To fabricate efficient formamidinium tin iodide (FASnI3) perovskite solar cells (PSCs), it is essential to deposit uniform and dense perovskite layers and reduce Sn(4+) content. Here we used solvent-engineering and nonsolvent dripping process with SnF2 as an inhibitor of Sn(4+). However, excess SnF2 induces phase separation on the surface of the perovskite film. In this work, we report the homogeneous dispersion of SnF2 via the formation of the SnF2-pyrazine complex. Consequently, we fabricated FASnI3 PSCs with high reproducibility, achieving a high power conversion efficiency of 4.8%. Furthermore, the encapsulated device showed a stable performance for over 100 days, maintaining 98% of its initial efficiency.

Objective White matter hyperintensities(WMH) are areas of increased signal on magnetic resonance imaging(MRI) scans that most commonly reflect small vessel cerebrovascular disease. Increased WMH volume is associated with risk and progression of Alzheimer’s disease(AD). These observations are typically interpreted as evidence that vascular abnormalities play an additive, independent role contributing to symptom presentation, but not core features of AD. We examined the severity and distribution of WMH in presymptomatic PSEN1, PSEN2, and APP mutation carriers to determine the extent to which WMH manifest in individuals genetically-determined to develop AD. Methods The study comprised participants(n=299, age=39.03±10.13) from the Dominantly Inherited Alzheimer Network, including 184(61.5%) with a mutation that results in AD and 115(38.5%) first-degree relatives who were non-carrier controls. We calculated the estimated years from expected symptom onset(EYO) by subtracting the affected parent’s symptom onset age from the participant’s age. Baseline MRI data were analyzed for total and regional WMH. Mixed effects piecewise linear regression was used to examine WMH differences between carriers and non-carriers with respect to EYO. Results Mutation carriers had greater total WMH volumes, which appeared to increase approximately 6 years prior to expected symptom onset. The effects were most prominent for the parietal and occipital lobe, which showed divergent effects as early as 22 years prior to estimated onset. Interpretation Autosomal dominant AD is associated with increased WMH well before expected symptom onset. The findings suggest the possibility that WMH are a core feature of AD, a potential therapeutic target, and a factor that should be integrated into pathogenic models of the disease.

Objective: To determine the predictive utility of baseline odor identification deficits for future cognitive decline and the diagnosis of Alzheimer disease (AD) dementia.Methods: In a multiethnic community cohort in North Manhattan, NY, 1,037 participants without dementia were evaluated with the 40-item University of Pennsylvania Smell Identification Test (UPSIT). In 757 participants, follow-up occurred at 2 years and 4 years.Results: In logistic regression analyses, lower baseline UPSIT scores were associated with cognitive decline (relative risk 1.067 per point interval; 95% confidence interval [CI] 1.040, 1.095; p , 0.0001), and remained significant (relative risk 1.065 per point interval; 95% CI 1.034, 1.095; p , 0.0001) after including covariates. UPSIT, but not Selective Reminding Test-total immediate recall, predicted cognitive decline in participants without baseline cognitive impairment. During follow-up, 101 participants transitioned to AD dementia. In discrete time survival analyses, lower baseline UPSIT scores were associated with transition to AD dementia (hazard ratio 1.099 per point interval; 95% CI 1.067, 1.131; p , 0.0001), and remained highly significant (hazard ratio 1.072 per point interval; 95% CI 1.036, 1.109; p , 0.0001) after including demographic, cognitive, and functional covariates.Conclusions: Impairment in odor identification was superior to deficits in verbal episodic memory in predicting cognitive decline in cognitively intact participants. The findings support the crosscultural use of a relatively inexpensive odor identification test as an early biomarker of cognitive decline and AD dementia. Such testing may have the potential to select/stratify patients in treatment trials of cognitively impaired patients or prevention trials in cognitively intact individuals.Neurology ® 2015;84:182-189 GLOSSARY AD 5 Alzheimer disease; AUC 5 area under the curve; CI 5 confidence interval; HR 5 hazard ratio; MCI 5 mild cognitive impairment; ROC 5 receiver operating characteristic; RR 5 relative risk; SRT 5 Selective Reminding Test; SRT-TR 5 Selective Reminding Test-total immediate recall; UPSIT 5 University of Pennsylvania Smell Identification Test; WHICAP 5 Washington Heights/Inwood Columbia Aging Project.

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Objective Increased risk of psychopathology is observed in children exposed to maternal prenatal distress, and elevated maternal cortisol and epigenetic regulation of placental glucocorticoid-pathway genes are potential mechanisms. The authors examined maternal distress and salivary cortisol in relation to fetal movement and heart rate (“coupling”) and DNA methylation of three glucocorticoid pathway genes—HSD11B2, NR3C1, and FKBP5—in term placentas. Method Mood questionnaires and salivary cortisol were collected from 61 women between 24–27 gestational weeks, and fetal assessment was conducted at 34–37 weeks. Placental CpG methylation in the three genes was analyzed using 450K Beadchips and bisulfite sequencing; correlations between maternal and fetal variables and DNA methylation were tested; and maternal distress effects on fetal behavior via DNA methylation were investigated. Results Perceived stress (Perceived Stress Scale), but not cortisol, was associated with altered CpG methylation in placentas. In the highest tertile of the Perceived Stress Scale, the Beadchip data revealed modestly elevated methylation of HSD11B2, associated with lower fetal coupling (β=−0.51), and modestly elevated methylation of FKBP5, also with lower fetal coupling (β=−0.47). These increases in methylation were validated by bisulfite sequencing, where they occurred in a minority of clones. Conclusions This is the first study to link the effects of pregnant women’s distress on the fetus and epigenetic changes in placental genes. Since increased DNA methylation in HSD11B2 and FKBP5 are seen in a minority of bisulfite sequencing clones, these epigenetic changes, and functional consequences, may affect subpopulations of placental cells.

Currently, the efficiency of perovskite solar cells (PSCs) is ≈24%. For the fabrication of such high efficiency PSCs, it is necessary to use both electron and hole transport layers to effectively separate the charges generated by light absorption of the perovskite layer and selectively transfer the separated electrons and holes. In addition to the efficiency, the materials used for transporting charges must be resilient to light, heat, and moisture to ensure long-term stability of PSCs; furthermore, low-cost fabrication is required to form a charge transport layer at low temperatures by a solution process. For this purpose, metal oxides are best suited as charge transport materials for PSCs because of their advantages such as low cost, long-term stability, and high efficiency. In this Review, the metal oxide electron and hole transport materials used in PSCs are reviewed and preparation of these materials is summarized. Finally, the challenges and future research direction for metal oxide-based charge transport materials are described. 10% by using a submicrometer-thick mp-TiO 2 film and solid type hole transporting materials (HTM). [1a,16] We first reported an efficiency of 12% using an ≈400 nm thick mp-TiO 2 electrode and a polymeric HTM (poly-triarylamine, PTAA). [17] Subsequently, the thickness of mp-TiO 2 was reduced to less than 200 nm, and the efficiency was improved by over 22% by controlling the surface morphology, [4] composition, [18] and defect [19] of the perovskite optical absorber using the same PTAA.

Objective To examine the association between odor identification deficits and future mortality in a multiethnic community cohort of older adults. Methods Participants were evaluated with the 40-item University of Pennsylvania Smell Identification Test (UPSIT). Follow-up occurred at 2-year intervals with information on death obtained from informant interviews and the National Death Index. Results During follow-up (mean 4.1 SD 2.6 years), 349 of 1169 (29.9%) participants died. Participants who died were more likely to be older (p < 0.001), male (p < 0.001), have lower UPSIT scores (p < 0.001), and have a diagnosis of dementia (p < 0.001). In a Cox model, the association between lower UPSIT score and mortality (Hazard Ratio 1.07 per point interval, 95%CI 1.05 to 1.08, p<0.001) persisted after controlling for age, gender, education, ethnicity, language, modified Charlson medical comorbidity index, dementia, depression, alcohol abuse, head injury, smoking, Body Mass Index, vision and hearing impairment (Hazard Ratio=1.05, 95%CI 1.03 to 1.07, p<0.001). Compared to the fourth quartile with the highest UPSIT scores, hazard ratios for mortality for the first, second, and third quartiles of UPSIT scores were 3.81 (95%CI 2.71 to 5.34), 1.75 (95%CI 1.23 to 2.50), and 1.58 (95%CI 1.09 to 2.30), respectively. Participant mortality rate was 45% in the lowest quartile of UPSIT scores (anosmia) and 18% in the highest quartile of UPSIT scores. Interpretation Impaired odor identification, particularly in the anosmic range, is associated with increased mortality in older adults even after controlling for dementia and medical comorbidity.

Parkinson's disease (PD) presents clinically with varying degrees of resting tremor, rigidity, and bradykinesia. For decades, striatal-thalamo-cortical (STC) dysfunction has been implied in Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Disclosure:The authors have reported no conflicts of interest. Specific Contributions of AuthorsMechelle M. Lewis: Data acquisition, analysis, and interpretation; obtaining funding for the study, administrative support for the study; primary drafting and critical revision of the manuscript. Guangwei Du: Data analysis and interpretation, drafting and critical revision of the manuscript, Suman Sen: Data acquisition, critical revision of the manuscript. Atsushi Kawaguchi: Statistical analysis of the data and data interpretation. Young Truong: Statistical analysis of the data, data interpretation, critical revision of the manuscript. Seonjoo Lee: Statistical analysis of the data and critical revision of the manuscript. Richard Mailman: Data interpretation and critical revision of the manuscript. Xuemei Huang: Conception and design of the study; data acquisition, analysis, and interpretation; drafting and critical revision of the manuscript; obtaining funding for the study; administration and supervision of the project. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2012 March 17. Zetusky et al., 1985), is less reliably responsive to dopaminergic modulation (Marjama-Lyons and Koller, 2000), and does not worsen at the same rate as bradykinesia and rigidity (Zetusky et al., 1985;Louis et al., 1999;Jankovic and Kapadia, 2001). Recent PD imaging studies suggest dopamine transporter levels and myocardial sympathetic degeneration correlate with hypokinesia/rigidity but not tremor (Spiegel et al., 2007). Finally, there is no correlation between rest tremor and striatal 18 Ffluorodopa uptake in PD patients (Vingerhoets et al., 1997).The pathological hallmark of PD is dopamine neuron loss in the substantia nigra pars compacta (SNc) of the basal ganglia (BG). For decades, a classic model emphasized the role of the BG in modulating cortical function through striatal-thalamo-cortical (STC) circuits (DeLong et al., 1984;Alexander et al., 1986;Albin et al., 1989), the dysfunction of which may lead to bradykinesia and rigidity. This model does not, however, explain PD resting tremor. Emerging evidence suggests the necessity of incorpating cerebello-thalamo-cortical (CTC) circuitry into discussions of motor function in both normal (Kelly et al., 2009) and dysfunctional (Deiber et al., 1993;Neychev et al., 2008;A...