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in view of the requirements of satellite structure lightweight design, a thruster bracket is chosen as the research object. A topology optimization model of bracket is established, and the fundamental frequency is the constraint condition, the design scheme of minimum quality is obtained. A bracket model of rod structure is established through 3D print method. Some mechanical performances such as fundamental frequency, intensity and drawing force are analyzed in detail through multiple iterations, so as to realize the trussed bracket design of lightweight high-performance.

Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide. Novel and effective therapy is needed to prevent the secondary spread of damage beyond the initial injury. The aim of this study was to investigate whether berberine has a neuroprotective effect on secondary injury post-TBI, and to explore its potential mechanism in this protection. The mice were randomly divided into Sham-saline, TBI-saline and TBI-Berberine (50 mg/kg). TBI was induced by Feeney's weight-drop technique. Saline or berberine was administered via oral gavage starting 1 h post-TBI and continuously for 21 days. Motor coordination, spatial learning and memory were assessed using beam-walking test and Morris water maze test, respectively. Brain sections were processed for lesion volume assessment, and expression of neuronal nuclei (NeuN), cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), 8-hydroxy-2-deoxyguanosine (8-OHdG), ionized calcium-binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) were detected via immunohistochemistry and immunofluorescence. There were statistically significant improvement in motor coordination, spatial learning and memory in the TBI-Berberine group, compared to the TBI-saline group. Treatment with berberine significantly reduced cortical lesion volume, neuronal loss, COX-2, iNOS and 8-OHdG expression in both the cortical lesion border zone (LBZ) and ipsilateral hippocampal CA1 region (CA1), compared to TBI-saline. Berberine treatment also significantly decreased Iba1- and GFAP-positive cell number in both the cortical LBZ and ipsilateral CA1, relative to saline controls. These results indicated that berberine exerted neuroprotective effects on secondary injury in mice with TBI probably through anti-oxidative and anti-inflammatory properties.

Background Nocardiosis is a rare and life-threatening opportunistic infection in the immunocompromised patients. Myasthenia gravis (MG) patients have the potential risk of nocardia infection because of the use of immunosuppressive agents. To date, only 7 cases of patients with MG have been reported to have nocardiosis. Disseminated nocardiosis with ocular involvement in MG patient haven’t been reported. Case presentation A 66-year-old man with MG, receiving treatment of methylprednisolone and azathioprine, was found to have respiratory infection. He also had heterogeneous symptoms with skin, brain and ocular manifestations. Nocardia bacteria was verified by the culture of puncture fluid, and the diagnosis of disseminated nocardiosis was made. Except for the left eye blindness, the patient completely recovered from the disease with combination antibiotic therapy. To further understand nocardiosis in patients with MG, we reviewed previous relevant literatures. According to all the literatures, this is the first report of disseminated nocardiosis with ocular involvement in MG patient. Conclusions MG patients with immunosuppressant treatments have the potential risk of rare nocardia infection, and a favourable prognosis can be achieved through early diagnosis and appropriate antibiotic therapy.

Although both the heat shock protein 70 (HSP70) and the activating transcription factor 5 (ATF5) have been shown to promote cell survival of transformed cells but not survival of non-transformed cells, the relationship of the two molecules is unknown. Here we show that HSP70 and ATF5 are concomitantly up-regulated upon transient but down-regulated over prolonged cellular stress and apoptotic stimulation in the rat C6 glioma and human U87 glioma cells. HSP70 interacts strongly with the N-terminal activation domain of ATF5, which is expected to be rigid and uniquely structured under physiological conditions because of extraordinary high concentration (over 25%) of proline residues. Binding of HSP70 to ATF5 is an ATP-driven process and requires functional ATPase on the nucleotide binding domain of the HSP70 molecule. Overexpression of HSP70 dramatically stabilizes the ATF5 protein, which is otherwise subject to rapid degradation, facilitated by both proteasome-dependent and caspase-dependent processes, whereas HSP70 depletion leads to acceleration of ATF5 degradation and transcription repression of Bcl-2 and Egr-1, which are downstream targets of ATF5 in C6 and U87 glioma cells. Our data reveal an essential role for HSP70 in maintaining high levels of ATF5 expression in glioma cells and support the conclusion that ATF5 is an important substrate protein of HSP70 that mediates HSP70-promoted cell survival in glioma cells.

Mesenchymal stromal cells (MSC) are attractive candidates for the treatment of Duchenne muscular dystrophy (DMD) but how the donor MSC distribute in multiple organs and whether the increased dystrophin leads to a change in the pathology of mdx mice is still uncertain. In this research we detected the distribution of MSC and the pathology of mdx mice after MSC infusion.MSC were isolated from rat bone marrow (BM) and expanded in proliferation medium. MSC of the fifth passage were delivered intravenously into irradiated mdx mice. The distribution of MSC labeled by [3H]TdR into a recipient's organs was calculated by radioactivity. The expression of dystrophin was detected at weeks 4, 8, 12 and 16 after MSC transplantation by immunofluorescence staining, RT-PCR and Western blot. Serum creatine kinase (CK) and centrally nucleated fiber (CNF) were also detected to assess the change in pathology.24-48 h after transplantation, MSC were mainly found in the BM, liver and lung. The radioactivity in these organs decreased, whereas skeletal and myocardial muscle radioactivity increased gradually over time. In accordance with the increased radioactivity in skeletal muscle, the amount of dystrophin-positive myofibers increased. Furthermore, serum CK and CNF decreased slightly, suggesting specific pathophysiologic features of the dystrophic muscle were partially restored.Upon certification of the distribution of transplanted MSC in irradiated mdx mice, we found evidence of myogenic differentiation of MSC in skeletal muscle. This research may help us understand the mechanism of therapy of MSC transplantation.

The insulin/insulin-like growth factor signaling (IIS) pathway is a major conserved regulator of aging. Nematode, fruit fly and mouse mutants with reduced IIS signaling exhibit extended lifespan. These mutants are often dwarfs leading to the idea that small body mass correlates with longevity within species. However, when different species are compared, larger animals are typically longer-lived. Hence, the role of IIS in the evolution of life history traits remains unresolved. Here we used comparative approach to test whether IGF1R signaling changes in response to selection on lifespan or body mass and whether specific tissues are involved. The IGF1R levels in the heart, lungs, kidneys, and brains of sixteen rodent species with highly diverse lifespans and body masses were measured via immunoblot after epitope conservation analysis. We report that IGF1R levels display strong negative correlation with maximum lifespan only in brain tissue and no significant correlations with body mass for any organ. The brain-IGF1R and lifespan correlation holds when phylogenetic non-independence of data-points is taken into account. These results suggest that modulation of IGF1R signaling in nervous tissue, but not in the peripheral tissues, is an important factor in the evolution of longevity in mammals.

To construct the recombinant plasmid containing human microdystrophin cDNA, and study the microdystrophin expression in vivo and in vitro.Microdystrophin cDNA was obtained from recombinant plasmid pBSK-MICRO digested with restrictive endonuclease Not I, the product was inserted into plasmid pVAX1, resulting in pAMICDYS. And then 3T3 cells were transfected with pAMICDYS. Forty-eight hours after transfection, the expression of the microdystrophin was detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry. Finally, TA muscles of mdx mice were injected with the recombinant plasmid pAMICDYS through i.m. and the pathological change of TA was evaluated by histology, and the expression of microdystrophin in mdx TA was detected by immunohistochemical analysis.The recombinant plasmid containing human microdystrophin cDNA was constructed successfully. The recombinant plasmid was proved to be able to express microdystrophin protein both in vivo and in vitro. Moreover, treatment of the TA of mdx mice with the recombinant plasmid could decrease the number of centrally nucleated myofibers.Recombinant plasmid containing the microdystrophin gene was constructed successfully, and it could express microdystrophin protein both in vivo and in vitro. It provides basis for further study on microdystrophin as a target gene to treat Duchenne muscular dystrophy (DMD) by electrotransfer, i.v, arterial injection and combining with other exogenous gene to enhance microdystrophin expression.

To investigate whether the recombinant baculovirus (Bac-CMV-EGFP) can effectively transduce into rhesus Bone-marrow derived Mesenchymal Stem Cells (rBMSCs) in vitro, and whether there are some efficiency to the rBMSCs of viability, proliferational and differentiational capacity after recombinant baculovirus transducing.The rBMSCs were cultured in vitro. After passaged more than three times, the rBMSCs were transduced with various dose of baculovirus (Multiplicity Of Infection, MOI, the MOI is 50, 100, 200, 300, and 500 vector genome (vg)/cell, respectively). We used flow cytometry to detect different transductive efficiency of various dose of baculovirus to rBMSCs. Under a suitable dose of baculovirus (300 v.g/cell), we studied cell viability, proliferation and differentiation capacity, and compared results with the control.Baculovirus could be transduced into rBMSCs in vitro. The transductive efficiency reached about 80% when the MOI was 300 v.g/cell, at 25 degrees C, and incubated for 4 h. Furthermore, under a higher transductive efficiency of baculovirus, there were no obvious influence to the rBMSCs of viability, proliferation and differentiation capacity compared with that of the control.The baculovirus can be safely and effectively transduced into rBMSCs in vitro, without any negative efficiency to cell viability, proliferation and differentiation capacity.

Although Schwann cell (SC) transplantation can enhance peripheral and central nerve repair experimentally, it is difficult to generate sufficient SC quickly for clinical application. So alternative cell systems for SC are desired. SC-like cells induced from adipose-derived stem cells (ADSC) may be one of the ideal alternative cell systems for SC. However, myelin-forming ability, which is the most important characteristics and function of SC, has not been investigated in SC-like cells from ADSC up to now. In this experiment, ADSC were harvested from rat inguinal fat pad. Rat ADSC were fibroblast-like in shape, almost all the cells expressed mesodermal marker fibronectin, and only few cells expressed neural stem cell marker nestin. A mixture of glial growth factors (Heregulin, bFGF, PDGF and forskolin) could induce rat ADSC into SC-like cells. SC-like cells were spindle-like in shape and expressed glial markers GFAP and S100, similar to genuine SC. When intracellular cAMP was increased, SC-like cells could express myelin protein p0. More importantly, when co-cultured with rat pheochromocytoma cell line (PC12 cells), SC-like cells could induce the differentiation of PC12 cells rapidly and form myelin structures with PC12 cells in vitro. Our data further demonstrated that SC-like cells from ADSC were able to form myelins and these cells may benefit the treatment of peripheral and central nerve injuries.

Background Schwann cells (SC) which are myelin-forming cells in peripheral nervous system are very useful for the treatment of diseases of peripheral nervous system and central nervous system. However, it is difficult to obtain sufficient large number of SC for clinical use, so alternative cell systems are desired. Results Using a procedure similar to the one used for propagation of neural stem cells, we could induce rat adipose-derived stem cells (ADSC) into floating neurospheres. In addition to being able to differentiate into neuronal- and glial-like cells, neurospheres could be induced to differentiate into SC-like cells. SC-like cells were bi- or tri-polar in shape and immunopositive for nestin and SC markers p75, GFAP and S-100, identical to genuine SC. We also found that SC-like cells could induce the differentiation of SH-SY5Y neuroblastoma cells efficiently, perhaps through secretion of soluble substances. We showed further that SC-like cells could form myelin structures with PC12 cell neurites in vitro. Conclusion These findings indicated that ADSC could differentiate into SC-like cells in terms of morphology, phenotype and functional capacities. SC-like cells induced from ADSC may be useful for the treatment of neurological diseases.