Objective To evaluate the early effect of Wallis interspinous dynamic stabilization system (Wallis system) in treatment of lumbar degenerative disease. Methods From January 2008 to Jan-uary 2009,21 patients(23 intervertebral spaces) with early lumbar disc herniation and lumbar spinal stenosis were treated with Wallis system. Four intervertebral spaces of L_(3-4) 19 intervertebral spaces of L_(4-5). Observed the time of total operation and implantation,the blood loss,and early recovery. The patients' visual analogue scale (VAS) and Oswestry disability index (ODI) scores were evaluated before and after operation. Results All patients were followed up for average (12.5 ± 0.4) months (7-18 months) after operation. The VAS and ODI scores at 7 days after operation dropped from (7.5 ± 1.5), (40.0 ± 2.0) scores before operation to (2.5 ± 0.5), (23.0 ± 1.5) scores (P < 0.01). Conclusion It is safe and easy to use Wallis system in the treatment of lumbar degenerative disease, with the advantage of mini-invasion and early effect.

BACKGROUND: There is nearly no muscle tissue with satisfactory function and appearance applying in clinical repair and construction of injured muscles to date. OBJECTIVE: To investigate the feasibility of applying autologous fascia as a scaffold to construct muscle in vivo. DESIGN, TIME AND SETTING: The randomized, self-matched control experiment was carried out between January 2004and June 2006 at Department of Burns & Plastic Surgery, Second Hospital of Shenzhen, Shenzhen, Guangdong Province, China MATERIALS: Twenty-eight healthy New Zealand rabbits, weighing (1.7±0.5) kg, without sex restriction, establishing middle part defect model of anterior tibial muscle of rabbit hind legs. METHODS: One hind leg of each rabbit was randomized to the experimental group (n=28), the other hind leg was assigned to one of 3 control groups, scaffold-connected group (n=10), muscle particle implant group (n=10) and blank control group(n=8). In experimental group, the defect was connected with an autologous fascial scaffold and filled with the mutilated muscle particles, and subcutaneous tissue and skin were sutured in situ. In scaffold-connected group, the treatments were same to the experimental group only except muscle particle implantation. In muscle particle implant group, the defect was filled with muscle particles but without fascial scaffold and other treatments were same to the experimental group. The defect in blank control group received no treatment. MAIN OUTCOME MEASURES: The success rate of muscle transplantation, histological and ultra structural observation,and immunohistochemical identification of desmin were observed at 2, 3, 4, 6 and 9 weeks after operation. The middle parts of samples were also harvested for relative quantitative analysis of α-actin cDNA using reverse transcription-polymerase chain reaction in the experimental group and scaffold-connected group.RESULTS: In experimental group, 1 muscle broke near the proximal junction, the other 27 succeeded and the appearance of healed defects became near normal gradually. In scaffold-connected group, 4 muscles broke, 6 muscles still depressed in defect area; in muscle particle implant group and blank control group, the defects had no change. In experimental group, a large quantity of skeletal muscle satellite cells proliferated, which reached peak at 2-3 weeks, cells attached to the ends of fibrous connective tissue; in scaffold-connected group only fibrous connective tissue was seen. lmmunohistochemistry showed that 85% cells in experimental group were desmin-positive, while the positive rate in scaffold-connected group was < 25%. The relative quantitative analysis of α -actin cDNA showed that there were significant differences between the experimental group and scaffold-connected group at different time points(P < 0.05).CONCLUSION: The success rate of repairing muscle defect with autologous fascial scaffold reached 93.33%, which indicates that it is feasible to promote muscle regeneration with autologous fascial scaffold.

Objective:To reveal the abnormal topology of brain network in Alzheimer′s disease (AD), and evaluate the laterality of tau protein deposition in brains of AD patients based on 18F-APN-1607 PET brain imaging combined with graph theory. Methods:From November 2018 to January 2020, 23 clinically diagnosed AD patients (9 males, 14 females; age (61.3±10.7) years) and 13 normal controls (NC) (9 males, 4 females; age (61.6±4.5) years) who underwent 18F-APN-1607 PET imaging in Huashan Hospital, Fudan University were analyzed in this cross-sectional study. The brain network analysis method based on graph theory was used to construct the tau network of the NC group and the AD group, the network attributes (clustering coefficient, shortest path length, local efficiency, and small-worldness) were calculated, and the asymmetry index (AI) of each group to evaluate the laterality of tau protein deposition was obtained. Permutation test (1 000 times) was used to analyze the differences in brain network parameters between the NC group and the AD group. Results:The tau network of the AD group had obvious topological disorder, and the connections in the olfactory cortex and temporal lobe were weakened, while in the posterior cingulate gyrus, anterior wedge, and parietal occipital lobe, the connections were enhanced. Compared with NC group, clustering coefficient ( t values: 2.28-2.69), local efficiency ( t values: 2.34-3.06) and small-worldness ( t values: 2.26-3.32) were significantly decreased in AD group (all P<0.05) with the sparsity of 20%-50%, while the shortest path length was significantly increased ( t values: 2.13-2.85; all P<0.05). There was significant tau laterality in the posterior cingulate gyrus, superior parietal gyrus, paracentral lobule, superior temporal gyrus and middle temporal gyrus (AI: 10.5%(8.1%, 13.9%), 14.1%(7.6%, 20.3%), -12.4%(-15.7%, -7.8%), -10.8%(-15.3%, -2.1%) , -12.1%(-17.9%, -6.6%), respectively). Conclusion:The tau network analysis based on 18F-APN-1607 may be used to reveal abnormal topological changes of AD patients, and the tau deposition in the posterior cingulate gyrus, superior parietal gyrus, paracentral lobule, superior temporal gyrus and middle temporal gyrus has obvious laterality in AD patients.

Abstract: To develop novel live attenuated influenza vaccine, we explored the feasibility to attenuate influenza virus by codon deoptimization of NS1. According to the codon usage bias in influenza A virus, we designed and synthesized a condon-deoptimized NS gene by substituting codons of 110 amino acids in the NS1 gene of A/Puerto Rico/8/34(H1N1) with unpreferred synonymous codons. The influenza A virus with the codon deoptimized NS1 gene (deoNS virus) was rescued by reverse genetics. Plaque forming assay and virus growth curve showed that the growth of deoNS virus was reduced about 1000 times in MDCK cells compared to that of the wild-type virus. Intranasal inoculation with deoNS virus did not cause death or evident disease in infected BALB/c mice. Furthermore, the virus titer in the lungs of mice infected with deoNS virus was significantly lower (i.e. 100-1000 times) than that of wild-type virus. Our results indicated that influenza virus could be effectively attenuated by synonymous codon deoptimization of NS1 gene. This strategy will be useful to develop new attenuated candidates for the production of live attenuated influenza vaccines.
Animals ; Base Sequence ; Chick Embryo ; Codon ; genetics ; Influenza A virus ; genetics ; pathogenicity ; Influenza Vaccines ; immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Orthomyxoviridae Infections ; immunology ; prevention & control ; Recombination, Genetic ; Vaccines, Attenuated ; immunology ; Viral Nonstructural Proteins ; genetics ; Virulence ; genetics

Objective:To observe the expressions of SENP1, SENP2and SENP6proteins in human malignant glioma tissue and cells, and to elucidate the their effects in the development of malignant glioma.Methods:The samples of normal human brain tissue and malignant glioma tissue were obtained and used as normal control group and malignant glioma group, respectively.The Cos7cells and the malignant glioma LN443and U343cells were cultured;the Cos7cells were used as normal cell control group, and the LN443and U343cells as malignant glioma cell group.Western blotting method was used to detect the expression levels of SENP1, SENP2and SENP6proteins in human malignant glioma tissue and cells.Results:In brain tissue, the expression levels of SENP1, SENP2and SENP6proteins in malignant glioma group were higher than those in normal control group (P＜0.05) .Compared with normal cell control group, the expression levels of SENP1, SENP2and SENP6proteins in the LN443and U343cells in malignant glioma cell group were significantly increased (P＜0.05) .Conclusion:SENP1, SENP2and SENP6proteins highly express in the malignant glioma tissue and cells, and they may play an important role in promoting the occurrence of malignant glioma.

Objective:Exploring tau related disease pattern (tauRDP) in the brain of Alzheimer′s disease (AD) patients based on 18F-APN-1607 PET scan. Methods:18F-APN-1607 PET images were collected from 17 AD patients (6 males and 11 females, age: (61.7±12.3) years, Mini-Mental State Examination (MMSE) score: 17.6±7.9) and 10 normal controls (NC; 6 males and 4 females, age: (61.2±4.7) years) from Huashan Hospital of Fudan University. The scaled subprofile model (SSM) based on principal component analysis (PCA) technique was used to construct the tauRDP. Then the expression value of tauRDP in each sample was calculated. The differences on tauRDP expression values between AD patients and NC were compared by independent-sample t test. Pearson correlation analysis was used to analyze the correlation between tauRDP expression values and MMSE values in AD patients. Results:The tauRDP area mainly included: precentral gyrus, dorsolateral superior frontal gyrus, middle frontal gyrus, inferior frontal gyrus of opercular part, inferior frontal gyrus of triangular part, supplementary motor area, medial superior frontal gyrus, left median cingulate and paracingulate gyri, right cuneus, superior occipital gyrus, middle occipital gyrus, postcentral gyrus, superior parietal gyrus inferior parietal, but supramarginal and angular gyri, supramarginal gyrus, angular gyrus, precuneus and middle temporal gyrus. There were significant differences ( t=4.395, P<0.001) between AD group (12.6±8.0) and NC group (0.0±1.0) in tauRDP expression values. The tauRDP expression values were correlated with MMSE values in AD group significantly ( r=-0.566, P=0.018). Conclusions:TauRDP established basing on SSM/PCA method can be used to quantitatively express the abnormal spatial distributions of tau deposition. Expression value of tauRDP has the potential to initially assess the severity of AD.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare hereditary cerebrovascular disease caused by a NOTCH3 mutation. However, the underlying cellular and molecular mechanisms remain unidentified. Here, we generated non-integrative induced pluripotent stem cells (iPSCs) from fibroblasts of a CADASIL patient harboring a heterozygous NOTCH3 mutation (c.3226C>T, p.R1076C). Vascular smooth muscle cells (VSMCs) differentiated from CADASIL-specific iPSCs showed gene expression changes associated with disease phenotypes, including activation of the NOTCH and NF-κB signaling pathway, cytoskeleton disorganization, and excessive cell proliferation. In comparison, these abnormalities were not observed in vascular endothelial cells (VECs) derived from the patient's iPSCs. Importantly, the abnormal upregulation of NF-κB target genes in CADASIL VSMCs was diminished by a NOTCH pathway inhibitor, providing a potential therapeutic strategy for CADASIL. Overall, using this iPSC-based disease model, our study identified clues for studying the pathogenic mechanisms of CADASIL and developing treatment strategies for this disease.