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.

Background and purpose In the central nervous system, a multitude of changes have been described associated with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, such as microglial activation, perivascular lymphocyte cuffing, hypoxic‐ischaemic changes, microthrombosis, infarcts or haemorrhages. It was sought here to assess the vascular basement membranes (vBMs) and surrounding perivascular astrocytes for any morphological changes in acute respiratory syndrome (coronavirus disease 2019, COVID‐19) patients. Methods The light microscopy morphology of the vBMs and perivascular astrocytes from brains of 14 patients with confirmed SARS‐CoV‐2 infection was analysed and compared to four control patients utilizing fluorescent immunohistochemistry for collagen IV and astrocytes (GFAP), endothelia (CD31), tight junction 1 (TJ1) adhesion protein, as well as the aquaporin 4 (AQP4) water channel. On 2D and 3D deconvoluted images from the cortex and white matter, vessel densities, diameters, degree of gliosis, collagen IV/GFAP and GFAP/AQP4 colocalizations were calculated, as well as the fractal dimension of astrocytes and vBMs viewed in tangential planes. Results Fractal dimension analysis of the GFAP‐stained astrocytes revealed lower branching complexities and decreased GFAP/collagen IV colocalization for COVID‐19 patients. Interestingly, vBMs showed significantly increased irregularities (fractal dimension values) compared to controls. Vessel diameters were increased in COVID‐19 cases, especially for the white matter, TJ1 protein decreased its colocalization with the endothelia, and AQP4 reduced its co‐expression in astrocytes. Conclusions Our data on the irregularity of the basement membranes, loss of endothelial tight junction, reduction of the astrocyte end‐feet and decrease of AQP4 suggest subtle morphological changes of the blood–brain barrier in COVID‐19 brains that could be linked with indirect inflammatory signalling or hypoxia/hypercapnia.

This is an open-access article distributed under the terms of a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International Public License, which permits unrestricted use, adaptation, distribution and reproduction in any medium, non-commercially, provided the new creations are licensed under identical terms as the original work and the original work is properly cited. ORIGINAL PAPER The influence of gestational diabetes mellitus (GDM) and gestational hypertension (GH) on placental morphological changes ANCA-MARIA ISTRATE-OFIŢERU 1-3) , COSTIN BERCEANU 3) , SABINA BERCEANU 3) , CRISTINA JANA BUSUIOC 1) , GABRIELA-CAMELIA ROŞU 1,2) , DAMIAN DIŢESCU 4) , FLORIN GROSU 5) , NICOLETA-LOREDANA VOICU 3,6)

Ovarian ectopic pregnancy (OEP) represents the rarest type of ectopic pregnancy, accounting for 1-3% of this pathology. The diagnosis of this pathology is challenging due to the non-specific clinical aspects and the ultrasound examination hampered by the lack of visible gestational sac in the presence of hematocele and hemoperitoneum. The purpose of the extended histopathological (HP) examination was to identify particular aspects of the OEP trophoblast and to highlight potential local ovarian modifications which can determine pregnancy fixation at this level. The patient presented local favorable conditions for intraovarian nidation, conditions confirmed by the HP classical examination and by the immunohistochemical evaluation. We identified, using classical Hematoxylin-Eosin, Masson's trichrome and Periodic Acid-Schiff (PAS)-Hematoxylin, necrotic hemorrhage, accentuated vascular thrombosis and high density lymphoplasmocytary infiltrate. These modifications increased local adhesivity and cell destruction through hypoperfusion. Anti-cluster of differentiation antibodies (CD34, CD38, tryptase) revealed the low number of intravillous vessels and the high number of macrophages and mastocytes involved in the local inflammatory process heighten. We identified the presence of trophoblast tissue in the ovarian structure using anti-cytokeratin AE1/AE3 (CK AE1/AE3)/anticytokeratin 7 (CK7) antibodies. The anti-alpha-smooth muscle actin (α-SMA) and anti-vimentin (VIM) antibodies displayed the density of myofibroblasts and intravillous stromal cells and with the aid of anti-progesterone receptor (PR) antibody, we identified the corpus luteum hormonal response in the OEP. The placental villosities present a blocked multiplication process at the anti-apoptotic B-cell lymphoma 2 (BCL2) protein, confirmed by the Ki67 cell proliferation and tumor protein 63 (p63) immunomarkers. Anti-neuron specific enolase (NSE), anticalretinin and anti-inhibin A antibodies showed the particular aspects of the granulosa and internal theca cells, which may be involved in oocyte release blockage, intraluteal and extraluteal fecundation of the OEP.

Endometriosis is a benign gynecological pathology that mostly affects the organs of the pelvis,but also organs located at a distance maybe affected. Tissue immunohistochemically identified as ectopic endometrium may undergo certain structural and functional changes that may lead to preneoplastic alterations (hyperplasia, dysplasia) in normal cellswhich can evolve to neoplasia. Clinical, genetic, metabolic conditions and local factors may influence degenerationof a benign pathology into a malignant pathology. Endometriosis of the abdominal wall is more frequently encountered, as the number of casarean section has increased. Endometriomas surrounding tissue has a direct impact on the structure of the cells that form the mass. By remodeling cellular morphology, corroborated with the hormonal factors action and the inflammatory response ( via lymphocyte cell secretion), the cell cycle is altered and antiapoptotic activity may be promoted. Immune system via lymphocyte cell secretion, the pressure exerted on the tumor area by surrounding tissueswith its size change, conditioned by the fluctuation of hormonal factors, act directly on the cellular structure and can increase anti-apoptotic action and decrease cell cycle regulation. The presence of endometriomas is identified by the positivity of immunohistochemical reactions for estrogen receptors (ER), progesteron receptors (PR), Cytokeratin 7 (CK7) for endometrial tissue. Negative reaction at Cytokeratin 20 (CK20) shows that the studied area is not a metastasis of a digestive tumor. The presence of abundant inflammatory, peritumoral cells markedwith anti-CD68 / Tryptase for macrophages / mast cells demonstrates the involvement of the inflammatory system in the structural and functional modification of endometrial cells.The pronounced cell division was demonstrated by intense reaction with the anti-Ki67 antibody.The signigicant anti-apoptotic action of the endometrial tissue is shown by the positivity of anti-B cell Lymphoma 2 (BCL2) / anti-Phosphatase and tensin homolog (PTEN) / anti-p53 antibodies.