Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14-month-old female with familial dysautonomia was referred to the pediatric department with high fever (41.6 degrees C), watery diarrhea, and vomiting. A few hours later, signs of encephalopathy appeared. Laboratory tests revealed elevated levels of lactate dehydrogenase (3500 U/L), aspartate aminotransferase (640 U/L), alanine aminotransferase (320 U/L), and creatine kinase (28,420 U/L). The diagnosis was heat stroke. Impaired autonomic nervous system function may be another risk factor for the development of heat stroke in young children.
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PMID:Heat stroke in familial dysautonomia. 1458 Jun 63

To determine the effects on hemodynamics, laboratory parameters, and renal function of terlipressin used in septic-shock patients with hypotension not responsive to high-dose norepinephrine (>2.0 microg x kg(-1) x min(-1)) and dopamine (25 microg x kg(-1) x min(-1)), a prospective, open-label study was carried out in 17 patients. Patients received one or two boluses of 1 mg of terlipressin. In all patients terlipressin induced a significant increase in mean arterial pressure (MAP), systemic vascular resistance, pulmonary vascular resistance, and left and right ventricular stroke work. The increase in MAP was accompanied by a significant decrease in heart rate and cardiac index, but stroke volume remained unchanged. Oxygen delivery and consumption were significantly decreased. Blood lactate concentrations significantly decreased over the study period. Bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were significantly increased. Thrombocytes were significantly decreased. No change in prothrombin time was observed. Renal function, assessed by urine flow and creatinine clearance, was significantly improved. Pulmonary function assessed by Pao2/Fio2 ratio was not affected. A significant reduction in norepinephrine and dopamine infusion rates was observed in all patients. Eight patients died during their ICU stay from late multiple organ failure. Within the limitations of the present study (open-label design, small group of patients), it can be concluded that in septic shock patients with hypotension nonresponsive to fluid resuscitation and high-dose vasopressors, terlipressin can be effective to restore MAP. Cardiac index should be closely monitored because it was significantly decreased by terlipressin. Renal function was significantly improved. Mesenteric circulation was not evaluated, but hepatic function was altered during the study period. Further studies are required to determine whether terlipressin is safe in terms of outcome in septic shock patients.
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PMID:Terlipressin in catecholamine-resistant septic shock patients. 1537 85

To identify biochemical markers for carotid stroke outcome, blood serum levels of inflammation markers (C-reactive protein, orosomucoid, soluble p-selectin) and autoantibodies (AAB) to neurospecific antigens (glial fibrillary acidic protein, neuron specific enolase, S-100 protein) were studied in 27 patients (mean age 64 +/- 6 years) with acute ischemic stroke in inner carotid artery system on day 1-2 and 21 of the disease onset. To day 21, patients with good rehabilitation of neurological functions (group 1) demonstrated a decrease of C-reactive protein and soluble p-selectin concentrations, and unfavorable disease course was associated with a significant (p<0.05) increase of concentrations of these indices. On day 1 and 7, a level of AAT to glial fibrillary acidic protein was higher (p<0.05) in group 1 than in that with minimal rehabilitation and to day 21 it decreased relatively the baseline level. At the same time, patients with minimal rehabilitation had a stable AAT level. On day 7, the AAT level correlated with expression of neurological deficit on day 21 (r=0.510; p=0.019). No stroke-course-dependent differences were found in dynamics of orosomucoid as well as of AAT to neuron specific enolase and S-100 protein levels.
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PMID:[Markers of inflammation, autoantibodies to neurospecific antigens and outcome in patients with acute ischemic stroke]. 1562 89

Tissue damage after ischemia and reperfusion (I/R) is largely caused by the sequelae of neutrophil infiltration. This inflammatory process can be initiated as the result of stroke, coronary ischemia, trauma, and other related conditions. The infiltration of neutrophils is facilitated by the expression of adhesion molecules on the surface of endothelial cells. Particularly important are the selectin family of adhesion molecules at the onset of neutrophil-mediated injury. The aim of this study was to determine the role of selectin inhibition in the modulation of chemokine expression and Akt/MAPK signaling after liver I/R. In addition, we evaluated the optimal dose and time of administration of a small molecule selectin inhibitor, TBC-1269. Mice subjected to 90 min of partial (70-80%) hepatic ischemia followed by 3 h of reperfusion were divided into 15 groups (n = 4/group); sham, ischemic control, and 10, 20, and 40 mg/kg dose groups for the antiselectin molecule were studied at 3 times of drug administration: 1 h before reperfusion (but after ischemia), at the time of reperfusion, and at 15 min after reperfusion. The parameters measured after 3 h of reperfusion included liver function tests (ALT and AST), histopathology, and tissue myeloperoxidase (MPO). Chemokine expression (MIP-1alpha, MIP-1beta, MIP-2 and KC), Akt, MAPK (p44/p42), and RSK expressions were also measured in liver tissue by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis, respectively. It was demonstrated that the small molecule multi-selectin inhibitor (TBC-1269) offered the most significant protection for the ischemic liver when given at 40 mg/kg at the time ofreperfusion. AST significantly differed between the control group and the group receiving 40 mg/kg at the time of reperfusion (p = .01). MPO levels in the liver tissue of the ischemic controls were significantly increased when compared to the levels of this enzyme in the TBC-1269 group at 40 mg/kg. Histological examination reflected the same results, with a significant difference (p = .02) between these same two groups. The chemokine profile also showed that the same treatment group had a downregulation of MIP-lalpha, MIP-1beta, MIP-2, and KC, as well as a lower expression of Akt, MAPK(p44/42), and RSK when compared to the control group. Thus, we demonstrated that the small molecule selectin inhibitor, TBC-1269, offered significant functional and structural protection of the ischemic liver when given at 40 mg/kg at the time of reperfusion. Lower doses and different times of administration did not show as prominent a drug effect. This selectin inhibition modulated the expression of Akt, MAPK (p44/42), and RSK, as well as MIP-1alpha, MIP-1beta, MIP-2, and KC chemokines. These alterations in cellular signaling and chemokine expression represent potential mechanisms or pathways of inflammatory response in I/R.
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PMID:Selectin inhibition modulates Akt/MAPK signaling and chemokine expression after liver ischemia-reperfusion. 1576 97

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.
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PMID:Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress. 1699 Apr 81

With the present experiment we sought to investigate brain plasticity underlying language recovery in a group of seventeen patients with non-fluent aphasia mainly caused by stroke. Patients were screened along three domains of measures: analysis of linguistic components by the Aachener Aphasie Test, combined mapping of their lesion from CT/MRI scans, and functional measure of the reorganized linguistic processes by means of mapping of slow evoked potentials. The spatial dimension and temporal dynamics of word processing were measured in three tasks, Phonological, Semantic and Orthographic. Compared with the matched control group, patients showed relative inhibition (decreased negativity) of left central regions in perisylvian areas, which were damaged in most subjects. In addition, reorganization of linguistic functions occurred within the left hemisphere both at frontal and posterior sites corresponding to spared brain regions. Correlations between linguistic lateralization in the three tasks and AAT subtests point to functional reorganization of phonological processes over left frontal sites and dysfunctional reorganization of semantic processing over left posterior regions.
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PMID:Language plasticity in aphasics after recovery: evidence from slow evoked potentials. 1825 72

The present study was attempted to assess the prophylactic and the therapeutic effect of human recombinant activated protein C (APC; drotrecogin-alpha, activated) in experimental heat stroke. Anesthetized rats were divided into two groups and given vehicle solution 1 h before the start or immediately after the termination of heat stress (isotonic sodium chloride solution, 2 mL kg(-1) of body weight, i.v.) or APC (1-10 mg in 2 mL of isotonic sodium chloride solution per kilogram of body weight, i.v.). They were exposed to ambient temperature of 40 degrees C for 100 min to induce heat stroke. When the vehicle-pretreated rats underwent heat stress, their survival time values were found to be 57 to 71 min. Pretreatment or treatment with APC significantly increased survival time (122-221 min). All vehicle-pretreated heat stroke animals displayed systemic inflammation (evidenced by increased TNF-alpha, IL-1alpha, and IL-6) and activated coagulation (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer and decreased levels of both platelet count and protein C). Biochemical assay also revealed that both renal and hepatic dysfunction (e.g., increased plasma levels of blood urea nitrogen, creatinine, adenine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) were noted during heat stroke. A significant decrease in both cerebral blood flow and partial pressure of oxygen in hypothalamus were also observed in vehicle-pretreated heat stroke animals. These heat stroke reactions were all significantly reduced by pretreatment or treatment with human recombinant APC. The results indicate that human recombinant APC can be used as a prophylactic and a therapeutic agent for experimental heat stroke by ameliorating systemic inflammation, hypercoagulable state, and multiple organ dysfunction.
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PMID:Activated protein C can be used as a prophylactic as well as a therapeutic agent for heat stroke in rodents. 1929 93

In a retrospective study, acute renal failure (ARF) was found in 10 (3.3%) among 304 hospitalized adults with dengue hemorrhagic fever (DHF), and 6 (60%) of the 10 patients with ARF died, whereas all 294 patients without ARF (controls) survived (P < 0.001). Compared with the controls, DHF patients with ARF were found to be significantly older (P = 0.002) and male predominant (P < 0.001) and to have higher frequency of previous stroke (P = 0.005), chronic renal insufficiency (P = 0.046), dengue shock syndrome (DSS; P < 0.001), gastrointestinal bleeding (P < 0.001), and concurrent bacteremia (P = 0.009), lower hemoglobin (P = 0.003) and serum albumin levels (P = 0.003), and higher incidences of prolonged prothrombin time (P < 0.001), elevated aspartate aminotransferase (P < 0.001), and alanine aminotransferase levels (P < 0.001). Multivariate analysis showed DSS (odd ratio = 220.0; P < 0.001) was an independent risk factor for development of ARF in DHF patients. The high fatality rate in DHF patients complicated with ARF in our series underscore the importance of clinicians' alertness to this potentially fatal complication so that initiation of timely appropriate treatment is possible.
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PMID:Clinical characteristics, risk factors, and outcomes in adults experiencing dengue hemorrhagic fever complicated with acute renal failure. 1934 94

Neurospecific enolase (NSE), gliofibrillar acid protein (GFAP), S100 protein and autoantibodies (AAB) to these proteins have been measured in the blood of 42 patients with acute ischemic stroke. Concentrations of all parameters we re increased in patients compared to the control group. There were a positive correlations between contents of AAB to GFAP and AAB to NSE (r = 0.470; p < 0.015) and a reverse correlation between concentrations of NSE and AAT to NSE (r = -0.301; p < 0.028). A study of the relationship between intensity of neurological deficit and AAB concentrations revealed the reverse correlation between the level of AAB to GFAP and scores on the European Stroke scale (ESS) (r = -0.509; p < 0.009) at the first day of ischemic stroke, i.e. in patients with marked neurological deficit (low scores on ESS) the levels of AAB to GFAP were higher. The higher concentration of AAB to NSE was found for the satisfactory rehabilitation, while the neurological deficit was significantly more severe (p = 0.034) at the AAT to NSE level less than 1.19 relative units. The more complete rehabilitation to the 21st day was reverse-correlated to the NSE concentration (r = -0.309; p < 0.026). There was the positive correlation between the restoration of lost functions (the increase of ESS scores from the 1st to 21st days) and levels of AAB to GFAP (r = 0.505; p < 0.023) and AAB to S100 (r = 0.450; p < 0.046).
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PMID:[Neurospecific proteins and autoantibodies in serum of patients with acute ischemic stroke]. 1989 4

Our purpose was to use multiple inflow pulsed ASL to investigate whether hemodynamic AAT information is sensitive to hemispheric asymmetry in acute ischemia. The cohorts included 15 patients with acute minor stroke or TIA and 15 age-matched controls. Patients were scanned by using a stroke MR imaging protocol at a median time of 74 hours. DWI lesion volumes were small and functional impairment was low; however, perfusion abnormalities were evident. Prolonged AAT values were more likely to reside in the affected hemisphere (significant when compared with controls, P < .048). An advantage of this ASL technique is the ability to use AAT information in addition to CBF to characterize ischemia.
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PMID:Multiple inflow pulsed arterial spin-labeling reveals delays in the arterial arrival time in minor stroke and transient ischemic attack. 2011 Mar 75


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