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2019-nCoV Omicron (B.1.1.529) variant, which has brought new challenges to the prevention and control of COVID-19 pandemic, has the characteristics of stronger transmissibility and more rapid transmission and more significant immune evasion. It took only two months to become a predominant strain worldwide after its identification in South Africa in November 2021. Local epidemics caused by Omicron variant have been reported in several provinces in China. However, the epidemiological characteristics of highly mutated Omicron variant remain unclear. This article summarizes the progress in the research of functional mutations, transmissibility, virulence, immune evasion and cross-reactive immune responses of Omicron variant, to provide references for the effective prevention and control of COVID-19 pandemic caused by Omicron variant.新型冠状病毒Omicron（B.1.1.529）变异株具有传播力强、传播速度快、免疫逃逸显著等特点，给新型冠状病毒肺炎疫情防控带来新的挑战。该变异株于2021年11月在南非被发现后，历时2个月便成为全球主要流行株，我国已有多个省份报告Omicron变异株引发的本土疫情。然而，Omicron变异株的高度突变对其流行病学特征的影响仍不够明晰。本文基于现有研究证据，针对Omicron变异株与功能有关的突变、传播力、毒力、免疫逃逸能力及免疫交叉反应等重要方面进行综述，为新型冠状病毒肺炎疫情的科学防控提供参考。.

肝脏胆管腺纤维瘤是一种非常罕见的肝内胆管肿瘤，在2020年版WHO分类中被归类为良性肿瘤。迄今为止，检索国内外文献报道23例，其中8例发生恶变。当细胞表现为细胞核拉长拥挤，呈假复层，排列呈复杂的乳头状、背靠背或筛状结构时提示肿瘤进展或恶性转化。我们报道1例胆管腺纤维瘤癌变-高中分化胆管细胞癌，并复习文献，探讨其病理形态特征、诊断及鉴别诊断要点。.

新型冠状病毒导致的重症呼吸道感染发病机制为促炎/抗炎反应紊乱及免疫失衡，免疫系统过度反应、免疫细胞过度凋亡和功能耗竭、免疫抑制或免疫麻痹等是主要的免疫病理表现。针对其发病机制的免疫调节治疗主要包括激素、IL-6受体拮抗剂、康复期血浆、超免疫球蛋白等，但其应用时机及临床效果尚存争议，本文对新型冠状病毒肺炎免疫失衡与免疫调节治疗进行评价总结。.

Long noncoding RNAs (lncRNAs) play crucial roles in the development of human cancers. LncRNA small nucleolar RNA host gene 20 (SNHG20) has been reported to be an oncogene in several cancers, whereas the specific role of SNHG20 in glioblastoma is unclear. In this study, we found that SNHG20 was significantly upregulated in glioblastoma tissues and cell lines. Survival analysis suggested that high expression of SNHG20 indicated the low overall survival rate of glioblastoma patients. Subsequently, gain or loss-of-function assays were carried out to examine the effect of SNHG20 on glioblastoma cell proliferation and apoptosis. We found that SNHG20 knockdown obviously suppressed cell proliferation, increased cell apoptosis and impaired stem properties, while SNHG20 overexpression led to the opposite results. In vivo experiment demonstrated that knockdown of SNHG20 efficiently suppressed cell growth in vivo. Furthermore, western blotting demonstrated that the PI3K/Akt/mTOR signaling pathway was activated by SNHG20 in glioblastoma cells. At last, rescue assays validated that PI3K/Akt/mTOR signaling pathway involved in the glioblastoma progression mediated by SNHG20. Taken together, this study revealed that SNHG20 regulated PI3K/Akt/mTOR signaling pathway to promote tumorigenesis and stemness of glioblastoma.

Objective To investigate the characteristics and patterns of factors such as victims' information, injury tools and time of occurrence of intentional injury cases in southwest China. Methods One thousand three hundred and forty intentional injury cases from several places in southwest China from 2014 to 2016 assessed as minor injury level Ⅱ and above had been randomly selected. Data on victims' information, motives, injury tools, sites of occurrence, time of occurrence, injured parts and degrees of injury were classified and gathered, and then association analyses of motives and types of injury tools as well as degrees of injury and injury tools were made. Results Most of the victims were young adults between 20-50 years （65.2%）, male （82.3%）, rural household registration （62.8%）; the motives were mainly dispute （45.8%）. Injury tools were mostly blunt （54.6%） or sharp （36.0%）. Specifically, injuries were mostly made bare-handed （36.9%） and by cutting tools （33.2%）; the cases mainly occurred in public areas （59.0%）. Cases occurred more frequently in January （11.3%）, February （13.1%）, March （11.6%） and from 22：00 to 01：00 every night. Injuries mainly involved the craniofacial region. The wounds were mainly assessed as minor injury level Ⅱ （61.6%）. There was statistical significance in the difference of types of injury tools among cases with different motives （西南地区1 340例故意伤害案件的特征及相关因素分析.目的 探究我国西南地区故意伤害案件的伤者信息、致伤工具、发生时间等因素的特点及规律。 方法 随机抽取西南地区多地2014—2016年轻伤二级及以上故意伤害案件1 340例，分类汇总伤者信息、作案动机、致伤工具、发生场所、发生时间、损伤部位和损伤程度，并对作案动机与致伤工具类型，以及损伤程度与致伤工具作关联分析。 结果 所涉案件中，伤者多为20~50岁青壮年（65.2%）、男性（82.3%）、农村户籍（62.8%）；作案动机以纠纷为主（45.8%），致伤工具多为钝器（54.6%）和锐器（36.0%），尤以徒手（36.9%）和刀具（33.2%）多见；案件主要发生在公共场所（59.0%），1月（11.3%）、2月（13.1%）、3月（11.6%）及每天夜晚22：00~01：00（23.2%）是高发时期；损伤主要涉及颅面部，所致损伤程度以轻伤二级（61.6%）为主。不同作案动机中致伤工具的类型差异有统计学意义（法医学；创伤和损伤；回顾性研究；故意伤害；损伤程度；西南地区；案例分析.

Hepatocellular carcinoma (HCC) is a common malignancy worldwide with poor prognosis and high mortality. The aberrant expression or alteration of microRNAs (miRNAs) contributes to the development and progression of cancer. Studies have shown that miR-455 plays a regulatory role in the development of HCC. Therefore, in the present study, the role of miR-455 was analyzed in HepG2 cells proliferation and apoptosis using MTT and flow cytometry methods. Binding sites were predicted by bioinformatics and luciferase assay was used to verify the target relationship between miR-455 and RhoC-encoding gene RHOC. After that, the effects of miR-455 on RHOC and its product RhoC, were explored by qPCR and Western blotting. As PTEN is a key tumor suppressor gene in HCC, and Bcl-2 and Caspase 3 are important indication of apoptosis, expression levels of PTEN, Bcl2 and Caspase 3 proteins were determined in cells overexpressing RhoC. We show that miR-455 promotes HepG2 cells apoptosis and inhibits proliferation. Bioinformatics analysis and luciferase assay indicate that specific recognition sites for miR-455 are within the RhoC 3'-UTR. Luciferase activity was significantly lower in the cells co-transfected with miR-455 mimics and RhoC-WT (p0.01) as compared to that in control cells, pointing that RHOC gene is, indeed, targeted by miR-455. RHOC mRNA was significantly reduced after miR-455 transfection in HepG2 cells. In addition, we show that RhoC could activate the HCC cells proliferation ability and inhibit apoptosis rate (p0.01), and decrease expression of PTEN and Caspase 3 (p0.01), while upregulating levels of Bcl2. In conclusion, our study indicates that miR-455 plays a suppressive role in HCC development by targeting RhoC-encoding mRNA.

As a new generation of negative pressure drainage technology, vacuum-assisted closure (VAC) can provide stable and persistent negative pressure, and there are several modes to choose from. VAC plays an important role in closing wounds quickly, controlling infection, promoting angiogenesis, increasing blood flow, and promoting granulation tissue growth of wounds. It is now widely applied in all kinds of acute, chronic, and special wounds in clinic with good therapeutic results. However, we need to pay attention to contraindications and complications of VAC when it is used, avoiding secondary damage due to improper treatment. In this review, we summarize VAC dressings, treating pressure and mode choice, mechanism in promoting wound healing, and clinical application of VAC.

A sub-population of chemoresistant cells exhibits biological properties similar to cancer stem cells (CSCs), and these cells are believed to be a main cause for tumor relapse and metastasis. In our study, we explored the role of SOX8 and its molecular mechanism in the regulation of the stemness properties and the epithelial mesenchymal transition (EMT) of cisplatin-resistant tongue squamous cell carcinoma (TSCC) cells. We found that SOX8 was upregulated in cisplatin-resistant TSCC cells, which displayed CSC-like properties and exhibited EMT. SOX8 was also overexpressed in chemoresistant patients with TSCC and was associated with higher lymph node metastasis, advanced tumor stage and shorter overall survival. Stable knockdown of SOX8 in cisplatin-resistant TSCC cells inhibited chemoresistance, tumorsphere formation, and EMT. The Wnt/β-catenin pathway mediated the cancer stem-like properties in cisplatin-resistant TSCC cells. Further studies showed that the transfection of active β-catenin in SOX8 stable-knockdown cells partly rescued the SOX8 silencing-induced repression of stem-like features and chemoresistance. Through chromatin immunoprecipitation and luciferase assays, we observed that SOX8 bound to the promoter region of Frizzled-7 (FZD7) and induced the FZD7-mediated activation of the Wnt/β-catenin pathway. In summary, SOX8 confers chemoresistance and stemness properties and mediates EMT processes in chemoresistant TSCC via the FZD7-mediated Wnt/β-catenin pathway.

Early detection of adefovir dipivoxil-resistant mutants during long-term treatment of chronic hepatitis B virus (HBV) infection with this drug is of great clinical importance. We developed an improved reverse dot hybridization test for simple and rapid detection of the rtA181V/T and rtN236T mutations associated with adefovir dipivoxil resistance in chronic hepatitis B patients. Probes were designed for genotypes B, C, and D of this resistance characteristic; a total of 70 clinical samples were analyzed with this improved reverse dot hybridization assay. Its usefulness was validated by comparing with sequencing data. Discordant results were confirmed by subclone sequencing. This reverse dot hybridization assay was sufficiently sensitive to detect 10(3) copies/mL; it also detected adefovir dipivoxil-resistant mutant strains when they comprised more than 5% of a mixed virus population. This reverse dot hybridization array correctly identified adefovir dipivoxil-resistant mutants; it had high concordance (98.5%) with direct sequencing data. There was no clear relationship between the HBV genotype and the development of adefovir dipivoxil-resistant mutants. This reverse dot hybridization assay proved to be simple and rapid for detection of rtA181V/T and rtN236T mutations associated with resistance to adefovir dipivoxil.

From 1977 to 1994, 9 breast cancer were treated. All patients presented axillary node enlargement as first sign. Six patients were treated by radical or modified radical mastectomy and 3 by axillary node excision. All patients received postoperative adjuvant radiotherapy and chemotherapy. Among the 6 patients treated by radical or modified radical mastectomy, 4 survived over 10 years after surgery, 1 died of heart disease at 8 years, and 1 on chemotherapy is for 4 months. The three patients treated by axillary node excision, all died of the disease at 8-32 months. It is considered that radical or modified radical mastectomy with adjuvant radiotherapy and chemotherapy is a suitable treatment selection for occult breast cancer.