The final diagnosis is based on examination of the Pap smears and the cell blocks using standard cytologic criteria (36). Special cytology stains are used as indicated to diagnose neuroendocrine tumors. The sensitivity of EUS-FNA for diagnosing pancreatic cancer has ranged from

80-95% in various published studies (37)-(39). The performance characteristics of EUS-FNA for diagnosing PaCa seem to be influenced by presence of obstructive jaundice at initial clinical presentation and presence of underlying chronic Inhibitors,research,lifescience,medical pancreatitis. In patients without obstructive jaundice, the diagnostic accuracy of EUS-FNA is very high (98.3%) and is not significantly influenced by presence of underlying chronic pancreatitis. However, in patients presenting with obstructive

jaundice, the sensitivity(92.0%) and Inhibitors,research,lifescience,medical accuracy(92.5%) of EUS-FNA for diagnosing malignancy is significantly lower especially so in patients with chronic pancreatitis (40). Absence of an identifiable mass lesion on EUS rules out PaCa with almost 100% certainty in the hands of experienced endosonographers (41). The accuracy of EUS-FNA for PaCa diagnosis can be further improved with use of adjunctive immunostaining in slides obtained by smearing EUS-FNA specimens (42). EUS is helpful in further evaluation of patients with non-specific and subtle findings suggestive of PaCa on CT and MRI imaging. Inhibitors,research,lifescience,medical We had earlier reported in non-jaundiced patients with “enlarged head of pancreas” or “dilated PD with or without a dilated CBD” on CT/MRI, a pancreatic malignancy was present Inhibitors,research,lifescience,medical in 9.0% of patients and EUS-FNA diagnosed cancer in these patients with 99.1% accuracy (43). EUS probably has a role in preoperative staging of PaCa for determining resectability. Portal vein and splenic vein invasion are visualized better with EUS. Inhibitors,research,lifescience,medical However, tumor involvement of SMA and SMV is not reliably determined by EUS. In published studies , EUS has a T-stage accuracy of 78-94% and N-stage accuracy of 64-82% (44)-(49). However, the presence of biliary stent at the time of EUS examination reduced the T-stage accuracy to 72% (50). EUS also plays a role in identification and biopsy of metastatic peripancreatic, celiac and mediastinal

lymph nodes for tumor involvement. Ahmed et al., questioned the role of EUS for T-staging and found its accuracy between 49% and 69% in two different studies (51),(52). With recent advances in CT and MRI technology and ALOX15 the ability to perform image reconstruction, very detailed evaluation of vascular infiltration by tumors is nowpossible. EUS imaging probably has an adjunctive role in T-staging of pancreatic tumors. However, due to its ability to reliably identify lymph nodal metastasis in celiac and mediastinal lymph nodes, EUS- FNA can prove to be beneficial in pre-operative assessment of learn more resectability (53),(54). The main limitation of EUS is its operator dependence and limited availability of expert endosonographers for accurate reporting. EUS carries a 0.

We will separate two notions generally confounded in the literature: anatomical and functional connectivity. The rationale for this is that we suppose the latter to be related to the common pathophysiological pathway leading to the clinical expression of the disease. The anatomical aspect is assumed to be one of the possible causes for the dysfunction. We will also discuss two levels of connectivity:

a local level, mainly concerning the direct surroundings of the neurons in the gray matter, and a longrange level, mainly concerning the white fiber tracts Inhibitors,research,lifescience,medical connecting distant parts of the brain. A third anomaly of connectivity could be related to neurons connecting with erroneous targets. Gray matter connectivity Gray matter hypotrophy and atrophy have both been described in schizophrenic patients. Hypotrophy buy Imatinib refers Inhibitors,research,lifescience,medical to a congenital reduction in the quantity of gray matter. It has been shown that such a reduction exists in patients as early as the first episode, with

the most robust evidence in the external temporal lobe, but with Inhibitors,research,lifescience,medical reductions also in the hippocampus and frontal and parietal lobes/’ However, it might be that part of the reduction is already related to an earlier origin of the disorder. Indeed, the average duration of untreated psychosis is 2.4 years, and some markers can even be traced back to the disease process long before that.7 However, the presence of similar, although lesser, gray matter reduction in relatives of patients also speaks for a congenital problem. Atrophy refers

to an acquired reduction in gray matter. The acceleration of gray matter decrease seems to occur mainly during the first year(s) of the disease process. Inhibitors,research,lifescience,medical Later on, the slope of the decrement is less striking. This gray matter reduction does not seem to be related to neuronal loss occurring after the second trimester. Indeed, Inhibitors,research,lifescience,medical only a few studies have found evidence for gliosis, a reputedly robust marker of neuronal necrosis, in the brains of patients with schizophrenia.8,9 It might be possible that some neurons are lost by apoptosis not necessarily accompanied by gliosis, but the general consensus is that most gray matter atrophy represents a reduction in only neuronal volume.10 As a matter of fact, cortical neurons are generally described as being smaller with higher density in pathological studies. Many authors have pointed out that the compartment showing the larger reduction could be the volume of axons and dendrites. In other words, there should be a reduction in the connecting parts of the neurons. In line with these arguments, synaptic spines and synaptic markers are reduced,11 as well as synaptic gene expression.12 In short, there is evidence of a reduction in local connectivity in some cortical areas in schizophrenia.

How important it is to take into account the type of effect size when appraising the magnitude of effect can be seen from a different meta-analysis that calculated uncontrolled pre- to post-treatment effect sizes.9. That meta-analysis reported an effect size of 1.53 for CBT in panic disorder. Figure 1. Average effect size estimates and corresponding 95% confidence intervals of the acute treatment efficacy of cognitive-behavioral therapy as compared with placebo on the various anxiety disorders for the primary continuous anxiety measure (dark blue bars) … Effectiveness Inhibitors,research,lifescience,medical Several studies

examined the effectiveness of CBT in panic disorder.11 The calculated uncontrolled pre- to post-treatment effect size was 1.01 (95% CI 0.77-1.25) for panic attacks and 0.83 (95% CI 0.60-1.06) for avoidance. Generalized anxiety disorder Inhibitors,research,lifescience,medical Generalized anxiety disorder is marked by excessive and uncontrollable worry. It is believed to be maintained by cognitive (attention and judgment) biases toward threat-relevant stimuli and the use of worry (and associated tension) and overly

cautious behaviors as a means to avoid catastrophic images and associated autonomic Inhibitors,research,lifescience,medical arousal.8 CBT of generalized anxiety disorder involves cognitive therapy to address worry and cognitive biases and relaxation to address tension, as well as imaginal exposure to catastrophic images and exposure to stressful situations while response preventing overly cautious behaviors. Efficacy Inhibitors,research,lifescience,medical The controlled effect size for CBT in generalized anxiety disorder was 0.51 (95% CI 0.05-0.97), indicating a

medium effect (Figure 1) although only two studies using a randomized controlled design to examine CBT treatment in patients with generalized anxiety disorder were available. Nevertheless, these results were recently corroborated by a Cochrane meta-analysis Inhibitors,research,lifescience,medical examining psychological treatments of generalized anxiety disorder.14 Based on thirteen studies, the authors concluded that psychological therapies, all using a CBT approach, were more effective than treatment as usual or wait list control Methisazone in achieving clinical response at post-treatment (RR 0.64, 95% CI 0.55-0.74). However, those studies examining CBT against supportive therapy (nondirective therapy and attention-placebo conditions) did not find a significant difference in clinical response between CBT and supportive therapy at post-treatment (RR 0.86, 95%CI 0.70 to 1.06). Again, the meta-analysis calculating uncontrolled pre- to post-treatment effect sizes found much a larger overall effect size of 1.80. 9 Effectiveness In PKA inhibitor eleven effectiveness studies, the pre- to post-treatment effect size for CBT in generalized anxiety disorder was 0.92 (95% CI 0.77-1.07). Social anxiety disorder Social anxiety disorder (or social phobia) is characterized by marked fear of performance, excessive fear of scrutiny, and fear of acting in a way that may be embarrassing.

The x-axis represents the proportion of patients who were incorrectly assigned to the coronary … Views on rationality: from unbounded rationality and Docetaxel ic50 irrationality to ecological rationality What to diagnose, whom to treat, what to eat, or which stocks to invest in—our days are filled with decisions, yet how do we make them, and how should we make them? In the decision sciences and beyond, the answer to these two questions depends on one’s view of human rationality. There are at least three views. Unbounded rationality: optimization Inhibitors,research,lifescience,medical The study of unbounded rationality asks the question, if people were omniscient,

that is, if they Inhibitors,research,lifescience,medical could compute the future from what they know, how would they behave and how should they behave? Optimization models such as Bayesian inference and the maximization of subjective expected utility take this view.2 When judging, for instance, whom to treat, these models assume that decision makers will collect and evaluate all information, weight each piece of it according to some criterion, and then combine the pieces to maximize the chances of attaining their goals (eg, treating the needy while saving costs). Optimization under constraints,

a sub-branch of unboundedly rational optimization, refers Inhibitors,research,lifescience,medical to models that do not assume full knowledge but take into account constraints, such as information costs. Optimization models are common in fields such as economics or computer science. The spirit of optimization is also reflected in the workings of the Heart Disease Predictive

Instrument, Inhibitors,research,lifescience,medical which is a linear regression model that computes optimal beta weights. Irrationality: cognitive illusions and biases According to the second view, human reasoning is not characterized by optimization but by systematic deviations from optimization, also called cognitive illusions, errors, or simply irrationality. Inhibitors,research,lifescience,medical The heuristics-and-biases framework3 proposes that humans commit systematic errors when judging probabilities and making decisions. Although this framework differs therein from the optimization view, it still takes optimization — such as maximization of expected utility — as the normative yardstick against which to evaluate human decision making. Decisions that deviate from this standard can be explicated by assuming that people suffer Resveratrol from cognitive limitations, such as a suboptimal information processing capacity or insufficient knowledge. Following this view, one might argue that the physicians’ large false -positive rate and below-chance performance in making allocation decisions (Figure 2) reflect the workings of their limited cognitive abilities. Ecological rationality: fast and frugal heuristics There is, however, an alternative to optimization and irrationality.

64 CB and PG also share high trait impulsivity.19,113 Other evidence could come from family studies of CB, PG, or OCD. There are few family studies regarding these disorders, and none have supported a familial relationship among these disorders. In the only controlled family history study of CB, Black et al45 did not find a relationship with OCD. In two family studies, one

Inhibitors,research,lifescience,medical using the family history method, the other using the family interview method, the investigators were unable to establish a connection between PG and OCD.114,115 Looking at this connection through OCD family studies has also failed to find a connection. Neither Black et al114 nor Bienvenu et al115 were able to establish a familial relationship between OCD and PG. Demographic similarities are often used to suggest that disorders might be linked, for example the fact that both alcohol disorders and antisocial personality disorder are predominantly Inhibitors,research,lifescience,medical found in men. Yet, there is no similarity in gender distribution among these disorders. With PG there is a clear male preponderance; with CB a female preponderance; with OCD, the gender distribution is evenly split. If these disorders were related, their natural

Inhibitors,research,lifescience,medical history and course might be CO-1686 similar as well. CB and OCD appear to have an onset in the late teens or early 20s. PG appears to have a slightly later onset, with women developing the disorder much later than men, but having a briefer course from onset of gambling to development of a disorder. This is what is seen with alcohol disorders, but not OCD. With CB, PG, and OCD are all considered mostly chronic, but the Inhibitors,research,lifescience,medical similarity stops there. For CB and PG, while there are no careful, longitudinal studies, the data suggest that the disorders may be Inhibitors,research,lifescience,medical episodic, that is, may remit for varying lengths of time depending on a host of external factors such as fear of consequences, eg, bankruptcy or divorce, or lack of income; OCD rarely remits.

In terms of suicide risk, PG has been reported to carry a risk for suicide attempts and completed suicides; Bay 11-7085 with CB, there are anecdotal reports of suicide attempts, but not completed suicides; with OCD, the data is somewhat mixed, but overall, the risk of completed suicide is considered low. Here, too, when one considers treatment response, OCD is well known to respond well to serotonin reuptake inhibitor antidepressants, and to cognitive behavioral therapy. CB and PG have no clear response to medication, and the most robust treatment data suggests that PG may respond to opioid antagonists. Both CB and PG are reported to respond to CBT, but the completeness and quality of the response is unlike that seen with OCD. The presence of similar biological markers is another way to assess the connection between these disorders. This task is hampered by the fact that none of these disorders has reliable markers.

” The scale was anchored at each end with the qualifiers “not at all” and “very much so.” Spearman’s correlations (rs) were performed between

the question scores and the absolute value of the change in response bias (|Δc|). The absolute value of the change in response bias was used because it gives a measure of the magnitude Inhibitors,research,lifescience,medical of the change in response bias regardless of the direction of the change. fMRI click here analysis Data preprocessing and image analysis were conducted using Statistical Parametric Mapping (SPM8, http://www.fil.ion.ucl.ac.uk/spm/; Wellcome Trust Centre for Neuroimaging, London, UK). Motion was assessed using Inhibitors,research,lifescience,medical the TSDiffANA toolbox (http://sourceforge.net/projects/spmtools/), and no participants were found to have moved more than 3 mm in any direction. All volumes were realigned to the first volume (Friston et al. 1994), and the mean functional and anatomical images were coregistered. The images were

then spatially normalized to the Montreal Neurological Inhibitors,research,lifescience,medical Institute (MNI) EPI template (Evans et al. 1992), resampled to a voxel size of 3 × 3 × 3 mm, and smoothed using a 8 mm full-width at half-maximum Gaussian kernel. A high-pass filter using a cut-off value of 128 sec and the SPM8 AR1 function were applied. The data were analyzed by modeling three event types (stimulus, decision, and feedback) as stick functions convolved with a synthetic hemodynamic response function. The three events were specified for “yes” and for “no” decisions for each motivational condition. The six motion parameters estimated during realignment were entered Inhibitors,research,lifescience,medical into the model as multiple regressors. The stimulus and decision events were combined and contrasted against an implicit baseline at the first level. These

contrast images were moved up to a second level, random-effects, flexible–factorial model where the effects of negative Inhibitors,research,lifescience,medical (Neg > Neut-N) and positive SB-3CT (Pos > Neut-P) motivation as well as any differences between neutral conditions (Neut-N > Neut-P; Neut-P > Neut-N) were examined. Significant clusters were identified at pFWE < 0.05 (family-wise error corrected), k ≥ 10 (extent threshold). Activations were localized to a particular anatomical region using the SPM anatomy toolbox (Eickhoff et al. 2006, 2007). To identify regions where activity correlated with change in response bias, a second–level, linear regression model specifying the positive motivation contrast images (Pos > Neut-P) and the change in response bias (Δcpositive) as a covariate was used. A whole-brain analysis identified significant clusters at pFWE < 0.05, k ≥ 10.

In a series of preclinical studies, nanoliposomal CPT-11 demonstrated significantly superior efficacy when compared to free CPT-11 at the same or higher dose, including frequent cures in some models. The superiority of nanoliposomal CPT-11 over free CPT-11 has been observed in different tumor models including colorectal, gastric, breast, cervical, glioma, pancreatic and lung cancer models. In addition to superior efficacy, nanoliposomal

CPT-11 has shown a more favorable pharmacologic profile and MLN8237 supplier reduced toxicity in multiple Inhibitors,research,lifescience,medical preclinical models. In order to evaluate this novel agent as a potential therapy for pancreatic cancer, a bioluminescence-based orthotopic xenograft model of pancreas cancer was developed (28). COLO357, a human pancreatic cell line, was passaged multiple times in vivo to generate the subline L3.6pl. This cell line was then modified by lentiviral transduction (L3.6pl-T) to express Inhibitors,research,lifescience,medical firefly luciferase. L3.6pl-T cells were implanted during open surgery directly into the pancreas of a nude mouse to form an orthotopic tumor xenograft. Therapeutic studies in this model compared nanoliposomal CPT-11 versus free drug at the equivalent dose, along with Inhibitors,research,lifescience,medical vehicle control (Figure 1). All treatments were administered intravenously by tail vein beginning at 7 days post-tumor implantation and continued weekly for a total of

3 planned treatments. At 20 mg/kg, free CPT-11 showed some tumor growth inhibition, but all mice required euthanization after 2 doses due to massive tumor progression. In contrast, nanoliposomal CPT-11 at the equivalent 20 mg/kg dose showed potent antitumor Inhibitors,research,lifescience,medical activity, including complete tumor inhibition during the entire post-treatment period. Systemic toxicity was not observed with any treatment. These studies indicated that nanoparticle- mediated delivery via nanoliposomal CPT-11 greatly

enhances antitumor efficacy in the COLO357/L3.6pI-T orthotopic pancreatic xenograft model. Figure 1 Nude mice were orthotopically implanted with COLO357/L3.6pI-T Inhibitors,research,lifescience,medical xenografts into the pancreas. Following ip administration of luciferin, animals were immediately imaged using a Xenogen IVIS 100 bioluminescence Astemizole system, and subsequently imaged at weekly intervals. … In the first-in-human phase I trial, patients with standard therapy-failure solid tumor were enrolled to determine the maximum tolerated dose, safety profile and pharmacokinetics of nanoliposomal CPT-11 (formerly PEP02, PharmaEngine, Inc., Taiwan, and now under the designation of MM-398, Merrimack Pharmaceuticals, Inc, USA). The drug was delivered intravenously for 90 minutes, once every 3 weeks, with starting dose of 60 mg/m2. The maximum tolerated dose was 120 mg/m2. Two patients achieved partial response including cervical cancer in one and pancreatic cancer in one (29).

This randomized, six-site, controlled clinical trial featured rigorous diagnostic criteria at study entry and compared the relative effectiveness of treatments of well-established efficacy. The initial MTA findings reported that all groups showed improvement over baseline at the end of the 14-month treatment period; however, the Comb and MedMgt group participants showed significantly greater #Cell Cycle inhibitor keyword# improvements in ADHD symptoms than did the Beh or CC participants. By the next follow-up, 3 years after enrollment, there were no longer significant treatment group differences in ADHD symptoms or functioning (Jensen et al. 2007). Molina et al. (Molina et al. 2009) reported the next two follow-up assessments

of the MTA sample at 6 and 8 years after random assignment, when the sample ranged in age from 13 to 18 years and found similar findings. Prevalence of prescription stimulant misuse The misuse of a stimulant medication – taking a stimulant not prescribed by a physician or in a manner not Inhibitors,research,lifescience,medical in accordance with physician guidance – has been growing over the past two decades. In fact, in the past 10 years there has been a surge in prevalence rates of nonprescription stimulant use among both adolescents and young Inhibitors,research,lifescience,medical adults. In general, nonprescription

use of MPH in 2000 was reported as 1.2% and in 2006 this number had risen to 2%. Breaking the sample down by age, nonprescription use among adolescents (ages 12–17) went from 2.2%

to 1.8% between 2000 and 2006, a slight decrease. Among college-aged individuals (ages 18–25), however, usage increased significantly from 3.6% in 2000 to 5.4% by 2006. Finally, among those 26 and older, usage is the lowest of any group, but rates are rising. In 2000, only 0.7% reported any Inhibitors,research,lifescience,medical lifetime usage of MPH, but this number had doubled to 1.5% by 2006 (Bogle and Smith 2009). The majority of research on the misuse of prescription stimulants has focused on undergraduate college students. The nonprescription use of stimulants has increased in this population, to the extent that the misuse of prescription stimulants is second only to marijuana as the most Inhibitors,research,lifescience,medical common form of illicit drug use among college else students (Johnston et al. 2004). A 2001 nationwide self-reported survey of more than 10,000 students from 4-year universities in the United States reported a 6.9% lifetime prevalence of nonprescription stimulant misuse, including a past-year prevalence of 4.1% and a past-month prevalence of 2.1% (McCabe et al. 2005). Colleges with the highest past-year prevalence rates were typically located in the northeastern United States, which is corroborated by other reports (McCabe et al. 2005). A study by Teter et al. (2005) of 9161 undergraduates reported an 8.1% lifetime nonprescription stimulant misuse rate among college students, including 5.4% over the past year. According to a 2002 survey of a single US college, 35.

3). Sternotomy was performed, but the mass was not removed successfully due to adhesion to its adjacent large vessels. Histopathologic examinations of specimen obtained during this procedure showed pleomorphic high-grade malignant tumor cells without any definite differentiation features (Fig. 4). Immunohistochemical study showed positive reactivity for vimentin, epithelial membrane antigen (EMA), cytokeratin (CK), CD99 (Fig. 5), but negative reactivity for calretinin, CD56, S-100, chromogranin, Inhibitors,research,lifescience,medical synaptophysin, leukocyte common

antigen (LCA). Although positive reactivity for vimentin and CD99 could suggest the possibility of high-grade sarcoma and Ewing’s sarcoma/primitive neuroectodermal tumor, expression of epithelial differentiation markers of EMA and CK could not be explained in both tumors. Considered histopathologic and immunohistochemical findings, primary pericardial undifferentiated carcinoma was suspected. After 4 months later, TTE demonstrated significantly Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical increased pericardial mass compared with that of before (Fig. 6). Despite several sets of palliative radiation therapy, the patient’s dyspnea was not relieved and expired due to multiple organ failure just within four months after presentation. Fig. 3 Follow-up T2-weighted MR image after 3 month of initial presentation showed that a huge

mass (arrows) about 8×15 cm-sized, settled in transverse sinus was compressing right superior vena cava without evidence of invasion of adjacent vessels. Fig. 4 The tumor cells revealed pleomorphic and hyperchromatic nucleus with epithelioid feature without Inhibitors,research,lifescience,medical any definite differentiation (H&E, ×400). Fig. 5 In immunohistochemical study, tumor cells showed positive reactivity for EMA Inhibitors,research,lifescience,medical (A), CK (B), vimentin (C), and CD99 (D). EMA: epithelial membrane antigen, CK: cytokeratin. Fig. 6 Follow-up transthoracic echocardiography after 4 month of initial presentation revealed an increased huge mass (arrows) of inhomogenous all echogenecity that was located in juxtaaortic

valve area. Discussion We present an unusual case of rapidly progressive pericardial undifferentiated carcinoma. Primary AVL-301 mw cardiac tumors are rare, with an incidence of 0.02%.1) Majority of these tumors are benign, with myxoma comprising 50% of primary cardiac tumors. Malignant tumors account for 25% of primary cardiac tumors. Sarcoma is most common and accounting for 20% of primary malignant cardiac tumors. They are often poorly differentiated, making an exact histologic diagnosis difficult.2) The 2 most common types of sarcomas are angiosarcomas and undifferentiated sarcomas. Other groups include leiomyosarcomas, malignant fibrous histiocytomas, osteosarcomas, and fibrosarcomas.

This phenomenon was initially observed in patients with schizophrenia, where bone mineral density (BMD) values measured by dual-emission X-ray absorptiometry (DXA) scans were 14% lower than matched controls [Baastrup et al. 1980] with further research indicating that up to 44% of women treated with first-generation antipsychotics had BMD values Inhibitors,research,lifescience,medical at least 1 SD below age- and sex-matched controls [Halbreich et al. 1995]. To date the relationships between antipsychotics and changes in BMD or bone metabolism have predominantly been investigated in cross-sectional studies of chronically treated patients compared with healthy controls,

cross-sectional studies comparing BMD in

Inhibitors,research,lifescience,medical chronically treated patients prescribed either ‘prolactin-elevating’ COX inhibitor in vivo agents (e.g. risperidone or first-generation antipsychotics) to ‘prolactin-sparing’ agents (e.g. other second- generation antipsychotics with lower risks of prolactin elevation), or in smaller prospective studies examining change in bone density over the course of year in chronically treated patients [Baastrup et al. 1980; Halbreich et al. 1995; Abraham et al. 2003a; Abraham et al. 2003b; Meaney et al. 2004; Howes Inhibitors,research,lifescience,medical et al. 2005]. These data indicate that antipsychotic effects on BMD are often, but not always, [Howes et al. 2005] likely to be observed after chronic treatment. Furthermore, there is some preliminary indication that changes in bone metabolism Inhibitors,research,lifescience,medical may occur as early as 6 months after the initiation of therapy [Abraham et al. 2003b; Meaney and O’Keane, 2007]. No investigations to date have studied acute changes (<3 months) in bone turnover in patients with minimal prior antipsychotic exposure. Identifying and characterizing whether changes in bone metabolism occur early in treatment may help us better understand how Inhibitors,research,lifescience,medical and if antipsychotics acutely influence bone physiology. The potential relationship

between antipsychotic treatments and osteoporosis-related outcomes is difficult to assess in patients with chronic psychosis due to known confounding prior medication treatments. Therefore, the investigation of this relationship in relatively healthy patients, early in the course of illness, with minimal prior exposure to antipsychotic agents would be informative. over In this study we assessed hormone and selected bone metabolism measures during the first 4 weeks of risperidone treatment in patients who were antipsychotic free before the study, the majority of whom had little or no prior lifetime antipsychotic exposure and were receiving their first treatment for psychosis. We tested the hypothesis that markers of bone resorption and bone formation are associated with risperidone-associated prolactin elevation.