Noticias y tensiones cambiarias en Argentina

We study the association between the nominal exchange rate and the dissemination of macroeconomic news in Argentina through the estimation of a VARX-GARCH(1,1) model. Our main empirical results show that: 1) The transmission of adverse financial shocks occurs mostly from the United States and operates via the spread of interest rates (EMBI+ for Argentina); 2) The news compiled from local and foreign newspapers do not generate relevant economic effects to explain the dynamics of the nominal exchange rate; and 3) The conditional volatility of shocks associated with the endogenous variables of the VARX model can be formalized through a GARCH(1,1) specification.Se estudia la relación entre el tipo de cambio nominal y la difusión de noticias macroeconómicas en Argentina mediante la estimación de un modelo VARX-GARCH(1,1). Los principales resultados empíricos indican que: 1) La transmisión de shocks financieros adversos procede fundamentalmente desde Estados Unidos y opera mediante el spread de tasas de interés (EMBI+ para Argentina); 2) Las noticias recopiladas de periódicos locales y extranjeros no ejercen efectos económicos relevantes para explicar la dinámica del tipo de cambio nominal; y 3) La volatilidad condicional de los shocks aleatorios asociados a las variables endógenas del modelo VARX puede formalizarse mediante una estrategia GARCH(1,1)

News and exchange rate pressures in Argentina

Se estudia la relación entre el tipo de cambio nominal y la difusión de noticias macroeconómicas en Argentina mediante la estimación de un modelo VARX-GARCH(1,1). Los principales resultados empíricos indican que: 1) La transmisión de shocks financieros adversos procede fundamentalmente desde Estados Unidos y opera mediante el spread de tasas de interés (EMBI+ para Argentina); 2) Las noticias recopiladas de periódicos locales y extranjeros no ejercen efectos económicos relevantes para explicar la dinámica del tipo de cambio nominal; y 3) La volatilidad condicional de los shocks aleatorios asociados a las variables endógenas del modelo VARX puede formalizarse mediante una estrategia GARCH(1,1).We study the association between the nominal exchange rate and the dissemination of macroeconomic news in Argentina through the estimation of a VARX-GARCH(1,1) model. Our main empirical results show that: 1) The transmission of adverse financial shocks occurs mostly from the United States and operates via the spread of interest rates (EMBI+ for Argentina); 2) The news compiled from local and foreign newspapers do not generate relevant economic effects to explain the dynamics of the nominal exchange rate; and 3) The conditional volatility of shocks associated with the endogenous variables of the VARX model can be formalized through a GARCH(1,1) specification.Facultad de Ciencias Económica

Dopamine D2/3 occupancy of ziprasidone across a day : a within-subject PET study

Rationale Ziprasidone is an atypical antipsychotic recommended to be administered twice daily. Objectives The purpose of this study was to investigate whether occupancy of the dopamine D2/3 receptors by ziprasidone is maintained across a day employing a within subject design. Methods Positron emission tomography (PET) scans with [11C]-raclopride were performed in 12 patients with schizophrenia while treated with ziprasidone 60 mg twice daily. Each patient completed [11C]-raclopride PET scans at 5, 13 and 23 h after the last dose of ziprasidone. Dopamine D2/3 receptor occupancy was estimated with reference to binding potential data of 44 age- and sex-matched control subjects in the caudate, putamen and ventral striatum. Results Eleven scans were available at each time point, and the mean occupancies at 5-, 13- and 23-h scans were 66, 39 and 2 % in the putamen; 62, 35 and −6 % in the caudate; and 68, 47 and 11 % in the ventral striatum, respectively. The time-course of receptor occupancy across the regions indicated an occupancy half-life of 8.3 h. The serum level of ziprasidone associated with 50 % D2/3 receptors occupancy was estimated to be 204 nmol/L (84 ng/ml). Prolactin levels were highest at 5-h post-dose and none showed hyperprolactinemia at 23-h scans. Conclusions The absence of ziprasidone striatal D2/3 receptor binding 23 h after taking 60 mg under steady-state conditions is consistent with its peripheral half-life. The results support our earlier report that ziprasidone 60 mg administered twice daily appears to be the minimal dose expected to achieve therapeutic central dopamine D2/3 receptor occupancy (i.e. 60 %).peer-reviewe

Antipsychotics, Metabolic Adverse Effects, and Cognitive Function in Schizophrenia

Cognitive impairment is a core symptom domain of schizophrenia. The effect of antipsychotics, the cornerstone of treatment in schizophrenia, on this domain is not fully clear. There is some evidence suggesting that antipsychotics may partially improve cognitive function, and that this improvement may vary depending on the specific cognitive domain. However, this research is confounded by various factors, such as age, duration/stage of illness, medication adherence, and extrapyramidal side effects that complicate the relationship between antipsychotics and cognitive improvement. Furthermore, antipsychotics—particularly the second generation, or “atypical” antipsychotics—can induce serious metabolic side effects, such as obesity, dyslipidemia and type 2 diabetes, illnesses which themselves have been linked to impairments in cognition. Thus, the inter-relationships between cognition and metabolic side effects are complex, and this review aims to examine them in the context of schizophrenia and antipsychotic treatment. The review also speculates on potential mechanisms underlying cognitive functioning and metabolic risk in schizophrenia. We conclude that the available literature examining the inter-section of antipsychotics, cognition, and metabolic effects in schizophrenia is sparse, but suggests a relationship between metabolic comorbidity and worse cognitive function in patients with schizophrenia. Further research is required to determine if there is a causal connection between the well-recognized metabolic adverse effects of antipsychotics and cognitive deficits over the course of the illness of schizophrenia, as well as, to determine underlying mechanisms. In addition, findings from this review highlight the importance of monitoring metabolic disturbances in parallel with cognition, as well as, the importance of interventions to minimize metabolic abnormalities for both physical and cognitive health

Estimating Endogenous Dopamine at D2 and D3 Receptors in the Human Brain using the Agonist Radiotracer [11C]-(+)-PHNO: Clinical, Cognitive, and Metabolic Correlates

Using positron emission tomography (PET), and reversibly binding radiotracers which label the dopamine (DA) D2/3 receptors (D2/3R), it is possible to estimate endogenous DA levels in the brain of humans in vivo. This thesis has four themes. The first theme is validating the use of an agonist radiotracer for D2/3R to estimate endogenous DA levels. The second theme is applying this method to better understand differences in DA levels between healthy persons and persons with schizophrenia. The third theme is determining other biologically relevant factors which may affect endogenous DA levels in the human brain in vivo, in particular, factors related to metabolic health. The final theme combines those previous – attempting to extend the basic metabolic correlates relating to endogenous DA to better understand how abnormalities in DA levels may arise in persons with schizophrenia. For the first time, an agonist radiotracer for the DA D2/3R was used to provide in vivo estimates of endogenous DA in the brains of healthy humans. Furthermore, it was determined that this radiotracer could be used to estimate endogenous DA in the brains of persons with schizophrenia who were currently taking antipsychotics. Elucidating relevant cognitive and biological factors which may relate to differences in endogenous DA levels is pertinent for better understanding how abnormalities in DA tone may arise in neuropsychiatric diseases. Thus, for the first time it is demonstrated that differences in insulin sensitivity among healthy persons is related to differences in endogenous DA in the ventral striatum. Given that insulin resistance can be comorbid or concurrent in persons with schizophrenia, future studies are proposed.Ph.D

Trait impulsivity is not related to post-commissural putamen volumes : A replication study in healthy men

High levels of trait impulsivity are considered a risk factor for substance abuse and drug addiction. We recently found that non-planning trait impulsivity was negatively correlated with post-commissural putamen volumes in men, but not women, using the Karolinska Scales of Personality (KSP). Here, we attempted to replicate this finding in an independent sample using an updated version of the KSP: the Swedish Universities Scales of Personality (SSP). Data from 88 healthy male participants (Mean Age: 28.16 +/- 3.34), who provided structural T1-weighted magnetic resonance images (MRIs) and self-reported SSP impulsivity scores, were analyzed. Striatal sub-region volumes were acquired using the Multiple Automatically Generated Templates (MAGeT-Brain) algorithm. Contrary to our previous findings trait impulsivity measured using SSP was not a significant predictor of post-commissural putamen volumes (beta = .14, df = 84, p = .94). A replication Bayes Factors analysis strongly supported this null result. Consistent with our previous findings, secondary exploratory analyses found no relationship between ventral striatum volumes and SSP trait impulsivity (beta = -.05, df = 84, p = .28). An exploratory analysis of the other striatal compartments showed that there were no significant associations with trait impulsivity. While we could not replicate our previous findings in the current sample, we believe this work will aide future studies aimed at establishing meaningful brain biomarkers for addiction vulnerability in healthy humans

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment.

Depressive symptoms are frequently seen in patients with dementia and mild cognitive impairment (MCI). Evidence suggests that there may be a link between current depressive symptoms and Alzheimer disease (AD)-associated pathological changes, such as an increase in cortical amyloid-β (Aβ). However, limited in vivo studies have explored the relationship between current depressive symptoms and cortical Aβ in patients with MCI and AD. Our study, using a large sample of 455 patients with MCI and 153 patients with AD from the Alzheimer's disease Neuroimaging Initiatives, investigated whether current depressive symptoms are related to cortical Aβ deposition. Depressive symptoms were assessed using the Geriatric Depression Scale and Neuropsychiatric Inventory-depression/dysphoria. Cortical Aβ was quantified using positron emission tomography with the Aβ probe(18)F-florbetapir (AV-45).(18)F-florbetapir standardized uptake value ratio (AV-45 SUVR) from the frontal, cingulate, parietal, and temporal regions was estimated. A global AV-45 SUVR, defined as the average of frontal, cingulate, precuneus, and parietal cortex, was also used. We observed that current depressive symptoms were not related to cortical Aβ, after controlling for potential confounds, including history of major depression. We also observed that there was no difference in cortical Aβ between matched participants with high and low depressive symptoms, as well as no difference between matched participants with the presence and absence of depressive symptoms. The association between depression and cortical Aβ deposition does not exist, but the relationship is highly influenced by stressful events in the past, such as previous depressive episodes, and complex interactions of different pathways underlying both depression and dementia

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment.

Depressive symptoms are frequently seen in patients with dementia and mild cognitive impairment (MCI). Evidence suggests that there may be a link between current depressive symptoms and Alzheimer disease (AD)-associated pathological changes, such as an increase in cortical amyloid-β (Aβ). However, limited in vivo studies have explored the relationship between current depressive symptoms and cortical Aβ in patients with MCI and AD. Our study, using a large sample of 455 patients with MCI and 153 patients with AD from the Alzheimer's disease Neuroimaging Initiatives, investigated whether current depressive symptoms are related to cortical Aβ deposition. Depressive symptoms were assessed using the Geriatric Depression Scale and Neuropsychiatric Inventory-depression/dysphoria. Cortical Aβ was quantified using positron emission tomography with the Aβ probe(18)F-florbetapir (AV-45).(18)F-florbetapir standardized uptake value ratio (AV-45 SUVR) from the frontal, cingulate, parietal, and temporal regions was estimated. A global AV-45 SUVR, defined as the average of frontal, cingulate, precuneus, and parietal cortex, was also used. We observed that current depressive symptoms were not related to cortical Aβ, after controlling for potential confounds, including history of major depression. We also observed that there was no difference in cortical Aβ between matched participants with high and low depressive symptoms, as well as no difference between matched participants with the presence and absence of depressive symptoms. The association between depression and cortical Aβ deposition does not exist, but the relationship is highly influenced by stressful events in the past, such as previous depressive episodes, and complex interactions of different pathways underlying both depression and dementia