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Viral myocarditis

The effect of Astragalus membranaceus on lymphocytes was studied. It stimulated the proliferation of murine spleen cells in vitro. [164]. The efficacy of Astragalus membranaceus oral liquor combined with routine therapy on T-lymphocyte subset of peripheral blood in viral myocarditis patients has been reported [165]. [Pg.226]

Yang, D Yu, J., Luo, Z Carthy, C.M., Wilson, J.E., Liu, Z and McManus, B.M. (1999). Viral myocarditis identification of five differentially expressed genes in coxsackievirus B3-infected mouse heart. Circ Res 84, 704-712. [Pg.284]

Kanda T, McManus JE, Nagai R, et al. Modification of viral myocarditis in mice by interleukin-6. Circ Res 1996 78 848-56. [Pg.732]

For treatment of encephalitis convulsions, idiopathic thrombocytopenic purpura, atherosclerosis, viral myocarditis, cancer, secondary erythroderma, nitrite poisoning, bronchialasthma and acute viral hepatitis ... [Pg.242]

SeUier-Leclere A-L, BeUi E, Guerin V, Dorfmuller P, Deschenes G. Fulminant viral myocarditis after rituximab therapy in paediatric nephrotic syndrome. Pediatr Nephrol 2013 28(9) 1875-9. [Pg.589]

Older infants requiring heart transplantation often suffer from dilated cardiomyopathy as a consequence of viral myocarditis. Cardiac transplantation is carried out in the same fashion as in grown-ups. [Pg.21]

Nishio R, Matsumori A, Shioi T, Wang W, Yamada T, Ono K, Sasayama S. Denopamine, a beta 1-adrenergic agonist, prolongs survival in a murine model of congestive heart failure induced by viral myocarditis suppression of tumor necrosis factor-alpha production in the heart. J. Am. Coll. Cardiol. 1998 32(3) 808-815. [Pg.953]

Picornavimses are small, nonenveloped RNA vimses. Members of this family include rhino- and enteroviruses, which are responsible for a variety of human diseases (viral respiratory infection, viral meningitis, myocarditis, pericarditis, encephalitis, chronic meningoencephalitis, herpangina, otitis media, neonatal enteroviral disease, and acute exacerbations of asthma). [Pg.979]

Complications of influenza may include exacerbation of underlying comorbidities, primary viral pneumonia, secondary bacterial pneumonia or other respiratory illnesses (e.g., sinusitis, bronchitis, otitis), encephalopathy, transverse myelitis, myositis, myocarditis, pericarditis, and Reye s syndrome. [Pg.463]

Animal models have established that infections can induce autoimmune disease. For example, coxsackievirus B3 infection of susceptible strains of mice results in inflammation in the heart that resembles the myocarditis and dilated cardiomyopathy that occurs in humans.28 44 The same disease can be induced by injecting mice with cardiac myosin mixed with adjuvant, thereby reproducing the disease in the absence of virus infection, indicating that an active viral infection is not necessary for the development of autoimmune disease.9 29 44 Likewise, a number of autoimmune diseases can be... [Pg.428]

Despite the protective effect of NO against various viral infections, workers in several studies have shown a harmful role of NO in many systems. NO seems to play a part in the development of pneumonia caused by influenza virus [128], in the pathogenesis in mice of tick-borne encephalitis flavivirus infection [131], and in worsening the course of the murine myocarditis caused by coxsackievirus B3 [132]. In addition, pneumonia in mice induced by herpes simplex virus type 1 could be suppressed by the inhibitor of iNOS [133]. The issue of whether NO acts as an inhibitor of viral replication or as a harmful agent, therefore, remains unanswered. This issue is particularly evident in HIV-1 infection, since NO seems to act as a double-edged sword in the pathogenesis of HIV-1. [Pg.22]

The tubingensins A (379) and B (380) showed activity against the widespread crop pest Heliothis zea, and display in vitro anti-viral activity against herpes simplex virus type 1 with IC50 values of 8 and 9 pg/mL, respectively (346) (see Scheme 2.100). Some bis-basic ethers of carbazoles are anti-viral. When tested against Encephala myocarditis viral infection, several N-ethyl substituted bis-basic carbazoles of the general formula 490 were shown to be active (448) (Scheme 4.9). [Pg.189]

M1P-1q Reduced pulmonary mononuclear infiltrate to challenge with influenza virus resulting in higher titers of influenza virus Less severe autoimmune myocarditis after coxsackie viral infection Knockout has increased MODS mortality and CTL activity Reduced NK-mediated inflammation... [Pg.14]

It is difficult to assess the relationship of HEAR oils and other oils high in docosenoic acid content to the development of focal myocardial degenerative lesions in the monkey. In a recent study, a series of 312 hearts were selected at random from monkeys used in unrelated toxicological studies (Qureshi, 1979). The monkeys, which included squirrel (Saimiri sciureus) cynomolgus Macaca fascicularis), rhesus Macaca mulatta) and assam (Ma-caca assamensis) monkeys were of both sexes. Chronic interstitial myocarditis was found in 34% of the monkeys, approximately evenly distributed in males and females (Table IX). The lesions varied from slight necrosis to myocarditis with focal accumulation of lymphocytes, mononuclear cells, plasma cells, and some eosinophiles. Inflammation of the myocardium was distributed throughout the heart. These lesions, which occur frequently in primates, apparently are not related to bacterial, viral, or parasitic infections, but may be related to, and precipitated by, stress (Qureshi, 1979 Soto et al., 1964). [Pg.283]

The MIP-la-deficient mice were challenged in vivo with two viruses known to be dependent on T-cells and macrophages for clearance. Additionally, a role for an autoimmune component for viral inflammation has been suggested in several models. When mice were challenged with Coxsackie B3 virus (CVB3), which causes myocarditis in humans and mouse characterized by an early myeloid infiltrate (5 d postinfection) which is replaced by a T-cell infiltrate at day 10. The data presented suggest an amelioration of inflammation in the MIP-la-deficient mice as assessed by heart pathology score. Curiously, no inflammation was scored in knock-out mice at any time point (days 1,6, 10,15, or 21) whereas 5 of 14 wild types (day 6), 8 of 12 on day 10,3 of 5 on day 15 and... [Pg.45]


See other pages where Viral myocarditis is mentioned: [Pg.292]    [Pg.439]    [Pg.456]    [Pg.267]    [Pg.267]    [Pg.267]    [Pg.280]    [Pg.284]    [Pg.675]    [Pg.112]    [Pg.14]    [Pg.292]    [Pg.439]    [Pg.456]    [Pg.267]    [Pg.267]    [Pg.267]    [Pg.280]    [Pg.284]    [Pg.675]    [Pg.112]    [Pg.14]    [Pg.51]    [Pg.591]    [Pg.268]    [Pg.275]    [Pg.254]    [Pg.1155]    [Pg.1136]    [Pg.1809]    [Pg.66]    [Pg.398]    [Pg.308]    [Pg.46]    [Pg.356]    [Pg.1121]   
See also in sourсe #XX -- [ Pg.33 , Pg.37 ]




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