Ferret badger rabies in Zhejiang, Jiangxi and Taiwan, China.

Ferret badger (FB, Melogale moschata) rabies is an increasing public health threat to humans, with FBs being a major reservoir and vector of rabies in China. Based on 152 published nucleotide sequences of the FB rabies virus (RABV) nucleoprotein, phylogenetic analysis revealed them to be clustered into six FB-related lineages, FB-I to FB-VI. The genetic features of members of lineage FB-VI suggest that cross-species transmission occurs between FBs and dogs. Here, we describe the phylogenetic relationships between FB-RABVs, their geographic segregation, and their evolutionary dynamics in epizootic regions.

Leaching behavior of total organic carbon, nitrogen, and phosphorus from banana peel.

The leaching behavior of organic carbon and nutrient compounds from banana peel (BP) was investigated in batch assays with respect to particle size, contact time, pH value, and temperature. The granularity, contact time, pH, and temperature caused no significant effects on the leaching of total phosphorus (TP) from the BP. The maximum leached total nitrogen (TN) content was found at pH 5.0 and 90 minutes, while no significant effects were caused by the granularity and temperature. The maximum leached total organic carbon (TOC) content was found by using a powder of 40 mesh, 150 minutes and at pH 6.0, while the temperature had no effect on the TOC leaching. The proportions of the TN, TP, and TOC contents leached from the dried BP ranged from 33.6% to 40.9%, 60.4% to 72.7%, and 8.2% to 9.9%, respectively, indicating that BP could be a potential pollution source for surface and ground water if discharged as domestic waste or reutilized without pretreatment.

LMO1 is a novel oncogene in colorectal cancer and its overexpression is a new predictive marker for anti-EGFR therapy.

Colorectal cancer (CRC) is the third leading cause of cancer mortality in the world. We report that one oncogene amplified on chromosome 3q26, LMO1, a master transcriptional regulator of stemness, operates to drive strong growth phenotype in CRC. The gene expression changes of LMO1 in human CRC tissues compared with noncancerous tissues were detected using real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) analysis and immunohistochemistry, which identified the gene overexpression of LMO1 in CRC. Moreover, we discovered that LMO1 promoted cancer cell proliferation in vitro/in vivo and LMO1 expression correlated with elevated AKT phosphorylation in CRC while the AKT phosphorylation was required for oncogenic effects of LMO1. Next, our data point to the usefulness of LMO1 overexpression, as a new predictive marker for responsiveness to cetuximab. All in all, LMO1 is a commonly activated tumor promoter that activates AKT signaling in CRC and a new predictive marker for targeted therapy.

Optimizing adsorption of Pb(II) by modified litchi pericarp using the response surface methodology.

Litchi pericarp was chemically modified as a novel bioadsorbent (MLP) for Pb(II) adsorption in this study. Operating parameters such as contact time, adsorbent dosage, and initial pH of solution were investigated using batch assays and further optimized using response surface methodology (RSM). The results showed that the MLP exhibited a high adsorption efficiency of 99.97% for Pb(II), which was optimal at a contact time of 71.56min, a initial pH of 6.81, and an adsorbent dose of 3.80g/L. Adsorption processes of Pb(II) by MLP could be well described with Langmuir or Freundlich isotherms and a pseudo-second-order kinetic model. The maximum adsorption capacity of Pb(II) by MLP was determined as 163.93mg/g, suggesting a highly promising potential for MLP to be used as a new bioadsorbent. Additionally, the thermodynamic study indicated that the adsorption process of Pb(II) by MLP was spontaneously and exothermic.

Comparative study on the adsorption capacity of raw and modified litchi pericarp for removing Cu(II) from solutions.

The adsorption of Cu(II) onto raw litchi pericarp (LP) and modified litchi pericarp (MLP) as a function of pH, adsorbent dose and contact time, were investigated. Adsorption equilibrium isotherms, kinetics, and thermodynamics were studied to characterize the adsorption process. Leaching assays were also conducted to evaluate the potential contamination risk of LP and MLP to aqueous systems. The maximum adsorption of Cu(II) onto MLP was occurred at the pH of 6.0, adsorbent dose of 10.0 g/L, and contact time of 60 min, respectively. The adsorption process of Cu(II) onto LP and MLP were described well by both Langmuir and Freundlich isotherms, and the adsorption kinetics of Cu(II) on MLP was pseudo-second-order. Cu(II) adsorption onto LP and MLP are both exothermic, while it is spontaneous for MLP, and non-spontaneous for LP. The maximum adsorption capacity of Cu(II) onto MLP was 23.70 mg/g, which was about 2.7 times higher than that of LP. Additionally, as compared to LP, the leaching amounts of TOC, TN, and TP from MLP were significantly reduced by a percentage of 27.0%, 90.3%, and 35.3%, respectively.

Traditional Chinese Medicine Syndromes are Associated with Driver Gene Mutations and Clinical Characteristics in Patients with Lung Adenocarcinoma.

This study aimed to investigate the associations between traditional Chinese medicine (TCM) syndromes and driver gene mutations as well as the clinical characteristics of patients with lung adenocarcinoma. We performed a cross-sectional study in patients with lung adenocarcinoma between June 2020 and October 2021. The patient characteristics, such as age, sex, smoking history, clinical stage, metastasis, driver gene mutations, and the type of traditional Chinese medicine syndrome/element, were collected. The associations between each TCM syndrome and sex, smoking history, clinical stage, metastasis, and driver gene mutations were analyzed. The present study included 127 patients. The most frequent TCM syndromes were Qi and Yin deficiency (39, 30.7%) and lung-spleen Qi deficiency (32, 25.2%). Eighty-one (63.8%) patients had mutations in driver genes, especially in the EGFR gene (64, 79.0%). There was a statistically significant association between a driver gene mutation and TCM syndrome (P < 0.05). Genetic mutations presented more frequently in patients with Qi and Yin deficiency (37.0%), lung-spleen Qi deficiency (30.0%), or the cold element (59.3%). Male patients were more likely to have Qi stagnation and blood stasis, whereas female patients were more likely to have lung-spleen Qi deficiency or Qi and Yin deficiency. The patients with lung-spleen Qi deficiency were usually younger than those with Qi and Yin deficiency or Qi stagnation and blood stasis (P < 0.05). Compared with the patients with other TCM syndromes, the patients with Yin and Yang deficiency were more likely to have bone metastasis. TCM syndromes were associated with driver gene mutations, sex, age, and bone metastasis in patients with lung adenocarcinoma.

Frontier progress of the combination of modern medicine and traditional Chinese medicine in the treatment of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC, accounting for 90% of primary liver cancer) was the sixth most common cancer in the world and the third leading cause of cancer death in 2020. The number of new HCC patients in China accounted for nearly half of that in the world. HCC was of occult and complex onset, with poor prognosis. Clinically, at least 15% of patients with HCC had strong side effects of interventional therapy (IT) and have poor sensitivity to chemotherapy and targeted therapy. Traditional Chinese medicine (TCM), as a multi-target adjuvant therapy, had been shown to play an active anti-tumor role in many previous studies. This review systematically summarized the role of TCM combined with clinically commonly used drugs for the treatment of HCC (including mitomycin C, cyclophosphamide, doxorubicin, 5-fluorouracil, sorafenib, etc.) in the past basic research, and summarized the efficacy of TCM combined with surgery, IT and conventional therapy (CT) in clinical research. It was found that TCM, as an adjuvant treatment, played many roles in the treatment of HCC, including enhancing the tumor inhibition, reducing toxic and side effects, improving chemosensitivity and prolonging survival time of patients. This review summarized the advantages of integrated traditional Chinese and modern medicine in the treatment of HCC and provides a theoretical basis for clinical research.

The Shuganhuazheng Formula in Triple-Negative Breast Cancer: A Study Based on Network Pharmacology and In Vivo Experiments.

Breast cancer is the most common cancer in women. Among breast cancer subtypes, triple-negative breast cancer (TNBC) has the highest degree of malignancy and the worst prognosis. The Shuganhuazheng formula (SGHZF) is a traditional Chinese herbal formula for the treatment of TNBC, but the mechanism of SGHZF in the treatment of TNBC remains unclear. In this study, the therapeutic effect and mechanism of SGHZF against TNBC were preliminarily determined based on in vivo experimental verification and network pharmacology. In terms of therapeutic effects, the antitumour effect was verified by measuring and calculating tumour volume, and the expression of proto-oncogene c-Myc was verified by PCR. In terms of the mechanism, potential therapeutic targets were identified by overlapping the SGHZF-related and TNBC-related targets. After comprehensively analysing the results of the protein-protein interaction (PPI), gene ontology (GO) function, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, Akt and HIF-1α were selected for verification by using immunohistochemical and Western blot analyses. The results of the study indicated that SGHZF can inhibit breast tumour growth in mice and that the mechanism may be related to the inhibition of Akt and HIF-1α expression.

LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR­4310/LGR5/Wnt/ß­catenin signaling pathway.

Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor­Node­Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)­4310 that targeted LGR5. Through the inhibition of miR­4310, CASC15 promoted leucine­rich repeat­containing G­protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/ß­catenin signaling pathway. The results revealed that the inhibition of the Wnt/ß­catenin signaling pathway in CASC15­overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/ß­catenin signaling pathway in a miR­4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.

Erratum: Role of macrophage migration inhibitory factor in mesenchymal epithelial transition of cervical carcinoma cells.

[This corrects the article on p. 9621 in vol. 10, PMID: 31966840.].

Role of macrophage migration inhibitory factor in mesenchymal epithelial transition of cervical carcinoma cells.

Cervical cancer is a kind of female malignant tumor with increasing incidence recently. Macrophage migration inhibitory factor (MIF) is a major tumor facilitating factor. The previous study suggests that there was a correlation between MIF and migration or invasion of tumors. Epithelial mesenchymal transition (EMT) is the basis for tumor invasion and migration. Therefore, this study utilized MFI to treat cervical carcinoma Hela cells, and the mechanism of EMT was also further analyzed. Cervical carcinoma Hela cells were transfected with pFenesil MIF siRNA plasmids, following by real-time fluorescent quantitative PCR to detect MIF levels. MTT assay was then utilized for evaluate the proliferative activity of Hela cells after transfection. The cell invasion and migration were examined. The expression of E-cadherin and Vimentin were also detected. The results indicated that the MIF was positively expressed in Hela cells, whose MIF mRNA level was increased after the transfection (P<0.05). Compared to the control or blank group, the transfected group had elevated proliferative activity with elongated incubation time (P<0.05). Both invasion and migration functions of transfected cells were significantly potentiated (P<0.05) compared to the control or blank group. E-cadherin expression level was also decreased in experimental group. MIF was also expressed in cervical carcinoma Hela cells. Elevated MIF level could facilitate the cell invasion and migration, and elevate the Vimentin and decrease E-cadherin expression, thus facilitating EMT.

MicroRNA-217 regulates WASF3 expression and suppresses tumor growth and metastasis in osteosarcoma.

Osteosarcoma is the most common type of primary tumor of bone which mainly affects adolescents and young adults. Osteosarcoma causes large number of deaths because of its complex pathogenesis and resistance to conventional treatment. MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs, causing translational repression or degradation. In this study, we showed that miR-217 was down-regulated in osteosarcoma cell lines and tissues in comparison to that in normal bone cells or tissues. Meanwhile, the lower level of miR-217 was associated with metastasis in clinical osteosarcoma patients. Furthermore, we found that overexpession of miR-217 markedly suppressed cell proliferation, migration, and invasion of osteosarcoma cells. Conversely, the inhibition of miR-217 expression significantly accelerated the cell proliferation, migration, and invasion. Moreover, we identified WASF3 as a novel functional downstream target of miR-217. The ectopic expression of WASF3 can partially reverse the inhibition of cell proliferation and invasion caused by miR-217. Take together, our results demonstrate that miR-217 functions as a tumor-suppressive miRNA and inhibits the osteosarcoma tumorigenesis through targeting WASF3.

LMO1 is a novel oncogene in lung cancer, and its overexpression is a new predictive marker for anti-EGFR therapy.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality in the world. We report that one oncogene amplified on chromosome 3q26, LMO1, a master transcriptional regulator of stemness, operates to drive strong growth phenotype in NSCLC. We first validate gene expression changes of LMO genes by real-time quantitative RT-PCR real-time quantitative reverse transcriptase-polymerase chain reaction analysis and immunohistochemistry, and we identified gene overexpression of LMO1 compared with non-cancerous tissues (p < 0.01). Next, we discovered that LMO1 promoted cancer cell proliferation in our in vitro/vivo cell proliferation assay, and our cell signaling experiments showed that LMO1 expression correlated with elevated AKT phosphorylation in NSCLC, while the AKT phosphorylation was required for LMO1's oncogenic effects. In addition, we compared complete response rate, stable disease rate, disease progression rate, and the disease control rate of patient with different LMO1 gene expression which pointed to the usefulness of LMO1 overexpression, as a new predictive marker for responsiveness to cetuximab. All in all, LMO1 is a commonly activated tumor promoter that activates AKT signaling in NSCLC and a new predictive marker for targeted therapy.

Helicobacter hepaticus infection in primary hepatocellular carcinoma tissue.

INTRODUCTION: Helicobacter (H.) hepaticus infection causes chronic active hepatitis and induces hepatocellular tumours in A/JCr mice, but evidence of this in humans is scarce. This study aimed to demonstrate the correlation between H. hepaticus and human primary hepatocellular carcinoma (HCC). METHODS: The sera of 50 patients with primary HCC were tested for the presence of anti-H. pylori and anti-H. hepaticus immunoglobulin G (IgG) antibodies. The liver tissues of patients who tested positive for serum antibody were analysed for H. hepaticus-specific 16S rRNA, H. hepaticus cdtB, H. pylori cagA, H. pylori vacA and H. pylori ureC genes using polymerase chain reaction. RESULTS: After the anti-H. pylori antibodies in the serum samples were absorbed by H. pylori antigen, the anti-H. hepaticus IgG serum antibody detection rate was 50.0% in patients with primary HCC. This was significantly higher (p < 0.001) than the detection rate in the benign liver tumour (7.7%) and normal liver tissue (6.3%) groups. Of the 25 primary HCC samples that tested positive for anti-H. hepaticus IgG serum antibody, the H. hepaticus-specific 16S rRNA gene was detected in nine (36.0%) samples. Sequencing showed that the polymerase chain reaction-amplified product exhibited 95.5%-100% homology to the H. hepaticus-specific 16S rRNA gene. Among these nine primary HCC tissue samples, the H. hepaticus cdtB gene was detected in four (44.4%) samples, while no such expression was observed in the benign liver tumour or normal liver tissue groups. CONCLUSION: The present study identified the presence of H. hepaticus infection in patients with primary HCC using serological and molecular biological detection, suggesting that H. hepaticus infection may be involved in the progression of HCC.