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CaTiO3 is one of the most versatile oxides of the perovskite family for applications in areas such as electronics, photocatalysis and photovoltaics, due to its properties that it can present, such as ionic conduction, ferroelectric, or photoluminescence. Consequently, the study of the synthesis routes of the material is the fundamental importance. The CaTiO3 powders were synthesized using the sol–gel technique, with different treatment temperatures of 600–1000 °C. The structural, morphological, compositional, and optical properties were analyzed by means of X-ray diffraction (XRD), Raman spectroscopy, scanning electron spectroscopy (SEM), Energy dispersive X-ray (EDX), Fourier transform infrared spectroscopy (FTIR), and UV–Vis spectrophotometry. X-ray diffraction (XRD) indicated the formation of the perovskite phase with an orthorhombic structure from 600 °C with the presence of traces of TiO2 in the anatase and rutile phase, which decreases with increasing heat treatment temperature. The degradation of methylene blue under ultraviolet light irradiation was carried out with the samples that present the highest purity of CaTiO3 treated at 900 and 1000 °C, which were synthesized with an increase in the amount of catalyst and reaction temperature by the sol–gel method, which was viable for obtaining CaTiO3 powders at low temperatures compared to conventional methods for the purpose of applying the photocatalytic degradation of methylene blue, which registered a degradation of up to 97%. [ABSTRACT FROM AUTHOR]

The authors report the ultrastructural characteristics of myopericytoma, a recently described variant of perivascular (pericytic) tumors, mainly with regard to their myopericytic cells and vessels. Myopericytes range between pericytes and vascular smooth muscle cells (SMCs) in a morphologic continuum. The principal findings of the intermediate phenotypes are (1) elongated or annular morphology with processes of varying length and thickness (usually long and thin); (2) a continuous, irregularly thickened and zonally duplicated basement membrane; (3) heterocellular 'peg and socket' junctions with neighboring endothelial cells, and scarce specialized junctions between myopericytes; (4) numerous micropinocytotic vesicles, whether continuous or forming focal rows; (5) abundant thin microfilaments, grouped in bundles with dense bodies and adhesion plaques; (6) poorly developed synthetic system (RER and Golgi); (7) pseudointracellular bodies formed by invagination of basement and plasma membranes, with numerous endocytic vesicles; and (8) zones of cytoplasmic rarefaction near micropinocytotic vesicles and intracellular organelles. The ultrastructure of myopericytes therefore makes it possible to distinguish them from pericytes, SMCs, and fibroblast/myofibroblasts, which is useful for myopericytoma diagnosis. The main pattern of the vessels, with perivascular concentric and multilayered growth of myopericytes (a thick wall in contrast to a small lumen) and lack of elastic material, also supports an intermediate form between pericytic and muscular microvasculature. The presence of myopericytes more similar to SMCs and of hemangiopericytoma-like vessels concurs with transitional forms with angioleyomyoma and true hemangiopericytoma, histogenetically representing a morphologic continuum for the perivascular tumors. [ABSTRACT FROM AUTHOR]

Congophilic birefringent amyloid deposits, with immunostaining for transthyretin (TTR) and amyloid P, associated with numerous coarse, enlarged and thick elastic fibres, are reported in the stroma of two choroid plexus papillomas, a finding not previously described in choroid plexus tumours. TTR was expressed as aggregates of ‘doughnut-shaped’ bodies, in which the TTR-positive peripheral area encircled the elastic fibre (TTR-negative core). Ultrastructurally, the amyloid microfibrils surrounded the elastic fibres and appeared to continue into the microfibrillar mantle of the latter. The stromal TTR-amyloid deposits associated with abundant elastic fibres in tumours that occur in the choroid plexus may be related to the alteration (production/accumulation, insufficient breakdown and/or extracellular matrix modifications) of some of the choroid plexus functions (removal, target and source of polypeptides, including TTR synthesis) and may be of interest for future studies on choroid plexus polypeptide activity and on protein development into elastomeric and amyloidogenic microfibrils. [ABSTRACT FROM AUTHOR]

Electronic spectra of nine different types of organic colorants embedded in three different matrices (sol–gel SiO2 , PMMA, and SiO2–PMMA) were studied experimentally with the use of optical absorption, photoluminescence excitation, and emission techniques, as well as fluorescent microscopy and atomic force microscopy. We found a distinct set of energy levels for each type of dye. The type of matrix and the degree of aggregation of the organic molecules have relatively small effects on the spectra, although their influence on the optical density of the material is essential. The character of the energy spectra is mainly related with the shape of the dye molecule. A quantum mechanical description of the electronic spectra of these molecules was made on the basis of the free electron molecular orbitals approach. The molecules were considered as two-dimensional potential wells with different shapes. The effect of boundary conditions on the energy spectra was studied. The direct solution of the Schrödinger equation shows a good theory–experiment correlation. [ABSTRACT FROM AUTHOR]

Abstract Background Previous experimental studies have shown that injurious mechanical ventilation has a direct effect on pulmonary and systemic immune responses. How these responses are propagated or attenuated is a matter of speculation. The goal of this study was to determine the contribution of mechanical ventilation in the regulation of Toll-like receptor (TLR) signaling and interleukin-1 receptor associated kinase-3 (IRAK-3) during experimental ventilator-induced lung injury. Methods Prospective, randomized, controlled animal study using male, healthy adults Sprague-Dawley rats weighing 300-350 g. Animals were anesthetized and randomized to spontaneous breathing and to two different mechanical ventilation strategies for 4 hours: high tidal volume (VT) (20 ml/kg) and low VT (6 ml/kg). Histological evaluation, TLR2, TLR4, IRAK3 gene expression, IRAK-3 protein levels, inhibitory kappa B alpha (IκBα), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL6) gene expression in the lungs and TNF-α and IL-6 protein serum concentrations were analyzed. Results High VT mechanical ventilation for 4 hours was associated with a significant increase of TLR4 but not TLR2, a significant decrease of IRAK3 lung gene expression and protein levels, a significant decrease of IκBα, and a higher lung expression and serum concentrations of pro-inflammatory cytokines. Conclusions The current study supports an interaction between TLR4 and IRAK-3 signaling pathway for the over-expression and release of pro-inflammatory cytokines during ventilator-induced lung injury. Our study also suggests that injurious mechanical ventilation may elicit an immune response that is similar to that observed during infections.

This article focuses on the role of pericytes and endothelial cells (EC). Some of the general functions of pericytes which have been postulated are, contractibility, considerable mesenchymal potentiality and control of EC growth by a mechanism that requires contact and activation of latent transforming growth factor. The possible role of pericytes during angiogenesis and granulation tissue formation may be related to the two latter functions that is, as a modulator of EC growth and as a source of other cells.

Abstract: Neural injury triggers changes in the expression of a large number of gene families. Particularly interesting are those encoding proteins involved in the generation, propagation or restoration of electric potentials. The expression of the Na+,K+-ATPase subunit isoforms (α, β and γ) was studied in dorsal root ganglion (DRG) and sciatic nerve of the rat in normal conditions, after axotomy and during regeneration. In normal DRG, α1 and α2 are expressed in the plasma membrane of all cell types, while there is no detectable signal for α3 in most DRG cells. After axotomy, α1 and α2 expression decreases evenly in all cells, while there is a remarkable onset in α3 expression, with a peak about day 3, which gradually disappears throughout regeneration (day 7). β1 Is restricted to the nuclear envelope and plasma membrane of neurons and satellite cells. Immediately after injury, β1 shows a homogeneous distribution in the soma of neurons. No β2 expression was found. β3 Specific immunofluorescence appears in all neurons, although it is brightest in the smallest, diminishing progressively after injury until day 3 and, thereafter, increasing in intensity, until it reaches normal levels. FXYD7 is expressed weakly in a few DRG neurons (less than 2%) and Schwann cells. It increases intensely in satellite cells immediately after axotomy, and in all cell types at day 3. Transient switching of members of the Na+,K+-ATPase isoform family elicited by axotomy suggests variations in the sodium pump isozymes with different affinities for Na+,K+ and ATP from those in intact nerve. This adaptation may be important for regeneration. [Copyright &y& Elsevier]

The often well-developed microvasculature in pancreatic neuroendocrine tumors (PanNETs) has been studied from different perspectives. However, some detailed structural findings have received less attention. Our objective is to study an overlooked event in PanNETs: "enclosed vascular tufts" (EVTs). For this purpose, 39 cases of PanNETs were examined with conventional (including serial sections) and immunochemistry procedures. In typical EVTs, the results show: 1) an insulated terminal vascular area, with a globular (glomeruloid) aspect, formed by a cluster of coiled microvessels, presenting CD31-, CD34-positive endothelial cells, αSMA-positive pericytes, and perivascular CD34-positive stromal cells/telocytes, separated by a pseudoglandular space from the surrounding trabeculae of tumor neuroendocrine cells; and 2) a pedicle joining the insulated terminal vascular area, with connective tissue tracts around the enclosing tumor trabeculae. EVTs predominate in the trabecular and nested gyriform pattern of PanNETs, with tumor trabeculae that follow a ribbon coil (winding ribbon pattern) around small vessels, which acquire a tufted image. In EVTs, secondary modifications may occur (fibrosis, hyalinization, myxoid changes, and calcification), coinciding or not with those of the connective tracts. In conclusion, the typical characteristics of unnoticed EVTs allow them to be considered as a morphological sign of PanNETs (a vascular tuft sign). Further in-depth studies are required, mainly to assess the molecular pathways that participate in vascular tuft formation and its pathophysiological implications., (©The Author(s) 2024. Open Access. This article is licensed under a Creative Commons CC-BY International License.)

Background: Peripheral neuropathy (PN) constitutes a dose-limiting side effect of oxaliplatin chemotherapy that often compromises the efficacy of antineoplastic treatments. Sensory neurons damage in dorsal root ganglia (DRG) are the cellular substrate of PN complex molecular origin. Dehydropeptidase-1 (DPEP1) inhibitors have shown to avoid platin-induced nephrotoxicity without compromising its anticancer efficiency. The objective of this study was to describe DPEP1 expression in rat DRG in health and in early stages of oxaliplatin toxicity. To this end, we produced and characterized anti-DPEP1 polyclonal antibodies and used them to define the expression, and cellular and subcellular localization of DPEP1 by immunohistochemical confocal microscopy studies in healthy controls and short term (six days) oxaliplatin treated rats., Results: DPEP1 is expressed mostly in neurons and in glia, and to a lesser extent in endothelial cells. Rats undergoing oxaliplatin treatment developed allodynia. TNF-𝛼 expression in DRG revealed a pattern of focal and at different intensity levels of neural cell inflammatory damage, accompanied by slight variations in DPEP1 expression in endothelial cells and in nuclei of neurons., Conclusions: DPEP1 is expressed in neurons, glia and endothelial cells of DRG. Oxaliplatin caused allodynia in rats and increased TNF-α expression in DRG neurons. The expression of DPEP1 in neurons and other cells of DRG suggest this protein as a novel strategic molecular target in the prevention of oxaliplatin-induced acute neurotoxicity., (© 2024. The Author(s).)

Over the years, the origin of ovarian Leydig cells has been, and still is, a topic subject to deep debate. Seven years ago, we proposed that this origin resided in intraneural elements that came from a possible reservoir of neural crest cells, a reservoir that may be located in the ganglia of the celiac plexus. We believe we have found the evidence necessary to prove this hypothesis., (© 2024. The Author(s) under exclusive licence to Japan Human Cell Society.)

Intussusceptive angiogenesis (IA) and intussusceptive lymphangiogenesis (IL) play a key role in the growth and morphogenesis of vessels. However, there are very few studies in this regard in vessel tumors (VTs). Our objective is to assess the presence, characteristics, and possible mechanisms of the formation of intussusceptive structures in a broad spectrum of VTs. For this purpose, examples of benign and malignant blood and lymphatic VTs were studied via conventional procedures, semithin sections, and immunochemistry and immunofluorescence microscopy. The results demonstrated intussusceptive structures (pillars, meshes, and folds) in benign (lobular capillary hemangioma or pyogenic granuloma, intravascular papillary endothelial hyperplasia or Masson tumor, sinusoidal hemangioma, cavernous hemangioma, glomeruloid hemangioma, angiolipoma, and lymphangiomas), low-grade malignancy (retiform hemangioendothelioma and Dabska tumor), and malignant (angiosarcoma and Kaposi sarcoma) VTs. Intussusceptive structures showed an endothelial cover and a core formed of connective tissue components and presented findings suggesting an origin through vessel loops, endothelialized thrombus, interendothelial bridges, and/or splitting and fusion, and conditioned VT morphology. In conclusion, the findings support the participation of IA and IL, in association with sprouting angiogenesis, in VTs, and therefore in their growth and morphogenesis, which is of pathophysiological interest and lays the groundwork for in-depth molecular studies with therapeutic purposes.

Telocytes/CD34+ stromal cells (TCs/CD34+ SCs) have been studied in numerous organs and tissues, but their presence and characteristics in the parathyroid glands have not been explored. Using immunological and ultrastructural procedures, we assess the location, arrangement, and behavior of TCs/CD34+ SCs in normal human parathyroids, during their development and in their most frequent pathologic conditions. In normal parathyroids, TCs/CD34+ SCs show a small somatic body and long thin processes with a moniliform aspect, form labyrinthine systems, connect other neighboring TCs/CD34+ SCs, vessels, adipocytes, and parenchymal cells directly or by extracellular vesicles, and associate with collagen I. TCs/CD34+ SCs and collagen I are absent around vessels and adipocytes within parenchymal clusters. In developing parathyroids, TCs/CD34+ SC surround small parenchymal nests and adipocytes. In hyperplastic parathyroids, TCs/CD34+ SCs are prominent in some thickened internodular septa and surround small extraglandular parenchymal cell nests. TCs/CD34+ SCs are present in delimiting regions with compressed parathyroids and their capsule in adenomas but absent in most adenomatous tissue. In conclusion, TCs/CD34+ SCs are an important cellular component in the human parathyroid stroma, except around vessels within parenchymal nests. They show typical characteristics, including those of connecting cells, are present in developing parathyroids, and participate in the most frequent parathyroid pathology, including hyperplastic and adenomatous parathyroids.

Kaposi sarcoma (KS) is an angioproliferative lesion in which two main KS cell sources are currently sustained: endothelial cells (ECs) and mesenchymal/stromal cells. Our objective is to establish the tissue location, characteristics and transdifferentiation steps to the KS cells of the latter. For this purpose, we studied specimens of 49 cases of cutaneous KS using immunochemistry and confocal and electron microscopy. The results showed that delimiting CD34+ stromal cells/Telocytes (CD34+SCs/TCs) in the external layer of the pre-existing blood vessels and around skin appendages form small convergent lumens, express markers for ECs of blood and lymphatic vessels, share ultrastructural characteristics with ECs and participate in the origin of two main types of neovessels, the evolution of which gives rise to lymphangiomatous or spindle-cell patterns-the substrate of the main KS histopathological variants. Intraluminal folds and pillars (papillae) are formed in the neovessels, which suggests they increase by vessel splitting (intussusceptive angiogenesis and intussusceptive lymphangiogenesis). In conclusion, delimiting CD34+SCs/TCs are mesenchymal/stromal cells that can transdifferentiate into KS ECs, participating in the formation of two types of neovessels. The subsequent growth of the latter involves intussusceptive mechanisms, originating several KS variants. These findings are of histogenic, clinical and therapeutic interest.

The microvasculature of angiolipoma frequently presents thrombi. Our objectives are to assess whether intussusceptive angiogenesis (IA) participates in vasculature formation in non-infiltrating angiolipoma and, if so, to explore how thrombi are involved in the IA process. For this purpose, we studied angiolipoma specimens (n: 52), using immunohistochemistry, and confocal and electron microscopy. The results showed the presence of folds and pillars, hallmarks of IA, dividing the vessel lumen. Folds showed a cover formed by reoriented endothelial cells from the vessel wall, or from newly formed folds, and a core initially formed by thrombus fragments (clot components as transitional core), which was replaced by extracellular matrix and invaginating pericytes establishing numerous peg-and-socket junctions with endothelial cells (mature core). A condensed plasmatic electron-dense material surrounded and connected folds and pillars with each other and with the vascular wall, which suggests a clot role in fold/pillar arrangement. In conclusion, we contribute to IA participation in capillary network formation in angiolipoma and the immunohistochemical and ultrastructural events by which microthrombosis facilitates IA. Therefore, in addition to the histogenesis of angiolipoma, we provide an easily obtainable substrate for future studies on clot component action in IA, of clinical and therapeutic interest., (©The Author(s) 2023. Open Access. This article is licensed under a Creative Commons CC-BY International License.)

Perivascular cells in the pericytic microvasculature, pericytes and CD34+ stromal cells/telocytes (CD34+SCs/TCs), have an important role in angiogenesis. We compare the behavior of these cells depending on whether the growth of endothelial cells (ECs) from the pre-existing microvasculature is toward the interstitium with vascular bud and neovessel formation (sprouting angiogenesis) or toward the vascular lumen with intravascular pillar development and vessel division (intussusceptive angiogenesis). Detachment from the vascular wall, mobilization, proliferation, recruitment, and differentiation of pericytes and CD34+SCs/TCs, as well as associated changes in vessel permeability and functionality, and modifications of the extracellular matrix are more intense, longer lasting over time, and with a greater energy cost in sprouting angiogenesis than in intussusceptive angiogenesis, in which some of the aforementioned events do not occur or are compensated for by others (e.g., sparse EC and pericyte proliferation by cell elongation and thinning). The governing mechanisms involve cell-cell contacts (e.g., peg-and-socket junctions between pericytes and ECs), multiple autocrine and paracrine signaling molecules and pathways (e.g., vascular endothelial growth factor, platelet-derived growth factor, angiopoietins, transforming growth factor B, ephrins, semaphorins, and metalloproteinases), and other factors (e.g., hypoxia, vascular patency, and blood flow). Pericytes participate in vessel development, stabilization, maturation and regression in sprouting angiogenesis, and in interstitial tissue structure formation of the pillar core in intussusceptive angiogenesis. In sprouting angiogenesis, proliferating perivascular CD34+SCs/TCs are an important source of stromal cells during repair through granulation tissue formation and of cancer-associated fibroblasts (CAFs) in tumors. Conversely, CD34+SCs/TCs have less participation as precursor cells in intussusceptive angiogenesis. The dysfunction of these mechanisms is involved in several diseases, including neoplasms, with therapeutic implications.

Glioma stem cells (GSCs) live in a continuous process of stemness reprogramming to achieve specific cell commitment within the so-called GSC niches, specifically located in periarteriolar regions. In this review, we analyze the expression levels, cellular and subcellular location, and role of three scaffold proteins (IQGAP1, FKBP51, and AmotL2) in GSC niches. Scaffold proteins contribute to cell differentiation, migration, and angiogenesis in glioblastoma. It could be of diagnostic interest for establishing stages, for therapeutic targets, and for improving glioblastoma prognosis, which is still at the experimental level.

Platelets in atherosclerosis, bypass stenosis, and restenosis have been extensively assessed. However, a sequential ultrastructural study of platelets in angiogenesis during the early phases of these lesions has received less attention. Our objective was the study of platelets in angiogenesis and vessel regression during intimal thickening (IT) formation, a precursor process of these occlusive vascular diseases. For this purpose, we used an experimental model of rat occluded arteries and procedures for ultrastructural observation. The results show (a) the absence of platelet adhesion in the de-endothelialized occluded arterial segment isolated from the circulation, (b) that intraarterial myriad platelets contributed from neovessels originated by sprouting angiogenesis from the periarterial microvasculature, (c) the association of platelets with blood components (fibrin, neutrophils, macrophages, and eosinophils) and non-polarized endothelial cells (ECs) forming aggregates (spheroids) in the arterial lumen, (d) the establishment of peg-and-socket junctions between platelets and polarized Ecs during intussusceptive angiogenesis originated from the EC aggregates, with the initial formation of IT, and (e) the aggregation of platelets in regressing neovessels ('transitory paracrine organoid') and IT increases. In conclusion, in sprouting and intussusceptive angiogenesis and vessel regression during IT formation, we contribute sequential ultrastructural findings on platelet behavior and relationships, which can be the basis for further studies using other procedures.

Glioblastoma (GBM) is the most malignant tumor in the brain. In addition to the vascular pattern with thin-walled vessels and findings of sprouting angiogenesis, GBM presents a bizarre microvasculature (BM) formed by vascular clusters, vascular garlands, and glomeruloid bodies. The mechanisms in BM morphogenesis are not well known. Our objective was to assess the role of pericyte/endothelial proliferation and intussusceptive angiogenic mechanisms in the formation of the BM. For this purpose, we studied specimens of 66 GBM cases using immunochemistry and confocal microscopy. In the BM, the results showed (a) transitional forms between the BM patterns, mostly with prominent pericytes covering all the abluminal endothelial cell (EC) surface of the vessels, (b) a proliferation index high in the prominent pericytes and low in ECs (47.85 times higher in pericytes than in ECs), (c) intravascular pillars (hallmark of intussusceptive angiogenesis) formed by transcapillary interendothelial bridges, endothelial contacts of opposite vessel walls, and vessel loops, and (d) the persistence of these findings in complex glomeruloid bodies. In conclusion, disproportion in pericyte/EC proliferation and mechanisms of intussusceptive angiogenesis participate in BM formation. The contributions have morphogenic and clinical interest since pericytes and intussusceptive angiogenesis can condition antiangiogenic therapy in GBM.

We studied CD34+ stromal cells/telocytes (CD34+SCs/TCs) in pathologic skin, after briefly examining them in normal conditions. We confirm previous studies by other authors in the normal dermis regarding CD34+SC/TC characteristics and distribution around vessels, nerves and cutaneous annexes, highlighting their practical absence in the papillary dermis and presence in the bulge region of perifollicular groups of very small CD34+ stromal cells. In non-tumoral skin pathology, we studied examples of the principal histologic patterns in which CD34+SCs/TCs have (1) a fundamental pathophysiological role, including (a) fibrosing/sclerosing diseases, such as systemic sclerosis, with loss of CD34+SCs/TCs and presence of stromal cells co-expressing CD34 and αSMA, and (b) metabolic degenerative processes, including basophilic degeneration of collagen, with stromal cells/telocytes in close association with degenerative fibrils, and cutaneous myxoid cysts with spindle-shaped, stellate and bulky vacuolated CD34+ stromal cells, and (2) a secondary reactive role, encompassing dermatitis-e.g., interface (erythema multiforme), acantholytic (pemphigus, Hailey-Hailey disease), lichenoid (lichen planus), subepidermal vesicular (bullous pemphigoid), psoriasiform (psoriasis), granulomatous (granuloma annulare)-vasculitis (leukocytoclastic and lymphocytic vasculitis), folliculitis, perifolliculitis and inflammation of the sweat and sebaceous glands (perifolliculitis and rosacea) and infectious dermatitis (verruca vulgaris). In skin tumor and tumor-like conditions, we studied examples of those in which CD34+ stromal cells are (1) the neoplastic component (dermatofibrosarcoma protuberans, sclerotic fibroma and solitary fibrous tumor), (2) a neoplastic component with varying presentation (fibroepithelial polyp and superficial myxofibrosarcoma) and (3) a reactive component in other tumor/tumor-like cell lines, such as those deriving from vessel periendothelial cells (myopericytoma), epithelial cells (trichoepithelioma, nevus sebaceous of Jadassohn and seborrheic keratosis), Merkel cells (Merkel cell carcinoma), melanocytes (dermal melanocytic nevi) and Schwann cells (neurofibroma and granular cell tumor).

The first case of a placental tumor composed of benign hepatic tissue was published in 1986 and considered a placental benign hepatocellular adenoma. Since then, this lesion is better known as ectopic liver, and a total of 12 cases have been published. The ectopic liver located in the umbilical cord is an even rarer alteration, with only nine cases described to date. We report another case of ectopic liver, this time in an embryo of only five weeks of gestational age.

Several origins have been proposed for cancer-associated fibroblasts (CAFs), including resident CD34+ stromal cells/telocytes (CD34+SCs/TCs). The characteristics and arrangement of mammary CD34+SCs/TCs are well known and invasive lobular carcinoma of the breast (ILC) is one of the few malignant epithelial tumours with stromal cells that can express CD34 or αSMA, which could facilitate tracking these cells. Our objective is to assess whether tissue-resident CD34+SCs/TCs participate in the origin of CAFs in ILCs. For this purpose, using conventional and immunohistochemical procedures, we studied stromal cells in ILCs (n:42) and in normal breasts (n:6, also using electron microscopy). The results showed (a) the presence of anti-CD34+ or anti-αSMA+ stromal cells in varying proportion (from very rare in one of the markers to balanced) around nests/strands of neoplastic cells, (b) a similar arrangement and location of stromal cells in ILC to CD34+SCs/TCs in the normal breast, (c) both types of stromal cells coinciding around the same nest of neoplastic cells and (d) the coexpression of CD34 and αSMA in stromal cells in ILC. In conclusion, our findings support the hypothesis that resident CD34+SCs/TCs participate as an important source of CAFs in ILC. Further studies are required in this regard in other tumours.

Intussusceptive angiogenesis (IA) is the process by which pre-existing blood vessels split, expand and remodel through intravascular pillar formation. In previous works, we studied the morphologic characteristics of intravascular papillary endothelial hyperplasia (IPEH) and suggested the participation of IA in the histogenesis of the lesion. Our current goal is to demonstrate that myriad papillae in IPEH are in fact myriad pillars, the hallmarks of IA. For this purpose, specimens of 14 cases of IPEH were used for conventional histologic techniques, immunohistochemistry and immunofluorescence in confocal microscopy. The studies showed the following pillar characteristics: a) structural composition by an endothelial cell (EC) cover and a connective core, b) characteristic pillar image and its appearance and disappearance in whole-mounted and series of individual views in confocal microscopy (requirements for pillar identification), c) arrangement in masses, alignments and meshes, and d) formation from vein intimal ECs, which extend and originate loops that encircle vein wall components (interstitial tissue structures: ITSs) and fibrin. The encircling ECs form the pillar cover and the encircled ITSs or fibrin form the initial core. Intraluminal endothelial bridges also originate from the vessel wall and from the pillars (nascent and thin pillars). In conclusion, the formation of myriad pillars, predominantly in veins, is the basis of IPEH. This lesion may therefore be considered an excessive expression of IA: IA becomes a lesion.

We studied telocytes/CD34+ stromal cells (TCs/CD34+SCs) in pathologically affected white adipose tissue after briefly examining them in normal fat. To this aim, we reviewed pathological processes, including original contributions, in which TCs/CD34+SCs are conserved, increased, and lost, or acquire a specific arrangement. The pathologic processes in which TCs/CD34+SCs are studied in adipose tissue include inflammation and repair through granulation tissue, iatrogenic insulin-amyloid type amyloidosis, non-adipose tissue components (nerve fascicles and fibres in neuromas and hyperplastic neurogenic processes) and tumours (signet ring carcinoma with Krukenberg tumour and colon carcinoma) growing in adipose tissue, adipose tissue tumours (spindle cell lipoma, dendritic fibromyxolipoma, pleomorphic lipoma, infiltrating angiolipoma of skeletal muscle and elastofibrolipoma), lipomatous hypertrophy of the interatrial septum, nevus lipomatosus cutaneous superficialis of Hoffman-Zurhelle and irradiated adipose tissue of the perirectal and thymic regions. Two highly interesting issues emerged: (1) whether the loss of CD34 expression in TCs/CD34+SCs is by changes in marker expression or the disappearance of these cells (the findings suggest the first possibility) and (2) whether in some invasive and metastatic malignant tumours, TCs/CD34+SCs that completely surround neoplastic cells act as nurse and/or isolating cells. Further studies are required on adipose tissue TCs/CD34+SCs, mainly in lipomatosis and obesity.