Thirty-two functional (T2* weighted) and

Thirty-two functional (T2* weighted) and obviously anatomical (T1 weighted) oblique slice were acquired along the ac-pc plane (3 mm thick, no gap), covering the whole temporal lobe and most of the frontal lobe

(TR = 2500 msec, TE = 35 msec, flip angle = 90°, voxel size = 2.3 × 2.3 × 3 mm). In addition, selleck chem Imatinib Mesylate high-resolution anatomical images were acquired for each subject using fast spoiled gradient echo (SPGR) sequence. In-plane anatomical images were Inhibitors,research,lifescience,medical used to align the functional data with the high-resolution anatomical data, allowing volume-based statistical analyses of signal changes along time. Data analysis fMRI data were preprocessed, analyzed, and visualized using MATLAB (The Mathworks, Nattick, MA) and mrVista tools ( Individual subject analyses were applied at native space of each participant, without spatial smoothing, in order to maintain the high spatial resolution provided by MRI. The first five fMRI volume images of each run were excluded from analysis to ensure steady-state Inhibitors,research,lifescience,medical magnetization. General linear model (GLM) predictors were constructed to estimate the relative contribution of each condition to every Inhibitors,research,lifescience,medical voxel’s time course, using a boxcar function convolved with a

canonical hemodynamic response function (HRF). Spatial contrast maps were computed for each contrast of interest, based on voxel-wise t-tests between the weights of relevant predictors. Functional ROIs were selected by marking continuous clusters of voxels that passed the threshold of p < 10−3 (uncorrected) within anatomically Inhibitors,research,lifescience,medical defined borders, as detailed below. This threshold was equivalent to a false discovery rate (FDR) corrected

value of q < 0.1. ROIs were defined in left inferior frontal gyrus (LIFG), bilateral posterior superior temporal sulcus (pSTS), and bilateral anterior superior temporal sulcus (aSTS). The decision Inhibitors,research,lifescience,medical to focus on this particular set of ROIs was guided by numerous preceding studies of speech processing and current models of speech processing (e.g., Scott and Johnsrude 2003; Price et al. 2005; Friederici 2011 among many others), and by a general inspection of the individual data confirming the existence of consistent activation in these areas for speech versus rest. The anatomical Cilengitide borders of the ROIs were defined as follows: (a) IFG: pars opercularis and pars triangularis of the IFG; (b) pSTS: the posterior third of the superior temporal sulcus, including BA 39 bordering BA 37, BA 22; (c) aSTS: the anterior third of the STS, including BA 38 and the anterior part of BA 22, bordering BA 21. Mean cluster size was calculated by averaging the volumes of activated voxels within an ROI across all participants, considering null activation as zero. Time course data were collected from ROI voxels identified by Speech versus SCN contrast in the native in-plane slices to avoid smoothing and interpolation.

In parasitic diseases, human sleep was studied by our team in the

In parasitic diseases, human sleep was studied by our team in the Gambian form of human African trypanosomiasis, sleeping sickness, which is due to the injection of trypanosomes by tsetse flies. In both viral and bacterial infections, the initial host’s immune reaction and hypersomnia, especially centered on SWS, develop concomitantly. In some diseases, such as Whipple’s disease43 or human immunodeficiency

virus (HIV) infection, autoantibodies are produced in the second phase and a dramatic decrease in, or disappearance of, Inhibitors,research,lifescience,medical sleep may occur.44 On the contrary, despite an extensive immune reaction during the initial hemolymphatic stage of human African trypanosomiasis, sleep remains undisturbed.45 However, in the second meningoencephalitic stage, autoantibodies reference 4 against nervous structures are widely produced, and both sleep and wakefulness are Inhibitors,research,lifescience,medical impaired due to the penetration of the trypanosome

into the central nervous system. At this stage of sleeping sickness, a “complex polysomnographic syndrome” is observed with disappearance of circadian rhythmicity of the alternation of sleep and wake episodes, which occur at any moment of the day or night, and Inhibitors,research,lifescience,medical appearance of anomalies in sleep structure, and the occurrence of SOREMP45’46 In any case, sleeping sickness is not a hypersomnia per se, but rather a major disorder of sleep structure and its circadian regulation. Therefore, in bacterial and viral diseases sleep modifications are coupled with immune reactions. The uncoupling between the acute phase of the immune reaction in sleeping sickness and sleep-wake patterns is not yet understood. Inhibitors,research,lifescience,medical Hypersomnia associated with metabolic or endocrine diseases Rarely, hypersomnia may complicate diabetes, hepatic encephalopathy, hypothyroidism, and acromegaly.47 Breathing disorders and periodic leg movements that often accompany metabolic disorders should be explored in the genesis of such hypersomnia. Breathing-related sleep disorder and periodic limb movements in sleep and sleep apnea syndromes Sleep apnea syndromes3 and periodic limb movements in sleep48 are the most frequent causes

of Inhibitors,research,lifescience,medical excessive daytime sleepiness. Limb movement ilsoriers Limb movement disorders related to rest and sleep have been divided into two syndromes, restless legs syndrome and periodic limb movements Dacomitinib during sleep. The latter are commonly associated with the former, as well as with various sleep disorders, such as insomnia, narcolepsy, and sleep apnea syndrome, and also physiological aging. The limb movements arouse the patients who is unaware of his or her highly fragmented sleep.48 Polysomnography shows lengthened sleep latency, increased waking after sleep onset, and numerous sleep stage changes; stage 1 is elevated, while SWS is low. A chronic sleep-wake disorder may develop, causing excessive daytime sleepiness. Restless legs syndrome is a sensorimotor disorder characterized by an urge or a need to move the limbs.

1991) Australia and New Zealand (1) Questionnaire


1991) Australia and New Zealand (1) Questionnaire

survey of ECT practice and attitudes to medical superintendents at hospitals. Frequency of unilateral versus bilateral electrode placement main aim. Sparse ECT utilization data Galletly CA (Galletly et al. 1991) South Australia (4) Too old, use of ECT data at hospital in Adelaide from 1981 to 1985 (five years). [Decline in use over period due to reduction of ECT for patients with schizophrenia] Gassy JE (Gassy and Rey 1990) NSW, Inhibitors,research,lifescience,medical Australia (4) Too old, a general hospital psychiatry unit use of ECT from April 1982 to December 1987 Ikeji OC (Ikeji et al. 1999) Nigeria (2) A prospective open-label study of 70 unmodified ECT treated patients without rate or prevalence data Odejide AO (Odejide et al. 1987) Nigeria (4) Sparse data from <1990, records from 1982 and1984 examined. Unmodified bilateral Inhibitors,research,lifescience,medical ECT. Modified ECT was tried in 1979, but found too expensive. Thirty percent of patients ECT treated in 1984 and average no. of ECTs six, range 1–19 Okasha TA (Okasha 2007) Egypt (2) General article about ECT use, economic aspects, problems of training, ethical issues, and discrepancies between developed and developing countries

in its application. No ECT utilization Inhibitors,research,lifescience,medical data Alhamad AM (Alhamad and,al–Haidar 1999) Saudi Arabia (3) Parallel publication, same data presented as in other included reference by same author (Alhamad 1999) Hermann RC (Hermann et al. 1999) USA (1) Retrospective study of ECT use among beneficiaries of

a New England insurance company in 1994 and 1995 Inhibitors,research,lifescience,medical Olfson M (Olfson et al. 1998) USA, New York (1) ECT use for general hospital in patients with only recurrent major depression diagnoses and estimate of effect on prompt ECT on the length of stay and cost of inpatient care Fink M (Fink and Kellner 2007) USA (1) General about ECT practice, no primary Inhibitors,research,lifescience,medical data Eranti SV (Eranti and McLoughlin Drug_discovery 2003) UK, USA (2) Editorial article state of the art, no primary data Thompson JW (Thompson et al. 1994) USA (4) Too old, National Institute of Mental Health (NIMH) data, type 2 diabetes ECT-treated patients in 1975, 1980, and 1986, focusing on data from 1980 and 1986 Levav I (Levav and Gonzalez 1998) Latin America (3) Parallel publication in English, read me replication of primary data presented in earlier study/ publication in 1996 (Levav and Gonzalez 1996) Glen T (Glen and Scott 2000) Edinburgh, Scotland, UK (1) Calculated annual and aggregate rates of ECT use by consultant teams, not relevant Fergusson G (Fergusson et al. 2003) Scotland (3) Parallel publication, same data presented in included 2004 publication (Fergusson et al.

Negative factors

that decrease synaptogenesis in a circui

Negative factors

that decrease synaptogenesis in a circuit-specific manner (eg, stress, excess glucocorticoids, reduced trophic support, and increased inflammatory cytokines) increase vulnerability and/or cause depression, while treatments or conditions that enhance synaptogenesis and increase connectivity (eg, neurotrophic factors, NMDA antagonists) have antidepressant actions and reduce vulnerability. The current review will focus on the signaling pathways and targets that underlie neuronal atrophy, and conversely those that contribute to the reversal of synaptic deficits caused Inhibitors,research,lifescience,medical by stress and depression, notably the role of neurotrophic factors. However, there are also other dysregulated systems of interest that will not be covered in this review, including proinflammatory cytokines, sex steroids Inhibitors,research,lifescience,medical (notably estrogen), and metabolic/feeding factors (ie, insulin/diabetes, leptin, and grehlin) to name a few that play an important role in the pathophysiology of depression and that could provide new therapeutic targets.

Disrupted connectivity of cortical and limbic depression circuitry Brain imaging and postmortem studies have identified key structures involved in the regulation of mood and depression, including the prefrontal cortex (PFC), hippocampus, cingulate cortex, amygdala, and basal ganglia.5,10 Blood flow and functional Inhibitors,research,lifescience,medical imaging studies have identified regions with reduced (PFC and hippocampus) or increased (subcallosal cingulate cortex Inhibitors,research,lifescience,medical and amygdala) activity. Together these studies have contributed to the emergence of a functional depression circuit. Altered activity and functional connections between the regions within this circuit correlate with unbalanced behavior that characterizes depression (see refs 4,5,10 for a complete description and discussion of these models). One model is based on extensive

evidence of decreased Inhibitors,research,lifescience,medical function and activity of the PFC and connections to and from other limbic and subcortical structures implicated in depression.5 Decreased function of the PFC in depressed patients underlies certain abnormal responses (eg, decreased reaction time and cognitive function), as well as a corresponding gain of function of the amygdala (loss of control of emotion and mood, and increased fear anxiety and IIPA axis reactivity), which is negatively controlled by PFC. Anacetrapib Disruption of connections between the PFC and amygdala, as well as the ventral striatum, could also contribute to decreased motivation and reward in depression, which could underlie disrupted eating, sleeping, and libido. While this circuit model may be oversimplified, there is sufficient evidence from human, as well as animal studies (see below) to support the hypothesis that there is loss of function, in part from decreased connections between PFC and other brain regions.

Compelling evidence indicates that HAPE is a hydrostatic-induced

Compelling evidence indicates that HAPE is a hydrostatic-induced permeability leak with mild alveolar hemorrhage.62,64,65 Two explanations have been suggested. The first is that that hypoxic pulmonary vasoconstriction is not homogeneous; consequently, pulmonary capillaries supplied by dilated arterioles are exposed to high pressures which cause damage to the capillary walls (stress failure) and leads to a leak of high-protein edema fluid with erythrocytes.4 The second explanation hypothesizes an

increase in pulmonary capillary pressures due to hypoxic pulmonary venous constriction.62,65 Regardless of the mechanisms, successful Inhibitors,research,lifescience,medical prophylaxis and treatment of high-altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary

hypertension is crucial for the development of high-altitude pulmonary Inhibitors,research,lifescience,medical edema.63,66 There are no randomized controlled trials evaluating treatment strategies. Oxygen, rest, and descent are commonly agreed upon.59,66 When patients fail to respond to conservative measures or develop HAPE in remote settings, nifedipine is recommended, 10 mg orally initially and then 30 mg of the extended release formulation orally every 12–24 hours.66 Phosphodiesterase inhibitors such as tadalafil have been shown to prevent Inhibitors,research,lifescience,medical HAPE in susceptible individuals67 and may also be effective in patient management. Some physicians are now employing Inhibitors,research,lifescience,medical combination

therapy with nifedipine and phosphodiesterase inhibitors,68 although these are off-label uses. If descent is not possible, use of a portable hyperbaric chamber is recommended. AMS: PREVENTION AND TREATMENT Drugs used in the prevention and management of AMS click this include acetazolamide, Inhibitors,research,lifescience,medical dexamethasone, phosphodiesterase inhibitors, and analgesics. Strategies to prevent AMS include preacclimatization, copious water consumption, and a high-carbohydrate diet. ACETAZOLAMIDE Acetazolamide is a potent carbonic anhydrase inhibitor; AV-951 its efficacy in preventing and ameliorating AMS has been well demonstrated although there is still debate regarding the optimal dose.69–71 A recent double-blind, randomized, placebo-controlled study in the Everest region of Nepal showed that 125 mg twice a day was just as effective in preventing AMS as 375 mg twice a day.69 In this study, the incidence of AMS among subjects taking acetazolamide averaged about 22% compared to 51% for those taking a placebo. Acetazolamide is not a panacea; a substantial percentage of subjects taking acetazolamide still develop AMS. In fact, on Kilimanjaro, where the rate of ascent tends to be faster than in Nepal, the incidence of AMS in those taking acetazolamide (250 mg twice a day) was 55% versus 84% for a comparison/placebo group.

Responsibilities Holding a child responsible for certain obligat

Responsibilities. Holding a child responsible for certain obligations invites him or her to share in the adults’ reality, teaches mutual dependence, and dispels the notion of a perpetual free ride. Safely and subsistence. Freedom from fear and want is a prerequisite of freedom for growth, exploration, and opportunity. Opportunities. All children should have access

to quality medical care, education, recreational activities, and vocational choice. Traditions. Ritual and repetitive family, cultural, or religious events not only enhance the present; they also enrich the future and endow the past with a sense of continuity and community. Altruism. To receive a kindness or to bestow one can be a moving experience Inhibitors,research,lifescience,medical for anyone, at any age. Human beings seem to need reminding to bring altruism forth and to battle the fear that opposes Inhibitors,research,lifescience,medical it. Children do, in fact, model their parents’ generosity and altruism. Values. Young people need to be inspired, to believe in a reason for being beyond the mundanities of life. Their essential energies are longing to be stimulated and energized. Idealism can more readily be kindled in youth than at any other time of life. The tetrad of Bs In studies done on youth and young adults in a variety of settings,6,22-25 and in interview research with

elderly people,26 Inhibitors,research,lifescience,medical four particular determinants repetitively and consistently manifested themselves in evaluating the self-perceived satisfaction and worth of one’s Inhibitors,research,lifescience,medical life. They are: (Personal) being – a sense of self. This refers to one’s self-image and accommodation to one’s sense of identity. It includes an appreciation of strengths, as well as an awareness of one’s limitations, and reflects a perception of being “grounded,” comfortable in one’s skin

(“le confort dans sa peau”). Inhibitors,research,lifescience,medical (Social) belonging. This refers to a sense of being an integral, accepted, appreciated part of a community. It is more than merely being with like-minded people; support and nurturance are dc rigeur. It selleck chem encompasses the sharing of noteworthy personal (pain and pleasure) experiences, mutual empathy, common goals, and a Batimastat sense of being affiliated and “connected” in a basic, meaningful way. (Ideological) believing. This is the sense of personal embodiment of an overriding system of values and principles of life, beyond the everyday mundanities of living. This is especially so beyond unbridled competition, materialism, and acquisitiveness. It refers to a “higher order” raison d’être, a moral compass, and even a spiritual guide (although it need not be religious in nature). (Altruism) benevolence. This serves to complete the tetrad of Bs, but it is clearly related to the other Bs and really depends on the existence of the others. This encompasses the degree to which an individual is authentically generous and generative.

When a patient dies with cardiac arrest, the other vital organs

When a patient dies with cardiac arrest, the other vital organs can be preserved, but for a limited time only, until harvesting and implantation can take place. Actions to preserve the organs involve inserting special cannulas that can perfuse the kidneys or other organs with the adequate preservation solutions, until consent is obtained from the family, and until the surgery can take place. Obviously, family Inhibitors,research,lifescience,medical consent is mandatory in most promotion info countries before harvesting can take place; however, special cannulas must be inserted promptly during cardiopulmonary resuscitation, before consent is given. This can be viewed as a temporary organ preservation act until the family and patient’s

past requests can be validated. This assures that the rights of the patient or the family to agree to organ donation can be preserved until they can be

reached and consent sought. While such programs may require a special set-up and expertise, they can increase the availability of organs for donations by 10%–30% if done properly.26,27 Inhibitors,research,lifescience,medical In Israel such programs are not implemented yet, although planning is underway. Immunosuppressive therapy, preventing organ rejection, has been the landmark in organ transplantation, with calcineurin inhibitors (CNI) being the backbone of this treatment. Nevertheless, major adverse events and persistent risk of chronic graft rejection Inhibitors,research,lifescience,medical continue to be a challenge to transplantation. Development Inhibitors,research,lifescience,medical of new agents with modern techniques to monitor immunosuppressant activity has made significant progress.28 The mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus involve a class of drugs suppressing T cell proliferation and reducing tumor growth. In solid-organ transplantation, the combination of a CNI and an mTOR-inhibitor

is a potent immunosuppressive therapy that effectively prevents the incidence of acute rejection, although the potential nephrotoxic impact must be considered in the longer term. There is no doubt that increased understanding of immune responses to transplantation, with development of new therapeutic regimens, will lead to more potent and less risky adverse event profile Inhibitors,research,lifescience,medical and will continue to improve both the short- and long-term outcome of organ transplantation. Presumed consent for organ transplantation is legislated in several countries. It has been claimed that presumed consent may increase the rate of deceased organ transplantations. Cilengitide Rithalia et al.29 have reviewed five studies comparing donation rates before and after the introduction of legislation for presumed consent, eight studies comparing donation rates in countries with and without presumed consent systems, and 13 surveys of public and professional attitudes to presumed consent. The authors conclude that presumed consent is associated with increased organ donation rates; however, it is unlikely to be the sole explanation for the variation in organ donation rates between countries.

The latter group of patients also received clopidogrel, low molec

The latter group of patients also received clopidogrel, low molecular weight heparin, or glycoprotein IIb/IIIa inhibitors less frequently than the group PLK inhibition selleck referred for PPCI. Among patients treated with fibrinolysis, 96% underwent subsequent coronary angiography (38% within 3 hours of fibrinolysis, 23% between 3 and 24 hours, and 39% beyond 24 hours), with most of them (84%) undergoing PCI. 32% of patients in the fibrinolysis group required urgent referral for “rescue”

PCI. Survival at 5 years was 88% in patients receiving fibrinolysis and 84% for those undergoing PPCI (HR, 0.73; CI, 0.50–1.06; p = 0.1). When the timing of administration of fibrinolysis was considered, prehospital fibrinolysis was associated with lower 5-year mortality (HR, 0.57; CI, 0.36–0.88), while in-hospital fibrinolysis was associated with a trend toward increased 5-year mortality (HR, 1.19; CI, 0.72–1.96) compared to PPCI. The investigators also studied the subgroup of patients who sought medical attention within 180 minutes from the onset of symptoms (STREAM-like population). 5-year survival in this population was 88% and 81% in the fibrinolysis and PPCI groups

respectively (HR, 0.63; CI, 0.41–0.98; p = 0.039). However, in a propensity score-adjusted matched analysis, the benefit seen with prehospital fibrinolysis and with fibrinolysis (pre- or in-hospital) in the STREAM-like population did not remain statistically significant. Discussion In agreement with several recent studies 10–13 as well as the current American and European practice guidelines, 2,3 both STREAM and FAST-MI support the current recommendation of performing a coronary angiogram within 3–24 hours after successful fibrinolysis when timely PPCI is unavailable. However, extrapolating these findings

to other healthcare systems around the world should be done with caution for the following reasons: • STREAM randomized a very specific group of STEMI patients, namely those with a symptom onset-to-FMC of less than 3 hours. It is well recognized that the fibrinolytic agents are more effective early in the course Drug_discovery of STEMI because of the absence of fibrin cross-linking in the fresh thrombus, and this effect progressively declines after the first 3 hours. 14 Similarly, two-thirds of the FAST-MI patients receiving fibrinolysis did so prior to hospital admission. It remains unclear whether these finding are also applicable to late presenters. • The fibrinolytic agent used in STREAM and in the majority of FAST-MI patients was tenecteplase (TNK) which has an extended half-life allowing for a single bolus administration. TNK is more fibrin-specific, is associated with less intracranial hemorrhage, and higher rates of infarct artery patency compared to streprokinase – which remains the most frequently administered fibrinolytic agent worldwide.

Changes associated with DLB include preservation of hippocampal a

Changes associated with DLB include preservation of hippocampal and medial temporal lobe volume on magnetic resonance imaging

(MRI)35,36 and occipital hypoperfusion on single-photon emission computed tomography (SPECT).37,38 Other features, such as generalized atrophy,36 white matter changes,39 and rates of progression of whole brain atrophy,40 appear to be unhelpful in differential diagnosis. Dopamine transporter loss in the caudate and putamen, a marker of nigrostriatal degeneration can be detected by dopaminergic SPECT and, in preliminary studies, has shown specificity and sensitivity of 85% or higher, and may be particularly helpful.41,12 Fluctuating cognition The Inhibitors,research,lifescience,medical profile of neuropsychological impairments in patients with DLB differs from that of AD and other dementia syndromes,43 reflecting the combined involvement of cortical and subcortical pathways and relative sparing of

the hippocampus. Patients with DLB Inhibitors,research,lifescience,medical perform better than AD on tests of verbal memory,44 but worse on visuospatial performance tasks45 and tests of attention.46 Fluctuations in cognitive function, which may vary over minutes, hours, or days, occur in 50% to 75% of patients, and are associated with shifting levels of attention and alertness. The assessment of fluctuating cognitive impairment Inhibitors,research,lifescience,medical poses considerable difficulty to most clinicians and has been repeatedly Inhibitors,research,lifescience,medical cited as a reason for low clinical ascertainment of DLB.31,47 Newly proposed methods of assessment may be particularly helpful in this regard. These include caregiverand observer-rated scales.48 Questions such as whether there are episodes when the patient’s thinking seems quite clear and then becomes muddled may be useful probes,49,50 although one recent study51 found carers’ reports of fluctuation to be less reliable

predictors of DI B diagnosis than more objective questions about daytime sleepiness, episodes of staring blankly, or incoherent speech (Table III). Recording variation in attentional Inhibitors,research,lifescience,medical performance using a computer-based test system52 offers an independent method of measuring fluctuation, which is also sensitive to drug treatment effects.53 Table III. Assessing cognitive fluctuation in dementia with Lewy bodies GSK-3 (DLB). AD, Alzheimer’s disease. Neuropsychiatrie features Although the expression “noncognitive features of dementia“ is frequently used to describe a multiplicity of symptoms such as apathy, anxiety, delusions, hallucinations, and depression that, are common in dementia, this term implies, probably incorrectly, that such features are independent of cognitive dysfunction. ”Neuropsychiatrie features“54 is a more useful epithet to describe such symptoms, which are particularly common in DLB and which often prompt, referral for clinical assessment. Visual hallucinations are the most, characteristic neuropsychiatrie feature of DLB, and it.

g , d) computer software to be converted to a meaningful physical

g., d) computer software to be converted to a meaningful physical parameter describing the process being investigated; finally, the resulting quantity has to be presented through e) an interface to the human operator. Biosensors can be applied to a large variety of samples including body fluids, food samples, cell cultures and be used to analyze environmental samples.Figure 1.Elements and selected components of a typical biosensor [1, 2, 3].In order to construct a selleck chemical Palbociclib successful biosensor for the non-specialist market a number of conditions must be met:The biocatalyst must be highly specific for the purpose of the analysis, be stable under normal storage conditions and show a low variation between assays.The reaction should be as independent as manageable of such physical parameters as stirring, pH and temperature. This will allow analysis of samples with minimal pre-treatment. If the reaction involves cofactors or coenzymes these should, preferably, also be co-immobilized with the enzyme.The response should be accurate, precise, reproducible and linear over the concentration range of interest, without dilution or concentration. It should also be free from electrical or other transducer induced noise.If the biosensor is to be used for invasive monitoring in clinical situations, the probe must be tiny and biocompatible, having no toxic or antigenic effects. Furthermore, the biosensor should not be prone to inactivation or proteolysis.For rapid measurements of analytes from human samples it is desirable that the biosensor can provide real-time analysis.The complete biosensor should be cheap, small, portable and capable of being used by semi-skilled operators.Designed for the purpose, biosensors are generally highly selective due to the possibility to tailor the specific interaction of compounds by immobilizing biological recognition elements on the sensor substrate that have a specific binding affinity to the desired molecule [4]. Typical recognition elements used in biosensors are: enzymes, nucleic acids, antibodies, whole cells, and receptors. Of these, enzymes are among the most common [3]. To fully exploit the specific interaction through biorecognition, the surface architecture of the sensor also must suppress any non-specific interaction. A tremendous research effort has been invested to find surface modifications with specific interaction capabilities over prolonged periods of time in biological fluids [5].