This review considers the current status of knowledge of stress-i

This review considers the current status of knowledge of stress-induced inflammation in the brain. Interestingly, anti-inflammatory pathways are also activated in brain in response to stress, constituting a possible endogenous mechanism of defence against excessive inflammation. The possibility of pharmacological modulation of these pathways to prevent the accumulation Of PFO-inflammatory I-BET-762 solubility dmso mediators and subsequent brain damage in stress and in stress-related neuropsychological conditions is also reviewed. This dual response elicited by stress in brain, both pro- and anti-inflammatory deserves further attention in order to understand pathophysiological

changes as well as possible new therapeutic approaches KU55933 nmr of stress-related neuropsychopathologies. (C) 2008 Elsevier Ltd. All rights reserved.”
“Pseudorabies virus (PRV) glycoprotein C (gC) initiates virus attachment to cells by binding to heparan sulfate (HS) proteoglycans. The gC:HS interaction is not essential since gC null mutants still infect; however, they are more easily removed from cells during the initial stages of infection. The expendability of gC has facilitated a genetic mapping of the HS-binding domain, which is composed

of three independent heparin-binding domains (HBDs) of six to eight amino acids each. Previous results suggested that at least one of the HBDs (HBD 1) functioned in a context-dependent manner. To define the context better, a reversion analysis was performed in which a defective gC containing a nonfunctional but intact HBD 1 regained HS-binding ability. To increase the reversion frequency, an efficient method for targeted, yet random mutagenesis of the gC gene was developed. The method involves random mutagenesis of a plasmid-borne copy of gC, and highly efficient recombination of the plasmid-borne genes into the virus genome at the site of a double-strand break in the viral gC locus. Revertants were recovered readily, and their gC

alleles suggested that HS-binding could be restored by several different amino acid substitutions. pheromone This approach should be applicable to targeted mutagenesis of other herpesvirus genes. (C) 2008 Elsevier B.V. All rights reserved.”
“The enclocannabinoid system is a widely distributed, neuromodulatory system which serves an integral role in regulating synaptic transmission. The presence of this system in stress-responsive neural circuits suggests that it may play a critical role in regulating neuroendocrine and behavioral responses to stress. Enclocannabinoid content in limbic structures which regulate activation of the hypothalamic-pituitary-adrenal (HPA) axis is dynamically regulated by stress. Under conditions of acute stress, the enclocannabinoid system tonically constrains activation of the HPA axis.

The primary end point was newly acquired infection with HIV type

The primary end point was newly acquired infection with HIV type 1 or 2. The secondary end point was newly

acquired gonococcal or chlamydial infection. The primary analysis was based on a log-rank test of no difference in the distribution of time to HIV infection, stratified according to site.

Results: A total of AZD2014 1398 women were enrolled and randomly assigned to receive cellulose sulfate gel (706 participants) or placebo (692 participants) and had follow-up HIV test data. There were 41 newly acquired HIV infections, 25 in the cellulose sulfate group and 16 in the placebo group, with an estimated hazard ratio of infection for the cellulose sulfate group of 1.61 (P=0.13). This result, which is not significant, is in contrast to the interim finding that led to the trial being stopped prematurely (hazard ratio, 2.23; P=0.02) and the suggestive result of a preplanned secondary (adherence-based) analysis (hazard ratio, 2.18; P=0.03). No significant effect of cellulose sulfate as compared with placebo was found on the risk of gonorrheal infection (hazard ratio, 1.10; 95% confidence interval [CI], 0.74

to 1.62) or chlamydial infection (hazard ratio, 0.71; 95% CI, 0.47 to 1.08).

Conclusions: Cellulose sulfate did not prevent HIV infection and may have increased the risk of HIV acquisition. ( number, NCT00153777; and Current Controlled Trials number, ISRCTN95638385.).”
“Objectives. Although evidence suggests that physical disability and depression may be reciprocally related, questions of, causalily Versus spuriousness and MX69 in vivo the direction of causality remain to be confidently answered. This study considered the hypotheis of reciprocal influence the possibility of spuriousness in relation to pain, stress, and lifetime major depression; and the

possible mediating effects of pain and social stress.

Methods. We analyzed data from a two-wave panel Study of Miami-Dade County residents (n = 1,455) that included a substantial oversampling of individuals reporting a physical disability. Results. Results CYTH4 indicated that, although prior levels of physical limitations predicted changes in depressive symptoms, there was no evidence of the reversc association.

Results also indicated that pail of the association between prior physical limitations and changes in depressive symptoms was explained by intervening level of pain and, to a lesser extent, by the day-to-day experience of discrimination.

Discussion. Much of whatever causation may be involved in the linkage between physical limitations and depressive symptomatology flows from limitations to depression rather than in the reverse direction. Results also make clear that this linkage is not in artifact of shared associations with pain, social stress, or litetime major depression.

It continued bilaterally to temporal and frontal poles by 290 ms

It continued bilaterally to temporal and frontal poles by 290 ms. Subtraction of nonattended from attended conditions removed primarily the early contralateral sensory components. There was some indication of a preferred order of sensory processing that may express and optimize hemispheric computational specializations. Results indicate similar functional organizations for tactile and visual pattern recognition. NeuroReport 20:941-945 (C) 2009 Wolters Kluwer Health check details | Lippincott Williams & Wilkins.”
“MicroRNAs (miRNAs) represent a conserved

class of small noncoding RNAs that are found in all higher eukaryotes as well as some DNA viruses. miRNAs are 20 to 25 nucleotides in length and have important regulatory functions in biological processes such as embryonic development, cell differentiation,

hormone secretion, and metabolism. Furthermore, miRNAs have been implicated in the pathology of various diseases, including cancer. miRNA expression profiles not only classify different types of cancer but also may even help to characterize distinct tumor stages, therefore constituting a valuable tool for prognosis. Here we report the miRNA profile of Epstein-Barr virus (EBV)-positive nasopharyngeal carcinoma (NPC) tissue samples characterized by cloning and sequencing. We found that all EBV miRNAs LDN-193189 price from the BART region are expressed in NPC tissues, whereas EBV miRNAs from the BHRF1 region are not found. Moreover, we identified two novel EBV miRNA genes originating from the BART region that have not been found in other tissues or cell lines before. We also identified three new human miRNAs which might be specific for nasopharyngeal tissues. We further show that a number of different cellular miRNAs, including miR-15a Tideglusib and miR-16, are up- or downregulated in NPC tissues compared to control tissues. We found that the tumor suppressor BRCA-1 is a target of miR-15a as well as miR-16, suggesting a miRNA role in NPC pathogenesis.”
“TASK-2 is a member of tandem-pore domain potassium

channels that regulate neuronal excitability. In this study we investigated the expression of TASK-2 in neuronal elements in the inner retina of rat by immunofluorescence double labeling. In contrast to weak expression in the outer retina, TASK-2 is strongly expressed in the inner retina. TASK-2 immunoreactivity was diffusely distributed throughout the inner plexiform layer. Double-labeling experiments revealed that TASK-2 was expressed in gamma-aminobutyric acid amacrine cells (GABAergic amacrine cells), including both dopaminergic and cholinergic ones. The immunostaining appeared on the membrane, cytoplasm, and somatodendritic compartments of these cells. In All glycinergic amacrine cells, however, only faint punctuate staining, if any, was seen. In addition, ganglion cells were also intensely labeled by TASK-2. NeuroReport 20:946-950 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Our results showed that HO-1 is differently expressed


Our results showed that HO-1 is differently expressed

in various brain regions in db/db mice when compared to lean animals. Furthermore, Selleckchem MK 2206 silibinin provides DNA protection and reduces oxidative stress in a brain specific area, in part via the activation of the HO system. Silibinin may provide a valid tool to counteract oxidative stress in the diabetic status in the central nervous system under diabetic condition. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Gap formation and closure represent important disturbance events in forests, but the processes involved are still poorly understood. We use models, which we and others previously developed, to make long-term predictions of tropical forest gap dynamics based on Barro Colorado Island data. We first fit the models to the data by comparing their discrete Fourier transforms, and we propose a definition for the lifetime of a gap and predict a large-gap lifetime typically to be less than 50 years. We find that the gap lifetime diverges logarithmically for large-gap sizes. We examine the ‘memory’ of spatial gap patterns via spatiotemporal correlations and find a correlation time of about 160 years, suggesting that present gap patterns could have long-lasting A-1210477 purchase effects on forest spatial patterns. (C) 2011 Elsevier Ltd. All rights reserved.”
“The ability

to react fast and efficiently in threatening situations is paramount for the survival of organisms and has been decisive in our evolutionary history. Defense mechanisms in primates rely on the fast recognition of potential predators and facial expressions of conspecifics. The neural circuitry responsible for the detection of threat is generally thought to be centered on the amygdala. Although it is a pivotal structure in the processing of emotional stimuli, the amygdala Sunitinib research buy does not seem necessary for the early stages of this process. Here we show that bilateral neurotoxic lesions of the superior

colliculus in infant capuchins monkeys impaired the recognition of a rubber-snake in a threat-reward conflict task. Lesioned monkeys were uninhibited by a snake in a food-reward retrieval task. Lack of inhibition in the task was observed over the course of 15 weeks. The long lasting recognition impairment of a natural predator observed here is similar to the tameness aspects of Kluver Bucy syndrome, indicating an important role of this structure in threat recognition. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Mate choice depends on mating preferences and on the manner in which mate-quality information is acquired and used to make decisions. We present a model that describes how these two components of mating decision interact with each other during a comparative evaluation of prospective mates.

GAPDH, Drp1, mitochondrial complex I, matrix metalloprotease-9, P

GAPDH, Drp1, mitochondrial complex I, matrix metalloprotease-9, Parkin, XIAP and protein-disulphide isomerase can also be S-nitro(sy)lated, but the contribution of these reactions to neurodegeneration remains unclear. Neurons are sensitive to NO-induced excitotoxicity because NO rapidly induces both depolarization and glutamate release, which together

activate the NMDA receptor. nNOS activation (as a result of NMDA receptor activation) may contribute to excitotoxicity, probably Tozasertib via peroxynitrite activation of poly-ADP-ribose polymerase and/or mitochondrial permeability transition. iNOS is induced in glia by inflammation, and may protect; however, if there is also hypoxia or the NADPH oxidase is active, it can induce neuronal death. Microglial phagocytosis may contribute actively to neuronal loss. (C) 2010 Elsevier Inc. All rights reserved.”
“We recently clarified the physiological formation of 8-nitroguanosine 3′,5′-cyclic monophosphate (8-nitro-cGMP) and its critical roles in nitric oxide (NO) signal transductions. This discovery of 8-nitro-cGMP is the first demonstration of a nitrated cyclic nucleotide functioning as a new second messenger in mammals since the identification of cGMP more than 40 years ago. By means Palbociclib of chemical analyses, e.g., liquid chromatography-tandem

mass spectrometry, we unequivocally identified 8-nitro-cGMP formation, which depended on NO production, in several types of cultured cells, including macrophages and glial cells. Most important, we previously showed that 8-nitro-cGMP as an electrophile reacted with Aldehyde dehydrogenase particular sulfhydryls of proteins to generate a unique post-translational modification that we called protein S-guanylation. In fact, certain specific intracellular proteins, such as the redox-sensor protein Keap1, readily underwent S-guanylation induced by 8-nitro-cGMP. 8-Nitro-cGMP activated the Nrf2 signaling pathway

by triggering dissociation of Keap1, via S-guanylation of its highly nucleophilic cysteine sulfhydryls. We also determined that S-guanylation of Keap1 was involved in cytoprotective actions of NO and 8-nitro-cGMP by inducing oxidative stress response genes such as heme oxygenase-1. Such unique chemical properties of 8-nitro-cGMP shed light on new areas of NO and cGMP signal transduction. Protein S-guanylation induced by 8-nitro-cGMP may thus have important implications in NO-related physiology and pathology, pharmaceutical chemistry, and development of therapeutics for many diseases. (C) 2010 Elsevier Inc. All rights reserved.”
“It is hypothesized that in cells producing nitric oxide (NO), NO and its endogenous derivatives (low-molecular S-nitrosothiols and dinitrosyl iron complexes (DNIC) with thiol-containing ligands) can move in the intracellular space not only by diffusion but also in an autowave mode.

We demonstrated directly that the TetR repressor utilizes an extr

We demonstrated directly that the TetR repressor utilizes an extrinsic mechanism and CAP, the catabolite activator protein, utilizes an intrinsic mechanism.”

microcoronary endothelial cells (RCEs) from spontaneously hypertensive rats (SHR), the nitric oxide (NO)/cyclic guanosine monophosphate (GMP)-dependent proteinkinase I (cGKI) pathway cannot regulate the cytosolic calcium ([Ca2+](i)) dynamic as in RCEs from Wistar Kyoto rats (WKY). We investigated the altered downstream NO target in SHR cells and, since cGKI expression was low, whether the re-expression of cGKI alpha in SHR RCEs could restore NO calcium responsiveness. We measured Selleck Alvocidib [Ca2+](i) dynamic by fura-2 imaging analysis and the cGKI level by RT-PCR and Western blot in SHR and WKY RCEs. Plasmids encoding for enhanced green fluorescence protein or cGKI alpha-enhanced green fluorescence protein were transiently transfected in SHR RCEs, and [Ca2+](i) was evaluated. Angiotensin-II (AT-II) increased [Ca2+](i)

in a concentration-dependent way in both strains. Whereas in WKY, endogenously produced NO and cyclic GMP analog decreased the AT-II-induced [Ca2+](i); transient, they were ineffective in SHR RCEs. The cGKI level was low in SHR cells. However, after cGKI alpha re-expression, endogenous NO decreased the AT-II-induced [Ca2+](i) transient, while endothelial NO synthase and cGKI inhibition find more prevented it. The low

this website expression of cGKI in SHR accounts for the absent regulation of the agonist-induced [Ca2+](i) transient by the NO/cyclic GMP pathway. Studies on cGKI in humans could contribute to a better understanding of cardiovascular pathologies. Copyright (C) 2012 S. Karger AG, Basel”
“Recent evidence suggests that GABA(A) receptor ligands may regulate ethanol intake via effects at both synaptic and extrasynaptic receptors. For example, the endogenous neurosteroid, allopregnanolone (ALLO) has a similar pharmacological profile as ethanol, and it alters ethanol intake in rodent models. Additionally, recent evidence suggests that delta-subunit-containing extrasynaptic GABA(A) receptors may confer high sensitivity to both ethanol and neurosteroids. The purpose of the present study was to determine the effects of ganaxolone (CAN; an ALLO analog) and gaboxadol (THIP; a GABA(A) receptor agonist with selectivity for the extrasynaptic delta-subunit) on ethanol intake, drinking patterns, and bout characteristics in operant and limited-access self-administration procedures.

3 to 10 mg/kg p o , depending on the procedure These effects par

3 to 10 mg/kg p.o., depending on the procedure. These effects paralleled those obtained with the prototypical benzodiazepine anxiolytic diazepam or chlordiazepoxide. Moreover, when SR58611A was tested in acute or chronic

models of depression in rodents, see more such as the forced-swimming and the chronic mild stress tests, it produced antidepressant-like effects, which were comparable in terms of the magnitude of the effects to those of the antidepressant fluoxetine or imipramine. Supporting these behavioral data, SR58611A modified spontaneous sleep parameters in a manner comparable to that observed with fluoxetine. Importantly, SR58611A was devoid of side effects related to cognition (as shown in the Morris water maze and object recognition tasks), motor activity (in the rotarod), alcohol interaction, or physical dependence. Antagonism studies using pharmacological AZD6094 chemical structure tools targeting a variety of neurotransmitters involved in anxiety and depression and the use of mice lacking the beta(3) adrenoceptor suggested that these effects of SR58611A are mediated by beta(3) adrenoceptors. Taken as a whole, these findings indicate that the pharmacological stimulation

of beta(3) adrenoceptors may represent an innovative approach for the treatment of anxiety and depressive disorders.”
“To date, explanations for the origin and emergence of the alphabet of amino acids encoded by the standard genetic code have been largely qualitative and speculative. Here, with

the help of computational chemistry, we present the first quantitative exploration of nature’s “”choices”" set against various models for plausible alternatives. Specifically, we consider the chemical space defined by three fundamental biophysical properties (size, charge, and hydrophobicity) to ask whether the amino acids Suplatast tosilate that entered the genetic code exhibit a higher diversity than random samples of similar size drawn from several different definitions of amino acid possibility space.

We found that in terms of the properties studied, the full, standard set of 20 biologically encoded amino acids is indeed significantly more diverse than an equivalently sized group drawn at random from the set of plausible, prebiotic alternatives (using the Murchison meteorite as a model for pre-biotic plausibility). However, when the set of possible amino acids is enlarged to include those that are produced by standard biosynthetic pathways (reflecting the widespread idea that many members of the standard alphabet were recruited in this way), then the genetically encoded amino acids can no longer be distinguished as more diverse than a random sample.

Mammalian target of rapamycin (mTOR), a major downstream target o

Mammalian target of rapamycin (mTOR), a major downstream target of Akt, regulates p70S6 kinase and S6, both of which are involved in ribosomal biogenesis and protein synthesis. I investigated whether ferulic acid regulates mTOR, p70S6 kinase, and S6 phosphorylation during brain ischemic injury.

Rats were treated immediately with vehicle or ferulic acid (100 mg/kg, i.v.) after middle cerebral artery occlusion (MCAO). Brains tissues were removed at 24 h after the onset of MCAO and the cerebral cortex regions were collected. Selleck FHPI Ferulic acid reduced the MCAO-induced infarct volume. I showed previously that ferulic acid prevents the MCAO injury-induced decrease of Akt phosphorylation. In this study, MCAO injury induced decreases in mTOR, p70S6 kinase, and S6 phosphorylation levels, while ferulic acid attenuated the injury-induced decreases. Immunohistochemical staining demonstrated that ferulic acid prevented the MCAO-induced reduction in the number of positive cells for phosphorylated p70S6 kinase and phosphorylated S6. These findings suggest that ferulic acid has a neuroprotective function against focal cerebral ischemia by modulating p70S6 kinase expression and S6 phosphorylation. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Background: Low molecular weight iron dextran

(LMWID) is licensed for use as a total dose infusion (TDI) over 4-6 h. In order to improve patient convenience and cost-effectiveness of therapy, we investigated the safety and efficacy of adopting accelerated dosing regimens and compared this with a standard rate LMWID infusion.

Methods: A retrospective study of patients undergoing accelerated Selonsertib mouse and standard rate TDI of LMWID was conducted across three centres. A total of 1904 doses of LMWID were administered at an accelerated rate of 1

g over 1 h 40 min. This was compared with 395 patients who had standard rate infusion of 1 g LMWID over 3-4 h.

Results: There were eight minor adverse events in patients receiving accelerated dose LMWID (8/1904, 0.42%) in comparison to one adverse Tryptophan synthase event in patients receiving a standard regimen (1/395, 0.25%). No serious adverse events occurred. Serum haemoglobin and ferritin significantly improved in both groups.

Conclusion: TDI LMWID is a safe and efficacious method of iron replacement. Accelerated infusion regimen is safe and compares well with standard rate infusion regimen. Furthermore, accelerated TDI of LMWID enables greater numbers of patients to be treated and consequently there appear to be advantages for both patient and health resources.”
“The genome from the Saccharomyces pastorianus industrial lager brewing strain Weihenstephan 34/70, a natural Saccharomyces cerevisiae/Saccharomyces eubayanus hybrid, indicated the presence of two different maltotriose transporter genes: a new gene in the S.eubayanus subgenome with 81% of homology to the AGT1 permease from S.cerevisiae, and an amplification of the S.

Microinjection of the NMDA receptor antagonist MK-801 or the non-

Microinjection of the NMDA receptor antagonist MK-801 or the non-NMDA receptor antagonist DNQX into the RN blocked this excitatory effect induced by glutamate. However, microinjection of the metabotropic glutamate receptor (mGluR) antagonist (+/-)-MCPG into the RN had no effect. These results suggest that simulated microgravity can reduce excitability of RN neurons following a functional

impairment of glutamate receptors. NMDA and non-NMDA receptors, but not mGluRs, are involved in the mediation of glutamate-evoked excitation of RN neurons. The decrease in excitability of RN neurons tray be involved in simulated microgravity-induced muscle atrophy. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Opioids like morphine produce antinociception after MLN0128 research buy intrathecal administration. Being hydrophilic in nature, morphine also spreads rostrally which leads to respiratory depression.

Loperamide has been reported to produce antinociception after learn more both intracisternal and intrathecal administration. It is also hydrophobic, which could restrict its diffusion in the spinal canal. However, the mechanism of its anti nociceptive action after intrathecal administration is not definitely known. In the present study, the antinociceptive effect of loperamide was evaluated by the formalin test. It significantly inhibited Phase II flinching behavior. This antinociceptive effect was reversed by pre-administration of naloxone indicating that it was predominantly due to activation of opioid receptors. (C) 2008 Published by Elsevier Ireland Ltd.”
“Using a prospective design, this study examines the mediating effect of perceived control in explaining the predictive role of socioeconomic status (SES) in long-term changes in functional status as a consequence of the occurrence of coronary heart disease (CHD). We followed 221 older CHD patients

by using a community-based survey. We collected data on patients’ functional status before the onset of disease and I year after the diagnosis. Multiple linear regressions show, that SES predicts functional changes only in relation to physical functioning. Furthermore, self-efficacy, but not mastery, mediates the predictive role of SES in changes in physical functioning in CHD patients. Self-efficacy is the only aspect of control that Dichloromethane dehalogenase mediates the relation between SES and changes in physical functioning. Our findings provide a basis for future interventions in disadvantaged groups of older persons and ne v theoretical models of recovery processes.”
“Antipsychotics are often administered to traumatic brain injured (TBI) patients as a means of controlling agitation, albeit the rehabilitative consequences of this intervention are not well known. Hence. the goal of this study was to evaluate the effects of risperidone (RISP) and haloperidol (HAL) on behavioral outcome after experimental TBI.

By using in situ cleavage we generated the mature form of APRIL,

By using in situ cleavage. we generated the mature form of APRIL, comprising its N-terminal basic region, which has full biological activity: receptor binding capability and

proliferation induction activity. (C) 2009 Elsevier Inc. All rights reserved.”
“Few studies have investigated whether neuronal function in the amygdaloid complex is necessary for the occurrence of the cardiovascular response to natural (unconditioned) Selleck Rigosertib environmental threats. In the present investigation in conscious unrestrained Sprague Dawley rats we inactivated neuronal function in the amygdaloid complex acutely (bilateral muscimol injections) or chronically (unilateral or bilateral ibotenic acid injections) and measured the effect on sudden falls in tail artery blood flow elicited by non-noxious salient stimuli (sympathetic cutaneous vasomotor alerting responses, SCVARs). After acute bilateral injection of vehicle (200 nl Ringer’s solution) the SCVAR index was 81 +/- 2%, indicating that tail blood flow was reduced by 81% in response to the salient stimuli. After acute bilateral injection of muscimol (1 nmol in 200 nl of Ringer’s solution) into the amygdaloid complex the SCVAR index was 49 +/- 5%, indicating

that tail blood flow was reduced by 49% in response to the salient stimuli (p < 0.01 versus vehicle, n = 7 rats for vehicle and 6 for muscimol). One week after unilateral ibotenic acid lesions, the SCVAR index was 68 +/- 3%, significantly less than 90 +/- 1%, the corresponding value after unilateral injection of vehicle (p < 0.01, n = 6 rats in each group). After bilateral ibotenic acid Veliparib solubility dmso lesions the SCVAR Histone demethylase index was 52 +/- 4%, significantly

less than 93 +/- 1%, the corresponding value after bilateral injection of vehicle (p < 0.001, n = 6 rats in each group). lbotenic acid caused extensive neuronal destruction of the whole amygdaloid complex, as well as lateral temporal lobe structures including the piriform cortex. Our results demonstrate that the amygdaloid complex plays an important role in mediating the tail artery vasoconstriction that occurs in rats in response to the animal’s perception of a salient stimulus, redirecting blood to areas of the body with more immediate metabolic requirements. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Aims: To reveal the cause of the difference in activity of chitinase A from Vibrio proteolyticus and chitinase A from a strain of Vibrio carchariae (a junior synonym of Vibrio harveyi), we investigated the pH-dependent activity of full-length V. proteolyticus chitinase A and a truncated recombinant corresponding to the V. harveyi form of chitinase A.

Methods and Results: After overexpression in Escherichia coli strain DH5 alpha, the full-length and truncated recombinant chitinases were purified by ammonium sulphate precipitation and anion exchange column chromatography.