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Electronic relaxation dynamics of solution-phase redox-exfoliated molybdenum disulfide (MoS2) monolayer and multilayer ensembles are described. MoS2 was exfoliated using polyoxometalate (POM) reductants. This process yields a colloidal heterostructure consisting of MoS2 2D sheet multilayers with surface-bound POM complexes. Using two-dimensional electronic spectroscopy, transient bleaching and photoinduced absorption signals were detected at excitation/detection energies of 1.82/1.87 and 1.82/1.80 eV, respectively. Approximate 100-fs bandgap renormalization (BGR) and subsequent defect- and phonon-mediated relaxation on the picosecond timescale were resolved for several MoS2 thicknesses spanning from 1 to 2 L to ∼20 L. BGR rates were independent of sample thickness and slightly slower than observations for chemical vapor deposition-grown MoS2 monolayers. However, defect-mediated relaxation accelerated ∼10-fold with increased sample thicknesses. The relaxation rates increased from 0.33 ± 0.05 to 1.2 ± 0.1 and 3.1 ± 0.4 ps−1 for 1–2 L, 3–4 L, and 20 L fractions. The thicknesses-dependent relaxation rates for POM-MoS2 heterostructures were modeled using a saturating exponential function that showed saturation at thirteen MoS2 layers. The results suggest that the increased POM surface coverage leads to larger defect density in the POM-MoS2 heterostructure. These are the first descriptions of the influence of sample thickness on electronic relaxation rates in solution-phase redox-exfoliated POM-MoS2 heterostructures. Outcomes of this work are expected to impact the development of solution-phase exfoliation of 2D metal-chalcogenide heterostructures. [ABSTRACT FROM AUTHOR]

Chemical sensors based on solution‐processed 2D nanomaterials represent an extremely attractive approach toward scalable and low‐cost devices. Through the implementation of real‐time impedance spectroscopy and development of a three‐element circuit model, redox exfoliated MoS2 nanoflakes demonstrate an ultrasensitive empirical detection limit of NO2 gas at 1 ppb, with an extrapolated ultimate detection limit approaching 63 ppt. This sensor construct reveals a more than three orders of magnitude improvement from conventional direct current sensing approaches as the traditionally dominant interflake interactions are bypassed in favor of selectively extracting intraflake doping effects. This same approach allows for an all solution‐processed, flexible 2D sensor to be fabricated on a polyimide substrate using a combination of graphene contacts and drop‐casted MoS2 nanoflakes, exhibiting similar sensitivity limits. Finally, a thermal annealing strategy is used to explore the tunability of the nanoflake interactions and subsequent circuit model fit, with a demonstrated sensitivity improvement of 2× with thermal annealing at 200 °C. [ABSTRACT FROM AUTHOR]

Chemical sensors based on solution‐processed 2D nanomaterials represent an extremely attractive approach toward scalable and low‐cost devices. Through the implementation of real‐time impedance spectroscopy and development of a three‐element circuit model, redox exfoliated MoS2 nanoflakes demonstrate an ultrasensitive empirical detection limit of NO2 gas at 1 ppb, with an extrapolated ultimate detection limit approaching 63 ppt. This sensor construct reveals a more than three orders of magnitude improvement from conventional direct current sensing approaches as the traditionally dominant interflake interactions are bypassed in favor of selectively extracting intraflake doping effects. This same approach allows for an all solution‐processed, flexible 2D sensor to be fabricated on a polyimide substrate using a combination of graphene contacts and drop‐casted MoS2 nanoflakes, exhibiting similar sensitivity limits. Finally, a thermal annealing strategy is used to explore the tunability of the nanoflake interactions and subsequent circuit model fit, with a demonstrated sensitivity improvement of 2× with thermal annealing at 200 °C. [ABSTRACT FROM AUTHOR]

• Childhood trauma (CT) is a major risk factor for neuropsychiatric disorders • Long-term epigenetic changes occur in the brain of adults with a history of CT • Affected pathways include the HPA axis, BDNF, oxytocin and neurotransmitter signaling • Pharmacological and psychological interventions may counteract CT-induced changes. Childhood trauma (CT) can have persistent effects on the brain and is one of the major risk factors for neuropsychiatric diseases in adulthood. Recent advances in the field of epigenetics suggest that epigenetic factors such as DNA methylation and histone modifications, as well as regulatory processes involving non-coding RNA are associated with the long-term sequelae of CT. This narrative review summarizes current knowledge on the epigenetic basis of CT and describes studies in animal models and human subjects examining how the epigenome and transcriptome are modified by CT in the brain. It discusses psychological and pharmacological interventions that can counteract epigenetic changes induced by CT and the need to establish longitudinal assessment after CT for developing more effective diagnostics and treatment strategies based on epigenetic targets. [ABSTRACT FROM AUTHOR]

The possibility that parental life experiences and environmental exposures influence mental and physical health across generations is an important concept in biology and medicine. Evidence from animal models has established the existence of a non-genetic mode of inheritance. This form of heredity involves transmission of the effects of parental exposure to the offspring through epigenetic changes in the germline. Studying the mechanisms of epigenetic inheritance in humans is challenging because it is difficult to obtain multigeneration cohorts, to collect reproductive cells in exposed parents, and to exclude psychosocial and cultural confounders. Nonetheless, epidemiological studies in humans exposed to famine, stress/trauma, or toxicants have provided evidence that parental exposure can impact the health of descendants, in some cases, across several generations. A few studies have also started to reveal epigenetic changes in the periphery and sperm after certain exposures. This article reviews these studies and evaluates the current evidence for the potential contribution of epigenetic factors to heredity in humans. The challenges and limitations of this fundamental biological process, its implications, and its societal relevance are also discussed. This review evaluates the current evidence for the effects of parental exposure on offspring health in humans and the potential contribution of epigenetic factors toward such transmission. It discusses the challenges and limitations of studying epigenetic inheritance in humans. It also addresses the implications of the concept of epigenetic inheritance on human health and its societal relevance. [ABSTRACT FROM AUTHOR]

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder with limited therapeutic options. Clinical trials of several drugs shown to be effective in the superoxide dismutase (SOD1) model of ALS have shown no or negative effects when tested in humans. Here we discuss the role of pioglitazone, a peroxisome proliferator-activated receptor-γ agonist, which failed to show efficacy in a recently published phase II clinical trial of ALS patients. The antioxidant and anti-inflammatory properties of pioglitazone make it an attractive therapeutic candidate for neurodegenerative disorders. However, its antidiabetic and antidyslipidemic effects might be detrimental, as emerging evidence suggests that some features of the metabolic syndrome may be protective in ALS. A number of clinical studies show that dyslipidemia, high body mass index, and possibly diabetes mellitus type 2 are associated with better clinical outcomes in ALS. This is further corroborated by studies on transgenic animal models and immortalized neuronal cell lines. Finally, the intricate interplay between glucose/lipid metabolism and susceptibility to oxidative damage in neurons warrants a judicious approach in further trials of antidiabetic drugs in ALS. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Ultrasensitive Molecular Sensors In article number 2106830, Nicholas R. Glavin and co‐workers describe a real‐time impedance spectroscopy approach, which enables ultrasensitive molecular sensors in solution processed 2D nanomaterials. Through bypassing traditionally dominant interflake interactions and selectively extracting intraflake doping effects, detection of NO2 vapor down to 1 ppb is readily achievable with an ultimate limit of detection approaching 63 ppt. Image by Dr. Jo Richers (www.jorichers.com). [ABSTRACT FROM AUTHOR]

Ultrasensitive Molecular Sensors Based on Real-Time Impedance Spectroscopy in Solution-Processed 2D Materials (Adv. Funct. Keywords: 2D materials; impedance spectroscopy; liquid phase exfoliation; molybdenum disulfide; sensors EN 2D materials impedance spectroscopy liquid phase exfoliation molybdenum disulfide sensors 1 1 1 03/21/22 20220316 NES 220316 B Ultrasensitive Molecular Sensors b In article number 2106830, Nicholas R. Glavin and co-workers describe a real-time impedance spectroscopy approach, which enables ultrasensitive molecular sensors in solution processed 2D nanomaterials. 2D materials, impedance spectroscopy, liquid phase exfoliation, molybdenum disulfide, sensors. [Extracted from the article]

This article, published in Advanced Functional Materials, discusses the development of ultrasensitive molecular sensors using real-time impedance spectroscopy in solution-processed 2D nanomaterials. The researchers, led by Nicholas R. Glavin, were able to achieve detection of NO2 vapor down to 1 ppb, with an ultimate limit of detection approaching 63 ppt. By bypassing interflake interactions and selectively extracting intraflake doping effects, the team was able to enhance the sensitivity of the sensors. This research has potential applications in various fields, such as environmental monitoring and healthcare. [Extracted from the article]

Our objective was to test the hypothesis that changes in body mass index (BMI) are associated with changes in the clinical course of ALS. We examined the relationships between BMI at first clinical visit and changes in BMI up to a two-year follow-up, and multiple clinical variables related to ALS: age of onset, rate of progression of motor symptoms, and survival. Baseline BMI was classified according to the World Health Organization (WHO) criteria. Changes in BMI were classified as a loss of >1 unit, no change, or a gain of >1 unit. Our results showed that baseline BMI was not associated with age of onset, rate of progression or survival. In contrast, a loss of BMI >1 over two years was associated with significantly shorter survival and a faster rate of progression. In a multiple regression model, these results were independent of gender, site of onset, history of diabetes mellitus and apolipoprotein (ApoE) genotype. In summary, a change in BMI after ALS diagnosis was significantly associated with rate of progression and survival. This raises the possibility that early changes in BMI may identify patients likely to have a more malignant course of the disease. However, further research is needed to clarify the relationship between BMI and ALS. [ABSTRACT FROM AUTHOR]

Background: Vascular dementia (VaD) is the second most common dementing illness. Multiple risk factors are associated with VaD, but the individual contribution of each to disease onset and progression is unclear. We examined the relationship between diabetes mellitus type 2 (DM) and the clinical variables of VaD. Methods: Data from 593 patients evaluated between June, 2003 and June, 2008 for cognitive impairment were prospectively entered into a database. We retrospectively reviewed the charts of 63 patients who fit the NINDS-AIREN criteria for VaD. The patients were divided into those with DM (VaD-DM, n=29) and those without DM (VaD, n=34). The groups were compared with regard to multiple variables. Results: Patients with DM had a significantly earlier onset of VaD (71.9 ± 6.54 vs. 77.2 ± 6.03, p< 0.001), a faster rate of decline per year on the mini mental state examination (MMSE; 3.60 ± 1.82 vs. 2.54 ± 1.60 points, p= 0.02), and a greater prevalence of neuropsychiatric symptoms at the time of diagnosis (62% vs. 21%, p=0.02). Conclusions: A history of pre-morbid DM was associated with an earlier onset and faster cognitive deterioration in VaD. Moreover, DM was associated with neuropsychiatric symptoms in patients with VaD. A larger study is needed to verify these associations. It will be important to investigate whether better glycemic control will mitigate the potential effects of DM on VaD. [ABSTRACT FROM AUTHOR]

Several studies have demonstrated impaired cognition in amyotrophic lateral sclerosis (ALS) patients, but it has been difficult to identify risk factors for this impairment. An association between cognitive changes and bulbar site of onset or dysarthria has been suggested, but the findings are variable. We tested for both associations in a large cohort of ALS patients. At the time of diagnosis of sporadic ALS, all patients ( n=355) in this prospective study underwent comprehensive neuropsychological testing. In addition, a subset of 175 patients underwent a detailed assessment of dysarthria, which was quantified using the Appel ALS Score (AALSS). ALS patients with bulbar site of onset performed significantly worse than limb onset patients on a few timed ((VSAT-time, p<0.05), (Stroop Color, p<0.05), (Stroop Word, p<0.05)) tests of frontal lobe functions, but the significance could not be replicated when motor impairment was accommodated into the tests ((VSAT-errors, p=0.73), (Stroop interference, p=0.08)). ALS patients with dysarthria performed significantly worse than non-dysarthrics on multiple timed ((BD, p<0.05), (VSAT-time, p<0.05), (Stroop Color, p<0.05), (Stroop Word, p<0.05), (Trails A, p<0.05), (Trails B, p<0.05)) neuropsychological tests, and the significance was maintained when motor impairment was accommodated into one of these tests (Stroop interference, p<0.05). Additionally, dysarthrics performed significantly worse on two untimed measures of cognition ((Similarities, p<0.05), (Rey Copy, p<0.05)). Cognitive functioning in ALS does not associate with the site of onset and has a moderate association with dysarthria. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented concerning research examining the macro role microglia plays in mental depression following a stroke and research on conversion of mild cognitive impairment to Alzheimer's disease which provides indirect support to the theory of microglial activation's role in post-stroke depression.

We read with great interest the paper of Riby et al. regarding atypical, unfamiliar face processing in Williams syndrome (WS; Riby, Doherty-Sneddon, & Bruce, 2008a). It offers considerable insight into the mechanism of facial perception in humans and a further elaboration of the hypersociability observed in patients with Williams syndrome. We would like to suggest that the neurologic mechanisms underlying the hypersociability in WS may be attributable to an impaired recognition of facial expressions of threat, a feature that localises to the amygdala. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented concerning research into possible associations between the use of acetylcholinesterase inhibitors, drugs used in the treatment of Alzheimer's disease and dementia with Lewy bodies, with increased anxiety and depression in older patients.

Small non-coding RNAs (sncRNAs) are potential vectors at the interface between genes and environment. We found that traumatic stress in early life altered mouse microRNA (miRNA) expression, and behavioral and metabolic responses in the progeny. Injection of sperm RNAs from traumatized males into fertilized wild-type oocytes reproduced the behavioral and metabolic alterations in the resulting offspring. [ABSTRACT FROM AUTHOR]

Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are two fatal neurodegenerative disorders with considerable clinical, pathological and genetic overlap. Both disorders are characterized by the accumulation of pathological protein aggregates that contain a number of proteins, most notably TAR DNA binding protein 43 kDa (TDP-43). Surprisingly, recent clinical studies suggest that dyslipidemia, high body mass index, and type 2 diabetes mellitus are associated with better clinical outcomes in ALS. Moreover, ALS and FTLD patients have a significantly lower incidence of cardiovascular disease, supporting the idea that an unfavorable metabolic profile may be beneficial in ALS and FTLD. The two most widely studied ALS/FTLD models, super-oxide dismutase 1 (SOD1) and TAR DNA binding protein of 43 kDA (TDP-43), reveal metabolic dysfunction and a positive effect of metabolic strategies on disease onset and/or progression. In addition, molecular studies reveal a role for ALS/FTLD-associated proteins in the regulation of cellular and whole-body metabolism. Here, we systematically evaluate these observations and discuss how changes in cellular glucose/lipid metabolism may result in abnormal protein aggregations in ALS and FTLD, which may have important implications for new treatment strategies for ALS/FTLD and possibly other neurodegenerative conditions. [ABSTRACT FROM AUTHOR]

Environmental factors can change phenotypes in exposed individuals and offspring and involve the germline, likely via biological signals in the periphery that communicate with germ cells. Here, using a mouse model of paternal exposure to traumatic stress, we identify circulating factors involving peroxisome proliferator‐activated receptor (PPAR) pathways in the effects of exposure to the germline. We show that exposure alters metabolic functions and pathways, particularly lipid‐derived metabolites, in exposed fathers and their offspring. We collected data in a human cohort exposed to childhood trauma and observed similar metabolic alterations in circulation, suggesting conserved effects. Chronic injection of serum from trauma‐exposed males into controls recapitulates metabolic phenotypes in the offspring. We identify lipid‐activated nuclear receptors PPARs as potential mediators of the effects from father to offspring. Pharmacological PPAR activation in vivo reproduces metabolic dysfunctions in the offspring and grand‐offspring of injected males and affects the sperm transcriptome in fathers and sons. In germ‐like cells in vitro, both serum and PPAR agonist induce PPAR activation. Together, these results highlight the role of circulating factors as potential communication vectors between the periphery and the germline. Synopsis: Exposure of mice to traumatic stress in early life leads to phenotypic changes that are transmitted to the progeny via mechanisms that remain poorly characterized. In vivo and in vitro findings from mice and humans implicate serum‐induced peroxisome proliferating‐activated receptor (PPAR) signaling in transmission of environmentally‐induced paternal traits via germline. Lipid metabolism pathways are altered in plasma of adult male mice exposed to postnatal trauma and their adult offspringLipid metabolism is also altered in plasma and saliva of human orphan children.Serum from mice with postnatal trauma activates PPAR nuclear receptors in spermatogonial cells in vitro.Pharmacological PPAR activation in vivo recapitulates trauma‐induced metabolic phenotypes in adult mice and their offspring and sperm RNA alterations in fathers.Injection of serum from trauma‐exposed males into control males recapitulates metabolic symptoms in their offspring. [ABSTRACT FROM AUTHOR]

A letter is presented from a reader commenting on a study that showed age-related memory impairment in older mice could be improved by plasma infusions from younger mice.

Summary Microglia coordinate various functions in the central nervous system ranging from removing synaptic connections, to maintaining brain homeostasis by monitoring neuronal function, and clearing protein aggregates across the lifespan. Here we investigated whether increased microglial phagocytic activity that clears amyloid can also cause pathological synapse loss. We identified TDP-43, a DNA-RNA binding protein encoded by the Tardbp gene, as a strong regulator of microglial phagocytosis. Mice lacking TDP-43 in microglia exhibit reduced amyloid load in a model of Alzheimer’s disease (AD) but at the same time display drastic synapse loss, even in the absence of amyloid. Clinical examination from TDP-43 pathology cases reveal a considerably reduced prevalence of AD and decreased amyloid pathology compared to age-matched healthy controls, confirming our experimental results. Overall, our data suggest that dysfunctional microglia might play a causative role in the pathogenesis of neurodegenerative disorders, critically modulating the early stages of cognitive decline. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented concerning prevention of dementia in older patients with diabetes mellitus using angiotensin converting enzyme (ACE) inhibitors.

Frontotemporal lobar degeneration with TAR-DNA-binding protein inclusions (FTLD-TDP) is the most common pathological subtype of frontotemporal dementia (FTD). Mutations leading to a loss of function in the progranulin gene (PGRN) are the most common known cause of FTLD-TDP. In agreement with the proposed loss of function disease mechanism, several groups have reported decreased plasma levels of PGRN in patients carrying PGRN mutations compared to individuals without PGRN mutations. We propose that traumatic brain injury (TBI), an environmental factor, may also increase the risk of FTD by altering PGRN metabolism. TBI may lead to an increase in the central nervous system levels of microglial elastases, which proteolyze PGRN into proinflammatory products called granulins causing a reduction in PGRN levels. Hence, inhibiting microglial activation may have an important implication for the prevention of FTD in patients with TBI. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

A letter to the editor is presented about the use of antiplatelet and anticoagulant medications in patients with cerebral amyloid angiopathy (CAA).

A letter to the editor is presented about research which needs to be done on the relationship between diabetes mellitus and dementia in older people.

Microglia, the resident immune cells of the brain, are increasingly implicated in the regulation of brain health and disease. Microglia perform multiple functions in the central nervous system, including surveillance, phagocytosis and release of a variety of soluble factors. Importantly, a majority of their functions are closely related to changes in their metabolism. This natural inter-dependency between core microglial properties and metabolism offers a unique opportunity to modulate microglial activities via nutritional or metabolic interventions. In this review, we examine the existing scientific literature to synthesize the hypothesis that microglial phagocytosis of amyloid beta (Aβ) aggregates in Alzheimer's disease (AD) can be selectively enhanced via metabolic interventions. We first review the basics of microglial metabolism and the effects of common metabolites, such as glucose, lipids, ketone bodies, glutamine, pyruvate and lactate, on microglial inflammatory and phagocytic properties. Next, we examine the evidence for dysregulation of microglial metabolism in AD. This is followed by a review of in vivo studies on metabolic manipulation of microglial functions to ascertain their therapeutic potential in AD. Finally, we discuss the effects of metabolic factors on microglial phagocytosis of healthy synapses, a pathological process that also contributes to the progression of AD. We conclude by enlisting the current challenges that need to be addressed before strategies to harness microglial phagocytosis to clear pathological protein deposits in AD and other neurodegenerative disorders can be widely adopted. [ABSTRACT FROM AUTHOR]

A response by Thomas Floss to a letter to the editor about his paper "Mitochondrial Dysfunction and Decrease in Body Weight of Transgenic Knock-in Mouse Model for TDP-43" that was published in a 2014 issue is presented.

The nonlinear optical (NLO) response of photonic materials plays an important role in the understanding of light–matter interaction as well as pointing out a diversity of photonic and optoelectronic applications. Among the recently studied materials, 2D-LTMDs (bi-dimensional layered transition metal dichalcogenides) have appeared as a beyond-graphene nanomaterial with semiconducting and metallic optical properties. In this article, we review most of our work in studies of the NLO response of a series of 2D-LTMDs nanomaterials in suspension, using six different NLO techniques, namely hyper Rayleigh scattering, Z-scan, photoacoustic Z-scan, optical Kerr gate, and spatial self-phase modulation, besides the Fourier transform nonlinear optics technique, to infer the nonlinear optical response of semiconducting MoS2, MoSe2, MoTe2, WS2, semimetallic WTe2, ZrTe2, and metallic NbS2 and NbSe2. The nonlinear optical response from a thermal to non-thermal origin was studied, and the nonlinear refraction index and nonlinear absorption coefficient, where present, were measured. Theoretical support was given to explain the origin of the nonlinear responses, which is very dependent on the spectro-temporal regime of the optical source employed in the studies. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which says a psychosocial model of extremism and hostile behavior needs to be developed by researchers in Switzerland.

A letter to the editor is presented which discusses the use of alteplase for treating ischemic stroke.

A letter to the editor is presented concerning the significance of patient literacy which is helpful on understanding prescription drug labels and medication.

Schizophrenia (SZP) has been historically referred to as 'dementia praecox' because of the recognition that its onset is associated with deficits in memory, attention and visuospatial orientation. We wondered whether there is evidence for additional cognitive decline late in the course of chronic SZP. This review examined the evidence (1) for cognitive decline late in the course of chronic SZP, (2) for how often the late cognitive decline occurs, and (3) whether the cognitive decline in late-life SZP is related to pathophysiology of SZP versus the superimposition of another type of dementia. A PUBMED search was performed combining the MESH terms schizophrenia and dementia, cognitive decline, cognitive impairment and cognitive deficits. A manual search of article bibliographies was also performed. We included longitudinal clinical studies employing standard tests of cognition. Cross-sectional studies and those that did not test cognition through standard cognitive tests were excluded. The initial search produced 3898 studies. Employing selection criteria yielded twenty-three studies. Our data extraction tool included the number of patients in the study, whether a control group was present, the age of patients at baseline and follow-up, the study setting (inpatients versus outpatients), the cognitive tests employed, study duration, and results. Only three longitudinal studies tested for dementia using Diagnostic and statistical manual of mental disorder (DSM) or International classification of disease (ICD) criteria and compared them to controls: two studies demonstrated an increase in the prevalence of dementia and one did not. Twenty longitudinal studies tested for one or more cognitive domains without employing standard criteria for dementia: twelve studies demonstrated a heterogeneous pattern of cognitive decline and eight did not. Studies generally did not control for known risk factors for cognitive impairment such as education, vascular risk factors, apolipoprotein (ApoE) genotype and family history. The evidence for late cognitive decline in SZP is mixed, but, slightly more studies suggest that it occurs. If it occurs, it is unclear whether it is related to SZP or other risks for cognitive impairment. Hence, prospective, longitudinal, controlled studies are needed to confirm that there is progressive cognitive decline in chronic SZP which occurs independent of other risk factors for cognitive impairment. [ABSTRACT FROM AUTHOR]

Background: Despite an alarming rise in the global prevalence of dementia, the available modalities for improving cognition and mental wellbeing of dementia patients remain limited. Environmental enrichment is an experimental paradigm that has shown promising anti-depressive and memory-enhancing effects in pre-clinical studies. However, its clinical utility has remained limited due to the lack of effective implementation strategies. Objective: The primary objective of this study was to evaluate the usability (tolerability and interactivity) of a long-term virtual reality (VR)- based environmental enrichment training program in older adults with mild cognitive impairment (MCI) and mild dementia. A secondary objective was to assess the effect of VR-based environmental enrichment on stabilization of cognitive functioning and improvement of mental wellbeing in older adults with MCI and mild dementia. Methods: A total of seven participants (four patients with MCI and three with mild dementia) received biweekly VR-based environmental enrichment over a course of 6 months. The tolerability and interactivity of the participants in the VR training was serially assessed via virtual reality sickness questionnaire (VRSQ) and recording of input-error ratio. Cognitive functioning was assessed through Montreal cognitive assessment (MoCA) before and after the study. Mental wellbeing was assessed through Warwick-Edinburgh Mental Well Being Scale (WEMWBS). Results: VR-based environmental enrichment was well-tolerated by the patients with significant decrease in VRSQ scores (p < 0.01) and input-error ratio (p < 0.001) overtime. VR training was also effective in stabilization of MoCA scores over the course of therapy (non-significant difference in the MoCA scores before and after the therapy) and was associated with a trend (p < 0.1) towards improvement in WEMWBS scores between the first and the last assessments. Qualitative observations by the care-givers further corroborated a noticeable improvement in mental wellbeing of patients. Conclusions: This pilot study shows that VR can be a feasible, tolerable, and potentially effective tool in long-term support of older adults with MCI and mild dementia. [ABSTRACT FROM AUTHOR]

[Display omitted] Electronic circuits, the backbone of modern electronic devices, require precise integration of conducting, insulating, and semiconducting materials in two- and three-dimensional space to control the flow of electric current. Alternative strategies to pattern these materials outside of a cleanroom environment, such as additive manufacturing, have enabled rapid prototyping and eliminated design constraints imposed by traditional fabrication. In this work, a transformative manufacturing approach using laser processing is implemented to directly realize conducting, insulating, and semiconducting phases within an amorphous molybdenum disulfide thin film precursor. This is achieved by varying the incident visible (514 nm) laser intensity and raster-scanning the thin film a -MoS 2 sample (900 nm thick) at different speeds for micro-scale control of the crystallization and reaction kinetics. The overall result is the transformation of select regions of the a -MoS 2 film into MoO 2 , MoO 3 , and 2H-MoS 2 phases, exhibiting conducting, insulating, and semiconducting properties, respectively. A mechanism for this precursor transformation based on crystallization and oxidation is developed using a thermal model paired with a description of the reaction kinetics. Finally, by engineering the architecture of the three crystalline phases, electrical devices such as a resistor, capacitor, and chemical sensor were laser-written directly within the precursor film, representing an entirely transformative manufacturing approach for the fabrication of electronic circuitry. [ABSTRACT FROM AUTHOR]

Zirconium telluride, a transition metal dichalcogenide, was synthesized by a redox exfoliated method to obtain a 2D monolayer semi-metal. After being characterized for compositional and optical analysis, its third-order nonlinear optical (NLO) properties were studied by the Z-scan technique in the femtosecond (100 fs) regime at 800 nm. Interestingly, in this spectro-temporal regime and in the intensity range exploited, the only third-order NLO effect observed was nonlinear refraction, giving rise to a positive value of the nonlinear refractive index coefficient, n2 = +(4.2 ± 0.3) × 10−16 cm2/W. Based on the calculated band structure and the excitation photon energies employed, the physical origin of the refractive nonlinearity is discussed. [ABSTRACT FROM AUTHOR]

The goal of this retrospective cohort study was to determine whether stressors related to military service, determined by a diagnosis of chronic post-traumatic stress disorder (cPTSD) or receiving a Purple Heart (PH), are associated with an increased risk of vascular risk factors and disease, which are of great concern for veterans, who constitute a significant portion of the aging US population. The Veterans Integrated Service Network (VISN) 16 administrative database was searched for individuals 65 years or older between October 1, 1997 to September 30, 1999 who either received a PH but did not have cPTSD (PH+/cPTSD-; n = 1499), had cPTSD without a PH (PH-/cPTSD+; n = 3593), had neither (PH-/cPTSD-; n = 5010), or had both (PH+/cPTSD+; n = 153). In comparison to the control group (PH-/cPTSD-), the PH+/cPTSD- group had increased odds ratios for incidence and prevalence of diabetes mellitus, hypertension, and hyperlipidemia. The PH-/cPTSD+ group had increased odds ratios for prevalence of diabetes mellitus and for the incidence and prevalence of hyperlipidemia. The PH-/cPTSD+ and PH+/cPTSD- groups were associated with ischemic heart disease and cerebrovascular disease, but not independently of the other risk factors. The PH+/cPTSD+ group was associated only with an increase in the incidence and prevalence of hyperlipidemia, though this group's much smaller sample size may limit the reliability of this finding. We conclude that certain physical and psychological stressors related to military service are associated with a greater incidence of several vascular risk factors in veterans aged 65 years or older, which in turn are associated with greater rates of ischemic heart disease and cerebrovascular disease. [ABSTRACT FROM AUTHOR]

Rapid fabrication of large area, ordered assemblies of polymer grafted (hairy) nanoparticles (PGNs) will enable additive manufacturing of novel membrane, electronic, and photonic elements. Herein, we discuss the relationship between select processing conditions, substrate surface energy, and canopy architecture on the hierarchical structure of sub- to monolayer PGN assemblies. Varying concentrations (10, 20, and 70 nM) of polystyrene (PS) grafted (σ - 1 chain/nm2) gold nanoparticles (AuNP, r0 = 9 nm) were flow-coated onto surface-modified silicon wafers (γs - 20 mN/m, hydrophobic to 80 mN/m, hydrophilic). The profile of an isolated gold-polystyrene (PS) PGN depends on substrate-canopy interface energy. At low substrate-PS interface energy (20 mN/m), the PS canopy spreads to maximize contact with the surface, whereas at high substrate-PS interface energy (80 mN/m), the chains minimize contact area resulting in a more compact, thicker PGN corona. This behavior is translated up to monolayer assemblies, where rougher, less-ordered assemblies with smaller AuNP-surface separation form on substrates with low interface energy. These films are also thinner with greater Au volume fraction, indicating that the segment density within the PS canopy depends on substrate surface energy. The impact of these processing parameters on PGN film formation parallels classic colloidal deposition even though the PS concentration is within the Landau-Levich regime for film formation from linear chains. The factors influencing local morphology, however, resemble those that affect polymer thin films. Using this understanding, we demonstrate fabrication within seconds of large area monolayer films with close-packed order. [ABSTRACT FROM AUTHOR]

We report the second harmonic scattering experiments from acetonitrile liquid suspensions of two-dimensional metal dichalcogenide nanoflakes , : the semiconducting MoS 2 and WS 2 , the metallic NbS 2 , and the semi-metallic ZrTe 2. Because the study is directly performed in the liquid phase, no symmetry breaking can be attributed to a supporting substrate as it is often the case in the investigation of the second harmonic generation efficiency for these materials. A comparative look of the origin of the nonlinear response using polarization analysis of the hyper Rayleigh scattering intensity is performed. Retardation is clearly exhibited by all nanoflakes considering their average dimensions but remains weak. This is attributed to the non-negligible role played by the nanoflake edges or the presence of surface absorbed polyoxometalates (POMs), in all cases. [Display omitted] • 2D materials were prepared by redox exfoliation and characterized them. • Hyper Rayleigh Scattering intensity of 2D materials was performed. • The Hyper Rayleigh Scattering response of 2D materials exhibits retardation. • Edge contribution is confirmed with a model based on nonlinear dipoles. [ABSTRACT FROM AUTHOR]

Highlights: [•] Long living exictons (8ns) are observed in water-soluble colloidal CdZnS nanoparticles. [•] Passivation with ZnS results in longer living excitation (20ns) in CdZnS/ZnS nanoparticles. [•] Rapid (250ps) exciton quenching is observed due to electron tunneling through the ZnS shell in CdZnS/ZnS·Pd adducts. [•] Type-I core/shell architecture allows for the mitigation of photo-oxidation while allowing for efficient direct catalysis. [ABSTRACT FROM AUTHOR]

Abstract: The primary exciton dynamics of colloidal indirect bandgap AlP nanocrystals are characterized with ultrafast transient absorption spectroscopy. A 400-nm excitation results in a high yield formation of an emissive exciton with a ∼1-ns lifetime and a 50-nm bandwidth red-shifted emission. Multi-wavelength target analysis is used to decompose the measured signals into sequential and parallel models, which interpret the measured data as an emissive exciton with a 1.2-ns decay time and a dark exciton which is attributed to surface trapping. Reconstructed nonlinear absorption spectra resolve a broad optical gain persisting for >1ns. The 15% emission yield demonstrates that colloidal AlP nanocrystals are useful as a potential broadband, high efficiency optoelectronics material. [Copyright &y& Elsevier]

Accumulation of the DNA/RNA binding protein fused in sarcoma as cytoplasmic inclusions in neurons and glial cells is the pathological hallmark of all patients with amyotrophic lateral sclerosis with mutations in FUS as well as in several subtypes of frontotemporal lobar degeneration, which are not associated with FUS mutations. The mechanisms leading to inclusion formation and fused in sarcoma-associated neurodegeneration are only poorly understood. Because fused in sarcoma belongs to a family of proteins known as FET, which also includes Ewing’s sarcoma and TATA-binding protein-associated factor 15, we investigated the potential involvement of these other FET protein family members in the pathogenesis of fused in sarcoma proteinopathies. Immunohistochemical analysis of FET proteins revealed a striking difference among the various conditions, with pathology in amyotrophic lateral sclerosis with FUS mutations being labelled exclusively for fused in sarcoma, whereas fused in sarcoma-positive inclusions in subtypes of frontotemporal lobar degeneration also consistently immunostained for TATA-binding protein-associated factor 15 and variably for Ewing’s sarcoma. Immunoblot analysis of proteins extracted from post-mortem tissue of frontotemporal lobar degeneration with fused in sarcoma pathology demonstrated a relative shift of all FET proteins towards insoluble protein fractions, while genetic analysis of the TATA-binding protein-associated factor 15 and Ewing’s sarcoma gene did not identify any pathogenic variants. Cell culture experiments replicated the findings of amyotrophic lateral sclerosis with FUS mutations by confirming the absence of TATA-binding protein-associated factor 15 and Ewing’s sarcoma alterations upon expression of mutant fused in sarcoma. In contrast, all endogenous FET proteins were recruited into cytoplasmic stress granules upon general inhibition of Transportin-mediated nuclear import, mimicking the findings in frontotemporal lobar degeneration with fused in sarcoma pathology. These results allow a separation of fused in sarcoma proteinopathies caused by FUS mutations from those without a known genetic cause based on neuropathological features. More importantly, our data imply different pathological processes underlying inclusion formation and cell death between both conditions; the pathogenesis in amyotrophic lateral sclerosis with FUS mutations appears to be more restricted to dysfunction of fused in sarcoma, while a more global and complex dysregulation of all FET proteins is involved in the subtypes of frontotemporal lobar degeneration with fused in sarcoma pathology. [ABSTRACT FROM PUBLISHER]

Amyotrophic lateral sclerosis (ALS) has been associated with changes in frontal and temporal lobe-mediated cognitive and behavioral functions. Verbal fluency, a sensitive measure to these changes, was utilized to investigate phonemic and semantic abilities in 49 ALS patients and 25 healthy controls (HCs). A subset of the ALS patients was classified as ALS-intact, ALS with mild cognitive impairments (ALS-mild), and ALS with fronto-temporal dementia (ALS-FTD) based on a comprehensive neuropsychological evaluation. Clustering and switching, the underlying component processes of verbal fluency, were analyzed using Troyer's (Troyer, Moscovitch, & Winocur, 1997) and Abwender's (Abwender, Swan, Bowerman, & Connolly, 2001) scoring systems. ALS patients exhibited decreased fluency versus HCs. For phonemic fluency, the intact ALS sample generated fewer clusters and more switches than the ALS-mild and ALS-FTD patients using both scoring systems. This suggests temporal involvement in ALS patients, with increasing frontal lobe involvement in patients with greater cognitive dysfunction. For semantic fluency, similar results were obtained with a greater emphasis on declines in clustering or increased temporal lobe dysfunction. These results suggest that verbal fluency measures identify frontal and temporal lobe involvement in the cognitive decline associated with ALS, particularly when the component processes are evaluated. The clinical utility of these scoring systems with ALS patients is also discussed. [ABSTRACT FROM AUTHOR]