scholarly journals STUDIES ON THE ETIOLOGY OF HEARTWATER

1926 ◽  
Vol 44 (6) ◽  
pp. 803-814 ◽  
Author(s):  
E. V. Cowdry

The Rickettsiæ of heartwater are more definitely restricted to the vascular endothelial cells of infected animals than are those of typhus or Rocky Mountain spotted fever. They likewise form more pronounced spherical colonies within the cells. Their presence does not injure the endothelial cells to a degree at all comparable with that caused by the other pathogenic Rickettsiæ. The rupture of endothelial cells and discharge of Rickettsiæ, which are apparently viable, into the circulation constitute phenomena not thus far reported in the case of typhus or Rocky Mountain spotted fever.

1923 ◽  
Vol 37 (2) ◽  
pp. 221-230 ◽  
Author(s):  
F. M. Nicholson

The Rickettsia of Rocky Mountain spotted fever were easily differentiated from mitochondria, phagocytosed blood pigment, nuclear debris, and all other known cellular constituents. Although they were lodged within the cytoplasm of endothelial cells, they were not observed to establish any definite relations with the nucleus or with other cellular components. Their number varied in contiguous cells which sustained the same degree of injury as evidenced by nuclear changes, and alterations in their mitochondria content. The mitochondria, on the other hand, showed similar modifications, characterized by a decrease in number and a rounding up into spherules, in all the endothelial cells seen in a section of an affected blood vessel. Diplobacillary forms were most abundant in the early stages of the reaction and single bacillary bodies towards its termination. Other slight differences in morphology from Wolbach's account were noted in the organisms as seen in the tissues of both ticks and guinea pigs. His study of the distribution of specific lesions with accompanying organisms in the tissues of guinea pigs was confirmed and extended.


1999 ◽  
Vol 277 (1) ◽  
pp. H28-H32 ◽  
Author(s):  
Bing Sun ◽  
Richard D. Vaughan-Jones ◽  
Jun-Ichi Kambayashi

Intracellular pH (pHi) regulation in human umbilical vein endothelial cells (HUVEC) was investigated. The pHi was recorded using seminaphthorhodafluor-1 (SNARF-1). Cells were intracellularly acid loaded with NH4Cl prepulse. In HEPES-buffered Tyrode (nominally [Formula: see text]free), pHi recovery from acid load was inhibited by 1.5 mM amiloride or Na+-free solution. Additionally, in [Formula: see text]-buffered Tyrode, a[Formula: see text]-dependent pHi recovery from acidosis was evident in the presence of 1.5 mM amiloride, which mediated complete recovery of pHi (7.26). In Na+-free solution, the[Formula: see text]-dependent acid extruder mediated pHi recovery after an acid load but only back to 7.09. These results suggest that there are two[Formula: see text]-dependent acid extruders in the HUVEC. One is Na+ dependent, and the other is Na+ independent. The former was further shown to be completely inhibited by 0.5 mM DIDS, whereas the latter was only inhibited by 24.6%. In Cl−-free solution, both of the [Formula: see text]-dependent pathways were inhibited. In conclusion, one[Formula: see text]-dependent acid extruder in the HUVEC resembles the Na+-dependent Cl−/[Formula: see text]exchange found in other tissues, and the other is Cl− dependent but Na+ independent.


1996 ◽  
Vol 75 (04) ◽  
pp. 600-606 ◽  
Author(s):  
Rui-Jin Shi ◽  
Patricia J Simpson-Haidaris ◽  
Victor J Marder ◽  
David J Silverman ◽  
Lee Ann Sporn

SummaryChanges in PAI-1 expression in human umbilical vein endothelial cells (HUVEC) were studied following in vitro infection with Rickettsia rickettsii. A 1.8-fold increase in secreted PAI-1 activity occurred in infected versus control cultures (p = 0.03) at 24 h but not at earlier timepoints. A similar increase (1.4-fold) in secreted PAI-1 antigen (p <0.005) was measured by ELISA. To determine whether this increase was due to increased synthesis of PAI-1, HUVEC were metabolically labeled with 35S-methionine concurrent with R. rickettsii infection. Such infection resulted in a 1.9-fold increase in labeled PAI-1 in the medium at 24 h (p = 0.036). Increase in steady-state levels of PAI-1 mRNA were detected as early as 18 h by Northern blot analysis, peaking (5.5-fold) at approximately 24 h. These results indicate that PAI-1 production is increased in RR-infected endothelial cells, an effect that may contribute to the vascular occlusions noted in Rocky Mountain spotted fever.


2013 ◽  
Vol 127 (5) ◽  
pp. 519-524 ◽  
Author(s):  
S Urata ◽  
M Ohki ◽  
T Tsutsumi ◽  
S Kikuchi

AbstractBackground and objectives:Organised haematomas of the maxillary sinus are rare, non-neoplastic, haemorrhagic lesions which can extend into the nasal cavity and/or the other paranasal sinuses. This study aimed to investigate the pathology of maxillary sinus organised haematoma, and also proposes a new aetiological hypothesis based on the observed pathology.Methods:Biopsies, computed tomography, magnetic resonance imaging and post-surgical histopathological examination of resected specimens were carried out.Conclusion:Distinct pathological differences were observed between the basal and peripheral portions of organised haematomas. We propose that an organised haematoma originates from the exudation of blood components between vascular endothelial cells. As a result, the basal portion consists of aggregated, dilated vessels around the natural ostium of the maxillary sinus. In addition, pseudovessels, without endothelial cells, arise from endocapillary vessels within the haematoma. Exudation of additional blood components from the pseudovessels advances the growth of the organised haematoma.


2018 ◽  
Author(s):  
Ling Zhou ◽  
Xuping Niu ◽  
Jiannan Liang ◽  
Junqin Li ◽  
Jiao Li ◽  
...  

AbstractObjectiveTo directionally-differentiate dermis-derived mesenchymal stem cells (DMSCs) into vascular endothelial cells (VECs) in vitro, providing an experimental basis for studies on the pathogenesis and treatment of vascular diseases.MethodsAfter separation by adherent culture, VEC line supernatant, vascular endothelial growth factor (VEGF), bone morphogenetic protein-4 and hypoxia were used for the differentiation of VECs from DMSCs. The cell type was authenticated by flow cytometry, matrigel angiogenesis assay in vitro, and immunofluorescent staining during differentiation. The VEGF concentration was investigated by enzyme-linked immunosorbent assay.ResultsAfter 28 days of differentiation, the cell surface marker CD31 was significantly positive (80%-90%) by flow cytometry in the VEC line-conditioned culture, which was significantly higher than in the other groups. Differentiated DMSCs had the ability to ingest Dil-ac-LDL and vascularize in the conditioned culture, but not in the other groups. In the VEC line supernatant, the concentration of VEGF was very low. The VEGF concentration changed along with the differentiation into VECs in the medium of the conditioned culture group.ConclusionVEC line supernatant can induce the differentiation of DMSCs into VECs, possibly through the pathway except VEGF.


Praxis ◽  
2005 ◽  
Vol 94 (47) ◽  
pp. 1869-1870
Author(s):  
Balestra ◽  
Nüesch

Eine 37-jährige Patientin stellt sich nach der Rückkehr von einer Rundreise durch Nordamerika mit einem Status febrilis seit zehn Tagen und einem makulösem extremitätenbetontem Exanthem seit einem Tag vor. Bei suggestiver Klinik und Besuch der Rocky Mountains wird ein Rocky Mountain spotted fever diagnostiziert. Die Serologie für Rickettsia conorii, die mit Rickettsia rickettsii kreuzreagiert, war positiv und bestätigte die klinische Diagnose. Allerdings konnte der beweisende vierfache Titeranstieg, möglicherweise wegen spät abgenommener ersten Serologie, nicht nachgewiesen werden. Nach zweiwöchiger antibiotischer Therapie mit Doxycycline waren Status febrilis und Exanthem regredient.


1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.


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