Field evidence of a natural capillary barrier in a gravel alluvial aquifer

Ozark streams commonly feature “composite” floodplains, in which the vadose zone consists of silt or silt loam soils (?1 m thick) overlying gravel subsoil. Previous work has shown that preferential flow paths can exist within the gravel subsoil, which can conduct water and P at rates exceeding the sorption capacity of the gravel. At a site on Barren Fork Creek, a 1- by 1-m infiltration plot was constructed and an infiltration experiment was performed using sequentially introduced solutes including P (the constituent of regulatory interest), Rhodamine-WT (Rh-WT, a visual tracer), and Cl− (an electrical tracer). The solute transport was measured with monitoring wells (MWs) placed 1 m from the plot boundary and 5 m down the groundwater flow gradient using an electrical resistivity imaging (ERI) array. The ERI method utilized differences between a pre-infiltration background image and subsequent temporal images taken during the test to quantify changes induced by the tracers. The infiltration test maintained a steady-state flow rate of 4.5 L min−1 for 84.75 h. Electrical resistivity imaging data showed significant changes in resistivity induced by the tracers within the soil vadose zone under the plot but no similar changes within the gravel, indicating that the interface was acting as a capillary barrier. Electrical resistivity images 5 m away from the plot showed tracer breakthrough into the gravel in areas not sampled by the MWs. Solute detection was limited in MWs, indicating that MWs could not adequately monitor movement below the capillary barrier because it controlled migration of solute to the heterogeneous phreatic zone

A Randomized Comparison of Aripiprazole and Risperidone for the Acute Treatment of First-Episode Schizophrenia and Related Disorders: 3-Month Outcomes

Research findings are particularly important for medication choice for first-episode patients as individual prior medication response to guide treatment decisions is unavailable. We describe the first large-scale double-masked randomized comparison with first-episode patients of aripiprazole and risperidone, 2 commonly used first-episode treatment agents. One hundred ninety-eight participants aged 15-40 years with schizophrenia, schizophreniform disorder, schizoaffective disorder or psychotic disorder Not Otherwise Specified, and who had been treated in their lifetime with antipsychotics for 2 weeks or less were randomly assigned to double-masked aripiprazole (5-30mg/d) or risperidone (1-6mg/d) and followed for 12 weeks. Positive symptom response rates did not differ (62.8% vs 56.8%) nor did time to response. Aripiprazole-treated participants had better negative symptom outcomes but experienced more akathisia. Body mass index change did not differ between treatments but advantages were found for aripiprazole treatment for total and low-density lipoprotein cholesterol, fasting glucose, and prolactin levels. Post hoc analyses suggested advantages for aripiprazole on depressed mood. Overall, if the potential for akathisia is a concern, low-dose risperidone as used in this trial maybe a preferred choice over aripiprazole. Otherwise, aripiprazole would be the preferred choice over risperidone in most situations based upon metabolic outcome advantages and some symptom advantages within the context of similar positive symptom response between medications

Pharmacogenetic Associations of Antipsychotic Drug-Related Weight Gain : A Systematic Review and Meta-analysis

Although weight gain is a serious but variable adverse effect of antipsychotics that has genetic underpinnings, a comprehensive meta-analysis of pharmacogenetics of antipsychotic-related weight gain is missing. In this review, random effects meta-analyses were conducted for dominant and recessive models on associations of specific single nucleotide polymorphisms (SNP) with prospectively assessed antipsychotic-related weight or body mass index (BMI) changes (primary outcome), or categorical increases in weight or BMI (≥7%; secondary outcome). Published studies, identified via systematic database search (last search: December 31, 2014), plus 3 additional cohorts, including 222 antipsychotic-naïve youth, and 81 and 141 first-episode schizophrenia adults, each with patient-level data at 3 or 4 months treatment, were meta-analyzed. Altogether, 72 articles reporting on 46 non-duplicated samples ( n = 6700, mean follow-up = 25.1wk) with 38 SNPs from 20 genes/genomic regions were meta-analyzed (for each meta-analysis, studies = 2–20, n = 81–2082). Eleven SNPs from 8 genes were significantly associated with weight or BMI change, and 4 SNPs from 2 genes were significantly associated with categorical weight or BMI increase. Combined, 13 SNPs from 9 genes (Adrenoceptor Alpha-2A [ ADRA2A ], Adrenoceptor Beta 3 [ ADRB3 ], Brain-Derived Neurotrophic Factor [ BDNF ], Dopamine Receptor D2 [ DRD2 ], Guanine Nucleotide Binding Protein [ GNB3 ], 5-Hydroxytryptamine (Serotonin) Receptor 2C [ HTR2C ], Insulin-induced gene 2 [ INSIG2 ], Melanocortin-4 Receptor [ MC4R ], and Synaptosomal-associated protein, 25kDa [ SNAP25 ]) were significantly associated with antipsychotic-related weight gain ( P -values < .05–.001). SNPs in ADRA2A , DRD2 , HTR2C , and MC4R had the largest effect sizes (Hedges’ g ’s = 0.30–0.80, ORs = 1.47–1.96). Less prior antipsychotic exposure (pediatric or first episode patients) and short follow-up (1–2 mo) were associated with larger effect sizes. Individual antipsychotics did not significantly moderate effect sizes. In conclusion, antipsychotic-related weight gain is polygenic and associated with specific genetic variants, especially in genes coding for antipsychotic pharmacodynamic targets

Pharmacogenetic Associations of Antipsychotic Drug-Related Weight Gain: A Systematic Review and Meta-analysis.

Although weight gain is a serious but variable adverse effect of antipsychotics that has genetic underpinnings, a comprehensive meta-analysis of pharmacogenetics of antipsychotic-related weight gain is missing. In this review, random effects meta-analyses were conducted for dominant and recessive models on associations of specific single nucleotide polymorphisms (SNP) with prospectively assessed antipsychotic-related weight or body mass index (BMI) changes (primary outcome), or categorical increases in weight or BMI (≥7%; secondary outcome). Published studies, identified via systematic database search (last search: December 31, 2014), plus 3 additional cohorts, including 222 antipsychotic-naïve youth, and 81 and 141 first-episode schizophrenia adults, each with patient-level data at 3 or 4 months treatment, were meta-analyzed. Altogether, 72 articles reporting on 46 non-duplicated samples (n = 6700, mean follow-up = 25.1wk) with 38 SNPs from 20 genes/genomic regions were meta-analyzed (for each meta-analysis, studies = 2-20, n = 81-2082). Eleven SNPs from 8 genes were significantly associated with weight or BMI change, and 4 SNPs from 2 genes were significantly associated with categorical weight or BMI increase. Combined, 13 SNPs from 9 genes (Adrenoceptor Alpha-2A [ADRA2A], Adrenoceptor Beta 3 [ADRB3], Brain-Derived Neurotrophic Factor [BDNF], Dopamine Receptor D2 [DRD2], Guanine Nucleotide Binding Protein [GNB3], 5-Hydroxytryptamine (Serotonin) Receptor 2C [HTR2C], Insulin-induced gene 2 [INSIG2], Melanocortin-4 Receptor [MC4R], and Synaptosomal-associated protein, 25kDa [SNAP25]) were significantly associated with antipsychotic-related weight gain (P-values &lt; .05-.001). SNPs in ADRA2A, DRD2, HTR2C, and MC4R had the largest effect sizes (Hedges' g's = 0.30-0.80, ORs = 1.47-1.96). Less prior antipsychotic exposure (pediatric or first episode patients) and short follow-up (1-2 mo) were associated with larger effect sizes. Individual antipsychotics did not significantly moderate effect sizes. In conclusion, antipsychotic-related weight gain is polygenic and associated with specific genetic variants, especially in genes coding for antipsychotic pharmacodynamic targets

Pharmacogenetic Associations of Antipsychotic Drug-Related Weight Gain : A Systematic Review and Meta-analysis

Although weight gain is a serious but variable adverse effect of antipsychotics that has genetic underpinnings, a comprehensive meta-analysis of pharmacogenetics of antipsychotic-related weight gain is missing. In this review, random effects meta-analyses were conducted for dominant and recessive models on associations of specific single nucleotide polymorphisms (SNP) with prospectively assessed antipsychotic-related weight or body mass index (BMI) changes (primary outcome), or categorical increases in weight or BMI (≥7%; secondary outcome). Published studies, identified via systematic database search (last search: December 31, 2014), plus 3 additional cohorts, including 222 antipsychotic-naïve youth, and 81 and 141 first-episode schizophrenia adults, each with patient-level data at 3 or 4 months treatment, were meta-analyzed. Altogether, 72 articles reporting on 46 non-duplicated samples ( n = 6700, mean follow-up = 25.1wk) with 38 SNPs from 20 genes/genomic regions were meta-analyzed (for each meta-analysis, studies = 2–20, n = 81–2082). Eleven SNPs from 8 genes were significantly associated with weight or BMI change, and 4 SNPs from 2 genes were significantly associated with categorical weight or BMI increase. Combined, 13 SNPs from 9 genes (Adrenoceptor Alpha-2A [ ADRA2A ], Adrenoceptor Beta 3 [ ADRB3 ], Brain-Derived Neurotrophic Factor [ BDNF ], Dopamine Receptor D2 [ DRD2 ], Guanine Nucleotide Binding Protein [ GNB3 ], 5-Hydroxytryptamine (Serotonin) Receptor 2C [ HTR2C ], Insulin-induced gene 2 [ INSIG2 ], Melanocortin-4 Receptor [ MC4R ], and Synaptosomal-associated protein, 25kDa [ SNAP25 ]) were significantly associated with antipsychotic-related weight gain ( P -values < .05–.001). SNPs in ADRA2A , DRD2 , HTR2C , and MC4R had the largest effect sizes (Hedges’ g ’s = 0.30–0.80, ORs = 1.47–1.96). Less prior antipsychotic exposure (pediatric or first episode patients) and short follow-up (1–2 mo) were associated with larger effect sizes. Individual antipsychotics did not significantly moderate effect sizes. In conclusion, antipsychotic-related weight gain is polygenic and associated with specific genetic variants, especially in genes coding for antipsychotic pharmacodynamic targets