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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that certain patients with cirrhosis have asymptomatic cardiac abnormalities that have not yet been explained. Thus, cardiac troponin I, a specific marker of myocardial injury, has been measured in patients with cirrhosis without previous cardiac disease. Thirty-two consecutive patients (age 49 +/- 11) with cirrhosis and normal ECG were selected, 22 of which were alcoholic. Hemodynamic investigations were performed. Left ventricular function and mass were evaluated by echocardiography. Serum creatine kinase MB mass, myoglobin, and cardiac troponin I concentrations were measured. Cardiac troponin I concentrations were elevated in 10 patients (32%) (range 0.06-0.25 microg/L) whereas creatine kinase MB mass and myoglobin were normal in all patients. Abnormal troponin I values were not related to the severity of cirrhosis, to the degree of portal hypertension, or to other hemodynamic values. In contrast, elevated serum cardiac troponin I concentrations were related to a decreased stroke-volume index (P <. 05) and a decreased left ventricular mass (P <.05). These results show a high prevalence of slightly elevated serum cardiac troponin I in patients with cirrhosis, especially in those with alcoholic cirrhosis. Elevated troponin I is associated with subclinical left ventricular myocardial damage. These findings may be linked to a lack of left ventricular adaptation in certain patients with cirrhosis and alcoholic cardiomyopathy.
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PMID:Elevated circulating cardiac troponin I in patients with cirrhosis. 1005 61

A number of medical applications of near-infrared spectroscopy are growing closer to clinical acceptance, and new techniques involving both spectroscopy and imaging are evolving rapidly. In vivo spectroscopy and, more recently, imaging techniques are largely based upon optical electronic transitions involving the metal centers of hemoglobin (blood), myoglobin (muscle) and cytochrome aa3 (mitochondria). The wide variety of near-IR based applications includes heart and stroke research, monitoring cerebral oxygenation of premature babies, and 'functional activation' (response of brain to mental tasks). All of these applications are founded upon changes in hemoglobin O2 saturation; these changes are monitored by following trends in the near-infrared absorptions of deoxyhemoglobin (760 nm) and oxyhemoglobin (920 nm). The same absorptions provide a basis for imaging regional variations in blood oxygenation. This report presents and discusses examples, both from the literature and from our recent work, of near-infrared spectroscopy and imaging in medical applications.
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PMID:In vivo optical/near-infrared spectroscopy and imaging of metalloproteins. 1083 Aug 79

To study the effect of age on serum myoglobin more clearly, the analytical, intra-individual and inter-individual components of variation were estimated from duplicate analyses of specimens collected from 18 healthy elderly subjects [ages 74-97 years; 9 men (EM)], and 14 healthy younger subjects [ages 25-31 years; 7 men (YM)] over a period of 6 weeks. The mean values (microgram/L) were EM: 53.7; EW: 44.9; YM: 34.2; YW:24.8. Estimated analytical (CVA), intra- (CVI) and inter-individual (CVG) variations as CV% were: CVA: 2.2. CVI: EM: 13; EW: 9.9; YM: 12.4; YW: 9.6. CVG: EM: 37.6; EW: 28; YM: 18.5; YW: 13.4. The data obtained were used to derive the desirable analytical goal for imprecision (i.e., < or = 6.5% in EM; < or = 4.9% in EW and < or = 6.2% in YM; < or = 4.8% in YW); inaccuracy (i.e., < or = 9.9% in EM; < or = 7.7 in EW and < or = 5.5% in YM; < or = 4.12% in YW); the change required for serial results to be significantly different (i.e., 36% in EM; 28% in EW and 34% in YM; 27.2% in YW), the numbers of specimen collections required to produce a more precise estimate of the homeostatic set point of an individual within 5% (i.e., 26 in EM; 16 in EW and 24 in YM; 15 in YW), and the index of individuality (i.e., 0.34 in EM; 0.35 in EW and 0.67 in YM; 0.71 in YW). This study shows that intra-individual biological variation of myoglobin in healthy elderly subjects is not different from that in young subjects. Inter-individual variation, instead, is greatly influenced by differences in age and sex.
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PMID:Biological variability of myoglobin in healthy elderly and younger subjects. 1096 74

To evaluate pathophysiological significance of post-mortem urinary myoglobin levels in determining the cause of death, we investigated 210 forensic autopsy cases, partially in comparison with serum levels. Post-mortem serum myoglobin levels were extraordinary high in most cases possibly due to post-mortem change. Urinary myoglobin levels did not correlate with the serum levels, showing possible post-mortem elevation in cases of a prolonged post-mortem period over 48h. A high (>1000 ng/ml), moderate (100-1000 ng/ml), slight (50-100 ng/ml) and not significant (<50 ng/ml) elevation of urinary myoglobin were observed in 26, 43, 31 and 110 cases, respectively. Half the highly elevated cases were those with a survival time over 24h. In cases of minor muscle injury such as head trauma, elevation of urinary myoglobin level was closely related to longer survival. In acute/subacute deaths with a post-mortem interval within 48h, a significant difference was observed in relation to the blood carboxyhemoglobin (COHb) levels of fire victims: myoglobinuria over 100 ng/ml was more frequently and markedly observed in cases with COHb below 60% than over 60%, suggesting muscle damage in fatal burns. Similar elevation was observed in heat stroke victims, and also in some cases of acute and subacute death from polytrauma, asphyxiation, drowning, electricity and spontaneous cerebral bleeding, but not in myocardial infarction. Thus, it was suggested that high post-mortem urinary myoglobin levels in acute and subacute death cases may be a possible indicator of antemortem massive skeletal muscle damage as well as exertional muscle hyperactivity or convulsive disorders associated with hypoxia.
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PMID:Post-mortem urinary myoglobin levels with reference to the causes of death. 1107 73

Myoglobinuria or rhabdomyolysis occurs when myoglobin escapes into the blood and then into the urine after acute muscle necrosis. It can be a serious medical condition leading to renal failure and death. There are many causes including exertion, crush syndromes, ischaemia, metabolic disorders, exogenous toxins and drugs, heat stroke and hereditary disorders such as malignant hyperthermia. We report the case of a 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles. Sodium monensin, the active principle of Rumensin(R), is a dietary additive used as a growth promoter for confined cattle. There are no previous reports of human intoxication. Accidental or experimental sodium monensin intoxication in animals produces similar findings to those seen in this case.
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PMID:Fatal rhabdomyolysis after acute sodium monensin (Rumensin) toxicity: case report. 1158 43

While the physiological adaptations that occur following endurance training in previously sedentary and recreationally active individuals are relatively well understood, the adaptations to training in already highly trained endurance athletes remain unclear. While significant improvements in endurance performance and corresponding physiological markers are evident following submaximal endurance training in sedentary and recreationally active groups, an additional increase in submaximal training (i.e. volume) in highly trained individuals does not appear to further enhance either endurance performance or associated physiological variables [e.g. peak oxygen uptake (VO2peak), oxidative enzyme activity]. It seems that, for athletes who are already trained, improvements in endurance performance can be achieved only through high-intensity interval training (HIT). The limited research which has examined changes in muscle enzyme activity in highly trained athletes, following HIT, has revealed no change in oxidative or glycolytic enzyme activity, despite significant improvements in endurance performance (p < 0.05). Instead, an increase in skeletal muscle buffering capacity may be one mechanism responsible for an improvement in endurance performance. Changes in plasma volume, stroke volume, as well as muscle cation pumps, myoglobin, capillary density and fibre type characteristics have yet to be investigated in response to HIT with the highly trained athlete. Information relating to HIT programme optimisation in endurance athletes is also very sparse. Preliminary work using the velocity at which VO2max is achieved (V(max)) as the interval intensity, and fractions (50 to 75%) of the time to exhaustion at V(max) (T(max)) as the interval duration has been successful in eliciting improvements in performance in long-distance runners. However, V(max) and T(max) have not been used with cyclists. Instead, HIT programme optimisation research in cyclists has revealed that repeated supramaximal sprinting may be equally effective as more traditional HIT programmes for eliciting improvements in endurance performance. Further examination of the biochemical and physiological adaptations which accompany different HIT programmes, as well as investigation into the optimal HIT programme for eliciting performance enhancements in highly trained athletes is required.
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PMID:The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. 1177 61

Neuroglobin (Ngb) is an O(2)-binding protein localized to cerebral neurons of vertebrates, including humans. Its physiological role is unknown but, like hemoglobin, myoglobin, and cytoglobin/histoglobin, it may transport O(2), detoxify reactive oxygen species, or serve as a hypoxia sensor. We reported recently that hypoxia stimulates transcriptional activation of Ngb in cultured cortical neurons and that antisense inhibition of Ngb expression increases hypoxic neuronal injury, whereas overexpression of Ngb confers resistance to hypoxia. These findings are consistent with a role for Ngb in promoting neuronal survival after hypoxic insults in vitro. Here we report that in rats, intracerebroventricular administration of an Ngb antisense, but not sense, oligodeoxynucleotide increases infarct volume and worsens functional neurological outcome, whereas intracerebral administration of a Ngb-expressing adeno-associated virus vector reduces infarct size and improves functional outcome, after focal cerebral ischemia induced by occlusion of the middle cerebral artery. We conclude that Ngb acts as an endogenous neuroprotective factor in focal cerebral ischemia and may therefore represent a target for the development of new treatments for stroke.
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PMID:Neuroglobin protects the brain from experimental stroke in vivo. 1262 Nov 55

Low oxygen levels (hypoxia) play a role in clinical conditions such as stroke, chronic ischemia, and cancer. To better understand these diseases, it is crucial to study the responses of vertebrates to hypoxia. Among vertebrates, some teleosts have developed the ability to adapt to extremely low oxygen levels. We have studied long-term adaptive responses to hypoxia in adult zebrafish. We used zebrafish that survived severe hypoxic conditions for 3 wk and showed adaptive behavioral and phenotypic changes. We used cDNA microarrays to investigate hypoxia-induced changes in expression of 15,532 genes in the respiratory organs (the gills). We have identified 367 differentially expressed genes of which 117 showed hypoxia-induced and 250 hypoxia-reduced expressions. Metabolic depression was indicated by repression of genes in the TCA cycle in the electron transport chain and of genes involved in protein biosynthesis. We observed enhanced expression of the monocarboxylate transporter and of the oxygen transporter myoglobin. The hypoxia-induced group further included the genes for Niemann-Pick C disease and for Wolman disease [lysosomal acid lipase (LAL)]. Both diseases lead to a similar intra- and extracellular accumulation of cholesterol and glycolipids. The Niemann-Pick C protein binds to cholesterol from internal lysosomal membranes and is involved in cholesterol trafficking. LAL is responsible for lysosomal cholesterol degradation. Our data suggest a novel adaptive mechanism to hypoxia, the induction of genes for lysosomal lipid trafficking and degradation. Studying physiological responses to hypoxia in species tolerant for extremely low oxygen levels can help identify novel regulatory genes, which may have important clinical implications.
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PMID:Gene expression profiling of the long-term adaptive response to hypoxia in the gills of adult zebrafish. 1599 72

Rhabdomyolysis is a common and potentially lethal clinical syndrome that results from acute muscle fiber necrosis with leakage of muscle constituents into blood. Myoglobinuria is the most significant consequence, leading to acute renal failure (ARF) in 15%-33% of patients with rhabdomyolysis. Rhabdomyolysis occurs from inherited diseases, toxins, muscle compression or overexertion, or inflammatory processes, among other disorders. In some cases, no cause is found. We describe 475 patients from the Johns Hopkins Hospital inpatient records between January 1993 and December 2001 for the following discharge diagnosis codes: myoglobinuria, rhabdomyolysis, myopathy, toxic myopathy, malignant hyperthermia, neuroleptic malignant syndrome, and polymyositis. Of 1362 patients, 475 patients with an acute neuromuscular illness with serum creatine kinase (CK) more than 5 times the upper limit of normal (>975 IU/L) were included. Patients with recent myocardial infarction or stroke were excluded. The etiology was assigned by chart review. For all, the highest values of serum CK, serum creatinine and urine myoglobin, hemoglobin, and red blood cells were recorded. Forty-one patients had muscle biopsy within at least 2 months from the onset of rhabdomyolysis.Of the 475 patients, 151 were female and 324 were male (median age, 47 yr; range, 4-95 yr). Exogenous toxins were the most common cause of rhabdomyolysis, with illicit drugs, alcohol, and prescribed drugs responsible for 46%. Among the medical drugs, antipsychotics, statins, zidovudine, colchicine, selective serotonin reuptake inhibitors, and lithium were the most frequently involved. In 60% of all cases, multiple factors were present. In 11% of all cases, rhabdomyolysis was recurrent. Underlying myopathy or muscle metabolic defects were responsible for 10% of cases, in which there was a high percentage of recurrence, only 1 etiologic factor, and a low incidence of ARF. In 7%, no cause was found. ARF was present in 218 (46%) patients, and 16 died (3.4%). A linear correlation was found between CK and creatinine and between multiple factors and ARF, but there was no correlation between ARF and death or between multiple factors and death. Urine myoglobin detected by dipstick/ultrafiltration was positive in only 19%. Toxins are the most frequent cause of rhabdomyolysis, but in most cases more than 1 etiologic factor was present. Patients using illicit drugs or on prescribed polytherapy are at risk for rhabdomyolysis. The absence of urine myoglobin, by qualitative assay, does not exclude rhabdomyolysis. With appropriate care, death is rare.
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PMID:Rhabdomyolysis: an evaluation of 475 hospitalized patients. 1626 12

The maximal oxygen uptake (V-dotO(2max)) is considered an important physiological determinant of middle- and long-distance running performance. Little information exists in the scientific literature relating to the most effective training intensity for the enhancement of V-dotO(2max) in well trained distance runners. Training intensities of 40-50% V-dotO(2max) can increase V-dotO(2max) substantially in untrained individuals. The minimum training intensity that elicits the enhancement of V-dotO(2max) is highly dependent on the initial V-dotO(2max), however, and well trained distance runners probably need to train at relative high percentages of V-dotO(2max) to elicit further increments. Some authors have suggested that training at 70-80% V-dotO(2max) is optimal. Many studies have investigated the maximum amount of time runners can maintain 95-100% V-dotO(2max) with the assertion that this intensity is optimal in enhancing V-dotO(2max). Presently, there have been no well controlled training studies to support this premise. Myocardial morphological changes that increase maximal stroke volume, increased capillarisation of skeletal muscle, increased myoglobin concentration, and increased oxidative capacity of type II skeletal muscle fibres are adaptations associated with the enhancement of V-dotO(2max). The strength of stimuli that elicit adaptation is exercise intensity dependent up to V-dotO(2max), indicating that training at or near V-dotO(2max) may be the most effective intensity to enhance V-dotO(2max) in well trained distance runners. Lower training intensities may induce similar adaptation because the physiological stress can be imposed for longer periods. This is probably only true for moderately trained runners, however, because all cardiorespiratory adaptations elicited by submaximal training have probably already been elicited in distance runners competing at a relatively high level.Well trained distance runners have been reported to reach a plateau in V-dotO(2max) enhancement; however, many studies have demonstrated that the V-dotO(2max) of well trained runners can be enhanced when training protocols known to elicit 95-100% V-dotO(2max) are included in their training programmes. This supports the premise that high-intensity training may be effective or even necessary for well trained distance runners to enhance V-dotO(2max). However, the efficacy of optimised protocols for enhancing V-dotO(2max) needs to be established with well controlled studies in which they are compared with protocols involving other training intensities typically used by distance runners to enhance V-dotO(2max).
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PMID:Is there an optimal training intensity for enhancing the maximal oxygen uptake of distance runners?: empirical research findings, current opinions, physiological rationale and practical recommendations. 1646 21


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