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Objective To determine the risk factors for human fascioliasis in Binchuan County. Methods Community-based case-control study was conducted in Binchuan County, by using a structured questionnaire from interview. Enrolled participants were 72, including 18 patients as cases in the hospital, and 54 community controls selected from the nearest households surrounding patient households. Cases and controls were matched with gender and age. Chi-square test and Logistic regression were employed for analysis of data. Results Eating salad vegetable three times every week, salad lettuce and salad vegetable purchased from market were risk factors for human fascioliasis. Conclusion The most effective public health measures include strengthening health education, improving food health awareness of residents, strengthening grazing management and domestic animal disease control, preventing fecal pollution and improving environment to avoid survival of Limnea peregra. [ABSTRACT FROM AUTHOR]

Purpose: The present study was carried out to investigate the global m 6 A-modified RNA pattern and possible mechanisms underlying the pathogenesis of keloid. Method: In total, 14 normal skin and 14 keloid tissue samples were first collected on clinics. Then, three samples from each group were randomly selected to be verified with the Western blotting to determine the level of methyltransferase and demethylase. The total RNA of all samples in each group was isolated and subjected to the analysis of MeRIP sequencing and RNA sequencing. Using software of MeTDiff and htseq- count, the m 6 A peaks and differentially expressed genes (DEGs) were determined within the fold change >2 and p- value < 0.05. The top 10 pathways of m 6 A-modified genes in each group and the differentially expressed genes were enriched by the Kyoto Encyclopedia of Genes and Genomes signaling pathways. Finally, the closely associated pathway was determined using the Western blotting and immunofluorescence staining. Results: There was a higher protein level of WTAP and Mettl3 in the keloid than in the normal tissue. In the keloid samples, 21,020 unique m 6 A peaks with 6,573 unique m 6 A-associated genetic transcripts appeared. In the normal tissue, 4,028 unique m 6 A peaks with 779 m 6 A-associated modified genes appeared. In the RNA sequencing, there were 847 genes significantly changed between these groups, transcriptionally. The genes with m 6 A-methylated modification and the upregulated differentially expressed genes between two tissues were both mainly related to the Wnt signaling pathway. Moreover, the hyper-m 6 A-modified Wnt/ β -catenin pathway in keloid was verified with Western blotting. From the immunofluorescence staining results, we found that the accumulated fibroblasts were under a hyper-m 6 A condition in the keloid, and the Wnt/ β -Catenin signaling pathway was mainly activated in the fibroblasts. Conclusion: The fibroblasts in the keloid were under a cellular hyper-m 6 A-methylated condition, and the hyper-m 6 A-modified highly expressed Wnt/ β -catenin pathway in the dermal fibroblasts might promote the pathogenesis of keloid., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Lin, Chen, Peng, Xiang, Xiao, Chen, Cui, Huang and Liu.)

Acute myeloid leukemia (AML) with nucleophosmin 1 (NPM1) mutations exhibits distinct biological and clinical features, accounting for approximately one-third of AML. Recently, the N 6 -methyladenosine (m 6 A) RNA modification has emerged as a new epigenetic modification to contribute to tumorigenesis and development. However, there is limited knowledge on the role of m 6 A modifications in NPM1-mutated AML. In this study, the decreased m 6 A level was first detected and high expression of fat mass and obesity-associated protein (FTO) was responsible for the m 6 A suppression in NPM1-mutated AML. FTO upregulation was partially induced by NPM1 mutation type A (NPM1-mA) through impeding the proteasome pathway. Importantly, FTO promoted leukemic cell survival by facilitating cell cycle and inhibiting cell apoptosis. Mechanistic investigations demonstrated that FTO depended on its m 6 A RNA demethylase activity to activate PDGFRB/ERK signaling axis. Our findings indicate that FTO-mediated m 6 A demethylation plays an oncogenic role in NPM1-mutated AML and provide a new layer of epigenetic insight for future treatments of this distinctly leukemic entity., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Xiao, Lei, Ren, Peng, Jing, Jiang, Huang, Tao, Lin, Yang, Sun, Tang, Wei, Yang and Zhang.)

Several studies have reported that FZD2 regulates tumor biology in a complex manner. The aim of the present study was to identify the role of FZD2 in the cell growth and metastasis of salivary adenoid cystic carcinomas (SACCs). The expression of FZD2 in ACC-83 and ACC-LM cells were measured with real-time PCR. Immunohistochemical staining was used to detect the expression of FZD2 in clinical SACC samples with or without metastasis. Cell proliferation and Transwell assays were performed to explore the effects of FZD2 on cell growth and migration following the silencing of FZD2 with small interference RNAs and the overexpression of FZD2 with plasmid. Our data showed that FZD2 was downregulated in ACC-LM cells, which are an adenoid cystic carcinoma cell line with high metastatic potential, compared to ACC-83 cells, which have low metastatic potential. Additionally, the expression of FZD2 was lower in SACC tissues with metastasis compared to SACC tissues without metastasis (P<0.05). Cell proliferation and migration of ACC-83 cells were increased after the knockdown of FZD2 and decreased following overexpression of FZD2. Knockdown of FZD2 downregulated the expression of PAI-1. Our results suggest that FZD2 may be a tumor suppressor gene in SACCs that inhibits cell growth and migration.

Objective: To carry out clinical diagnosis and treatment of Fasciola gigantica infection during an outbreak in Yunnan Province., Methods: Data on epidemiology, diagnosis and treatment were collected from 27 patients. A questionnaire survey to the patients and partial villagers was carried out including history of raw food-eating and pet-raising. Animal feces were collected and examined by precipitation method and eggs incubation method. Cattle from two patients families were dissected to find Fasciola infection. Serum samples from patients, family members, and villagers were detected. Possible intermediate snails were collected from the vicinity of streams and ponds in 15 villages where patients lived., Results: The earliest onset of symptoms among the patients was on March 10, 2011 and the last case was on January 10, 2012. The clinical manifestations were mainly fever with unknown reason, decreasing hemoglobin, increasing eosinophils, and hepatosplenomegaly. No parasite eggs were found in feces. Antibodies against F. gigantica were positive by ELISA in 23 patients. Fasciola eggs were then found in 4 patients' feces on February 16, 2012. F. gigantica eggs and adults were found in the hepatobiliary system of dissected cattle. Triclabendazole [10 mg/(kg x d) x2 d] was administered orally for the patients and the clinical symptoms eased. Snails including Physa acuta, Radix swinhoei and Galba pervia were collected and cercariae were found in only one snail., Conclusion: An outbreak of F. gigantica infection has been confirmed and the diagnosed cases effectively treated with triclabendazole.

Cadherins are found in almost all living organisms. In addition to their role in the formation and maintenance of normal tissue architecture, cadherins seem to play a crucial role in the cell-cell interactions of cancer cells in tumorigenesis, invasion and metastasis. The aim of the present study was to identify the role of CDH12 in the invasion and metastasis of salivary adenoid cystic carcinoma (SACC). Real-time PCR results showed that CDH12 is abnormally expressed in the highly metastatic SACC cell line ACC-M, compared to ACC-2, a SACC cell line with low metastatic ability. CDH12 expression was significantly higher in clinical samples with metastasis and recurrence than in those without metastasis and recurrence (P<0.05), as demonstrated by immunohistochemical analysis. Overexpression of the CDH12 protein in ACC-M cells infected with an adenovirus vector containing CDH12 enhanced the invasive and migratory ability of ACC-M cells in vitro compared to ACC-M cells infected with empty vector. Likewise, knockdown of CDH12 by small interfering RNA efficiently inhibited the invasion and migration of ACC-M cells in vitro. These results indicate that CDH12 may play an important role in the invasion and metastasis of SACC.

The Notch signaling pathway is important for cell-cell communication; it is involved in gene regulation mechanisms that control multiple cell differentiation processes during embryonic and adult life. Notch is present in all metazoans, and vertebrates possess four different Notch receptors: Notch-1, Notch-2, Notch-3, and Notch-4. The aim of the present study was to identify the role of Notch protein in the metastasis of salivary adenoid cystic carcinoma (SACC). Real-time PCR results showed that Notch-1, Notch-2, and Notch-4 were upregulated in the highly metastatic SACC cell line ACC-M, compared to ACC-2, a SACC cell line with low metastatic ability. Knockdown of Notch-4 by small interfering RNA efficiently inhibited the invasion of ACC-M cells. Notch-4 expression was significantly higher in the clinical samples with metastasis and recurrence compared to that in control (p<0.05), shown by immunohistochemistry analysis. These results indicate that Notch-4 may play an important role in SACC metastasis.

Purpose: To study the differential expression pattern of MMPs and TIMPs in ACC-M and ACC-2 tumor model., Methods: High and low metastatic tumor models were set up by transplantion of ACC-M and ACC-2 to nude mouse respectively. Then 3 mice in each group were selected randomly to detect the mRNA level of MMP-2, MMP-7, MMP-9, TIMP-1 and TIMP-2 using semiquantitative RT-PCR,GAPDH was used as internal control. Meanwhile, the expression of MMP-2, MMP-7, MMP-9, TIMP-1 and TIMP-2 in each transplanted tumor were determined by immunohistochemical assay, and IOD value of immunohistochemical reaction was measured. All data were analyzed by SPSS11.5 software package for Student's t test., Results: The results of RT-PCR and immunohistochemistry showed an up-regulation of MMP-2, MMP-7, MMP-9 and TIMP-1 in ACC-M tumor model compared with ACC-2 model (P < 0.05), while the expression of TIMP-2 showed no significant difference between the two models (P > 0.05)., Conclusion: The differential expression pattern of MMP-2, MMP-7, MMP-9, and TIMP-1 in 2 tumor models may result in different metastasis potential; The 2 tumor models provide good study model for investigation of the metastatic mechanism of salivary adenoid cystic carcinoma.

Objective: To construct differential expression profiles of adenoid cystic carcinoma cell lines for screening candidate genes related to metastasis and to verify some candidate genes in adenoid cystic carcinoma., Methods: Restriction fragments differential display PCR (RFDD-PCR) was used to set up gene expression profiles of adenoid cystic carcinoma cell lines-ACC-M and ACC-2, with high and low metastasis potential respectively. Candidate genes were screened through bioinformatics analysis. Then, a gene family of these candidate genes was checked using semi-quantitative reverse transcription-PCR(RT-PCR)., Results: Two gene expression profiles including 5420 gene fragments were constructed, 12 genes of a family called matrix metalloproteinase genes (MMPs) were observed obvious differentially expressed between two cell lines. Results of semi-quantitative RT-PCR also identified this different expression of MMP2,MMP7,MMP9,MMP14,MMP15 and MMP24., Conclusion: The construction of gene expression profiles of ACC-M and ACC-2 cell lines makes the foundation for seeking the target genes of adenoid cystic carcinoma. MMP2,MMP7,MMP9 and MMP15 may be relevant with carcinogenesis, development and metastasis of adenoid cystic carcinoma, and different metastasis potential may result from different subtype of MMPs gene family.