Endometriosis’s impact on reproductive structures and its treatment

Endometriosis is a painful, chronic disease affecting approximately 10% of all women at reproductive age, and from the most common locations where endometriosis is found: the ovary, fallopian tubes, and uterine ligaments, and, less commonly they are found in the lung, the bladder, rectum, and intestines. It is known that endometriosis, in the reproductive organs, causes pelvic pain before or during menstruation, difficulty in pregnancy or infertility, for reasons that are not entirely clear, but some theories have tried to explain this phenomenon and confirmed that it may be a result of a defect in the immune and hormonal system in addition to some factors that affect egg’s quality and the movement of the gametes and therefore reproduction function. Treatment options now focus on pain management and attempting to limit the progression of implants, using a range of hormonal medications such as anti-progesterone, progestin, oral contraceptives, and GnRH, also including surgical procedures such as endometriosis and adhesion tissue. In this review, weshed light on the damage and issues that women may face due to this disease. We discuss some alternative solutions used by specialists for patient susceptibility.

Immunocompetent cells in the tissue of adhesives of patients with adhesion process in the small pelvis

Objective: To study the morphological features and subpopulation composition of immunocompetent cells of adhesion tissue in women with adhesions of the pelvic organs.Materials and Methods: Th e study was carried out using surgical material obtained from 70 women aged 23 to 40 years. Of these, 50 tissue samples of peritoneal adhesions from patients with adhesions of organs in the small pelvis of I – II degree who underwent adhesiolysis and 20 samples of parietal peritoneum from healthy women who underwent endoscopic sterilization for contraception or completion of generative function. Th e authors used histological, immunohistochemical, and morphometric research methods.Results: Immunological changes in adhesion tissue were characterized by the activation of the T-cell link of immunity. It was confi rmed by a signifi cant increase in the content of CD4+ (p <0.001), CD8+ (p <0.001), a shift in the balance of immunoregulatory subpopulations towards CD8+, a lower indicator of the immunoregulatory index (p = 0.015), and insuffi ciency of the humoral link of immunity, namely, the absence of CD20+ content against the background of a slight increase in the CD138+ pool.Conclusion: To prevent the postoperative adhesion process in the small pelvis in patients of reproductive age, it is necessary to apply immunomodulatory therapy in the early postoperative period, which will improve the results of surgical treatment and is pathogenetically justifi ed.

TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells

Background. Postoperative abdominal adhesion remains one of the frequent complications after abdominal surgery and lacks effective intervention. Peritoneal mesothelial cell injury and healing play crucial roles in the process of adhesion formation, and identifying this mechanism might provide new insight into possible new therapeutic strategies for this disease. Transmembrane and immunoglobulin domain-containing 1 (TMIGD1) has been proven to protect renal epithelial cells from injury induced by oxidative stress and has also been identified as a novel adhesion molecule. Here, we investigated the role of TMIGD1 and its possible mechanism in adhesion formation. Materials and Methods. Immunohistochemistry (IHC), qPCR, and immunofluorescence (IHF) were used to detect the expression of TMIGD1. The grade and tenacity score of adhesion were used to evaluate the adhesion formation conditions. A TMIGD1-overexpressing HMrSV5 cell line was established. MTT assay, Western blotting, Annexin V apoptosis analysis, and CK19 staining were used to measure mesothelial cell viability, apoptosis, and completeness. ROS and MDA detection were used to measure mesothelial cell oxidative stress levels. JC-1 staining, IHF, and transmission electron microscopy were performed to assess mitochondrial function. Scratch-wound and adhesion assays were used to evaluate the adhesion ability of mesothelial cells. Results. First, we showed that TMIGD1 was decreased in mouse abdominal adhesion tissue and peritoneal mesothelial cells. Second, TMIGD1 overexpression inhibited adhesion formation. Third, TMIGD1 overexpression protected mesothelial cells from hydrogen peroxide- (H2O2-) induced oxidative stress injury. Fourth, TMIGD1 overexpression alleviated oxidative stress by protecting the mitochondrial function of mesothelial cells. In addition, TMIGD1 overexpression enhanced mesothelial cell adhesion. Conclusion. Our findings suggest that TMIGD1 protects mesothelial cells from oxidative stress injury by protecting their mitochondrial function, which is decreased in regular abdominal adhesion tissue. In addition, TMIGD1 enhances peritoneal mesothelial cell adhesion to promote healing.

Clinical Efficacy and Safety of Silicone Elastomer Sheet during Decompressive Craniectomy: Anti-Adhesive Role in Cranioplasty

(1) Background: Cranioplasty is a surgery to repair a skull bone defect after decompressive craniectomy (DC). If the process of dissection of the epidural adhesion tissue is not performed properly, it can cause many complications. We reviewed the effect of a silicone elastomer sheet designed to prevent adhesion. (2) Methods: We retrospectively reviewed 81 consecutive patients who underwent DC and subsequent cranioplasty at our institution between January 2015 and December 2019. We then divided the patients into two groups, one not using the silicone elastomer sheet (n = 50) and the other using the silicone elastomer sheet (n = 31), and compared the surgical outcomes. (3) Results: We found that the use of the sheet shortened the operation time by 24% and reduced the estimated blood loss (EBL) by 43% compared to the control group. Moreover, the complication rate of epidural fluid collection (EFC) in the group using the sheet was 16.7%, which was lower than that in the control group (41.7%, p < 0.023). Multivariate logistic regression analysis showed the sheet (OR 0.294, 95% CI 0.093–0.934, p = 0.039) to be significantly related to EFC. (4) Conclusions: The technique using the silicone elastomer sheet allows surgeons to easily dissect the surgical plane during cranioplasty, which shortens the operation time, reduces EBL, and minimizes complications of EFC.

TRIM21 Is Decreased in Colitis-associated Cancer and Negatively Regulates Epithelial Carcinogenesis

Background Tripartite motif-containing (TRIM)21 is reported to be associated with the regulation of immune response in gut mucosa. Here we studied the underlying mechanisms of TRIM21 in the pathogenesis of colitis-associated cancer (CAC). Methods We analyzed TRIM21 expression in tumor tissues from patients with colorectal cancer (CRC) and ulcerative colitis (UC)-associated cancer by immunohistochemistry and real-time polymerase chain reaction and established a CAC model in TRIM21−∕− and wild type mice by azoxymethane (AOM) and dextran sodium sulfate (DSS). Associated gene expression of tumor cell proliferation, adhesion, tissue remodeling and angiogenesis, and inflammatory cytokines were examined in normal colon and CAC by immunohistochemistry and real-time polymerase chain reaction. Results Expression of TRIM21 was found to be decreased in tumor tissues from patients with CRC and UC-associated cancer than that in controls, and TRIM21−∕− deficiency promoted AOM/DSS-induced CAC, characterized by more weight loss and multiple, large colon tumors in TRIM21−∕− mice. Moreover, associated gene expression of tumor cell proliferation (eg, Ki67), tissue remodeling and angiogenesis (eg, MMP10, HIF1-α, COX2, Ang4), and pro-inflammatory cytokines (eg, IL-6, TNF-α, IL-1β) markedly upregulated, whereas associated gene expression of tumor cell adhesion (E-cadherin) and inflammatory cytokines (eg, IL-10, TGF-β, Foxp3, IFN-γ) downregulated in tumor tissues from TRIM21–/– mice compared with controls. Conclusions TRIM21 is decreased in colitis-associated cancer and negatively regulates intestinal epithelial carcinogenesis by modulating epithelial cell proliferation, adhesion, tissue remodeling and angiogenesis, and pro-inflammatory responses. Therefore, TRIM21 may serve as a novel therapeutic target for CAC therapy.

TMIGD1 is Expressed at Low Levels in Abdominal Adhesion Tissue and Reduces Oxidative Stress in Peritoneal Mesothelial Cells

BackgroundPostoperative abdominal adhesion is one of the most commonly observed complications after abdominal surgery. However, there is no effective treatment for adhesion other than enterolysis. Mesothelial cell repair plays an extremely important role in the process of adhesion formation. Here, we hypothesize that transmembrane and immunoglobulin domain-containing 1 (TMIGD1) is expressed at low levels in abdominal adhesion tissue and can reduce oxidative stress and promote cell adhesion in peritoneal mesothelial cells.Materials and MethodsFirst, we performed gene microarray analysis and used qPCR, western blotting, immunohistochemistry and immunofluorescence to detect the expression of TMIGD1 in rat adhesion tissue and normal peritoneal tissue. Then, we established a TMIGD1-overexpressing HMrSV5 cell line and detected ROS, apoptosis, and the mitochondrial membrane potential by the MTT assay, western blotting, flow cytometry with 2’,7’-dichlorofluorescein diacetate (DCFH-DA) as a probe. Furthermore, we examined p38 phosphorylation in different TMIGD1-expressing cell lines and used a p38 inhibitor to determine whether the antioxidant effect of TMIGD1 is dependent on p38. Finally, we evaluated the adhesion ability of different TMIGD1 cell lines using scratch wound and adhesion assays.ResultsTMIGD1 was expressed at low levels in adhesion tissue and at lower levels in mesothelial cells. TMIGD1 overexpression alleviated H2O2-induced oxidative stress injury in human HMrSV5 cell lines. The phosphorylation level of p38 was higher in the TMIGD1-overexpressing cell line, and we found that the effect of TMIGD1 was inhibited by a p38 inhibitor. In addition, TMIGD1 overexpression inhibited mesothelial cell migration and promoted mesothelial cell adhesion.ConclusionTMIGD1 is expressed at low levels in abdominal adhesion tissue and can reduce H2O2-induced oxidative stress by promoting p38 phosphorylation. In addition, TMIGD1 can promote cell adhesion.# These authors contributed equally to this work.

The mechanics of flexor tendon adhesions

The mechanics of adhesions at a local tissue level have not been extensively studied. This study compared microstrains and macrostrains in adhesions of immobilized and mobilized partially lacerated flexor digitorum profundus tendons in a New Zealand White rabbit model. At 2 weeks, 50 digits were randomized to either gross tensile testing or micromechanical assessment, in which the movement of fluorescently labelled cell nuclei, acting as dynamic markers, was visualized using real-time confocal microscopy. The structural stiffness and load at failure of immobilized adhesions were 140% and 160% of that of mobilized adhesions, respectively, and both differences were statistically significant. Micromechanically, different patterns of loading and failure were observed. Mobilized adhesions exhibited over a three-fold higher local strain, which was less uniformly distributed. Confocal microscopy provided an accurate measure of local strain. For the first time, it has been possible to visualize, define, and quantify local adhesion tissue mechanics. Mobilization appears to favour the formation of sites expressing increased local strain responses or those predisposed to heterogeneity and localized failure.