Objective
To evaluate and discuss the plastic surgery treatment of asymmetric crying face.
Methods
From 2019 to 2022, 60 patients with asymmetric crying face were treated by fascia lata grafting. We ...evaluated the postoperative improvement, summarized experiences and reviewed literatures about the treatment of asymmetric crying face.
Results
59 patients showed varying degrees of improvement in the movement of the affected corner of mouth, and no complications were found during the follow-up period of 6 months to 24 months.
Conclusions
The cause of asymmetric crying face is still uncertain. Fascia lata grafting has shown a certain effect in the treatment of asymmetric crying face. This study evaluated this method with quite large sample. More researches are needed to explore the most appropriate treatment for asymmetric crying face.
Polysaccharides are the main active components of Grifola umbellate, most of which are β-glucans with (1→3)-β-glucose main chain and (1→6)-β-glucose side chain structures. Grifola umbellate ...polysaccharides (GUPs) have antioxidant, immune regulation, anti-tumor, and other effects. But so far, for different types of GUPs, the relationship between their structures and functions has not explicitly been classified and summarized. Herein, the extraction, isolation and purification, structures, derivatization, biological activities and applications of GUPs were reviewed. It provided a reference for the research and development of GUPs in the future.
Display omitted
•Preparation of GUPs was summed up.•The structure-function relationship of GUPs was discussed.•The application of GUPs was summarized and elaborated.
Background and Aim. miRNAs play an important role in the development of human fibrosis. However, miRNA expression profiles during different stages of chronic hepatitis B (CHB) are not well defined. ...In this study, we aimed to further validate the features of 5 miRNA candidates from our previous study during different fibrotic stages and the value of diagnosis for liver fibrosis. Methods. Differential expression of five selected miRNAs (hsa-mir-1225-3p, hsa-mir-1238, hsa-miR-3162-3P, hsa-miR-4721, and hsa-miR-H7) was verified by qRT-PCR in the plasma of 83 patients and 20 healthy controls. The relative expression of these miRNAs was analyzed in different groups to screen target miRNA. A logistic regression analysis was performed to assess factors associated with fibrosis progression. The receiver operating characteristic (ROC) curve and discriminant analyses validated the ability of these predicted variables to discriminate the nonsignificant liver fibrosis group from the significant liver fibrosis group. Furthermore, the established models were compared with other prediction models to evaluate the diagnostic efficiency. Results. These five tested miRNAs all had signature correlations with hepatic fibrotic level (p<0.05), and the upregulation trends were consistent with miRNA microarray analysis previously. The multivariate logistic regression analysis identified that a model of five miRNAs (miR-5) had a high diagnostic accuracy in discrimination of different stages of liver fibrosis. The ROC showed that the miR-5 has excellent value in diagnosis of fibrosis, even better than the Forns score, FIB-4, S index, and APRI. GO functions of different miRNAs mainly involved in various biological processes were markedly involved in HBV and revealed signaling pathways dysregulated in liver fibrosis of CHB patients. Conclusions. It was validated that the combination of these five miRNAs was a new set of promising molecular diagnostic markers for liver fibrosis. The diagnosis model (miR-5) can distinguish significant and nonsignificant liver fibrosis with high sensitivity and specificity.
Objective:
Inflammatory bowel disease (IBD) is characterized by gut microbiota dysbiosis, which is also frequently observed in patients with non-alcoholic fatty liver disease. Whether gut microbiota ...dysbiosis in IBD patients promotes the development of non-alcoholic steatohepatitis (NASH) remains unclear. We aimed to explore the role of gut microbiota dysbiosis in the development of NASH in mice with dextran sulfate sodium salt (DSS) induced colitis.
Design:
Dextran sulfate sodium salt was used to induce colitis, and high fat (HF), in combination with a high-fructose diet, was used to induce NASH in C57BL/6J male mice. Mice were treated with (1%) DSS to induce colitis in cycles, and each cycle consisted of 7 days of DSS administration followed by a 10-day interval. The cycles were repeated throughout the experimental period of 19 weeks. Pathological alterations in colitis and NASH were validated by hematoxylin and eosin (H&E), oil red O, Sirius red staining, and immunofluorescence. Gut microbiota was examined by 16S rRNA sequencing, and gene expression profiles of hepatic non-parenchymal cells (NPCs) were detected by RNA sequencing.
Results:
Dextran sulfate sodium salt administration enhanced the disruption of the gut–vascular barrier and aggravated hepatic inflammation and fibrosis in mice with NASH. DSS-induced colitis was accompanied by gut microbiota dysbiosis, characterized by alteration in the core microbiota composition. Compared with the HF group, the abundance of
p_Proteobacteria
and
g_Bacteroides
increased, while that of
f_S24-7
decreased in the DSS + HF mice. Specifically, gut microbiota dysbiosis was characterized by enrichment of lipopolysaccharide producing bacteria and decreased abundance of short-chain fatty acid-producing bacteria. Gene expression analysis of liver NPCs indicated that compared with the HF group, genes related to both inflammatory response and angiocrine signaling were altered in the DSS + HF group. The expression levels of inflammation-related and vascular development genes correlated significantly with the abundance of
p
_
Proteobacteria
,
g
_
Bacteroides
, or
f_S24-7
in the gut microbiota, implying that gut microbiota dysbiosis induced by DSS might aggravate hepatic inflammation and fibrosis by altering the gene expression in NPCs.
Conclusion:
Dextran sulfate sodium salt-induced colitis may promote the progression of liver inflammation and fibrosis by inducing microbiota dysbiosis, which triggers an inflammatory response and disrupts angiocrine signaling in liver NPCs. The abundance of gut microbiota was associated with expression levels of inflammation-related genes in liver NPCs and may serve as a potential marker for the progression of NASH.
Exosomal miRNAs activates hepatic stellate cell (HSC) and promote fibrosis. miR-222 was found to be increased in hepatitis B virus (HBV)-infected hepatocytes, and ferroptosis was reported to ...ameliorate liver fibrosis (LF). Although miR-222 and ferroptosis have been implicated in LF, the association between miR-222 and ferroptosis and how they coordinate to regulate LF are still not explicit. This study investigates the roles of miR-222 and transferrin receptor (TFRC) in LF. Lipid reactive oxygen species (ROS) level was analyzed by flow cytometry. FerroOrange staining was used to measure intracellular iron level. Luciferase reporter assay was adopted to confirm the binding of miR-222 and TFRC. Real-time quantitative PCR and immunoblots were applied to analyze gene and protein expression. The results showed that supplementation of exosomes derived from HBV-infected LO2 cells remarkably enhanced LX-2 cell activation, evidenced by elevated hydroxyprolin (Hyp) secretion and α-SMA and COL1A2 expression. miR-222 was significantly increased in HBV-Exo. Overexpressing miR-222 upregulated cell viability, secretion of Hpy, and expression of α-SMA and COL1A2, which were all blocked by overexpression of TFRC. Further study showed that TFRC was a target of miR-222, and miR-222 promoted LX-2 cell activation through suppressing TFRC-induced ferroptosis in LX-2 cells. Exosomal miR-222 derived from HBV-infected hepatocytes promoted LF through inhibiting TFRC and TFRC-induced ferroptosis. This study emphasizes the significance of miR-222/TFRC axis in LF and suggests new insights in clinical decision making while treating LF.
Graphical abstract
Exosomes derived from HBV-infected LO2 cells promote LX-2 cell activation and liver fibrosis in mouse
Exosomal miR-222 derived from HBV-infected LO2 cells promotes LX-2 cell activation
TFRC is a target of miR-222 and inhibits LX-2 cell activation induced by miR-222
miR-222 promotes LX-2 cell activation through inhibiting TFRC-induced ferroptosis
Liver sinusoidal endothelial cells (LSECs) undergo capillarization, or loss of fenestrae, and produce basement membrane during liver fibrotic progression. DLL4, a ligand of the Notch signaling ...pathway, is predominantly expressed in endothelial cells and maintains liver sinusoidal homeostasis. The aim of this study was to explore the role of DLL4 in LSEC capillarization. The expression levels of DLL4 and the related genes, capillarization markers and basement membrane proteins were assessed by immunohistochemistry, immunofluorescence, RT-PCR and immunoblotting as appropriate. Fenestrae and basement membrane formation were examined by electron microscopy. We found DLL4 was up-regulated in the LSECs of human and CCl4-induced murine fibrotic liver, consistent with LSEC capillarization and liver fibrosis. Primary murine LSECs also underwent capillarization in vitro, with concomitant DLL4 overexpression. Bioinformatics analysis confirmed that DLL4 induced the production of basement membrane proteins in LSECs, which were also increased in the LSECs from 4 and 6-week CCl4-treated mice. DLL4 overexpression also increased the coverage of liver sinusoids by hepatic stellate cells (HSCs) through endothelin-1 (ET-1) synthesis. The hypoxic conditions that was instrumental in driving DLL4 overexpression in the LSECs. Consistent with the above findings, DLL4 silencing in vivo alleviated LSEC capillarization and CCl4-induced liver fibrosis. In conclusion, DLL4 mediates LSEC capillarization and the vicious circle between fibrosis and pathological sinusoidal remodeling.
•LSECs undergo capillarization in the early stage of liver fibrosis.•DLL4 was up-regulated in LSECs of fibrotic liver tissues.•DLL4 overexpression accelerated LSECs capillarization.•Inhibiting DLL4 expression in vivo alleviated LSEC capillarization and CCl4-induced liver fibrosis.
Social media has become an important part of plastic surgeons' practices. Is it true that the more followers, the more efficient it is to the plastic surgeon's branding? This study is to verify the ...quantitative correlation between social media and clinical appointments and to optimize its utilization. One hundred and five plastic surgeons were divided into 3 groups according to titles. WEIBO served as a targeted platform and descriptive data, including numbers of followers and clinic appointments were collected for analysis. The promotive effect was quantified as and correlation analysis was conducted to quantify the relationship between followers and outpatient appointments. From this research, it was found that 62% of participants were social media users, while 38% were not. No statistical significance was found between them by comparing the number of clinic appointments. For surgeons with social media, a positive correlation was proven between followers and clinic appointments, whose Pearson's correlation was 0.266 (attending: 0.557, associate consultant: 0.315, consultant: 0.060). Meanwhile, the conversion rates in this study were 22.49±44.67% (attending), 13.10±24.57% (associate consultant), and 18.88±36.05% (consultant). Outpatient consultations of senior surgeons without social media (2652±14492) were significantly higher than young surgeons with social media (1800±1718, P <0.05). The regression equation was Clinical Appointments=ln (Followers)×316.906-992.588 ( R2 =0.270, P =0.023). In conclusion, this study proved that social media positively influenced clinic appointments but the traditional personal brandings like reputations, academic pedigree, and word of mouth still played an indispensable role in career development. Young surgeons benefited most from social media. The promotive effect of social media would reach its saturation when the followers were up to ∼50,000.
This study aimed to verify the correlation of the airway-facial phenotype and visualize the morphological variation in Crouzon syndrome patients. Additionally, to develop a non-radiation methodology ...for airway assessments.
In this study, 22 patients diagnosed with Crouzon syndrome (Age: 7.80 ± 5.63 years; Gender distribution: 11 females and 11 males) were analysed. The soft tissue surface and airway were three-dimensionally reconstructed, and the entire facial phenotype was topologized and converted into spatial coordinates. Geometric morphometrics was employed to verify the correlation and visualize dynamic phenotypic variation associated with airway volume. A total of 276 linear variables were automatically derived from 24 anatomical landmarks, and principal component analysis (PCA) identified the 20 most significant parameters for airway evaluation. Correlation analyses between parameters and airway volume were performed. Then, patients were classified into three groups based on airway volume, and the differences among the groups were compared for evaluating the differentiating effectiveness of parameters.
The facial phenotype was strongly correlated with the airway (coefficient: 0.758). Morphological variation was characterized by (i) mandibular protrusion and anticlockwise rotation; (ii) midface retrusion; (iii) supraorbital frontward and (iv) lengthening of the facial height. All the anthropometric parameters were strongly associated with the airway, and the differences among the groups were statistically significant.
This study confirmed the strong correlation between facial phenotype and airway parameters in Crouzon syndrome patients. Despite the development of the airway, pathological midface retrusion was still aggravated, suggesting that surgical intervention was inevitable. Three-dimensional facial anthropometry has potential as a non-radiation examination for airway evaluation.
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