Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Extensive data collected over the past decade demonstrate clearly that disease-active and disease-inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease-active and disease-inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline phosphatase, beta-glucuronidase, prostaglandin-E2, aspartate aminotransferase, and IgG4 antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on beta-glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with early-onset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE2 and Interleukin-1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site-specific disease activity. However, the capacity of an individual to mount an IgG2 subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility.
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PMID:Host response tests for diagnosing periodontal diseases. 157 49

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1 alpha, IL-1 beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1 beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.
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PMID:Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 173 70

The effect of prostaglandins (PG) in patients with fulminant and subfulminant viral hepatitis was studied. Seventeen patients presented with FHF secondary to hepatitis A (N = 3), hepatitis B (N = 6) and non-A, non-B (NANB) hepatitis (N = 8). Fourteen of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation, the mean AST was 1844 +/- 1246 units/liter, bilirubin 232 +/- 135 mumol/liter, PT 34 +/- 18 and PTT 73 +/- 26 sec, and coagulation factors V and VII were 8 +/- 4 and 9 +/- 51%, respectively. Twelve of 17 patients responded to PGE1 rapidly, with a decrease in AST from 1540 +/- 833 to 188 +/- 324 units/liter, a decrease in prothrombin time from 27 +/- 7 sec to 12 +/- 1 sec, PTT from 61 +/- 10 sec to 31 +/- 2 sec, and an increase in factor V from 9 +/- 4% to 69 +/- 18% and factor VII from 11 +/- 5% to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT but improvement was observed upon retreatment. After four weeks of intravenous therapy, oral PGE2 was substituted. Two patients have recovered completely and remain in remission six and 12 months following cessation of therapy. Two additional patients continue in remission after two and six months of PGE2. No relapses have been seen in patients with hepatitis A virus (HAV) or hepatitis B virus (HBV) infection. Liver biopsies in the 12 surviving patients have returned to normal. These results suggest efficacy of PGE for FHF. Further investigation is warranted.
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PMID:Treatment of fulminant viral hepatic failure with prostaglandin E. A preliminary report. 190 42

The effect of PG on patients with fulminant and subfulminant viral hepatitis (FHF) was studied. 17 patients presented with FHF secondary to hepatitis A (n = 3), hepatitis B (n = 6), and non-A, non-B (NANB) hepatitis (n = 8). 14 of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation the mean aspartate transaminase (AST) was 1,844 +/- 1,246 U/liter, bilirubin 232 +/- 135 mumol/liter, prothrombin time (PT) 34 +/- 18, partial thromboplastin time (PTT) 73 +/- 26 s, and coagulation Factors V and VII 8 +/- 4 and 9 +/- 5%, respectively. Intravenous PGE1 was initiated 24-48 h later after a rise in AST (2,195 +/- 1,810), bilirubin (341 +/- 148), PT (36 +/- 15), and PTT (75 +/- 18). 12 of 17 responded rapidly with a decrease in AST from 1,540 +/- 833 to 188 +/- 324 U/liter. Improvement in hepatic synthetic function was indicated by a decrease in PT from 27 +/- 7 to 12 +/- 1 s and PTT from 61 +/- 10 to 31 +/- 2 s, and an increase in Factor V from 9 +/- 4 to 69 +/- 18% and Factor VII from 11 +/- 5 to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT, and improvement was observed upon retreatment. After 4 wk of intravenous therapy oral PGE2 was substituted. Two patients with NANB hepatitis recovered completely and remained in remission 6 and 12 mo after cessation of therapy. Two additional patients continued in remission after 2 and 6 mo of PGE2. No relapses were seen in the patients with hepatitis A virus and hepatitis B virus infection. Liver biopsies in all 12 surviving patients returned to normal. In the five nonresponders an improvement in hepatic function was indicated by a fall in AST (3,767 +/- 2,611 to 2,142 +/- 2,040 U/liter), PT (52 +/- 25 to 33 +/- 18 s), and PTT (103 +/- 29 to 77 +/- 44 s), but all deteriorated and died of cerebral edema (n = 3) or underwent liver transplantation (n = 2). These results suggest efficacy of PGE for FHF, and further investigation is warranted.
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PMID:Biochemical and clinical response of fulminant viral hepatitis to administration of prostaglandin E. A preliminary report. 279 44

Ergot alkaloids possess some properties potentially beneficial in ischemia of organs. Therefore the effect of pretreatment by nicergoline and bromocriptine was established in ischemia-reperfusion injury of rat liver. PGE2 and verapamil were used as comparative agents. Hepatic ischemia (60 min) of anesthetized rats was induced by clamping of vessels supplying the median and left lateral lobe. Tested drugs were given i.v. 2 or 5 min prior to inducing ischemia. ALT and AST activities in serum two hours after the end of ischemia were used as markers of hepatocellular injury. Only PGE2 (0.1 mg.kg-1) pretreatment minimized the postischemic rise of both ALT and AST activities. Pretreatment with various doses of nicergoline (1 or 4 mg.kg-1), bromocriptine (1 or 4 mg.kg-1) and verapamil (0.9 or 4.5 mg.kg-1) did not influence significantly serum transaminases activities after ischemia. Bromocriptine (4 mg.kg-1) given together with PGE2 did not improve a protective effect against ischemia achieved by the administration of PGE2 (0.1 microgram.kg-1).
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PMID:The effect of pretreatment with prostaglandin E2 (PGE2), verapamil, nicergoline and bromocriptine on ischemia-reperfusion injury of rat liver in vivo. 776 87

The present study was undertaken to evaluate the cytoprotective activity in the gastric mucosa of rats subjected to CCl4-induced liver injury. Response of gastric mucosa to absolute ethanol insult or acid (pylorus ligation) after CCl4 challenge was analyzed. Intraperitoneal administration of CCl4 increased plasma AST and ALT, but liver protein and glycogen levels were decreased; in addition, gastric acid secretion was significantly increased with respect to control animals (1541 +/- 266 vs. 629 +/- 25 mu eq H+; p < 0.001). Microscopical gastric erosions were observed in 3/10 animals after CCl4 challenge. Pylorus-ligated as well as CCl4-challenged rats developed increased susceptibility to gastric lesions, compared to control (lesion indices: 4.6 +/- 0.20 vs 2.8 +/- 0.13; p < 0.05), while showing increased resistance to absolute ethanol-induced gastric damage (30.4 +/- 11.2 vs 89.7 +/- 9.7 mm, p < 0.01). PGE2 levels in the gastric mucosa were not influenced by exposure to CCl4. Ultrastructural studies revealed the presence of continuous ethanol-resistant and apparently more adherent layer of mucus in CCl4-challenged animals. Morphological evaluation revealed an increase in Alcian blue-stained mucus. A dual condition of enhanced sensitivity to HCl with increased tolerance to ethanol was observed in gastric mucosa of CCl4-treated animals. These observations could be explained by the amount and/or composition of protective mucus layer in the gastric mucosa.
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PMID:Cytoprotective activity in the gastric mucosa of rats exposed to carbon tetrachloride-induced liver injury. 934 46

Medium osmolarity sensitively regulates Kupffer cell functions like phagocytosis and prostaglandin (PG) and cytokine production. Betaine and taurine, recently identified as osmolytes in liver cells, interfere with these effects. Because Kupffer cell activation is an important pathogenic mechanism in ischemia-reoxygenation injury, the influence of osmolarity and osmolytes was investigated in a rat liver perfusion model of warm ischemia. Livers were perfused with different medium osmolarities for 60 to 90 minutes in the absence of oxygen, followed by another 90 minutes of reoxygenation. Lactate dehydrogenase (LDH) leakage into the effluent perfusate during the hypoxic and the reoxygenation period was eight- to 10-fold higher with a medium osmolarity of 385 mosmol/L than in normo-osmolarity, and further decreased with hypo-osmolar perfusion buffer. Betaine and taurine addition to the perfusate in near physiological concentrations decreased hypoxia-reoxygenation-induced LDH leakage, aspartate transaminase (AST) leakage, and perfusion pressure increase in hyperosmolar and normo-osmolar perfusions. Stimulation of PGD2, PGE2, thromboxane B2 (TXB2), and tumor necrosis factor alpha (TNF-alpha) release, as well as induction of carbon uptake by the liver during reoxygenation, were suppressed by betaine and taurine, pointing to an interference of these osmolytes with Kupffer cell function. In contrast, endothelial cell function as assessed by hyaluronic acid (HA) uptake was not influenced. It is concluded that warm ischemia-reoxygenation injury in rat liver is aggravated by hyperosmolarity and attenuated by hypo-osmolarity. The osmolytes betaine and taurine have a protective effect, presumably by inhibition of Kupffer cell activation.
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PMID:Cytoprotection by the osmolytes betaine and taurine in ischemia-reoxygenation injury in the perfused rat liver. 939 98

To study the role of Kupffer cells in the aggravation of liver injury, effects of zymosan on acute liver damage were explored using perfused livers of rats 24 h after intraperitoneal injection of D-galactosamine (800 mg/kg). The leakage of lactate dehydrogenase and aspartate aminotransferase into the effluent was used to indicate acute liver damage. Infusion of zymosan (30 microgram/ml) into the portal vein rapidly increased the leakage of lactate dehydrogenase and aspartate aminotransferase from galactosamine-treated liver with decreased perfusion flow. Pretreatment of animals with gadolinium, which diminished an immunostaining of resident macrophages in the injured liver, significantly attenuated the flow reduction induced by zymosan, whereas it did not affect the increases in enzyme leakage. Infusions of PGF2alpha, PGE2, and leukotriene D4, the eicosanoids mainly produced by Kupffer cells, decreased perfusion flow without rapid augmentation of enzyme leakage from galactosamine-treated liver. These results indicate that zymosan potentiates acute liver damage after galactosamine injection and suggest that certain types of nonparenchymal cells other than Kupffer cells are mainly involved in the action of zymosan.
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PMID:Aggravating action of zymosan on acute liver damage in perfused liver of rats treated with D-galactosamine. 984 73

The dried fruits of Crataegus pinnatifida, a local soft drink material and medical herb, demonstrated antioxidant effect in a previous study. The present study investigates the anti-inflammatory potential of flavonoid contents from dried fruit of C. pinnatifida (CF-Fs). The preliminary investigation showed that CF-Fs (0.25-0.75 mg/mL) decreased the release of PGE2 and nitric oxide as induced by lipopolysaccharide (LPS, an endotoxin) in macrophage RAW 264.7 cells. The in vivo assay showed that pretreatment of rats with CF-Fs (50-200 mg/kg dosed by gavage) for 5 days significantly decreased the serum levels of the hepatic enzyme markers alanine aminotransferase and aspartate aminotransferase induced by the 6-h treatment with LPS (i.p.; 5 mg/kg). Histopathological evaluation of the rat livers revealed that CF-Fs reduced the incidence of liver lesions such as neutrophil infiltration and necrosis induced by LPS. Furthermore, it was found that pretreatment with CF-Fs decreased the hepatic expression of iNOS and COX-2 induced by LPS in rats. These results demonstrate that CF-Fs present anti-inflammatory potential in vitro and in vivo and that they may play a role in hepatoprotection.
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PMID:Anti-inflammatory potential of flavonoid contents from dried fruit of Crataegus pinnatifida in vitro and in vivo. 1565 84

Prostaglandin E(2) (PGE(2)) mediates a variety of both innate and adaptive immunity responses through 4 distinct receptors, EP1-4. Recent studies have suggested the physiological and pathological role of EP4 in various inflammatory diseases. In this study, we investigated the importance of the EP4 receptor, and the efficacy of a selective EP4 agonist to alter hepatic ischemia/reperfusion (I/R) injury, an important cause of damage in liver resection and transplantation. We used an established murine I/R injury model, 70% partial hepatic ischemia for 90 minutes in male C57BL/6 mice. The local expression of EP4 messenger RNA (mRNA) in the naive and the ischemic liver at 2 hours after reperfusion was examined using RT-PCR analysis. Some mice received the EP4 selective agonist during I/R. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured as markers of hepatic injury. EP4 expression in the liver was significantly up-regulated at 2 hours after reperfusion. Furthermore, treatment with EP4 agonist significantly inhibited hepatic injury at 6 hours after reperfusion. Our data suggest an inhibitory role of EP4 PGE(2) receptor in hepatic I/R injury and the therapeutic efficacy of a selective EP4 agonist for liver protection.
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PMID:Role of EP4 prostaglandin E2 receptor in the ischemic liver. 1580 64


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