Witham et al.24 showed that single doses of 100,000 and 200,000 IU of vitamin D in diabetic type II patients increased serum vitamin D from 41 to 63 and from 48 to79 nmol./l respectively. However, they showed that the decrease of PTH did not reach statistical significance. Moreover, another study,18 showed that a single dose of 200,000 IU of vitamin D in the healthy youths was associated with a peak in vitamin D concentration after two weeks of treatment, Inhibitors,research,lifescience,medical but lower than that of our study at three months after treatment. Therefore, a single dose of 300,000 IU dose employed

in this study is of higher effectiveness compared with an oral dose, especially in people suffering from vitamin D deficiency. Our study was advantageous for the presence of a control group in which all measurements were Inhibitors,research,lifescience,medical made similar to those of the IG. However, our study is limited for not measuring urine calcium and creatinin, since these variables could confirm the presence of hypervitaminosis more exactly and more confidently. Moreover, serum vitamin D was measured by ELISA kit, which is of lower accuracy compared with HPLC and RIA methods. Further studies are needed to evaluate the effect of postpartum supplementation of vitamin D on antirachitic

factor of the mother’s milk, and infant’s health indexes. Moreover, additional clinical trial studies will have to be conducted to determine the Inhibitors,research,lifescience,medical effect of mega doses Inhibitors,research,lifescience,medical of vitamin D on other health-related parameters such as the factors related to metabolic syndrome as well as inflammatory markers. Conclusion The findings of the study indicate that intramuscular administration of a single dose of 300,000 IU of vitamin D is effective and safe to improve vitamin D status, and to ameliorate the factors related to the Inhibitors,research,lifescience,medical health of mothers and infants, particularly in the regions with severe vitamin D deficiency. Acknowledgment This study was funded by Faculty of Health, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. We would like to thank Margo C Honeymand and Leonard C Harrison for their I-BET151 supplier assistance in planning the research proposal, the staff

at Yazd Diabetes Research Center, particularly Mrs Leila Azodi and Mrs Fateme Zare for their cooperation in blood sampling and biochemical tests, lactating mothers who participated in the study, secondly and Yazd Health Faculty for funding of the project. Conflict of Interest: None declared.
Background: Bacteremia due to Enterococcus faecalis is usually caused by strains resistant to most antibiotics. Effective management of the disease is dependent on rapid detection and characterization of the bacteria, and determination its sensitivity pattern to antimicrobial drugs. The aim of this study was to investigate a more rapid and reliable assay for simultaneous diagnosis of enterococcal bacteremia and its sensitivity pattern to antimicrobial drugs.

Depression may also be associated with increased mortality. Unfortunately, this treatable cause of suffering is frequently misdiagnosed and poorly treated in patients with cancer who are dying. In addition to traditional psychosocial and pharmacological treatments, several novel approaches to end-of-life care have been shown to result in robust improvement in depressive symptoms for patients with terminal cancer. These comprehensive and patient-centered

interventions offer patients the incalculable benefits of less suffering and optimum communication with family, friends, and clinicians providing care for them at the end of life.
Major Inhibitors,research,lifescience,medical depressive disorder (MDD), one of the most common psychiatric illnesses in the adult Inhibitors,research,lifescience,medical population, is a major cause of disability1 and is associated with a twofold increase in nonsuicidal mortality in women.2 In addition to poor medical compliance and Small Molecule Compound Library lifestyle factors, endocrine, immune, and autonomic dysregulations may play a causative role in producing medical illnesses Inhibitors,research,lifescience,medical in patients with MDD.3,4 The goal of this article is to describe some of the most clinically relevant medical consequences of major depression by summarizing here the findings of the POWER (Premenopausal, Osteoporosis Women, Alendronate, Depression) Study. The medical consequences of depression, as observed in the POWER Study, included

osteoporosis, endocrine and immune alterations, subclinical inflammation and alterations in coagulability, Inhibitors,research,lifescience,medical chronic pain, and decreased quality of life. Some of the novel pathogenetic mechanisms unraveled will be discussed. This review will conclude by listing some implications for clinical practice and future research. Medical consequences of major depression in premenopausal mildly depressed women mostly in remission The POWER study Women with MDD

were characterized with a matched Inhibitors,research,lifescience,medical group of healthy women from an immune, endocrine, and inflammatory point of view and prospectively followed for 36 months, with evaluations at baseline, 6, 12, 24, and 36 months.5 In the POWER Study, the presence of a control group prevented artifacts secondary to a nonspecific “study effect” on mood and provided found a benchmark for the research measurements taken. Study design The POWER Study was a three-year prospective investigation of bone turnover and other measurements conducted at the NIH Clinical Center.5 Recruitment was conducted from July 2001 to February 2003 in the Washington, DC, metropolitan area by advertising in newspapers, radio, flyers and on the Internet. We enrolled 89 communitydwelling 21- to 45-year-old premenopausal women with current or recent MDD and 44 healthy control women. Women were enrolled if they met DSM-IV criteria for MDD, and had experienced a depressive episode in the preceding three years.

213,214 In addition, many recent reports have correlated degree of γ oscillation disturbance with degree of schizophrenia symptoms including the cognitive impairment classical in schizophrenia, positive symptoms (ie, hallucinations and delusions) and negative symptoms (ie, affective blunting, anhedonia, avolitional state).213,215,217 Finally, these γ disturbances are also present Inhibitors,research,lifescience,medical in first-degree relatives of schizophrenic patients without classical schizophrenia symptoms per se and therefore may be a traceable endophenotype.211,218,219 The rekindled interest in the study of γ oscillations mainly lies in the understanding

of the critical involvement of parvalbumin-immunoreactive basket interneurons in γ oscillations13 and the relatively selective degeneration of this parvalbumin class of neurons in schizophrenia.220 Schizophrenic patients also show a significant reduction in sleep spindles221,222 and θ-γ phase coupling.223 γ oscillation disturbances may Inhibitors,research,lifescience,medical also point to alterations in the glutamatergic system, given that glutamate neurons are the primary backbone of neural signaling. Indeed data have shown that glutamate-targeted treatments for schizophrenia may have efficacy in schizophrenic patients.224 While schizophrenia is perhaps the most pervasive and debilitating psychiatric disease, Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical depression is the most prevalent, with roughly

20% lifetime incidence in Western populations and it inflicts the third largest measured disease burden of all illnesses in the world.225,226 Numerous studies have noted oscillation-related differences between depressed patients versus controls: increased Inhibitors,research,lifescience,medical α and β rhythm power, increased β asymmetric a in the frontal aspects of the hemispheres, and sensory-evoked responses.227,228 Such differences may be leveraged in

better treating this debilitating and sometimes-lethal disease. At the moment, while a variety of treatments exist for depression, the current state of the art in drug-based treatment is based on statisticallyinformed trial and error.229 This is due to the fact that there is no reliable means of determining which medication will work for which individual patient. A number of researchers have begun to PAK6 use EEG to not only point to differences between depressed patients and healthy controls, but have also begun to find correlates between brain rhythms and likelihood of response.227,228 Treatment response is IWR 1 predicted by a number of electrical parameters including baseline α power, α power asymmetry, frontal θ concordance measures within a few days of treatment, evoked responses to auditory stimuli and combinations of these measures. In general these parameters are able to predict responsivity at rates of approximately 60% to 80% accuracy.

The intestine was cut into 0.5-cm pieces. The pieces were incubated twice in media containing 0.15 μg/ml dithiothreitol (Sigma) and stirred at 37 °C for 20 min. Supernatants were collected and the IELs were collected at the interface of 40/80% Percoll gradients (Sigma). The purified IELs were cultured at 5 × 105/2 ml/24-well-plate in the presence of Con Ruxolitinib A (5 μg/ml). Supernatant were collected after 3 days culture and frozen at −80 °C

for ELISA analyses. Interleukin-2 (IL-2) activity was determined using a bio-assay on IL-2 dependent CTLL-2 cells as described elsewhere [16]. Each sample was tested in duplicate. IL-2 levels are expressed as mean counts per minute (cpm). Standard deviation was below 10% when not indicated. A typical international standard curve of this assay has been referred to [17]. IFN-γ, IL-4, IL-10 and TGF-β in the supernatant of IELs cultured with Con A by day 6 were determined by selleck inhibitor ELISA assay (R&D Systems, Minneapolis, MN, USA) of the culture supernatant following the manufacture’s instruction. In brief, diluted capture antibody was added to each well of the ELISA plate (Costar, Cambridge, MA, USA). Plates were sealed and incubated overnight at 4 °C. Plates were washed three times with 300 μl PBS-Tween, blocked and emptied. Samples and standards were added to

triplicate wells and plates were incubated at RT for 2 h. After washing, biotinylated detection antibody was added for 60 min at RT, followed by 100 μl horseradish peroxidase avidin for 30 min at RT. TMB substrate (Merck, Darmstadt, Germany) was added to each well. After 10 min at RT 50 μl stop solution (2 N H2SO4) was added and Adenylyl cyclase absorbance measured at a wavelength of 450 nm. Target cells were Ag85A cDNA transfected P815 cell line (kindly provided by inhibitors Professor Huygen, Pasteur Research Institute, Brussels, Belgium). These cells were incubated at 37 °C with 250 μCi of 51Cr (China Institute of Atomic Energy, China) in 1 ml of 20% FCS RPMI 1640 medium for 45 min. Labeled targets were washed three times with HBSS and

resuspended in 20% FCS RPMI at 105 cells/ml. 51Cr-labeled target cells (104 cells in 100 μl) were placed into each well of 96-well plates, and 100 μl/well of each dilution of IELs as effectors was added. Plates were incubated at 37 °C for 4 h. The supernatant from each well was harvested, and the amount of 51Cr released was counted in a gamma counter. The percentage of specific lysis was calculated as [(experimental release − spontaneous release)/(100% release − spontaneous release)] × 100. All determinations of cytotoxicity were conducted in triplicate, with a minimum of three E:T cell ratios. IELs (2 × 105 per well) purified from the immunized mice were incubated for 48 h at 37 °C in 96-well round-bottom tissue culture plates (Greiner Bio-One GmbH, Frickenhausen, Germany) in the presence of Ag85A protein.

In terms of these criteria, the opener-interneuron A3-AO and T3-DO and the closer interneurons recorded

in A2 and A3 qualify as components of the singing CPG. The ascending and descending opener-interneuron A3-AO and T3-DO occurred both as pairs of bilateral mirror-image sibling cells, and in both cases, intracellular depolarizing current injection in either the right or left interneuron was Pfizer Licensed Compound Library cell assay sufficient to elicit singing motor activity. If the singing CPG consists of bilateral-symmetrical hemioscillators (Ronacher 1989; Hennig and Otto 1995), at some point the left and right subcircuits need to be coupled Inhibitors,research,lifescience,medical to ensure coordinated movement of the two forewings for sound production. A common mechanism for synchronizing CPG neurons is electrical coupling via gap junctions (Marder and Calabrese 1996; Kiehn and Tresch 2002), which is often indicated by dye coupling (Ewadinger et Inhibitors,research,lifescience,medical al. 1994; Antonsen and Edwards 2003; Fan et al. 2005). Labeling an A3-AO with neurobiotin reliably stained the contralateral A3-AO sibling neuron as well, whereas for T3-DO even intense neurobiotin labeling never indicated any dye coupling. This points toward electrical synapses between the A3-AO sibling cells providing bilateral synchronization of the motor pattern.

Besides graded synaptic transmission (Simmons 1982; Manor et al. 1997), electrical coupling would explain how subthreshold Inhibitors,research,lifescience,medical shifting of the A3-AO membrane potential modulated the singing rhythm (cf. Mulloney et al. 1981; Mamiya et al. 2003). Similar subthreshold interaction has been reported between flight CPG neurons in the locust (Robertson Inhibitors,research,lifescience,medical and Reye 1988). The spatial overlap of the T3-DO main dendrite with axonal arborization of both A3-AO neurons and vice versa (Fig. 10) indicate mutual synaptic connections between these CPG neurons. As spike activity in the ascending A3-AO neurons strictly preceded the first T3-DO spike by about 3 Inhibitors,research,lifescience,medical msec, the depolarization of T3-DO could be driven by excitatory A3-AO inputs, whereas the depolarization of A3-AO cannot primarily result from descending T3-DO inputs and may involve the

descending command neurons. Some flight CPG interneurons directly activate motoneurons (Robertson and Pearson 1985). As mesothoracic and prothoracic motoneurons contribute to singing (Kutsch 1969; Pfau and Koch 17-DMAG (Alvespimycin) HCl 1994), the meso- and prothoracic axon collaterals of A3-AO may allow such direct connections. The opener-inter neuron A1-AO forward the rhythmic CPG output from the metathoracic ganglion to the mesothoracic motor network without interfering with pattern generation. Generation of syllable and chirp rhythm Our experiments clearly indicate A3-AO and T3-DO as crucial elements of the syllable–rhythm-generating network (cf. Figs. 2C–E and 6C–E). The membrane potential oscillations in A3-AO and T3-DO seem to result from excitatory inputs as well as inhibitory connections with yet unidentified closer interneurons like those we recorded in the anterior abdominal neuromeres.

Subjects were instructed to determine if the array contained a blue circle and to respond yes (right index finger

click) or no (left index finger click) as soon as possible. Upon logging a response, the array was again blurred so that the shapes could not be determined, preventing the subjects from continuing to search. The total time window allotted to view the array and log a response for both rest and task periods was 7 sec. Figure 1 Overview of the conjunctive visual search (CVS) task. Presentation of an X indicates a period without searching, and presentation of an O indicates a Inhibitors,research,lifescience,medical period of searching. Upon response, the array is blurred to impair searching. Neuroimaging A 1.5 Tesla (T) MR scanner (Siemens Magnetom Avanto; Siemens, Erlangen, Germany) with an eight-channel birdcage head coil was used for all acquisitions. Participants were positioned on the scanner table supine with their arms at their side and their head stabilized using locking pads attached to the head coil. A video projection system (BrainLogics MRI Digital Projection System; Psychology Software Inhibitors,research,lifescience,medical Tools Inc., Sharpsburg, PA) was used for delivery of visual information to a mirror affixed to the top of the head coil. Audio communication with the subject was enabled using noise-canceling headphones. An MR safe vision correction lens system (Psychology Software Tools

Inhibitors,research,lifescience,medical Inc.) was used to assist patients not able to clearly visualize test letters on the mirror. After positioning the center of each participant’s head at the magnet isocenter, a high-resolution T1-weighted anatomical scan was acquired using a 3D magnetization-prepared Inhibitors,research,lifescience,medical rapid acquisition gradient-echo (MPRAGE) Epacadostat nmr sequence with a 512 × 512 element

matrix, 120 slices, 1 × 1 × 1 mm voxel size, TR/TE = 500/15 msec, and flip angle = 15°. A single fMRI acquisition Inhibitors,research,lifescience,medical was then acquired using a gradient recalled echo sequence with a 64 × 64 element matrix, 24 slices, 4.5 × 4.5 × 5 mm voxel size, 1 mm slice gap, TR/TE = 2000/10 msec, and flip angle = 90°. The stimulus presentation was synced to the pulse sequence using a 5-V transistor-transistor logic pulse received from the imager at the start of every new TR. Consistent with the stimulus outlined in section 2009, 192 volumes were acquired for a total acquisition time of 6 min 24 sec. Data processing and analysis Individual image processing The FMRIB Software Urease Library (Smith et al. 2004; Woolrich et al. 2009) was used for processing of all fMRI data sets. Individual (first-level) analysis was first performed on each of the 4D fMRI data sets. This individual processing began with a high-pass temporal filter with cutoff = 32 sec applied to the 4D fMRI data. Motbion correction was applied by registering each volume to the center volume in the 4D data set by minimizing a correlation ratio cost function with motion estimated based on a rigid-body 12-parameter model (Jenkinson et al. 2002).

To optimize its safety use as a plant-based medicine, one should, beside the historical documentation on C. edulis, have

a toxicity assessment of this medicinal plant. Thus, the evaluation of the acute and sub-acute toxicities of C. edulis in the present study appears to be biologically essential. Acute Toxicity With the LD50 of 16.8 and kg in male and female mice respectively, the crude extract of C. edulis may be Inhibitors,research,lifescience,medical considered fairly toxic.22,23 These result indicate that female mice are more tolerant to the C. edulis extract than males after oral administration. This is in contrary to the observation of Drici and Clement,24 and Liechti and co-workers,25 who showed that the adverse effects of drugs and toxic substances were more

pronounced in women than in men. A reduced reaction to noise was observed suggesting that the extract may have a depressant or sedative effect on the central nervous system.11 The administration of the extract to mice caused a reduced reaction to pinch. This decreased sensitivity may be due to the action of the extract Inhibitors,research,lifescience,medical on the SCH772984 nociceptors or to the inhibition of the production of algogenic substances (e.g. prostaglandins or histamines), or Inhibitors,research,lifescience,medical to the inhibition of the painful message transmission at the central level.26 Sub-Acute Toxicity Changes in body weight are used as an indicator of adverse effects of drugs and chemicals.27 In the sub-acute toxicity study, significant decreases in total weight gain were observed in the rats, which received the extract at

the dose of 200 mg/kg BW as compared to the control. This suggests that C. edulis had negative effect on Inhibitors,research,lifescience,medical the normal growth of rats. The reduction in total weight gain may be due to less food and water intake,28 after the administration of C. edulis extract. This growth retardation may also be due to the antilipidaemic effect of C. edulis extract as shown by the decrease of serum total cholesterol. The hematopoietic system is one of the most sensitive targets for toxic compounds, and is an important Inhibitors,research,lifescience,medical index of physiological and pathological status in man and animal,29 In this study, a significant decrease in hematocrit values was also observed Non-specific serine/threonine protein kinase in male from the dose of 200 mg/kg BW as compared to that of the control group, suggesting that the extract at high doses may have some effect on the red blood cells. This was confirmed by the decrease, though not significant, observed in red blood cells count of rats treated with the same doses. However, the normal values for hematocrit range from 34% to 48% in Wistar albino rats.30 In the present study, hematocrit value (45.0±1.2) of the male rats receiving the extract at the dose of 200 mg/kg BW was within the normal range. The biochemical parameters (i.e. serum levels of ALT, AST and creatinine) also showed significant increases in the group receiving the highest dose as compared to that of the control group.

A small number of participants failed to complete the study questionnaires at isolated measurement points, as presented in Tables 2 and 3. At

the end of the 2-week check details intervention period, the experimental and control groups did not have significantly different scores on the modified Oswestry Disability Index, with a mean between-group difference in change from baseline of 0 points (95% CI –6 to 7). Also at this time, the groups did not differ significantly on the any of the secondary outcomes, as presented in Tables 2 and 3 (individual data are presented in Table 4 on the eAddenda). The percentage of the experimental group using medication for their low back pain at the end of the 2-week intervention (88%, 38/43) was not significantly different from the control group (73%, 32/44), relative risk 1.22 (95% CI 0.98 to 1.50). A significant difference was found in global rating of change between groups immediately following the intervention. The experimental group had a mean rating of 2.9 points (SD 1.1) while the control group had a mean of 3.5 points (SD 1.4). The mean between-group difference was 0.6

points in favour of the experimental group (95% CI 0.1 to 1.1). At the 6-week and 28-week follow-up points, no statistically significant differences were identified for any outcomes, even before Bonferroni correction, as presented in Tables 2 and 3. There was no significant difference in the number of treatments received after the Trametinib manufacturer 2-week allocated intervention period. The percentage of the experimental group using medication for their low back pain at 6 weeks (83%, 34/41) was not significantly different from the control group (73%3, 0/41), relative

risk 1.13 (95% CI 0.90 to 1.43). There were no adverse effects reported during the trial in either group. This study was the first to examine the treatment of acute low back pain using Strain-Counterstrain techniques. Adding the Strain-Counterstrain intervention did not substantially improve outcomes over exercise therapy alone. The best estimates of the effect of the intervention at the three outcome assessment points were only 2 points or less the on a 100-point scale. However, the upper limits of the 95% CIs around these estimates all still included the pre-specified minimum clinically important difference of 6 points. Therefore it is possible, although Modulators unlikely, that further research could identify a clinically worthwhile difference by further refining these estimates. We consider Strain-Counterstrain to be a form of spinal manipulative therapy, because the pelvis, sacrum, and lower limbs are used to position the lumbar and sacral regions passively in degrees of flexion, extension, lateral flexion, and rotation.

It is worth remembering that antipsychotics and antidepressants were shown to be effective (to just about everyone’s satisfaction) without the ‘advantage’ of randomized, controlled trials. Each paper, in its own way, calls for better integration of evidence-based ideals with clinical observation.
The International Classification of Diseases 10 [World Health Organization, 1992] characterizes depression Inhibitors,research,lifescience,medical by three core symptoms: low mood, anhedonia and low energy levels. Other symptoms include reduced concentration and self-esteem, ideas of self-harm, disturbed sleep and diminished appetite, which must persist for 2 weeks minimum. Variation in symptomatology Inhibitors,research,lifescience,medical distinguishes

between mild, moderate and severe depression. In regards to management, antidepressants are first-line

treatment for moderate and severe depression, whereas ‘watchful-waiting’, exercise and problem solving are recommended for mild depression [Anderson et al. 2008]. The serendipitous discovery that iproniazid and imipramine elevate mood implicated a central role of the monoamine system in depression pathology. Thus, all commercially available antidepressants increase levels of serotonin (5HT), norepinephrine (NE) and/or dopamine (DA) via different therapeutic mechanisms. First-generation antidepressants include tricyclic Inhibitors,research,lifescience,medical antidepressants (TCAs) Inhibitors,research,lifescience,medical and monoamine oxidase inhibitors (MAOIs), XL184 however they frequently possess undesirable side-effects, and toxic effects in overdose, limiting their application. Newer-generation antidepressants, including the well-known

selective serotonin reuptake inhibitors (SSRIs) are more selective and offer improved safety and tolerability (see Table 1 for a selective review of antidepressants; note, however, that this table does not represent an exhaustive review of the antidepressants currently available [Gelder et al. 2006]). Table 1. Review of antidepressants: therapeutic mechanism and side-effects. Efficacy of antidepressant: a picture of bliss Clinical Inhibitors,research,lifescience,medical trials provide compelling evidence for antidepressant effectiveness, with thousands of positive trials over the past five decades [Hollon et al. 2002]. Randomized controlled trials (RCTs) are the before gold-standard methodology for assessing efficacy, in which patients are assigned in a double-blind fashion to a placebo (inert ‘sugar pill’) or active-drug group. Meta-analyses of RCTs typically report antidepressants as 20–30% more effective than placebo, with higher response rates (50% reduction in Hamilton Depression Rating Scale [HDRS] scores) and improved remission rates (HDRS score of less than 8) [Davis et al. 1993; Walsh et al. 2002; Arroll et al. 2005]. Meta-analyses indicate antidepressant effectiveness varies as a function of symptom severity, with greatest efficacy in severe depression.

This plight is further worsened by the fact that there is a significant, lag time, up to 4 to 6 weeks, before the full www.selleckchem.com/products/iox1.html benefit of the medication can be determined. Thus, for each “failed” treatment, substantive and perhaps critical time is lost, which might lead to dire consequence including further deterioration, dropping out, and a further increase of the risk for mortality. Similarly, clinicians currently have little means for determining the optimal starting dose of any of the ADs being prescribed. This is so despite the fact that huge Inhibitors,research,lifescience,medical interindividual variations (up to 100 times) have

been demonstrated for most, if not all, Inhibitors,research,lifescience,medical ADs (and most of the other medications). For a substantive proportion of the patients, the “standard” initial doses (as suggested in package inserts and in textbooks) represent, only a small fraction of the optimal dose needed for therapeutic response, for others, such doses lead to severe side effects. The titration is essentially “trial and error,” time-consuming, and contributes

further to the delay in treatment response and recovery. Inhibitors,research,lifescience,medical Although the determination of the concentration of drugs and their metabolites in bodily fluids (typically plasma or serum) could be useful in this regard, it is usually not available in clinical settings (it may not. be feasible to have “blood level” measurements of various ADs available on a routine basis), and is typically Inhibitors,research,lifescience,medical done at steadystate, requiring patients to be on a particular medication for at. an extended period of time before the measurement (single dose kinetics

is even harder to do and more difficult to interpret in the clinical settings). Thus, although ADs are efficacious, neither their choice nor the dosing Inhibitors,research,lifescience,medical strategy are based on rational principles, leading to substantial “false starts,” delay in response, diminished medication adherence, “under- or overtreatment,” iatrogenic problems, morbidity, and even mortality. The promise of pharmacogenetics/pharmacogenomics about In such a context, it may be particularly surprising that knowledge derived from the field of pharmacogenctics/pharmacogenomics has not. yet. made inroads into enhancing clinicians’ ability to “individualize” or “personalize” pharmacotherapy. Evolving over the past half century, the field of pharmacogenetics has provided the basis for our understanding of many “idiosyncratic” drug reactions. In recent, years, it elucidated much of the genetic basis of individual variations in pharmacokinetics (especially genes determining drug metabolism) and pharmacodynamics (therapeutic target responses). Their relevance for ADs is summarized below.