scholarly journals CHANGE IN CONTENT OF GLYCOPROTEINS ON THE SURFACE OF ENDOTHELIAL CELL CULTURE EA.HY 926 AND INTIMA OF INTERNAL CAROTID ARTERIES UNDER THE INFLUENCE OF MAGNESIUM OROTATE

2017 ◽  
Vol 13 (1) ◽  
pp. 88-94
Author(s):  
L. V. Didenko ◽  
E. A. Ulubieva ◽  
T. G. Borovaya ◽  
A. G. Avtandilov ◽  
N. V. Shevlyagina ◽  
...  
Author(s):  
Е.А. Улубиева ◽  
Т.Г. Боровая ◽  
Д.В. Диденко ◽  
А.Г. Автандилов ◽  
К.В. Чельдиев ◽  
...  

Цель исследования состояла в изучении структурных особенностей и механизмов формирования патологической извитости внутренних сонных артерий с оценкой влияния терапии магния оротатом. Материал и методы. С помощью световой микроскопии и иммуногистохимичекого анализа исследовали фрагменты артерий, полученные при последовательно выполненной билатеральной резекции внутренних сонных артерий (ВСА) у пациентов с двусторонней патологической извитостью до и после лечения магния оротатом. Результаты. До лечения в средней оболочке артерий наблюдалась слабо выраженная гистохимическая реакция гладких миоцитов на эластин, фрагментация внутренней эластической мембраны и визуальное уменьшение численности эластических волокон. Наружная оболочка во всех исследованных образцах выглядела в разной степени «разрыхленной». После лечения магния оротатом структура средней оболочки ВСА выглядела более компактной с тесным расположением пучков гладких миоцитов во всех образцах. Коллагеновые волокна наружной оболочки располагались более компактно лишь на периферии, где наружная оболочка ВСА практически сливается с тканями рядом расположенных органов. При этом наблюдались признаки разобщения и сетчатая архитектура волокон. Выраженная иммуногистохимическая реакция клеток средней и наружной оболочек на металлопротеиназу-9 (МПП-9) до лечения магния оротатом позволяет рассматривать активацию синтеза этого фермента в качестве одного из механизмов, вызывающих разобщение (а, возможно, - и деградацию) пучков гладких миоцитов, волокон коллагена и эластина при формировании патологической извитости. Лечение магнием оротатом достоверно оптимизирует гистологическую структуру стенки артерий. Заключение. В основе формирования патологической извитости ВСА может быть нарушение соотношения продукции коллагена и эластина гладкими миоцитами, фибробластами средней и наружной оболочек, и/или активация синтеза этими же клетками матриксной МПП-9. Магния оротат способствует восстановлению гистологической архитектоники стенки ВСА, возможно, вследствие ингибирования образования ММП-9 клетками артериальных оболочек, и восстановлению компактной архитектурной конструкции последних. The aim is to identify the structural features and mechanisms of formation of pathological tortuosity of the internal carotid arteries (ICA) with evaluation of the effect of therapy with magnesium orotate. Material and methods. With the help of light microscopy, immunohistochemical analysis, fragments of arteries obtained with successively performed bilateral rezection of the ICA in patients with their bilateral pathological tortuosity before and after treatment with magnesium orotate were studied. Results. Before the treatment in the middle shell arteries revealed weakly expressed in histochemical reaction of smooth muscle cells on elastin, the fragmentation of the internal elastic membrane and visual decrease in the number of elastic fibers. The outer shell in all the investigated samples looked different degrees of «loosened». After treatment with magnesium orotate structure of the middle shell of the ICA look more compact close bundles of smooth myocytes in all samples. Collagen fibers of the outer shell was located in a more compact, only on the periphery, where the outer sheath of the ICA almost merges with the tissues of adjacent organs was present signs of separation and mesh architecture of the fibers. Pronounced immunohistochemical reaction of cells of middle and outer shells on metalloproteinase-9 to the treatment of magnesium orotate allows us to consider the activation of the synthesis of this enzyme as one of the mechanisms that lead to dissociation (and, perhaps, - and degradation) bundles of smooth myocytes, collagen fibers and elastin in the formation of pathological tortuosity. Treatment with magnesium orotate significantly optimizes histological structure of the walls of the arteries. Conclusion. At the basis of the formation of pathological tortuosity of the ICA, there may be a disruption in the ratio of production of collagen and elastin to smooth myocytes, fibroblasts of the middle and outer membranes, and / or activation of the synthesis by these cells of matrix metalloproteinase-9. Magnesium orotate contributes to the restoration of the histological architectonics of the wall of the ICA due to a decrease in the activity of MMP-9 formation by cells of the arterial membranes and restoration of the compact architectural structure of the latter.


Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 362-365 ◽  
Author(s):  
H Ishii ◽  
HH Salem ◽  
CE Bell ◽  
EA Laposata ◽  
PW Majerus

Abstract Protein C activation by thrombin is significantly accelerated by the endothelial cell cofactor, thrombomodulin. In this study, we have developed a radioimmunoassay for thrombomodulin and have measured the cofactor content in several human tissues. The assay method detects as little as 2 ng of thrombomodulin. The highest thrombomodulin content was found in lung and placenta, but the antigen was also detected in spleen, pancreas, liver, kidney, skin, heart, and aorta. Unexpectedly, thrombomodulin was absent from brain. Extracts from cerebral cortex, cerebellum, centrum semiovale, midbrain, basal ganglia, pons, and medulla were devoid of thrombomodulin. In contrast, thrombomodulin antigen is present in extracerebral intracranial vessels, including basilar and internal carotid arteries and choroid plexus, as well as in endothelium of the pia-arachnoid.


Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 362-365 ◽  
Author(s):  
H Ishii ◽  
HH Salem ◽  
CE Bell ◽  
EA Laposata ◽  
PW Majerus

Protein C activation by thrombin is significantly accelerated by the endothelial cell cofactor, thrombomodulin. In this study, we have developed a radioimmunoassay for thrombomodulin and have measured the cofactor content in several human tissues. The assay method detects as little as 2 ng of thrombomodulin. The highest thrombomodulin content was found in lung and placenta, but the antigen was also detected in spleen, pancreas, liver, kidney, skin, heart, and aorta. Unexpectedly, thrombomodulin was absent from brain. Extracts from cerebral cortex, cerebellum, centrum semiovale, midbrain, basal ganglia, pons, and medulla were devoid of thrombomodulin. In contrast, thrombomodulin antigen is present in extracerebral intracranial vessels, including basilar and internal carotid arteries and choroid plexus, as well as in endothelium of the pia-arachnoid.


Author(s):  
Novikova I.N. ◽  
Popova T.F. ◽  
Gribacheva I.A. ◽  
Petrova E.V. ◽  
Marushchak A.A. ◽  
...  

Moya-Moya disease is a rare progressive chronic cer-ebrovascular disease characterized by a narrowing of the lumen of the intracranial segments of the internal carotid arteries, as well as the initial segments of the anterior and middle cerebral arteries with the devel-opment of a network of small vascular anastomoses. Violations of blood supply due to occlusion lead to the development of ischemic strokes in the correspond-ing pools, and ruptures of vascular anastomoses - to the development of hemorrhagic strokes, causing a variety of neurological disorders. The article presents a clinical case of Moya-Moya disease in a 31-year-old patient. The disease was manifested by acute disorders of cerebral circulation in ischemic and hemorrhagic types. The diagnosis was made in accordance with the diagnostic criteria of the disease based on the data of endovascular cerebral angiography.


2001 ◽  
Vol 176 (1) ◽  
pp. 263-264 ◽  
Author(s):  
Rodolfo A. Ibarra ◽  
Prabhakar Kesava ◽  
John L. Fewins

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1119.3-1120
Author(s):  
L. Nacef ◽  
H. Ferjani ◽  
H. Riahi ◽  
Y. Mabrouk ◽  
E. Labbene ◽  
...  

Background:Patients with rheumatoid arthritis (RA) are at higher cardiovascular risk (CVR) than the general population due to chronic inflammation. Several factors, both modifiable and non-modifiable, can increase this risk. Intima-media thickness (IMT) was considered as a marker for atherosclerosis.Objectives:This study aimed to identify predictor factors of increasing IMT.Methods:The prospective study was carried out on patients with RA who met the 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria. These patients were followed in the rheumatology department of the Kassab Institute. The socio-demographic data, biological and immunological parameters were collected.Framingham’s score quantified the cardiovascular risk at 10-years. Carotid Ultrasonography (US) using a high resolution B mode carotid measured intima-media thickness (IMT) as a subclinical marker of atherosclerosis. Carotid US was performed in the supine position, according to American Society of Echocardiography guidelines. IMT was measured in the left (LCC) and right (RCC) common carotid arteries, the left (LIC) and right (RIC) internal carotid arteries, and the left (LEC) and right (RIC) internal carotid arteries. An increased IMT was defined as ≥0.9 mm.We analyzed data by the SPSS statistical package. A p-value <0.05 was considered significant.Results:Of the 47 patients surveyed, 78.7% were female. The mean age was 52.5 ±11.06 [32-76]. The duration disease was 86.25 ±63 months [5-288] and was erosive in 81.6% of cases. The rheumatoid factor (RF) was positive in 57.8% of patients, and citrullinated antipeptide antibodies (ACPA) were present in 62.2%. Eight patients had a previous CV history (hypertension, diabetes or dyslipidemia) and 16.4% were active smokers. Among women, 43.6% were postmenopausal. ITM was significantly higher in men at LIC (0.037) and LEC (0.025). Older age was associated with increased ITM in LIC (p=0.046; r=0.295), LEC (p=0.05; r=0.412), RCC (p=0.034; r=0.317), and REC (p=0.009; r=0.382). The ITM for LCC, LIC, LEC, RCC, RIC, and REC was higher in postmenopausal women, with no significant difference (p=0.782, p=0.208, p=0.877, r=0.734, p=0.808, p=0.437, respectively).Among the modifiable factors, active smoking was associated with a higher ITM at the REC level (p=0.047). However, weight was not associated with an increased ITM (LCC: p=0.092; LIC: p=0.985; LEC: p=0.952; RCC: p=0.744; RIC: p=0.210; REC: p=0.510). In our study, there was no significant association between DAS28 disease activity or inflammatory marks and ITM (LCC: p=0.784; LIC: p=0.316; LEC: p=0.420; RCC: p=0.784; RIC: p=0.484; REC: p=0.754).Conclusion:In our study, the non-modifiable factors associated with increased ITM were advanced age and male gender. The modifiable factor impacting ITM was primarily active smoking. Surprisingly, disease activity and biological inflammation did not influence ITM.References:[1]S. Gunter and al. Arterial wave reflection and subclinical atherosclerosis in rheumatoid arthritis. Clinical and experimental rheumatology 2018; 36: clinical e.xperimental.[2]Aslan and al. Assessment of local carotid stiffness in seronegative and seropositive rheumatoid Arthritis. Scandinavian cardiovascular journal, 2017.[3]Martin i. Wah-suarez and al, carotid ultrasound findings in rheumatoid arthritis and control subjects: a case-control study. Int j rheum dis. 2018;1–7.Disclosure of Interests:None declared


1999 ◽  
Vol 26 (7) ◽  
pp. 469-473
Author(s):  
Mikimasa Noguchi ◽  
Takashi Tatezawa ◽  
Shigeyuki Nakajima ◽  
Osamu Ishikawa

2004 ◽  
Vol 114 (8) ◽  
pp. 1037-1040 ◽  
Author(s):  
Ralph L. Nachman ◽  
Eric A. Jaffe

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