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)

Acute ethanol exposure depresses ventricular contractility and contributes to alcoholic cardiomyopathy in both men and women chronically consuming ethanol. However, a gender-related difference in the severity of myopathy exists with female being more sensitive to ethanol-induced tissue damage. Acetaldehyde (ACA), the major oxidized product of ethanol, has been implicated to play a role in the pathogenesis and gender-related difference of alcoholic cardiomyopathy, possibly due to its direct cardiac effect and interaction with estrogen. This study was designed to compare the effects of cardiac overexpression of alcohol dehydrogenase (ADH), which converts ethanol into ACA, on the cardiac contractile response to ethanol in ventricular myocytes isolated from age-matched adult male and female transgenic (ADH) and wild-type (FVB) mice. Mechanical properties were measured with an IonOptix SoftEdge system. ACA production was assessed by gas chromatography. The ADH myocytes from both genders exhibited similar mechanical properties but a higher efficacy to produce ACA compared to FVB myocytes. Exposure to ethanol (80-640 mg/dl) for 60 min elicited concentration-dependent decrease of cell shortening in both FVB and ADH groups. The ethanol-induced depression on cell shortening was significantly augmented in female but not male ADH group. ADH transgene did not exacerbate the ethanol-induced inhibition of maximal velocity of shortening/relengthening in either gender. In addition, neither ethanol nor ADH transgene affect the duration of shortening and relengthening in male or female mice. These data suggest that females may be more sensitive to ACA-induced cardiac contractile depression than male, which may attribute to the gender-related difference of alcoholic cardiomyopathy.
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PMID:Influence of gender on ethanol-induced ventricular myocyte contractile depression in transgenic mice with cardiac overexpression of alcohol dehydrogenase. 1260 Jun 69

Oculopharyngodistal-myopathy (OPDM) is an autosomal dominant, heredofamilial myopathy accompanied with slowly progressive ptosis and extraocular palsy, and weakness of the masseter, facial, and bulbar muscles, as well as distal involvement of the limbs starting around 40 years of age or later. A 54-year-old female with OPDM underwent resection of the uterus for uterus body cancer. We speculated the patient might be at the risk of aspiration pneumonia, prolonged respiratory depression, and malignant hyperthermia, and chose spinal and epidural anesthesia. The operation was performed successfully and the patient was discharged uneventfully.
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PMID:[Anesthetic management of a patient with oculopharyngodistal-myopathy]. 1264 70

Despite recent advances in pharmacological therapy, chronic heart failure remains a major cause of morbidity and mortality in older people. Studies of exercise training in younger, carefully selected patients with heart failure have shown improvements in symptoms and exercise capacity and in many pathophysiological aspects of heart failure, including skeletal myopathy, ergoreceptor function, heart rate variability, endothelial function, and cytokine expression. Data on mortality and hospitalization are lacking, and effects on everyday activity, depression, and quality of life are unclear. Exercise therapy for patients with heart failure appears to be safe and has the potential to improve function and quality of life in older people with heart failure. To realize these potential benefits, exercise programs that are suitable for older, frail people need to be established and tested in an older, frail, unselected population with comorbidities.
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PMID:Exercise training as a therapy for chronic heart failure: can older people benefit? 1275 48

We report on clinical, histological and genetic findings in two patients carrying novel heteroplasmic mutations in the mitochondrial cytochrome c oxidase subunit genes COII and COIII. The first patient, a 35 year-old man had a multisystemic disease, with clinical symptoms of bilateral cataract, sensori-neural hearing loss, myopathy, ataxia, cardiac arrhythmia, depression and short stature and carried a 7970 G>T (E129X) nonsense mutation in COII. A sudden episode of metabolic encephalopathy caused by extremely high blood lactate lead to coma. The second patient developed exercise intolerance and rhabdomyolysis at age 22 years. A heteroplasmic missense mutation 9789 T>C (S195P) was found in skeletal muscle, but not in blood and myoblasts pointing to a sporadic mutation. Our report of two patients with isolated COX deficiency and new mutations in COX subunit genes may help to draw more attention to this type of mtDNA defects and provide new aspects for counselling affected families.
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PMID:Mutations in mtDNA-encoded cytochrome c oxidase subunit genes causing isolated myopathy or severe encephalomyopathy. 1628 75

Inadvertent ingestion of thiafentanil oxalate by a captive adult female mountain lion (Puma concolor) caused a prolonged clinical syndrome that included sedation and depression, muscle tension, and myopathy that was incompletely antagonized by naltrexone HCl. A serum chemistry profile revealed markedly elevated creatinine phosphokinase (CK; 490,450 IU/l), alanine aminotransferase (ALT; 1,896 IU/l), and aspartate aminotransferase (AST; 4,321 IU/l) 2 days after onset. The affected animal's condition gradually improved over the next 15 days in response to supportive therapy that included diazepam (5 mg as needed), Normasol R (3 l/day), dexamethasone (tapering dose starting at 1 mg/kg), and ketoprofen (1 mg/kg). She eventually recovered completely. Based on these observations, carcasses of animals immobilized with thiafentanil should be marked and disposed of properly to preclude opportunities for secondary exposure and potential intoxication in scavenging species. In addition, caution is advised when using thiafentanil in animals that could be preyed upon before full metabolism of the drug.
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PMID:Suspected secondary thiafentanil intoxication in a captive mountain lion (Puma concolor). 1645 79

Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain. These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission, and play an important role in regulating central noradrenergic and GABA function. Thyroid deficiency during the perinatal period results in mental retardation. Hypothyroidism of the adults causes most frequently dementia and depression. Other less common clinical pictures include myxoedema coma, dysfunction of cerebellum and cranial nerves. Hypothyroidism also increases predisposition of stroke. Peripheral diseases frequently include polyneuropathy, carpal tunnel syndrome, myalgic state, and rarely myokymia. Nearly all the hyperthyroid patients show minor psychiatric signs, and infrequently psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur. The peripheral complications may be indicated by chronic thyrotoxic myopathy, infiltrative ophthalmopathy, myasthenia gravis, periodic hypokalemic paralysis and polyneuropathy. Generalized resistance to thyroid hormone was confirmed in a number of patients with attention deficit-hyperactivity disorder. Significantly elevated antithyroid antibody titers characterize Hashimoto's encephalopathy. This condition is a rare, acute - subacute, serious, life threatening, but steroid-responsive, relapsing-remitting, autoimmune disease.
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PMID:[Some neurologic and psychiatric complications in endocrine disorders: the thyroid gland]. 1734 50

An Asian multiparous woman weighing 47 kg, who suffered from a rare myopathy, congenital fibre type disproportion, was given morphine 10 mg intramuscularly for labour analgesia. After delivery, she had diastolic hypertension and proteinuria and was prescribed magnesium sulphate. Some hours later she became unresponsive with little respiratory effort. Blood gas analysis revealed a respiratory acidosis. Naloxone administration reversed the symptoms. Further doses were required as the respiratory depression recurred. Opioid-related narcosis is the most likely diagnosis in this case. Other possible differential diagnoses were magnesium overdose or a post-ictal state. The presence of a myopathy could render this patient susceptible to the respiratory effects of opioids. Other explanations for an exaggerated and delayed response to opioids include co-administration of other respiratory depressant drugs such as magnesium sulphate, co-morbidity such as renal impairment and genetic variability in the metabolism of morphine. Robust guidelines and highlighting patients with risk factors are required to prevent this complication from recurring.
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PMID:Opioid-related narcosis in a woman with myopathy receiving magnesium. 1764 82

Glucocorticoids (GC) are used widely for the treatment of patients with various disorders, including autoimmune diseases, allergies, and lymphoproliferative disorders. Glucocorticoid therapy is often limited by several adverse reactions associated with GC excess. Excess GC can elicit a variety of symptoms and signs, including growth retardation in children; immunosuppression; cardiovascular disorders like hypertension and atherosclerosis; osteoporosis; myopathy; and diabetes mellitus. Currently, attention is focused on oxidative stress as one of the major determinants of endothelial dysfunction and cardiovascular senescence. The main reason for all unwanted effects of GC is that dexamethasone induces the overproduction of reactive oxygen species, causing dysregulation of physiological processes. Humans and animals with GC-induced hypertension exhibit reduced nitric oxide levels; patients with excess GC levels also suffer from depression as a consequence of low levels of serotonin and melatonin. The common cofactor for the production of these vasoactive molecules is tetrahydrobiopterin (BH4), which is required for nitric oxide synthesis.
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PMID:Glucocorticoids and oxidative stress. 1771 67

Apical hypertrophic cardiomyopathy (AHC) is associated with neurological abnormalities such as transient ischemic attack, stroke, limb-girdle muscular dystrophy, or eosinophilic myositis in single cases. The association of AHC and metabolic myopathy has not been reported. In an 84-year-old woman with long-standing gait disturbance, dementia, Parkinson syndrome, ptosis, ophthalmoparesis, tetraparesis, polyneuropathy, lactacidosis, polyarthralgia, dorsalgia, and osteoporosis, cardiac examination for long-standing anginal chest pain and palpitations, revealed supraventricular and monomorphic ventricular ectopic beats, hypertrophic signs, ST-depression and negative T waves on electrocardiogram (ECG), diastolic dysfunction with impaired relaxation, and AHC on transthoracic echocardiography. AHC was confirmed by cardiac magnetic resonance imaging, which additionally showed a small left ventricular apical aneurysm with a wall-thickness of only 3 mm. The patient was suspected to additionally have a multisystem disease, most likely due to impaired oxidative metabolism. This case shows that AHC may take a mild course and be associated with a number of extracardiac abnormalities.
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PMID:Apical hypertrophic cardiomyopathy in encephalomyopathy. 1816 25

The ionophores (polyether compounds) have been the predominant means of chemical control of coccidiosis in the past 15 years because of the slow development of resistant strains to them relative to other anticoccidial drugs. However, the ionophores have a narrow range of safety, and it is sometimes difficult to ensure an even distribution of the drug throughout the feed. Diagnosis of toxicity is difficult because of the reversibility of clinical signs and the variability of pathological lesions ranging from none to non-specific. This paper reviews the known pathology of ionophore toxicity and the inadequacies of present diagnostic approaches. Analysis for ionophores in feed may be made by silica gel and high performance thin layer chromatography, but tissue analyses for toxic levels, a more specific diagnostic aid, are not commonly carried out. Limited studies suggest that residues in even severely intoxicated birds remain low. Diagnosis relies upon clinical signs of incoordination, leg weakness, diarrhoea and depression, non-specific histopathological lesions of myopathy and the presence of high levels of ionophores in the feed. If, however, toxicity is due to uneven distribution, feed samples may return false negative results. Current diagnostic criteria are, therefore, unsatisfactory and there is a clear need to investigate other diagnostic approaches.
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PMID:Ionophore toxicity in chickens: a review of pathology and diagnosis. 1867 Sep 51


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