“
“Type 2 diabetes (T2D) is one of the major risk factors

associated with Alzheimer’s disease (AD). Recent studies have found similarities in molecular mechanisms that underlie AS1842856 datasheet the respective degenerative developments in the two diseases. Pharmacological agents, such as dipeptidyl peptidase-4 (DPP-4) inhibitors, which increase the level of glucagon-like peptide-1 (GLP-1) and ameliorate T2D, have become valuable candidates as disease modifying agents in the treatment of AD. In addition, endogenous GLP-1 levels decrease amyloid beta (A beta) peptide and tau phosphorylation in AD. The present study examines the efficacy of Saxagliptin, a DPP-4 inhibitor in a streptozotocin (STZ) induced rat model of AD. Three months following induction of AD by intracerebral administration of streptozotocin, animals were orally administered Saxagliptin (0.25, 0.5 and 1 mg/kg) for 60 days. The effect of the

DPP-4 inhibitor on hippocampal GLP-1 levels, A beta burden, tau phosphorylation, inflammatory markers and memory retention were evaluated. The results reveal an attenuation of A beta, tau phosphorylation and inflammatory markers and an improvement in hippocampal GLP-1 and memory retention following treatment. This remarkable therapeutic effect of Saxagliptin mediated through DPP-4 inhibition GW3965 mouse demonstrates a unique mechanism for A beta and tau clearance by increasing GLP-1 levels and reverses the behavioural deficits and pathology observed in AD. (C) 2013 Elsevier Ltd. All rights reserved.”
“There has been little investigation of the possible lasting adverse effects of gamma-hydroxybutyrate (GHB).

This study aims to study whether GHB produces residual adverse effects on memory and social behaviour in rats and lasting changes

Trichostatin A in brain monoamines and oxytocin-related gene expression.

Rats received daily intraperitoneal injections of GHB (500 mg/kg), methylenedioxymethamphetamine (MDMA; 5 mg/kg) or their combination (GHB/MDMA) over ten consecutive days. Locomotor activity and body weight were assessed during the dosing period and withdrawal-related anxiety was assessed 24 h after drug cessation. After a washout of 4 weeks, rats were tested on the emergence, social interaction, and object recognition tasks over a 2-week period. Monoamine levels in cortex and striatum, and hypothalamic oxytocin and oxytocin receptor mRNA, were then assessed.

MDMA and GHB/MDMA caused modest sensitization of locomotor activity over time, while sedative effects of GHB diminished with repeated exposure. GHB-treated rats showed reduced social interaction 24 h after the final dose, indicating GHB withdrawal-induced anxiety. All drug-treated groups displayed residual deficits in social interaction and object recognition. No changes in monoamine levels were detected 8 weeks post-drug. However, MDMA pre-exposure increased hypothalamic oxytocin mRNA while GHB pre-exposure upregulated oxytocin receptor mRNA.

“
“Objective: Aortic aneurysm size is a critical determinant of the need for intervention, yet the maximal diameter will often Selleckchem BI-D1870 vary depending on the modality and method of measurement. We aimed to define the relationship between commonly used computed tomography (CT) measurement techniques and those based on current reporting standards and to compare the values obtained with diameter measured using ultrasound (US).

Methods. CT scans from patients with US-detected aneurysms were analyzed using three-dimensional reconstruction software. Maximal aortic diameter

was recorded in the anteroposterior (CT-AP) plane, along the maximal ellipse (CT-ME), perpendicular to the maximal ellipse (CT-PME), or perpendicular to the centerline of flow (CT-PCLF). Diameter measurements were compared with each other and with maximal AP diameter according to US (US-AP). Analysis was performed according to the principles of Bland and Altman.

Results are expressed as mean +/- standard deviation. Results. CT and US scans from 109 patients (92 men,

17 women), with a mean age of 72 +/- 8 years, were included. The mean of each series of readings on CT was significantly larger than the mean US-AP measurement (P < .001), and they also differed significantly from each other (P < .001). The CT-PCLF diameter was larger than CT-AP find more and CT-PME by mean values of 3.0 +/- 6.6 and 5.9 +/- 6.0 mm, respectively. The CT-ME diameter was larger than CT-PCLF by a mean of 2.4 +/- 5 mm. The US-AP diameter was smaller than CT-AP diameter by 4.2 +/- 4.9 mm, CT-ME by 9.6 +/- 8.0 mm, CT-PME by 1.3 +/- 5 mm, and smaller than CT-PCLF by 7.3 +/- 7.0 mm. Aneurysm size did not significantly affect these differences. Seventy-eight 17-DMAG (Alvespimycin) HCl percent of 120 pairs of intraobserver CT measurements and 65% of interobserver CT measurements differed

by <2 mm.

Conclusions: CT-based measurements of aneurysm size tend to be larger than the US-A-P measurement. CT-PCLF diameters are consistently larger than CT-PME as well as CT-AP measurements. These differences should be considered when applying evidence from previous trials to clinical decisions. (J Vasc Surg 2009;50:263-8.)”
“Following CNS injury there is a period of vulnerability when cells will not easily tolerate a secondary insult. However recent studies have shown that following traumatic brain injury (TBI), as well as hypoxic-ischemic injuries, the CNS may experience a period of protection termed “”preconditioning.”" While there is literature characterizing the properties of vulnerability and preconditioning in the adult rodent, there is an absence of comparable literature in the developing rat. To determine if there is a window of vulnerability in the developing rat, post-natal day 19 animals were subjected to a severe lateral fluid percussion injury followed by pilocarpine (Pc)-induced status epilepticus at 1, 6 or 24 In post TBI.

(C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The midbrain periaqueductal gray (PAG) is part of the brain system involved in active defense reactions to threatening stimuli. Glutamate N-methyl-d-aspartate (NMDA) receptor activation within the dorsal column of the PAG (dPAG) leads to autonomic and behavioral responses characterized as the fear

reaction. Nitric oxide (NO) has been proposed to be a mediator of the aversive action of glutamate, since the activation of NMDA receptors in the brain increases NO synthesis.

We investigated the effects see more of intra-dPAG infusions of NMDA on defensive behaviors in mice pretreated with a neuronal nitric oxide synthase (nNOS) inhibitor [N omega-propyl-l-arginine (NPLA)], in the same midbrain site, during a confrontation with a predator in the rat exposure test (RET).

Male Swiss mice received intra-dPAG injections of NPLA (0.1 or 0.4 nmol/0.1 mu l), and 10 min later, they were infused with NMDA (0.04 nmol/0.1 mu l) into the dPAG. After 10 min, each mouse was placed in the RET.

NMDA treatment enhanced avoidance behavior from the predator and markedly increased freezing behavior. These proaversive effects of NMDA were prevented by prior injection of NPLA. Furthermore, defensive behaviors (e.g., avoidance, risk assessment, freezing) were consistently reduced

by the highest dose of NPLA alone, suggesting an intrinsic effect of nitric oxide on defensive behavior in mice exposed to the RET.

These findings suggest a potential role of glutamate NMDA receptors and NO in the dPAG AR-13324 order in the regulation of defensive behaviors in mice during a confrontation with a predator in the RET.”
“The participation

of the brain-derived neurotrophic factor (BDNF) in the benefits of physical exercise on cognitive functions has been widely investigated. Flavopiridol manufacturer Different from voluntary exercise, the effects of treadmill running on memory and BDNF are still controversial. Importantly, the impact of the frequency of physical exercise on memory remains still unknown. In this study, young adult and middle-aged rats were submitted to 8 weeks of treadmill running at moderate intensity and divided into 4 groups of frequency: 0, 1, 3 and 7 days/week. Aversive and recognition memory were assessed as well as the immunocontent of proBDNF, BDNF and tyrosine kinase receptor type B (TrkB) in the hippocampus. Frequencies did not modify memory in young adult animals. The frequency of 1 day/week increased proBDNF and BDNF. All frequencies decreased TrkB immunocontent. Middle-aged animals presented memory impairment along with increased BDNF and downregulation of TrkB receptor. The frequency of 1 day/week reversed age-related recognition memory impairment, but worsened the performance in the inhibitory avoidance task. The other frequencies rescued aversive memory, but not recognition memory.

To further investigate the roles of these proteins in viral pathogenicity, we constructed chimeric recombinant viruses by exchanging the G and M genes of the attenuated SN strain with those of the highly pathogenic SB strain. Infection of mice with these chimeric viruses revealed a significant increase

in the pathogenicity of the SN strain bearing the RV G from the pathogenic SB strain. Moreover, the pathogenicity was further increased when both G and M from SB were introduced into SN. Interestingly, the replacement of the G or M gene or both in SN by AZD2281 chemical structure the corresponding genes of SB was associated with a significant decrease in the rate of viral replication and viral RNA synthesis. In addition, a chimeric SN virus bearing both the M and G genes from SB exhibited more efficient cell-to-cell spread than a chimeric SN virus in which only the G gene was replaced. Together, these data indicate that both G and M play an important role in RV pathogenesis by regulating virus replication and facilitating cell-to-cell spread.”
“Tourette’s Syndrome (TS) is a neuropsychiatric disorder https://www.selleckchem.com/products/chir-99021-ct99021-hcl.html characterized by motor and vocal tics, often

associated with behavioral disorders. Symptoms often disappear before or during adulthood. The pathophysiology of TS is still a matter of considerable debate. Current knowledge of cortico-basal ganglia-thalamocortical circuits provide explanations for the beneficial effects of deep brain stimulation (DBS) on tics. When conservative treatment fails in patients with severe TS, DBS may be a therapeutic option. In 1999, thalamic DBS was introduced for intractable TS. Since then, multiple targets have been used in a small number of patients, including the globus pallidus pars interna and the nucleus accumbens. Inclusion and exclusion criteria have been formulated to identify good candidates for DBS.”
“The binding of

herpes simplex virus type 1 ICP4, TATA-binding protein (TBP), and RNA polymerase II (polII) to the promoter regions of representative immediate-early (IE) (ICP0), early (E) (thymidine kinase [tk]), and late (L) (glycoprotein C [gC]) genes on the viral genome was examined as a function of time postinfection, MEK162 mw viral DNA replication, cis-acting sites for TFIID in the Ilk and gC promoters, and genetic background of ICP4. The binding of TBP and poles to the IE ICP0 promoter was independent of the presence of ICP4, whereas the binding of TBP and poles to the tk and gC promoters occurred only when ICP4 also bound to the promoters, suggesting that the presence of ICP4 at the promoters of E and L genes in virus-infected cells is crucial for the formation of transcription complexes on these promoters. When the TATA box of the tk promoter or the initiator element (INR) of the gC promoter was mutated, a reduction in the amount of TBP and poles binding was observed.

035). The mean T-score for response time on the CPT was higher in the subjects with TT genotype in the rs6489630 SNP compared to those with the CC or CT genotype, even after adjusting for the effect of IQ (p = 0.021).

Conclusions: These results provide preliminary evidence of an association between NTF3 and the intelligence and selective attention deficit in the Korean population. (C) 2010 Elsevier Inc. All rights reserved.”
“Background

Intermittent preventive treatment for malaria during infancy (IPTi) is the administration of a full therapeutic course of antimalarial drugs to infants living in settings where malaria is endemic, at the time of routine vaccination in the first year of life. We investigated whether IPTi with sulfadoxine-pyrimethamine or other antimalarial drug combinations adversely affected MK-0518 serological responses to vaccines used in the Expanded Programme on Immunization (EPI).

Methods The study was JQ1 done in a subset of children enrolled in

five randomised controlled trials in Navrongo, Ghana; Kilimanjaro, Tanzania; Manhica, Mozambique; Kisumu, Kenya; and Bungoma, Kenya. All infants presenting for the second dose of the diphtheria-tetanus-pertussis vaccination (given at 8-10 weeks of age) were eligible, and analyses included all children who had received measles vaccination (at 9 months of age) and at least one dose of IPTi or placebo. Blood samples were collected before and after vaccination, and antibody titres were measured by plaque reduction neutralisation (measles, yellow fever), microneutralisation (polio serotypes

1 and 3), and ELISA (all other EPI antigens). Laboratory personnel were unaware of the randomisation groups. We compared the proportion of infants in the IPTi and placebo groups who did not attain protective antibody titres after vaccination, using a one-sided significance non-inferiority margin of 5% for measles (the primary endpoint) and 10% for other EPI antigens.

Findings Between September, 2000, and May, 2008, 8416 children were enrolled in the five studies. Paired samples from 2368 children from sites where sulfadoxine-pyrimethamine learn more was compared with placebo were analysed for measles antibodies. 464 children with detectable measles antibody in their sample before vaccination were excluded, leaving 1904 individuals (934 placebo and 970 sulfadoxine-pyrimethamine) in the study. IPTi with sulfadoxine-pyrimethamine did not have a clinically significant effect on immune responses to measles vaccine; 61 of 970 (6.3%) children who received IPTi did not develop a protective antibody response after measles vaccination compared with 60 of 934 (6.4%) who received placebo, a difference of -0.14% (95% CI -2.3 to 2.1). When other antimalarial drugs were used for IPTi the results were much the same.

Electron cryomicroscopy revealed two major particle populations of similar to 60 and similar to 45 nm in diameter. The similar to 60-nm particles

were characterized by a membrane bilayer (presumably an envelope) that is spatially separated from an internal structure (presumably a capsid), VE-821 mouse and they were enriched in fractions that displayed a high infectivity-to-HCV RNA ratio. The similar to 45-nm particles lacked a membrane bilayer and displayed a higher buoyant density and a lower infectivity-to-HCV RNA ratio. We also observed a minor population of very-low-density, >100-nm-diameter vesicular particles that resemble exosomes. This study provides low-resolution ultrastructural information of particle populations displaying differential biophysical properties and specific infectivity. Correlative analysis of the abundance of the different particle populations with infectivity, LB-100 solubility dmso HCV RNA, and viral antigens suggests that infectious particles

are likely to be present in the large similar to 60-nm HCV particle populations displaying a visible bilayer. Our study constitutes an initial approach toward understanding the structural characteristics of infectious HCV particles.”
“A number of neurotoxin- and gene-based rodent models of acute neurodegeneration of nigrostriatal dopamine (DA) neurons are used to study Parkinson’s disease (PD). The rapid degeneration achieved by many of these current models limits the capacity of the model to develop pathogenic mechanisms and display the various stages of motor degradation representative of the human Parkinsonian condition. Chronic rodent models have been the only ones to reproduce these characteristics, yet do not show correlated progress of DA loss with multiple to stepwise behavioral deficits as seen in humans. In the present

study, we have developed a progressive model of increasing DA loss and motor dysfunction via progressively increased administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), in the C57BI/6J mouse. Mice were administered a daily (5 d/wk) dose of MPTP that increased weekly over the course of 4 weeks (4 mg/kg, 8 mg/kg, 16 mg/kg and 32 mg/kg). Each treatment group was tested for exploratory and motor behavioral changes after every week leading up to their final dose, as well as changes in tyrosine hydroxylase immunoreactivity (TH-ir) of the substantia nigra pars compacta (SNpc) and caudate putamen (CPu). We detected a 24% decrease in the mean number of TH-ir SNpc neurons/section after 1 week, and a 62% decrease after 4 weeks as compared to the vehicle group. CPu TH-ir began at a 35% loss after 1 week and increased to a 74% loss after 4 weeks compared to the vehicle group. CPu DA content showed an initial decrease of 20% after 1 week, and a final decrease of 70% following week 4 versus the vehicle group.

Failure to detect associations between postnatal exposure and health outcomes may stem from the limitations of commonly selleck compound employed approaches to assess lactational exposure. The aim of the present study was to assess whether lactational exposure to polychlorinated biphenyl-153 (PCB-153), dichlorodiphenyldichloroethylene (DDE), or hexachlorobenzene (HCB) as estimated with a physiologically based

pharmacokinetic (PBPK) model, is associated with decrements in mental and psychomotor development scores of the Bayley Scales of Infant Development (BSID) test in children aged around 14-months of a subsample (N = 1175) of the Spanish INMA birth cohort, and to compare this with the effects of prenatal exposure. Although in the present study population PCB-153, DDE and HCB exposure increased within the first months of postnatal life, no associations were found between different periods of postnatal exposure to these compounds and mental or psychomotor scores. Increasing prenatal PCB-153 concentrations were associated with worse mental and psychomotor scores, although significance was only reached for psychomotor development (beta [95%CI] = -1.36 [-2.61, -0.11]). Indeed, the association between exposure and effects observed during prenatal life weakened gradually across periods of postnatal life. Results of the present study suggest that,

although breastfeeding increases children’s blood persistent organic pollutants (POPs) levels Verteporfin in vivo during postnatal life, deleterious effects of PCB-153 on neuropsychological development are mainly attributable to prenatal exposure. (c) 2012 Elsevier Inc. All rights reserved.”
“Beta-amyloid (A beta) is a major pathogenic peptide in Alzheimer’s disease (AD) and is generated by the processing of amyloid precursor protein (APP). We have previously reported that the brown algae Ecklonia cava, which has anti-oxidant and anti-inflammatory functions, Dichloromethane dehalogenase decreased A beta production and further aggregation in HEK293 cells expressing the APP Swedish mutation. Here, we show

the reduction mechanism of A beta production using the butanol extract of Ecklonia cava through the examination of expression and activity of alpha-, beta-, and gamma-secretase. Treatment with the extract resulted in the activation of alpha-secretase with a contrasting decrease in its mRNA and protein expression. This activation was consistent with the translocation of the extract into the plasma membrane of the secretase. Gamma-secretase activity was lowered by E. cava, and this effect may be due to the decreased expression of PSEN1 mRNA and protein. In addition, the basal nuclear location of PSEN1, which may affect chromosome missegregation in neurodegenerative disease, was reduced by the extract, despite the significance of this finding remains unclear.

Moreover, a temperature-sensitive mutation in U(L)15 precluded coimmunoprecipitation of pU(L)15 with the U(L)28 and U(L)33 proteins at the nonpermissive temperature. We conclude that interactions between putative terminase components are tightly linked to successful viral DNA cleavage and packaging.”
“People can solve problems in more than one way. Two general strategies involve (A) methodical, conscious, search of problem-state transformations, and (B) sudden insight, with abrupt emergence of the solution into consciousness. This study elucidated the influence of initial resting brain-state on subjects’ subsequent strategy choices. High-density electroencephalograms

(EEGs) were recorded from subjects at rest who were subsequently directed to solve a series of anagrams. Subjects were divided into two groups based on the proportion of anagram solutions derived with self-reported insight versus search. Reaction time this website and accuracy results were consistent with different cognitive problem-solving strategies used for OTX015 mouse solving anagrams with versus without insight. Spectral analyses yielded group differences in resting-state EEG supporting hypotheses concerning insight-related attentional diffusion and right-lateralized hemispheric asymmetry. These results reveal a relationship between resting-state brain activity and problem-solving strategy, and, more generally, a dependence of event-related

neural computations on the preceding resting state. (c) 2007 Elsevier Ltd. All rights reserved.”
“Cytolytic T lymphocytes (CTL) play a major role in controlling human immunodeficiency virus type I (HIV-1) infection. To evade immune pressure, HIV-1 is selected at targeted CTL epitopes, which may consequentially alter viral replication fitness. In our longitudinal investigations

of the interplay between T-cell immunity and viral evolution following acute HIV-1 infection, we observed in a treatment-naive patient the emergence of highly avid, gamma interferon-secreting, CD8(+) CTL recognizing second an HLA-Cw*0102-restricted epitope, NSPTRREL (NL8). This epitope lies in the p6(Pol) protein, located in the transframe region of the Gag-Pol polyprotein. Over the course of infection, an unusual viral escape mutation arose within the p6(Pol) epitope through insertion of a 3-amino-acid repeat, NSPT(SPT)RREL, with a concomitant insertion in the p6(Gag) late domain, PTAPP(APP). Interestingly, this p6(Pol) insertion mutation is often selected in viruses with the emergence of antiretroviral drug resistance, while the p6(Gag) late-domain PTAPP motif binds Tsg101 to permit viral budding. These results are the first to demonstrate viral evasion of immune pressure by amino acid insertions. Moreover, this escape mutation represents a novel mechanism whereby HIV-1 can alter its sequence within both the Gag and Pol proteins with potential functional consequences for viral replication and budding.

Although the precise cause of GWI is still unknown, combined exposure to a nerve gas prophylaxis drug pyridostigmine bromide

(PB) and pesticides DEET and permethrin during the war has been proposed as one of the foremost causes of GWI. We investigated the effect of 4 weeks of exposure to Gulf war illness-related (GWIR) chemicals in the absence www.selleckchem.com/products/jq1.html or presence of mild stress on mood and cognitive function, dentate gyrus neurogenesis, and neurons, microglia, and astrocytes in the hippocampus. Combined exposure to low doses of GWIR chemicals PB, DEET, and permethrin induced depressive-and anxiety-like behavior and spatial learning and memory dysfunction. Application of mild stress in the period of exposure to chemicals exacerbated the extent of mood and cognitive dysfunction. Furthermore, these behavioral impairments were associated with reduced hippocampal volume and multiple cellular alterations such as chronic reductions in neural stem cell activity and neurogenesis, partial loss of principal neurons, and mild inflammation comprising sporadic occurrence

of activated microglia and significant hypertrophy of astrocytes. The results show the first evidence of an association between mood and cognitive dysfunction and hippocampal pathology epitomized by decreased neurogenesis, partial loss of principal neurons, and mild inflammation in a model of GWI. Hence, treatment strategies that are efficacious for enhancing neurogenesis and suppressing inflammation may be helpful for alleviation of mood and Crenolanib cognitive dysfunction observed in GWI.”
“This review summarizes the current knowledge of Cl- transport in vascular smooth muscle cells (VSMCs). VSMCs accumulate Cl- intracellularly using two secondary-active transport mechanisms. The Cl- equilibrium potential is more positive than Avapritinib the resting membrane potential enabling Cl- to be a depolarizing ion upon activation of a Cl- conductance. Cl- currents are involved in different vascular responses suggesting

a number of different Cl- channels. All known Cl- channel families, with the exception of the GABA-/glycinereceptor family, have been identified in VSMCs. At least one member of the voltage-activated ClC family – ClC-3 – has been suggested to be involved in myogenic constriction, in cell proliferation and to have an anti-apoptotic action. The cystic fibrosis transmembrane conductance regulator is also demonstrated in VSMCs. The molecular identity of the major anion conductance in VSMCs – a Ca2+ – activated Cl – cur rent – is uncertain. Several candidates have been suggested with bestrophin and TMEM16 protein families the current favorites. Specific pharmacological tools are lacking for Cl channels but recent molecular biology developments have made selective gene manipulations possible.

Materials and Methods: Subjects were recruited from the Division of Urogynecology at the University of Rochester. Inclusion criteria were overactive bladder refractory to anticholinergic medications, multiple daily incontinence episodes and a 24-hour pad weight of 100 gm or greater. Subjects with low leak point pressures, increased post-void residual volume or neurological etiologies were excluded from study. Subjects were randomized to placebo or to 1 of 2 doses of botulinum-A

toxin. The detrusor was injected at 8 to 10 sites above the trigone. Evaluations were performed at baseline, and at 3 and 6 weeks after injection, and included bladder diaries, pad weights, quality of life questionnaires and urodynamic studies.

Results: A total of 22 subjects participated in stage 1 of this 2-stage study. We report https://www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html on the outcomes of stage 1 of this study. Because stage 2 is still ongoing and investigators remain blind to the doses of botulinum-A toxin, the 2 botulinum-A toxin groups were combined for this report. There were no differences in mean baseline measurements between the 2 groups. Statistically significant improvements in daily selleck incontinence episodes, pads changed

per day and quality of life questionnaires were seen in the botulinum-A toxin group with no changes in the placebo group. No change in nocturia, daily voiding frequency, peak flow or detrusor pressure was seen in either group. Of 15 subjects 4 (26%) receiving botulinum-A toxin had a post-void residual volume of 200 cc or greater and 1 subject required intermittent catheterization. Four subjects experienced a urinary tract infection, 2

(13%) in the botulinum-A toxin group and 2 (28%) in the placebo group (not significant).

Conclusions: Botulinum.-A toxin can significantly reduce urge urinary incontinence due to overactive bladder at 6 weeks. However, there is a risk of urinary retention requiring self-catheterization.”
“An intracellularly produced constitutive heparinase was isolated from the periplasmic space of Acinetobacter calcoaceticus by freeze fracturing and purified 51.2-fold by ion exchange and gel filtration chromatography. Specific activity of the purified enzyme was found to be 41 IU/mu g protein with a 120 000 Da molecular mass. The enzyme activity was maximum at 35 degrees OSI-027 solubility dmso C in the presence of 250 mM NaCl at pH 7.5. The enzyme activity was inhibited in the presence of Ba(2+), Hg(2+), Cd(2+), IAA and DEPC, and enhanced by the presence Of Cu(2+), Fe(2+) ions and reducing agents. Inhibition of enzyme activity by iodoacetic acid and enhancement of enzyme activity in the presence of reducing agents indicated that free sulfohydryl groups of cysteine residues were necessary for catalytic activity of the enzyme. The affinity of the enzyme for different glycosaminoglycans studied varied and showed high affinity for heparin with a K(m). value of 0.026 mM.