Delirium tremens is characterized by hyperactivity and hypervigilance with EEG showing sparse normal alpha, but increased beta activity. Clinical features of delirium Delirium is the most frequently seen mental dysfunction in the critically ill.14 Particularly prevalent in the elderly, it can be seen about 20% of hospitalized patients15,16 as described by Lipowski17: Delirium is a transient organic mental syndrome of acute onset, characterized by global impairment of cognitive functions, reduced level of consciousness, attentional abnormalities,

Inhibitors,research,lifescience,medical increased or decreased psychomotor function, and a disordered sleep-wake cycle. The clinical features of delirium predominantly involve impairment of cognition and awareness. Motor activity may be decreased or increased, but it often is characterized by agitation with behavioral

disturbance. The clouding of consciousness typically impairs insight and a change Inhibitors,research,lifescience,medical in outlook, bringing the patient to medical attention. There is impaired orientation to time, place, and occasionally person, with the patient appearing to wander in space and time (usually in the past), confusing even close family members, the unfamiliar hospital surroundings, the seasons, Inhibitors,research,lifescience,medical and years. Nocturnal-diurnal sleep-wake cycles are often impaired and may be ABT 737 inverted, with sundowning characterized by agitation at the day’s end, but lethargy or sleep during the daylight Inhibitors,research,lifescience,medical hours. It may engender lethargy or passivity with decreased eating and responsiveness during the

day, alternating with agitation, anxiety, hallucinations, and hyperphasia at night. Any particular patient may have one or more of these disturbances, but the individual patient may have a highly variable temporal course and manifestations of these features. Physicians on their brief rounds may fall to note the fluctuating Inhibitors,research,lifescience,medical mental status so characteristic of delirium, while the nursing staff with a more prolonged observation bring the key signs to clinical attention.18 Delirium may be differentiated into two forms.18,19 The first type Is characterized by excitation, anxiety, anger, and changes in behavior with hypervigilance and typically signs of autonomic excess. This type follows benzodiazepine, alcohol, or barbiturate withdrawal, or the use of central nervous system-stimulating drugs such almost as cocaine or amphetamines. A second type is characterized by psychomotor retardation, indifference and apathy, impaired cognition, and physical activity with a decreased level of consciousness. The distinction may not be clear, and one state may give way to the other, for example, following a period of excitation with alcohol withdrawal, a patient may pass over into a state of obtundation and lethargy. Higher cortical function Delirium is characterized by impairment of higher cortical functions, involving defective thinking, memory, and spatial, temporal, and personal orientation.

7% of the variance. For the DAT1, no significant main effect was observed but at least a trend. Both effects like hypothesized, reduced Sadness in Met-carriers as well as in 10R-carriers.

As postulated, the accumulation of both resilience factors for depression results in PF-02341066 clinical trial lowest Sadness scores and was visible in an interaction effect of both polymorphisms increasing the explained variance to 1.1%. This led us to the suggestion that only the combination Inhibitors,research,lifescience,medical of the previously independent with PEM-associated alleles (Met-/10R-) results in decreased NEM. From a theoretical point of view, the genotype configuration 9R/9R (10R-) and Val/Val (Met-) that is related to the lowest Sadness scores, results in balanced DA levels due to lower reuptake (more DA in the synaptic cleft) in combination with faster degradation of DA Inhibitors,research,lifescience,medical (leading to an adaptation to the DAT1 10R-induced increase in synaptic DA levels). Of course, it is

in general problematic to conclude on DA levels by taking into account only two DA polymorphisms even if COMT and DAT1 have great impact on DA levels due to their function in DA clearance. However, a balanced DA level as inferred from the DA transporter density and DA catabolism cannot be an explanation for the Inhibitors,research,lifescience,medical present results. The genotype configuration Met+/10R+ (low DA catabolism and high DA reuptake) that is related to high Sadness scores would theoretically Inhibitors,research,lifescience,medical result in balanced DA levels, too. This problem can be solved if we take the distribution of the proteins within the different brain regions into consideration. DAT1 is most abundantly expressed in the striatum and midbrain and COMT in the prefrontal cortex (PFC), where DAT1 is only marginally present (Sesack et al. 1998; Lewis et al. 2001). This raises the question if a direct interplay Inhibitors,research,lifescience,medical of both proteins in the regulation of DA neurotransmission with a strong dampening effect on NEM is dependent on a balanced DA level with low DA levels in the PFC (Met-) and high DA levels in the striatum (10R-). This idea is corroborated

by neuroimaging studies demonstrating the importance of DA gene variations in regulating brain circuitry involved in processing negative emotional stimuli (Prata et al. 2009). Several lines of evidence indicate that both cortical and subcortical regions are activated during aminophylline the presentation of emotional stimuli (Zubieta et al. 2003) and are associated with Sadness and depression (Haber and Brucker 2009). A recent fMRI-study by Prata et al. (Prata et al. 2009) demonstrated significant epistasis between DAT1 and COMT genes on cortical activation during task-tapping executive functions in relation to schizophrenia, whereas the epistatic effect of DAT1 and COMT varied in different brain areas. For this reason they speculated that their findings possibly reflect expression and activity levels of the two proteins in different brain areas.

93 The currently available epidemiological and clinical data on use of lipids lowering drugs (statins) and risk of AD give a rather mixed picture. Several cross-sectional and case-control

studies have reported that statin users have a considerable lower prevalence of AD.94,95 While the follow-up data from the Rotterdam Study showed that use of statins was associated with a lower risk of AD independent of lipophilicity of statins,96 other prospective studies have indicated that there is no beneficial effect or only modestly decreased risk of AD related to statin use.97,98 Neuropathological studies also showed inconsistent findings as to whether the use of statins was associated with the burden of Alzheimer pathological Inhibitors,research,lifescience,medical changes and infarcts in the brain.99,100 Experimental studies suggest that statins may reduce β-amyloid

Inhibitors,research,lifescience,medical production in vitro and in vivo. Statins also have a variety of actions that may benefit the central nervous system and reduce the risk of AD, including endothelial protection via actions on the nitric oxide synthase system, antioxidant, anti-inflammatory, and antiplatelet effects. Nutritional and dietary factors Several follow-up studies have reported a decreased risk of AD associated with increasing dietary or supplementary intake, of antioxidants (eg, vitamins E and C),101,102 although some Pemetrexed mouse negative Inhibitors,research,lifescience,medical findings were also reported.103 Furthermore, studies found that higher adherence to “Mediterranean diet” (ie, a dietary pattern with higher intake of fish, fruits, and vegetables rich in antioxidants) was associated with a reduced risk of AD independent of vascular pathways.104,105 In addition, mixed results have been reported on the association of serum vitamin Inhibitors,research,lifescience,medical B12, folate, and

homocysteine with the risk of dementia and AD.106 Hie Cochrane systematic Inhibitors,research,lifescience,medical review concluded that folic acid and vitamin B12 supplementations have no benefits on cognition, although folate plus vitamin B12 are effective in reducing serum homocysteine.107 Finally, it has been reported that a diet rich in saturated fats and cholesterol increases the risk of AD,108 whereas polyunsaturated fatty acids and fish may be protective against dementia.109,110 Sitaxentan Unsaturated fatty acids may confer protection through anti-inflammatory properties. Fatty acids may also play a part in the synthesis and fluidity of nerve cell membranes and for synaptic plasticity and neuronal degeneration. In addition, oxidative stress is one of the central features in the Alzheimer brain. Hius, it may be plausible that supplementation or diet rich in antioxidants such as fruits, vegetables, and vitamins E and C might protect against AD. Diabetes An increased risk of not only vascular dementia but also neurodegenerative type dementia among persons with diabetes has been reported in several longitudinal studies,111-113 and the risk effect was confirmed by a systematic review.114 Midlife diabetes or a longer duration of diabetes may play a crucial role in dementia and AD.

For better or for worse, drugs are not individually developed; they do not target the individual biological system. However, human individuals are, biologically as well as socially, highly varied, and a common medical

problem is that people with similar symptoms, or the same illness, may react quite differently to a prescribed drug. Even if available data justify the prescription of a given drug, the effects of this drug can vary extensively between distinct individuals. Whereas one individual may be greatly helped by the drug, another may be more or less nonresponsive to it; and whilst one patient Inhibitors,research,lifescience,medical will suffer severe side effects, Inhibitors,research,lifescience,medical another will not. From the point of view of the patient, it is clearly of interest to know if one belongs to the group (normally, the majority) that is helped by the drug, or to the minority that is not, whether one will suffer side effects, and, if so, of what type and degree. For society, adverse drug responses (ADRs) are a major medical and economic problem. ADRs

cause thousands of deaths and Rapamycin in vitro serious injuries yearly, and have even been suggested to constitute between the fourth and the sixth leading cause of death in the US, which Inhibitors,research,lifescience,medical would rank ADRs ahead of pneumonia and diabetes.4 Thus the concern felt by many people regarding what side effects they are likely to experience is very valid:

Inhibitors,research,lifescience,medical even a brief glance at the most common or important side effects may be rather alarming. The side effects of psychopharmacological drugs can be very serious, including loss of muscular coordination, slowing of reactions, addiction, and psychiatric conditions other than the one targeted by the drug (eg, depression or anxiety). The prescription of drugs that may have serious side effects is not a satisfactory area for a trial-and-error strategy, by which one might prescribe or take a drug with reasonable hope for good results but without knowing in advance what will happen. Even Inhibitors,research,lifescience,medical if side-effect profiles are admittedly dynamic, the risk:benefit ratio positive, serious side effects statistically- uncommon, and prescription of the drug in agreement with the gold standard of psychiatric Carnitine dehydrogenase treatment in a given context, a physician or a patient might still hesitate to prescribe or take it, and wish to know if her/his individual biological structure is compatible with the drug or not. Will the drug help? If so, at what price? What can be done to optimize its therapeutic effects? Until recently, there were no options available other than a probability calculus based on data collected from previous and ongoing experience. There were scant possibilities to determine in advance how the patient as an individual would react to the drug.

3).

T2WI and FLAIR imaging showed no abnormality such as vascular disease or metal deposits in any patient. The arterial flow void was also intact (figures not shown). click here Figure 3 Three axial views and one sagittal view from T1-weighted MRI images in (A) 1-year-old, (B) 9-year-old, and (C) 18-year-old XPA patients. Diffusion tensor imaging (DTI) We calculated mean FA values and plotted the results Inhibitors,research,lifescience,medical against the age of patients (Fig. 4). For most XPA patients between 6 and 9 years of age, FA values at any region differed little from those in the 1-year-old patient. Furthermore, FA values were lower in patients No.9 and No.10 compared with younger patients, especially in the CC and WMP. Figure 4 Inhibitors,research,lifescience,medical FA values in XPA patients are plotted against the age of patients. Magnetic resonance spectroscopy (MRS) Peaks for lactate and lipid were not detected in any patient. The NAA/Cre ratios were plotted against the patients’ age shown in Figure 5. The NAA/Cre ratios ranged from 1.5 to 2.5 for patients No.1 through No.8 but fell below 1.5 for patients No.9 and No.10. Cho/Cre ratios had no differences

between Inhibitors,research,lifescience,medical all patients (data not shown). Figure 5 NAA/Cre ratios in the centrum semiovale (open circles) and gyrus cinguli (filled circles) in XPA patients are plotted against the age of patients. Discussion The molecular mechanism for neuronal damage in XPA is yet to be elucidated. Recently, it has been discussed that acquired factors such as oxidative stress or excitatory amino acid toxicity Inhibitors,research,lifescience,medical are related to CNS disorders in XPA. It was reported that metabolic products of oxidative stress were exhibited in the basal ganglia in the brain of XPA patients, while apoptosis, neurofibrillary tangles, or senile plaques were not noted (Hayashi et al.

2005). Due to the inability Inhibitors,research,lifescience,medical to repair DNA in XPA patients, acquired damage could be a factor in the neurodegenerative changes. DNA damage from oxidative stress, however, is commonly corrected by “base” excision repair (Robertson et al. 2009). Oppositely, XPA is a disorder of “nucleotide” excision repair system. Unknown mechanism, other than malfunction in DNA repair, is assumed to play an important role in neuronal damage in XPA. Neurological symptoms are common Terminal deoxynucleotidyl transferase in XPA patients, though its precise mechanism remains still unclear. The onset of neurological symptoms in XPA seems to occur between 3 and 8 years of age (Anttinen et al. 2008). In our study, however, even 1-year-old patients showed neurological abnormalities such as a decline of DTRs. Some patients had history of several months delay of initial walking. Contrary to general understanding, careful observation can detect neurological symptoms in infancy in XPA patients. Conventional MRI sequences showed brain atrophy and expansion of frontal sinuses in adolescent patients. Every region of the brain, including cortex, brain stem, and cerebellum, remarkably reduced in size in adult patients.

A threshold of 10% above and below 100% efficiency was applied. Endogenous control Relative quantification is the most widely adopted approach whereby quantification of gene expression is normalised relative to an endogenously expressed control (EC) gene(s). Central to the reliable determination of gene expression is the choice of control gene. B2M and PPIA have previously been identified as the most stably expressed genes

in a large cohort of colorectal tissues (33) and were used to normalise expression values in the present study. RT-PCR of mRNA The expression of each EC gene was analysed by RQ-PCR using TaqMan gene expression assays using a 7900HT instrument (Applied Biosystems). All Inhibitors,research,lifescience,medical reactions were performed in 10 µL reactions, in triplicate within the same PCR run. Negative controls were included for each

gene target under assay. On each plate, an interassay Inhibitors,research,lifescience,medical control was included to account for any variations between runs. For each well 2 µL of cDNA from each sample was added to 18 µL of PCR reaction mix which http://www.selleckchem.com/products/ink128.html consisted of 10 µL TaqMan master mix, nuclease free water and 1 µL gene expression assay primer-probe mix (Applied Biosystems). Standard fast thermal cycling parameters of 40 cycles of 95 °C for 15 seconds and 60 °C for 60 seconds were applied in accordance with Inhibitors,research,lifescience,medical the manufacturer’s recommendations. Relative quantification Inhibitors,research,lifescience,medical Cycle threshold (Ct) is defined as the PCR cycle number at which the fluorescence generated from amplification of the target gene within a sample increases to a threshold value of 10 times the standard deviation of the base line emission and is inversely proportionate to the Inhibitors,research,lifescience,medical starting amount of the target cDNA. QBasePlus software (Biogazelle) was used to calculate expression values of each chemokine target. Relative quantities were corrected for efficiency of amplification and fold change in gene expression between groups was calculated

as E-ΔΔCt ± s.e.m. The lowest expressed sample was used as a calibrator. -ΔΔCt = (Ct target gene, test sample – Ct endogenous control, test sample) – (Ct target gene, calibrator sample – Ct endogenous control, calibrator sample). Statistical analysis Statistical analysis was carried out with IBM SPSS Statistics 17.0 (SPSS Inc.). Data was tested for normal distribution Terminal deoxynucleotidyl transferase graphically using histograms and also using the Kolmogorov-Smirnov and Shapiro-Wilk tests. Parametric tests were used where appropriate. One-way ANOVA and independent t-test were used to determine association and comparisons between independent groups. Correlation analysis used Spearman’s Rho and Pearson’s correlations coefficient for nonparametric and parametric data respectively. Univariate analysis and paired-T test were used to assess related samples.

Behavior, in this context, is thought, language, feeling, perception, learning, movement, sensing, planning, creativity, and other meanings that are

attached to the word behavior in everyday use. However, the actual nature of the psychobiological transform is extremely vague. The reason for this vagueness is the apparent complexity of the biological and behavioral realms, which include an immense number of states and of transitions between states that might be relevant. Operationally, behavioral and brain scientists find themselves in a situation where it is not at all clear what biological level of organization a psychological phenomenon should be transformed to, without losing the explanatory power of the transformation. Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical For some researchers the state

of single synapses, potentiated or depressed, with all the molecular intricacies involved, is behaviorally relevant. There are neuroscientists for whom neuronal excitability, determined by the molecular states of membrane-embedded ionic channels, is behaviorally relevant. For others, the mere fact that a cortical neuron is a target for many thousands of other input neurons, none of which is capable on its own of firing the target neuron, suggests that the states of single synapses or single neurons cannot possibly be behaviorally relevant. For these scientists, the behaviorally relevant state concept may be Inhibitors,research,lifescience,medical realized in the form of a temporally structured firing pattern, or as an http://www.selleckchem.com/products/BKM-120.html average firing rate in a population of neurons. Neural network theoreticians Inhibitors,research,lifescience,medical might reason in terms of abstract attractor states, while neurophysiologists might stress, for instance, the state of a rewarding system as defined in terms of electrical or neuro-pharmacological activity. Thus, the question of what biological level of organization a psychological phenomenon should be transformed to, without losing the explanatory power Inhibitors,research,lifescience,medical of that transformation, is open. The assumption underlying the studies reviewed here is that the most relevant

level of description is the level of neuronal populations and interactions between such populations. There is a significant body of data suggesting that even the simplest kind of mammalian behavior imaginable involves at least thousands of neurons, thousands of spikes, and hundreds of thousands of synapses. Indeed, much attention has been devoted to population level descriptions, resulting in theories such as neuronal assemblies, neuronal groups, GPX6 synfire chains, population codes, etc., in attempts to understand development and functionality of neural systems. As will be shown below, the study of the dynamical properties at the neuronal networks level gives hope that the gap between levels of description may be partially bridged. The central hypothesis of neuroscience is that behavior can and should be understood in terms of representational processes in the brain.

It should be pointed out that in spite of being a hypertensive patient, her blood pressure, monitored daily, stayed within the normal range of 130 mmHg/70 mmHg. Biochemical parameters, creatinine, liver function laboratory

tests, TSH and EKG showed no changes with the combined treatment. Lithaemia was 0.66 mEq/L at the sixth week. No adverse effects were reported Inhibitors,research,lifescience,medical with the exception of dry mouth and moderate constipation, both well tolerated by the patient. Discussion The combination of high doses of both clomipramine [Gervasoni et al. 2009] and mirtazapine achieved a high level of synergy, acting at pharmacodynamic level through triple serotoninergic DNA Damage antagonist enhancement (reuptake inhibition by clomipramine, alpha-2 and 5-HT2 antagonistic effects of mirtazapine) and dual noradrenergic enhancement

(reuptake inhibition by clomipramine and its active metabolite desmethylclomipramine, antagonistic alpha-2 effect of mirtazapine). In addition, blockage of the 5-HT2 and 5-HT3 receptors achieved Inhibitors,research,lifescience,medical with mirtazapine can help to reduce the serotoninergic sexual (5-HT2) and digestive (5-HT3) adverse effects of clomipramine. It is also known that sustained 5-HT2 blockage improves sleep and increases the gene expression of the 5-HT1A receptor (synergy between 5-HT2 antagonism and 5-HT1A stimulation) [Ruiz-Doblado Inhibitors,research,lifescience,medical et al. 2010]. In addition, both clomipramine and mirtazapine were considered two of the most effective antidepressant drugs in a recent review of the evidence [Montgomery et al. 2007]. Furthermore, lithium enhancement has a stabilizing effect on membranes and also Inhibitors,research,lifescience,medical on sodium cellular transportation, as well as the upregulation of gene expression associated with neurotransmission Inhibitors,research,lifescience,medical via second messengers (phosphatidylinositol). Finally, partial rapid eye movement sleep deprivation, during

the second half of the night, can enhance pharmacological effect. Although its efficacy is known at the empirical level, the mechanism of action of its antidepressant effect remains unclear. Nowadays there are ‘cleaner’ combinations in treatment algorithms for resistant melancholia, such as those associating venlafaxine or duloxetine (both dual 5-HT-NA ADP ribosylation factor antidepressants) with a second antidepressant or mood regulator [Hannan et al. 2007; De la Gándara et al. 2008; Yazici, 2009], but some works have shown that the noradrenergic effect of these new drugs may be inferior to that of clomipramine, which achieves a powerful noradrenaline reuptake inhibition due to both the drug itself and its metabolite (clomipramine + desmethylclomipramine) [Gillman, 2007]. According to our current state of knowledge, this is the first documented case of response to this combination of drugs in resistant melancholia at these doses.

The interaction between ethnicity and the degree of density of the minority in the local neighborhood, for example, has been examined in South London.112 The risk of schizophrenia appears to be particularly increased among ethnic groups when they comprise a smaller proportion of the local population.

In order to further investigate the role of social factors, Mallett et al conducted a first-onset matched case-control study in London between 1991 and 1993.113 Three socioenvironmental variables separated African-Caribbean cases from both their peers and normal controls: Inhibitors,research,lifescience,medical unemployment, living alone, and a long period of separation from their parents in childhood. Eaton and Harrison reviewed 17 population-based studies from the UK and the Netherlands and found that the studies consistently reported higher incidence rates for immigrant groups whose position in society could be described as disadvantaged, with the relative incidence varying from 1.7 to 13.2. 114 Urbanicity An increased Inhibitors,research,lifescience,medical prevalence of psychosis in urban compared to rural settings is one of the most consistent findings in schizophrenia research.115 Prospective incidence studies are more Inhibitors,research,lifescience,medical suited

to examining urbanicity as a risk factor for schizophrenia since prevalence studies are limited by migration to urban areas after illness onset. A number of such prospective studies have demonstrated an association between urbanicity at birth or during childhood and later development of psychosis.108,116 In a recent follow-up study of the entire Swedish population, those living in the most densely populated areas had 68% to 77% more risk of developing psychosis (12%-20% for depression) than the control group living in the least densely populated areas.117 On the basis Inhibitors,research,lifescience,medical of a similar population-based Inhibitors,research,lifescience,medical register study in Denmark, the proportion of schizophrenia risk PF 562271 attributable to urbanicity was estimated

to be as high as 35%.108 Using the same Danish registers, Pedersen et al recently reported a dose-response relationship between duration of urban exposure during upbringing, rather than at birth, and risk of schizophrenia-evidence that enhances notions of causality.118 They also found that the RR of schizophrenia increased with changing residence to a relatively more urban area during childhood and adolescence. Mortensen has reviewed the role of urbanicity and suggested a number of intermediate risk factors to explain the association, Mannose-binding protein-associated serine protease including toxic exposures, infection, social class, and overcrowding.119 There have been concerns about the conceptual validity of urbanicity, the mechanism of causation, and the problem of residual confounding. Van Os has reviewed such concerns and argues that the exposure acts between birth and illness onset, is associated with “at-risk mental states” as well as psychotic disorder, and is likely to reflect social environmental factors such as isolation and poor cohesion.

Motion trajectories are typically rendered based on an algorithm resulting in “Brownian motion like” object motion (cf. Pylyshyn and Storm 1988; “Brownian motion” is a term used in physical chemistry to describe the movement of particles in suspension, resulting from collisions with rapidly moving atoms or molecules). There are restrictions regarding sudden and large velocity changes (a factor referred to as object inertia, Pylyshyn 2004), giving object motion a certain appearance of Inhibitors,research,lifescience,medical “biologicity.” Moreover, motion trajectories are affected by object

“behavior”: in the incidence of intersection, two objects can overlap with each other (Pylyshyn 2004), bounce off each other (Bahrami 2003), or go round each other (Alvarez and Franconeri 2007). Such constraints restrict the set of possible spatial coordinates to which an object can proceed from one frame to another. However, from the remaining set, coordinates are usually Inhibitors,research,lifescience,medical chosen in an arbitrary manner, yielding essentially unpredictable object motion. Cognitive processes during MOT Behavioral results on MOT cannot readily be explained by “spotlight” theories of attention (Posner 1980). Rather, Yantis (1992) found empirical evidence that target objects are

“grouped,” that is, cognitively represented as if belonging to one AZD2281 supplier virtual Inhibitors,research,lifescience,medical object. During tracking, instead of continuously shifting the locus of attention back and forth between objects, target identity is supposedly maintained via a holistic representation in the form of said virtual Inhibitors,research,lifescience,medical object. Furthermore, Pylyshyn and Storm (1988) suggested that object identity is maintained through “mental reference tokens.” In an early stage of visual perception, salient objects in a visual display can be “indexed,” a mechanism that individuates and keeps track of said objects without the necessity to categorize or conceptualize them (Pylyshyn 2001). On a similar notion, Kahneman and colleagues suggested the existence Inhibitors,research,lifescience,medical of object files, that is, temporary visual representations of real world

objects (Kahneman and Treisman 1984; Kahneman et al. 1992). Object files tuclazepam store information on object surface features, such as shape or texture, and spatiotemporal characteristics (Mitroff and Alvarez 2007). Depending on their availability and reliability in a given situation, both types of information can be used to maintain object correspondence in the incidence of brief occlusions of an observed moving object, (Hollingworth and Franconeri 2009; Papenmeier et al. in press). However, in situations where no distinguishing surface information is available (such as in the MOT paradigm), spatiotemporal information appears to be of key significance to the maintenance of object file representations. Indeed, while random changes in object shape or object color did not impair tracking performance (Bahrami 2003; unless, for instance, targets and distractors swapped colors during occlusion, see Huff et al.