Enzymatic hydrolysis of PTT polymers and oligomers.

Oligomers and polymers (film, fabrics) of the linear aromatic polyester poly(trimethylene terephthalate) (PTT) were treated with polyesterases from Thermomyces lanuginosus, Penicillium citrinum, Thermobifida fusca and Fusarium solani pisi. The cutinase from T. fusca was found to release the highest amounts of hydrolysis products from PTT materials and was able to open and hydrolyse a cyclic PTT dimer according to RP-HPLC-UV detection. In contrast, the lipase from T. lanuginosus also showed activity on the PTT fibres and on bis(3-hydroxypropyl) terephthalate (BHPT) but was not able to hydrolyse the polymer film, mono(3-hydroxypropyl) terephthalate (MHPT) nor the cyclic dimer of PTT. As control enzymes inhibited with mercury chloride were used. Surface hydrophilicity changes were investigated with contact angle measurements and the degree of crystallinity changes were determined with DSC.

Canadian Stroke Best Practice Recommendations for Acute Stroke Management: Prehospital, Emergency Department, and Acute Inpatient Stroke Care, 6th Edition, Update 2018.

The 2018 update of the Canadian Stroke Best Practice Recommendations for Acute Stroke Management, 6th edition, is a comprehensive summary of current evidence-based recommendations, appropriate for use by healthcare providers and system planners caring for persons with very recent symptoms of acute stroke or transient ischemic attack. The recommendations are intended for use by a interdisciplinary team of clinicians across a wide range of settings and highlight key elements involved in prehospital and Emergency Department care, acute treatments for ischemic stroke, and acute inpatient care. The most notable changes included in this 6th edition are the renaming of the module and its integration of the formerly separate modules on prehospital and emergency care and acute inpatient stroke care. The new module, Acute Stroke Management: Prehospital, Emergency Department, and Acute Inpatient Stroke Care is now a single, comprehensive module addressing the most important aspects of acute stroke care delivery. Other notable changes include the removal of two sections related to the emergency management of intracerebral hemorrhage and subarachnoid hemorrhage. These topics are covered in a new, dedicated module, to be released later this year. The most significant recommendation updates are for neuroimaging; the extension of the time window for endovascular thrombectomy treatment out to 24 h; considerations for treating a highly selected group of people with stroke of unknown time of onset; and recommendations for dual antiplatelet therapy for a limited duration after acute minor ischemic stroke and transient ischemic attack. This module also emphasizes the need for increased public and healthcare provider's recognition of the signs of stroke and immediate actions to take; the important expanding role of paramedics and all emergency medical services personnel; arriving at a stroke-enabled Emergency Department without delay; and launching local healthcare institution code stroke protocols. Revisions have also been made to the recommendations for the triage and assessment of risk of recurrent stroke after transient ischemic attack/minor stroke and suggested urgency levels for investigations and initiation of management strategies. The goal of this updated guideline is to optimize stroke care across Canada, by reducing practice variations and reducing the gap between current knowledge and clinical practice.

External validation of a six simple variable model of stroke outcome and verification in hyper-acute stroke.

We aimed to validate a previously described six simple variable (SSV) model that was developed from acute and sub-acute stroke patients in our population that included hyper-acute stroke patients. A Stroke Outcome Study enrolled patients from 2001 to 2002. Functional status was assessed at 6 months using the modified Rankin Scale (mRS). SSV model performance was tested in our cohort. 538 acute ischaemic (87%) and haemorrhagic stroke patients were enrolled, 51% of whom presented to hospital within 6 h of symptom recognition. At 6 months post-stroke, 42% of patients had a good outcome (mRS < or = 2). Stroke patients presenting within 6 h of symptom recognition were significantly older with higher stroke severity. In our Stroke Outcome Study dataset, the SSV model had an area under the curve of 0.792 for 6 month outcomes and performed well for hyper-acute or post-acute stroke, age < or > or = 75 years, haemorrhagic or ischaemic stroke, men or women, moderate and severe stroke, but poorly for mild stroke. This study confirms the external validity of the SSV model in our hospital stroke population. This model can therefore be utilised for stratification in acute and hyper-acute stroke trials.

A case-control study of tissue plasminogen activator for acute ischemic stroke.

BACKGROUND: Randomized trials demonstrate that intravenous tissue plasminogen activator (tPA) improves outcome in acute ischemic stroke (AIS). To assess translation of this efficacy into effectiveness in routine clinical practice we performed a case-control study of tPA treatment for AIS in a single hospital. METHODS: 151 tPA-treated AIS patients (1996-2005) were matched 1:1 with blinding to outcome to controls from a prospective registry based on age, gender, pre-stroke Oxford handicap scale (OHS), stroke severity, and subtype. The outcomes were in-hospital death, symptomatic intracranial hemorrhage (SICH), length-of-stay (LOS), discharge OHS and long-term survival. RESULTS: In-hospital mortality (23% vs. 24%) or long-term survival (median follow-up of 2 years) was not different between cases and controls (p = 0.83). SICH occurred in 7.8% (95% CI 4.2-13.5%) of tPA-treated patients. Median LOS was non-significantly shorter for cases (13 [7-29] vs. 16 [8-32] days, p = 0.14) but significantly shorter in tPA-treated vs. non-treated women (14 [7-28] vs. 20 [11-34] days, p = 0.04). At discharge 6.6% (95% CI 1.1-12.0%) more tPA-treated patients than controls had no disability (OHS < or = 1, p = 0.02). However, there was no difference in discharge independence rates or proportion discharged home. CONCLUSION: We demonstrate minor improvements in early recovery after stroke with tPA but the impact is less dramatic than that reported in randomized trials. This may relate to timing of treatment and the type of patients treated.

Sonochemical substrate selectivity and reaction pathway of systematically substituted azo compounds.

The sonochemical degradation of the systematically substituted azo compound 2,7-dihydroxy-1-phenylazonaphthaline-3,6-disulfonic acid was investigated using a frequency of 850 kHz and an acoustic input power of 61 W. All derivatives were degraded completely within 6h by the ultrasonic treatment. Trifluoromethyl substituted azo compounds exhibited 2-3-fold higher degradation rates in comparison to the reference hydrogen substituted azo compound (k=0.54 h(-1)). In contrast to enzymatic processes (azoreductase or laccase), the ultrasonic treatment for these ortho-, meta-, and para-substituted azo compound showed 1.5-50-fold higher degradation rates. Additionally the ultrasound treatment was characterized by shorter reaction times. As a result of the detection and identification of specific intermediates using LC-MS a reaction pathway of the sonochemical degradation of the analysed azo compound is proposed indicating the formation of cyclohexadienone and naphthalene quinone derivatives.

Influence of redox mediators and metal ions on synthetic acid dye decolourization by crude laccase from Trametes hirsuta.

In this paper, the effect of redox mediators on synthetic acid dye decolourization (Sella Solid Red and Luganil Green) by laccase from Trametes hirsuta cultures has been investigated. All the redox mediators tested, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 1-hydroxybenzotriazole (HBT) and Remazol Brilliant Blue R (RBBR), led to higher activities than those obtained without mediators addition showing the suitability of the laccase/mediator system (LMS) in the decolourization of acid dyes. HBT was by far the most effective mediator, showing a decolourization percentage of 88% in 10 min for Sella Solid Red and of 49% in 20 min for Luganil Green. On the other hand, the stability of laccase against several metal ions, normally found in textile wastewater, was assessed. Laccase was stable at a concentration of 1mM for 7d against all the metal ions tested except for Zn+2, CrO4(-2), Cd+2, Cr2O7(-2), Fe+2, Cu+2 and especially Hg+2. When the concentration was increased to 10mM laccase stability decreased against all the metals assayed, in particular against Fe+2. In addition, the effect of metal ions on the decolourization process was also studied. It was found that Hg+2 inhibited the dye decolourization process, being the presence of HBT absolutely required for dye decolourization.

Central effects of vasopressin and 1-desamino-8-D-arginine vasopressin (DDAVP) on interleukin-1 fever in the rat.

The intracerebroventricular administration of arginine vasopressin suppressed significantly the fever evoked by interleukin-1. This antipyretic action of arginine vasopressin was blocked completely by the antivasopressor analog d(CH2)5Tyr(Me)arginine vasopressin, an antagonist of the V1 subtype of peripheral vasopressin receptor. However, in contrast to AVP, the V2 receptor agonist, 1-desamino-8-D-arginine vasopressin, did not alter the normal time course or magnitude of interleukin-1 fever. These data suggest that arginine vasopressin induced antipyresis is mediated via central receptors which may resemble the V1 subtype of peripheral vasopressin receptor. The V2 subtype of vasopressin receptor is unlikely to be involved since an agonist of this receptor did not exhibit any antipyretic activity against interleukin-1 fever.

Hydrolysis of isolated coffee mannan and coffee extract by mannanases of Sclerotium rolfsii.

Different mannanase preparations obtained from the filamentous fungus Sclerotium rolfsii were used for the hydrolysis of coffee mannan, thus reducing significantly the viscosity of coffee extracts. Mannan is the main polysaccharide component of these extracts and is responsible for their high viscosity, which negatively affects the technological processing of instant coffee. Coffee mannan was isolated from green defatted Arabica beans by delignification, acid wash and subsequent alkali extraction with a yield of 12.8%. Additionally, coffee extract polysaccharides were separated by alcohol precipitation and were found to form nearly half of the coffee extract dry weight. These isolated mannans as well as the mannan in the coffee extract were efficiently hydrolysed by the S. rolfsii mannanase, which resulted in significant viscosity reductions. Concurrently, the reducing sugar content increased continuously due to the release of various mannooligosaccharides including mannotetraose, mannotriose, and mannobiose. Both a partially purified, immobilised and a soluble, crude mannanase preparation were successfully employed for the degradation of coffee mannan.

Indigo degradation with purified laccases from Trametes hirsuta and Sclerotium rolfsii.

The degradation of the textile dye indigo with purified laccases from the fungi Trametes hirsuta (THL1 and THL2) and Sclerotium rolfsii (SRL1) was studied. All laccases were able to oxidize indigo yielding isatin (indole-2,3-dione), which was further decomposed to anthranilic acid (2-aminobenzoic acid). Based on the oxygen consumption rate of the laccases during indigo degradation, a potential mechanism for the oxidation of indigo involving the step-wise abstraction of four electrons from indigo by the enzyme was suggested. Comparing the effect of the known redox-mediators acetosyringone, 1-hydroxybenzotriazole (HOBT) and 4-hydroxybenzenesulfonic acid (PHBS) on laccase-catalyzed degradation of indigo, we found a maximum of about 30% increase in the oxidation rate of indigo with SRL1 and acetosyringone. The particle size of indigo agglomerates after laccase treatment was influenced by the origin of the laccase preparation and by the incubation time. Diameter distributions were found to have one maximum and compared to the indigo particle size distribution of the control, for all laccases, the indigo agglomerates seemed to have shifted to smaller diameters. Bleaching of fabrics by the laccases (based on K/S values) correlated with the release of indigo degradation products.

Esterase and lipase activity in Jatropha curcas L. seeds.

Two new esterases (JEA and JEB) and a lipase (JL) were extracted from the seeds of Jatropha curas L. Lipase activity was only found during germination of the seeds and increased to a maximum after 4 days of germination. All enzymes were found to be most active in the alkaline range at around pH 8 and the purified (fractionated precipitation with ethanol and gel filtration) esterases were very stable at high temperatures. The molecular weight (SDS-PAGE) of both esterases was determined to be 21.6-23.5 kDa (JEA) and 30.2 kDa (JEB) and the isoelectric point was 5.7-6.1 for esterase JEA and 9.0 for esterase JEB. Most ions caused a negative influence on the activity of both esterases. Using p-nitrophenyl butyrate as a substrate JEA showed a K(m) of 0.02 mM and a v(max) of 0.26 micromol mg(-1) min(-1). Under the same conditions JEB showed a K(m) of 0.07 mM and a v(max) of 0.24 micromol mg(-1) min(-1). Both esterases hydrolyzed tributyrin, nitrophenyl esters up to a chain length of =C4 and naphtylesters up to a chain length =C6. In transesterification reactions, JL was found to be most active at very low water activities (0.2) and in high water activities, the lipase hydrolysed triglycerides into conversions above 80%. The lipase hydrolysed both short chain and long chain triglycerides at about the same rate but was inactive on alpha-methylbenzyl acetate. JL is a potentially useful biocatalyst in the hydrolysis of triglycerides in organic solvents.

Thermo-alkali-stable catalases from newly isolated Bacillus sp. for the treatment and recycling of textile bleaching effluents.

Three thermoalkaliphilic bacteria, which were grown at pH 9.3-10 and 60-65 degrees C were isolated out of a textile wastewater drain. The unknown micro-organisms were identified as thermoalkaliphilic Bacillus sp. Growth conditions were studied and catalase activities and stabilities compared. Catalases from Bacillus SF showed high stabilities at 60 degrees C and pH 9 (t1/2=38 h) and thus this strain was chosen for further investigations, such as electron microscopy, immobilization of catalase and hydrogen peroxide degradation studies. Degradation of hydrogen peroxide with an immobilized catalase from Bacillus SF enabled the reuse of the water for the dyeing process. In contrast, application of the free enzyme for treatment of bleaching effluents, caused interaction between the denaturated protein and the dye, resulting in reduced dye uptake, and a higher color difference of 1.3DeltaE* of dyed fabrics compared to 0.9DeltaE* when using the immobilized enzyme.

Application of ligand-exchange capillary electrophoresis to the chiral separation of alpha-hydroxy acids and beta-blockers.

The application of the principle of ligand-exchange capillary electrophoresis to two substance classes is described. As chiral selector N-(2-hydroxyoctyl)-L-4-hydroxyproline-copper(II) complex was used. This principle was applied to the chiral separation of alpha-hydroxy acids and drugs containing amino alcohol structure such as beta-blockers. The enantioselectivity was found to be strongly dependent on pH corresponding to the optimal conditions for complex formation for each structure class.

Aspirin and heparin in acute ischaemic stroke in older patients.

Over four-fifths of all strokes are due to thrombotic or embolic occlusion of cerebral arteries. There is a strong rationale for considering antithrombotic therapy for the treatment of patients with acute ischaemic stroke. Antiplatelet therapy with 150 to 300 mg of aspirin (acetylsalicylic acid) started within the first 48 hours of an ischaemic stroke improves patient outcome in the short and long term, with a low risk of adverse effects. Anticoagulants such as heparin may reduce the risk of developing deep venous thrombosis and pulmonary embolism in patients with stroke, but randomised controlled trials have demonstrated a significant and dose-dependent risk of intracranial haemorrhage. The routine use of parenteral anticoagulants, including unfractionated heparin, low-molecular-weight heparins and heparinoids in the acute phase of ischaemic stroke is not associated with any net short or long term benefit. Aspirin is, therefore, the antithrombotic drug of choice in the treatment of acute ischaemic stroke.

Chiral ligand-exchange capillary electrophoresis.

This review summarizes the application of capillary electrophoresis and capillary electrochromatography for the chiral separation of various substance classes using the principle of ligand exchange. The application of this principle to various substance classes is reported.

Antiplatelet therapy for acute ischaemic stroke.

BACKGROUND: In patients with acute ischaemic stroke, platelets become activated. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and reduce the risk of early recurrent ischaemic stroke. This might reduce the risk of early death and improve long-term outcome in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage. OBJECTIVES: The aim of this review is to assess the net result of antiplatelet therapy in acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (most recent date of search March 1999), the register of trials held by the Antiplatelet Trialists' Collaboration, and MedStrategy (1995). We also contacted relevant pharmaceutical companies. SELECTION CRITERIA: Randomised trials comparing antiplatelet therapy started within 14 days of the stroke with control in patients with definite or presumed ischaemic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria and assessed trial quality, and for the included trials, extracted and cross-checked the data. MAIN RESULTS: Eight trials involving 41,325 patients were included. Two trials testing aspirin 160 to 300 mg once daily started within 48 hours of onset contributed 98% of the data. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (OR = 0.94; 95% CI 0.91 - 0.98). In absolute terms, 13 more patients were alive and independent at the end of follow-up for every 1000 patients treated. Furthermore, treatment increased the odds of making a complete recovery from the stroke (OR = 1.06; 95% CI 1.01 - 1.11). In absolute terms, 10 patients made a complete recovery for every 1000 patients treated. Antiplatelet therapy was associated with a small but definite excess of 2 symptomatic intracranial haemorrhages for every 1000 patients treated, but this was more than offset by a reduction of 7 recurrent ischaemic strokes for every 1000 patients treated. REVIEWER'S CONCLUSIONS: Antiplatelet therapy with aspirin 160 to 300 mg daily, given orally (or per rectum in patients who cannot swallow), and started within 48 hours of onset of presumed ischaemic stroke reduces the risk of early recurrent ischaemic stroke without a major risk of early haemorrhagic complications and improves long-term outcome.

Anticoagulants for acute ischaemic stroke.

BACKGROUND: Most ischaemic strokes are caused by blood clots blocking an artery in the brain. Clot prevention with anticoagulant therapy could have a significant impact on patient survival, disability and stroke recurrence. OBJECTIVES: The objective of this review was to assess the effect of anticoagulant therapy versus control in the early treatment of patients with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (last searched 30 October 2003). For previous updates of this review, we searched the register of the Antithrombotic Trialists' (ATT) Collaboration, consulted MedStrategy (1995), and contacted relevant drug companies. SELECTION CRITERIA: Randomised trials comparing early anticoagulant therapy (started within two weeks of stroke onset) with control in patients with acute presumed or confirmed ischaemic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion, assessed trial quality and extracted the data. MAIN RESULTS: Twenty-two trials involving 23,547 patients were included. The quality of the trials varied considerably. The anticoagulants tested were standard unfractionated heparin, low-molecular-weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. Based on nine trials (22,570 patients) there was no evidence that anticoagulant therapy reduced the odds of death from all causes (odds ratio (OR) = 1.05, 95% confidence interval (CI) 0.98 to 1.12) at the end of follow-up. Similarly, based on six trials (21,966 patients), there was no evidence that anticoagulants reduced the odds of being dead or dependent at the end of follow-up (OR = 0.99; 95% CI 0.93 to 1.04). Although anticoagulant therapy was associated with about 9 fewer recurrent ischaemic strokes per 1000 patients treated (OR = 0.76; 95% CI 0.65 to 0.88), it was also associated with a similar sized 9 per 1000 increase in symptomatic intracranial haemorrhages (OR = 2.52; 95% CI 1.92 to 3.30). Similarly, anticoagulants avoided about 4 pulmonary emboli per 1000 (OR = 0.60, 95% CI 0.44 to 0.81), but this benefit was offset by an extra 9 major extracranial haemorrhages per 1000 (OR = 2.99; 95% CI 2.24 to 3.99). Sensitivity analyses did not identify a particular type of anticoagulant regimen or patient characteristic associated with net benefit. REVIEWERS' CONCLUSIONS: Immediate anticoagulant therapy in patients with acute ischaemic stroke is not associated with net short- or long-term benefit. The data from this review do not support the routine use of any type of anticoagulant in acute ischaemic stroke. People treated with anticoagulants had less chance of developing deep vein thrombosis (DVT) and pulmonary embolism (PE) following their stroke, but these sorts of blood clots are not very common, and may be prevented in other ways.

Antiplatelet therapy for acute ischaemic stroke.

BACKGROUND: In patients with acute ischaemic stroke, platelets become activated. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and reduce the risk of early recurrent ischaemic stroke. This might reduce the risk of early death and improve long-term outcome in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage. OBJECTIVES: The aim of this review is to assess the efficacy and safety of antiplatelet therapy in acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched August 2002), the Cochrane Controlled Trials Register (CCTR) (Cochrane Library Issue 1 2002), MEDLINE (June 1998-October 2001), and EMBASE (June 1998-February 2002). In 1998, for previous versions of this review, we searched the register of the Antiplatelet Trialists Collaboration, MedStrategy and contacted relevant drug companies. SELECTION CRITERIA: Randomised trials comparing antiplatelet therapy (started within 14 days of the stroke) with control in patients with definite or presumed ischaemic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria and assessed trial quality, and for the included trials, extracted and cross-checked the data. MAIN RESULTS: Nine trials involving 41,399 patients were included. Two trials testing aspirin 160 to 300 mg once daily started within 48 hours of onset contributed 98% of the data. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (OR = 0.94; 95% CI 0.91 to 0.98). In absolute terms, 13 more patients were alive and independent at the end of follow-up for every 1000 patients treated. Furthermore, treatment increased the odds of making a complete recovery from the stroke (OR = 1.06; 95% CI 1.01 to 1.11). In absolute terms, 10 more patients made a complete recovery for every 1000 patients treated. Antiplatelet therapy was associated with a small but definite excess of 2 symptomatic intracranial haemorrhages for every 1000 patients treated, but this was more than offset by a reduction of 7 recurrent ischaemic strokes and about one pulmonary embolus for every 1000 patients treated. REVIEWER'S CONCLUSIONS: Antiplatelet therapy with aspirin 160 to 300 mg daily, given orally (or per rectum in patients who cannot swallow), and started within 48 hours of onset of presumed ischaemic stroke reduces the risk of early recurrent ischaemic stroke without a major risk of early haemorrhagic complications and improves long-term outcome.

Anticoagulants for acute ischaemic stroke.

BACKGROUND: Most ischaemic strokes are caused by blood clots blocking an artery in the brain. Clot prevention with anticoagulant therapy could have a significant impact on patient survival, disability and recurrence of stroke. OBJECTIVES: The objective of this review was to assess the effect of anticoagulant therapy in the early treatment of patients with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (most recent search: March 1999) and consulted MedStrategy (1995). We also contacted drug companies. SELECTION CRITERIA: Randomised trials comparing early anticoagulant therapy (started within two weeks of stroke onset) with control in patients with acute presumed or confirmed ischaemic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion, assessed trial quality and extracted the data. MAIN RESULTS: Twenty-one trials involving 23,427 patients were included. The quality of the trials varied considerably. The anticoagulants tested were standard unfractionated heparin, low-molecular-weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. Based on eight trials (22,450 patients) there was no evidence that anticoagulant therapy reduced the odds of death from all causes (odds ratio 1.05, 95% confidence intervals 0.98-1.12). Similarly, based on five trials (21, 846 patients), there was no evidence that anticoagulants reduced the odds of being dead or dependent at the end of follow-up (odds ratio 0.99, 95% confidence intervals 0.94-1.05). Although anticoagulant therapy was associated with about 9 fewer recurrent ischaemic strokes per 1000 patients treated, it was also associated with a similar sized 9 per 1000 increase in symptomatic intracranial haemorrhages. Similarly, anticoagulants avoided about 4 pulmonary emboli per 1000, but this benefit was offset by an extra 9 major extracranial haemorrhages per 1000. Sensitivity analyses did not identify a particular type of anticoagulant regimen or patient characteristic associated with net benefit. REVIEWER'S CONCLUSIONS: Immediate anticoagulant therapy in patients with acute ischaemic stroke is not associated with net short- or long-term benefit. The data from this review do not support the routine use of any type of anticoagulant in acute ischaemic stroke.

Decolorization of textile dyes by laccases from a newly isolated strain of Trametes modesta.

Four ligninolytic fungi, Trametes modesta, Trametes hirsuta, Trametes versicolor and Sclerotium rolfsii, were compared for their ability to produce laccases. The fungal laccases were screened for their ability to decolorize eight synthetic dyes (anthraquinone, azo, indigo and triarylmethane). The decolorization rate depended both on the source of the enzyme preparation and on the structure of the dye. Based on laccase production and dye decolorizing ability, T. modesta was selected for further studies. All the tested dyes were decolorized by the T. modesta laccase most efficiently under acid conditions (pH 3-6) but the optimum pH for decolorization of the individual dye varied. The decolorization rate of this laccase increased with the rise in temperature to 50-60 degrees C. The decolorization efficiency of T. modesta laccase was improved remarkably in the presence of mediators like 1-hydroxybenzotriazole and 2-methoxyphenothiazine.

Chiral separation of beta-methyl-amino acids by ligand exchange using capillary electrophoresis and HPLC.

This paper deals with the chiral separation of optical isomers of beta-methyl-amino acids by CE and HPLC using the principle of ligand-exchange. Capillary zone electrophoresis was carried out using Cu(II) complexes of L-4-hydroxyproline (L-4-Hypro), N-(2-hydroxypropyl)-L-4-hydroxyproline (HP-L-4-Hypro) and N-(2-hydroxyoctyl)-L-4-hydroxyproline (HO-L-4-Hypro) as chiral selectors, added to the electrolyte. The HPLC separations were performed on a chiral stationary ligand-exchange chromatography phase containing L-4-Hypro chemically bonded to silica gel. With both techniques nearly all compounds investigated are baseline resolved using different background electrolytes and mobile phases, respectively.