Office of Drug Control Policy, Agency Performance Plan

Annual Report, Agency Performance Plan

Neuroplasticity of inhibitory control

Executive control refers to a set of abilities enabling us to plan, control and implement our behavior to rapidly and flexibly adapt to environmental requirements. These adaptations notably involve the suppression of intended or ongoing cognitive or motor processes, a skill referred to as "inhibitory control". To implement efficient executive control of behavior, one must monitor our performance following errors to adjust our behavior accordingly. Deficits in inhibitory control have been associated with the emergènce of a wide range of psychiatric disorders, ranging from drug addiction to attention deficit/hyperactivity disorders. Inhibitory control deficits could, however, be remediated- The brain has indeed the amazing possibility to reorganize following training to allow for behavioral improvements. This mechanism is referred to as neural and behavioral plasticity. Here, our aim is to investigate training-induced plasticity in inhibitory control and propose a model of inhibitory control explaining the spatio- temporal brain mechanisms supporting inhibitory control processes and their plasticity. In the two studies entitled "Brain dynamics underlying training-induced improvement in suppressing inappropriate action" (Manuel et al., 2010) and "Training-induced neuroplastic reinforcement óf top-down inhibitory control" (Manuel et al., 2012c), we investigated the neurophysiological and behavioral changes induced by inhibitory control training with two different tasks and populations of healthy participants. We report that different inhibitory control training developed either automatic/bottom-up inhibition in parietal areas or reinforced controlled/top-down inhibitory control in frontal brain regions. We discuss the results of both studies in the light of a model of fronto-basal inhibition processes. In "Spatio-temporal brain dynamics mediating post-error behavioral adjustments" (Manuel et al., 2012a), we investigated how error detection modulates the processing of following stimuli and in turn impact behavior. We showed that during early integration of stimuli, the activity of prefrontal and parietal areas is modulated according to previous performance and impacts the post-error behavioral adjustments. We discuss these results in terms of a shift from an automatic to a controlled form of inhibition induced by the detection of errors, which in turn influenced response speed. In "Inter- and intra-hemispheric dissociations in ideomotor apraxia: a large-scale lesion- symptom mapping study in subacute brain-damaged patients" (Manuel et al., 2012b), we investigated ideomotor apraxia, a deficit in performing pantomime gestures of object use, and identified the anatomical correlates of distinct ideomotor apraxia error types in 150 subacute brain-damaged patients. Our results reveal a left intra-hemispheric dissociation for different pantomime error types, but with an unspecific role for inferior frontal areas. Les fonctions exécutives désignent un ensemble de processus nous permettant de planifier et contrôler notre comportement afin de nous adapter de manière rapide et flexible à l'environnement. L'une des manières de s'adapter consiste à arrêter un processus cognitif ou moteur en cours ; le contrôle de l'inhibition. Afin que le contrôle exécutif soit optimal il est nécessaire d'ajuster notre comportement après avoir fait des erreurs. Les déficits du contrôle de l'inhibition sont à l'origine de divers troubles psychiatriques tels que l'addiction à la drogue ou les déficits d'attention et d'hyperactivité. De tels déficits pourraient être réhabilités. En effet, le cerveau a l'incroyable capacité de se réorganiser après un entraînement et ainsi engendrer des améliorations comportementales. Ce mécanisme s'appelle la plasticité neuronale et comportementale. Ici, notre but èst d'étudier la plasticité du contrôle de l'inhibition après un bref entraînement et de proposer un modèle du contrôle de l'inhibition qui permette d'expliquer les mécanismes cérébraux spatiaux-temporels sous-tendant l'amélioration du contrôle de l'inhibition et de leur plasticité. Dans les deux études intitulées "Brain dynamics underlying training-induced improvement in suppressing inappropriate action" (Manuel et al., 2010) et "Training-induced neuroplastic reinforcement of top-down inhibitory control" (Manuel et al., 2012c), nous nous sommes intéressés aux changements neurophysiologiques et comportementaux liés à un entraînement du contrôle de l'inhibition. Pour ce faire, nous avons étudié l'inhibition à l'aide de deux différentes tâches et deux populations de sujets sains. Nous avons démontré que différents entraînements pouvaient soit développer une inhibition automatique/bottom-up dans les aires pariétales soit renforcer une inhibition contrôlée/top-down dans les aires frontales. Nous discutons ces résultats dans le contexte du modèle fronto-basal du contrôle de l'inhibition. Dans "Spatio-temporal brain dynamics mediating post-error behavioral adjustments" (Manuel et al., 2012a), nous avons investigué comment la détection d'erreurs influençait le traitement du prochain stimulus et comment elle agissait sur le comportement post-erreur. Nous avons montré que pendant l'intégration précoce des stimuli, l'activité des aires préfrontales et pariétales était modulée en fonction de la performance précédente et avait un impact sur les ajustements post-erreur. Nous proposons que la détection d'erreur ait induit un « shift » d'un mode d'inhibition automatique à un mode contrôlé qui a à son tour influencé le temps de réponse. Dans "Inter- and intra-hemispheric dissociations in ideomotor apraxia: a large-scale lesion-symptom mapping study in subacute brain-damaged patients" (Manuel et al., 2012b), nous avons examiné l'apraxie idémotrice, une incapacité à exécuter des gestes d'utilisation d'objets, chez 150 patients cérébro-lésés. Nous avons mis en avant une dissociation intra-hémisphérique pour différents types d'erreurs avec un rôle non spécifique pour les aires frontales inférieures.

Report of Recommendations to the Governor's Office of Drug Control Policy, June 30, 2002

State Agency Audit Report

Governor's Office of Drug Control Policy, Notification Letter, July 25, 2005

State Audit Reports - Notification Letter

Concordância dos referenciais de crescimento propostos pelo Center of Disease Control e Organização Mundial de Saúde

O objetivo deste estudo foi verificar a concordância dos referenciais recomendados pelo Center of Disease Control (CDC) e pela Organização Mundial da Saúde (OMS) na avaliação do estado nutricional. Trata-se de um estudo transversal, com participação de 254 crianças de 3 a 11 meses e 29 dias de idade de São Paulo e Ribeirão Preto, nos meses de junho de 2005 a julho de 2006. Os índices antropométricos foram calculados em programas disponibilizados nos sites do CDC e OMS, respectivamente. Aplicado Teste Kappa para as variáveis nominais (comprimento/idade) e Kappa-ponderado para variáveis ordinais (peso/comprimento) evidenciou-se que os referenciais CDC e OMS apresentam diferenças na avaliação nutricional infantil, sendo encontrados resultados com maior discordância nas crianças de 3 a 6 meses.

Office of Drug Control Policy Performance Report, FY 2004

Agency Performance Report

Office of Drug Control Policy Performance Report, FY 2005

Agency Performance Report

Guidleines for Removal of Traffic Control Devices in Rural Areas, October 2005

It is commonly regarded that the overuse of traffic control devices desensitizes drivers and leads to disrespect, especially for low-volume secondary roads with limited enforcement. The maintenance of traffic signs is also a tort liability concern, exacerbated by unnecessary signs. The Federal Highway Administration’s (FHWA) Manual on Uniform Traffic Control Devices (MUTCD) and the Institute of Transportation Engineer’s (ITE) Traffic Control Devices Handbook provide guidance for the implementation of STOP signs based on expected compliance with right-of-way rules, provision of through traffic flow, context (proximity to other controlled intersections), speed, sight distance, and crash history. The approach(es) to stop is left to engineering judgment and is usually dependent on traffic volume or functional class/continuity of system. Although presently being considered by the National Committee on Traffic Control Devices, traffic volume itself is not given as a criterion for implementation in the MUTCD. STOP signs have been installed at many locations for various reasons which no longer (or perhaps never) met engineering needs. If in fact the presence of STOP signs does not increase safety, removal should be considered. To date, however, no guidance exists for the removal of STOP signs at two-way stop-controlled intersections. The scope of this research is ultra-low-volume (< 150 daily entering vehicles) unpaved intersections in rural agricultural areas of Iowa, where each of the 99 counties may have as many as 300 or more STOP sign pairs. Overall safety performance is examined as a function of a county excessive use factor, developed specifically for this study and based on various volume ranges and terrain as a proxy for sight distance. Four conclusions are supported: (1) there is no statistical difference in the safety performance of ultra-low-volume stop-controlled and uncontrolled intersections for all drivers or for younger and older drivers (although interestingly, older drivers are underrepresented at both types of intersections); (2) compliance with stop control (as indicated by crash performance) does not appear to be affected by the use or excessive use of STOP signs, even when adjusted for volume and a sight distance proxy; (3) crash performance does not appear to be improved by the liberal use of stop control; (4) safety performance of uncontrolled intersections appears to decline relative to stop-controlled intersections above about 150 daily entering vehicles. Subject to adequate sight distance, traffic professionals may wish to consider removal of control below this threshold. The report concludes with a section on methods and legal considerations for safe removal of stop control.

Predictors of asthma control in everyday clinical practice in Switzerland.

OBJECTIVE: To identify predictors of improved asthma control under conditions of everyday practice in Switzerland. RESEARCH DESIGN AND METHODS: A subgroup of 1380 patients with initially inadequately controlled asthma was defined from a cohort of 1893 asthmatic patients (mean age 45.3 + or - 19.2 years) recruited by 281 office-based physicians who participated in a previously-conducted asthma control survey in Switzerland. Multiple regression techniques were used to identify predictors of improved asthma control, defined as an absolute decrease of 0.5 points or more in the Asthma Control Questionnaire between the baseline (V1) and follow-up visit (V2). RESULTS: Asthma control between V1 and V2 improved in 85.7%. Add-on treatment with montelukast was reported in 82.9% of the patients. Patients with worse asthma control at V1 and patients with good self-reported adherence to therapy had significantly higher chances of improved asthma control (OR = 1.24 and 1.73, 95% CI 1.18-1.29 and 1.20-2.50, respectively). Compared to adding montelukast and continuing the same inhaled corticosteroid/fixed combination (ICS/FC) dose, the addition of montelukast to an increased ICS/FC dose yielded a 4 times higher chance of improved asthma control (OR = 3.84, 95% CI 1.58-9.29). Significantly, withholding montelukast halved the probability of achieving improved asthma control (OR = 0.51, 95% CI = 0.33-078). The probability of improved asthma control was almost 5 times lower among patients in whom FEV(1) was measured compared to those in whom it was not (OR = 0.23, 95% CI = 0.09-0.55). Patients with severe persistent asthma also had a significantly lower probability of improved control (OR = 0.15, 95% CI = 0.07-0.32), as did older patients (OR = 0.98, 95% CI = 0.97-0.99). Subgroup analyses which excluded patients whose asthma may have been misdiagnosed and might in reality have been chronic obstructive pulmonary disease (COPD) showed comparable results. CONCLUSIONS: Under conditions of everyday clinical practice, the addition of montelukast to ICS/FC and good adherence to therapy increased the likelihood of achieving better asthma control at the follow-up visit, while older age and more severe asthma significantly decreased it.

Governor’s Office of Drug Control Policy Agency Performance Reporting, 2006

The Agency Performance Report for the Governor’s Office of Drug Control Policy is published in accordance with the Accountable Government Act. The information provided within this report is to aid in decision-making and to illustrate accountability to stakeholders and citizens. The report is indicative of the agency’s progress in meeting performance targets and achieving goals consistent with the enterprise strategic plan, the agency strategic plan and agency performance plan.

Governor’s Office of Drug Control Policy Agency Performance Reporting, 2007

The Agency Performance Report for the Governor’s Office of Drug Control Policy is published in accordance with the Accountable Government Act. The information provided within this report is to aid in decision-making and to illustrate accountability to stakeholders and citizens. The report is indicative of the agency’s progress in meeting performance targets and achieving goals consistent with the enterprise strategic plan, the agency strategic plan and agency performance plan.

Audit report of the Governor's Office of Drug Control Policy for the year ended June 30, 2006

Audit report of the Governor's Office of Drug Control Policy for the year ended June 30, 2006

Total exposure and exposure rate effects for alcohol and smoking and risk of head and neck cancer: a pooled analysis of case-control studies.

Although cigarette smoking and alcohol consumption increase risk for head and neck cancers, there have been few attempts to model risks quantitatively and to formally evaluate cancer site-specific risks. The authors pooled data from 15 case-control studies and modeled the excess odds ratio (EOR) to assess risk by total exposure (pack-years and drink-years) and its modification by exposure rate (cigarettes/day and drinks/day). The smoking analysis included 1,761 laryngeal, 2,453 pharyngeal, and 1,990 oral cavity cancers, and the alcohol analysis included 2,551 laryngeal, 3,693 pharyngeal, and 3,116 oval cavity cancers, with over 8,000 controls. Above 15 cigarettes/day, the EOR/pack-year decreased with increasing cigarettes/day, suggesting that greater cigarettes/day for a shorter duration was less deleterious than fewer cigarettes/day for a longer duration. Estimates of EOR/pack-year were homogeneous across sites, while the effects of cigarettes/day varied, indicating that the greater laryngeal cancer risk derived from differential cigarettes/day effects and not pack-years. EOR/drink-year estimates increased through 10 drinks/day, suggesting that greater drinks/day for a shorter duration was more deleterious than fewer drinks/day for a longer duration. Above 10 drinks/day, data were limited. EOR/drink-year estimates varied by site, while drinks/day effects were homogeneous, indicating that the greater pharyngeal/oral cavity cancer risk with alcohol consumption derived from the differential effects of drink-years and not drinks/day.

Dietary folates and cancer risk in a network of case-control studies.

Background Folate deficiency leads to DNA damage and inadequate repair, caused by a decreased synthesis of thymidylate and purines. We analyzed the relationship between dietary folate intake and the risk of several cancers. Patients and methods The study is based on a network of case-control studies conducted in Italy and Switzerland in 1991-2009. The odds ratios (ORs) for dietary folate intake were estimated by multiple logistic regression models, adjusted for major identified confounding factors. Results For a few cancer sites, we found a significant inverse relation, with ORs for an increment of 100 μg/day of dietary folate of 0.65 for oropharyngeal (1467 cases), 0.58 for esophageal (505 cases), 0.83 for colorectal (2390 cases), 0.72 for pancreatic (326 cases), 0.67 for laryngeal (851 cases) and 0.87 for breast (3034 cases) cancers. The risk estimates were below unity, although not significantly, for cancers of the endometrium (OR = 0.87, 454 cases), ovary (OR = 0.86, 1031 cases), prostate (OR = 0.91, 1468 cases) and kidney (OR = 0.88, 767 cases), and was 1.00 for stomach cancer (230 cases). No material heterogeneity was found in strata of sex, age, smoking and alcohol drinking. Conclusions Our data support a real inverse association of dietary folate intake with the risk of several common cancers.

Diabetes mellitus and cancer risk in a network of case-control studies.

Diabetes has been associated to the risk of a few cancer sites, though quantification of this association in various populations remains open to discussion. We analyzed the relation between diabetes and the risk of various cancers in an integrated series of case-control studies conducted in Italy and Switzerland between 1991 and 2009. The studies included 1,468 oral and pharyngeal, 505 esophageal, 230 gastric, 2,390 colorectal, 185 liver, 326 pancreatic, 852 laryngeal, 3,034 breast, 607 endometrial, 1,031 ovarian, 1,294 prostate, and 767 renal cell cancer cases and 12,060 hospital controls. The multivariate odds ratios (OR) for subjects with diabetes as compared to those without-adjusted for major identified confounding factors for the cancers considered through logistic regression models-were significantly elevated for cancers of the oral cavity/pharynx (OR = 1.58), esophagus (OR = 2.52), colorectum (OR = 1.23), liver (OR = 3.52), pancreas (OR = 3.32), postmenopausal breast (OR = 1.76), and endometrium (OR = 1.70). For cancers of the oral cavity, esophagus, colorectum, liver, and postmenopausal breast, the excess risk persisted over 10 yr since diagnosis of diabetes. Our data confirm and further quantify the association of diabetes with colorectal, liver, pancreatic, postmenopausal breast, and endometrial cancer and suggest forthe first time that diabetes may also increase the risk of oral/pharyngeal and esophageal cancer. [Table: see text] [Table: see text].