Abstract Background Clonorchis sinensis infection could trigger strong immune responses in mice and humans. However, whether the C.sinensis infection has an impact on arthritis is unknown. Here we investigated the effect of C.sinensis infection on type II collagen-induced arthritis in BALB/c mice. Results The mice were firstly infected with 45 C.sinensis metacercariae by oral gavage. Four weeks later, arthritis in mice was induced by type II collagen. Joint inflammation with severe redness and swelling in hind paws was observed in type II collagen-induced arthritis (CIA) mice. Besides, the physical activity was significantly reduced, but the respiratory exchange ratio was increased in CIA mice. Compared with CIA mice, C.sinensis infection could increase the severity of arthritis in CIA mice, based on the results of disease score and pathological changes. Compared to CIA mice, increased neutrophils and Ly6C hi monocytes, decreased B cells and CD4 + T cells, were found in C.sinensis infected CIA mice. Besides these, C.sinensis infected mice also displayed significantly higher levels of serum IL-4 and IL-17 than those in CIA mice. Conclusions Taken together, our data suggest that C.sinensis infection have a bad effect on arthritis, and could induce the abnormality of the immune response in mice with CIA.
Abstract Although pain is frequently accompanied with depression, little is known about the risk factors contributing to individual differences to the comorbidity of pain and depression. In this study, we examined whether cytokines and brain-derived neurotrophic factor (BDNF) might contribute to the individual differences in the development of neuropathic pain-induced depression. Rats were randomly subjected to spared nerved ligation (SNI) or sham surgery. The SNI rats were divided into two groups by the data from depression-related behavioral tests. Rats with depression-like phenotype displayed higher levels of pro-inflammatory cytokines (e.g., interleukin (IL)-1β, IL-6) as well as imbalance of pro/anti-inflammatory cytokines compared with rats without depression-like phenotype and sham-operated rats. Levels of BDNF in the prefrontal cortex of rats with depression-like phenotype were lower than those of rats without depression-like phenotype and sham-operated rats. A single dose of ketamine ameliorated depression-like behaviors in the rats with depression-like phenotype. Interestingly, higher serum levels of IL-1β and IL-6 in the rat with depression-like phenotype were normalized after a single dose of ketamine. These findings suggest that alterations in the inflammatory cytokines and BDNF might contribute to neuropathic pain-induced depression, and that serum cytokines may be predictable biomarkers for ketamine’s antidepressant actions.
Objective To determine the role of Video-assisted thoracoscopic surgery in spontaneous hemopneumothorax(SPH).Methods From feburary 2005 to august 2011,15 patients with spontaneous hemopneumothorax were treated.Results All 15 operations were successfully performed.14 patients were successfully received in Video-assisted thoracoscopic surgery and 1 patient was treated with open thoracotomy.The outcome of the operation revealed mean operation time of 57 minutes(rang from 30~128 minutes),mean drainage of 168 ml during 24 hours after operation.The mean time for chest tube removal was 2.9 days(rang from 1~6 days),and the mean postoperative stay was 8.2 days(rang from 4~12 days).All patients recovered well after surgery and had no perioperative complications or postoperative complications.Conclusion VATS was an safe,minimal invasion and feasible treatment for patients with spontaneous hemopneumothorax.
Postoperative cognitive decline (POCD) is a recognized clinical phenomenon characterized by cognitive impairments in patients following anesthesia and surgery, yet its underlying mechanism remains unclear. Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal plasticity, learning, and memory via activation of TrkB-full length (TrkB-FL) receptors. It has been reported that an abnormal truncation of TrkB mediated by calpain results in dysregulation of BDNF/TrkB signaling and is associated with cognitive impairments in several neurodegenerative disorders. Calpains are Ca2+-dependent proteases, and overactivation of calpain is linked to neuronal death. Since one source of intracellular Ca2+ is N-methyl-d-aspartate receptors (NMDARs) related and the function of NMDARs can be regulated by neuroinflammation, we therefore hypothesized that dysregulation of BDNF/TrkB signaling mediated by NMDAR/Ca2+/calpain might be involved in the pathogenesis of POCD.In the present study, 16-month-old C57BL/6 mice were subjected to exploratory laparotomy with isoflurane anesthesia to establish the POCD animal model. For the interventional study, mice were treated with either NMDAR antagonist memantine or calpain inhibitor MDL-28170. Behavioral tests were performed by open field, Y maze, and fear conditioning tests from 5 to 8 days post-surgery. The levels of Iba-1, GFAP, interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), NMDARs, calpain, BDNF, TrkB, bax, bcl-2, caspase-3, and dendritic spine density were determined in the hippocampus.Anesthesia and surgery-induced neuroinflammation overactivated NMDARs and then triggered overactivation of calpain, which subsequently led to the truncation of TrkB-FL, BDNF/TrkB signaling dysregulation, dendritic spine loss, and cell apoptosis, contributing to cognitive impairments in aging mice. These abnormities were prevented by memantine or MDL-28170 treatment.Collectively, our study supports the notion that NMDAR/Ca2+/calpain is mechanistically involved in anesthesia and surgery-induced BDNF/TrkB signaling disruption and cognitive impairments in aging mice, which provides one possible therapeutic target for POCD.
Abstract Background Toxoplasma gondii ( T. gondii ) is a neuroinvasive parasite causing neuroinflammation, which in turn is associated with a higher risk for several psycho-behavioral disorders. There is an urgent need to identify drugs capable of improving cognitive deficits induced by T. gondii infection. β-Glucan, an active ingredient in mushrooms, could significantly enhance immunity. However, the effects of β-glucan against neuroinflammation and cognitive decline induced by T. gondii infection remain unknown. The present study aimed to investigate the neuroprotective effect of β-glucan on goal-directed behavior of mice chronically infected by T. gondii Wh6 strain. Methods A mice model of chronic T. gondii Wh6 infection was established by infecting mice by oral gavage with 10 cysts of T. gondii Wh6. Intraperitoneal injection of β-glucan was manipulated 2 weeks before T. gondii infection. Performance of the infected mice on the Y-maze test and temporal order memory (TOM) test was used to assess the goal-directed behavior. Golgi-Cox staining, transmission electron microscopy, immunofluorescence, real-time PCR and western blot assays were used to detect prefrontal cortex-associated pathological change and neuroinflammation. Results The administration of β-glucan significantly prevented T. gondii Wh6-induced goal-directed behavioral impairment as assessed behaviorally by the Y-maze test and TOM test. In the prefrontal cortex, β-glucan was able to counter T. gondii Wh6-induced degeneration of neurites, impairment of synaptic ultrastructure and decrease of pre- and postsynaptic protein levels. Also, β-glucan significantly prevented the hyperactivation of pro-inflammatory microglia and astrocytes, as well as the upregulation of proinflammatory cytokines caused by chronic T. gondii Wh6 infection. Conclusions This study revealed that β-glucan prevents goal-directed behavioral impairment induced by chronic T. gondii infection in mice. These findings suggest that β-glucan may be an effective drug candidate to prevent T. gondii- associated psycho-behavioral disorders including goal-directed behavioral injury. Graphical Abstract
Interleukin 18(IL_18)is a novel potent inducer of IFN_γ production and plays an important role in Th1 type immune response.In this study,specific primers for chicken inteleukin_18(chIL_18)cDNA have been designed and synthesized according to the previously reported nucleic acid sequence of chicken interleukin_18 cDNA.Using total RNA from ConA_stimulated chicken splenocytes,chicken IL_18 cDNA encoding mature protein was amplified by reverse transcription polymerase chain reaction(RT_PCR).Sequence analysis indicated that there is one nucleotide different from the pubilshed chIL_18 cDNA sequence in 482(T_C).It is the first chicken IL_18 cDNA that has been cloned in China and this study has paved a way for future study about the expression and biological function of chIL_18.
To construct the yeast two-hybrid bait vectors with VP1,VP2 and VP3 genes of chicken anemia virus(CAV) and identify their self-activations,the VP1,VP2 and VP3 genes were amplified by PCR from the CAV M9905 strain total genomic DNA and then cloned them into pDEST32 and pDEST22 vectors using Gateway technology,respectively.The restriction enzyme digestion,PCR and sequence analysis were performed to confirm the fact that those genes had been inserted successfully into the vectors,then pDEST32-VP1/VP2/VP3,pDEST22,pDEST22-VP1/VP2/VP3 and pDEST32 were co-transformed into the yeast strain Mav203 by PE g/LiAC method and amplified by yeast in 3AT plates with SC/-Leu/-Trp/-His,SC/-Leu/-Trp/-Ura and YPAD with NC filter and their self-activations were tested by both selective plate and X-gal assay.The yeast two-hybrid tests showed that Mav203 transfected with the vectors did not grow in plates containing SD/-Leu/-Trp/-His with 3AT concentration higher than 30 mmol/L or in SD/-Leu/-Trp/-Ura plates,and the situation also happened in the X-gal color assay,indicating that the bait plasmid pDEST32-VP1/VP2/VP3 had no autonomous activation,therefore could serve as bait vector in researching the interactions of the three proteins of CAV.
Low germination rate is a key factor influencing seed germination of the European Mountain-Ash(Sorbus aucuparia).This study focused on the effects of the treatments of stratification and gibberellin soaking on the seed germination rate of 5 different Sorbus aucuparia provenances from different altitudes of European Alps.Compared with the stratification under a varying temperature within the range of 5—6℃(at an average of 5.6℃),the time for beginning germination after the stratification with a two-stage temperature treatment(firstly 2.9 ℃ for 60 days and then 5℃ till sowing) was postponed by 0—24 days,indicating the temperature of the stratification affects the germination speed.However,the germination rate after the two-stage temperature stratification was obviously higher than those after the stratification with a varying temperature in range of 5—6℃.For example,the germination rate for the provenances of No.2,3 and 6 was increased from less than 1% to 15%,57.8% and 14% respectively.However,there was no difference in germination rate between the 2 stratification treatments for the provenances of No.4 and 5,indicating different characters among provenances.A treatment of a 6—8 h soaking in gibberellin solution was helpful to break the seed dormancy and increase the germination rate obviously.The germination rate after the soaking in gibberellin solution with the concentration of 50—300 mg/L increased the germination rate of the provenance No.2 from 0.32%(as blank control) to 12.6%—42.0%,with an maximum rate from the gibberellin concentration of 200 mg/L.
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