Objective The aim of this study is to detect the expression of purinergic 2X7 receptor(P2X7R)and the NLRP3 inflammasome in benign prostatic hyperplasia(BPH)tissues and to analyze the clinical correlations.Methods Twelve patients undergoing surgery for BPH were enrolled.Based on the presence or absence of inflammatory cell infiltration in HE-stained tissue sections,the patients were divided into inflammation group and non-inflammation group.Preoperative routine ex-aminations excluded surgical contraindications,and International Prostate Symptom Score(IPSS)questionnaires,urinary flow rate measurements,expressed prostatic secretions(EPS)analysis,and prostate-specific antigen(PSA)tests were conducted.Prostate tissues obtained during surgery were subjected to HE staining,immunofluorescence/Western blot to detect the expression of NLRP3,P2X7R,Caspase-1,Cleaved-Caspase-1,IL-1 β,and TNF-α,and immunofluorescence to assess lymphocyte infiltra-tion.SPSS 26.0 software was used to analyze correlations between the expression levels of NLRP3 and P2X7R in prostate tissues and indicators including Caspase-1,Cleaved-Caspase-1,IL-1 β,TNF-α,lymphocyte count,IPSS score,urinary flow rate,EPS,and PSA.Results In BPH tissues,the expression levels of NLRP3 and P2X7R were positively correlated(P＜0.05).The ex-pression levels of NLRP3 and P2X7R were positively correlated with Caspase-1,Cleaved-Caspase-1,IL-1 β,TNF-α,and lym-phocyte count(P＜0.05).NLRP3 and P2X7R expression levels were positively correlated with white blood cell count in EPS,but showed no correlation with IPSS score,lecithin body count in EPS,maximum urinary flow rate and PSA(P＜0.05).Conclusion P2X7R and NLRP3 in prostate tissues exacerbate local inflammatory responses,which may be an important mecha-nism in BPH development.However,they are not correlated with IPSS score,lecithin body count in EPS,maximum urinary flow rate and PSA.

Abstract Prenatal stress is a common, systemic, nonspecific stress response that occurs during pregnancy. The gut microbiota, which is known as the “second genome” of the human body, interacts with all major systems of the body. Changes in the gut microbiota can impact the development and health of infants and young children. Advances in research technology have allowed us to uncover the relationship between prenatal stress and imbalances in offspring intestinal microbiota, as well as the development of multiple systemic diseases. However, the exact mechanisms through which prenatal stress disrupts the gut microbiota of offspring remain incompletely understood. This review summarizes the existing research on diseases caused by prenatal stress disrupting the offspring intestinal flora, and seeks future research directions to expand the understanding of the pathogenesis of infant diseases.

Abstract Asthma is a well-characterized heterogeneous disease marked by airway remodeling and chronic airway inflammation. Clinically, the treatment of asthma primarily relies on hormonal drugs. However, the long-term use of these medications can lead to significant side effects. Mitophagy is a biological process that selectively transports damaged mitochondria to lysosomes for degradation. Recent research has revealed the crosstalk between mitophagy and asthma. Accordingly, taking mitophagy as an entry point, summarizing the key molecular mechanisms and regulators of mitophagy in asthma will facilitate the development of novel intervention targets and strategies for asthmatic treatment.

Objective The aim of this study is to detect the expression of purinergic 2X7 receptor(P2X7R)and the NLRP3 inflammasome in benign prostatic hyperplasia(BPH)tissues and to analyze the clinical correlations.Methods Twelve patients undergoing surgery for BPH were enrolled.Based on the presence or absence of inflammatory cell infiltration in HE-stained tissue sections,the patients were divided into inflammation group and non-inflammation group.Preoperative routine ex-aminations excluded surgical contraindications,and International Prostate Symptom Score(IPSS)questionnaires,urinary flow rate measurements,expressed prostatic secretions(EPS)analysis,and prostate-specific antigen(PSA)tests were conducted.Prostate tissues obtained during surgery were subjected to HE staining,immunofluorescence/Western blot to detect the expression of NLRP3,P2X7R,Caspase-1,Cleaved-Caspase-1,IL-1 β,and TNF-α,and immunofluorescence to assess lymphocyte infiltra-tion.SPSS 26.0 software was used to analyze correlations between the expression levels of NLRP3 and P2X7R in prostate tissues and indicators including Caspase-1,Cleaved-Caspase-1,IL-1 β,TNF-α,lymphocyte count,IPSS score,urinary flow rate,EPS,and PSA.Results In BPH tissues,the expression levels of NLRP3 and P2X7R were positively correlated(P＜0.05).The ex-pression levels of NLRP3 and P2X7R were positively correlated with Caspase-1,Cleaved-Caspase-1,IL-1 β,TNF-α,and lym-phocyte count(P＜0.05).NLRP3 and P2X7R expression levels were positively correlated with white blood cell count in EPS,but showed no correlation with IPSS score,lecithin body count in EPS,maximum urinary flow rate and PSA(P＜0.05).Conclusion P2X7R and NLRP3 in prostate tissues exacerbate local inflammatory responses,which may be an important mecha-nism in BPH development.However,they are not correlated with IPSS score,lecithin body count in EPS,maximum urinary flow rate and PSA.

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 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 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.