Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030794 (pelvic pain)
 4,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Placental site nodules or plaques (PSN-Ps) are nodular benign lesions of the intermediate trophoblast (IT) cells in the endometrium, endocervix, superficial myometrium or fallopian tube, occurring after a remote intrauterine pregnancy. We present a study of 25 cases of PSN-Ps These lesions occurred in patients aged 18 to 44 years. Most were discovered incidentally in endometrial curettage specimens. The specimens were received as part of clinical investigations for menorrhagia, per vaginal bleeding or pelvic pain. None of the PSN-Ps was visible grossly. Microscopically, they were mostly multiple, well-circumscribed, oval or plaque-like cellular nodules. The IT cells typically had abundant vacuolated or eosinophilic cytoplasm. The nuclei were irregular, large, hyperchromatic, often degenerate-looking and either mononucleated, multinucleated or multiclefted. Hyalinization surrounding individual or groups of IT cells, or located in the centre of the nodules, was a constant feature in all cases. The lesional cells were strongly immunoreactive to CAM 5.2, 34 beta E12, AE1/AE3, EMA and vimentin. Some cases showed focal positivity to HCG and HPL. PLAP staining was consistently negative. Ultrastructurally, the IT cells showed prominent nuclear variation in size and shape. The abundant, vacuolated cytoplasm contained some rough endoplasmic reticulum and loosely arranged filaments. This study describes the clinicopathological and immunophenotypic features of 25 cases of PSN-Ps including the ultrastructural findings of one case.
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PMID:Placental site nodules and plaques: a clinicopathological and immunohistochemical study of 25 cases with ultrastructural findings. 1064 2

Endometriosis is clinically associated with pelvic pain and infertility, with implantation failure strongly suggested as an underlying cause for the observed infertility. Eutopic endometrium of women with endometriosis provides a unique experimental paradigm for investigation into molecular mechanisms of reproductive dysfunction and an opportunity to identify specific markers for this disease. We applied paralleled gene expression profiling using high-density oligonucleotide microarrays to investigate differentially regulated genes in endometrium from women with vs. without endometriosis. Fifteen endometrial biopsy samples (obtained during the window of implantation from eight subjects with and seven subjects without endometriosis) were processed for expression profiling on Affymetrix Hu95A microarrays. Data analysis was conducted with GeneChip Analysis Suite, version 4.01, and GeneSpring version 4.0.4. Nonparametric testing was applied, using a P value of 0.05, to assess statistical significance. Of the 12,686 genes analyzed, 91 genes were significantly increased more than 2-fold in their expression, and 115 genes were decreased more than 2-fold. Unsupervised clustering demonstrated down-regulation of several known cell adhesion molecules, endometrial epithelial secreted proteins, and proteins not previously known to be involved in the pathogenesis of endometriosis, as well as up-regulated genes. Selected dysregulated genes were randomly chosen and validated with RT-PCR and/or Northern/dot-blot analyses, and confirmed up-regulation of collagen alpha2 type I, 2.6-fold; bile salt export pump, 2.0-fold; and down-regulation of N-acetylglucosamine-6-O-sulfotransferase (important in synthesis of L-selectin ligands), 1.7-fold; glycodelin, 51.5-fold; integrin alpha2, 1.8-fold; and B61 (Ephrin A1), 4.5-fold. Two-way overlapping layer analysis used to compare endometrial genes in the window of implantation from women with and without endometriosis further identified three unique groups of target genes, which differ with respect to the implantation window and the presence of disease. Group 1 target genes are up-regulated during the normal window of implantation but significantly decreased in women with endometriosis: IL-15, proline-rich protein, B61, Dickkopf-1, glycodelin, N-acetylglucosamine-6-O-sulfotransferase, G0S2 protein, and purine nucleoside phosphorylase. Group 2 genes are normally down-regulated during the window of implantation but are significantly increased with endometriosis: semaphorin E, neuronal olfactomedin-related endoplasmic reticulum localized protein mRNA and Sam68-like phosphotyrosine protein alpha. Group 3 consists of a single gene, neuronal pentraxin II, normally down-regulated during the window of implantation and further decreased in endometrium from women with endometriosis. The data support dysregulation of select genes leading to an inhospitable environment for implantation, including genes involved in embryonic attachment, embryo toxicity, immune dysfunction, and apoptotic responses, as well as genes likely contributing to the pathogenesis of endometriosis, including aromatase, progesterone receptor, angiogenic factors, and others. Identification and validation of selected genes and their functions will contribute to uncovering previously unknown mechanism(s) underlying implantation failure in women with endometriosis and infertility, mechanisms underlying the pathogenesis of endometriosis and providing potential new targets for diagnostic screening and intervention.
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PMID:Expression profiling of endometrium from women with endometriosis reveals candidate genes for disease-based implantation failure and infertility. 1281 May 42

Apigenin is a plant-derived flavonoid having antiproliferative, anti-inflammatory, and anti-angiogenic properties in chronic and metabolic diseases, and cancers. However, the functional role of apigenin remains to be identified in human endometriosis that is a benign inflammatory disease causing infertility, dysmenorrhea, dyspareunia, and chronic abdominal or pelvic pain. In the present study, we determined the effects of apigenin on two well-established human endometriosis cell lines (VK2/E6E7 and End1/E6E7). Apigenin reduced proliferation and induced cell cycle arrest and apoptosis in the both endometriosis cell lines. In addition, it disrupted mitochondrial membrane potential (MMP) which was accompanied by an increase in concentration of calcium ions in the cytosol and in pro-apoptotic proteins including Bax and cytochrome c in the VK2/E6E7 and End1/E6E7 cells. Moreover, apigenin treated cells accumulated excessive reactive oxygen species (ROS), and experienced lipid peroxidation and endoplasmic reticulum (ER) stress with activation of the unfolded protein response (UPR) regulatory proteins. Furthermore, the apigenin-induced apoptosis in endometriosis cells was regulated via the ERK1/2, JNK, and AKT cell signaling pathways. Taken together, apigenin is a potential novel therapeutic agent to overcome current limitations in the treatment to endometriosis.
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PMID:Apigenin induces ROS-dependent apoptosis and ER stress in human endometriosis cells. 2861 56