Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies [G. S. Hudson et al. (1989) J. Biol. Chem. 265, 808-814] showed that the faster turnover rates and lower affinities for CO2 of ribulosebisphosphate carboxylase/oxygenases from C4 plants, compared to C3 and C3/C4 plants, were specified by the chloroplast-encoded large subunits. In pairs of closely related C3 and C4 species from three genera, these kinetic changes were accompanied by only three to six amino acid residue substitutions, depending on the genus. None of these substitutions occurred near the active site and only one, 309Met (C3) to Ile (C4), was common to all three genera. Unlike the plant carboxylases, the highly homologous enzyme from the cyanobacterium Synechococcus PCC 6301 folds and assembles properly when its rbcL and rbcS genes are coexpressed in Escherichia coli. Furthermore, the cyanobacterial enzyme has Ile at position 309 of the large subunit, a high turnover number, and a poor affinity for CO2. 309Ile was replaced with Met and several other residues by site-directed mutagenesis of the cyanobacterial rbcL. Met and Leu were tolerated at this position with no alteration in the kinetic or structural properties of the assembled holoenzyme. However, substitution with Val, Gly, Trp, or Arg prevented the assembly of the subunits. The indifference to Met or Ile at this position, as well as the tolerance for Leu which is not observed with any natural ribulosebisphosphate carboxylase, leads to the conclusion that either the 309Met/Ile substitution has no effect on the kinetic properties of the plant enzyme, despite the correlation apparent in previous studies, or the cyanobacterial enzyme is sufficiently different from the plant enzyme in other respects that the influence of residue 309 is masked.
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PMID:Effects of mutations at residue 309 of the large subunit of ribulosebisphosphate carboxylase from Synechococcus PCC 6301. 144 69

A 43 year-old woman suffered a cardio-circulatory arrest with a post-anoxic coma during 24 hours. This was followed by and akinetic-hypertonic syndrome. There was also dystonia of both hands and of right big toe. After and initial mutism, the patient spoke with dysarthria, a monotonous weak voice of poor timbre and low vocal volume. She had in addition mood disturbances with indifference to her condition and compulsive activity. Extrapyramidal syndromes after ischemic anoxia are rare, when compared to their relative frequency after carbon monoxide poisoning. Early CT scan with contrast can identify symmetrical and bilateral lenticulocaudal high densities and MRI is also useful for the diagnosis.
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PMID:[Extrapyramidal syndrome after cardiocirculatory incompetence]. 274 Jun 88

A summary of clinical data is presented on 34 men and 52 women patients with brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Their ages ranged from 34 to 82 years, with peak incidence in the sixth and seventh decade. Possible etiological factors were age, duration of unconsciousness on acute intoxication, and previous physical illness. The onset was relatively sudden after the apparent clear period which ranged from 2 to 40 days (mean 22.5 days). The most frequent symptoms were apathy, dull facial expressions, dementia, such as amnesia and disorientation, hypokinesia, mutism, irritable distractibility, urinary and/or fecal incontinence, gait disturbance and abnormal neurological signs and reflexes. EEG was abnormal in 33 of the 57 cases (58%). Of 27 patients who were given a computed tomographic brain scan, 15 patients were abnormal. The prognosis was relatively good in the follow-up study of 56 patients. Only age was related to a better prognosis.
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PMID:A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. 396 7

Thermal stress was induced experimentally in the hybrid pigs LW X L, weighing 45 to 52 kg. The trials were repeated in boxes heated to the temperature of 43 to 47 degrees C. The pigs were examined for the values of tremor, pH, partial pressure of carbon dioxide (pCO2), base excess (BE), buffer base (BB), standard and actual bicarbonate (SB and AB), total carbon dioxide (tCO2) and partial oxygen pressure in blood (pO2). Thermal stress caused marked tachycardia, polypnoea, higher body temperature, increased blood pH, reduction of partial carbon dioxide pressure. Respiratory alkalosis was accompanied by cardiovascular weakness, general excitation followed by apathy, cyanosis and dyspnoea.
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PMID:[The effect of heat stress on acid-base homeostasis in pigs]. 643 33

Two patients who had suffered severe carbon monoxide intoxication showed lasting neuropsychologic sequelae: 1) deep inertia involving the whole behaviour and expressed by an almost complete lack of activity if not induced by someone else; a mental gap when the patients were left to themselves and a tendency to give up the mental activity when stimuli ceased; an apparent affective indifference connected with a lack of spontaneous expression of the affects; 2) pseudo-obsessionnal activities: coprolalia with sexual themes in one patient, obsessive collecting and tidying up activities in the other one. Neurologic examination was normal, particularly no parkinsonian syndrome was present. CT scans showed bilateral pallidal low density areas. Both patients had moderate intellectual impairment in psychometric tests and amnestic disorders. There is a possible relationship between memory and cognitive impairment and mental inertia. The onset of pseudo-obsessional signs following basal ganglia lesions is emphasized. The central semeiological fact seems to be a disorder of the initiation and the carrying on of any external action as well as mental activity itself. This may be related with the activity disorders represented at a more elementary level by motion impairment in parkinsonian akinesia.
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PMID:[Behavior and mental activity disorders after carbon monoxide poisoning. Bilateral pallidal lesions]. 646 94

The in-vitro activity of a combination of ranitidine bismuth citrate (RBC) and metronidazole against metronidazole-resistant Helicobacter pylori strains (MIC > or = 8 mg/L) was evaluated by agar dilution chequerboard and killing curve methods. Twenty-five metronidazole-resistant strains were used in the chequerboard method, using Mueller-Hinton agar plus 7% lysed horse blood, an inoculum of 10(6) cfu/spot and incubation in a 10% CO2 atmosphere at 37 degrees C for 3-5 days. Synergy was defined as a fractional inhibitory concentration (FIC) index of < or = 0.5, partial synergy as 0.5 < FIC < or = 1, indifference as 1 < FIC < or = 4 and antagonism as FIC > 4. For nine strains, killing curves were constructed for metronidazole and RBC individually and in combination at 1 x MIC. The number of viable colonies was counted at time 0 and after 2, 4, 6, 8 and 24 h; the combination was defined as synergic if it produced a decrease of > or = 2 log10 cfu/mL compared with the most active single agent. Metronidazole MICs ranged from 8 to 128 mg/L and RBC MICs from 0.125 to 4 mg/L. The minimum FIC ranged from 0.28 to 1 and the maximum FIC from 1 to 1.25. When RBC and metronidazole were combined, all the metronidazole-resistant H. pylori strains revealed partial (68%) or total (32%) synergy. Five out of the nine strains also exhibited synergy at 4, 6 or 8 h incubation when tested by the killing curve method although three other strains exhibited no synergy. In the last strain, a 2log10 decrease in the initial number was observed with RBC alone or combined with metronidazole.
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PMID:Study of the combination of ranitidine bismuth citrate and metronidazole against metronidazole-resistant Helicobacter pylori clinical isolates. 978 70

A 69-year-old woman was admitted to our hospital due to an interval form of carbon monoxide (CO) poisoning one month after acute CO poisoning. On admission, she had disorientation, memory disturbance, apathy, masked face, muscle rigidity, bradykinesia and parkisonian gait. An MRI (FLAIR image) revealed high signal intensity lesions in the bilateral globus pallidus and the white matter of the frontal lobe. Hyperbaric oxygen (HBO) therapy at 2 atmospheres for 60 min was given every day, in addition to citicoline, levodopa/DCI and selegiline hydrochloride. Cognitive disturbance and parkinsonism gradually decreased, and abnormal signals in the bilateral globus pallidus and the cerebral white matter were attenuated after the treatment. Neuropsychiatric abnormalities except for a slight gait disturbance disappeared one and a half month after starting the treatment. In addition to HBO therapy, administration of citicoline, lovodopa and selegiline may be useful in the case of the interval form of CO poisoning.
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PMID:[A case of interval form of carbon monoxide poisoning with a remarkable recovery]. 1598 66

A 59-year-old patient presented with compulsive behaviors and lasting apathy after carbon monoxide intoxication. The apathy could be overcome by external stimulation (self-activation deficit). There was severe neuronal loss bilaterally in the anterior part of the pallidum and in the substantia nigra, pars reticulata. This first clinico-pathological case of a self-activation deficit illustrates the dissociation between motor and behavioral symptoms in lesions of the pallido-nigral complex, with the behavioral symptoms being related to lesions of the substantia nigra, pars reticulata and of the anterior part of the pallidum.
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PMID:Behavioral symptoms after pallido-nigral lesions: a clinico-pathological case. 1856 36

The caudate nucleus, which is vulnerable to hypoxic-ischemic brain injury (HI-BI), is important to cognitive function because it is connected to the prefrontal cortex. Using diffusion tensor tractography (DTT), no study on injury of the prefronto-caudate tract in a patient with HI-BI has been reported so far. Here, we report a patient with severe apathy who showed injury of the prefronto-caudate tract following HI-BI, which was demonstrated by DTT. A 38-year-old female patient suffered HI-BI induced by carbon monoxide poisoning following attempted suicide for a period of approximately four hours. From the onset, the patient showed severe apathy (7 months after onset-the Apathy Scale score was 24 [full score: 42]). Brain MR images taken at seven months after onset showed no abnormality. On 7-month DTT, the neural connectivity of the caudate nucleus to the medial prefrontal cortex (Brodmann area: 10 and 12) and orbitofrontal cortex (Brodmann area: 11 and 13) was decreased in both hemispheres. Using DTT, injury of the prefronto-caudate tract was demonstrated in a patient who showed severe apathy following HI-BI. We believe that injury of the prefronto-caudate tract might be a pathogenetic mechanism of apathy in patients with HI-BI.
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PMID:Severe Apathy Due to Injury of Prefronto-caudate Tract. 3141 Feb 97