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Biomedical subjects

R Khatib

Publications and source records attributed to R Khatib.

At least 73 records · Page 4Linked to original sources
PubMed1989

Coxsackievirus B3 myocarditis in C3H/HeJ mice: description of an inbred model and the effect of exercise on virulence.

The effect of forced exercise on the development of coxsackievirus B3 myocarditis in inbred C3H/HeJ mice was studied. Four groups of mice (30 per group) were formed: infected-exercised (Group I); infected-unexercised (Group II); uninfected-exercised (Group III); and uninfected-unexercised (Group IV). Infected mice were inoculated intraperitoneally with 1.0 x 10(2.1) TCID50 coxsackievirus B3. Exercised animals were swum daily for 60 minutes on days 1-9. Myocardial viral titers were acutely elevated on day 3 of infection and were augmented significantly by exercise on days 6 and 9. Exercise increased the overall mortality from 0-10% to 20-40%; significantly increased heart: body weight ratios on days 6, 9 and 13; and increased the extent of myocardial fiber necrosis. We have reproduced the acceleration of CB3 myocarditis by exercise in the inbred C3H model.

Animals↗
PubMed1989

Detection of experimental myocarditis by monoclonal antimyosin antibody, Fab fragment.

The purpose of this study was to determine whether monoclonal antimyosin Fab (antigen binding fragment) was capable of labeling hearts with experimental coxsackievirus myocarditis, and to determine whether Fab could be used for detecting myocardial damage in either early or chronic phases of the disease. Sixty-five, 3-week-old cesarean-derived 1 (CD 1) mice were divided into two groups: group I (noninfected animals) and group II (infected with coxsackievirus B3). Mice from each group were killed on days 7, 17, 30, or 90 of infection. Forty-eight hours before killing, mice were injected with monoclonal I125 antimyosin, Fab (25 microCi/injection) and radioactivity was counted in the heart. Selected heart sections were also examined by autoradiography. Heart radioactivity, count/m/mg (m +/- SEM) on days 7, 17, 30, and 90 of infection was 10.8 +/- 1.7, 21.3 +/- 1.1, 11.2 +/- 3.4, and 12.4 +/- 1.5 for group I, versus 36.7 +/- 8.0 (p less than 0.01), 50.0 +/- 4.5 (p less than 0.001), 33.4 +/- 16.1 (p = NS), and 40.6 +/- 8.5 (p less than 0.01) for group II, respectively. Autoradiography revealed focal uptake within areas of necrotic myocardium. We conclude that I125 Fab may be useful in detecting myocardial damage in the experimental model of murine myocarditis up to day 90 of infection.

Animals↗
PubMed1988

Effect of metoprolol in acute coxsackievirus B3 murine myocarditis.

Recent studies suggest that beta-adrenergic blocking agents show promise in the management of cardiomyopathies; however, their role in acute myocarditis is unknown. One hundred 3 week old mice were infected with coxsackievirus B3 and were given either metoprolol (n = 50) or normal saline solution (n = 50) intraperitoneally for 10 days. Twenty mice from each group were observed for mortality for 30 days. Of the remaining 60 mice, 10 from each group were killed on day 3, 6 or 10 and examined for heart viral titers and pathologic changes. Mortality rate in the metoprolol group was 60% compared with 0% in the saline group (p less than 0.005). Viral titers on day 10 of infection were 10(2.6 +/- 0.2) median tissue culture infective dose for the metoprolol group versus 10(2.1 +/- 0.1) for the saline group (p less than 0.05). Whereas pathologic changes at days 3, 6 and 10 of infection were similar in both groups, on day 30 of infection, inflammation, necrosis and mineralization scores (mean +/- SEM) were 1.1 +/- 0.3, 2.1 +/- 0.4, 2.2 +/- 0.5 for the metoprolol group versus 0.3 +/- 0.1, 0.4 +/- 0.3, 0.4 +/- 0.3 for the saline group, respectively (p less than 0.01). Six noninfected mice received metoprolol intraperitoneally for 10 days; there was no mortality during 30 days of observation. In conclusion, metoprolol administration exerts deleterious effects in acute coxsackievirus B3 murine myocarditis.

Animals↗
PubMed1988

Effect of indomethacin in the late phase of coxsackievirus myocarditis in a murine model.

Previous studies have shown that indomethacin administered during the early phase of experimental myocarditis may exacerbate the disease process. It is unknown whether late administration of this agent is safe. Therefore, the effect of indomethacin administration during the late phase of coxsackievirus B3 murine myocarditis was investigated. Forty 3-week-old CD1 mice each received a 3 x 10(4) median tissue culture-infective dose of coxsackievirus intraperitoneally. On day 10 of infection, mice were randomized to receive either indomethacin or normal saline solution for 10 days, and 10 mice from each group were killed on days 20 and 30 of infection. Heart weight and size and serum atrial natriuretic peptide were similar in both groups on days 20 and 30. On day 20, pathologic scores for the degree of inflammation and necrosis were 1.7 and 1.0 for the indomethacin group versus 1.4 and 1.7 for the saline solution group. On day 30, pathologic scores were 0.3 and 0.6 for the indomethacin group versus 0.5 and 0.6 for the saline solution group. In addition, mineralization was absent in indomethacin-treated animals on day 20 after infection, but it was present in half of the control animals at that time. The degree of mineralization did not differ on day 30 between the two groups. These findings suggest that indomethacin given in the late phase of coxsackievirus myocarditis has no deleterious effects at 30 days.

Animals↗
PubMed1986

Coxsackievirus B3 murine myocarditis: deleterious effects of nonsteroidal anti-inflammatory agents.

The effect of salicylates or indomethacin usage during viral infection was investigated in a murine model of coxsackievirus B3 myocarditis. Eighty-two 3-week-old CD1 mice received 3 x 10(5) median tissue culture infective dose (TCID50) of coxsackievirus B3 intraperitoneally. Then they received salicylates, indomethacin, or saline solution daily for 10 days. Mortality, viral and antibody titers, interferon levels, and pathologic changes in the heart were compared. Mortality (2/33, 4/15, and 0/34, respectively) and virus titers (10(4.72), 10(4.78), and 10(3.4) TCID50, respectively) were higher, interferon levels (300, 267, and 980 IU, respectively) were lower, and pathologic changes were worse in treated animals (antibody titers were similar). These findings indicate that nonsteroidal anti-inflammatory agents adversely affect the course of acute coxsackievirus B3 murine myocarditis. Determination of the pathogenesis of this deleterious effect requires thorough evaluation of virus-host interactions.

Animals↗
PubMed1985

Characteristic manifestations of clostridium induced spontaneous gangrenous myositis.

Spontaneous clostridial myonecrosis occurred in 30- and 69-year-old patients with pancytopenia (after treatment of acute myelogenous leukemia) and diabetes with neutropenia respectively. They presented with fever and sudden onset of pain plus tenderness in involved muscles. They rapidly deteriorated and died within hours after admission. A review of the literature for previous reports of this condition disclosed 31 additional cases. Mean age of patients was 50 years, male to female ratio was 2.2:1, and an underlying condition was present in all of them. Presenting manifestations were spontaneously occurring excruciating pain in the involved muscle (67%), generalized sepsis and shock (24%), nonpainful swelling in the involved muscles (6%) and pain, swelling and shock (3%). Mortality rate was 91% (30/33). The clostridial strains associated with this condition were identified in 31 cases, with Clostridium perfringens and C. septicum causing 28 of them. Bacteremia was described in 10 cases. Awareness of this rare catastrophe may aid in early recognition and surgical intervention which are essential for patient survival.

Adult↗
PubMed1983

Carcinoma of the breast and meningioma. Association and management.

An association between carcinoma of the breast and meningioma has been recognized recently. Three more cases are added to the few previously reported in the literature. An awareness of this association together with modern techniques of investigation, particularly CAT scanning, may permit earlier diagnosis and treatment of more cases. Meningioma as well as carcinoma of the breast is more common in women and the incidence of both tumors reaches a peak in the fifth and sixth decades. Both are related to pregnancy and have an estrogen-receptor protein. Lesions of the central nervous system following the diagnosis and treatment of breast cancer are usually presumed to be metastatic. Therefore, these lesions may be irradiated without complete clinical investigation. If the clinician is aware of this association, appropriate diagnostic procedures could lead to the surgical removal of a benign meningioma. Skull x-rays, bone scan, brain scan, CAT scan, and cerebral angiograms are useful in making a diagnosis. Besides surgery, radiation therapy and hormonal therapy may play a role in the management.

Aged↗
PubMed1983

Alterations in coxsackievirus B4 heart muscle disease in ICR Swiss mice by anti-thymocyte serum.

Coxsackievirus B4 (CB4) infection in infant ICR Swiss mice induces synchronous peaks in both virus titres and pathologic changes in the heart. Among surviving mice, transmural necrosis is followed by fibrosis and ventricular aneurysm. Rabbit antimouse thymocyte serum (ATS) was given before CB4 infection to determine the effects of thymus-dependent functions upon the course of disease. The mortality in ATS-treated mice was 75.9% (65 of 83 mice died) compared to 21.3% (16 of 75 mice died) in normal rabbit serum-treated controls. Pathologic studies showed that ATS-treated mice had more extensive myofibre necrosis and subsequent mineralization, but during the first 10 days of infection, leukocytic infiltration was decreased. Splenic follicles were not present until the 17th day after infection in this treated group. Serum CB4-neutralizing antibodies were similar in mice from the group treated with ATS and normal rabbit serum. These findings indicate that ATS-suppressible functions contribute importantly to virus elimination, perhaps by an increase in macrophage phagocytosis of CB4.

Animals↗
PubMed1982

A mouse model of transmural myocardial necrosis due to coxsackievirus B4: observations over 12 months.

The course of coxsackievirus B4 necrotizing myocarditis was studied over a 12-month period in 712 ICR Swiss mice inoculated at less than 48 h of age. Affected animals were sacrificed at intervals until 1 year. Microscopically, focal myocardial necrosis, which was often transmural in extent with mixed inflammatory exudate, and subsequent fibrous replacement were induced in 75% of the examined animals. The left ventricle (63 of 69 subjects, 91.3%), interventricular septum (39 of 69 subjects, 56.5%) and right ventricle (26 of 69 subjects, 37.7%) were most frequently involved. Thinning of the ventricular wall and grossly apparent localized ventricular bulges (aneurysms) were seen in 22 subjects (the left ventricle 16 times, the right ventricle 5 times, and the interventricular septum 5 times). Coronary arteries were normal in all instances.

Animals↗
PubMed1980

Age-dependent pathogenicity of group B coxsackieviruses in Swiss-Webster mice: infectivity for myocardium and pancreas.

Coxsackieviruses B1-B4 were inoculated intraperitoneally into 48-hr-old, 14-day-old, and three- to five-month-old Swiss-Webster mice. Immediate death occurred only among mice less than 48 hr old, which died from fulminant encephalitis. Older mice usually survived. Myocarditis ensued in mice less than 48 hr old that were infected with coxsackieviruses B1 and B4. Several of the surviving mice developed left ventricular aneurysms, which resulted from transmural necrotizing myocarditis. In this group (coxsackieviruses B1 and B4), pathologic changes in the heart were synchronous with maximal cardiac titers of virus. Fourteen-day-old mice infected with coxsackieviruses B2 and B3 developed nontransmural necrotizing myocarditis in which maximal pathologic changes followed peak cardiac titers of virus by several days, whereas three- to five-month-old mice infected with coxsackieviruses B1, B2, B3, or B4 showed maximal susceptibility to destructive lesions in the exocrine glandular pancreas. Therefore, specific susceptibilities to infection with coxsackieviruses group B vary with age of the mouse, virus type (and strain), and organ.

Aging↗