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At least 973 records · Page 54Linked to original sources
PubMed1989

Partial purification, and some properties and reactivities of cetraxate benzyl ester hydrochloride-hydrolyzing enzyme.

Debenzylating enzyme from Aspergillus niger enzyme (commercial crude cellulase) catalyzes the hydrolysis of cetraxate benzyl ester hydrochloride (2), a precursor of the antiulcer agent (1). The enzyme was highly purified by three kinds of chromatographies (hydrophobic, ion exchange, gel filtration) with a recovery of 36%. The content of the debenzylating enzyme was about 0.1% in the crude cellulase, but the enzyme showed no cellulase activity. The purified enzyme was inactivated by Hg2+, and diisopropyl phosphorofluoridate (DFP). It was a monomer with a molecular weight of about 35,000, and its isoelectric point was estimated to be 5.3. It showed a debenzylating activity for the phenylpropionic acid benzyl ester moiety of various benzyl ester derivatives, and the benzyl ester of phenylalanine or that of tyrosine was also well hydrolyzed.

Aspergillus niger↗
PubMedDate not supplied

[Effect of cicloxilic acid on biliary dynamics].

This work was developed in order to estimate, with objective methods, the pharmacodynamic activities of a new choleretic and antilithogenic drug, the cicloxilic acid. It was determined the changes of daily biliary flow and bile composition in 8 patients with biliary system surgical intervention and "T" (Kehr) tube inserted. The cicloxilic acid was given in the dose of 240 mg/day. The results showed, after treatment, an emphasized middle volume increase of the excreted bile, as well as a significant decrease of the biliary cholesterol, while pH and density maintained constants. The results corroborated the pharmacodynamic activities given to cicloxilic acid as a "true" choleretic to be utilized in clinic situations where it's wished a biliary flow increase and the possibility to avoid a cholesterol lithiasis or relieve consequent disturbances.

Aged↗
PubMed1998

A summary of mechanistic hypotheses of gabapentin pharmacology.

Although the cellular mechanisms of pharmacological actions of gabapentin (Neurontin) remain incompletely described, several hypotheses have been proposed. It is possible that different mechanisms account for anticonvulsant, antinociceptive, anxiolytic and neuroprotective activity in animal models. Gabapentin is an amino acid, with a mechanism that differs from those of other anticonvulsant drugs such as phenytoin, carbamazepine or valproate. Radiotracer studies with [14C]gabapentin suggest that gabapentin is rapidly accessible to brain cell cytosol. Several hypotheses of cellular mechanisms have been proposed to explain the pharmacology of gabapentin: 1. Gabapentin crosses several membrane barriers in the body via a specific amino acid transporter (system L) and competes with leucine, isoleucine, valine and phenylalanine for transport. 2. Gabapentin increases the concentration and probably the rate of synthesis of GABA in brain, which may enhance non-vesicular GABA release during seizures. 3. Gabapentin binds with high affinity to a novel binding site in brain tissues that is associated with an auxiliary subunit of voltage-sensitive Ca2+ channels. Recent electrophysiology results suggest that gabapentin may modulate certain types of Ca2+ current. 4. Gabapentin reduces the release of several monoamine neurotransmitters. 5. Electrophysiology suggests that gabapentin inhibits voltage-activated Na+ channels, but other results contradict these findings. 6. Gabapentin increases serotonin concentrations in human whole blood, which may be relevant to neurobehavioral actions. 7. Gabapentin prevents neuronal death in several models including those designed to mimic amyotrophic lateral sclerosis (ALS). This may occur by inhibition of glutamate synthesis by branched-chain amino acid aminotransferase (BCAA-t).

Acetates↗
PubMed1983

Tranexamic acid for the treatment of advanced ovarian carcinoma.

In the present phase II trial, 26 heavily pretreated patients with advanced recurrent ovarian carcinoma were treated with tranexamic acid, 4-6 g per os daily for at least 3 months. Of these 26 patients, 3 had stage IIb, 21 stage III and 2 stage IV. Histologic examination revealed serous adenocarcinoma in 13, mucinous in 3, endometroid in 4, 1 anaplastic and 5 unspecified adenocancer. Twenty of the tumors were poorly differentiated and 5 highly-moderately differentiated. No objective response was noted but all the highly-moderately differentiated tumors showed a stable disease state with a median duration of 6 months (range 4-36 months). The patients with poorly differentiated tumors had a median survival of 4 months. Most of the patients had some form of gastro-intestinal side effect. This investigation has shown that treatment with tranexamic acid was not particularly helpful in poorly differentiated cases in which modern combined chemotherapy already had failed. The effect in highly-moderately differentiated cases needs further evaluation.

Adenocarcinoma↗
PubMed1986

Adjuvant effects of tranexamic acid to chemotherapy in ovarian cancer patients with large amount of ascites.

Eleven patients with advanced ovarian carcinoma who had large quantities of ascites during the course of previous chemotherapy were tested with intraperitoneal injections of tranexamic acid, followed by combination chemotherapy. A 4-g dose of tranexamic acid was administered intraperitoneally every day for at least 2 weeks. Seven out of 11 patients (63.6%) showed changes from positive to negative in Papanicolaou smears of the ascitic fluid after treatment with tranexamic acid. A marked reduction of ascitic fluids was observed in 4 of 11 patients (36.4%). If 2 cases with partial reduction of ascites are included, the response rate improved to 54.5%. Median survival time after initiation of treatment with tranexamic acid was significantly longer in patients with good response to tranexamic acid than in patients with poor response. Proliferation of cells in cultures established from ovarian cancer tissue of a patient with good response to tranexamic acid was inhibited at all concentrations of tranexamic acid used in this study, in contrast to non-inhibition of similar cells cultured from a patient with poor response, at any concentration of tranexamic acid. These results suggest that treatment with tranexamic acid suppresses malignant cells in the ascites, followed by reduction of ascites themselves, and an improvement in the response rate to subsequent chemotherapy.

Adult↗
PubMed1991

Method for the biological monitoring of hexahydrophthalic anhydride by the determination of hexahydrophthalic acid in urine using gas chromatography and selected-ion monitoring.

A method for the determination of hexahydrophthalic acid, a metabolite of hexahydrophthalic anhydride, in human urine has been developed. The urine was worked-up by liquid-solid extraction, esterified with boron trifluoride-methanol, and analysed by capillary gas chromatography and selected-ion monitoring. Hexadeuterium-labelled hexahydrophthalic acid was used as the internal standard. The precision was 4% at 0.7 microgram/ml and 5% at 0.07 microgram/ml. The recovery of the acid for the overall method was 101% at 0.07 micrograms/ml of urine (with a coefficient of variation of 4%) and 95% at 0.7 microgram/ml (coefficient of variation 2%). The limit of detection was 20 ng/ml urine.

Chromatography, Gas↗
PubMed1978

Secondary haemorrhage following traumatic hyphaema. A comparative study of conservative and tranexamic acid treatment.

Three out of 56 consecutively admitted patients with traumatic hyhaema, treated conservatively, developed secondary haemorrhage. Of the following 64 patients treated with tranexamic acid, none developed secondary haemorrhage. Statistical analysis, using chi2 test with Yate's correction showed no statistical difference with regard to the occurrence of secondary haemorrhage between the two groups.

Adolescent↗
PubMed1989

Short-term tranexamic acid treatment in aneurysmal subarachnoid hemorrhage.

Antifibrinolytic treatment for 4 weeks after a subarachnoid hemorrhage has been shown to have no effect on outcome since a reduction in the rate of rebleeding was offset by an increase in ischemic events. To determine if a shorter course (4 days) of antifibrinolytic treatment before the expected onset of ischemic complications might reduce the rate of rebleeding yet avoid ischemic complications, we prospectively studied a series of 119 patients with subarachnoid hemorrhage; 479 patients with subarachnoid hemorrhage from our previous randomized double-blind study (238 treated with placebo, 241 with long-term tranexamic acid) served as historical control groups. At 3 months' follow-up, the outcome of patients treated with short-term tranexamic acid was not different from that of patients treated with long-term tranexamic acid. The rate of rebleeding (24 of 119, 20%) was near that with placebo (56 of 238, 24%). In contrast, the rate of cerebral infarction (33 of 119, 28%) was almost identical to that after long-term tranexamic acid (59 of 241, 24%), although mortality from cerebral infarction was reduced. Compared with historical control groups, treatment with tranexamic acid for 4 days fails to reduce the incidence of rebleeding but still increases the rate of cerebral infarction.

Cerebral Angiography↗
PubMed1974

Comparative effects of proteinase inhibitors, plasminogen antiactivators, heparin and acetylsalicylic acid on the experimental disseminated intravascular coagulation induced by thormbin.

In an experimental study in the rabbit, the modifications of some haemostasis parameters (platelet count, platelet retention and aggregation, platelet factors 3 and 4, platelet and plasma plasmin inhibiting activities, fibrinogen and other plasma factor levels, FDP), and histological findings are compared in both the normal animal and the animal with disseminated intravascular coagulation (DIC) induced by thrombin perfusion after administration of fibrinolytic inhibitors (plasminogen antiactivators and proteinase inhibitors). In the normal animal, the administration of fibrinolytic inhibitors is followed by haemostatic changes similar to those found in thrombophilic states. The modifications are more pronounced with plasminogen antiactivators than with proteinase inhibitors. In the animal with DIC, the administration of fibrinolytic inhibitors enhances the haemostatic and the biological disorders produced by thrombin perfusion. The effect of the plasminogen antiactivators is even more evident. The preventive administration of heparin reduces or abolishes the biological and histological disorders induced by thrombin; its beneficial effect is considerably reduced when thrombin is combined with fibrinolytic inhibitors. The administration of acetylsalicylic acid appears to be ineffective for the prevention of haemostatic and histological changes induced by thrombin perfusion.

Aminocaproates↗
PubMed1979

Cicloxilic acid and the bile lipids in oral contraceptive users.

Cholesterol supersaturation of gallbladder bile induced by oral contraceptives is significantly reduced by the administration of cis-2-hydroxy-2-phenyl-cyclohexane-carboxilic acid (cicloxilic acid), a choleretic substance which has been demonstrated to exert an antilithogenic effect in the rat and in man.

Adolescent↗
PubMed1978

Enzyme-activated irreversible inhibitors of L-ornithine:2-oxoacid aminotransferase. Demonstration of mechanistic features of the inhibition of ornithine aminotransferase by 4-aminohex-5-ynoic acid and gabaculine and correlation with in vivo activity.

L-Ornithine:2-oxoacid aminotransferase is a specific enzyme with respect to the amino group donor. Nevertheless it was found that this enzyme is inhibited by some 4-aminobutyrate analogs, 4-aminohex-5-ynoic acid and 5-amino-1,3-cyclohexadienyl-carboxylic acid (gabaculine), which are currently considered to be enzyme-activated irreversible inhibitors of 4-aminobutyrate:2-oxoglutarate aminotransferase. The inhibitory mechanisms for the two omega-aminotransferases are identical. A close structural analog of these inhibitors, 4-aminohex-5-enoic acid, is not inhibitory for ornithine aminotransferase, whereas it effectively inhibits 4-aminobutyrate aminotransferase. The reasons for this difference are discussed. The in vitro findings are entirely transferable to the in vivo situation: 4-aminohex-5-ynoic acid and gabaculine cause a long-lasting inhibition of ornithine aminotransferase in brain and liver, and reduce significantly in vivo ornithine degradation, whereas 4-aminohex-5-enoic acid is inactive both in vivo and in vitro toward this enzyme. The enzyme-activated irreversible inhibitors allow one for the first time to study the physiological consequences of irreversible ornithine aminotransferase inhibition.

Aminocaproates↗
PubMed1986

Effects of tranexamic acid on fibrinolysis, fibrinogenolysis and amidolysis.

When Glu-plasminogen (Glu-plg) was activated by urokinase (UK) in the presence of fibrinogen or fibrinogen plus tranexamic acid (1 mM), or else tranexamic acid (1 mM), the activation as measured by the hydrolysis of S-2251 was enhanced by tranexamic acid or fibrinogen or both. When plasma or clotted plasma was activated by UK in the presence of 1 mM tranexamic acid, fibrinolysis was completely inhibited. When Lys-plg was activated by UK in the presence of tranexamic acid and fibrin or fibrinogen, fibrinolysis was completely inhibited by 1 mM tranexamic acid, but some inhibition of fibrinogenolysis was observed. The release of B beta 15-42 from fibrin in clotted plasma activated by UK was inhibited to some extent by 1 mM tranexamic acid. The release of B beta 15-42 from fibrin after UK-activation of Lys-plg was partly inhibited by tranexamic acid. In conclusion, tranexamic acid in the concentration of 1 mM enhanced amidolysis, but inhibted fibrinolysis measured by the generation of fibrin-degradation products. Fibrinogenolysis and the release of B beta 15-42 from fibrin were partly inhibited.

Blood Coagulation↗
PubMed1993

Localization of [3H]gabapentin to a novel site in rat brain: autoradiographic studies.

The autoradiographical distribution of [3H]gabapentin, the tritiated analogue of the novel anticonvulsant gabapentin (1-(aminomethyl)cyclohexaneacetic acid) was measured in rat brain. Binding to sections was uniformly inhibited by non-radioactive gabapentin and 3-isobutyl-gamma-aminobutyric acid (3-isobutyl-GABA). Specific gabapentin binding sites were unevenly distributed throughout the brain with the highest level being found in the outer layers of the cerebral cortex (38 +/- 7 fmol/mm2; n = 3) and the lowest amounts in the white matter. In the hippocampus, the distribution of the binding site paralleled the excitatory neuronal input with the highest levels of binding being measured in the outer layers of the dentate gyrus and in the dendritic regions of the CA1 pyramidal cell layer. The binding site appeared absent from the cell body region of granule and pyramidal cells. Lesions performed unilaterally in the striatum using quinolinic acid resulted in a marked loss of [3H]gabapentin binding sites as compared with sham-lesioned animals, suggesting the binding site was localized on neuronal cell bodies. These data complement and extend the results of experiments using [3H]gabapentin with homogenates of rat brain and show the discrete localization of this novel binding site in regions associated with excitatory amino acid input. The data do not support previous indications of an association of the gabapentin binding site and NMDA/glycine receptor complex.

Acetates↗
PubMed1987

Tranexamic acid as an aid to reducing blood transfusion requirements in gastric and duodenal bleeding.

A prospective randomised double blind study examined the effect of the antifibrinolytic drug tranexamic acid compared with placebo in 154 patients bleeding from verified benign lesions in the stomach or duodenum or both. Three out of 72 patients receiving tranexamic acid underwent emergency surgery compared with 15 out of 82 given placebo (p = 0.010). Nineteen patients receiving placebo rebled during their admission as compared with 10 in the active treatment group (p = 0.097). Blood transfusion requirements were significantly reduced by tranexamic acid (p = 0.018). Side effects occurred in six patients, of which an uncomplicated deep venous thrombosis was the most severe. Tranexamic acid reduces the blood transfusion requirement and need for emergency surgery in patients bleeding from a benign gastric or duodenal lesion.

Adolescent↗
PubMed2001

GABA agonists and gabapentin for spastic hypertonia.

Spasticity is a result of an imbalance between the afferent excitatory and descending inhibitory pathways after central nervous system damage. Its pharmacologic control is believed to result from the antagonism of inhibitory mechanisms (gamma-aminobutyric acid [GABA] or glycine-mediated antagonism of excitatory mechanisms), or both. Because GABA receptor sites are widely present in the central nervous system, it is amenable to pharmacologic manipulation.

Acetates↗
PubMed1996

Periodic limb movements of sleep and the restless legs syndrome.

Periodic limb movements of sleep and the restless legs syndrome are not diagnoses but rather an indication that there is some CNS disturbance and are associated with an ever-growing number of conditions. They are very common, exist in many forms and are often overlooked by physicians. It is the author's opinion that they are parts of what has been called an akathisia syndrome in the most severe situations and may include the same mechanisms that underlie attention disorders, chronic fatigue syndrome and "sun-downing." They are likely parts of a syndrome caused by dysfunction in a complex brainstem center. This center's normal function is to maintain a smooth electrical template on which discrete neuronal impulses sculpture the rich repertoire we recognize as sensory and motor function awake and to effect a smooth "switching" mechanism allowing sleep to occur without motor and sensory input invading consciousness (awakening). While the DA-ergic CNS pathways have been thought to be the primary neurotransmitter involved, the opioids secondary, there is mounting evidence that the situation is far more complicated, that many neurotransmitter, including stimulating and inhibiting amino acids, play a part. These patients agonize with their indisposition but can be helped by various treatments. Treatment alleviates not only the distress caused by the symptoms but also the devastating insomnia and excessive daytime sleepiness associated with it.

Acetates↗