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)

In acute-phase response, the use of amino acids is redirected to supporting the synthesis of proteins for host defence and tissue repair. Fibrinogen is one of these proteins, and its plasma levels commonly increase in acute-phase conditions. After hepatectomy, this pattern may be modified by the variable impact of postoperative liver dysfunction. Our study was performed to specifically assess and quantify this aspect. Data were collected prospectively on 82 hepatectomized patients; 62 recovered normally, 20 had major complications (most commonly sepsis). Plasma fibrinogen and a large series of complementary variables were determined preoperatively and at postoperative days 1, 3 and 7 in all patients and until recovery, or death in those with complications. Multiple regression analysis showed that postoperative changes in fibrinogen (deltaFIB, micromol/l) were simultaneously related to the number of resected liver segments (NSEG), total bilirubin (BIL, micromol/l), aspartate aminotransferase (AST, U/l, n.v. 5-45), albumin (ALB, g/l), prothrombin activity (PA, % of standard reference), age (AGE, years) and basal preoperative fibrinogen (PFIB, micromol/l): deltaFIB = -0.51(NSEG) - 0.71(Log(n)BIL) - 0.74(Log(n)AST) + 0.11(ALB) + 0.09(PA) - 0.06(AGE) - 0.55(PFIB) + 7.74 (n=362, r2=0.68, p<0.001). In addition, an early postoperative tendency for low fibrinogen was associated with the subsequent development of complications or death. Our study quantifies the impact of size of hepatectomy and dysfunction of residual liver in modulating postoperative fibrinogen level and suggests that failure of fibrinogen to increase may signal an unfavorable condition limiting up-regulation of acute-phase response and increasing liability to complications.
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PMID:Modulation of plasma fibrinogen levels in acute-phase response after hepatectomy. 1508 May 57

In this study, we evaluated the effect of prostaglandin E2 (PGE2) on renal and hepatic function using an experimental cirrhosis model plus acute liver damage (ALD). Male Wistar rats treated with carbon tetrachloride (CCl4) for 8 weeks were used for the cirrhosis model. Cirrhotic rats were further exposed to an additional acute dose of CCl4 to induce ALD and then treated with PGE2 intramuscularly twice a day for 7 days (200 microg/Kg/day). PGE2 administration started 3 h after the additional dosing of CCl4 and PGE2 effect on hepatorenal function was examined on days 1, 2, 3, and 7. PGE2-treatment ameliorated the decrease in urinary sodium excretion, and normalized serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and plasma renin observed in cirrhotic rats with ALD. In addition, PGE2-treatment decreased mean arterial pressure, glomerular hypercellularity and thickening of the kidney capillary wall, and liver steatosis and cellular necrosis. Also, PGE2 increased the number of regenerative nodules. Finally, PGE2-treatment inhibited the increase in Alpha 1-acid glycoprotein (pAGP), fibrinogen, and Apo A-1 mRNA expression by 83%, 59%, and 77%, respectively. These results suggest that PGE2 administration may decrease the expression of acute phase proteins. In conclusion, PGE2-treatment improved hepatic and renal function and may be useful to down-regulate the acute phase response in cirrhotic rats presenting ALD induced by CCl4.
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PMID:PGE2 alleviates kidney and liver damage, decreases plasma renin activity and acute phase response in cirrhotic rats with acute liver damage. 1581 58

In the present study, Nigella unguicularis (Lam.) Spenner (Ranunculaceae) (Nu) fixed oil was administered orally to Wistar Kyoto rats for 4 weeks. The effects of the oil on serum lipid profile, haematological parameters and oxidant/antioxidant balance were investigated. The study showed that daily administration of the oil (1 ml/kg orally for 4 weeks) caused a significant decrease in serum total cholesterol, VLDL-cholesterol, triglycerides, glucose levels and a significant elevation of serum high-density lipoprotein level. The serum transaminases ( aspartate transaminase (AST), alanine transaminase (ALT)), alkaline phosphatase, bilirubin, blood urea nitrogen, urea, mean corpuscular haemoglobin concentration decreased significantly while albumin, mean corpuscular volume and fibrinogen levels increased significantly compared to control values. The administration of the oil (1 ml/kg orally for 4 weeks) caused a significant increase total antioxidant status in rats. Treatment with Nigella unguicularis oil did not effect malondialdehyde (MDA) concentrations. It is concluded that Nigella unguicularis oil possesses favourable metabolic effects on blood biochemistry and oxidant/antioxidant balance in rats.
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PMID:Effects of Nigella unguicularis fixed oil on blood biochemistry and oxidant/antioxidant balance in rats. 1584 32

It is possible that women with triplet pregnancies are more likely to exhibit pregnancy-induced antithrombin deficiency, gestational thrombocytopenia, and perinatal elevation in serum aspartate aminotransferase (AST) than women with twin pregnancies. We retrospectively reviewed changes in antithrombin activity, platelet count, and blood chemistry in 23 twin and seven triplet pregnancies in which the mothers received antenatal care and gave birth in our hospital during 1999 and 2001. Both antithrombin activity and platelet counts gradually decreased until delivery, then promptly increased after delivery in both twin and triplet pregnancies. A significantly larger number of women developed gestational thrombocytopenia of < 100 x 10 (9)/L (43% [three of seven] versus 4.3% [one of 23]; p < 0.01) and pregnancy-induced antithrombin deficiency of < 60% of normal activity (57% [four of seven] versus 17% [four of 23]; p < 0.05) in triplet than in twin pregnancies. Eight women with pregnancy-induced antithrombin deficiency, including three women with gestational thrombocytopenia, were significantly more likely to develop perinatal elevations of AST, lactate dehydrogenase, serum creatinine, fibrin/fibrinogen degradation products, and D-dimer than were those without pregnancy-induced antithrombin deficiency. These findings suggest that women with triplet pregnancies are at an increased risk of the HELLP syndrome and acute fatty liver of pregnancy compared with women with twin pregnancies.
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PMID:Changes in antithrombin activity and platelet counts in the late stage of twin and triplet pregnancies. 1605 99

There are few extensive studies about clinicopathological findings of spontaneous canine babesiosis caused by a large form of the parasite found in Europe. To further characterize and describe clinicopathological findings in dogs affected with this large form of Babesia in northeastern Italy, we evaluated 23 Italian dogs with canine babesiosis by means of clinical history, physical examination, hematological, biochemical, hemostatic tests, serum electrophoresis and urinalysis. Seventeen dogs (74%) had recently traveled on a hunting trip (within 5-15 days of being presented to the clinic) to Bosnia and Herzegovina (n=7), to Croatia (n=8) and to Hungary (n=2). The duration of clinical signs ranged from 1 to 5 days prior to the arrival at the clinic. The main clinical signs were dehydration (100%), apathy (74%), anorexia or decrease appetite (70%) and fever (68%). The anemia was present in 74% of the dogs and classified as mild (35%), moderate (59%) and severe (6%). In all cases, the anemia was normocytic and normochromic. Only three dogs presented erythrocyte regeneration. Seventy percent of dogs had hemolytic anemia and 30% had non-hemolytic anemia. Sixty-nine percent of dogs showed leucopenia and 74% neutropenia. Leucocitosis, due to mature neutrophilia and lymphocytosis, was present in one dog. Activated lymphocytes were noted in 61% of dogs. In all dogs, thrombocytopenia and an elevated hyperfibrinogenemia were present. Significant prolonged activated partial thromboplastin time (aPTT) was only found in one case. In four dogs, both plasma fibrinogen/fibrin degradation products (FDPs) and D-Dimer were increased. Antithrombin (AT) was slightly decreased in 11 of the 23 dogs. In the majority of cases, mild elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), creatinekinase (CK), total bilirubin and lactic acid and decrease of total iron and total iron binding capacity (TIBC) were present. In conclusion, the main clinicopathological findings were a mild to severe thrombocytopenia, a mild to moderate hemolytic anemia, neutropenia and hyperfibrinogenemia.
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PMID:Clinicopathological findings in naturally occurring cases of babesiosis caused by large form Babesia from dogs of northeastern Italy. 1611 10

Total plasma exchange (TPE) corrects coagulopathy in patients with liver disease and removes hepatotoxins/cytokines. This improvement is transient but can be used as a bridge until an organ is identified for liver transplantation (LTx) or the liver itself regenerates. Our aim was to retrospectively assess the efficacy of TPE in fulminant hepatic failure (FHF) and its impact on liver function tests. Between 1995-2001, 39 patients with FHF who had undergone TPE were reviewed. FHF was defined according to the O'Grady criteria based on the duration of encephalopathy as well as jaundice. TPE was performed using the Cobe Spectra TPE (Gambro) in Liver Intensive Care Unit, continued on a daily basis, until either adequate clinical response was achieved, the patient expired, or transplantation occurred. INR, PTT, Fibrinogen, ALT, AST, GGT, BUN, Ammonia, and Total Bilirubin were analyzed before and after TPE. Student's t-test and chi-square test and ANOVA were used for statistical analysis. Thirty-nine patients with FHF (31 females, 8 males with mean age of 32.3, range: 7-64) underwent TPE. Coagulopathy, hyperbilirubinemia, hyperammonemia were significantly improved (P < 0.05). Twenty-one patients survived (54%), 12 required LTx, and 18 patients (including one after LTx) expired. TPE was found to be significantly effective for correction of coagulopathy and improvement of liver tests. This intervention can be considered for temporary liver support until recovery or liver transplantation.
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PMID:The effect of total plasma exchange on fulminant hepatic failure. 1614 21

In vivo protective effects of s-allyl cysteine (SAC) and s-propyl cysteine (SPC) against acetaminophen-induced hepatotoxicity in Balb/cA mice were studied. SAC and SPC at 1g/L were added into drinking water for four weeks and followed by acetaminophen treatment. Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). SAC or SPC intake alleviated AT-III and protein C reduction (P < 0.05); but did not affect PAI-1 activity and plasma fibrinogen level (P > 0.05). These data suggest that SAC and SPC are potential multiple-protective agents against acetaminophen-induced hepatotoxicity.
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PMID:Protective effect of s-allyl cysteine and s-propyl cysteine on acetaminophen-induced hepatotoxicity in mice. 1618 16

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear transcription factor that comprises the primary molecular target for thiazolidinedione (TZD) insulin-sensitizing drugs. Whilst expressed in many tissues in humans, its abundant expression in adipose tissue is believed to be the focal point through which TZDs regulate genes involved in glucose and lipid metabolism and via which these agents ultimately improve the hyperglycemia of type 2 diabetes. However, TZDs exhibit many additional properties, not least an array of effects which suggest a broad attack on the inflammatory process. Thus, TZDs have been shown to reduce plasma levels of the chemokine, monocyte chemotactic protein-1 (MCP-1), the anti-fibrinolytic protein, plasminogen activator inhibitor-1 (PAI-1), the endothelial cell adhesion molecules, e-selectin and inter-cellular adhesion molecule-1 (ICAM-1), the leucocyte-activating molecule, CD40L, and the tissue-remodeling enzyme, matrix metalloproteinase-9 (MMP-9). Further tangible evidence of a reduction by TZDs of systemic inflammation in patients with the classical metabolic syndrome stems from falls in the white blood cell count, P-selectin-positive platelets and in the acute-phase inflammatory proteins, C-reactive protein, serum amyloid A and fibrinogen. At the tissue level, TZDs improve vascular endothelial function, and reduce the rate of progression of intimal-medial thickening of the carotid artery and the microalbuminuria of type 2 diabetes. Further, TZDs have been shown to be efficacious in inflammatory diseases as wide-ranging as psoriasis, ulcerative colitis and non-alcoholic steatohepatitis (NASH). In the case of the latter, a broad spectrum of TZD-related properties is visible. Here, these drugs improve insulin sensitivity for glucose metabolism, reduce hyperinsulinemia, hepatic steatosis, inflammation and fibrosis, and lower the circulating levels of liver transaminases (ALT, AST), alkaline phosphatase and gamma glutamyl transferase. These effects in humans are also well-supported by investigative animal and in vitro studies. The ameliorative effects on liver fibrosis are of particular interest since they suggest that TZDs are able to activate a program of corrective tissue-remodeling. The basis for this action may be partly an ability to inhibit matrix protein secretion by hepatic stellate cells. An analogous action has also been seen in kidney mesangial cells. In conclusion, TZDs are important new drugs, presently indicated for the treatment of type 2 diabetes but with a spectrum of properties which suggests their potential for treating a number of degenerative inflammatory diseases, including NASH. However, full-scale, long-term clinical trials are needed with TZDs to test their potential to treat NASH, not least because of the (hepatotoxic) legacy of the prototype TZD, troglitazone, but also in view of the escalating burden of liver disease which is accompanying the increasing global prevalence of clinical obesity and type 2 diabetes.
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PMID:Thiazolidinediones: Pleiotropic drugs with potent anti-inflammatory properties for tissue protection. 1619 19

Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a kind of inborn errors of metabolism, with the main clinic manifestations of jaundice, hepatomegaly, and abnormal liver function indices. As a mitochondrial solute carrier protein, citrin plays important roles in aerobic glycolysis, gluconeogenesis, urea cycle, and protein and nucleotide syntheses. Therefore citrin deficiency causes various and complicated metabolic disturbances, such as hypoglycemia, hyperlactic acidemia, hyperammonemia, hypoproteinemia, hyperlipidemia, and galactosemia. This paper reported a case of NICCD confirmed by mutation analysis of SLC25A13, the gene encoding citrin. The baby (male, 6 months old) was referred to the First Affiliated Hospital with the complaint of jaundice of the skin and sclera, which it had suffered from for nearly 6 months. Physical examination showed obvious jaundice and a palpable liver 5 cm below the right subcostal margin. Liver function tests revealed elevated enzymatic activities, like GGT, ALP, AST, and ALT, together with increased levels of TBA, bilirubin (especially conjugated bilirubin), and decreased levels of total protein/albumin and fibrinogen. Blood levels of ammonia, lactate, cholesterol, and triglyceride were also increased, and in particular, the serum AFP level reached 319,225.70 microg/L, a extremely elevated value that has rarely been found in practice before. Tandem mass analysis of a dried blood sample revealed increased levels of free fatty acids and tyrosine, methionine, citrulline, and threonine as well. UP-GC-MS analysis of the urine sample showed elevated galactose and galactitol. The baby was thus diagnosed with suspected NICCD based on the findings. It was then treated with oral arginine and multiple vitamins (including fat-soluble vitamins A, D, E, and K), and was fed with lactose-free and medium-chain fatty acids enriched formula instead of breast feeding. After half a month of treatment, the jaundice disappeared, and the laboratory findings, including liver function indices, blood levels of ammonia, lactate and AFP, were returned to normal level. The baby was followed up for 6 months. It developed well, and the abnormal laboratory findings, including MS-MS and UP-GC-MS analysis results, have been corrected, except a slightly elevated lactate level sometimes. SLC25A13 gene mutation analysis for the patient revealed a compound heterozygote of mutation 851del4 and 1638ins23 and therefore NICCD was definitely diagnosed.
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PMID:[A difficult and complicated case study: neonatal intrahepatic cholestasis caused by citrin deficiency]. 1661 6

This study was conducted to evaluate some anticoagulants' (protein C, protein S and antithrombin) activities among epileptic children treated with VPA and to learn if thromboembolic events occur among these children or their parents. Twenty-five boys and 15 girls using VPA for at least 3 months were included in the VPA group. The control group consisted of 28 boys and 12 girls who had no infection and did not use any medication that could alter protein C activity. Complete blood counts, ALT, AST, PT, aPTT, fibrinogen, protein C, protein S and AT tests were studied in both groups. Serum VPA levels were determined in the VPA group. Protein C and protein S activities of the children in the VPA group were significantly lower than those in the control group (89.5+/-19.3% vs 104.9+/-21.7% and 44.6+/-16.3% vs 59.4+/-28.4%, respectively). Neither children using VPA, nor their parents had any thromboembolic events in medical history. Platelet counts, ALT and fibrinogen levels in the VPA group were significantly lower than those in the controls. A negative correlation was found between serum VPA level and platelet counts. There were also negative correlations between fibrinogen and serum VPA levels, and between fibrinogen level and protein S activity. The children in the VPA group had lower PT and higher aPTT levels than the children in the control group. Since other factors known to alter the anticoagulant activities and liver functions were eliminated initially, the decreases of protein C and protein S activities, thrombocyte counts, ALT, PT and fibrinogen levels and increase in aPTT level may be attributed to VPA. VPA hepatotoxicity can be the cause of decreased pro- and anticoagulant activities.
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PMID:Protein C, protein S and other pro- and anticoagulant activities among epileptic children using sodium valproate. 1684 52


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