference in the percentage of freezing time during training,total distance and time of staying in the central zone among the 3 groups (P ＞ 0.05).Conclusion Hippocampal histone acetylation is involved in the regulation of isoflurane-induced amnestic effect in mice.

Objective To develop a special stool collector for paraplegic patients with constipation,and to observe the clinical effects. Methods 52 paraplegic patients with constipation were divided into group A(30 cases) and group B(22 cases ).Group A used type one stool collector and goup B chose type two stool collector. The time of dealing with defecation, exposure time, pollution area, the usage of urinal pad, toilet paper, clean water before and after the special toilets were observed between the two groups. Results Each indicator significantly changed after using two types of stool collectors in the two groups of patients and above were significantly decreased. Conclusions The special stool collector for the paraplegic patients with constipation can effectively avoid the soakage of the anal and buttocks skin, reduce the environment pollution of the odor, reduce labor intensity and lower care costs.

Gut dysbiosis,a well-known risk factor to triggers the progression of Alzheimer's disease(AD),is strongly associated with metabolic disturbance.Trimethylamine N-oxide(TMAO),produced in the dietary choline metabolism,has been found to accelerate neurodegeneration in AD pathology.In this study,the cognitive function and gut microbiota of TgCRND8(Tg)mice of different ages were evaluated by Morris water maze task(MWMT)and 16S rRNA sequencing,respectively.Young pseudo germ-free(PGF)Tg mice that received faecal microbiota transplants from aged Tg mice and wild-type(WT)mice were selected to determine the role of the gut microbiota in the process of neuropathology.Excessive choline treatment for Tg mice was used to investigate the role of abnormal choline metabolism on the cognitive functions.Our results showed that gut dysbiosis,neuroinflammation response,Aβ deposition,tau hyper-phosphorylation,TMAO overproduction and cyclin-dependent kinase 5(CDK5)/transcription 3(STAT3)activation occurred in Tg mice age-dependently.Disordered microbiota of aged Tg mice accelerated AD pathology in young Tg mice,with the activation of CDK5/STAT3 signaling in the brains.On the contrary,faecal microbiota transplantation from WT mice alleviated the cognitive deficits,attenuated neuro-inflammation,Aβ deposition,tau hyperphosphorylation,TMAO overproduction and suppressed CDK5/STAT3 pathway activation in Tg mice.Moreover,excessive choline treatment was also shown to aggravate the cognitive deficits,Aβ deposition,neuroinflammation and CDK5/STAT3 pathway activation.These findings provide a novel insight into the interaction between gut dysbiosis and AD progression,clarifying the important roles of gut microbiota-derived substances such as TMAO in AD neuropathology.

Acute spinal cord injury（ASCI），commonly seen in spinal surgery，is usually caused by mechanical injury to the spine. ASCI can lead to secondary lung injury and even acute respiratory distress syndrome（ARDS），seriously endangering the life safety of patients. Damage-associated molecular pattern（DAMP）is a sort of endogenous substances released after injury，including intracellular proteins，extracellular matrix，secretory factors and nucleic acid-related products. DAMP released after ASCI activates downstream signaling pathways and participates in lung injuries. DAMP-related studies have revealed molecular mechanism of lung injury after ASCI，and explored the possible therapeutic targets of lung injury. In this study，the authors review the mechanism of action of DAMP in lung injury after ASCI and the role of different kinds of DAMP in lung injury，so as to provide new ideas for clinical treatment of lung injury after ASCI.

To investigate the effect of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) on () biofilm. biofilms were constructed on a cell slide and treated with ALA-PDT.According to different light doses,the biofilms were divided into six groups:ALA-PDT group [ALA-PDT1 (50 J/cm),ALA-PDT2 group (100 J/cm),ALA-PDT3 group (200 J/cm)],ALA-only group (ALA group),light-only group (LED),and a negative control group (ALA-PDT-group).The biofilm structure and the ratio of the dead bacteria/live bacteria were observed using a laser confocal microscope (CLSM).Biofilm viability was measured using the XTT assay. CLSM showed that the biofilm structures of ALA group and LED group were not significantly different from that of ALA-PDT-group,whereas the biofilm structure was more seriously damaged in ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group than in the ALA-PDT-group.The ratios of the dead/live bacteria in ALA-PDT-group,ALA group,LED group,ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group were 0.350±0.033, 0.305±0.046, 0.330±0.032, 1.525±0.439, 2.293±0.148 and 3.092±0.189,respectively.ALA group(=0.003, =1.000)and LED group(=-0.025, =1.000)did not significantly differ from the ALA-PDT-group.However,the ratio of dead/live bacteria in ALA-PDT-group was significantly lower than those in ALA-PDT1 group (=-0.162, <0.001),ALA-PDT2 group (=-0.254, <0.001),and ALA-PDT3 group (=-0.352, <0.001).The values of the XTT assay were were 0.462±0.028,0.465±0.044,0.437±0.047,0.301±0.040,0.207±0.001,and 0.110±0.007,respectively,in ALA-PDT-group,ALA group,LED group,ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group.Although the values of XTT assay in ALA(=-0.044, =1.000)and LED groups (=-0.020, =1.000)did not significantly differ from that in ALA-PDT-group,it was significantly higher in ALA-PDT-group than in ALA-PDT1 group (=1.175, <0.001),ALA-PDT2 group (=1.942, <0.001),and ALA-PDT3 group (=-0.352, =2.742, <0.001). ALA-PDT has an inhibitory effect on biofilm.ALA-PDT destroys biofilm structure and inhibits biofilm viability.
Aminolevulinic Acid ; Biofilms ; Photochemotherapy ; Photosensitizing Agents ; Propionibacterium acnes