177Lu-prostate specific membrane antigen(PSMA)radio-ligand therapy has been approved abroad for advanced prostate cancer and has been in several clinical trials in China.Based on domestic clinical practice and experimental data and referred to international experience and viewpoints,the expert group forms a consensus on the clinical application of 177Lu-PSMA radio-ligand therapy in prostate cancer to guide clinical practice.

OBJECTIVE To provide reference for safe use of risperidone in clinic. METHODS Data mining and analysis of risperidone-related adverse drug event （ADE） reports from the first quarter of 2017 to the third quarter of 2021 in the United States FAERS database were carried out using reported odds ratio and composite criteria methods from Medicines and Healthcare Products Regulatory Agency. RESULTS There were 101 181 ADE reports with risperidone as the primary suspect drug，involving a total of 33 179 patients. Among those reports，the male-to-female ratio was about 6.21 to 1； most of them were ＜18 years old （15.01%）； ADE was mainly reported by consumers （69.74%） and mainly reported by the United States （79.72%）； oral dosage form was the most used，accounting for 83.71%. A total of 409 ADE signals were obtained，including male breast development， pseudogynecomastia，abnormal increase in body mass，hyperprolactinemia and Wellens syndrome，etc. Twenty-six systems and organs were involved，mainly including reproductive system and breast diseases，various injuries，poisoning and operational complications， mental diseases，metabolic and nutritional diseases，and various nervous system diseases，etc. CONCLUSIONS The common ADE signals of risperidone and the system involved are consistent with the instructions，but we should also be alert to the ADE not recorded in the instruction，such as Wellens syndrome，fibroproliferative endocarditis，cavernous degeneration of portal vein，rabbit syndrome，etc.

Objective:To analyze the molecular epidemiological characteristics of the Corona virus disease 2019 (COVID-19) cases in Shijiazhuang, which can reveal the origin of the outbreak and provide a scientific basis for COVID-19 prevention and control.Methods:From January 2 to January 8, 2021, a total of 404 samples from 170 COVID-19 cases were collected from the Shijiazhuang Fifth Hospital. The consensus sequence of 2019 novel Coronavirus(2019-nCoV) was obtained through multiplex polymerase chain reaction-based sequencing. The sequences of 170 COVID-19 cases were analyzed by the PANGOLIN, and the data were statistically analyzed by T-test.Results:Among the 404 COVID-19 samples, a total of 356 samples obtained high quality genome sequences (>95%,100×sequencing depth). The whole genome sequences of 170 COVID-19 cases were obtained by eliminating repeated samples. All 170 sequences were recognized as lineage B1.1 using PANGOLIN. The number of single nucleotide polymorphism arrange from 18-22 and most of the single nucleotide polymorphism were synonymous variants. All of 170 genomes could be classified into 48 sub-groups and most of the genomes were classified into 2 sub-groups (66 and 31, respectively).Conclusions:All cases in this study are likely originated from one imported case. The viruses have spread in the community for a long time and have mutated during the community transmission.

The importance of structural variants(SVs)for human phenotypes and diseases is now recognized.Although a variety of SV detection platforms and strategies that vary in sensitivity and specificity have been developed,few benchmarking procedures are available to confidently assess their performances in biological and clinical research.To facilitate the validation and application of these SV detection approaches,we established an Asian reference material by characterizing the genome of an Epstein-Barr virus(EBV)-immortalized B lymphocyte line along with identified benchmark regions and high-confidence SV calls.We established a high-confidence SV callset with 8938 SVs by integrating four alignment-based SV callers,including 109x Pacific Biosciences(PacBio)continuous long reads(CLRs),22 x PacBio circular consensus sequencing(CCS)reads,104x Oxford Nanopore Technologies(ONT)long reads,and 114×Bionano optical mapping plat-form,and one de novo assembly-based SV caller using CCS reads.A total of 544 randomly selected SVs were validated by PCR amplification and Sanger sequencing,demonstrating the robustness of our SV calls.Combining trio-binning-based haplotype assemblies,we established an SV benchmark for identifying false negatives and false positives by constructing the continuous high-confidence regions(CHCRs),which covered 1.46 gigabase pairs(Gb)and 6882 SVs supported by at least one diploid haplotype assembly.Establishing high-confidence SV calls for a benchmark sample that has been characterized by multiple technologies provides a valuable resource for investigating SVs in human biology,disease,and clinical research.

Objective:This study was performed to investigate the feasibility of preservation of internal branch of superior laryngeal nerve(ibSLN) during transoral endoscopic surgery for hypopharyngeal squamous cancer(HSCC) and the influence on patient′s swallowing function after operation.Methods:From May 2020 to June 2021, the data of 29 HSCC patients who required for transoral endoscopic surgery in the Department of Otorhinolaryngology Head and Neck Surgery, the Second Xiangya Hospital of Central South University were prospectively included, and the included patients were divided into two groups randomly by lottery. According to whether ibSLN was actively dissected during operation, they were divided into ibSLN preservation group ( n=15) and control group ( n=14, without ibSLN preservation). Operation time, intraoperative hemorrhage, intraoperative neck dissection, postoperative radiotherapy, postoperative recurrence within 1 year, retention and swallowing function, the recovery of oral soft diet and the quality of life were compared between two groups. SPSS 25.0 software was used for statistical analysis. Results:The study included 29 eligible patients, including 25 males and 4 females.The age ranged from 42 to 67 (56.07±5.93) years. There were no significant differences( P>0.05) between 2 groups in the following data,including age( t=-0.56), gender( χ2=0.01), TNM stage(T stage χ2=0.29, N stage χ2=0.02), pathological diagnosis( χ2=0.03), preoperative swallowing function( χ2=0.00) and M. D. Anderson Dysphagia Inventory(MDADI) score(global t=0.55, emotional t=0.16, functional t=0.60, physical t=0.64), operation time( t=1.62) and intraoperative hemorrhage( t=-1.46), intraoperative neck dissection( χ2=0.01), postoperative radiotherapy( χ2=0.32), postoperative recurrence within 1 year( P>0.050). The swallowing function was evaluated by water swallowing test after operation. The swallowing function of ibSLN preservation group was better than control group, and the difference between two groups was statistically significant on the 1st ( χ2=4.44, P=0.035), 5th ( χ2=4.24, P=0.039) and 7th ( χ2=4.55, P=0.033) day after operation. On the 14th day after operation, the MDADI scores of patients in the ibSLN preservation group were higher than those in the control group in global ( t=2.45, P=0.021), functional ( t=2.54, P=0.017) and physical ( t=2.24, P=0.034) dimensions, except for emotional dimension ( t=1.89, P=0.070). The median time of oral soft diet( U=23.00, P<0.001), normal oral diet( U=21.00, P<0.001) and the nasogastric tube removal time ( U=18.50, P<0.001) in ibSLN preservation group was 2 days, 5 days and 6 days respectively, earlier than that in control group, which had statistically significant difference. Conclusion:Our results show that it is feasible to preserve the ibSLN during HSCC transoral endoscopic surgery, which can achieve rapid recovery of postoperative swallowing function.

Objective:To explore the effect of microRNA (miRNA)-3126-5p on the proliferation and migration of colorectal cancer cells by inhibiting the expression of LIM and SH3 protein 1 ( LASP1). Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-3126-5p in colorectal cancer cell lines (HT-29, HCT116, LoVo, SW480) and normal intestinal mucosal epithelial cells (HIEC). The cell line with the lowest expression level was selected as the experimental object. The experiment was divided into 2 groups: the negative control group (transfected with miR-NC) and the miR-3126-5p group (transfected with miR-3126-5p). Cells of each group were collected 48h after transfection. qRT-PCR method was used to detect the expression level of miR-3126-5p in each group. The MTS method and the scratch healing experiment were used to detect the proliferation level and migration ability of the cells in each group. The bioinformatics software microRNA.org and the dual-luciferase reporter gene experiment were used to predict and verify the target genes of miR-3126-5p, respectively. qRT-PCR and Western blot were used to detect the expression levels of target genes in each group of cells. Measurement data were expressed as mean±standard deviation ( Mean± SD), t test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with normal intestinal mucosal epithelial cells (HIEC), the expression level of colorectal cancer cell line miR-3126-5p was significantly reduced ( P<0.05), and the cell line with the lowest expression level was HCT116 cells ( P<0.01). The expression of miR-3126-5p in HCT116 cells in the negative control group and miR-3126-5p group were (1.05±0.16) and (7.91±1.26) respectively, and the difference was statistically significant ( t=5.40, P<0.01). Compared with the negative control group, the proliferation ability of HCT116 cells in the miR-3126-5p group was significantly reduced ( t=4.52, P<0.05), and the migration ability was significantly reduced ( P<0.01). microRNA.org shows that miR-3126-5p has complementary binding sites with LIM and SH3 protein 1 ( LASP1) gene mRNA. miR-3126-5p can target LASP1 mRNA ( P<0.01). Compared with the negative control group, the expression of LASP1 gene in HCT116 cells of the miR-3126-5p group was significantly reduced ( t=4.56, P<0.01). Conclusion:The expression of miR-3126-5p in colorectal cancer cell lines is low, and miR-3126-5p can reduce the proliferation and migration ability of colorectal cancer HCT116 cells by inhibiting the expression of the target gene LASP1.

Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups. Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells ( P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group ( t=7.87, P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced ( P<0.05), and the scratch healing rate was significantly reduced ( P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p ( P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced ( P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (all P<0.01). Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.

Objective:To observe the expression of long non-coding RNA (lncRNA) PP7080 in gastric cancer tissues and cell lines, and clarify its effect on the migration and proliferation of gastric cancer cell MGC803 and its molecular mechanism.Methods:Real-time PCR was used to detect the expression of lncRNA PP7080 in gastric cancer tissues and adjacent tissues, gastric cancer cell lines and immortalized normal gastric mucosal epithelial cell lines. The gastric cancer cell line with the least expression was selected, and the expression plasmid of lncRNA PP7080 and the negative control plasmid were transfected into gastric cancer cells, respectively, and named as lncRNA PP7080 group and NC group. Real-time PCR to verify the effect of transfection. Cell scratch test and CCK-8 test were used to detect the regulation of lncRNA PP7080 on the migration and proliferation of gastric cancer cells.The statistical saftware SPSS 20.0 was used for statistical analysis, the measurement data of normal distribution were expressed as ( Mean± SD). Real-time PCR and Western blot were used to detect the expression of tumor metastasis suppressor gene 1 ( TMSG-1) in the transfected cells. The t test was used for comparison between groups. Results:The expression of lncRNA PP7080 in gastric cancer tissue was less than that in adjacent tissues [(0.85±0.34) vs (5.33 ± 0.76), P<0.01]. The expression of lncRNA PP7080 in gastric cancer cell lines is less than that of immortalized normal gastric mucosal epithelial cells ( P<0.05), and the least expression in MGC803 cells ( P<0.01). The expression of lncRNA PP7080 in the lncRNA PP7080 group was significantly higher than that in the NC group, and the difference was statistically significant ( P<0.01). The cell migration rates of NC group and lncRNA PP7080 group were (72.67±6.39)% and (26.45±6.63)%, respectively, and the cell migration ability of lncRNA PP7080 group was significantly reduced ( P<0.01). Compared with the NC group, the cell proliferation ability of the lncRNA PP7080 group was significantly reduced ( P<0.05). Compared with the NC group, the expression of TMSG-1 in MGC803 cells of the lncRNA PP7080 group was significantly reduced ( P<0.01). Conclusion:lncRNA PP7080 is lowly expressed in gastric cancer tissues and cell lines. lncRNA PP7080 can inhibit the migration and proliferation of gastric cancer cell MGC803 by promoting the expression of TMSG-1 gene.

Objective:To explore the inhibition of microRNA (miRNA, miR)-5590-3p on the expression of transforming growth factor beta typeⅡreceptor (TGFBR2) gene and its effect on the invasion and proliferation of gastric cancer cell line HS-746T.Methods:The gastric cancer cell line was cultured in vitro. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to analyze the expression of miR-5590-3p in gastric cancer tissues and cell lines. The miR-NC and miR-5590-3p mimic were transfected into gastric cancer cell line HS-746T by lipofection, and named as miR-NC group and miR-5590-3p group, respectively. qRT-PCR was used to measure transfection effects. Transwell assay and cell counting kit-8 (CCK-8) assay were used to detect cell invasion and proliferation after transfection. The bioinformatics software predicts and the dual luciferase reporter gene system validates the target gene of miR-5590-3p. qRT-PCR and western blot were used to measure the expression of TGFBR2 and its downstream proteins in the transfected cells. Results:The expression of miR-5590-3p in gastric cancer tissues was significantly lower than that in adjacent tissues ( P<0.01). The expression of miR-5590-3p in gastric cancer cell lines was significantly lower than that in normal gastric mucosal epithelial cells ( P<0.05), and lowest in HS-746T cells ( P<0.01). After transfection, the expression of miR-5590-3p in miR-5590-3p group (11.76±0.21) was significantly higher than that in miR-NC group (1.06±0.21), with statistically significant difference ( P<0.01). The number of invasive cells in miR-NC group and miR-5590-3p group were (101.20±15.47) and (26.53±6.53), respectively, and the invasion ability of miR-5590-3p group was significantly decreased ( P<0.01). Compared with the miR-NC group, the cell proliferation ability of the miR-5590-3p group was significantly decreased ( P<0.05). Bioinformatics software showed that the target gene for miR-5590-3p is TGFBR2. The dual luciferase reporter gene system confirmed that miR-5590-3p can target the TGFBR2 gene ( P<0.01). Western blot results showed that compared with miR-NC group, the expression of TGFBR2 in HS-746T cells in miR-5590-3p group was significantly decreased ( P<0.01), the expression of ZEB-1 and ZEB-2, and the expression of CDK1 and cyclin B proteins were decreased as well. Conclusions:miR-5590-3p can inhibit the invasion and proliferation of gastric cancer cell HS-746T by targeting and regulating the expression of TGFBR2 gene.

Objective:To explore the regulation of microRNA (miRNA, miR)-7856-5p on the expression of EPH receptor A3 (EPHA3) gene and its effect on the migration and proliferation of colorectal cancer cell line SW480.Methods:Real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of miR-7856-5p in colorectal cancer tissues and cell lines. The miR-7856-5p mimic and miR-NC were transfected into colorectal cancer cell line SW480 by lipofection, respectively, and defined as miR-7856-5p group and miR-NC group, respectively. Real-time PCR was used to detect transfection effects. Transwell assay and CCK-8 assay were used to detect cell migration and proliferation after transfection. The bioinformatics software predicts and the dual luciferase reporter gene system validates the target gene of miR-7856-5p. Real-time PCR and Western blot were used to detect the expression of EPHA3 in the transfected cells. The measurement data in accordamce with normal distribution were expressed as mean±standard deviation, t test was used for inter grap comparison, and single factor analysis of variance was used for multi group comparison. Results:The expression of miR-7856-5p in colorectal cancer tissues was significantly lower than that in adjacent tissues ( P<0.01). The expression of miR-7856-5p in colorectal cancer cell lines was significantly lower than that in normal intestinal mucosal epithelial cells ( P<0.05), and lowest in SW480 cells ( P<0.01). The expression of miR-7856-5p in miR-7856-5p group was significantly higher than that in miR-NC group, the difference was statistically significant [(9.49 ± 1.09) vs (1.06 ±0.18), P<0.01]. The number of migrated cells in miR-NC group and miR-7856-5p group were (125.70±14.05) and (42.01±8.98), respectively, and the migration ability of miR-7856-5p group was significantly decreased ( P<0.01). Compared with the miR-NC group, the cell proliferation ability of the miR-7856-5p group was significantly decreased ( P<0.05). Bioinformatics software showed that the target gene for miR-7856-5p was EPHA3. The dual luciferase reporter gene system confirmed that miR-7856-5p can target the EPHA3 gene ( P<0.05). Compared with the miR-NC group, the expression of EPHA3 in the SW480 cells of the miR-7856-5p group was significantly decreased ( P<0.05). Conclusion:miR-7856-5p can inhibit the migration and proliferation of colorectal cancer cell SW480 by regulating the expression of EPHA3.