Morita therapy has been bom for more than 100 years.Inpatient Morita therapy is highly oper-able and easy to master.It can improve many refractory neuroses through four-stage treatment.But more neuroses are treated in outpatient clinics,and Morita therapy cannot be used in hospitalized patients.Therefore,the formula-tion of expert opinions on outpatient operations is particularly important.This paper is based on domestic and for-eign references,and after many discussions by domestic Morita therapy experts,and then drew up the first version of the expert opinions on operation of outpatient Morita therapy.Meanwhile the operation rule of Morita therapy in three stages of outpatient treatment was formulated:in the etiological analysis stage,under the theoretical guidance of Morita therapy,analyze the pathogenic factors,to improve treatment compliance and reduce resistance;during the operating stage,guide patients to engage in constructive and meaningful actions,realizing the achievement of letting nature take its course principle;in the cultivating character and enriching life stage,pay attention to positive infor-mation,expanding the scope and content of actions,improving the ability to adapt to complex life,and preventing recurrence caused by insufficient abilities.It will lay a foundation for the promotion of Morita therapy in domestic outpatient clinics,so that more patients with neurosis and other psychological diseases could receive characteristic Morita therapy treatment in outpatient clinics.

Primary prostate synovial sarcoma (PPSS) is rare in clinic. One patient was admitted to our hospital in May 2021. The patient was admitted to the hospital because of the physical examination. Preoperative pelvic enhanced MR, PETCT and preoperative puncture pathology suggested that pelvic soft tissue sarcoma was likely. Robot-assisted radical resection of pelvic tumor was performed, and the unilateral PPSS was diagnosed by postoperative pathology, immunohistochemistry and gene detection. Patients were treated with ifosfamide + adriamycin adjuvant chemotherapy one month after operation, and Proton therapy radiotherapy five months after operation. Follow-up for more than 2 years showed that the patients were generally in good condition, and no recurrence or metastasis was found in imaging.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3375 patients, of which 1822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. 14 different pathogenic/ probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%. The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1 , TCF12, EFNB1 , and FGFR3) . The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3375 patients, of which 1822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. 14 different pathogenic/ probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%. The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1 , TCF12, EFNB1 , and FGFR3) . The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3 375 patients, of which 1 822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. Fourteen different pathogenic/probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%(19/109). The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1, TCF12, EFNB1, and FGFR3). The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3 375 patients, of which 1 822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. Fourteen different pathogenic/probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%(19/109). The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1, TCF12, EFNB1, and FGFR3). The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.

Objective To explore the use of new media technology to estimate the size of the online MSM population in Pudong New Area, to understand the frequency of new media software use, HIV testing and high-risk behavior, and to provide a basis for AIDS prevention and control. Methods The online MSM registration information in Pudong New Area was collected through a gay dating APP. At five time points on March 28 and April 11, 2019, MSM who logged into the gay dating APP were counted. The MSM were confirmed by comparing the login name and registration information. The capture-recapture (C-R) method was used to calculate the MSM population size. Meanwhile, a questionnaire survey was conducted on the online MSM. Results The MSM population size in Pudong New Area was estimated at 13 174 [95% CI: 9,672~16,676] through the C-R method. The proportion of multiple sexual partners accounted for 72.5%. According to the ordered multi-classification logistics analysis, age, education level, experience of attending a talk on AIDS, and experience of receiving AIDS publicity and education in the VCT clinic were the influencing factors of AIDS awareness. Conclusion New media technology provided new technical means for estimating the size of MSM population. The MSM population^’s awareness of AIDS risk and prevention still needs to be strengthened. It is worthy of further studies on the role of new media technology in AIDS prevention and health education in the future.

An essential step for cancer vaccination is to break the immunosuppression and elicit a tumor-specific immunity. A major hurdle against cancer therapeutic vaccination is the insufficient immune stimulation of the cancer vaccines and lack of a safe and efficient adjuvant for human use. We discovered a novel cancer immunostimulant, trichosanthin (TCS), that is a clinically used protein drug in China, and developed a well-adaptable protein-engineering method for making recombinant protein vaccines by fusion of an antigenic peptide, TCS, and a cell-penetrating peptide (CPP), termed an "all-in-one" vaccine, for transcutaneous cancer immunization. The TCS adjuvant effect on antigen presentation was investigated and the antitumor immunity of the vaccines was investigated using the different tumor models. The vaccines were prepared

Objective:To compare the baseline difference in the quantitative hepatitis B core antibody levels (qAnti-HBc) between non-response and response group in children with HBeAg-positive chronic hepatitis B (CHB) who received antiviral therapy, and further explore the proportion and functional activity of CD8 + memory T lymphocyte subsets with different qAnti-HBC levels in peripheral blood of children.Methods:The baseline anti-HBc quantification (qAnti-HBc) levels of 85 children with HBeAg-positive CHB who visited the Department of Infectious Diseases, Children's Hospital of Chongqing Medical University from June 2018 to December 2020 were detected retrospectively. The relationship between the baseline qAnti-HBc level and HBeAg serological response in 37 children who received antiviral therapy was analyzed. The proportion of CD8 + memory T lymphocyte subsets and the secretion levels of interferon (IFN) γ, and tumor necrosis factor (TNF) α in peripheral blood of 59 children at baseline were detected by flow cytometry. The relationship between qAnti-HBc level and the proportion and functional activity of CD8 + memory T lymphocyte subsets was analyzed. Pearson’s Chi-square test was used to compare the count data. Mann-Whitney U test or Kruskal-Wallis test was used to compare measurement data between two or more groups, and Spearman’s rank correlation analysis was used for the correlation between continuous variables. Results:Among 37 children who received entecavir (ETV, 21/37 cases) or pegylated interferon (Peg-IFN, 16/37 cases), 18 cases had developed HBeAg seroconversion (10/ 21 cases in the ETV group, 8/16 cases in the Peg-IFN group). The baseline qAnti-HBc level was significantly higher in the response group [4.71 (4.64~4.81) log 10IU/ml] than the non-response group children [4.54 (4.45~4.64) log 10IU/ml, Z = -3.316, P = 0.001]. The proportion of CD8 + Tem, CD38 +CD8 + Tem, CD38 +CD8 + Temra cells and the levels of IFNγ and TNFα secreted by CD8 + T lymphocytes were significantly higher in the high-qAnti-HBc group than the low-qAnti-HBc group ( P < 0.05). The proportion of CD8 + Tem, CD38 +CD8 + Tem and CD38 +CD8 + Temra cells was significantly higher in ALT > 1× upper limit of normal value (ULN) group than ALT≤1×ULN group ( P < 0.05). However, there were no significant differences in the levels of IFNγ and TNFα secreted by CD8 + T lymphocytes between the two groups ( P > 0.05). Spearman’s correlation analysis showed that qAnti-HBc was positively correlated with the proportion of CD8 + Tem, CD38 +CD8 + Tem, CD38 +CD8 + Temra cells and the level of IFNγ secreted by CD8 +T lymphocytes ( P < 0.05). Additionally, ALT was only positively correlated with the proportion of CD38 +CD8 + TEM and CD38 + CD8 + Temra cells ( P < 0.05). Conclusion:Raised baseline qAnti-HBc level is related to the HBeAg serological response to antiviral therapy in children with CHB. Peripheral blood effector CD8+ T lymphocytes of CHB children with higher qAnti-HBc show stronger phenotype and functional activation characteristics, which may shed some light on the underlying immune mechanism related to antiviral therapy efficacy in children with CHB.

OBJECTIVE: To identify pathogenic mutation for a family with neurofibromatosis type 1(NF1) and provide prenatal diagnosis for them. METHODS: Mutation analysis of the sporadic family with NF1 was performed with target captured next generation sequencing and Sanger sequencing. RNA samples were extracted from the lymphocytes of NF1 patient and her parents. RT-PCR and Sanger sequencing were performed to analyze the relative mRNA expression in the samples. Prenatal diagnosis of the pathogenic mutation was offered to the fetus. RESULTS: A novel splicing mutation c.1260+4A>T in the gene was found in the proband of the family, but was not found in her parents.cDNA sequencing showed that 13 bases inserted into the 3' end of exon 11 in the gene lead to a frameshift mutation. Prenatal diagnosis suggested that the fetus did not carried the mutant. CONCLUSIONS The : c.1260+4A>T mutation found in the NF1 patient is considered to be pathogenic, which provides information for family genetic counseling and prenatal diagnosis.
DNA Mutational Analysis ; Female ; Frameshift Mutation ; Genetic Testing ; Humans ; Male ; Neurofibromatosis 1 ; diagnosis ; genetics ; Pregnancy ; Prenatal Diagnosis