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)

The purpose of this study is to investigate the daily life and care condition of elderly people living in Korea, and to observe the symptom of senile dementia among them. In the first survey, 713 subjects were screened and 42 subjects were diagnosed as suffering from senile dementia. In the second survey, 26 elderly and their caregivers who agreed to participate in this program, were interviewed. The results were as follows. 1. About 25% of the 713 subjects needed some kind of help in their daily life. 2. 85% of the subjects could go out and about their houses without help. Only 5% of them had a complete or a partial loss of activity. 3. Of all the subjects, 42 were diagnosed as suffering from senile dementia. The prevalence of this disease was calculated at 5.6% in the survey. 4. Each demented elderly person had 5.3 mental symptoms on the average. Depression was observed more among women and violence was observed more among men. 5. The elderly who had a lower CPR score (Caretaker-Patient Relationship Score), indicating a poor relationship between the patient and caretaker, had a higher prevalence of mental symptoms than those who had a higher CPR score.
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PMID:[The study of senile symptoms and home care on the elderly living in Korea]. 824 57

Resuscitation decisions during the first 6 weeks were analysed for 97 admissions to a psychogeriatric ward of a general teaching hospital. Seventy-seven patients (79%) had a written 'do not resuscitate' (DNR) order on admission and 74 patients (875) had a written DNR order after 6 weeks. Morbidity was assessed with a pre-arrest morbidity (PAM) index and a modified PAM index (MPI). Dementia influenced the presence of a DNR order, both because lack of effectiveness of CPR and lack of quality of life. Age was related to a DNR order. The MPI was associated with the presence of a written DNR order, while the PAM score failed to reach significance. Six weeks after admission DNR orders were predictable by the four variables of dementia, the use of antidepressants, age and PAM, in that order. The association of the use of antidepressants with the presence of a written DNR order was surprising. The use of antidepressants is not the same as the diagnosis of depression. Because of the design, our results cannot permit any conclusion whether depression acts as an additional factor considered in decision-making in psychogeriatric patients. We suggest that depression and its correlates should be considered in discussions and studies about DNR.
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PMID:Dementia in resuscitation policy: a prospective study of a psychogeriatric ward in a Dutch general teaching hospital. 867 May 60

We describe a cardiac arrest which occurred during general anaesthesia in the prone position for surgical correction of lumbar kyphosis in a patient with Marfan's syndrome. Peroperative monitoring was routine with ECG, non-invasive arterial pressure, oximetry, PETCO2 and central venous pressure, plus aortic blood flow and and systolic time intervals via an oesophageal echo-Doppler device. Forty-five minutes after the start of surgery, a sudden decrease in aortic blood flow followed by a decrease in PETCO2 suggested acute cardiac failure despite continuation of the ECG signal. Initial CPR in the prone position produced a slight increase in PETCO2. When the patient was turned to the supine position and the legs elevated, chest compression was more efficient and spontaneous circulation was rapidly restored. Circulatory arrest could be explained by incompletely treated hypovolaemia, or by myocardial depression (decrease in aortic blood flow and lengthened pre-ejection period) combined with excessive hypotension in a patient with Marfan's syndrome, thus compromising coronary blood flow producing ST segment depression. Continuous non-invasive aortic blood flow and PETCO2 monitoring proved valuable in the early detection and treatment of circulatory arrest and in the evaluation of the efficiency of peroperative CPR.
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PMID:Non-invasive continuous haemodynamic and PETCO2 monitoring during peroperative cardiac arrest. 870 1

Previous studies from our laboratory have shown that mitochondrial dysfunction may be an important early event in S-[(1 and 2)-phenyl-2-hydroxyethyl]cysteine (PHEC)-induced cytotoxicity in isolated rat renal proximal tubules. The present study has therefore examined in more detail PHEC-induced mitochondrial dysfunction, both in vivo and in vitro, using isolated renal cortical mitochondria. Renal cortical mitochondria isolated from PHEC-treated rats in vivo showed depressed effects on the mitochondrial respiration and oxidative phosphorylation in both a dose (0, 250, and 500 micromol/kg iv)- and time (0-24 h)-dependent manner in the presence of both succinate (Site 2) and malate plus alpha-ketoglutarate (Site 1) as respiratory substrates, with initial significant depression occurring as early as 4 h following treatment with 500 micromol PHEC/kg. Similar mitochondrial dysfunctions were observed in vitro in concentration- and time-dependent manners with both respiratory substrates. PHEC also caused a marked dose-dependent inhibition of mitochondrial succinate dehydrogenase and NADH cytochrome c reductase activities both in vivo and in vitro, with initial inhibition occurring as early as 4 h after in vivo administration and 45 min after exposure to PHEC in vitro, while the NADH dehydrogenase activity was not considerably inhibited. The mitochondrial ATPase activity was significantly decreased 4 and 24 h following treatment with PHEC (500 micromol/kg). These results suggest that PHEC exerts its inhibitory effect on the mitochondrial respiration and oxidative phosphorylation through the action on the mitochondrial electron transport chain. PHEC significantly reduced the activity of adenine nucleotide translocase as well as the net uptake of substrates by mitochondria without affecting their efflux within 2-4 h after its injection (500 micromol/kg). On the other hand, significant renal damage, as assessed by morphological study, appeared as early as 24 h following such treatment. The observation of similar effects after both in vivo and in vitro exposures may suggest that the effect on mitochondria may have a pathogenic role in PHEC-induced renal injury in rats. PHEC produces mitochondrial toxicity that results from an inactivation of mitochondrial anionic substrate transporters as well as from an inhibition of activities of adenine nucleotide translocase and dehydrogenases.
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PMID:S-[(1 and 2)-phenyl-2-hydroxyethyl]cysteine-induced alterations in renal mitochondrial function in male Fischer-344 rats. 970 95

We investigated the functional changes in the mitochondrial respiratory chain at the rostral ventrolateral medulla (RVLM), the medullary origin of sympathetic vasomotor tone, in an experimental model of endotoxemia that mimics systemic inflammatory response syndrome. In Sprague-Dawley rats maintained under propofol anesthesia, intravenous administration of Escherichia coli lipopolysaccharide (LPS; 30 mg/kg) induced a reduction (Phase I), followed by an augmentation (Phase II) and a secondary decrease (Phase III) in the power density of vasomotor components (0-0.8 Hz) in systemic arterial pressure signals. LPS also elicited progressive hypotension, and death ensued within 4 h. Enzyme assay revealed significant depression of the activity of nicotinamide adenine dinucleotide cytochrome c reductase (Complexes I + III) and cytochrome c oxidase (Complex IV) in the RVLM during all three phases of endotoxemia. On the other hand, the activity of succinate cytochrome c reductase (Complexes II + III) remained unaltered. We conclude that selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain at the RVLM, whose neuronal activity is intimately related to the death process, is closely associated with fatal endotoxemia in the rat.
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PMID:Dysfunction of the mitochondrial respiratory chain in the rostral ventrolateral medulla during experimental endotoxemia in the rat. 1237 92

Many chromones, especially those having 2-substituents, manifest a remarkable variety of biological activities, such as the important cytotoxicity against human leukaemia cells, antiallergic, anticancer activities; unfortunately chromones normally disturb mitochondrial bioenergetics. A new 2-styrylchromone has been synthesized by the Baker-Venkataraman method and a classical approach has been used to assess the effects of 2-styrylchromone (3'-allyl-4',5,7-trimethoxy-2-styrylchromone) on rat liver mitochondrial bioenergetic. Mitochondrial respiratory rate and transmembrane potential were measured polarographically using a Clark oxygen electrode and with a selective electrode, respectively. All the disturbance induced by 2-styrylchromone on the enzymatic activities (succinate dehydrogenase, succinate cytochrome c reductase, and cytochrome c oxidase) and in the mitochondrial osmotic volume were determined spectrophotometrically. State 4, state 3, and uncoupled (presence of carbonylcyanide p-trifluoromethoxyphenylhydrazone) respiration rates were decreased by 2-styrylchromone in a concentration-dependent manner. Depression of respiratory activity promoted by 2-styrylchromone is essentially mediated through partial inhibition of succinate cytochrome c reductase. Phosphorylation capacity was strongly depressed as a result of an inhibition on the enzymatic complex (F(0)F(1)-ATPase) and also because of a deleterious effect on the integrity of the mitochondrial membrane, which uncoupled the respiration-generated proton gradient with the proton-driven phosphorylation. The structural integrity of the outside membrane is severely affected since cytochrome c can be released. 2-Styrylchromone uncouples oxidative phosphorylation by an inhibitory action on the redox chain and ATP synthase activity. Additionally, it can release cytochrome c. Cell death can probably result due to the induction of procaspase-9 and other procaspases and by a strong decrease of the available ATP.
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PMID:Interactions of a new 2-styrylchromone with mitochondrial oxidative phosphorylation. 1243 63

Depression can be the first sign of dementia or can occur in the follow-up of a clearly demented patient. One must be able to distinguish symptoms of depression and dementia, and recognize depression superimposed on dementia in order to provide optimal treatment. Suicidal risk must be assessed, and major depressive episodes must be appropriately treated. Useful drugs to treat depression in demented patients are reviewed. At this stage of the dementing illness, the patient still needs medical attention for other medical problems, periodic health exams, other chronic conditions, etc. It is also important to address the issues of CPR and level of care, if it has not been done previously. Legal aspects must also be clarified at this stage. The patient's ability to consent or to make financial decisions must be assessed. Some objective criteria are suggested. At this stage of the disease, the family physician can really make the difference between a premature nursing home placement and a patient staying at home with his family.
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PMID:[My patient has dementia, but so far, it is not that bad...]. 1508 7

We investigated possible changes in bioenergetics at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. In Sprague-Dawley rats maintained under propofol anesthesia, microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive hypotension that was accompanied by an early augmentation (80-100 min post-Mev; Phase I), followed by a decrease (>100 min post-Mev; Phase II) in the power density of the vasomotor components (0-0.8 Hz) in systemic arterial pressure (SAP) signals. Enzyme assay revealed that local application of Mev into the RVLM also significantly and progressively depressed the activity of NADH cytochrome c reductase (marker for Complexes I and III) and cytochrome c oxidase (marker for Complex IV) in the mitochondrial respiratory chain of the RVLM, but not the heart. On the other hand, the activity of succinate cytochrome c reductase (marker for Complexes II and III) remained unaltered. Both the cardiovascular consequences and depression of mitochondrial respiratory chain enzymes elicited by Mev were significantly antagonized on comicroinjection of atropine (3.5 or 7 nmol) bilaterally into the RVLM. We conclude that Mev adversely effects cardiovascular control by acting as a cholinesterase inhibitor in the RVLM, whose neuronal activity is intimately related to the death process. The resulting accumulation of acetylcholine and prolonged activation of muscarinic receptors in the RVLM is manifested by a selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain that underlies cardiovascular toxicity associated with organophosphate poisons such as Mev.
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PMID:Depression of mitochondrial respiratory enzyme activity in rostral ventrolateral medulla during acute mevinphos intoxication in the rat. 1517 37

Coenzyme Q10 (CoQ10, ubiquinone) is a highly mobile electron carrier in the mitochondrial respiratory chain that also acts as an antioxidant. We evaluated the cardiovascular protective efficacy of CoQ10 at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. Experiments were carried out in adult male Sprague-Dawley rats that were maintained under propofol anesthesia. Microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive hypotension and minor bradycardia, alongside significant depression of the activity of NADH cytochrome c reductase (enzyme marker for Complexes I and III) or cytochrome c oxidase (enzyme marker for Complex IV) in the mitochondrial respiratory chain, reduction in ATP concentration, or tissue hypoxia in the RVLM. On the other hand, the activity of succinate cytochrome c reductase (enzyme marker for Complexes II and III) remained unaltered. The Mev-induced hypotension, bioenergetic failure, or hypoxia was significantly reversed when CoQ10 (4 microg) was coadministered bilaterally into the RVLM with the organophosphate poison. We conclude that CoQ10 confers cardiovascular protection against acute Mev intoxication by acting on the RVLM, whose neuronal activity is intimately related to the "life-and-death" process. We also showed that amelioration of the selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain, the reduced ATP level, and the induced tissue hypoxia in the RVLM are among some of the underlying mechanisms for the elicited protection.
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PMID:Coenzyme q10 confers cardiovascular protection against acute mevinphos intoxication by ameliorating bioenergetic failure and hypoxia in the rostral ventrolateral medulla of the rat. 1580 59

We evaluated the functional changes in the mitochondrial respiratory chain at the rostral ventrolateral medulla (RVLM), the medullary origin of sympathetic vasomotor tone, in an experimental model of fatal organophosphate poisoning using the insecticide mevinphos (Mev). We also investigated the neuroprotective role of coenzyme Q10 (CoQ10) in this process. Intravenous administration of Mev (1 mg/kg) in Sprague-Dawley rats maintained with propofol elicited an initial hypertension followed by hypotension, accompanied by bradycardia, with death ensuing within 10 min. Enzyme assay revealed a significant depression of the activity of nicotinamide adenine dinucleotide cytochrome c reductase, succinate cytochrome c reductase, and cytochrome c oxidase in the RVLM during this fatal Mev intoxication. ATP production also underwent a significant decrease. Pretreatment by microinjection bilaterally of CoQ10 (4 microg) into the RVLM significantly prevented mortality, antagonized the cardiovascular suppression, and reversed the depressed mitochondrial respiratory enzyme activities, or reduced ATP production in the RVLM induced during Mev intoxication. Our results indicated that dysfunction of mitochondrial respiratory chain and energy production at the RVLM takes place during fatal Mev intoxication. We further demonstrated that CoQ10 provides neuroprotection against Mev-induced cardiovascular depression and fatality through maintenance of activity of the key mitochondrial respiratory enzymes in the RVLM.
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PMID:Neuroprotective role of coenzyme Q10 against dysfunction of mitochondrial respiratory chain at rostral ventrolateral medulla during fatal mevinphos intoxication in the rat. 1596 63


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