BACKGROUND: Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is a severe congenital disorder characterized by vaginal hypoplasia caused by dysplasia of the Müllerian duct. Patients with MRKH syndrome often require nonsurgical or surgical treatment to achieve satisfactory vaginal length and sexual outcomes. The extracellular matrix has been successfully used for vaginal reconstruction. METHODS: In this study, we developed a new biological material derived from porcine vagina (acellular vaginal matrix, AVM) to reconstruct the vagina in Bama miniature pigs. The histological characteristics and efficacy of acellularization of AVM were evaluated, and AVM was subsequently transplanted into Bama miniature pigs to reconstruct the vaginas. RESULTS: Macroscopic analysis showed that the neovaginas functioned well in all Bama miniature pigs with AVM implants. Histological analysis and electrophysiological evidence indicated that morphological and functional recovery was restored in normal vaginal tissues. Scanning electron microscopy showed that the neovaginas had mucosal folds characteristics of normal vagina. No significant differences were observed in the expression of CK14, HSP47, and a-actin between the neovaginas and normal vaginal tissues. However, the expression of estrogen receptor (ER) was significantly lower in the neovaginas than in normal vaginal tissues. In addition, AVM promoted the expression of b-catenin, c-Myc, and cyclin D1. These results suggest that AVM might promotes vaginal regeneration by activating the b-catenin/cMyc/cyclin D1 pathway. CONCLUSION This study reveals that porcine-derived AVM has potential application for vaginal regeneration.

Inflammation is the basic pathological process of a variety of diseases, which involved in the occurrence and development of female infertility-related diseases, especially in bacteria and viruses infection of reproductive system, resulting in infertility. However, inflammatory reactions and factors also exist in normal physiological processes, such as endometrial morphologic changes in menstrual cycles, follicle genesis, ovulation, luteinization, pregnancy, etc. In addition, inflammation is also involved in the occurrence of some reproductive endocrine and metabolic diseases, such as obesity, endometriosis, polycystic ovary syndrome and so on. In the past, the understanding to inflammation in reproductive system was mostly limited to the inflammatory diseases and resulted in fertility decline or sterility, infertility, and other problems, which was not comprehensive. This review summarized the normal physiological inflammation and disease-related inflammation in the reproductive system, and described the evaluation of inflammatory state, as well as relevant prevention and treatment suggestions.

Autophagy is an important metabolic process that maintains homeostasis of cells, tissues and organisms. In endometrial cells, autophagy is involved in regulating endometrial growth and receptivity through a variety of pathways, including AMPK/TSC/mTOR signaling pathway, PI3K/AKT/mTOR signaling pathway, ATG4C, ULK4, RB1CC1/FIP200 and other related signaling pathways. These pathways are essential for maintaining intracellular environmental homeostasis and the health of the female reproductive system. At the same time, abnormal autophagy can lead to decreased endometrial receptivity and is associated with the occurrence and development of a variety of endometria-related diseases, and the level of autophagy presents dynamic changes in different periods of disease. In this paper, the role and mechanism of autophagy in endometrium were reviewed in order to provide relevant evidence for new drug development and treatment strategies. Deep understanding of the role and mechanism of autophagy in endometrium is expected to provide new ideas and directions for the treatment of endometrial diseases.

Autophagy is an important metabolic process that maintains homeostasis of cells, tissues and organisms. In endometrial cells, autophagy is involved in regulating endometrial growth and receptivity through a variety of pathways, including AMPK/TSC/mTOR signaling pathway, PI3K/AKT/mTOR signaling pathway, ATG4C, ULK4, RB1CC1/FIP200 and other related signaling pathways. These pathways are essential for maintaining intracellular environmental homeostasis and the health of the female reproductive system. At the same time, abnormal autophagy can lead to decreased endometrial receptivity and is associated with the occurrence and development of a variety of endometria-related diseases, and the level of autophagy presents dynamic changes in different periods of disease. In this paper, the role and mechanism of autophagy in endometrium were reviewed in order to provide relevant evidence for new drug development and treatment strategies. Deep understanding of the role and mechanism of autophagy in endometrium is expected to provide new ideas and directions for the treatment of endometrial diseases.

Background: Classical swine fever virus (CSFV), the causative agent of classical swine fever (CFS), is a highly contagious disease that poses a serious threat to Chinese pig populations. Objectives: Many provinces of China, such as Shandong, Henan, Hebei, Heilongjiang, and Liaoning provinces, have reported epidemics of CSFV, while the references to the epidemic of CSFV in Yunnan province are rare. This study examined the epidemic characteristics of the CSFV in Yunnan province. Methods: In this study, 326 tissue samples were collected from different regions in Yunnan province from 2015 to 2021. A reverse transcription-polymerase chain reaction (RT-PCR), sequences analysis, and phylogenetic analysis were performed for the pathogenic detection and analysis of these 326 clinical specimens. Results: Approximately 3.37% (11/326) of specimens tested positive for the CSFV by RTPCR, which is lower than that of other regions of China. Sequence analysis of the partial E2 sequences of eleven CSFV strains showed that they shared 89.0–100.0% nucleotide (nt) and 95.0–100.0% amino acid (aa) homology, respectively. Phylogenetic analysis showed that these novel isolates belonged to the subgenotypes 2.1c and 2.1d, with subgenotype 2.1c being predominant. Conclusions The CSFV was sporadic in China’s Yunnan province from 2015 to 2021. Both 2.1c and 2.1d subgenotypes were found in this region, but 2.1c was dominant.

Objective:To investigate the relationship between NOD-like receptors 3 (NLRP3) inflammasomes mediated inflammatory response and the pathogenesis of depression, and to investigate the effect of fluoxetine on this process.Methods:120 male C57BL/6J (wild-type) mice were randomly divided into control group 1, control group 2, chronic unpredictable mild stress (CUMS) group, and CUMS plus fluoxetine group. Another 30 male C57BL/6J (NLRP3-/-) mice were selected as NLRP3-/- group. Control group 1 and control group 2 had No treatment; CUMS group, CUMS plus fluoxetine group, and NLRP3-/- group were given chronic unpredictable mild stimulation for six weeks. After modeling, mice in control group 2 and CUMS plus fluoxetine group were intraperitoneally injected with fluoxetine (10 mg/(kg·d)). In contrast, mice in the other three groups were injected with the same amount of normal saline every day for four weeks. Behavioral tests were performed once a week before and after stress stimulation. Tail venous blood was drawn immediately before stress stimulation, three weeks later and six weeks after stress stimulation and was centrifuged at 3000 r/min for 10 min. The supernatant was kept and frozen for future use. Serum levels of interleukin-1β(IL-1β) and interleukin-18 (IL-18) were detected by enzyme-linked immunosorbent assay. After drug intervention (10 mg/(kg·d) fluoxetine or the same volume of normal saline), the mice in each group underwent behavioral tests once a week. The results included the sugar water preference test, forced swimming test (FST), and tail suspension test (TST). Tail venous blood was drawn from mice in each group at 1, 3, and 4 weeks after fluoxetine administration, and the supernatant was centrifuged and stored for later use. Serum levels of IL-1β and IL-18 were detected by enzyme-linked immunosorbent assay. At the above time points, 5 mice in each group were sacrificed each time, and fresh hippocampal tissues were collected and stored at a low temperature. NLRP3, urinary winter peptidase (caspase-1), the induction of transcription factors-KB (nuclear factor-κB, NF-κB), IL-1β and the IL-18 in the hippocampus brain regions were detected by using Western Blot.Results:(1) Model establishment: After six weeks of CUMS, compared with control group 1 and control group 2, the sugar water consumption of mice in CUMS group and CUMS+fluoxetine group was significantly reduced, and the immobility time of FST and TST was significantly prolonged, which proved that the model establishment was successful. After CUMS, NLRP3-/- group mice did not show depression-like changes in FST, sugar water preference test, and TST, which indicated that the model failed to be established. (2) After intraperitoneal fluoxetine injection, there were no significant differences in sugar water consumption, FST and TST immobility time between control group 2 and control group 1 ( P>0.05), and the sugar water consumption of mice in CUMS plus fluoxetine group was significantly increased, compared with CUMS group ( P<0.05). The immobility time of FST and TST was significantly shortened ( P<0.05). (3) The results of the enzyme-linked immunosorbent assay showed that after stimulation of CUMS, compared with control group 1 and control group 2, the serum levels of IL-1β and IL-18 in CUMS group and CUMS plus fluoxetine group were significantly increased ( P<0.05), while NLRP3-/- group had no significant change ( P>0.05). After fluoxetine administration, the serum levels of IL-1β and IL-18 in CUMS plus fluoxetine group were significantly lower than those in CUMS group ( P<0.05). (4) Western blotting results showed that after stimulation of CUMS, compared with control group 1 and control group 2, mice brain hippocampus NLRP3 expression, caspase-1 activation and induction of transcription factors-κB (nuclear factor-κB, NF-κB), IL-1β, IL-18 expression significantly increased ( P<0.05) in CUMS and CUMS plus fluoxetine group. After fluoxetine treatment, mice brain hippocampus NLRP3 expression, caspase-1 activation, NF-κB, IL-1β, and IL-18 expression in CUMS plus fluoxetine group had a significant reduction (restored to control 1 group by 99%, 91%, 97%, 95%, and 97% respectively). Conclusion:(1) CUMS may bring more NLRP3, caspase-1, NF-κB, IL-1β, and IL-18 expression in mice hippocampus, which cannot be seen, in the NLRP3 gene knockout mice; (2) The fluoxetine treatment may significantly decrease the NLRP3, caspase-1, NF-κB, IL-1β, IL-18 expression on depressive model mice, and improve depressive behavior.

Objective:To investigate the relationship between NOD-like receptors 3 (NLRP3) inflammasomes mediated inflammatory response and the pathogenesis of depression, and to investigate the effect of fluoxetine on this process.Methods:120 male C57BL/6J (wild-type) mice were randomly divided into control group 1, control group 2, chronic unpredictable mild stress (CUMS) group, and CUMS plus fluoxetine group. Another 30 male C57BL/6J (NLRP3-/-) mice were selected as NLRP3-/- group. Control group 1 and control group 2 had No treatment; CUMS group, CUMS plus fluoxetine group, and NLRP3-/- group were given chronic unpredictable mild stimulation for six weeks. After modeling, mice in control group 2 and CUMS plus fluoxetine group were intraperitoneally injected with fluoxetine (10 mg/(kg·d)). In contrast, mice in the other three groups were injected with the same amount of normal saline every day for four weeks. Behavioral tests were performed once a week before and after stress stimulation. Tail venous blood was drawn immediately before stress stimulation, three weeks later and six weeks after stress stimulation and was centrifuged at 3000 r/min for 10 min. The supernatant was kept and frozen for future use. Serum levels of interleukin-1β(IL-1β) and interleukin-18 (IL-18) were detected by enzyme-linked immunosorbent assay. After drug intervention (10 mg/(kg·d) fluoxetine or the same volume of normal saline), the mice in each group underwent behavioral tests once a week. The results included the sugar water preference test, forced swimming test (FST), and tail suspension test (TST). Tail venous blood was drawn from mice in each group at 1, 3, and 4 weeks after fluoxetine administration, and the supernatant was centrifuged and stored for later use. Serum levels of IL-1β and IL-18 were detected by enzyme-linked immunosorbent assay. At the above time points, 5 mice in each group were sacrificed each time, and fresh hippocampal tissues were collected and stored at a low temperature. NLRP3, urinary winter peptidase (caspase-1), the induction of transcription factors-KB (nuclear factor-κB, NF-κB), IL-1β and the IL-18 in the hippocampus brain regions were detected by using Western Blot.Results:(1) Model establishment: After six weeks of CUMS, compared with control group 1 and control group 2, the sugar water consumption of mice in CUMS group and CUMS+fluoxetine group was significantly reduced, and the immobility time of FST and TST was significantly prolonged, which proved that the model establishment was successful. After CUMS, NLRP3-/- group mice did not show depression-like changes in FST, sugar water preference test, and TST, which indicated that the model failed to be established. (2) After intraperitoneal fluoxetine injection, there were no significant differences in sugar water consumption, FST and TST immobility time between control group 2 and control group 1 ( P>0.05), and the sugar water consumption of mice in CUMS plus fluoxetine group was significantly increased, compared with CUMS group ( P<0.05). The immobility time of FST and TST was significantly shortened ( P<0.05). (3) The results of the enzyme-linked immunosorbent assay showed that after stimulation of CUMS, compared with control group 1 and control group 2, the serum levels of IL-1β and IL-18 in CUMS group and CUMS plus fluoxetine group were significantly increased ( P<0.05), while NLRP3-/- group had no significant change ( P>0.05). After fluoxetine administration, the serum levels of IL-1β and IL-18 in CUMS plus fluoxetine group were significantly lower than those in CUMS group ( P<0.05). (4) Western blotting results showed that after stimulation of CUMS, compared with control group 1 and control group 2, mice brain hippocampus NLRP3 expression, caspase-1 activation and induction of transcription factors-κB (nuclear factor-κB, NF-κB), IL-1β, IL-18 expression significantly increased ( P<0.05) in CUMS and CUMS plus fluoxetine group. After fluoxetine treatment, mice brain hippocampus NLRP3 expression, caspase-1 activation, NF-κB, IL-1β, and IL-18 expression in CUMS plus fluoxetine group had a significant reduction (restored to control 1 group by 99%, 91%, 97%, 95%, and 97% respectively). Conclusion:(1) CUMS may bring more NLRP3, caspase-1, NF-κB, IL-1β, and IL-18 expression in mice hippocampus, which cannot be seen, in the NLRP3 gene knockout mice; (2) The fluoxetine treatment may significantly decrease the NLRP3, caspase-1, NF-κB, IL-1β, IL-18 expression on depressive model mice, and improve depressive behavior.

Objective To study the effect of menopause status and the time of taking tamoxifen (TAM) on endometrial lesions after breast cancer surgery. Methods A total of 330 patients with postoperative vaginal irregular bleeding after breast cancer surgery or endometrial lesions after B ultrasonic from August 2007 to August 2017 in Northern Jiangsu People 's Hospital were retrospectively analyzed, including 180 cases of taking TAM treatment (medicine-taking group), and 150 cases of not taking TAM treatment (non medicine-taking group). The patients were also divided into the menopause group and the premenopausal group. According to the time of taking TAM, the patients were divided into < 2 years group, 2-5 years group and > 5 years group. Chi-square and Fisher test were used to compare the differences. Results The endometrial lesions incidence in the medicine-taking group was higher than that in the non medicine-taking group [84.44 ％ (152/180) vs. 56.00％(84/150);χ2=51.701, P=0.000]. The endometrial lesions rate in the menopause group was higher than that in the premenopause group [medicine-taking group: 69.70 ％ (46/66) vs. 92.98 ％ (106/114), χ2= 17.254, P= 0.000; non medicine-taking group: 46.15 ％ (35/65) vs. 63.53 ％(54/85), χ2 = 4.513, P= 0.034]. For the patients in the menopause group and the premenopause group, the incidence of endometrial lesions for those who took medicine for>5 years [96.00％(48/50), 85.19％(23/27)] was higher than that in the<2 years group and 2-5 years group [78.26％(18/23), 42.86％(6/14);95.12％(39/41), 72.00％(18/25) respectively], and there were statistical differences (χ2=7.619, P=0.022;χ2= 8.070, P= 0.018). The menopause was not correlated with staging, muscular lawyer infiltration and lymph metastasis postoperative (P> 0.05), but with the type of endometrial cancer (P= 0.013); the length of taking medicine was related with the type of endometrial cancer and the lymph metastasis (P=0.027). With the prolonged time of medicine-taking for postmenopause patients, the incidence of type Ⅱendometrial cancer and positive rate of lymph metastasis were also increased. Conclusions Taking TAM after surgery for breast cancer patients increases the risk of endometrial lesions. The longer the patients take the medicine, the greater risk of the lesions take, and the worse the pathological, histological type and prognosis of endometrial carcinoma are, which is more obvious for postmenopausal women who take TAM for more than 5 years.

The magnamosis device for stage-one repair of the rectovaginal tistula consists of two arc magnets. Drawing the interrupting thread along the fistula margin via the vaginal side, and pulling the string to arrange the magnets at the fistula base along the long axis of the vagina, we made the magnamosis device automatically clipped to seal the fistula. After removing the threads we kept the device for 2-4 weeks till the natural detachment of it when the compressed tissue in between healed after vascular necrosis. This device utilizing the unique ability of magnamosis to fulfill anastomosis under inflammatory infected state reduces the current high relapse rate and colostomy drawbacks of the conventional rectovaginal neoplasty.
Female ; Gynecologic Surgical Procedures ; instrumentation ; methods ; Humans ; Magnetics ; Magnets ; Pressure ; Rectovaginal Fistula ; surgery ; Wound Healing

Objective To build the relationship model of childhood aubuse, personality, insecurity and dissociative trait in medical students. Methods Through stratified sampling,262 medical students were investiga?ted by the Personal Report of Childhood Abuse( PRCA) ,Dissociative Trait Scale( DTS) ,Self?Rating Feeling of In?security Scale( SRFIS) ,Revised NEO Five?Factor Inventory( NEO?FFI?R) . A path analysis was applied by AMOS (Analysis of Moment Structures) version 7.0. Results ①Childhood abuse was positively related to insecurity, dissociative trait and neuroticism( r=0.248~0.361, P<0.01) ,but was passively related to extraversion,agreeable?ness and conscientiousness( r=-0.168~-0.250, P<0.01). Insecurity was positively related to dissociative trait and neuroticism( r=0.479~0.522, P<0.01) ,but was passively related to extraversion,agreeableness and conscien?tiousness( r=-0.234~-0.324, P<0.01). Dissociative trait was positively related to neuroticism( r=0.597, P<0.01) ,but was passively related to openness, extraversion, agreeableness and conscientiousness ( r=-0. 133~-0.453, P<0.05). ②The path analysis showed that childhood abuse was directly related to insecurity(B=0.339, P<0.01)and personality(B=-0.226, P<0.01)of medical students. Personality was directly related to insecurity and dissociative( B=-0.609~-0.363, P<0.01) . Insecurity was directly related to dissociative trait( B=0.448, P<0.01) . Personality and insecurity mediated entirely the relationship between childhood abuse and dissociative trait of medical students. The model fit indexes were χ2/ df =1.151<3.000, P=O.080>0.05,RMSEA=0.024<0.050, GFI=0.935,AGFI=0.909,NFI=0.923,RFI=0.902,IFI=0.989,TLI=0.986 and CFI=0.989. Conclusion Per?sonality and insecurity as mediated variable mediate the relationship between childhood abuse and dissociative trait of medical students. Childhood abuse has no direct effect on dissociative trait of medical students.