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Given that lumbar disc herniation (LDH) is a prevalent spinal condition that causes significant individual suffering and societal costs, the genetic basis of LDH has received relatively little research. Our aim is to increase understanding of the genetic factors influencing LDH. We perform a genome-wide association analysis (GWAS) of LDH in the FinnGen project and in Estonian and UK biobanks, followed by a genome-wide meta-analysis to combine the results. In the meta-analysis, we identify 41 loci that have not been associated with LDH in prior studies on top of the 23 known risk loci. We detect LDH-associated loci in the vicinity of genes related to inflammation, disc-related structures, and synaptic transmission. Overall, our research contributes to a deeper understanding of the genetic factors behind LDH, potentially paving the way for the development of new therapeutics, prevention methods, and treatments for symptomatic LDH in the future. A genome-wide association study suggests 41 previously unreported loci on top of the 23 known loci that influence the disease risk for lumbar disc herniations. Many of these loci harbour genes implicated in disc structure and inflammation, as well as genes related to the nervous system and nerve function. [ABSTRACT FROM AUTHOR]

Background: Fried food consumption has been associated with obesity; little is known about whether genetic background modifies this association. Methods: We analyzed interactions between a genetic risk score (GRS) based on 32 BMI-associated variants and fried food consumption on body mass index (BMI) and obesity in 9623 women from the Nurses' Health Study (NHS) and 6379 men from the Health Professionals Follow-up Study (HPFS) and in a replication cohort of 21426 women from the Women's Genome Health Study (WGHS). Results: An interaction between fried food consumption and the GRS on BMI was identified in both NHS and HPFS (P for interaction≤0.001). Among participants in the highest tertile of the GRS, the differences in BMI between individuals who consumed fried foods ≥4times/week and those consumed <1time/week amounted to 1.0 in women and 0.7 kg/m2 in men, whereas the corresponding differences were 0.5 and 0.4 kg/m2 in the lowest tertile of the GRS. The gene-diet interaction was replicated in the WGHS (P for interaction<0.001). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.2, 1.6, and 2.4 kg/m2 for fried food consumption<1, 1-3 and ≥4times/week (P for interaction<0.001) (Figure); and the odds ratios (95% CI) for obesity per 10 risk alleles were 1.60 (1.38-1.84), 2.13 (1.74-2.60) and 2.65 (2.08- 3.39) across the three categories of consumption (P for interaction=0.002). In addition, we found that the individual variants in genes highly expressed or known to act in the central nervous system showed significant interactions, with the FTO variant showing the strongest result (P for interaction<0.001). Conclusion: Fried food consumption may interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity. [ABSTRACT FROM AUTHOR]

In search of novel breast cancer (BC) risk variants, we performed a whole-exome sequencing and variant analysis of 69 Finnish BC patients as well as analysed loss-of-function variants identified in DNA repair genes in the Finns from the Genome Aggregation Database. Additionally, we carried out a validation study of SERPINA3 c.918-1G>C, recently suggested for BC predisposition. We estimated the frequencies of 41 rare candidate variants in 38 genes by genotyping them in 2482–4101 BC patients and in 1273–3985 controls. We further evaluated all coding variants in the candidate genes in a dataset of 18,786 BC patients and 182,927 controls from FinnGen. None of the variants associated significantly with cancer risk in the primary BC series; however, in the FinnGen data, NTHL1 c.244C>T p.(Gln82Ter) associated with BC with a high risk for homozygous (OR = 44.7 [95% CI 6.90–290], P = 6.7 × 10–5) and a low risk for heterozygous women (OR = 1.39 [1.18–1.64], P = 7.8 × 10–5). Furthermore, the results suggested a high risk of colorectal, urinary tract, and basal-cell skin cancer for homozygous individuals, supporting NTHL1 as a recessive multi-tumour susceptibility gene. No significant association with BC risk was detected for SERPINA3 or any other evaluated gene. [ABSTRACT FROM AUTHOR]

Successful development of novel therapies requires that clinical trials are conducted in patient cohorts with the highest benefit-to-risk ratio. Population-based biobanks with comprehensive health and genetic data from large numbers of individuals hold promise to facilitate identification of trial participants, particularly when interventions need to start while symptoms are still mild, such as for Alzheimer's disease (AD). This study describes a process for clinical recall studies from FinnGen. We demonstrate the feasibility to systematically ascertain customized clinical data from FinnGen participants with ICD10 diagnosis of AD or mild cognitive disorder (MCD) in a single-center cross-sectional study testing blood-based biomarkers and cognitive functioning in-person, computer-based and remote. As a result, 19% (27/140) of a pre-specified FinnGen subcohort were successfully recalled and completed the study. Hospital records largely validated registry entries. For 8/12 MCD patients, other reasons than AD were identified as underlying diagnosis. Cognitive measures correlated across platforms, with highest consistencies for dementia screening (r = 0.818) and semantic fluency (r = 0.764), respectively, for in-person versus telephone-administered tests. Glial fibrillary acidic protein (GFAP) (p < 0.002) and phosphorylated-tau 181 (pTau-181) (p < 0.020) most reliably differentiated AD from MCD participants. We conclude that informative, customized clinical recall studies from FinnGen are feasible. [ABSTRACT FROM AUTHOR]

Narcolepsy type 1 (NT1) is caused by a loss of hypocretin/orexin transmission. Risk factors include pandemic 2009 H1N1 influenza A infection and immunization with Pandemrix®. Here, we dissect disease mechanisms and interactions with environmental triggers in a multi-ethnic sample of 6,073 cases and 84,856 controls. We fine-mapped GWAS signals within HLA (DQ0602, DQB1*03:01 and DPB1*04:02) and discovered seven novel associations (CD207, NAB1, IKZF4-ERBB3, CTSC, DENND1B, SIRPG, PRF1). Significant signals at TRA and DQB1*06:02 loci were found in 245 vaccination-related cases, who also shared polygenic risk. T cell receptor associations in NT1 modulated TRAJ*24, TRAJ*28 and TRBV*4-2 chain-usage. Partitioned heritability and immune cell enrichment analyses found genetic signals to be driven by dendritic and helper T cells. Lastly comorbidity analysis using data from FinnGen, suggests shared effects between NT1 and other autoimmune diseases. NT1 genetic variants shape autoimmunity and response to environmental triggers, including influenza A infection and immunization with Pandemrix®. Narcolepsy has genetic and environmental risk factors, but the specific genetic risk loci and interaction with environmental triggers are not well understood. Here, the authors identify genetic loci for narcolepsy, suggesting infection as a trigger and dendritic and helper T cell involvement. [ABSTRACT FROM AUTHOR]

Uterine leiomyomata (UL) are the most common tumours of the female genital tract and the primary cause of surgical removal of the uterus. Genetic factors contribute to UL susceptibility. To add understanding to the heritable genetic risk factors, we conduct a genome-wide association study (GWAS) of UL in up to 426,558 European women from FinnGen and a previous UL meta-GWAS. In addition to the 50 known UL loci, we identify 22 loci that have not been associated with UL in prior studies. UL-associated loci harbour genes enriched for development, growth, and cellular senescence. Of particular interest are the smooth muscle cell differentiation and proliferation-regulating genes functioning on the myocardin-cyclin dependent kinase inhibitor 1 A pathway. Our results further suggest that genetic predisposition to increased fat-free mass may be causally related to higher UL risk, underscoring the involvement of altered muscle tissue biology in UL pathophysiology. Overall, our findings add to the understanding of the genetic pathways underlying UL, which may aid in developing novel therapeutics. Many genetic factors that contribute to uterine leiomyomata (UL) - the most common tumours of the female genital tract - remain to be discovered. Here, the authors conduct a UL meta-genome-wide association study, and find loci related to altered muscle tissue biology that are associated with UL. [ABSTRACT FROM AUTHOR]

Among the colloidal quantum dots, 2D nanoplatelets present exceptionally narrow optical features. Rationalizing the design of heterostructures of these objects is of utmost interest; however, very little work has been focused on the investigation of their electronic properties. This work is organized into two main parts. In the first part, we use 1D solving of the Schrödinger equation to extract the effective masses for nanoplatelets (NPLs) of CdSe, CdS, and CdTe and the valence band offset for NPL core/shell of CdSe/CdS. In the second part, using the determined parameters, we quantize how the spectra of the CdSe/CdS heterostructure get affected by (i) the application of an electric field and (ii) by the presence of a dull interface. We also propose design strategies to make the heterostructure even more robust. [ABSTRACT FROM AUTHOR]

Large-scale biobank initiatives and commercial repositories store genomic data collected from millions of individuals, and tools to leverage the rapidly growing pool of health and genomic data in disease prevention are needed. Here, we describe the derivation and validation of genomics-enhanced risk tools for two common cardiometabolic diseases, coronary heart disease and type 2 diabetes. Data used for our analyses include the FinnGen study (N = 309,154) and the UK Biobank project (N = 343,672). The risk tools integrate contemporary genome-wide polygenic risk scores with simple questionnaire-based risk factors, including demographic, lifestyle, medication, and comorbidity data, enabling risk calculation across resources where genome data is available. Compared to routinely used clinical risk scores for coronary heart disease and type 2 diabetes prevention, the risk tools show at least equivalent risk discrimination, improved risk reclassification (overall net reclassification improvements ranging from 3.7 [95% CI 2.8–4.6] up to 6.2 [4.6–7.8]), and capacity to be improved even further with standard lipid and blood pressure measurements. Without the need for blood tests or evaluation by a health professional, the risk tools provide a powerful yet simple method for preliminary cardiometabolic risk assessment for individuals with genome data available. Max Tamlander et al. combine polygenic risk scores and clinical assessments to improve prediction of coronary artery disease and type 2 diabetes in European cohorts. Taken together, their results provide a useful method for preliminary cardiometabolic risk assessment in patients. [ABSTRACT FROM AUTHOR]

Nanocrystals (NCs) have reached a high level of maturity, enabling their integration into optoelectronic devices. The next challenge is the combination of several types of devices into one complex system to achieve better on‐chip integration. Here, an all‐HgTe‐NC active imaging setup operating in the short‐wave infrared (IR) is focused on. First, the design of an optimized IR light‐emitting diode (LED) is focused on. It is shown that a halide technology processing enables an increase of the electroluminescence signal by a factor of 3, while preserving a low turn‐on voltage and a high brightness (3 W sr−1 m−2). Then the degradation mechanism of this LED under continuous operation is unveiled and a shift from band edge to trap emission is shown. This degradation process can be strongly reduced thanks to the encapsulation and the thermal control of the LED. Lastly, the IR emission of the LED is imaged using a focal plane array whose active layer is also made of HgTe NCs, paving the way for all‐NC‐based active imaging setups. [ABSTRACT FROM AUTHOR]

For short wave infrared (SWIR) sensing, InGaAs is the leading technology combining high carrier mobility, high homogeneity, and complete control over the n-to-p doping. In the meanwhile, numerous alternative materials have tried to compete with InGaAs. Among them, colloidal nanocrystals with narrow bandgap can address the current issue in designing cost-effective sensors for the SWIR range. Rather than putting these two materials against each other, we design here a synergistic duo in which HgTe nanocrystals are used to broaden the spectral range of InGaAs while lifting the lattice matching constraints. We propose a diode geometry where a p-type HgTe NC array is coupled with n-type InGaAs wires, which are used as high mobility (μ > 1000 cm2 V−1 s−1) minority carrier extractors. This approach also demonstrates that Van der Waals heterostructures are not limited to graphene-like materials, and that bulk-like III–V semiconductors can also be light sensitized by colloidal nanoparticles. This work paves the way toward further synergies between epitaxially grown and colloidally grown semiconductors for infrared detection. [ABSTRACT FROM AUTHOR]

Visible nanocrystal-based light-emitting diodes (LEDs) are about to become commercially available. However, their infrared counterparts suffer from two key limitations. First, III–V semiconductor technologies are strong competitors. Second, their potential for operation beyond 1.7 µm remains unexplored. The range from 1.5 to 4 µm corresponds to a technological gap in which the efficiency of interband quantum-well-based devices vanishes and quantum cascade lasers are not efficient enough. Powerful infrared LEDs in this range are needed for applications such as active imaging, organic molecule sensing and airfield lighting. Here we report the design of a HgTe nanocrystal-based LED with luminescence between 2 and 2.3 µm. With an external quantum efficiency of 0.3% and radiance up to 3 W Sr−1 m−2, these HgTe LEDs already present a competitive performance for emission above 2 µm. Near-infrared emission at around 2 µm is observed from HgTe nanocrystals. LEDs based on this material platform could prove to be a useful low-cost, convenient light source for applications in gas sensing and other tasks. [ABSTRACT FROM AUTHOR]

Obesity and its associated metabolic syndrome are a leading cause of morbidity and mortality in the United States. Given the disease's heavy burden on patients and the healthcare system, there has been increased interest in identifying pharmacological targets for the treatment and prevention of obesity. Towards this end, genome-wide association studies (GWAS) have identified hundreds of human genetic variants associated with obesity. The next challenge is to experimentally define which of these variants are causally linked to obesity, and could therefore become targets for the treatment or prevention of obesity. Here we employ high-throughput in vivo RNAi screening to test for causality 293 C. elegans orthologs of human obesity-candidate genes reported in GWAS. We RNAi screened these 293 genes in C. elegans subject to two different feeding regimens: (1) regular diet, and (2) high-fructose diet, which we developed and present here as an invertebrate model of diet-induced obesity (DIO). We report 14 genes that promote obesity and 3 genes that prevent DIO when silenced in C. elegans. Further, we show that knock-down of the 3 DIO genes not only prevents excessive fat accumulation in primary and ectopic fat depots but also improves the health and extends the lifespan of C. elegans overconsuming fructose. Importantly, the direction of the association between expression variants in these loci and obesity in mice and humans matches the phenotypic outcome of the loss-of-function of the C. elegans ortholog genes, supporting the notion that some of these genes would be causally linked to obesity across phylogeny. Therefore, in addition to defining causality for several genes so far merely correlated with obesity, this study demonstrates the value of model systems compatible with in vivo high-throughput genetic screening to causally link GWAS gene candidates to human diseases. Author summary: Human GWAS have identified hundreds of genetic variants associated with human obesity. The genes being regulated by these variants at the protein or expression level represent potential anti-obesity targets. However, for the vast majority of these genes, it is unclear whether they cause obesity or are coincidentally associated with the disease. Here we use a high-throughput genetic screening strategy to test in vivo in Caenorhabditis elegans the potential causal role of human-obesity GWAS hits. Further, we combined the results of the genetic screen with analyses of mouse and human GWAS databases. As a result, we present 17 genes that promote or prevent C. elegans obesity, and the early onset of organismal deterioration and death associated with obesity. Further, the sign of the correlation between the expression levels of the human genes and their associated clinical traits matches, for the most part, the phenotypic effects of knocking down these genes in C. elegans, suggesting conserved causality and pharmacological potential for these genes. [ABSTRACT FROM AUTHOR]

The limited investigation of the optical properties of HgTe nanocrystal (NC) thin films has become a bottleneck for the electromagnetic design of devices. Using broadband ellipsometry, the refractive index (n) and the extinction coefficient (k) are determined for a series of HgTe NC films relevant to infrared sensing applications. Electromagnetic simulations reveal that the n value of HgTe NC thin films can conveniently be approximated by its mean spectral value n = 2.35 ± 0.15. This complex optical index is then used to design a diode with i) a reduced amount of Hg containing material (thin film < 150 nm) and ii) a thickness of the device better‐matched with the carrier diffusion length. It is demonstrated that introducing an aluminum grating onto the transparent conductive electrode leads to an enhanced absorption while reinforcing the work‐function difference between the two electrodes. Broadband (≈1 µm), non‐polarized, and strong absorption up to 100% is designed. This leads to a responsivity of 0.2 A W−1 and a detectivity of 2 × 1010 Jones for 2 µm cut‐off wavelength at room‐temperature, while the time response is as short as 110 ns. [ABSTRACT FROM AUTHOR]

Autosomal genetic analyses of blood lipids have yielded key insights for coronary heart disease (CHD). However, X chromosome genetic variation is understudied for blood lipids in large sample sizes. We now analyze genetic and blood lipid data in a high-coverage whole X chromosome sequencing study of 65,322 multi-ancestry participants and perform replication among 456,893 European participants. Common alleles on chromosome Xq23 are strongly associated with reduced total cholesterol, LDL cholesterol, and triglycerides (min P = 8.5 × 10−72), with similar effects for males and females. Chromosome Xq23 lipid-lowering alleles are associated with reduced odds for CHD among 42,545 cases and 591,247 controls (P = 1.7 × 10−4), and reduced odds for diabetes mellitus type 2 among 54,095 cases and 573,885 controls (P = 1.4 × 10−5). Although we observe an association with increased BMI, waist-to-hip ratio adjusted for BMI is reduced, bioimpedance analyses indicate increased gluteofemoral fat, and abdominal MRI analyses indicate reduced visceral adiposity. Co-localization analyses strongly correlate increased CHRDL1 gene expression, particularly in adipose tissue, with reduced concentrations of blood lipids. The influence of X chromosome genetic variation on blood lipids and coronary heart disease (CHD) is not well understood. Here, the authors analyse X chromosome sequencing data across 65,322 multi-ancestry individuals, identifying associations of the Xq23 locus with lipid changes and reduced risk of CHD and diabetes mellitus. [ABSTRACT FROM AUTHOR]

Primary open-angle glaucoma (POAG), is a heritable common cause of blindness world-wide. To identify risk loci, we conduct a large multi-ethnic meta-analysis of genome-wide association studies on a total of 34,179 cases and 349,321 controls, identifying 44 previously unreported risk loci and confirming 83 loci that were previously known. The majority of loci have broadly consistent effects across European, Asian and African ancestries. Cross-ancestry data improve fine-mapping of causal variants for several loci. Integration of multiple lines of genetic evidence support the functional relevance of the identified POAG risk loci and highlight potential contributions of several genes to POAG pathogenesis, including SVEP1, RERE, VCAM1, ZNF638, CLIC5, SLC2A12, YAP1, MXRA5, and SMAD6. Several drug compounds targeting POAG risk genes may be potential glaucoma therapeutic candidates. Primary open-angle glaucoma (POAG) is highly heritable, yet not well understood from a genetic perspective. Here, the authors perform a meta-analysis of genome-wide association studies in 34,179 POAG cases, identifying 44 previously unreported risk loci and mapping effects across multiple ethnicities. [ABSTRACT FROM AUTHOR]

Infrared nanocrystals are promising building blocks for the design of low-cost infrared sensors. Vertical geometry diode is, among possible geometries, the one that has led to the best performance so far. However, this geometry suffers from a lack of tunability after its fabrication, slowing down possible improvements. Here, we demonstrate gate control on a vertical diode in which the active layer is made of HgTe NCs absorbing in the extended short-wave infrared (2.5 μm). To reach this goal, we take advantage of the electrostatic transparency of graphene, combined with the high capacitance LaF3 ionic glass to design a gate tunable photodiode. The latter behaves as a work function-tunable electrode which lets the gate-induced electric field tune the carrier density within the nanocrystal film. In particular, we show that the gate allows to tune the band profile leading to more efficient charge extraction and thus an enhanced photoresponse (×4 compared to the device with a floating gate). This work also demonstrates that photoelectron extraction can still be improved in the existing diode, by better controlling the doping profile of the stack. [ABSTRACT FROM AUTHOR]

Polygenic risk scores (PRS) for breast cancer have potential to improve risk prediction, but there is limited information on their utility in various clinical situations. Here we show that among 122,978 women in the FinnGen study with 8401 breast cancer cases, the PRS modifies the breast cancer risk of two high-impact frameshift risk variants. Similarly, we show that after the breast cancer diagnosis, individuals with elevated PRS have an elevated risk of developing contralateral breast cancer, and that the PRS can considerably improve risk assessment among their female first-degree relatives. In more detail, women with the c.1592delT variant in PALB2 (242-fold enrichment in Finland, 336 carriers) and an average PRS (10–90th percentile) have a lifetime risk of breast cancer at 55% (95% CI 49–61%), which increases to 84% (71–97%) with a high PRS (> 90th percentile), and decreases to 49% (30–68%) with a low PRS (< 10th percentile). Similarly, for c.1100delC in CHEK2 (3.7–fold enrichment; 1648 carriers), the respective lifetime risks are 29% (27–32%), 59% (52–66%), and 9% (5–14%). The PRS also refines the risk assessment of women with first-degree relatives diagnosed with breast cancer, particularly among women with positive family history of early-onset breast cancer. Here we demonstrate the opportunities for a comprehensive way of assessing genetic risk in the general population, in breast cancer patients, and in unaffected family members. Identifying women at high risk of breast cancer has important implications for screening. Here, the authors demonstrate that polygenic risk scores improve breast cancer risk prediction in the population, in women with mutations in high-risk genes and in women with close relatives with the disease. [ABSTRACT FROM AUTHOR]

Myeloproliferative neoplasms (MPNs) are blood cancers that are characterized by the excessive production of mature myeloid cells and arise from the acquisition of somatic driver mutations in haematopoietic stem cells (HSCs). Epidemiological studies indicate a substantial heritable component of MPNs that is among the highest known for cancers1. However, only a limited number of genetic risk loci have been identified, and the underlying biological mechanisms that lead to the acquisition of MPNs remain unclear. Here, by conducting a large-scale genome-wide association study (3,797 cases and 1,152,977 controls), we identify 17 MPN risk loci (P < 5.0 × 10−8), 7 of which have not been previously reported. We find that there is a shared genetic architecture between MPN risk and several haematopoietic traits from distinct lineages; that there is an enrichment for MPN risk variants within accessible chromatin of HSCs; and that increased MPN risk is associated with longer telomere length in leukocytes and other clonal haematopoietic states—collectively suggesting that MPN risk is associated with the function and self-renewal of HSCs. We use gene mapping to identify modulators of HSC biology linked to MPN risk, and show through targeted variant-to-function assays that CHEK2 and GFI1B have roles in altering the function of HSCs to confer disease risk. Overall, our results reveal a previously unappreciated mechanism for inherited MPN risk through the modulation of HSC function. A genome-wide association study identifies 17 genetic loci that are associated with the risk of myeloproliferative neoplasms (MPNs), and shows that the modulation of haematopoietic stem cell function drives MPN risk. [ABSTRACT FROM AUTHOR]

In response to activism by student survivors of sexual violence beginning in the early 2010s, respondents--those students named as abusers and harassers in sexual misconduct cases--and their advocates have recently turned to the courts. To date, respondents have filed over 500 due process claims to challenge the fairness of their schools' sexual misconduct disciplinary proceedings. Courts assessing these due process claims apply the Mathews v. Eldridge balancing test, the governing procedural due process framework. The Mathews balancing test instructs courts to weigh: 1) the private interests at stake; 2) the risk of erroneous deprivation using current procedures; and 3) the public interests at stake. The underlying facts in Mathews concerned two parties--the party facing a deprivation and the charging institution. But Mathews did not contemplate the structure of cases where one student has allegedly harmed another, meaning there is an additional party to consider: a complaining student. Sexual misconduct cases, like other harassment, discrimination, and violence cases, have this unique three-party structure. By applying the Mathews balancing test--a due process framework built on a two-party case--to what are in fact three-party cases, courts fail to adequately account for all of the interests at stake. As a result, student survivors have been pushed off the scales of justice when courts consider what process is due to student respondents. But the Mathews framework, when properly applied, includes universities' broader goals as well as survivors' interests. To preserve the rights and respect the interests of all respondents, survivors, and schools alike, the courts must adequately balance all of the interests at stake, accounting for survivors' interests in the realms of education, reputation, and future prospects under the third Mathews factor. While there are legislative, administrative, and institutional ways to pursue fairness in campus sexual misconduct disciplinary proceedings, the courts are the constitutional backstop for each of these avenues. Only once survivors' interests have been restored to the scales in Mathews analyses will advocates have the opportunity to achieve truly fair, balanced processes. [ABSTRACT FROM AUTHOR]

HgTe nanocrystals offer a unique combination of broadly tunable optical absorption in the infrared from 1 to 100 μm and photoconductive properties. Herein, some of the recent developments related to their integration into photodiodes are discussed. Concepts such as the development of colloidal unipolar barrier, development of ink to achieve strongly absorbing and conductive film, and the recent proposition of intraband photodiode are also discussed. [ABSTRACT FROM AUTHOR]

This Note argues that policy proposals mandating law enforcement involvement in campus sexual assault cases are harmful to survivors of sexual assault and are inconsistent with Title IX. Title IX’s gender-equality goals require schools to address sexual assault as a civil rights issue, with a focus on its impact on survivors’ continued access to education. Mandatory police involvement proposals will frustrate that goal. These proposals take a criminal law view rather than a civil rights approach, and in doing so, import obstacles that survivors have long faced in the criminal system into the campus process. What is more, these proposals will have the effect of making it more difficult for survivors, particularly those from marginalized communities, to report their sexual assaults to their schools. If survivors are not able to report, they will not be able to access the accommodations they need to continue their education, and schools will not have the information they need to adequately combat sexual assault on campus. Efforts at reform would be better served by focusing on improving the campus process than on limiting survivors’ options. [ABSTRACT FROM AUTHOR]

Germanane is a two-dimensional, strongly confined form of germanium. It presents an interesting combination of (i) ease of integration with CMOS technology, (ii) low toxicity, and (iii) electronic confinement which transforms the indirect bandgap of the bulk material into a direct bandgap featuring photoluminescence. However, the optoelectronic properties of this material remain far less investigated than its structural properties. Here, we investigate the photoluminescence and transport properties of arrays of methyl-terminated germanane flakes. The photoluminescence appears to have two contributions, one from the band edge and the other from trap states. The dynamics of the exciton appear to be in the range of 1–100 ns. Conduction in this material appears to be p-type, while the photoconduction time response can be made as short as 100 μs. [ABSTRACT FROM AUTHOR]