Repository logo
  • English
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Latviešu
  • Magyar
  • Nederlands
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Log In
    New user? Click here to register.
Repository logo

Repositorio Institucional de la Universidad de Murcia

Repository logoRepository logo
  • Communities & Collections
  • All of DSpace
  • menu.section.collectors
  • menu.section.acerca
  • English
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Latviešu
  • Magyar
  • Nederlands
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Log In
    New user? Click here to register.
  1. Home
  2. Browse by Subject

Browsing by Subject "Thrombus"

Now showing 1 - 2 of 2
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Publication
    Open Access
    Crosstalk between endothelial cell and thrombus in chronic thromboembolic pulmonary hypertension: perspective
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Sakao, Seiichiro; Tatsumi, Koichiro
    It is generally accepted that chronic thromboembolic pulmonary hypertension (CTEPH) results from pulmonary emboli originating from deep vein thrombosis. However, this consensus opinion has been challenged, and the concept that some aspects of CTEPH exacerbation might result from a small-vessel disease leading to secondary thrombosis has been suggested. In addition to the effect of recurrent thromboembolism, a number of lines of clinical evidence indicate that progressive worsening is contributed to by remodeling in the small pulmonary arteries. Histopathological studies of the microvascular changes in CTEPH have identified vascular lesions similar to those seen in idiopathic pulmonary arterial hypertension (IPAH). Especially in in vitro and ex vivo experiments, pulmonary artery endothelial cells (ECs) in pulmonary hypertensive diseases are suggested to exhibit an unusual hyperproliferative potential with decreased susceptibility to apoptosis, indicating that dysfunctional ECs may contribute to the progression of the diseases. Although the degree and mechanisms of EC dysfunction as a contributor to CTEPH are unclear, EC dysfunction may occur in small arteries. Indeed, the cells stimulated by the microenvironment created by the unresolved clot may release substances that induce EC dysfunction. The EC dysfunctions in CTEPH may lead to disorders of the anti-coagulation properties in ECs and may result in additional clots in situ. Moreover, these may lead to the progression, not only of distal thrombus, but also of proximal clotting. This article reviews the pathobiological concepts of CTEPH and explains a crosstalk between EC dysfunction and in situ thrombi which may contribute to the vascular lesions of CTEPH.
  • Loading...
    Thumbnail Image
    Publication
    Open Access
    Impact of COVID-19 disease on placental histopathology. PLAXAVID study
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Montáns Araújo, J.; Suy Franch, A.; García Ruiz, I.; Maíz, N.; Garcia Aguilar, E.; Hidalgo Bermejo, F.J.
    Background. The impact of COVID-19 on pregnancy has been analyzed suggesting an increased risk of placental lesions that might lead to maternal and neonatal complications. However, the current published evidence is not conclusive because contradictory results. Methods. PLAXAVID is an observational, retrospective, histopathological, single-center study that aimed to evaluate the prevalence of vascular and inflammatory lesions in placental and umbilical cord samples of one hundred women infected by SARS-CoV2 during pregnancy. Results. The histopathological analysis showed that in most of the placentas (77.8%) there were signs of maternal vascular malperfusion (MVM; primary endpoint). The most common MVM features were an accelerated villous maturation (37.4%), central villous infarcts (33.3%), and villous agglutination (46.5%). Fetal vascular malperfusion (FVM) was identified in 57.6% of samples, and the most frequent features were hyalinized avascular villi (38.4%), fetal vascular thrombi (20.2%) and umbilical cord at risk of partial obstruction (14.1%). Acute and chronic inflammatory pathology were noticed in 22.2% and 49.5% of placentas, respectively. No significant correlations were found between MVM presence and the time, duration, and severity of infection, nor with the duration of pregnancy. However, in critically ill patients, the pregnancy duration (p=0.008), newborn weight (p=0.003), and APGAR test scores (p<0.001) were significantly lower. The same trend was observed considering the presence of infection at the time of delivery and in preterm births. Conclusion. A very high percentage of placentas with vascular and/or inflammatory lesions was found in the analyzed cohort. Therefore, PLAXAVID study results supported that COVID-19 should be considered a risk factor during gestation and requires close monitoring of pregnancy.

DSpace software copyright © 2002-2025 LYRASIS

  • Cookie settings
  • Accessibility
  • Send Feedback