Objective To observe the effect of repetitive transcranial magnetic stimulation (rTMS) on behavior in response to chronic but unpredictable mild stress and explore potential neuroendocrine mechanisms.Methods Forty adult SD male rats were randomly divided into a control group (n =8) and a model preparation group (n=32).The control group was given normal care while a model of depression was induced in the model preparation group through giving an unpredictable mild stimulus (CUMS).The depressive rats were randomly divided into a model group,an rTMS group and a sham rTMS group (8 cases in each group).The rTMS group and sham rTMS groups accepted the rTMS or sham stimulation for 3 weeks.The changes in behavior in each group were quantified using body weight,sucrose consumption and an open field test before and after stimulation.Enzyme-linked immunosorbent assays (Elisas) were conducted to detect plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels.Reverse-transcription polymerase chain reactions (RT-PCRs) were carried out to allow the detection of mRNA expression in hypothalamus related to levels of adrenocorticotropic hormone releasing hormone (CRH).Results After the modeling there were significant differences between the model preparation group and the control group in terms of weight increase,sucrose consumption and open field test results.After rTMS the rate of weight increase,sucrose consumption and the scores in the open field test of the rTMS group had increased significantly more than in the control group.Elisas showed significantly higher plasma ACTH and CORT levels in the model group as well.The average expression of CRH mRNA in the model group was significantly higher than in either of the other two groups.Conclusions rTMS can relieve depression-like behavior induced by chronic stress,at least in rats.This may be related to a downgrading of the hyperactive functioning of the hypothalamus-pituitary-adrenal axis.

Objective To investigate the expression of miR-155 in rats exposed to PM2.5 and its signifi-cance.Methods Thirty-two 12-weeks-old healthy male SD rats were randomly divided into PM2.5-primary expo-sure group (P1),PM2.5-three times exposure group (P3), saline-control group and blank-control group (O), with 8 rats in each group. The pathological changes of lung tissue of each group were observed by HE staining and the expressions of miR-155 in lung tissue of each group were measured by RT-PCR. The expressions of TNF-α, IL-6 and IL-1β in serum of each group were measured by ELISA.One-way ANOVA and LSD-t test were used for statistical analysis,and Pearson′s correlation analysis was used to evaluate the relationship between the levels of miR-155 and TNF-α,IL-6 and IL-1β. Results The expression of inflammatory cytokines TNF-α,IL-6 and IL-1β in P1 and P3 increased when compared with that in saline control group and blank-control group, and the amount of expression increased with the increase of the number of exposure and dose;the difference between groups was statistically sig-nificant(P<0.01).At the same time,with the increase of the dose and number of PM2.5,the inflammatory damage of lung tissue was enhanced.The expression of miR-155 in lung tissue also increased with the increase of the dose and number of PM 2.5,and it had significantly positive correlation with serum inflammatory cytokines(P<0.01),and had statistical significance. Conclusions The lung tissue of rats exposed to PM2.5 can produce inflammatory injury, and the damage is enhanced with the increase of exposure times and dose.The expression of miR-155 is positively correlated with inflammatory injury in rats.Consequently,miR-155 may participate in PM2.5-induced inflammatory lung injury in rats.

Objective:To explore the protective role and possible mechanism of neural stem cells combined with edaravone in cortical neurons after oxygen-glucose deprivation/reperfusion (OGD-R).Methods:(1) Neural stem cells from brain tissues of SD fetal rats aged 14-16 d were cultured in vitro, and identified with Nestin, glial fibrillary acidic protein (GFAP), and microtubule-associated protein 2 (MAP2) immunofluorescent staining. Expressions of neuron-specific nuclear protein (NeuN) and β-Tubulin were detected by immunofluorescent staining in primary cortical neurons from SD rats born within 24 h. (2) Primary cortical neurons were divided into normal group (normal culture), OGD-R model group (re-oxygenated culture for 24 h after hypoxia for 1.5 h), OGD-R+neural stem cells group (re-oxygenated co-culture with cortical neurons and neural stem cells for 24 h after hypoxia for 1.5 h), OGD-R+edaravone group (re-oxygenated culture for 24 h after hypoxia for 1.5 h; 100 μmol/L edaravone before hypoxia), OGD-R+neural stem cells+edaravone group (re-oxygenated co-culture with cortical neurons and neural stem cells for 24 h after hypoxia for 1.5 h; 100 μmol/L edaravone before hypoxia); 24 h after each treatment, neuron proliferation in each group was detected by cell counting Kit 8 (CCK8), apoptosis rate was detected by flow cytometry, contents of interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) in neuronal supernatant were detected by enzyme-linked immunosorbent assay (ELISA), and real-time quantitative fluorescent polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the mRNA and protein expressions of Notch1, Hes1 and Hes5, respectively. Results:(1) Immunofluorescent staining results showed that neural stem cells were positive for Nestin, GFAP and MAP2, and cortical neurons were positive for NeuN and β-Tubulin; all of them were successfully identified. (2) Compared with normal group, OGD-R model group, OGD-R+neural stem cell group and OGD-R+edaravone group had decreased neuron viability, increased apoptosis, increased supernatant IL-1β and TNF-α contents, and increased Notch1 mRNA and protein expressions, with significant differences ( P<0.05). Compared with OGD-R model group, OGD-R+neural stem cells+edaravone group had increased neuron viability, decreased apoptosis, decreased supernatant IL-1β and TNF-α contents, and decreased mRNA and protein expressions of Hes1 and Hes5, with significant differences ( P<0.05). Compared with the OGD-R model group, OGD-R+edaravone group and OGD-R+neural stem cell+edaravone group had significantly decreased Notch1 mRNA and protein expressions ( P<0.05). Conclusion:Combination of edaravone and neural stem cell therapy can reverse the neuronal damage caused by OGD-R, whose mechanism may be by inhibiting the expressions of inflammatory factors and key signaling molecules in Notch signaling pathway, such as Notch1, Hes1, and Hes5.

The causes of pyogenic liver abscess has been known as biliary tract disease or intrabadominal infection but the large proportions of the patients has no apparent underlying disorders. Recently colonic mucosal lesions were reported in patients with cryptogenic liver abscess and it has been suggested that colonic mucosal break may play a role in developing liver abscess in otherwise healthy patients. We experienced a patient of severe recurrent liver abscess complicated with endophthalmitis only 3 months after successful treatment of initial cryptogenic liver abscess and a polypoid colon cancer was discovered by chance. It seems prudent to proceed colonoscopic examination in patients with cryptogenic liver abscess especially when it is recurrent.
Biliary Tract Diseases ; Colon ; Colonic Neoplasms ; Endophthalmitis ; Humans ; Klebsiella pneumoniae ; Liver ; Liver Abscess ; Liver Abscess, Pyogenic ; Recurrence

Objective:To report a case with frontotemporal dementia (FTD) characterized by involuntary laughter.Methods:The clinical manifestations and imaging characteristics of a patient diagnosed as FTD was analyzed. Then the results of cerebrospinal fluid, positron emission tomography-computed tomography (PET-CT) and single-photon emission computed tomography examinations were collected. Blood samples were tested for related genes of FTD.Results:The patient is a 66 years old woman with insidious onset and progressing symptoms and she was mainly manifested as laughing out loud involuntarily when looking at others, childishness, stubbornness, loss of interest, irritability and other personal changes. Mild motor and language disorders were also manifested as moving slowly and speaking unclearly. The magnetic resonance imaging showed the atrophy of bilateral frontal, temporal lobe and bilateral hippocampal while the image of PET-CT showed the metabolism was reduced in different degrees. Eventually, behavioural variant of FTD was diagnosed. The result of ANXA11 gene sequencing revealed the mutation of c.107C>G(p.P36R).Conclusions:This is the first case in which a heterozygous mutation of ANXA11 gene, which is related to amyotrophic lateral sclerosis (ALS), is found in simple FTD patient, suggesting that ANXA11 gene may play an important role in the pathogenesis of FTD. This further supports the theory that ALS and FTD are spectrum disorders.