Currently, lithium, valproate, carbamazepine, chlorpromazine, hal

Currently, lithium, valproate, carbamazepine, chlorpromazine, haloperidol, risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole are indicated for the treatment of acute mania in the majority of European countries and North America, with some minor variations from country to country, and lithium, valproate, lamotrigine, olanzapine, aripiprazole, and quetiapine are indicated for maintenance treatment, Inhibitors,research,lifescience,medical again depending on the country. However, the gap between evidence base and clinical practice is still huge, and the majority of patients have to be treated with combinations of several drugs and psychosocial interventions Inhibitors,research,lifescience,medical in order to achieve

a. reasonable outcome from the clinical as well as functional point, of view. This may be particularly true for patients with rapid-cycling bipolar disorder, who may need complex combinations of therapies and sometimes physical treatments such as electroconvulsive Crenolanib CP-868596 therapy to achieve clinical stability. For these patients, as well as for those with

mixed states, for those with enduring subsyndromal symptoms, and ultimately Inhibitors,research,lifescience,medical for the majority of people with bipolar disorder, more efficacious, tolerable treatments are badly needed.
Bipolar affective disorder, type I (BP-I) is a severe mental illness marked by periodic extremes of mood state (manias), as well as (in most cases) episodes of depression and (in many cases) psychosis. The consequences of BP-I are severe, and involve both direct, and indirect, issues. Rates of suicide in BP-I patients are high,1,2 and =BP-I subjects also suffer from poorer quality of life and lower productivity than unaffected individuals.3 Inhibitors,research,lifescience,medical Annual public health costs Inhibitors,research,lifescience,medical (combined direct, and indirect) of BP have been estimated to be between 24 billion and 45 billion dollars.4,5 BP-I occurs in all populations that have been studied, with lifetime prevalence rates worldwide

of the order of one per every 100 individuals.6 Segregation analyses, Entinostat adoption studies, and twin studies have consistently shown that, regardless of the population studied, genetic factors play an important role in determining one’s risk of developing BP-I.7-9 Since little is known about the actual etiology of BP, it would be a major contribution to our understanding of the pathophysiology of BP if the genes responsible for the neurobiologie changes which underlie this disorder could be identified. The difficulty in finding genetic loci that, are involved in BP most likely derives from the complex nature of the illness. When multiple transmission inhibitor manufacture models for BP-I (the most, severe form of BP) have been tested, oligogenic epistatic models arc found to be the best fit, rather than models which purport one major locus.

By “reaction” we understand the whole class of voluntary and invo

By “reaction” we understand the whole class of voluntary and involuntary reflexes … in which … the affects are discharged. If this reaction takes place to a sufficient amount a large part of the affect disappears as a result. … If a reaction is suppressed [the affect] stays attached to the memory. The injured person’s reaction to the trauma only exercises a complete “cathartic” Inhibitors,research,lifescience,medical effect if it is an adequate reaction – as, for instance, revenge… . Abreaction, however, is not the only method of dealing with the situation that is open to a normal person who has this website experienced a psychical trauma. But language serves as a substitute for action: with its help, an affect can be “abreacted” almost as effectively. … If

there is no such reaction, in either deeds or words, any recollection of the event retains its affective tone. … A memory of such a trauma, even if it has not been abreacted, enters the great complex of associations, it comes alongside other experiences, which Inhibitors,research,lifescience,medical may contradict it, and

is subjected to rectification by other ideas. … In this way a normal person is able to bring about the disappearance of the accompanying affect through the process of association It may therefore be said that the. ideas which have become pathological have persisted with such freshness and affective strength Inhibitors,research,lifescience,medical because they have been denied the normal wearing-away processes by means of abreaction and. reproduction in states of uninhibited association (italicized Inhibitors,research,lifescience,medical in original). We have become convinced that the splitting of consciousness … under the form of “double

conscience” is present to a rudimentary degree in every hysteria and that a tendency to dissociation, and with it, the contain emergence of abnormal states of consciousness, is the basic phenomenon of this neurosis … in this view we concur with Janet … we must, however, mention another remarkable fact … Inhibitors,research,lifescience,medical namely, that these memories, unlike the memories of the rest of their lives, are not at the patients’ disposal. On the contrary these experiences are completely absent from the patient’s memory when they are in a normal psychical state, or are only present in a highly summary form ….( 1893, pp 7-11).26 Over time, Freud Dacomitinib came to disbelieve the reality of his patients’ tales of trauma. In his Autobiographical Study (1925),27 he wrote: I believed these stories and consequently supposed that I had discovered the roots of the subsequent neurosis… . If the reader feels inclined to shake his head at my credulity, I cannot altogether blame him. I was at last obliged to recognize that these scenes of seduction had never taken place, and that they were only fantasies which my patients had made up (p 34 ).27 However, like Janet before him, Freud kept being fascinated with the issue of patients’ apparent compulsion to arrange their lives in such a way that they would repeat their trauma over and over again.

2009, 2010) Of these, matched subsets of 39 and 46 also complete

2009, 2010). Of these, matched subsets of 39 and 46 also completed functional magnetic resonance imaging (fMRI) (Williams et al. 2009, 2010). Assessments: Heart rate and fMRI were recorded during a facial emotion viewing task, under both conscious and nonconscious conditions. DNA was extracted from cheek swab samples and genotyped for the polymorphism of the serotonin transporter gene (5-HTT-LPR) and COMT Val108/158Met genotypes (for details of Methods, Williams et al. 2009, 2010). selleck bio Validation outcomes: Greater fear reactivity Inhibitors,research,lifescience,medical indexed by both heart rate and

activation of brainstem, amygdala, and medial prefrontal cortex circuitry was associated with greater negativity relative to positivity bias. This association was pronounced in individuals with the “risk” alleles, 5 HTT-LPR Short and COMT Met. The findings indicate that a higher negativity bias is underpinned by genetic and fear circuitry susceptibility for emotional disorder. Ecological validation with real-world functional capacities The association between the Inhibitors,research,lifescience,medical full BRISC and proxy measures of real-world functional outcomes was established in the same sample of 55 participants used to assess construct validation against the ERQ and IC. These proxy measures included the following: Quality Inhibitors,research,lifescience,medical of Life assessed by

the World Health Organizations Qualify of Life scale, brief version (WHOQOL-BREF) scale (World Health Organization Group 1998) Satisfaction with Life Scale (SWLS; Diener et al. 1985) Work productivity, in terms of both absenteeism (hours absent from work) and presenteeism (performance level), assessed Inhibitors,research,lifescience,medical using the Health and Work Performance Questionnaire (HPQ; Kessler et al. 2003) Validation outcomes: Correlation analyses between the BRISC scales and the WHOQOL-BREF, SWLS, and HPQ, at a corrected P-value of 0.01, demonstrated the following associations: Negative correlations between lower negativity–positivity bias and higher WHOQOL-BREF psychological (r = −0.50, P < 0.0001) and social relationships (P = −0.39, P = 0.003) components of quality of life, and the presenteeism component of the screening libraries productivity on the HPQ (r = −0.39, P = 0.01) Inhibitors,research,lifescience,medical Positive correlations between higher emotional

resilience and higher scores on the WHOQOL-BREF psychological component (r = 0.52, P < 0.0001) and satisfaction with life on the SWLS (r = 0.34, P = 0.01) Positive correlations between higher social skills and higher scores on the WHOQOL-BREF components GSK-3 of physical health (r = 0.45, P = 0.001) and environment (r = 0.56, P < 0.0001), satisfaction with life (r = 0.42, P = 0.001) and presenteeism on the HPQ (r = 0.37, P = 0.008) Study research sites Participants were recruited from 12 medical research or clinical research sites. These sites agreed to collaborate as partners with Brain Resource to evaluate brain health in patients using a standardized set of assessments and contribute the data to a centralized library (the Brain Resource International Database).

Long-term effects beyond the neonatal period, however, are not su

Long-term effects beyond the neonatal period, however, are not sufficiently studied. Agonist maintenance: methadone Pioneering work by Dole and Nyswander in the 1960s55-57 provided the initial scientific basis for using the long-acting opioid agonist methadone for maintenance. Numerous studies since then58-62 have demonstrated that methadone maintenance of opioid addicts substantially reduces mortality and morbidity, the risk of new human immunodeficiency virus Inhibitors,research,lifescience,medical (HIV) infection, criminal activity, and illicit opioid

use, especially when used with enhanced ancillary services.63 Unfortunately, many programs do not provide these services, both because of decreased technical support government funding and increased private ownership. In the US, there are over 240 000 individuals maintained on methadone, while in some other countries, eg, Russia, government opposition Inhibitors,research,lifescience,medical to agonist maintenance prevents its use, even when high HIV rates exist. Federal regulations With a few exceptions, methadone may only be dispensed for opioid detoxification or maintenance treatment by opioid treatment programs certified by the Substance Abuse and Mental Health Administration (SAMHSA) and approved by the appropriate state

agency. Inhibitors,research,lifescience,medical Depending on criteria such as continued illicit drug use and employment, an increasing number of takehome doses is permitted, up to a maximum of a 1 -month supply after 2 years or longer. Pharmacology While heroin is short-acting and relatively ineffective orally, methadone is a long-acting, and orally effective, opioid. It is excreted primarily Inhibitors,research,lifescience,medical in the urine and is an agonist at li and 8 opiate receptors. Methadone is primarily metabolized through cytochrome P450 (CYP) enzymes, predominantly involving the CYP3A4 pathway. Drugs that increase the P450 enzymes, such as the retroviral agents for treating HIV, may increase methadone metabolism and lead to withdrawal symptoms, even in stable maintained patients. In Inhibitors,research,lifescience,medical contrast, drugs that inhibit these enzymes, such

as some selective serotonin selleck chemicals llc reuptake inhibitor (SSRI) antidepressants, may increase methadone levels and sedation.64-68 Effects are more likely early in treatment before plasma levels have stabilized.69 Physicians using methadone are advised to consult tables of drug interactions for complete listings. Dosing Methadone’s plasma GSK-3 half-life, once stabilized, averages 24 to 36 hours70 with a range of 13 to 50 hours, making it a useful once-daily maintenance medication compared with morphine or heroin. However, up to 10 days may be needed for such a steady state and before that, new patients, either in maintenance or given methadone for analgesia, are at risk of fatal overdose.8,71 Doses should not exceed 40 mg/day the first day of dosing or be increased over the next 2 weeks by more than 5 to 10 mg every 2 to 3 days.

A smaller, but still significant, sib-sib intraclass correlation

A smaller, but still significant, sib-sib intraclass correlation was found for Factor III (contamination/cleaning; P=.02) and

Factor II (symmetry/ordering/arranging). Limiting the sample to female subjects more than doubled the sib-sib intraclass correlations for Factor II. Another much smaller study of 40 sibling pairs from Brazil found significant, sib-sib intraclass correlations when both siblings were female for Factor IV (hoarding).94 When both siblings were male, they also reported a significant sib-sib intraclass correlation for Factor III (contamination/washing). Future efforts to define the genetically determined host, factors that may predispose someone to develop PANDAS is also clearly needed. Thus far, the only Inhibitors,research,lifescience,medical hint, Inhibitors,research,lifescience,medical has been that patients with rheumatic fever typically have positive family

histories of OCD, and that PANDAS cases have a higher rate of rheumatic fever in their familes.69,95 In sum, the use of quantitative traits that are familial may provide a powerful approach for detecting the genetic susceptibility loci that contribute to OCD. Our prediction is that some genes will be specific to certain OC symptom dimensions, while others will be “generalist” genes that influence the expression of OCD and closely related disorders including tic Inhibitors,research,lifescience,medical disorders, trichotillomania, body dysmorphic disorder, and various eating disorders. These generalist genes may exist within modules of coexpressed genes that are functionally related. Using this framework, it will be worthwhile

to determine whether overlapping transcriptional networks underlie the expression of the OC spectrum of normal phenomena as they are Inhibitors,research,lifescience,medical regulated by specific evolutionarily conserved neural networks. Then when these networks become dysregulated, for whatever reason, OCD and related disorders emerge as disorders of mind, brain, and behavior. Nongenetic risk factors Despite our enthusiasm for the identification of dimension specific and Inhibitors,research,lifescience,medical subtype specific OCD vulnerability genes, it should also be noted that environmental factors doubtless play an important, role in the transmission of these traits across generations. Indeed, the bulk Brefeldin_A of the evidence concerning familial risk has come from affected sibling-pair studies and genetic family studies. In contrast to twin and adoption studies, the design of these studies simply tests for familial transmission; they do not exclude the likely role of nongenetic familial transmission, in which family members can serve as inhibitor Pazopanib models for dysfunctional behaviors. More work is needed to identify the environmental factors that foster the onset and course of these symptoms. To date, the strongest evidence points to maternal adverse perinatal events,96-98 and early psychosocial adversities as being associated with the future development of OCD.99-103 Psychosocial stress is also a powerful determinant of future OCD severity, which in turn is predictive of the severity of future depressive symptoms.

11 This issue was resolved with the help of a conditional mouse

11 This issue was resolved with the help of a conditional mouse mutant, where the CRHR1 was deleted in specific brain areas.12 These studies made it clear that CRH produces depression-like symptoms independently of its pituitary action. What is badly needed is a set of gene tests and biomarkers identifying patients who are likely to respond to CRHR1 antagonists. In search of such information, CRH overexpressing mice were studied

in a specialized sleep laboratory, and it was found that these mice have REM-sleep disinhibition, ie, increased activity of Inhibitors,research,lifescience,medical paradoxical sleep where enhanced eye movements occur. This abnormality disappears once these transgenic mice are treated with CRHR1 antagonists.13 Likewise, patients that fulfilled

the criteria for major depression but had different sleep EEG signatures responded much better to a CRHR1 antagonist if they had increased REM density. That prompts quite unexpectedly the Inhibitors,research,lifescience,medical question of whether a sleep EEG analysis might help to identify patients that would benefit from a CRHR1 antagonist.11 Such a Inhibitors,research,lifescience,medical mechanism-based approach is required to make progress in the field, which will see a departure from blockbusters and the generation of individualized treatments based on gene tests and biomarkers. This proposition is further exemplified for mifepristone, which blocks the progesterone and glucocorticoid receptors (GR). Research led by Alan Schatzberg postulated that the hypercortisolemia observed in many patients with psychotic

depression is enhancing dopaminergic neuro-transmission.14 Therefore, blocking GR in dopaminoceptive Inhibitors,research,lifescience,medical neurons could be beneficial for these patients. In fact, mifepristone, by blocking GR, is a successful treatment for many, but not all patients with psychotic Inhibitors,research,lifescience,medical depression. Here again, the need for biomarkers allowing to identify GR antagonist responders is Ivacaftor EC50 obvious. Similar to the results from CRH overexpressing mice, an animal model that generates biomarkers helping the clinician to identify responders to GR antagonists is much more helpful than struggling endlessly with the generation of Dacomitinib a mouse model for psychotic depression.15 The lesson we have learned in the past is that there is no chance of developing a mouse model that fits closely to a set of diagnostic criteria for human psychiatric disorders.16 The forced swim test, for example, is not telling us anything about depression, and is even counterproductive for discovery of antidepressants beyond monoaminergic mechanisms of action. It is unlikely that complex human diseases such as schizophrenia, depression, obsessive-compulsive disorder, anorexia, or panic disorder can be modeled in a mouse, fish, or fly.

These results suggest that SBE7-β-CyD increased the bioavailabili

These results suggest that SBE7-β-CyD increased the bioavailability and persistence of the blood-glucose lowering effect of insulin glargine after subcutaneous administration of an insulin glargine solution to rats. Table 3 In vivo pharmacodynamics parameters of insulin glargine with or without SBE7-β-CyD (200mM). (1) Time to nadir blood glucose concentration. (2)

Nadir blood glucose concentration. (3) The cumulative percentage of change in serum glucose Inhibitors,research,lifescience,medical … 4. Conclusions In the present study, we revealed that Sul-β-CyD and SBE7-β-CyD increased solubility of insulin glargine. Furthermore, SBE7-β-CyD suppressed the formation of oligomer and enhanced the dissolution rate of insulin glargine from its precipitate, compared to that of Sul-β-CyD. In addition, we Inhibitors,research,lifescience,medical demonstrated that SBE7-β-CyD increased the bioavailability and persistence of the blood-glucose lowering effect of insulin glargine after subcutaneous administration of an insulin glargine solution to rats, probably due to the inhibitory effects of SBE7-β-CyD on the enzymatic degradation at the injection site, resulting from

the interaction with insulin glargine molecules. These findings indicate that SBE7-β-CyD can be a useful excipient for a cisplatin synthesis peakless profile of insulin Inhibitors,research,lifescience,medical glargine. Acknowledgments The work described in this paper presents additional results from a Joint Research Project by Kumamoto University and its collaboration partner CyDex

Pharmaceuticals, Inc. and the authors wish to acknowledge this collaboration as well as funding support from CyDex Pharmaceuticals, Inc. The authors oblige Inhibitors,research,lifescience,medical to Sanofi-Aventis for the supply of insulin glargine.
Doxorubicin (Adriamycin) is a commonly used anti-cancer drug. It is most often used against breast and esophageal carcinomas, Inhibitors,research,lifescience,medical osteosarcoma and soft-tissue sarcomas, and Hodgkin’s and non-Hodgkin’s lymphomas [1]. The effectiveness of doxorubicin (DOX) in treating various types of cancers is greatly limited by the serious side effects caused by the drug. The initial side effects caused as a result of DOX administration include less serious symptoms, such as nausea, vomiting, myelosuppression, and arrhythmia, which are usually reversible [1]. However, DOX-associated cardiomyopathy Anacetrapib and congestive heart failure have raised grave concern among health practitioners [2]. A widely researched approach of increasing the efficacy, while lowering the deleterious side effects caused by anti-cancer agents such as doxorubicin, is of selleck screening library developing nanoparticle-based drug delivery systems [3–5]. Various kinds of nanoparticles have been studied for the delivery of DOX, which include poly(butylcyanoacrylate) [6], poly(isohexylcyanoacrylate) [7], poly(lactic-co-glycolic acid [8], chitosan [9], gelatine [10], and liposomes [11]). In addition, Dreis et al.

Notably, miR-21 exerts its actions by regulating

Notably, miR-21 exerts its actions by regulating Gefitinib the

expression of the same target genes as mouse/human miR-21, namely Sprouty, Pdcd4, and Ptenb. 58 MiR-138, which was specifically expressed in the developing ventricular chamber, was shown to be required for establishment of chamber-specific gene expression patterns. MiR-138 acts by targeting multiple members of the retinoic acid signaling pathway, to prevent ventricular expansion of gene expression normally restricted to the atrio-ventricular valve region. 59 Last, but not least, a recent study reported a putative mutual cross-regulation mechanism between the TF Tbx5 and miR-218-1, and demonstrated its implication in heart development in zebrafish. 60 Of note, Tbx5 gene expression levels have an overt effect on heart development, and their dysregulation has been related with the establishment of congenital heart defects. Similarly, the Tbx5 downstream targets miR-218-1 and its host gene Slit2 are

known to be involved in heart development. Specifically, miR-218-1 was shown to suppress the expression of Robo receptors (Robo1,2), which interact with Slit family ligands to facilitate cell guidance during development. Evidently, the miR-218-1 and Slit/Robo form a regulatory loop required for heart tube formation in zebrafish. 61 The exact role of miR-218-1 in Tbx-5 regulation, though, is still being explored. 60 Additional information on cardiac development-related miRNAs has emerged from studies in the Mexican axolotl (salamander). Interestingly, a group investigated the role of a human fetal heart microRNA which is thought to be related to the human miR-499 family, and was therefore named miR-499c, in mutant axolotl hearts in organ culture. Accordingly, the axolotl hearts with abnormal development (without tropomyosin expression, sporadically beating etc) were incubated with the miR-499c, which was able to induce expression of cardiac markers (tropomyosin, troponin, α-syntrophin) in these hearts. 62 Evidently, miR-499c treatment promoted the formation AV-951 of cardiac myofibrils in mutant

axolotl hearts, thus showing the potential to restore normal embryonic heart development in this species. 62 As presented in the following section, miR-499 possibly plays a key role during human cardiomyocyte (CMC) differentiation, and hence the role of the new miR-499c in cardiac development requires further investigation. miRNA expression in embryonic stem cell-derived cardiomyocytes However informative studies in animal models may be, they still have to be validated in humans. To this end, human embryonic stem cell-derived cardiomyocytes (hESC-derived CMCs) are now providing valuable new insights. The first miRNA profiling study of hESC-derived CMCs led to the identification of 711 unique miRNAs.

The current task can be contrasted with two popular measures of

The current task can be contrasted with two popular measures of working memory (e.g., n-back; Owen et al. 2005) and the Sternberg tasks (Sternberg 1966; Manoach et al. 2003). Although a working memory task, our task differs in theoretically interesting ways from the classic paradigms that gave it an advantage for answering our hypotheses. We used a variant of a 1-back task in which difficulty in cognitive processes increased with the number of relevant cues, in this case colors.

Inhibitors,research,lifescience,medical In terms of cognitive load and methodology, what sets our fMRI research paradigm apart is the following: First, difficulty was parametrically graded across classes of items (according to theoretical modeling and prior developmental work, Arsalidou et al. 2010). Second, executive demand was Inhibitors,research,lifescience,medical useful site controlled (i.e., constant across levels). Third, most other imaging studies fail to consider a sufficient number of graded difficulty levels (Rypma et al. 2002 being an exception in the verbal domain). Without these many levels, it is impossible to account for the capacity limitations in mental attention proposed by both working memory (Cowan 2005) and developmental researchers (e.g., Pascual-Leone 1970; Halford et al. 1998). Fourth, in terms of statistical power, the current task was designed as a block paradigm with relatively short trials in order Inhibitors,research,lifescience,medical to accommodate

six levels of difficulty. In this regard, it should be noted that fMRI studies that have many conditions face a trade-off between the number of trials needed for sufficient statistical power and the time participants Inhibitors,research,lifescience,medical can stay in the scanner, particularly so in studies with children (Gaillard et al. 2001). The range of levels of working memory capacity that can be assessed using our tasks is very relevant for the study of developmental and clinical populations. With a future aim to use the tasks for neuroimaging with developmental Inhibitors,research,lifescience,medical populations, we were interested

in methods that minimize extraneous developmental-laden factors (we used short runs, child friendly content, etc.; see Gaillard et al. 2001; Luna et al. 2010). To facilitate comparisons across populations, Luna et al. (2010) recommended the use of tasks with well-understood neural correlations in the adult literature. Thus, prior to this study, our working memory task was validated behaviorally in adults as well as in children (Arsalidou Anacetrapib et al. 2010). Behavioral performance followed a graded age-dependent growth pattern such that 7–8, 9–10, 11–12, 13–14 year olds, and adults could cope with working memory demands up to 3, 4, 5, 6, and 7 units, respectively (Arsalidou et al. 2010). These observations point to a linear pattern in working memory development that is captured by our task. It is on this basis that our current hypotheses and analyses investigate particularly a linear pattern.

Studies of GSH interactions with toxic heavy metals (Hg, Cd, Pb)

Studies of GSH interactions with toxic heavy metals (Hg, Cd, Pb) are important to gain better understanding of the environmental effects on human health. In particular, the elucidation of mechanisms leading to increased susceptibility to autism [19, 20], diabetes [21], and other diseases [21-26] due to diminished active GSH levels in cells and body fluids and the reduced antioxidation capacity [27] to protecting against radicals, should enable us to devise preventive measures to effectively diminish the spread and decrease the occurrence of these diseases. The involvement of GSH in counteracting heavy metal poisoning and organic peroxide neutralization is associated with its rich functionality and its key role in the GSH/GSSG system of redox regulation in living organisms.In this work, we have investigated the immobilization of GSH on a cysteamine-SAM (CA-SAM) formed on Au piezoelectrodes by adsorptive dissociation of a disulphide, cystamine. The change in film permeability was investigated using Hg(II) ion probe which offers rich reactivity for voltammetric analysis and large molar mass easily detectable by the electrochemical quartz crystal nanogravimetry (EQCN) [28, 29]. The electrochemistry of Hg(II) on noble metal electrodes has been studied extensively on polycrystalline Au [30-37], Au nanoparticles on glassy carbon [38] and on single crystal Au(111) surface [39-49]. Hg deposition on graphite [50, 51] and platinum [52] electrodes have been investigated using EQCN. Thin Hg films on glassy carbon [53-56] and Ag microdisk [57] have been developed for heavy metal speciation by stripping voltammetric methods. In our recent studies of GSH-SAM on Au [3, 4], we have observed easy penetration of Hg(II) ions and their discharge at the bottom of ion-channels. In the present work, the films were modified by immobilization of GSH on CA-SAM to control the film permeability and to selleck screening library uncover the thiol group of GSH to enhance functionality of the film.2.?Results and Discussion2.1. EQCN voltammetric analysis of Hg(II) processes at Au/CA and Au/CA-GSH piezoelectrodesThe electrochemical processes on a cysteamine-SAM (CA-SAM) modified Au electrode are hindered by blocking the access of electroactive species to the electrode surface. However, due to the short length of the carbon chain, the CA-SAM films are less compact and more disordered than aminothiol films with longer alkyl chains. On the other hand, the glutathione-SAM films (GSH-SAM) with longer peptide branches form gated ion channels with high ion permeability [1-5, 65-67]. In the following experiments, we have examined the effect of GSH bound to the CA-SAM on Hg(II) permeability and reactivity and found rather unusual behavior of these films.