Objective To observe the significance of rehabilitation integrated system for stroke patients. Methods From October, 2013 to June, 2015, 95 stroke patients were divided randomly into experimental group (n=48) and control group (n=47). The experimental group received rehabilitation under the guide of rehabilitation integrated system, while the control group in the routine process. They were assessed with simplified Fugl-Meyer Assessment (FMA) and Barthel Index (BI) before and 3 months after treatment. The satisfaction was also inves-tigated. Results There was no significant difference between groups in the differences of scores of FMA and BI before and after treatment (t<1.044, P>0.05), while the satisfaction was higher in the experimental group (t=4.287, P<0.01). Conclusion The application of rehabilitation integrated system may improve the process of treatment and the efficiency of management, and result in more satisfaction of the stroke pa-tients.

Objective:To investigate the protective effect of ergosterol on neurons in CA1 area of the hippocampus and its mechanism in rats anesthetized with propofol.Methods:Forty-five SD rats were randomly divided into control group, propofol group and propofol+ergosterol group ( n=15). Rats in the control group were injected intraperitoneally with 100 mg/kg fat emulsion solvent; rats in the propofol group were injected intraperitoneally with 50 mg/kg propofol first, and after the righting reflex was restored, they were injected with 50 mg/kg propofol; propofol+ergosterol group was intraperitoneally injected with 30 mg/kg ergosterol, followed by propofol injection, and the propofol injection method was the same as that of the propofol group. Injection was given continuously for 7 d. After the last injection, the rats in each group were awake for 2 h. The ultrastructure of neurons in hippocampal CA1 area was observed by transmission electron microscopy. HE staining, TUNEL and neuronal nuclear antigen (NeuN) staining, and Western blotting were used to detect the morphology, apoptosis, and postsynaptic density protein 95 (PSD95) expression of neurons in the hippocampal CA1 area, respectively. Western blotting was used to determine the expressions of apoptosis-related proteins and phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway proteins in hippocampal CA1 area of rats. Results:Transmission electron microscopy and HE staining showed that the damage of neurons in the hippocampal CA1 area of the propofol+ergosterol group was slighter than that of the propofol group. As compared with control group, propofol group had significantly higher neuronal apoptosis, significantly higher levels of activated Caspase 3 and Bax protein expressions, significantly decreased Bcl-2 and PSD95 expressions, significantly increased apoptosis inducing factor (AIF) and Cytochrome (Cyt)-C protein expressions, statistically lower Sirt1 protein expression, and significantly lower phosphorylated (p)-PI3K/PI3K level and p-Akt/Akt ratio in the hippocampal CA1 area ( P<0.05). As compared with propofol group, propofol+ergosterol group had significantly lower neuronal apoptosis in the hippocampal CA1 area (27.33±1.37% vs. 17.47±0.87%, P<0.05). As compared with propofol group, propofol+ergosterol group had significantly lower activated Caspase 3 and Bax protein expressions, significantly increased Bcl-2 and PSD95 expressions, significantly decreased AIF and Cyt-C protein expressions, statistically higher Sirt1 protein expression, and significantly higher p-PI3K/PI3K level and p-Akt/Akt ratio in the hippocampal CA1 area ( P<0.05). Conclusion:Ergosterol pretreatment can inhibit propofol-induced neuron apoptosis and alleviate the neuronal damage in the hippocampal CA1 area, whose mechanism may be mediated by PI3K-Akt signaling pathway.

Objective:To explore the cellular heterogeneity and the differences in branched trajectory of pericytes between keloids and localized scleroderma, and to provide new clues for the pathogenesis and therapeutic targets of the two skin fibrotic diseases.Methods:Single cell transcriptome sequencing (scRNA-seq) data of 3 cases of scleroderma, 4 cases of keloid and their corresponding 4 cases of adjacent normal skin samples were selected from GEO and GSA-Human databases, and the expression matrix of the data was drawn. Seurat 4.3.0 of R (4.2.2) was used to process the t-distributed stochastic neighbor embedding ( t-SNE) visualization map. Monocle 2.24.0 was used to analyze the pseudo-temporal trajectory of pericytes. Results:The unsupervised clustering of keloid and scleroderma skin tissues revealed 19 different cell populations, among which C7 and C11 cells were pericytes, marked by high expression levels of PDGFRB and RGS5 genes, accounting for 7.53% of the total cells. Pericytes can be further divided into 8 subgroups. Pseudo-temporal analysis revealed a branched trajectory with two major branches, that is, cell fate 1 and cell fate 2, which could be further divided into 5 cellular states of pericytes (S1-S5). S4 constituted the most of the prebranch, which represented the cellular state of the initial pericyte phenotype. S5 constituted the most of the cell fate 1 branch, which represented the early differentiation state of the pericyte phenotype. S1, S2, S3 constituted the most of the cell fate 2 branch. S3 represented the intermediate differentiation state of the pericyte phenotype, while S1 and S2 represented the terminal differentiation states of the pericyte phenotype. Compared with the uniform distribution of various differentiation states of pericytes in normal skin, the keloid pericytes mainly distributed in the prebranch (S4), cell fate 1 (S5) and the first half of cell fate 2 (S3), representing cellular states of the initial, early and intermediate phases of the pericyte phenotype. Branched expression analysis modeling revealed the overexpression of SOX4, COL4A1, COL6A3, AHR, CXCL3 and IL1R1 genes, et cetera. On the other hand, the localized scleroderma pericytes mainly distributed in the bottom half of cell fate 2 (S1, S2), representing the final differentiated phase of pericyte phenotype, which overexpressed ACTA2 and MYH11 genes.Conclusion:Pericytes in keloid and scleroderma are heterogenous and have different differentiation trajectories. Pericytes in keloid have stem-like characteristics, and play an important role in the pathologic characteristics of invasiveness and recurrence through high expression of genes related to cell stemness, epithelial-mesenchymal transition, invasiveness, and immune microenvironment regulation. However, pericytes in localized scleroderma may mainly transdifferentiate into myofibroblasts, leading to their fibrotic pathological phenotype.

Objective:To explore the cellular heterogeneity and the differences in branched trajectory of pericytes between keloids and localized scleroderma, and to provide new clues for the pathogenesis and therapeutic targets of the two skin fibrotic diseases.Methods:Single cell transcriptome sequencing (scRNA-seq) data of 3 cases of scleroderma, 4 cases of keloid and their corresponding 4 cases of adjacent normal skin samples were selected from GEO and GSA-Human databases, and the expression matrix of the data was drawn. Seurat 4.3.0 of R (4.2.2) was used to process the t-distributed stochastic neighbor embedding ( t-SNE) visualization map. Monocle 2.24.0 was used to analyze the pseudo-temporal trajectory of pericytes. Results:The unsupervised clustering of keloid and scleroderma skin tissues revealed 19 different cell populations, among which C7 and C11 cells were pericytes, marked by high expression levels of PDGFRB and RGS5 genes, accounting for 7.53% of the total cells. Pericytes can be further divided into 8 subgroups. Pseudo-temporal analysis revealed a branched trajectory with two major branches, that is, cell fate 1 and cell fate 2, which could be further divided into 5 cellular states of pericytes (S1-S5). S4 constituted the most of the prebranch, which represented the cellular state of the initial pericyte phenotype. S5 constituted the most of the cell fate 1 branch, which represented the early differentiation state of the pericyte phenotype. S1, S2, S3 constituted the most of the cell fate 2 branch. S3 represented the intermediate differentiation state of the pericyte phenotype, while S1 and S2 represented the terminal differentiation states of the pericyte phenotype. Compared with the uniform distribution of various differentiation states of pericytes in normal skin, the keloid pericytes mainly distributed in the prebranch (S4), cell fate 1 (S5) and the first half of cell fate 2 (S3), representing cellular states of the initial, early and intermediate phases of the pericyte phenotype. Branched expression analysis modeling revealed the overexpression of SOX4, COL4A1, COL6A3, AHR, CXCL3 and IL1R1 genes, et cetera. On the other hand, the localized scleroderma pericytes mainly distributed in the bottom half of cell fate 2 (S1, S2), representing the final differentiated phase of pericyte phenotype, which overexpressed ACTA2 and MYH11 genes.Conclusion:Pericytes in keloid and scleroderma are heterogenous and have different differentiation trajectories. Pericytes in keloid have stem-like characteristics, and play an important role in the pathologic characteristics of invasiveness and recurrence through high expression of genes related to cell stemness, epithelial-mesenchymal transition, invasiveness, and immune microenvironment regulation. However, pericytes in localized scleroderma may mainly transdifferentiate into myofibroblasts, leading to their fibrotic pathological phenotype.

Petrochemical-derived polyester plastics such as polyethylene terephthalate (PET) and polybutylene adipate terephthalate (PBAT) have been widely used. However, the difficulty to be degraded in nature (PET) or the long biodegradation cycle (PBAT) resulted in serious environmental pollution. In this connection, treating these plastic wastes properly becomes one of the challenges of environment protection. From the perspective of circular economy, biologically depolymerizing the waste of polyester plastics and reusing the depolymerized products is one of the most promising directions. Recent years have seen many reports on polyester plastics degrading organisms and enzymes. Highly efficient degrading enzymes, especially those with better thermal stability, will be conducive to their application. The mesophilic plastic-degrading enzyme Ple629 from the marine microbial metagenome is capable of degrading PET and PBAT at room temperature, but it cannot tolerate high temperature, which hampers its potential application. On the basis of the three-dimensional structure of Ple629 obtained from our previous study, we identified some sites which might be important for its thermal stability by structural comparison and mutation energy analysis. We carried out transformation design, and performed expression, purification and thermal stability determination of the mutants. The melting temperature (T_m) values of mutants V80C and D226C/S281C were increased by 5.2 ℃ and 6.9 ℃, respectively, and the activity of mutant D226C/S281C was also increased by 1.5 times compared with that of the wild-type enzyme. These results provide useful information for future engineering and application of Ple629 in polyester plastic degradation.
Plastics/metabolism* ; Polyethylene Terephthalates/metabolism* ; Biodegradation, Environmental ; Metagenome