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Amaç: Koroner arter cerrahisinde greft açık kalma süresi endotel fonksiyonuna bağlıdır. Nitrik Oksitin (NO) endotel fonksiyonuna yararlı etkisi bilinmektedir. Greftlerdeki Nitrik Oksit düzeyi ve Losartan’ın Nitrik Oksit üzerine etkisi invitro olarak araştırılmıştır. Yöntem: Çalışma 13 hasta da 78 örnek ile yapıldı. İnternaltorasik arter, radial arter ve safenvengreft örnekleri “Kontrol Grubu” ve “Losartan Grubu” olmak üzere ikiye ayrıldı. Losartan grubu örnekleri 1 x 10-5molar Losantanlı Troyde’s solüsyonu çözeltisi içinde inkübe edildi. Nitrik Oksit, Griess yöntemi kullanılarak ölçüldü. İstatistiksel değerlendirme. Kruskal Wallis Oneway ANOVA, İndependentsample T ile Tukey ve Bonferroni testleri kullanılarak yapıldı. Bulgular: Kontrol grubu bazal Nitrik Oksit değeri, internaltorasik arter greftinde anlamlı olarak yüksek bulunmuştur (p

Although metallic stents improved the safety and efficacy of percutaneous coronary intervention (PCI), even the latest generation of drug-eluting stents (DES) is still limited by several factors. The limitations of DES are mainly related to the permanent metallic caging in vessel, chronic inflammatory response to the polymer and adverse effects of antiproliferative drug on endothelial tissue, leading to impaired physiological vasomotor response and late stent-related adverse events such as stent thrombosis and neoatherosclerosis. Bioresorbable vascular scaffold (Absorb BVS; Abbott Vascular) was designed to overcome these drawbacks of DES by disappearing from the vessel wall. Absorb BVS, however, was withdrawn from the world market because of increased incidence of scaffold thrombosis compared with DES. Importantly, only very limited long-term post-BVS implantation data are available, especially with regard to neoatherosclerosis, which can lead to very late adverse events even after resorption of the scaffold. Therefore, the goal of this review was to highlight the mid to long term clinical outcomes published to date, and to describe the features of the intimal healing process and neoatherosclerosis in the 5 years following Absorb BVS implantation, mainly based on our previous study. This may provide important information on the pathophysiology of the scaffolded vessel for clinicians, and promote identification of future bioresorbable materials for PCI that will minimize the stimulus for neoatherosclerosis.

The treatment of corneal endothelial dysfunction has experienced a revolutionary change in the past decades with the emergence of endothelial keratoplasty techniques: descemet stripping automated endothelial keratoplasty (DSAEK) and descemet membrane endothelial keratoplasty (DMEK). Recently, new treatments such as cultivated endothelial cell therapy, Rho-kinase inhibitors (ROCK inhibitors), bioengineered grafts, and gene therapy have been described. ,ese techniques represent new lines of treatment for endothelial dysfunction. ,eir advantages are to help address the shortage of quality endothelial tissue, decrease the complications associated with tissue rejection, and reduce the burden of postoperative care following transplantation. Although further randomized clinical trials are required to validate these findings and prove the long-term efficacy of the treatments, the positive outcomes in preliminary clinical studies are a stepping stone to a promising future. Our aim is to review the latest available alternatives and advancements to endothelial corneal transplant.

Submitted by Celio Junior da Costa Fernandes (celio.fernandes@unesp.br) on 2021-08-09T18:20:16Z No. of bitstreams: 1 Tese_Celio_30_March_2021.pdf: 204900028 bytes, checksum: 877d007d43b3628fe94ab22133db75a0 (MD5) Approved for entry into archive by Tais de Almeida (tais.almeida@unesp.br) on 2021-08-09T18:54:29Z (GMT) No. of bitstreams: 1 fernandes_cjc_dr_bot.pdf: 204900028 bytes, checksum: 877d007d43b3628fe94ab22133db75a0 (MD5) Made available in DSpace on 2021-08-09T18:54:29Z (GMT). No. of bitstreams: 1 fernandes_cjc_dr_bot.pdf: 204900028 bytes, checksum: 877d007d43b3628fe94ab22133db75a0 (MD5) Previous issue date: 2021-04-08 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Compreender os mecanismos envolvidos na manutenção e homeostase óssea requer elucidar o comportamento de células em seu microambiente. O objetivo deste estudo foi investigar como células ósseas (MC3t3-E1, HOEL) ou mesenquimais são moduladas através da sinalização parácrina desencadeada por fibroblastos (3t3-NIH), células endoteliais de veias (HUVEC) e de aorta (HCAEC), além de células de músculo liso (AoSMC/VSMC). Para avaliar essa capacidade de modulação de células ósseas, fibroblastos, células endoteliais e de musculatura lisa foram mantidas em cultura por 72 horas com o intuito de condicionar o meio, o qual foi coletado e utilizado para tratar MC3T3 ou HOEL ou células mesenquimais, com o intuito de fazer uso de ferramentas de biologia celular e molecular para investigar alterações de expressão gênica e fenotípica. Nossos resultados mostram que 3T3-NIH é capaz de modular a expressão de marcadores de diferenciação osteoblasto-osteócito (DMP1. SOST, RankL e OPG). Além disso, vimos que AoSMC em duas condições distintas - Estatico e Shear-Stress - são capazes de promover uma transição osteoblasto-osteócito através de vesículas extracelulares (EVs), ativando a expressão de biomarcadores moleculares deste processo (miR23-a, DMP1, SOST, FGF23 e GP38) e, neste contexto, nossos dados também mostram que o meio condicionado por HUVEC modula marcadores de diferenciação de osteoblastos (Runx2, Osterix e ALP) e genes que são traduzidos em proteínas e que atuam na homeostase dos minerais da matriz óssea (NPP1 e TNAP). Considerando que as células AoSMC e HUVEC são capazes de modular a osteocitogênese e a osteoblastogênese, respectivamente, o meio condicionado por essas células foi coletado e as vesículas foram extraídas coletadas para melhor caracterização em termos de tamanho, concentração, biomarcadores de membrana, carga elétrica de membrana e conteúdo proteico, o que revelou que o perfil AoSMC não apresentou diferença em termos de condições experimentais (estática e Shear-Stress), também vimos que as células mesenquimais que recebem o tratamento com meio de cultura condicionado por AoSMC aumentou os marcadores de osteocitogênese, enquanto os EVs isolados do meio condicionado por HUVEC modularam positivamente esses mesmos marcadores (PHEX, MEPE, MMP-14, GP-38, DMP1). Esses dados permitem concluir que o tecido endotelial e os fibroblastos contribuem para a homeostase do osso e sua remodelação dinâmica é modulada pela transição osteoblastos-osteócitos por meio de fatores tróficos e vesículas extracelulares. Understanding the mechanisms involved in bone maintenance and homeostasis requires elucidating the behavior of bone tissue in relation to communication with other adjacent tissues. The aim of this study was to investigate how bone cells (MC3t3-E1, HOEL) or mesenchymal cells are modulated through paracrine signaling triggered by fibroblasts (3t3-NIH), vein endothelial cells (HUVEC) and aortic endothelial cells (HCAEC), in addition to smooth muscle cells (AoSMC/VSMC). The cells of the tissues adjacent to the bone remained in culture for 72 hours to condition the medium, this same medium was collected and used to treat MC3t3 or HOEL or mesenchymal cells. Our results show that 3t3-NIH is capable of modulating the expression of osteoblast-osteocyte differentiation markers (DMP1. SOST, RankL and OPG). In addition, we saw that AoSMC in two different conditions: Static and Shear-Stress, are capable of promoting an osteoblast-osteocyte transition through extracellular vesicles (EVs), activating the expression of molecular biomarkers of this process (miR23-a, DMP1, SOST, FGF23 and GP38), in this context our data also show that the medium conditioned by HUVEC modulates osteoblast differentiation markers (Runx2, Osterix and ALP) and genes that are translated into proteins and that act in the homeostasis of bone matrix minerals (NPP1 and TNAP). Considering that AoSMC and HUVEC cells are capable of modulating osteocytogenesis and osteoblastogenesis, respectively, the medium conditioned by these cells was collected and the vesicles were extracted for treatment: 1. medium rich in vesicles and other trophic factors, and 2. treatment only with vesicles. EVs were characterized in terms of size, concentration, membrane biomarkers, membrane electrical charge and protein content, which revealed that the AoSMC profile showed no difference in terms of experimental conditions (static and Shear-Stress), we also saw that the mesenchymal cells receiving treatment with AoSMC-conditioned culture medium increased osteocytogenesis markers, while EVs isolated from HUVEC-conditioned medium positively modulated these same markers (PHEX, MEPE, MMP-14, GP-38, DMP1). These data allow us to conclude that the endothelial tissue and fibroblasts contribute to bone balance by modulating the osteoblast-osteocyte transition through trophic factors and extracellular vesicles. FAPESP: 2016/08888-9; 2018/10856-3; 2019/21807-6

Active smokers are people who are smoking continuously. The population of active smokers in Central Kalimantan was 26,5% in 2013. The farmer, fish farmer, and laborer had a large proportion (44.5%) as an active smoker than another job that reported according to types of jobs. Cigarettes contain many toxic and addictive chemicals. Majority of active smokers that was living in Kelurahan Tanjung Pinang Kota Palangka Raya, especially who live in Jl. Bengaris works as a farmer, fish farmer, or laborer. Active smokers have a high risk of suffering from heart disease. Cigarette compound that harmful can cause endothelial tissue dysfunction in heart blood vessels and following by thrombus formation that due to increased platelet counts and platelet aggregation. This study aimed to describe of platelet count in active smokers in Jl. Bengaris Kelurahan Tanjung Pinang, Palangka Raya. The descriptive observational method was used in this study. The sample obtained by 48 people with purposive sampling technique with criteria such as active smokers, men, working as farmers, fish farmers, or laborers, no history of the disease, and willing to be respondent. Examination of platelet count was done by hematology analyzer. The average of respondents aged 20-30 years (35.4%) and 31-40 years (31.2%), worked as farmers (43.7%) and laborers (41.7%), duration of smoking were 1-10 year (37.5%), consumption of smoking was 11-20 cigarettes / day (41.7%), and rest periods were > 6 hours / day (64.6%). There was one person of the active smoker with a high platelet count (2.1%) and normal platelet count of 47 people (97.9%).

Passive smokers that exposure to cigarette smoke in their house has been reached 78,4%. Inhaled of cigarette smoke in the room was more dangerous than in an open place. Every puff of cigarette smoke from active smoker contains 1015 of free radicals which can cause oxidative stress. The presence of free radicals will trigger of activation of inflammatory genes, and then they can be activated of endothelial cells, dysfunction, and injury. Oxidative stress also stimulates large production of platelet (thrombogenesis) and followed by excessive formation of fibrin and thrombin. So that can cause thrombus in endothelial tissue, and it subsequently develops into atherosclerosis. This study aimed to describe thrombocytosis as a risk factor for increased of atherosclerosis in passive smokers in Kecamatan Pahandut, Kota Palangka Raya. This study used a descriptive observational method with a cross-sectional design. The sample obtained by 45 people with purposive sampling technique with criteria such as respondents were passive smokers, housewives, exposed to cigarette smoke more than five years, no history of the disease, and willing to become respondents. Examination of platelet counts was analyzed by an automatic method using Hematology Analyzer. The results showed that 6.7% of passive smokers had high platelet counts (thrombocytosis). High platelet counts in 6.7% of passive smokers caused by exposure of cigarette smoke from active smokers can endanger passive smoking, especially the risk of atherosclerosis. Therefore, a preventive and educative method for both passive and active smokers are needed to prevent the dangers of cigarette smoke to the risk of atherosclerosis

This article reports a combined technique of sutureless intrascleral fixated intraocular lens implantation and Descemet membrane endothelial keratoplasty in a patient with anterior pseudophakic bullous keratopathy. Two scleral tunnels were created, corneal incisions were made, and a foldable intraocular lens was cut and removed from the anterior chamber. After performing anterior vitrectomy, a 3-piece foldable intraocular lens was implanted into the anterior chamber. One of the intraocular lens haptics was grasped with a forceps and pulled out from the scleral tunnel. Then, the end of the haptic was cauterized. Similar maneuvers were applied for the other haptic. Next, an 8-mm-diameter donor tissue was prepared, and the recipient endothelial tissue was peeled and removed from the center of the recipient cornea. The prepared donor tissue was injected into the anterior chamber. After proper opening and placement of the donor tissue, an air bubble was injected below the tissue. There were no postoperative complications during the 1-month follow-up.

Background:Endothelial progenitor cells (EPC), involved in vasculogenesis and endothelial tissue repair, have been described as relevant players in vascular and connective tissue diseases [1-2]. In this regard, a previous study of our group disclosed that the degree of EPC frequency may help to identify the presence of interstitial lung disease (ILD) in rheumatoid arthritis patients [3]. Given that ILD is the main cause of mortality in patients with systemic sclerosis (SSc) [1, 4-6], the understanding of the role of EPC in the mechanism of SSc-ILD+ vasculopathy is crucial.Objectives:To assess the potential role of EPC on vascular dysfunction associated with the presence of ILD in patients with SSc.Methods:Peripheral venous blood was collected from a total of 39 patients with SSc, 20 with ILD (SSc-ILD+) and 19 without ILD (SSc-ILD-). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by flow cytometry. EPC were considered as CD34+, CD45Low, CD309+ and CD133+.Results:Statistically significant differences in EPC frequency between patients with SSc-ILD+ and patients with SSc-ILD- were disclosed. Specifically, an increase of EPC frequency was observed in SSc-ILD+ patients when compared to patients with SSc-ILD- (mean ± standard deviation: 0.033 ± 0.012 versus 0.021 ± 0.017, respectively, p=0.012).Conclusion:Our results suggest a potential role of EPC on vascular damage associated with the manifestation of ILD in patients with SSc.References:[1]Eur J Rheumatol 2020;7(Suppl 3):S139-S146.[2]Arthritis Rheum 2009;60(11):3168-79.[3]J Clin Med 2020;9(12):4098.[4]Ann Rheum Dis 2007;66(7):940-4.[5]Rheumatology (Oxford) 2010;49(12):2375-80.[6]Eur Respir Rev 2015;24(135):102-14.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

Retained descemet’s membrane is a rare complication of penetrating keratoplasty. It can lead to graft failure by compromising the endothelial tissue of the cornea. We report a case which was diagnosed as retained descemet’s membrane post penetrating keratoplasty by anterior segment optical coherence tomogram and was managed surgically by descemetorhexis without compromising the graft integrity which led to good visual gain.

We present a characterization of chemically treated cells using atomic force microscopy (AFM) which can observe changes in morphology and elasticity of cells. Since AFM has the significant advantage that it does not require fixation of samples, the method is simple and can capture various properties of living cells. In this study, corneal epithelial and endothelial cells were examined. The topography images of the corneal cells without glutaraldehyde (GA) fixation were successfully obtained. The images showed a natural three-dimensional shape of these cells, which scanning electron microscope (SEM) images could not provide. The AFM images of GA-fixed cells were taken and compared with a SEM image reported in the literature. Our results show that longer time for GA fixation makes the surface of the corneal endothelial tissue stiffer. Also, longer treatment results in relatively large structural variation in samples. Combined with conventional histochemical methods, this approach helps us gain an overall understanding of the influence of such chemical treatment.

Corneal blindness affects over 10 million people worldwide and current treatment strategies often involve replacement of the defective layer with healthy tissue. Due to a worldwide donor cornea shortage and the absence of suitable biological scaffolds, recent research has focused on the development of tissue engineering techniques to create alternative therapies. This review will detail how we have refined the simple engineering technique of plastic compression of collagen to a process we now call Real Architecture for 3D Tissues (RAFT). The RAFT production process has been standardised, and steps have been taken to consider Good Manufacturing Practice compliance. The evolution of this process has allowed us to create biomimetic epithelial and endothelial tissue equivalents suitable for transplantation and ideal for studying cell-cell interactions in vitro.

Eye-bank preparation of endothelial tissue for keratoplasty continues to evolve. Although eye-bank personnel have become comfortable and competent at Descemet's stripping automated endothelial keratoplasty (DSAEK), tissue preparation and tissue transport, optimization of preparation methods continues. Surgeons and eye-bank personnel should be up to date on the research in the field. As surgeons transit to Descemet's membrane endothelial keratoplasty (DMEK), eye banks have risen to the challenge of preparing tissue. Eye banks are refining their DMEK preparation and transport techniques.This article covers refinements to DSAEK tissue preparation, innovations to prepare DMEK tissue, and nuances to improve donor cornea tissue quality.As eye bank-supplied corneal tissue is the main source of tissue for many corneal surgeons, it is critical to stay informed about tissue handling and preparation. Ultimately, the surgeon is responsible for the transplantation, so involvement of clinicians in eye-banking practices and advocacy for pursuing meaningful research in this area will benefit clinical patient outcomes.

Caffeic acid phenethyl ester (CAPE) is a component of honeybee hives with various beneficial properties. Tissue factor (TF), the key trigger of thrombosis, is expressed in human endothelial cells. This study was designed to investigate whether CAPE modulates TF expression in human aortic endothelial cells (HAECs). Western blots and real-time polymerase chain reactions were performed. CAPE (10(-7)-10(-5) M) inhibited tumor necrosis factor (TNF)-α induced endothelial TF protein expression by 2.1-fold at 10(-5) M (p

Background/Aims: End-stage renal disease (ESRD) is associated with a prothrombotic phenotype and substantial activation of platelets can occur in the course of hemodialysis. However, the underlying mechanisms for increased platelet reactivity remain unclear. Increased levels of oxidized albumin, termed “advanced oxidation protein products (AOPPs)” accumulate in subjects with renal disease. Methods: Platelet aggregation was assessed with platelet aggregometry. Platelet activation, formation of reactive oxygen species and tissue factor expression on the surface of platelets and endothelial cells was measured by flow cytometry. Platelet adherence was assessed under flow using the Cellix system. The oxidative status of albumin isolated from ESRD patients was determined by photometric analysis. Tissue factor levels in serum samples were determined using a commercially available ELISA kit. Results: Albumin isolated from hemodialysis patients as well as in vitro generated AOPP-albumin promoted platelet activation via CD36, dependent on the AOPP-content of albumin. AOPP-albumin mediated platelet activation was prevented by scavenging superoxide anions and inhibitors of phospholipase C and protein kinase C. Furthermore, AOPP and serum tissue factor levels were considerably increased in ESRD patients on hemodialysis and a significant correlation of AOPP and serum tissue factor was found. Conclusion: Interaction of platelet CD36 with endogenous oxidized albumin may link oxidative stress with a prothrombotic phenotype in ESRD.

Aortic cross-clamping during cardiac operations may injure the vessel wall and cause tissue lesions. This experimental study analyses the influence of the intravascular and external pressure and the duration of aortic cross-clamping on endothelial tissue damage. Fresh porcine aortas (n=20) were tested with intravascular pressures from 30 to 80 mmHg. The external clamp pressure, necessary to occlude the aorta, was applied by using the second cog of a commercial aortic clamp and cross-clamping was performed for 1 and 30 min. The observed pressure curves were compared to the histological findings. For occlusion of the aorta, an external pressure of at least 10-fold higher than the intravascular pressure (max. 812 mmHg) had to be applied. After 30 min of clamping, a complete endothelial destruction was observed, irrespective of intra-aortic pressure. The aortic media remained intact. After 1 min clamping, fractions of intact endothelial cells were left, ranging from 40 to 70% at different intra-aortic pressures. These results indicate that endothelial tissue lesions due to aortic cross-clamping are not avoidable, even in moderate clamp application. The duration of aortic cross-clamping but not intravascular pressure is the pivotal factor. The integrity of the aortic media can be preserved if low-force cross-clamping is achieved.

Cell-cell junctions are essential for epithelial and endothelial tissue formation and communication between neighboring cells. We report here that migfilin, a recently identified component of cell-extracellular matrix adhesions, is recruited to cell-cell junctions in response to cadherin-mediated cell-cell adhesions. Migfilin is detected at cell-cell junctions in both epithelial and endothelial cells. It forms detergent-resistant, discrete clusters that associate with actin bundles bridging neighboring cells. Immunoelectron microscopic analyses reveal that migfilin is closely associated with β-catenin, but not desmosomes, at cell-cell junctions. Furthermore, we show that the C-terminal LIM domains, but not its N-terminal domain, mediates migfilin localization to cell-cell junctions. The site mediating the localization of migfilin to cell-cell junctions at least partially overlaps with that mediating the localization of migfilin to cell-ECM adhesions. Finally, siRNA-mediated depletion of migfilin compromised the organization of adherens junctions and weakened cell-cell association. These results identify migfilin as a component of adherens junctions and suggest an important role for migfilin in the organization of the cell-cell adhesion structure.

In healthy blood vessels with a laminar blood flow, the endothelial cell division rate is low, only sufficient to replace apoptotic cells. The division rate significantly increases during embryonic development and under halted or turbulent flow. Cells in barrier tissue are connected and their motility is highly correlated. Here we investigate the long-range dynamics induced by cell division in an endothelial monolayer under non-flow conditions, mimicking the conditions during vessel formation or around blood clots. Cell divisions induce long-range, well-ordered vortex patterns extending several cell diameters away from the division site, in spite of the system’s low Reynolds number. Our experimental results are reproduced by a hydrodynamic continuum model simulating division as a local pressure increase corresponding to a local tension decrease. Such long-range physical communication may be crucial for embryonic development and for healing tissue, for instance around blood clots., Endothelial cell division is highly sensitive to fluid conditions and essential for blood vessel healing. Here Rossen et al. demonstrate how cell division triggers the emergence of long-range votex patterns in endothelial tissue under conditions that mimic blood vessel formation and blood clots.

A combination of experimental, theoretical, and imaging methodologies is used to examine the hierarchical structure and function of intramyocardial arteriolar trees in porcine hearts to provide a window onto a region of myocardial microvasculature which has been difficult to fully explore so far. A total of 66 microvascular trees from 6 isolated myocardial specimens were analyzed, with a cumulative number of 2438 arteriolar branches greater than or equal to 40 μm lumen diameter. The distribution of flow rates within each tree was derived from an assumed power law relationship for that tree between the diameter of vessel segments and flow rates that are consistent with that power law and subject to conservation of mass along hierarchical structure of the tree. The results indicate that the power law index increases at levels of arteriolar vasculature closer to the capillary level, consistent with a concomitant decrease in shear stress acting on endothelial tissue. These results resolve a long standing predicament which could not be resolved previously because of lack of data about the 3D, interconnected, arterioles. In the context of myocardial perfusion, the results indicate that the coefficient of variation of flow rate in pre-capillary distal arterioles is high, suggesting that heterogeneity of flow rate in these arterioles is not entirely random but may be due at least in part to active control.

Hemangiopericytoma (HPC) may develop in every site where the endothelial tissue exits and primarily develops in the skeletal-muscular system or the skin. Adult cases of HPC generally exhibit a benign course. 20–30% of the cases may show a malign course. The tumors that show more than four mitoses, a focal area of necrosis, and increased cellularity on a magnification ×10 are considered as malign. In our paper, we presented our case who showed a lung metastasis at the end of 4 years and who developed a pathological fracture of the right humerus at the end of approximately 2 years, because hemangiopericytoma is rarely seen in the chest wall as a primary tumor.

Hemangiopericytoma (HPC) is an uncommon highly vascular neoplasm that originated from Zimmerman's pericytes which surrounds the endothelial tissue. Primary epidural HPC of the sacrum is extremely rare. We reported an unusual case of primary epidural malignant HPC of the sacrum that invaded vertebral bone and caused rectum compression in a 57-year-old male for the first time. The patient presented progressive low back pain and ribbon-like stool over 3 months. The surgical intervention involved sacrectomy and en bloc resection of the tumor. We described the clinical, radiological, and histological features of this tumor and reviewed the literature.

The objective of this study is elucidating the mechanisms by which the wettability of nanofibrous electrospun mats varies in polymer blends, and highlighting how this can play a pivotal role in enhancing the viability of cultured microvascular endothelial cells (EC). A functional microvascular network is essential for supplying bioengineered tissues with oxygen and nutrients while removing metabolic wastes. An in vitro pre-vascularization strategy consists of seeding EC on scaffolds, which in turn promotes cells infiltration, adhesion and functionality. We use electrospun poly-L-lactic acid (PLLA) and gelatin (Gel) as prototype materials for realizing nanofibrous scaffolds as bioartificial architectures to improve the proliferation and the functionality of human microvascular ECs (HMEC-1). HMEC-1 seeded on electrospun scaffolds adhere, remain viable, proliferate and positively express the endothelial cell marker CD31 particularly on blend PLLA/Gel fibers, which exhibit wettability enhanced with respect to both the constituent polymers, and are therefore especially promising constructs for promoting the formation of functional endothelial tissue. The wettability characteristics of the blend polymer fibrous scaffolds are modeled and discussed. These results can be valuable for the future design of pre-vascularized scaffolds with enhanced wettability properties for functional tissue engineered implants, with ECs able to form in perspective an effectively functioning vasculature upon implantation.

Retention of the host’s Descemet’s membrane is a complication which can occur during the course of a penetrating keratoplasty and which eventually leads to loss of graft clarity by clouding or by coming into contact with the graft endothelium. The retained Descemet’s membrane can compromise endothelial tissue by contact injury or by limiting diffusion of aqueous humour nutrients. In our study we discuss the pathogenesis, diagnosis and treatment of this complication. In addition we report some our cases treated with three different approaches.

Ureteral stents represent a minimally invasive alternative to preserve urinary drainage whenever ureteral patency is deteriorated or is under a significant risk to be occluded due to extrinsic or intrinsic etiologies. The ideal stent that would combine perfect long-term efficacy with no stent-related morbidity is still lacking and stent usage is associated with several adverse effects that limit its value as a tool for long-term urinary drainage. Several new ideas on stent design, composition material and stent coating currently under evaluation, foreseen to eliminate the aforementioned drawbacks of ureteral stent usage. In this article we review the currently applied novel ideas and new designs of ureteral stents. Moreover, we evaluate potential future prospects of ureteral stent development adopted mostly by the pioneering cardiovascular stent industry, focusing, however, on the differences between ureteral and endothelial tissue.

IL-1β is a pleotropic cytokine that may mediate increased procoagulant activity and permeability in endothelial tissue during inflammatory conditions. The procoagulant effects of IL-1β are mediated through induction of tissue factor (TF) but its alterations on vascular permeability are not well characterized. We found that IL-1β induced a rapid and dose-dependent increase in TF activity in human umbilical vein endothelial cells (ECs) under routine culture conditions. However, IL-1β caused a rapid and marked increase in permeability across confluent EC monolayers using a two-compartmentin vitromodel only in the presence of factor VIII-deficient plasma that was completely abrogated by neutralizing anti-TF antibody pre-treatment.In vitropermeability was associated with loss of EC surface expression of VE-cadherin and contraction of F-actin cytoskeletal elements that resulted in EC intercellular gap formation. These data demonstrate that IL-1β induces marked changes in permeability across activated endothelium via a TF dependent mechanism and suggest that modulation of TF activity may represent a strategy to treat various acute and chronic inflammatory conditions mediated by this cytokine.

While gene transfer has been difficult to accomplish in the kidney, reports have indicated that tissue cavitation may facilitate such genetic modifications. Accordingly, we investigated this theory, and designed and characterized a method that utilizes renal vein-guided, retrograde pressurized injections to illicit prompt transgene expression in mammalian kidneys. In devising this approach we hypothesized that the hydrodynamic forces generated from pressured injections were sufficient to facilitate the widespread delivery of exogenous matter throughout the kidney. As a consequence, this infusion process would assist the passage of transgenes across epithelial and endothelial tissue layers, and ultimately support their cellular uptake. We tested this hypothesis by introducing naked plasmid DNA and baculovirus vectors, which express fluorescent proteins, into 60 rodent kidneys. Gene expression was then examined in live animals using intravital multiphoton fluorescence microscopy, and in vitro with confocal laser scanning microscopy and electron microscopy. We recorded transgene expression in various glomerular, tubular and vascular segments throughout a period of 3 weeks. Moreover, we were able to generate transient, yet stable targeted and non-specific genetic modifications. Overall, these results outline a potentially attractive approach for renal gene transfer in live animals.View Large Image | View Hi-Res Image | Download PowerPoint Slide

The present knowledge of the morphology of cephalopod central hearts is presented. The cytological characteristics of the epicardial, myocardial and endothelial tissue layers are reviewed. Myocardial cells are characterized as obliquely striated myocytes with a high level of oxidative metabolism. The voluminous myocardium is intensively penetrated by nerve fibers controlling the myogenic heart rhythm by different chemical transmitter systems. Catecholaminergic fluorophores and acetylcholinesterase activity could be localized by means of histochemical and cytochemical investigations. A glio-interstitial cell system is shown to be present in connection with nerve fibers and also uncombined between heart muscle cells. Its content of large different-sized inclusions is described and their function discussed.

To the Editor: Between the ages of 45 and 65 years, the incidence of myocardial infarction is three times higher in men compared with women. In addition, the prevalence of thrombotic stroke is ∼50% greater in men than women ([1][1]). The mechanisms behind this gender difference in

Freeze-fracture of fixed and unfixed tissue, lanthanum tracer and conventional thin-section studies have revealed 2 new types of septate junction in the class Anthozoa, phylum Coelenterata. These new junctions have the 15−18-nm intercellular spacing of all other described septate junctions and are found around the apical circumference of cells lining a lumen or outside edge. However, in freeze-fracture replicas and tangential views of lanthanum-impregnated tissue, they are seen to be quite different from other known septate junction types. One of the new junctions is found in endothelial tissue such as that lining the gut or the inside of the tentacles. In tangential view it is seen to consist of relatively short, straight, double septa, again with lateral projections. Tn freeze-fracture of unfixed tissue, the junction consists of double rows of particles on the P face, the particles of one row being rounded, those of the other being elongated at right angles to the line of the septum. This dichotomy in particle size is unexpected, as the 2 halves of the septa as seen in tangential view are symmetrical. In freeze-fracture of fixed material the particle arrays remain on the P face and appear similar to those of unfixed material, but never as clear. In fixed tissue, some distortion has occurred and in extreme cases septa appear as a single broad jumbled row of particles. In this double septa junction, the rows of particles seen in freeze-fracture are occasionally seen to anastomose with a septum dividing into 2 and a third row of particles aligning with the 2 new septa to form their double particle rows. In both fixed and unfixed tissues, the E face of the junction consists of wide, shallow grooves. The second of the new junctions occurs in epithelial tissue, such as around the outer edge of sea-anemone tentacles, and consists of long wavy septa with lateral projections. In views where these projections appear longest, they arise predominantly from one side of the septa. In freeze-fracture of both fixed and unfixed tissue, this junction appears as rows of closely spaced particles on the P face. Occasionally rows of particles are seen on the E face, but usually this face is characterized by shallow grooves. In some aspects these 2 new junctions have features in common with the Hydra type junction also found in the Coelenterata. In all 3 types septa are relatively straight, rather than pleated, and there are lateral projections on the septa.

THE distribution of the blood group A antigen in human tissues as shown by fluorescent rabbit antibody against human ovarian cyst A substance has been previously described1,2. It was found that the A antigen in epithelial tissues was not soluble in ethanol and thus differed from the A antigen found in the vascular endothelium, which was removed by ethanol treatment.