Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two pregnant mares diagnosed as having equine monocytic ehrlichiosis based on history, clinical signs, and high serum antibody titers to Ehrlichia risticii aborted subsequent to recovery from illness. Mare 1 and mare 2 experienced clinical illness at 120 and 143 days of gestation and aborted at 203 and 226 days of gestation, respectively. The fetuses were expelled in fresh condition, and both mares retained their placentas upon abortion. Gross findings for the fetuses included meconium staining and petechiation of external surfaces. Internally, there was increased volume of feces within the small and large intestines and liver discoloration with enlargement. Microscopic findings included lymphohistiocytic enterocolitis, hepatitis, and myocarditis. Lymphoid hyperplasia and depletion were present in spleen, thymus, and lymph nodes. Ehrlichia risticii was recovered from bone marrow, spleen, lymph node, colon, and liver of the first fetus and bone marrow and colon of the second fetus. Electron microscopic evaluation of the organism isolated in cell culture revealed morphology consistent with E. risticii. The isolated organism was inoculated into a naive pony, and this pony developed high levels of antibody against E. risticii, became ehrlichemic, and developed clinical signs of depression, anorexia, and mild diarrhea. These findings confirm that E. risticii is an abortifacient under conditions of natural infection and should be considered as a differential diagnosis of equine abortions.
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PMID:Identification of Ehrlichia risticii as the causative agent of two equine abortions following natural maternal infection. 761 2

We report the clinical and instrumental data, including the endomyocardial biopsy findings, of six young athletes presenting with minor arrhythmias and/or echocardiographic abnormalities. In one of them, a left ventricular dilation with moderate depression of the systolic function had been attributed to an athlete's heart. A diagnosis of arrhythmogenic right ventricular dysplasia had been made in three others, one with right ventricular dilation and apical hypokinesia, and two with ventricular arrhythmias with QRS morphology of left bundle branch block. A myocarditis could be unequivocally established in four athletes (two with and two without fibrosis). In the remaining two, with a clinical history strongly suggesting a previously acute myocarditis, the endomyocardial biopsy specimen revealed a nonspecific fibrosis compatible but not definitely pathognomonic of a healed myocarditis. Our report suggests that a myocarditis may be a cause of minor rhythm disturbances and/or echocardiographic abnormalities in athletes. A prevalent localization of the inflammatory process in the right ventricle with or without the occurrence of ventricular arrhythmias with left bundle branch block morphology can mimic an arrhythmogenic right ventricular dysplasia. An early diagnosis of myocarditis in athletes is useful to avoid the risk of fatal arrhythmias, also considering that rest still keeps on being one of the most effective strategies in myocarditis management.
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PMID:Role of myocarditis in athletes with minor arrhythmias and/or echocardiographic abnormalities. 777 5

Using methods of cytochemical investigation of the blood polymorphonuclear leucocytes (PMNL), parameters have been studied, characterizing the systems of biological defence and bioenergetics in patients with dilated cardiomyopathy (DCMP), infectious allergic myocarditis (IAM) and myocarditic cardiosclerosis (MCS). DCMP patients showed depression of NBT--test against the background of the increase in the cationic proteins (CP) level in the blood PMNLs, which was a major cytochemical feature. G-6-PhDG activity was increased in IAM patients against the background of high values of NBT-test. Increased values for G-6-PhDG, CP, phosphatases in the presence of low levels of myeloperoxidase in the blood PMNL suggest chronic inflammatory process in the myocardium. Investigation into the cytochemical parameters of bioenergetic and biological defence of the blood PMNL in patients with DCMP, IAM and MCS permits optimization of the diagnosis and treatment policy in the aforementioned nosological entities.
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PMID:[The cytochemical characteristics of the blood polymorphonuclear leukocytes in dilated cardiomyopathy and an inflammatory myocardial lesion]. 790 Mar 29

Nine children in the age group of new born to 10 years were seen during the period October 1989 to January 1993 with varying manifestations of Myocarditis. This ranged from cardiogenic shock due to fulminant cardiac failure, recurrent wheezy episodes (mistakenly treated as bronchial asthma) bronchiolitis and rhythm disturbances. Clinical picture was collaborated by radiological evidence of cardiomegaly, ECG changes of low voltage QRS complexes with ST depression, T wave inversion or signs of left ventricular dilatation. SGOT, SGPT, CPK, LDH were elevated significantly in 7 cases. Echocardiographic changes ranged from left ventricular dilatation to global hypokinesia and mild mitral incompetence. Viral studies suggested infection with Coxsackie B1 in 4 cases, B4 in 2, B5 in 2 and Dengue 3 in 1 case. All the children recovered well with routine anti failure measures and treatment of arrhythmias and 2 children needed steroid therapy. At the end of follow up of 6 months to 1 year there has been complete reversal of ECHO changes to normal. Viral Myocarditis can manifest in varied ways in children and if treated adequately may lead to complete recovery.
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PMID:Varied manifestations of viral myocarditis. 792 2

Six Indonesian buffaloes (Bubalus bubalis) were inoculated intravenously with 10(5) Trypanosoma evansi, examined clinically, haematologically and serologically, and then killed 1, 2, 3, 4, 8 or 12 weeks after infection for detailed pathological study. Relapsing fever was related to the waves of parasitaemia and fluctuations of pulse and respiration rates. Anaemic mucous membranes, depression, weakness, refusal to walk, loss of appetite and emaciation were seen. Body weight, packed cell volume, total platelet and red cell counts, and haemoglobin values were below those of two uninfected control buffaloes, as well as below the normal range; on the other hand antibody titres against T. evansi in infected animals were all above those in controls. Emaciation, serous atrophy of fat, hydropericardium, petechial to larger haemorrhages in the pericardium, pneumonia, congested liver and spleen, oedematous enlargement of the superficial lymph nodes and hyperplastic bone marrow were the major gross pathological changes. Histologically, the severity of the disease increased from 1 to 7 weeks after infection and became less obvious at 12 weeks. The most consistent lesions were interstitial pneumonia, interstitial myocarditis, splenic multifocal necrosis, interstitial myositis and hyperplastic bone marrow. The last three lesions appear not to have been reported previously in T. evansi infection in buffaloes or other animals. The clinicopathological findings in this study show that T. evansi is both an intravascular and extravascular parasite.
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PMID:The pathology of experimental Trypanosoma evansi infection in the Indonesian buffalo (Bubalus bubalis). 804 Mar 89

In susceptible DBA/2 mice coxsackievirus B 3-induced myocarditis leads to inflammatory and necrotic lesions in the myocardium 7-10 days after virus inoculation. The purpose of this study was to determine whether hemodynamic changes occur in murine coxsackievirus B 3 myocarditis and whether they are correlated to histological cardiac lesions throughout the infection. Left ventricular function was determined by open chest puncture of the left ventricle in the course of acute coxsackievirus B 3 infection. Histological cross sections of the heart were stained with hematoxylin/eosin and scored blindly for myocarditic lesions. Left ventricular function was preserved until day 7 post-virus inoculation Left ventricular systolic pressure, +dP/dtmax and -dP/dtmax and heart rate declined significantly from day 7 to day 10. The decrease in these parameters did not correlate with viral concentrations in the heart on the day of hemodynamic measurements. The decrease was related to histological changes on day 10, but not on day 7 of the infection. The data suggest (a) that a cumulative loss of cardiac myofibers, induced either by the virus and/or by immune reactions to the heart, is likely to lead to a late depression of cardiac function, and (b) that there is a weak and only temporary structure-function relationship in the heart in coxsackievirus B 3 myocarditis. Therefore, in addition to an analysis of histological changes, the measurement of cardiac function appears to be very important in order to completely evaluate the severity of myocarditis and the usefulness of any therapy.
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PMID:Left ventricular hemodynamic parameters in the course of acute experimental coxsackievirus B 3 myocarditis. 852 20

Four 4-mo-old elk calves (Cervus elaphus) obtained from northeastern Oregon (USA) each were inoculated orally with 250,000 sporocysts of Sarcocystis spp., including S. sybillensis and S. wapiti. Three similar elk calves of comparable ages and weights served as uninoculated controls maintained with the inoculated elk during the experimental period between September and December 1993. Body weights were evaluated at 0 and 90 days postinoculation (PI); packed cell volumes of whole blood were evaluated at 0, 30, and 60 days PI, and numbers of sarcocysts in histologic sections from 11 selected tissues were evaluated at 90 days PI. Significant differences in blood packed cell volumes were not detected between groups (P > 0.05). Except for weight gain, elk remained healthy. Mean (+/- SE) weight gain of inoculated elk (27.1 +/- 1.6 kg) was significantly (P < 0.05) less than that of controls (40.2 +/- 4.9 kg). Mean (+/- SE) number of sarcocysts in tissues of inoculated (114.4 +/- 25.7 cm2) and controls (4.5 +/- 1.4 cm2) differed significantly (P < 0.05). Heart, esophagus and skeletal muscle contained the most sarcocysts. No sarcocysts were detected in brain, spinal cord, or testicles. Histologically, mononuclear myositis and myocarditis, with numerous intralesional sarcocysts were seen. Less severe, but widespread inflammation occurred in brain, spinal cord, and optic nerve. Mortality and anemia were not seen, but weight gain depression was detected in the inoculated elk over the 90 day experimental period.
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PMID:Experimental infections of Sarcocystis spp. in Rocky Mountain elk (Cervus elaphus) calves. 859 75

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

We found recently autoantibodies against the adenine nucleotide translocator (ANT), a carrier in the inner mitochondrial membrane, in sera of patients with myocarditis and dilated cardiomyopathy. To elucidate whether these antibodies are of pathophysiological importance, we investigated the function and expression of the adenine nucleotide translocator (ANT) in the heart muscle tissue of patients suffering from myocarditis and DCM. We found a markedly lowered transport capacity of the translocator accompanied by an elevation in total ANT protein content. The alteration in ANT protein amount is caused by an ANT isoform shift characterized by an increase in ANT 1 isoform protein associated with a decrease in ANT 2 isoform and an unchanged ANT 3 content. It could be shown that the isoform shift is not a progressive process during the disease period but an event in the early period of illness which becomes permanent. Simulating the effect of pathogenetic factors of autoimmunological diseases, we infected A/J mice with the enterovirus Coxsackie B3 and immunized guinea pigs with myocardial ANT protein. Both treatments led to autoimmunological responds and to a lowered myocardial transport capacity of ANT, to a disturbed energy metabolism and consequently to a depression of heart function.
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PMID:Significance of the adenine nucleotide translocator in the pathogenesis of viral heart disease. 897 71

An explanation was sought for the fact that an enhancement of myocarditis occurs when Trypanosoma cruzi infected mice is treated with cyclophosphamide (CY). Several schedules were tested in mice and two polar models were achieved--one presenting parasite exacerbation without inflammatory reaction and the other presenting only cellular infiltrate in function of timing and different dosage of drug. In those receiving the drug after infection, an enhancement of the parasite load was detected and it was associated with an inflammatory reaction when mice were treated every other day with low doses of CY (3 mg/kg), but such inflammation was not present if a single dose of 200 mg/kg was used 5 days after infection. On the other hand, in schedules using 200 mg/kg of CY 2 days before infection an enhancement of myocarditis was observed on day 12 post infection, but this was not associated with parasite proliferation. Finally when employing a single intermediate dose of 40 mg/kg, a parasite load as well as a myocarditis enhancement was observed. A correlation between blood monocytes rebound and the intensity of myocarditis has been observed, and the varying time of drug injection suggested that this cellular infiltrate modulates the parasite load. If the immunosuppressive period of the drug occurred during parasite tissue invasion, parasite load amplification would occur without myocarditis. This was achieved using a single dose (200 mg/kg) of CY five days after infection, since monocytosis occurs 7-8 days after drug injection, allowing for parasite multiplication in tissues. The present data bring a strong suggestion that the modulation of myocarditis and parasite load are directly correlated with the leukocytes rebound occurring after the depression period promoted by CY treatment.
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PMID:Chagas' disease: enhancement of systemic inflammatory reaction in cyclophosphamide treated mice. 902 90


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