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International Journal of Molecular... Jul 2023Phytoestrogens (PEs) are estrogen-like nonsteroidal compounds derived from plants (e.g., nuts, seeds, fruits, and vegetables) and fungi that are structurally similar to... (Review)
Review
Phytoestrogens (PEs) are estrogen-like nonsteroidal compounds derived from plants (e.g., nuts, seeds, fruits, and vegetables) and fungi that are structurally similar to 17β-estradiol. PEs bind to all types of estrogen receptors, including ERα and ERβ receptors, nuclear receptors, and a membrane-bound estrogen receptor known as the G protein-coupled estrogen receptor (GPER). As endocrine-disrupting chemicals (EDCs) with pro- or antiestrogenic properties, PEs can potentially disrupt the hormonal regulation of homeostasis, resulting in developmental and reproductive abnormalities. However, a lack of PEs in the diet does not result in the development of deficiency symptoms. To properly assess the benefits and risks associated with the use of a PE-rich diet, it is necessary to distinguish between endocrine disruption (endocrine-mediated adverse effects) and nonspecific effects on the endocrine system. Endometriosis is an estrogen-dependent disease of unknown etiopathogenesis, in which tissue similar to the lining of the uterus (the endometrium) grows outside of the uterus with subsequent complications being manifested as a result of local inflammatory reactions. Endometriosis affects 10-15% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhea, dyspareunia, and infertility. In this review, the endocrine-disruptive actions of PEs are reviewed in the context of endometriosis to determine whether a PE-rich diet has a positive or negative effect on the risk and course of endometriosis.
Topics: Female; Humans; Receptors, Estrogen; Endometriosis; Phytoestrogens; Diet; Endocrine System
PubMed: 37569571
DOI: 10.3390/ijms241512195 -
Heliyon Mar 2024Vulvovaginal candidiasis (VVC) is the second most common cause of vaginal infection globally after bacterial vaginosis (BV) and associated with adverse reproductive and... (Review)
Review
Vulvovaginal candidiasis (VVC) is the second most common cause of vaginal infection globally after bacterial vaginosis (BV) and associated with adverse reproductive and obstetric outcomes, including preterm delivery, sexually transmitted infections and pelvic inflammatory disease. Although effective control of VVC is achievable with the use of traditional treatment strategies (i.e., antifungals), the possibility of drug intolerance, treatment failure and recurrence, as well as the appearance of antifungal-resistant species remain critical challenges. Therefore, alternative therapeutic strategies against VVC are urgently required. In recent years, an improved understanding of the dysbiotic vaginal microbiota (VMB) during VVC has prompted the consideration of administering -biotics to restore the balance of the VMB within the context of VVC prevention and treatment. Here, we aim to summarize the current evidence of the anti- effects of probiotics, postbiotics and synbiotics and their potential use as an alternative/complementary therapy against VVC. Additionally, this review discusses advantages and challenges associated with the application of -biotics in VVC to provide guidance for their later use. We also review new developments in VVC therapy, i.e., vaginal microbiota transplantation (VMT) as an emerging live biotherapeutic therapy against VVC and discuss existing shortcomings associated with this nascent field, expecting to stimulate further investigations for introduction of new therapies against VVC.
PubMed: 38463778
DOI: 10.1016/j.heliyon.2024.e27239 -
Skeletal Radiology Dec 2023To describe the frequency of MR and CT features of infectious sacroiliitis (ISI) and assess its extent and complications MATERIALS AND METHODS: This retrospective study...
OBJECTIVE
To describe the frequency of MR and CT features of infectious sacroiliitis (ISI) and assess its extent and complications MATERIALS AND METHODS: This retrospective study included patients with ISI who were evaluated between 2008 and 2021 in a single center. Two radiologists reviewed MRI and CT images to determine the anatomical distribution (unilateral/bilateral, iliac/sacral bone, proximal/middle/distal), severity (bone marrow edema [BME]/periostitis/erosions), concurrent infection (vertebral/nonvertebral), and complications (abscess/probable adjacent osteomyelitis/cavitation/devitalized areas/sequestrum/pelvic venous thrombosis) of ISI. Interobserver reproducibility was assessed. Correlation analysis evaluated the effect of the causative microorganism on severity. Two human bodies were dissected to outline possible ways that ISI can spread.
RESULTS
Forty patients with ISI (40 years ± 22; 26 women) were evaluated. Ten patients had bilateral ISI. Concurrent vertebral infection was associated in 15% of cases. Reproducibility of sacral BME, periostitis, and reactive locoregional abnormalities was perfect (κ = 1). Reproducibility was low for erosion count (κ = 0.52[0.52-0.82]) and periarticular osteopenia (κ = 0.50[0.18-0.82]). Inflammatory changes were BME (42/42 joints), muscle edema (38/42), and severe periostitis along the ilium (33/37). Destructive structural changes occurred with confluent erosions (iliac, 20/48; sacral, 13/48), sequestrum (20/48), and cavitation (12/48). Complications occurred in 75% of cases, including periarticular abscesses (n = 30/47), probable adjacent osteomyelitis (n = 16/37), and pelvic thrombophlebitis (n = 3). Tuberculous ISI (6/40) correlated with sclerosis (rs = 0.45[0.16; 0.67]; p < 10) and bone devitalization (rs = 0.38[0.16; 0.67]; p = .02). The anatomical study highlighted the shared venous vascularization of sacroiliac joints, pelvic organs, and mobile spine.
CONCLUSION
Complications of ISI are frequent, including abscesses, adjacent osteomyelitis, and periostitis. ISI had bilateral involvement nonrarely and is commonly associated with another spinal infection.
PubMed: 38110777
DOI: 10.1007/s00256-023-04535-w -
Neurourology and Urodynamics Aug 2023We identified a subset of patients with noninfectious cystitis who develop refractory symptoms marked by diffuse inflammatory changes, reduced bladder capacity, and...
PURPOSE
We identified a subset of patients with noninfectious cystitis who develop refractory symptoms marked by diffuse inflammatory changes, reduced bladder capacity, and vesicoureteral reflux (VUR), termed here as "progressive inflammatory cystitis" (PIC). Our objective was to describe the phenotype, disease outcomes, and pathologic findings of PIC.
MATERIAL AND METHODS
A single institution retrospective cohort study of patients with PIC. Patients with a history of pelvic radiation, urologic malignancy, or neurogenic bladder were excluded. We describe cohort characteristics and use bivariate analyses to compare subgroups. Kaplan-Meier methods estimate time to urinary diversion.
RESULTS
From 2008 to 2020, 46 patients with PIC were identified. The median age of symptom onset was 63 years old (interquartile range [IQR]: 56, 70) and the most common presenting symptoms were urinary urgency/frequency (54%) and incontinence (48%). Urodynamics showed a median maximum bladder capacity of 80 mL (IQR: 34, 152), commonly with VUR (68%) and hydronephrosis (59%). Ultimately 36 patients (78%) underwent urinary diversion at a median of 4.5 years (IQR: 2, 6.5) after symptom onset. Significant pathologic findings include presence of ulceration (52%), acute and chronic inflammation (68%), including eosinophils (80%), lymphoid follicles (56%), and mast cells in both lamina and muscularis propria (76%).
CONCLUSIONS
PIC is a newly defined entity characterized by significantly diminished bladder capacity, upper tract changes, and relatively quick progression to urinary diversion. Larger prospective cohort studies are required to further characterize this severe phenotype of chronic noninfectious cystitis, aid earlier diagnosis, and guide management decisions.
Topics: Humans; Urinary Bladder; Retrospective Studies; Prospective Studies; Cystitis; Urinary Incontinence; Vesico-Ureteral Reflux
PubMed: 37126389
DOI: 10.1002/nau.25195 -
Journal of Reproductive Immunology Dec 2023Chronic endometritis has a high incidence in infertile women, which is caused by endometrial microbiome infection. In response to microbial infection, the role of...
Chronic endometritis has a high incidence in infertile women, which is caused by endometrial microbiome infection. In response to microbial infection, the role of defensins during chronic endometritis need explored. Besides, the expression of estrogen and its receptors vary in different menstrual cycles, but their roles in chronic endometritis are still unclear. In this study, we used the human endometrial tissues to examine the expression of antimicrobial peptides (AMPs) α-defensin hNP-1 and β-defensins hBD-1, hBD-2, hBD-3, hBD-4 and LCN2. We found the expression of hBD-1 and LCN2 were downregulated in endometritis tissues, while the expressions of hBD-2, hBD-3, hBD-4, hNP-1, and estrogen and ERα were upregulated in chronic endometritis tissues compared to normal tissues. The expression and phosphorylation of STING, which is a crucial mediator of mammalian innate immunity in response to pathogens, was regulated with the treatment of ERα inhibitor raloxifene (Rx). Furthermore, using with the estrogen receptor inhibitor Rx and STING inhibitor H-151 significantly decreases the LCN2 expression. Taken together, these results suggested ERα was upregulated to modulate STING expression inducing LCN2 antimicrobial peptide expression to modulate the mucosal immunity during chronic endometritis.
Topics: Animals; Female; Humans; Defensins; Down-Regulation; Endometritis; Estrogen Receptor alpha; Estrogens; Infertility, Female; Lipocalin-2; Mammals; Receptors, Estrogen
PubMed: 37952294
DOI: 10.1016/j.jri.2023.104167 -
Hepatology (Baltimore, Md.) Mar 2024Primary sclerosing cholangitis (PSC) is linked to inflammatory bowel disease (IBD). However, there is limited overlap between IBD and PSC risk genes, but a stronger...
BACKGROUND AND AIMS
Primary sclerosing cholangitis (PSC) is linked to inflammatory bowel disease (IBD). However, there is limited overlap between IBD and PSC risk genes, but a stronger association between PSC and other autoimmune conditions. We aimed to assess the coexistence and familial association of autoimmune disorders in PSC, and the influence of autoimmune comorbidity on severe outcomes.
APPROACH AND RESULTS
In a matched cohort study, 1378 individuals with PSC and 13,549 general population comparators and their first-degree relatives were evaluated. National registries provided data on diagnoses and outcomes (liver transplantation, hepatobiliary cancer, and liver-related death). The OR of autoimmune disease was estimated by logistic regression. The Fine and Gray competing risk regression estimated HRs for severe outcomes. The prevalence of non-IBD, non-autoimmune hepatitis, and autoimmune disease was 18% in PSC and 11% in comparators, OR: 1.77 (95% CI: 1.53-2.05). Highest odds were seen for celiac disease [OR: 4.36 (95% CI: 2.44-7.49)], sarcoidosis [OR: 2.74 (95% CI: 1.29-5.33)], diabetes type 1 [OR: 2.91 (95% CI: 2.05-4.05)], and autoimmune skin disease [OR: 2.15 (95% CI: 1.52-2.96)]. First-degree relatives of individuals with PSC had higher odds of developing IBD, autoimmune hepatitis, and any autoimmune disease than relatives of the comparators [OR: 3.25 (95% CI: 2.68-3.91); OR: 5.94 (95% CI: 2.82-12.02); OR: 1.34 (95% CI: 1.19-1.50)]. Autoimmune comorbidity in PSC was not associated with poorer outcomes [HR: 0.96 (95% CI: 0.71-1.28)].
CONCLUSIONS
Individuals with PSC and their first-degree relatives had higher odds of autoimmune disease compared to matched comparators. This finding provides validation for prior genetic discoveries at a phenotypic level. Autoimmune comorbidity did not impact severe outcomes.
PubMed: 38441983
DOI: 10.1097/HEP.0000000000000823 -
Medicine Mar 2024Endometriosis (EMT) a common gynecological condition in women, an inflammatory disease characterized by the presence of endometrial tissue on organs and tissues in the...
BACKGROUND
Endometriosis (EMT) a common gynecological condition in women, an inflammatory disease characterized by the presence of endometrial tissue on organs and tissues in the pelvis, and is mainly associated with chronic pelvic pain and infertility. As the etiology has not been fully elucidated, current treatment is limited to surgery, hormones and painkillers, with more side effects and difficulty in achieving long-term relief. Oxidative stress manifests itself as an overproduction of reactive oxygen species, which has an integral impact in the pathology of female reproductive disorders. In this review, we evaluate the mechanisms of iron overload-induced oxidative stress and ferroptosis in EMT and their pathophysiological implications.
METHODS
Because the etiology has not been fully elucidated, current treatments are limited to surgery, hormones, and painkillers, which have many side effects and are difficult to achieve long-term relief.
RESULTS
We interpreted that antioxidants as well as ferroptosis inducers show promising results in the treatment of EMT, but their application in this population needs to be further investigated.
CONCLUSION
In combination with the interpretation of previous studies, it was shown that iron overload is present in the peritoneal fluid, endometriotic lesions, peritoneum and macrophages in the abdominal cavity. However, the programmed cellular ferroptosis associated with iron overload is resisted by endometriotic foci, which is critical to the pathophysiology of EMT with local iron overload and inflammation.
Topics: Female; Humans; Endometriosis; Ferroptosis; Oxidative Stress; Iron Overload; Hormones
PubMed: 38489713
DOI: 10.1097/MD.0000000000037421 -
Frontiers in Genetics 2023Inflammatory bowel disease (IBD) is a complex and multifactorial inflammatory condition, comprising Crohn's disease (CD) and ulcerative colitis (UC). While numerous...
Transcriptome profiling of intact bowel wall reveals that PDE1A and SEMA3D are possible markers with roles in enteric smooth muscle apoptosis, proliferative disorders, and dysautonomia in Crohn's disease.
Inflammatory bowel disease (IBD) is a complex and multifactorial inflammatory condition, comprising Crohn's disease (CD) and ulcerative colitis (UC). While numerous studies have explored the immune response in IBD through transcriptional profiling of the enteric mucosa, the subtle distinctions in the pathogenesis of Crohn's disease and ulcerative colitis remain insufficiently understood. The intact bowel wall specimens from IBD surgical patients were divided based on their inflammatory status into inflamed Crohn's disease (iCD), inflamed ulcerative colitis (iUC) and non-inflamed (niBD) groups for RNA sequencing. Differential mRNA GO (Gene Ontology), and KEGG (Kyoto Encyclopedia of Genes and Genomes), and GSEA (Gene Set Enrichment Analysis) bioinformatic analyses were performed with a focus on the enteric autonomic nervous system (ANS) and smooth muscle cell (SMC). The transcriptome results were validated by quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC). A total of 2099 differentially expressed genes were identified from the comparison between iCD and iUC. Regulation of SMC apoptosis and proliferation were significantly enriched in iCD, but not in iUC. The involved gene PDE1A in iCD was 4-fold and 1.5-fold upregulated at qPCR and IHC compared to that in iUC. Moreover, only iCD was significantly associated with the gene sets of ANS abnormality. The involved gene SEMA3D in iCD was upregulated 8- and 5-fold at qPCR and IHC levels compared to iUC. These findings suggest that PDE1A and SEMA3D may serve as potential markers implicated in enteric smooth muscle apoptosis, proliferative disorders, and dysautonomia specifically in Crohn's disease.
PubMed: 37727374
DOI: 10.3389/fgene.2023.1194882 -
Heliyon Sep 2023The pathogenesis of recurrent pelvic organ prolapse (POP) is currently unclear. Therefore, developing targeted preventive measures is difficult. This study identified...
BACKGROUND
The pathogenesis of recurrent pelvic organ prolapse (POP) is currently unclear. Therefore, developing targeted preventive measures is difficult. This study identified potential key pathways, crucial genes, comorbidities, and therapeutic targets associated with the occurrence and development of recurrent POP.
METHODS
The original microarray data GSE28660, GSE53868, and GSE12852 were downloaded from the GEO database. Identification and validation of differentially expressed genes (DEGs) and hub genes associated with recurrent POP were performed using R software and cytoHubba of Cytoscape. Protein-protein interaction (PPI) networks were constructed using the STRING tool and visualized using Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) enrichment analyses were effectively performed using DAVID platforms. In addition, the NetworkAnalyst platform was used to explore and visualize the miRNA-hub gene network, TF-hub gene network, hub gene-disease network, and hub gene-drug/chemical network.
RESULTS
A total of 110 DEGs and 6 hub genes (ADIPOQ, IL6, PPARG, CEBPA, LPL, and LIPE) were identified in this study. These genes were primarily enriched in the PPAR, AMPK, and adipocytokine, non-alcoholic fatty liver disease, and signaling pathways related to glycerol metabolism. Moreover, 96 miRNAs and 97 TFs were identified to as being associated with recurrent POP. These genes were closely linked to adipocyte metabolism and distribution, energy metabolism, and the longevity regulatory pathway. In addition, 192 diseases or chronic complications were potentially related to the recurrence of POP, including diabetes, hypertension, obesity, inflammatory diseases, and chronic obstructive pulmonary disease. Furthermore, 954 drugs or compounds were shown to have therapeutic potential for recurrent POP, and the most critical target drugs were dexamethasone, bisphenol A, efavirenz, 1-methyl-3-isobutylxanthine, and estradiol.
CONCLUSIONS
The results of this study revealed that ADIPOQ, IL6, PPARG, CEBPA, LPL, and LIPE as potential hub genes associated with recurrent POP, and these hub genes may aid in the understanding of the mechanism underlying POP recurrence and the development of potential molecular drugs.
PubMed: 37681155
DOI: 10.1016/j.heliyon.2023.e19440 -
Pain Research & Management 2023Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is one of the most common diseases of the male urological system while the etiology and treatment of CP/CPPS... (Review)
Review
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is one of the most common diseases of the male urological system while the etiology and treatment of CP/CPPS remain a thorny issue. Cumulative research suggested a potentially important role of glial cells in CP/CPPS. This narrative review retrospected literature and grasped the research process about glial cells and CP/CPPS. Three types of glial cells showed a crucial connection with general pain and psychosocial symptoms. Microglia might also be involved in lower urinary tract symptoms. Only microglia and astrocytes have been studied in the animal model of CP/CPPS. Activated microglia and reactive astrocytes were found to be involved in both pain and psychosocial symptoms of CP/CPPS. The possible mechanism might be to mediate the production of some inflammatory mediators and their interaction with neurons. Glial cells provide a new insight to understand the cause of complex symptoms of CP/CPPS and might become a novel target to develop new treatment options. However, the activation and action mechanism of glial cells in CP/CPPS needs to be further explored.
Topics: Humans; Animals; Male; Chronic Disease; Prostatitis; Pelvic Pain; Central Nervous System; Neuroglia; Chronic Pain
PubMed: 38023826
DOI: 10.1155/2023/2061632