In addition to the physical deformity, there is often great psychological burden of facial scars for patients. In this study, we use condensed nanofat combined with fat grafts in a novel technique to improve atrophic facial scars by raising both the surface and the bottom of the affected area.OBJECTIVE To assess whether the use of condensed nanofat combined with fat grafting can be effective in treating atrophic facial scars from both an aesthetic and a functional perspective. DESIGN, SETTING, AND PARTICIPANTSIn this prospective case series of 20 patients with 25 atrophic facial scars, each scar was treated with condensed nanofat combined with fat grafts at the

Hepatocellular carcinoma (HCC) is a highly heterogeneous, multigene-driven malignant tumor. ZNF384 is an overexpressed gene with a high frequency of alteration in HCC, but research on the function of ZNF384 in HCC is lacking. In this study, the expression level of ZNF384 in HCC was analyzed through immunohistochemical (IHC) staining, Western blot analysis and qRT-PCR. We also generated ZNF384 knockdown and knockout HCC cell lines using short hairpin RNA (shRNA) and CRISPR/Cas9 systems. MTS, colony formation, and 5-ethynyl-20-deoxyuridine (EdU) assays; flow cytometry; and a xenograft mouse model were used to evaluate the effects of ZNF384 on cell proliferation. Western blot analysis, a dual luciferase reporter assay and a ChIP assay were performed to explore the potential mechanism. We found that overexpression of ZNF384 in HCC and elevated expression of ZNF384 in HCC tissues was significantly correlated with tumor recurrence ( P = 0.0097). Kaplan–Meier survival analysis revealed that high expression levels of ZNF384 were correlated with poor overall survival ( P = 0.0386). Downregulation of ZNF384 expression suppressed HCC cell proliferation by inhibiting the expression of Cyclin D1. These findings suggest that ZNF384 tends to act as an oncogene in the development of HCC. ZNF384 promotes the proliferation of HCC cells by directly upregulating the expression of Cyclin D1 and might serve as a prognostic predictive factor for HCC patients.

The incidence of inflammatory bowel diseases (IBD), including Crohn's diseases and ulcerative colitis, is increasing by time and showing a trend of younger age. Precise diagnosis and effective treatments for IBD have attracted growing attention in recent years. However, diagnosing and locating inflammatory lesions remain a great challenge for IBD. In this study, assisted by a kind of aggregation‐induced emission (AIE) nanoprobes (BPN‐BBTD nanoparticles [NPs]), the second near‐infrared (NIR‐II) fluorescence imaging is first utilized to accurately trace inflammatory lesions, monitor inflammation severity and detect the response to the drug intervention in IBD mouse models. Through the advantages of high signal‐to‐background ratio (SBR) and sharp spatial resolution of bio‐imaging in NIR‐II region, the NIR‐II fluorescence imaging‐guided surgery can help to achieve a complete resection of severe inflammatory bowls and a secure surgical anastomosis. In addition, with the help of NIR‐II fluorescence wide‐field microscopy, the distribution of BPN‐BBTD NPs can be directly detected in tissue level and found to be mainly accumulated in mucosa and submucosa layers. This study highlights that AIE NPs‐assisted NIR‐II fluorescence imaging hold a great potential value for future diagnosis and imaging‐guided surgery in IBD.

Lymph node metastasis is a major metastatic route of cancer and significantly influences the prognosis of cancer patients. Radical lymphadenectomy is crucial for a successful surgery. However, iatrogenic normal organ injury during lymphadenectomy is a troublesome complication. Here, this paper reports a kind of organic nanoprobes (IDSe-IC2F nanoparticles (NPs)) with excellent second near-infrared (NIR-II) fluorescence and photothermal properties. IDSe-IC2F NPs can effectively label lymph nodes and helped achieve high-contrast lymphatic imaging. More importantly, by jointly using IDSe-IC2F nanoparticles and other kinds of nanoparticles with different excitation/emission properties, a multichannel NIR-II fluorescence imaging modality and imaging-guided lymphadenectomy is proposed. With the help of this navigation system, the iatrogenic injury can be largely avoided. In addition, NIR-II fluorescence imaging-guided photothermal treatment ("hot" strategy) can ablate those metastatic lymph nodes which are difficult to deal with during resection ("cold" strategy). Nanoprobes-assisted and multichannel NIR-II fluorescence imaging-guided "cold" and "hot" treatment strategy provides a general new basis for the future precision surgery.

Objective: Conflicting results existed about the role of prognostic nutritional index (PNI) for hepatocellular carcinoma (HCC) patients who received curative hepatectomy. The aim of this study is to identify the predictive capacity of PNI for survival after hepatectomy. Methods: Preoperative PNI, neutrophil-to-lymphocyte ratio (NLR), tumor feature and clinical information of 187 patients with HCC from Sir Run Run Shaw hospital were evaluated. We also conducted a meta-analysis of seven cohort studies. Results: Our study showed that HCC patients with a low PNI of <45 had a poor recurrence-free survival (RFS) rate (hazard ratio [HR] 1.762, 95% confidence interval [CI] 1.066-2.911, p ¼ 0.027, respectively). The 5-year OS and RFS rates of the high PNI (!45) vs low PNI (<45) were 76.7% vs 50.1% (p ¼ 0.001) and 47.0% vs 28.9% (p ¼ 0.001), respectively. In HCC TNM I patients (n ¼ 144), a low PNI remained an independent prognostic factor of OS and RFS (HR 2.305, 95% CI 1.008-5.268, p ¼ 0.048; HR 2.122, 95% CI 1.149-3.920, p ¼ 0.016). The 5-year OS and RFS rates of the high PNI vs low PNI were 81.3% vs 62.4% (p ¼ 0.041) and 53.4% vs 45.6% (p ¼ 0.013), respectively. In the pooled analysis, the data showed that a low PNI was significantly associated with poor OS and RFS (HR 2.27, 95% CI 1.03-4.07, p < 0.001 and HR 1.68, 95% CI 1.45-1.94, p < 0.001, respectively). Conclusions: The preoperative PNI was an independent prognostic factor for OS and RFS rates in HCC patients who received hepatectomy.

Altered metabolic patterns in tumor cells not only meet their own growth requirements but also shape an immunosuppressive microenvironment through multiple mechanisms. Noncoding RNAs constitute approximately 60% of the transcriptional output of human cells and have been shown to regulate numerous cellular processes under developmental and pathological conditions. Given their extensive action mechanisms based on motif recognition patterns, noncoding RNAs may serve as hinges bridging metabolic activity and immune responses. Indeed, recent studies have shown that microRNAs, long noncoding RNAs and circRNAs are widely involved in tumor metabolic rewiring, immune cell infiltration and function. Hence, we summarized existing knowledge of the role of noncoding RNAs in the remodeling of tumor metabolism and the immune microenvironment, and notably, we established the TIMELnc manual, which is a free and public manual for researchers to identify pivotal lncRNAs that are simultaneously correlated with tumor metabolism and immune cell infiltration based on a bioinformatic approach.

Although many approaches have been used to treat hepatocellular carcinoma (HCC), the clinical benefits remain limited, particularly for late stage HCC. In recent years, studies have focused on immunotherapy for HCC. Immunotherapies have shown promising clinical outcomes in several types of cancers and potential therapeutic effects for advanced HCC. In this review, we summarize the immune tolerance and immunotherapeutic strategies for HCC as well as the main challenges of current therapeutic approaches. We also present alternative strategies for overcoming these limitations.

E-cadherin is well known as a growth and invasion suppressor and belongs to the large cadherin family. Loss of E-cadherin is widely known as the hallmark of epithelial-tomesenchymal transition (EMT) with the involvement of transcription factors such as Snail, Slug, Twist and Zeb1/2. Tumor cells undergoing EMT could migrate to distant sites and become metastases. Recently, numerous studies have revealed how the expression of E-cadherin is regulated by different kinds of genetic and epigenetic alteration, which are implicated in several crucial transcription factors and pathways. E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%). Combining the data from The Cancer Genome Atlas (TCGA) database and previous studies, we have summarized the roles of gene mutations, chromosome instability, DNA methylation, histone modifications and non-coding RNA in E-cadherin in HCC. In this review, we discuss the current understanding of the relationship between these modifications and HCC. Perspectives on E-cadherin-related research in HCC are provided.