OBJECTIVE:To provide reference for chemical composition analysis in Angiopteris fokiensis. METHODS:The fat-soluble components in A. fokiensis were extracted and separated. The separated fat-soluble compounds were analyzed and identi-fied by GC-MS after methyl esterification. RESULTS & CONCLUSIONS:Totally 52 compounds were detected and 43 of those were identified. They were mainly organic acids and sterols compounds. The 43 components are first identified in A. fokiensis.

OBJECTIVETo examine the prevalence and the sequence of the genes of new genotypes of hepatitis G virus (HGV) in Guangxi, China.

METHODSSerum samples were collected from 85 intravenous drug abusers (IVDAs), 80 patients with liver diseases (PLDs) and 50 blood donors (BDs). All sera (n=215) were tested by using EIA for HBsAg, anti-HCV and anti-HIV, and by using nested PCR for HGV RNA. In 62 subjects positive for HGV, HGV RNA was sequenced, and a phylogenetic tree was constructed for analyzing genotypes of HGV.

RESULTSHGV RNA was detected in 85 of 215 serum samples (39.53%). The positivity rates for HBsAg, anti-HCV and anti-HIV were 39.07%, 42.79% and 0, respectively. First, 11 nucleotide sequences were determined and the isolates were grouped into three clusters with HGV. 5 of 11 HGV isolates clustered in a distinct phylogenetic branch (genotype Asia) which was different from the described GBV-C and HGV sequences, suggesting the presence of a new genotype of HGV in this locality. Second, 51 nucleotide sequences were determined and analyzed for their genotypes of HGV, and showed genotype GBV-C (3.23%), genotype HGV 30-65% and new genotype (genotype Asia) 64.51%, respectively.

CONCLUSIONSThere were subgenotypes in 3 genotypes of HGV; The predominant genotypes of HGV were genotype Asia and genotype HGV among IVDAs, PLDs, and BDs patients in Guangxi, China.

Adult ; Blood Donors ; China ; epidemiology ; Female ; GB virus C ; genetics ; isolation & purification ; Genotype ; Hepatitis C ; epidemiology ; Humans ; Liver Diseases ; virology ; Male ; Polymerase Chain Reaction ; RNA, Viral ; genetics ; Sequence Analysis, RNA ; Substance Abuse, Intravenous ; virology

Exocrine ductal carcinoma is an important part of malignant tumors of exocrine glands, including invasive breast ductal carcinoma, salivary duct carcinoma, pancreatic ductal adenocarcinoma and cholangiocarcinoma. Most of these diseases are aggressive, highly malignant and endanger human health. Early detection and diagnosis are the key to a good prognosis for exocrine ductal carcinoma. Different exocrine ductal carcinomas also have certain connections, and their molecular biological characteristics, pathological characteristics and molecular mechanisms have similarities. Surgical resection combined with adjuvant radiotherapy and chemotherapy is currently a common treatment method for exocrine ductal carcinoma. At the same time, its related targeted therapy and immunotherapy sites can also learn from each other. Human epidermal growth factor receptor-2 (HER-2) and the family markers have become breast ductal carcinoma and salivary duct carcinoma targeted therapy sites, and immunotherapy at programmed death ligand 1 (PD-L1) sites has also been involved in many studies, but there is no clear conclusion yet.

Ferroptosis is a new form of regulated cell death discovered in recent years, which is iron-dependent cell death characterized by peroxidation of polyunsaturated fatty acid phospholipids. Recent studies have shown that radiotherapy can induce ferroptosis in cancer cells via ionizing radiation. Targeting ferroptosis plays a synergistic role in tumor suppression with radiation, which not only further deepens the connotation of radiobiology, but also provides a new perspective for tumor radiosensitization. This review systematically summarizes the occurrence and defense of ferroptosis, focusing on the key role of ferroptosis in the radiobiological effects of tumor cells and the potential application of ferroptosis in radiosensitization.

Objective:To screen and verify the key radioresistance genes regulated by m6A methylation in nasopharyngeal carcinoma (NPC) based on the chip data and cell experiments.Methods:The microarray data of NPC radioresistance genes, m6A regulated genes and mRNA expression profiles of NPC genes were downloaded from Gene Expression Omnibus (GEO) database. The differential genes were screened and statistically analyzed by R software. The biological processes, signal pathways and interaction networks of these genes were analyzed by bioinformatics. The m6A regulatory factors were knocked down and the radioresistant strains were constructed. The above m6A differential radioresistant genes of NPC were screened and verified by real-time reverse transcription PCR (qRT-PCR) and Western blot. The m6A modification of screened genes and their direct binding ability with methyltransferase 3 (METTL3) were verified by methylated RNA immunoprecipitation qPCR (MeRIP-qPCR). The siRNA of selected genes was transfected into NPC cells, and after treatment with ionizing radiation, cell proliferation was detected by CCK-8 assay and EdU, apoptosis and cell cycle were detected by flow cytometry, and radiosensitivity was detected by clone formation assay. The trend of differences in the abundance of Fe 2+ and lipid peroxidation between the control and EGLN3 knockdown groups after ionizing radiation treatment was compared by paired t-test. Results:Chip data GSE48501 intersected with GSE200792 and GSE53819 to obtain 6 differential genes, including EGLN3, FOSL2, ADM, JUN, VEGFA and PRDM1. The target genes of EGLN3 and FOSL2 were further screened by TNMplot and KMplot, etc. The mRNA of the target genes directly bound to METTL3 and were subjected to its mediated modification of m6A. The target genes were up-regulated in the parental cells after irradiation in a dose and time gradient manner, which were also significantly up-regulated in radioresistant cells. After EGLN3 and FOSL2 were down regulated, the proliferation activity of NPC cells was more significantly decreased after irradiation, and the radiosensitization ratio was statistically significant compared with that of NPC cells without EGLN3 and FOSL2 down-regulation. After irradiation, EGLN3 down-regulated NPC cells significantly down-regulated glutathione peroxidase 4 (GPX4) expression, increased the abundance of Fe 2+ and lipid peroxidation, which played a role in radiosensitization by inducing ferroptosis. Conclusions:EGLN3 and FOSL2 play a role in radioresistance in NPC through METTL3 mediated m6A methylation. Down-regulation of EGLN3 combined with ionizing radiation can increase the intracellular Fe 2+ abundance and lipid peroxidation and down-reuglate the expression of GPX4 in NPC cells, which can enhance radiosensitization for NPC radiotherapy by the ferroptosis pathway.

Objective:To observe the possible toxicity of long-term intravenous injection of Tanreqing injection in Beagle dogs， so as to provide experimental data for its clinical safe medication. Method:A total of 32 Beagle dogs （16 males and 16 females） were randomly divided into the low- （2.5 mL·kg^-1）， medium- （5.0 mL·kg^-1）， and high-dose （10.0 mL·kg^-1） Tanreqing injection groups and control group according to their body mass indices， with eight dogs in each group. In the waking state， the dogs were treated with intravenous injection of corresponding drugs into the medial cephalic vein of forelimb for 13 weeks， followed by four-week drug withdrawal. After the observation of general condition， body mass， and food consumption， the Beagle dogs were subjected to electrocardiography， ophthalmoscopy， hematological examination， serum biochemistry， and blood coagulation test in the middle of medication （week 6）， at the end of medication （week 13）， and during recovery （week 17）. Then the gross anatomy was conducted for calculating the major organ coefficients and observing the histopathological changes. Result:No obvious toxic reaction was found in each group， but the decreased fibrinogen and increased Kupffer's cells phagocytizing yellow-brown pigment in hepatic sinusoids were observed in the high-dose Tanreqing injection group following three months of medication. Reduction of fibrinogen was not observed in recovery period， but Kupffer's cells that phagocytized yellow-brown pigment still existed. Conclusion:The intravenous injection of Tanreqing injection at 2.50 mL·kg^-1 （low dose）， 5.00 mL·kg^-1 （medium dose） or 10.00 mL·kg^-1 （high dose） for three months in Beagle dogs resulted in no obvious toxic reaction. However， it is still suggested to test the liver function and blood coagulation after long-term administration of high-dose Tanreqing injection.

Resection of oral and maxillofacial tumors is often accompanied by the inferior alveolar nerve neurectomy, resulting in abnormal sensation in lower lip. It is generally believed that spontaneous sensory recovery in this nerve injury is difficult. However, during our follow-up, patients with inferior alveolar nerve sacrifice showed different degrees of lower lip sensory recovery. In this study, a prospective cohort study was conducted to demonstrate this phenomenon and analyze the factors influencing sensory recovery. A mental nerve transection model of Thy1-YFP mice and tissue clearing technique were used to explore possible mechanisms in this process. Gene silencing and overexpression experiments were then conducted to detect the changes in cell morphology and molecular markers. In our follow-up, 75% of patients with unilateral inferior alveolar nerve neurectomy had complete sensory recovery of the lower lip 12 months postoperatively. Patients with younger age, malignant tumors, and preservation of ipsilateral buccal and lingual nerves had a shorter recovery time. The buccal nerve collateral sprouting compensation was observed in the lower lip tissue of Thy1-YFP mice. ApoD was demonstrated to be involved in axon growth and peripheral nerve sensory recovery in the animal model. TGF-β inhibited the expression of STAT3 and the transcription of ApoD in Schwann cells through Zfp423. Overall, after sacrificing the inferior alveolar nerve, the collateral compensation of the ipsilateral buccal nerve could innervate the sensation. And this process was regulated by TGF-β-Zfp423-ApoD pathway.
Mice ; Animals ; Lip/innervation* ; Prospective Studies ; Mandibular Nerve/pathology* ; Sensation/physiology* ; Trigeminal Nerve Injuries/pathology*