Endometriosis (E) and adenomyosis (A) are associated with a wide spectrum of symptoms and may present various histopathological transformations, such as the presence of hyperplasia, atypia, and malignant transformation occurring under the influence of local inflammatory, vascular and hormonal factors and by the alteration of tumor suppressor proteins and the inhibition of cell apoptosis, with an increased degree of lesion proliferation. Material and methods: This retrospective study included 243 patients from whom tissue with E/A or normal control uterine tissue was harvested and stained by histochemical and classical immunohistochemical staining. We assessed the symptomatology of the patients, the structure of the ectopic epithelium and the presence of neovascularization, hormone receptors, inflammatory cells and oncoproteins involved in lesion development. Atypical areas were analyzed using multiple immunolabeling techniques. Results: The cytokeratin (CK) CK7+/CK20− expression profile was present in E foci and differentiated them from digestive metastases. The neovascularization marker cluster of differentiation (CD) 34+ was increased, especially in areas with malignant transformation of E or A foci. T:CD3+ lymphocytes, B:CD20+ lymphocytes, CD68+ macrophages and tryptase+ mast cells were abundant, especially in cases associated with malignant transformation, being markers of the proinflammatory microenvironment. In addition, we found a significantly increased cell division index (Ki67+), with transformation and inactivation of tumor suppressor genes p53, B-cell lymphoma 2 (BCL-2) and Phosphatase and tensin homolog (PTEN) in areas with E/A-transformed malignancy. Conclusions: Proinflammatory/vascular/hormonal changes trigger E/A progression and the onset of cellular atypia and malignant transformation, exacerbating symptoms, especially local pain and vaginal bleeding. These triggers may represent future therapeutic targets.

Objective: Omentum involvement resulting from uterine perforation is a rare complication following intrauterine procedures that might require immediate intervention due to severe ischemic consequences. This review examines the prevalence of this complication, risk factors, the mode and timing of diagnosis, the proper management and the outcome. Methods: A systematic literature search was conducted on PubMed, PubMed Central and Scopus using uterine perforation, D&C, abortion and omentum as keywords. The exclusion criteria included the presence of the uterus or placenta’s malignancy and uterine perforation following delivery or caused by an intrauterine device. Results: The review included 11 articles from 133 screened papers. We identified 12 cases that three evaluators further analysed. We also present the case of a 32-year-old woman diagnosed with uterine perforation and omentum involvement. The patient underwent a hysteroscopic procedure with resectioning the protruding omentum into the uterine cavity, followed by intrauterine device insertion. Conclusion: This paper highlights the importance of a comprehensive gynaecological evaluation following a D&C procedure that includes a thorough clinical examination and a detailed ultrasound assessment. Healthcare providers should not overlook the diagnosis of omentum involvement in the presence of a history of intrauterine procedures.

Objective: To evaluate the potential of the first-trimester ultrasound (US) features for the detection of central nervous system (CNS) anomalies. Methods/Methodology: This is a prospective one-center three-year study. Unselected singleton pregnant women were examined using an extended first-trimester anomaly scan (FTAS) that included the CNS assessment: the calvaria shape, the septum (falx cerebri), the aspect of the lateral ventricles, the presence of the third ventricle and aqueduct of Sylvius (AS) and the posterior brain morphometry: the fourth ventricle, namely intracranial translucency (IT), brain stem/brain stem–occipital bone ratio (BS/BSOB) and cisterna magna (CM). The spine and underlying skin were also evaluated. The cases were also followed during the second and third trimesters of pregnancy and at delivery. FTAS efficiency to detect major CNS abnormalities was calculated. Results: We detected 17 cases with CNS major abnormalities in a population of 1943 first-trimester (FT) fetuses, including spina bifida with myelomeningocele, exencephaly-anencephaly, holoprosencephaly, hydrocephaly, cephalocele and Dandy-Walker malformation. The CNS features in the abnormal group are presented. In the second trimester (ST), we further diagnosed cases of corpus callosum agenesis, cerebellar hypoplasia, vein of Galen aneurysm and fetal infection features (ventriculomegaly, intraventricular bands, intraventricular cyst and hyperechoic foci), all declared normal at the FTAS. During the third trimester (TT) scan we identified a massive fetal cerebral haemorrhage absent at previous investigations. We report a detection rate of 72.7% of fetal brain anomalies in the FT using the proposed CNS parameters. The sensitivity of the examination protocol was 72.7%, and the specificity was 100%. Conclusion: A detailed FT CNS scan is feasible and efficient. The majority of cases of major CNS abnormalities can be detected early in pregnancy. The visualization rates of the CNS parameters in the FT are great with short, if any, additional investigation time. FT cerebral disorders such as haemorrhage or infections were missed in the FT even when an extended evaluation protocol was used.

INTRODUCTION: Deficiency in the aquaporin‐4 (AQP4) water channel has been linked to impaired amyloid beta (Aβ) clearance. However, a detailed morphopathological analysis of amyloid deposition following AQP4 therapeutic modulation remains unexplored.METHODS: Two‐month‐old amyloid precursor protein presenilin 1 (APPPS1) mice were treated daily for 28 days with either the AQP4 facilitator N‐(3‐(Benzyloxy)pyridin‐2‐yl) benzene‐sulfonamide (TGN‐073) or the AQP4 inhibitor N‐(1,3,4‐thiadiazol‐2‐yl)pyridine‐3‐carboxamide dihydrochloride (TGN‐020) (both at 200 mg/kg). Controls included vehicle‐treated APPPS1 and WT C57BL/6J mice. Comprehensive histopathological, biochemical, and behavioral analyses were conducted.RESULTS: Mice treated with AQP4 facilitator showed a significant reduction in total Aβ, fibrillar deposits, and soluble Aβ, while the AQP4 inhibitor caused a substantial increase in brain Aβ. AQP4‐facilitator treatment also reduced Aβ40 levels and Aβ40/Aβ42 ratio, whereas the inhibitor treatment increased both Aβ40 and Aβ42. Additionally, facilitator‐treated mice demonstrated reduced anxiety and improved memory performance.DISCUSSION: These findings suggest that AQP4 modulation is a promising strategy to enhance Aβ clearance and a potential therapeutic target in Alzheimer's disease.Highlights: Intramural periarterial drainage of the interstitial fluid mediated by aquaporin‐4 (AQP4) is a key element that ensures clearance of catabolites/Aβ peptide from within the brain parenchyma. Inhibition of AQP4 in an APPPS1 mouse model of AD leads to increased amyloid deposition and deficient behavior compared to untreated transgenic animals. Pharmaceutical facilitation of AQP4 in the same APPPS1 mouse model leads to a massive decrease in amyloid burden and improves the behavioral performance of the animals compared to untreated control APPPS1 mice.

Ectopic endometrial epithelium associates a wide spectrum of symptomatology. Their evolution can be influenced by inflammatory and vascular changes, that affect not only the structure and cell proliferation rate, but also symptoms. This prospective study involved tissue samples from surgically treated patients, stained using classical histotechniques and immunohistochemistry. We assessed ectopic endometrial glands (CK7+, CK20−), adjacent blood vessels (CD34+), estrogen/progesterone hormone receptors (ER+, PR+), inflammatory cells (CD3+, CD20+, CD68+, Tryptase+), rate of inflammatory cells (Ki67+) and oncoproteins (BCL2+, PTEN+, p53+) involved in the development of endometriosis/adenomyosis. A CK7+/CK20− expression profile was present in the ectopic epithelium and differentiated it from digestive metastases. ER+/PR+ were present in all cases analyzed. We found an increased vascularity (CD34+) in the areas with abdominal endometriosis and CD3+−:T-lymphocytes, CD20+−:B-lymphocytes, CD68+:macrophages, and Tryptase+: mastocytes were abundant, especially in cases with adenomyosis as a marker of proinflammatory microenvironment. In addition, we found a significantly higher division index-(Ki67+) in the areas with adenomyosis, and inactivation of tumor suppressor genes-p53+ in areas with neoplastic changes. The inflammatory/vascular/hormonal mechanisms trigger endometriosis progression and neoplastic changes increasing local pain. Furthermore, they may represent future therapeutic targets. Simultaneous-multiple immunohistochemical labelling represents a valuable technique for rapidly detecting cellular features that facilitate comparative analysis of the studied predictors.

The placenta is an essential organ in the proper development of pregnancy, and it can present a lot of structural and vascular lesions that can affect fetal development. One of the pathologies associated with pregnancy, which can change the placental structure is thrombophilia (TPh), and this can be correlated with an intrauterine growth restriction (IUGR) of the fetus. Maternal clinical aspects (age, weight) can be correlated with fetal ones (weight, gender), but also with the structural and vascular aspect of the placenta. The placental structure associated with TPh and IUGR shows macroscopic changes, such as fibrin deposition, calcifications and placental infarctions, but microscopic lesions are best highlighted by classical staining techniques: Hematoxylin-Eosin (HE), Masson's trichrome (MT) and Periodic Acid-Schiff (PAS)-Hematoxylin, but also by immunohistochemistry technique with the help of anti-cluster of differentiation 34 (CD34) antibody that could make it possible to quantify vascular density depending on the pathology. Microscopic changes were massive infarcts caused by vascular ischemia, intravenous and extravillous fibrin deposits, calcifications, and vascular thrombosis. All these clinical, morphological and morphopathological data are interconnected and may vary in the presence of TPh and IUGR.