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1.
Int J Prev Med ; 14: 38, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37351036

RESUMO

Introduction: COVID-19 is a respiratory disease caused by infection with severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2). Thrombotic complications appear to be of particular importance in patients with COVID-19. This study aimed to investigate Changes in the level of Antiphospholipid antibodies (Anticardiolipin and Anti-ß2-glycoprotein-I) and thromboembolic indices in COVID-19 patients during 3 weeks. Methods: This cross-sectional study was performed on adults with Covid-19 hospitalized at Al-Zahra Hospital in Isfahan. The case group includes the patients admitted to the internal ward or ICU who despite receiving prophylactic or anticoagulant doses suffer from thrombotic complications and the control group includes COVID-19 patients without thromboembolic events. The sample size of 120 people was considered. Anticardiolipin and anti-ß2-glycoprotein-I antibodies, coagulation profiles including Fibrinogen, PTT, PT Troponin, ESR, CRP, and D-dimer were examined. After collection, the data were entered into spss24 software and analyzed. Results: The results showed that there was no statistically significant difference in the changes of anticardiolipin and anti-beta-2 glycoprotein in IgM and IgG as well as in the changes of ESR, CRP, PTT, PT, and fibrinogen in the two groups (P > 0.05). Conclusions: Our study showed that there was no statistically significant relationship between anti-phospholipid antibodies (anticardiolipin and anti-beta-2 glycoprotein) and thromboembolic events. Therefore anticardiolipin and anti-beta-2 glycoprotein is probably the puzzles causing thrombosis in COVID-19 patients, and other inflammatory responses should be examined among the cases.

2.
Biomed Pharmacother ; 93: 1220-1229, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28738538

RESUMO

OBJECTIVE: Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities in humans. Clinically, it is essential to limit the progress of cognitive impairment after TBI. It is reported that diosmin has a neuroprotective effect that can limit the progress of the impairment. The aim of this study was to evaluate the effects of diosmin on neurological score, memory, tumor necrosis factor-α (TNF-α) level and long-term potentiation in hippocampal dentate gyrus after the injury. METHODS: A total of ninety six adult male Wistar rats were used as test subjects in this study. The animals were randomly assigned into one of the following three groups (n=32/group): Sham, TBI and diosmin (100mg/kg, p.o for seven consecutive days before TBI induction). TBI was induced into the animals by Marmarou's method. Briefly, a 200g weight was dropped from a 1m height through a free-falling tube onto the head of the anesthetized rats. RESULTS: The veterinary coma scale scores, memory and long-term potentiation in TBI group showed significant decrease at different times after the onset of TBI when compared with Sham (p<0.001). The TNF-α level in the hippocampus of the TBI group of animals was significantly higher than that found in the test subjects from the Sham group (p<0.001). The pre-treatment of the TBI group with diosmin significantly improved their neurological scores, memory and long-term potentiation (p<0.001) when compared with the TBI group. The TNF-α level in hippocampus of the diosmin group was significantly lower than the TBI group (p<0.001). CONCLUSION: Based on the results of the present study, pre-treatment with diosmin has protective effects against TBI-induced memory and long-term potentiation impairment. The effects of diosmin may be mediated through a decrement in the TNF-α concentration of hippocampus as a pro-inflammatory cytokine.


Assuntos
Lesões Encefálicas Traumáticas/tratamento farmacológico , Cognição/efeitos dos fármacos , Disfunção Cognitiva/tratamento farmacológico , Diosmina/farmacologia , Hipocampo/efeitos dos fármacos , Animais , Lesões Encefálicas Traumáticas/metabolismo , Disfunção Cognitiva/metabolismo , Citocinas/metabolismo , Modelos Animais de Doenças , Hipocampo/metabolismo , Potenciação de Longa Duração/efeitos dos fármacos , Masculino , Memória/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/metabolismo
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