Selective Defect Research Articles

Tannic Acid Selective Modulation Defects to Enhance the Photocatalytic CO2 Reduction Activity of Layered Double Hydroxides.

Recently, layered double hydroxides (LDH) have shown great potential in photoreduction of CO2 owing to its flexible structural adjustability. In this study, the mild acidic property of tannic acid (TA) is exploited to etch the bimetal LDH to create abundant vacancies to gain the coordination unsaturated active centers. Based on the different chelating abilities of TA to various metal ions, the active metals are remained by selective chelation while the inert metals are removed during the etching process of bimetal LDH. Furthermore, selective chelating with metal ions not only increases the percentage of highly active metals but also compensates for the structural damage caused by the etch, which achieves a scalpel-like selective construction of vacancies. The NiAl-LDH etched and functionalized by TA for 3h exhibits superior photo-reduction of CO2 performance without co-catalysts and photo-sensitizers, which is 14 times that of the pristine NiAl-LDH. The fact that many bimetal LDHs can be functionalized by TA and exhibit significantly improved photocatalytic efficiency is confirmed, suggesting this strategy is generalized to functionalize double- or multi-metal LDH. The method provided in this work opens the door for polyphenol-functionalized LDHs to enhance their ability for light-driven chemical transformations.

A gain of function variant in RGS18 candidate for a familial mild bleeding syndrome.

Inherited platelet diseases (IPDs) are bleeding disorders characterized by either defect in platelet count or in platelet function, the latter being less common and very heterogeneous. Numerous gene variants associated with abnormal receptors, granules, and signaling pathways have been reported. Despite significant advancements in our understanding, many patients still lack a precise diagnosis. To identify the genetic basis of a novel mild bleeding syndrome in a family exhibiting a selective defect of platelet aggregation. Our study included 6 family members across three generations, who displayed reduced platelet aggregation in response to ADP, PAR1-AP, arachidonic acid, and epinephrine, but not collagen. Platelet morphology, granule content and expression of major surface glycoproteins were all found to be normal. Whole exome sequencing was performed for affected and non-affected family members. We identified RGS18, which encodes the regulator of G protein signaling (RGS) 18, as a candidate gene for the platelet function defect observed in this family. The RGS18 protein serves as a crucial negative regulator of G protein-coupled receptor (GPCR) signaling and coordinates the signaling pathways of natural platelet inhibitors. The heterozygous RGS18 c.643C>T, p.Arg215* variant was found to co-segregate among all six affected subjects. Truncation at Arg215 removes the S216 and S218 phosphorylation sites, which are crucial regulatory domains for RGS18 activation. The impaired platelet function is thought to arise from excessive platelet downregulation due to constitutive activation of RGS18, resulting from a loss of association of the truncated form with the 14-3-3 protein.

Application of Object Detection Algorithms in Non-Destructive Testing of Pressure Equipment: A Review.

Non-destructive testing (NDT) techniques play a crucial role in industrial production, aerospace, healthcare, and the inspection of special equipment, serving as an indispensable part of assessing the safety condition of pressure equipment. Among these, the analysis of NDT data stands as a critical link in evaluating equipment safety. In recent years, object detection techniques have gradually been applied to the analysis of NDT data in pressure equipment inspection, yielding significant results. This paper comprehensively reviews the current applications and development trends of object detection algorithms in NDT technology for pressure-bearing equipment, focusing on algorithm selection, data augmentation, and intelligent defect recognition based on object detection algorithms. Additionally, it explores open research challenges of integrating GAN-based data augmentation and unsupervised learning to further enhance the intelligent application and performance of object detection technology in NDT for pressure-bearing equipment while discussing techniques and methods to improve the interpretability of deep learning models. Finally, by summarizing current research and offering insights for future directions, this paper aims to provide researchers and engineers with a comprehensive perspective to advance the application and development of object detection technology in NDT for pressure-bearing equipment.

A selective defect in the glial wedge as part of the neuroepithelium disruption in hydrocephalus development in the mouse hyh model is associated with complete corpus callosum dysgenesis.

Dysgenesis of the corpus callosum is present in neurodevelopmental disorders and coexists with hydrocephalus in several human congenital syndromes. The mechanisms that underlie the etiology of congenital hydrocephalus and agenesis of the corpus callosum when they coappear during neurodevelopment persist unclear. In this work, the mechanistic relationship between both disorders is investigated in the hyh mouse model for congenital hydrocephalus, which also develops agenesis of the corpus callosum. In this model, hydrocephalus is generated by a defective program in the development of neuroepithelium during its differentiation into radial glial cells. In this work, the populations implicated in the development of the corpus callosum (callosal neurons, pioneering axons, glial wedge cells, subcallosal sling and indusium griseum glial cells) were studied in wild-type and hyh mutant mice. Immunohistochemistry, mRNA in situ hybridization, axonal tracing experiments, and organotypic cultures from normal and hyh mouse embryos were used. Our results show that the defective program in the neuroepithelium/radial glial cell development in the hyh mutant mouse selectively affects the glial wedge cells. The glial wedge cells are necessary to guide the pioneering axons as they approach the corticoseptal boundary. Our results show that the pioneering callosal axons arising from neurons in the cingulate cortex can extend projections to the interhemispheric midline in normal and hyh mice. However, pioneering axons in the hyh mutant mouse, when approaching the area corresponding to the damaged glial wedge cell population, turned toward the ipsilateral lateral ventricle. This defect occurred before the appearance of ventriculomegaly. In conclusion, the abnormal development of the ventricular zone, which appears to be inherent to the etiology of several forms of congenital hydrocephalus, can explain, in some cases, the common association between hydrocephalus and corpus callosum dysgenesis. These results imply that further studies may be needed to understand the corpus callosum dysgenesis etiology when it concurs with hydrocephalus.

Highly Sensitive and Selective Defect WS2 Chemical Sensor for Detecting HCHO Toxic Gases

The gas sensitivity of the W defect in WS2 (VW/WS2) to five toxic gases—HCHO, CH4, CH3HO, CH3OH, and CH3CH3—has been examined in this article. These five gases were adsorbed on the VW/WS2 surface, and the band, density of state (DOS), charge density difference (CDD), work function (W), current–voltage (I–V) characteristic, and sensitivity of adsorption systems were determined. Interestingly, for HCHO-VW/WS2, the energy level contribution of HCHO is closer to the Fermi level, the charge transfer (B) is the largest (0.104 e), the increase in W is more obvious than other adsorption systems, the slope of the I–V characteristic changes more obviously, and the calculated sensitivity is the highest. To sum up, VW/WS2 is more sensitive to HCHO. In conclusion, VW/WS2 has a great deal of promise for producing HCHO chemical sensors due to its high sensitivity and selectivity for HCHO, which can aid in the precise and efficient detection of toxic gases.

Charged-Particle-Irradiated Tin Oxyhydroxide Nanoparticle Anodes for Lithium-Ion Batteries

Metal oxyhydroxides have been promising ceramic materials in miscellaneous electrochemical fields due to their multiple redox states, interlayer conductivity, and structural stability as well as electrocatalytic activity. When applied to anode active materials for secondary batteries, particularly lithium-ion batteries, metal oxyhydroxides have a much larger theoretical capacity than that of commercial graphite by conversion and/or alloying reactions with lithium ions rather than intercalation. However, the inevitable volume variation of metal oxyhydroxides during battery operation impinges other primary components in anode materials such as binders and conducting agents, leading to pulverizing the anode materials. Moreover, metal oxyhydroxides are not electrically conductive so much that electrochemical reactions cannot be facilitated efficiently during cycling. Accordingly, many efforts, for example, nanostructuring, constructing hierarchical configurations or hollow structures, and hybridization with carbonaceous materials, have been attempted to overcome the limitations of metal oxyhydroxide anode active materials. In addition, crystal defects in anode materials are greatly helpful to promote electrochemical activity by tuning electronic and chemical properties. Hydrogen annealing, plasma treatment, and chemical reduction method are common approaches to inducing a large number of defects in materials, but they are generally employed at high temperatures or under controlled-pressure circumstances. Therefore, we deploy charged particle irradiation to generate numerous defects in the metal oxyhydroxide anode materials. Incident charged particles interact with a lot of atoms in the anode materials, causing atomic displacement. As a result of the displacement, diverse kinds of defects are produced, which change the electronic and chemical structures of the anode materials. Charged particle irradiation introduces a high density of defects and selective defect types for short time at room temperature. Amorphization is also induced by charged particle irradiation, which is beneficial to improve the electrochemical performance of metal oxyhydroxide anode materials. Herein, we first synthesize tin oxyhydroxide nanoparticles (SnOOH NPs), one of the potential anode active materials using simple nanostructuring, via an electrochemical route, anodization. Anodization is a very fast and concise process to obtain nanostructured metal oxides as well as NPs. Electrodes with SnOOH NPs are irradiated with various charged particles including electrons, protons, helium ions, nitrogen ions, and argon ions, and the irradiation effects are investigated. SnOOH NP anodes irradiated with each type of charged particle show different electrochemical performances from each other, but all of the irradiated SnOOH NP anodes exhibit enhanced discharge capacity or cycle life compared with a pristine SnOOH NP anode. Plausible mechanisms of the irradiation effects depending on charged particles are also proposed. Charged particle irradiation can be utilized for not only metal oxyhydroxides but any kind of ceramic materials in diverse applications including lithium-ion batteries. Figure 1

Near-infrared photoluminescent detection of serum albumin using single-walled carbon nanotubes locally functionalized with a long-chain fatty acid

Serum albumin (SA) is a protein found in biofluids that is useful for diagnosing kidney and liver-related diseases. Single-walled carbon nanotubes (SWCNTs) showing photoluminescence (PL) in the near-infrared (NIR) region are prospective candidates for diagnosis NIR probes. Their NIR PL enhancement has been reported by defect introduction techniques based on local chemical functionalization of SWCNTs. The locally functionalized (lf-)SWCNTs exhibit a bright defect PL (>1000 nm) from the defect sites and its sensitive wavelength shifts in response to surrounding dielectric atmospheres have been reported. Here, we used the sensitive defect PL responses of lf-SWCNTs to establish a NIR sensing system for SA detection. A palmitic acid group that binds to SA strongly and selectively, was functionalized at the defect site of lf-SWCNTs (lf-SWCNTs-p). Compared to typical PL of unmodified SWCNTs, selective defect PL red-shifts (of 2.5 nm max.) were clearly observed according to the addition of SA in phosphate-buffered saline. The defect PL responsiveness could detect different SA from human, bovine, and mouse. The red-shifts of the defect PL occurred by formation of a high dielectric environment based on the specific binding between SA and the palmitic acid groups on the defect sites. The lf-SWCNTs-p detected SA-spiked serum and albuminuria of diabetic mouse in body fluids. The findings show that the lf-SWCNTs-p offer an NIR PL analytical tool for SA in body fluids applicable to a disease diagnosis and expand the bioapplications of lf-SWCNTs based on their molecular design-based defect engineering.

(Digital Presentation) Deconstructing Proton Transport through Atomically Thin Monolayer CVD Graphene Membranes

Selective proton (H+) permeation through the atomically thin lattice of graphene and other 2D materials offers new opportunities for energy conversion/storage and novel separations. Practical applications necessitate scalable synthesis via approaches such as chemical vapor deposition (CVD) that inevitably introduce sub-nanometer defects, grain boundaries and wrinkles, and understanding their influence on H+ transport and selectivity for large-area membranes is imperative but remains elusive. Using electrically driven transport of H+ and potassium ions (K+) we probe the influence of intrinsic sub-nanometer defects in monolayer CVD graphene across length-scales for the first time. At the micron scale, the areal H+ conductance of CVD graphene (∼4.5–6 mS cm−2) is comparable to that of mechanically exfoliated graphene indicating similarly high crystalline quality within a domain, albeit with K+ transport (∼1.7 mS cm−2). However, centimeter-scale Nafion|graphene|Nafion devices with several graphene domains show areal H+ conductance of ∼339 mS cm−2 and K+ conductance of ∼23.8 mS cm−2 (graphene conductance for H+ is ∼1735 mS cm−2 and for K+ it is ∼47.6 mS cm−2). Using a mathematical-transport-model and Nafion filled polycarbonate track etched supports, we systematically deconstruct the observed orders of magnitude increase in H+ conductance for centimeter-scale CVD graphene. The mitigation of defects (>1.6 nm), wrinkles and tears via interfacial polymerization results in a conductance of ∼1848 mS cm−2 for H+ and ∼75.3 mS cm−2 for K+ (H+/K+ selectivity of ∼24.5) via intrinsic sub-nanometer proton selective defects in CVD graphene. We demonstrate atomically thin membranes with significantly higher ionic selectivity than state-of-the-art proton exchange membranes while maintaining comparable H+ conductance. Our work provides a new framework to assess H+ conductance and selectivity of large-area 2D membranes and highlights the role of intrinsic sub-nanometer proton selective defects for practical applications.

Half-Heusler alloys as emerging high power density thermoelectric cooling materials

To achieve optimal thermoelectric performance, it is crucial to manipulate the scattering processes within materials to decouple the transport of phonons and electrons. In half-Heusler (hH) compounds, selective defect reduction can significantly improve performance due to the weak electron-acoustic phonon interaction. This study utilized Sb-pressure controlled annealing process to modulate the microstructure and point defects of Nb0.55Ta0.40Ti0.05FeSb compound, resulting in a 100% increase in carrier mobility and a maximum power factor of 78 µW cm−1 K−2, approaching the theoretical prediction for NbFeSb single crystal. This approach yielded the highest average zT of ~0.86 among hH in the temperature range of 300-873 K. The use of this material led to a 210% enhancement in cooling power density compared to Bi2Te3-based devices and a conversion efficiency of 12%. These results demonstrate a promising strategy for optimizing hH materials for near-room-temperature thermoelectric applications.

Role of HLA class-I antigen peptide loading complex components in immune evasion and treatment sensitivity in human lung cancer.

2623 Background: Determinants of sensitivity and resistance to immune checkpoint inhibitors (ICIs) are poorly understood. An intact HLA class-I antigen presentation machinery (APM) is necessary for tumor-antigen recognition by effector T-cells and disruptions to the APM can cause ICI resistance. The peptide loading complex (PLC) is a multi-chaperone complex located in the endoplasmic reticulum in which tapasin (Tap), calreticulin (CalR) and ERp57 play major roles. The PLC allows for optimal peptide selection and loading onto HLA class-I heavy chain and is critical for adequate cell surface presentation of peptide-HLA complexes. We studied the frequency and clinical significance of cancer-cell selective PLC protein defects in human NSCLC. Methods: Multiplex quantitative immunofluorescence (mQIF) was performed to simultaneously and spatially measure cytokeratin (CK), Tap, CalR, ERp57 and CD8 protein levels in 1,031 primary NSCLCs from 5 independent cohorts represented in tissue microarrays. The protein levels were measured in CK-positive cancer-cells and in CK-negative stromal cells. The presence of lower marker levels in malignant cells relative to stromal cells within the same sample was considered as cancer-cell selective downregulation. Cohorts #1-3 included baseline samples from patients treated without ICIs and Cohort #4 included samples from patients treated with ICIs. Cohort #5 contained lung adenocarcinomas clinically tested for EGFR and KRAS mutations. The association between the levels of Tap, CalR and ERp57, their association with clinicopathologic variables, CD8+ T-cell levels and outcomes were studied. Results: mQIF analysis identified cancer-cell selective downregulation of Tap, CalR and/or ERp57 in 73%, 81%, 68% and 75% of cases from Cohorts #1-4, respectively. The most common PLC alterations were cancer-cell downregulation of Tap alone in Cohorts #1 (32%), #3 (34%) and #4 (36%); and Tap-CalR in Cohort #2 (29%). Tap and ERp57 levels were significantly higher in stage IV than in earlier stage tumors. The PLC marker levels and the frequency of cancer-cell selective downregulation were comparable across EGFR and KRAS mutated samples. NSCLCs with cancer-cell Tap downregulation had lower CD8+ T-cell infiltration and shorter OS across all cohorts that reached statistical significance in Cohort #4 (median OS 12.08 vs 21.00, HR=1.72, 95% CI 1.02-2.89, p=0.034). The cancer-cell selective downregulation of CalR was associated with shorter OS in cohorts #1 and #3. Conclusions: HLA class-I PLC components show variable levels in treatment naïve NSCLCs. Downregulation of Tap in cancer-cells, alone or in combination with other PLC members occurs in up to 60% of cases and is associated with reduced CD8+ TILs and shorter OS preferentially in patients treated with ICIs. Cancer-cell Tap downregulation could mediate primary ICI resistance and has biomarker potential.

UBL5 Modulates Expression of Crucial TLR Pathway Genes and Inflammasome Activation in Human Macrophage Cells

Abstract We conducted a genome-wide siRNA screen for regulators of LPS-driven TNF expression in macrophages. We used a splicing-independent reporter for the screen, and while we identified very few core spliceosome components among the strongest screen hits, we observed a clear enrichment for peripheral splicing regulators. Among these, a novel putative splicing regulator, UBL5, gave a strong screen phenotype, and a UBL5 shRNA-expressing cell line showed a selective defect in LPS-driven gene expression. While many genes were induced normally by LPS in the UBL5 deficient cells, a subset of genes, including core components of the LPS-activated TLR4 signaling pathway, were substantially diminished in UBL5-deficient cells. We conducted both Illumina and Pacbio long-read sequencing, and we observed marked defects in the LPS-induced splicing of numerous genes, however the primary impact on known components of the TLR4 pathway was observed at the level of overall gene expression rather than alternative splicing. Our data suggests that the putative splicing regulator UBL5 also has key roles in the maintenance and induction of gene expression for several core components of the TLR4 signaling pathway. Key role of UBL5 in the induction of TLR4 signaling pathway was further evidenced by the defective NLRP3 inflammasome activation and protection of OC43 coronavirus infection in UBL5-deficient cells. This work was supported by the Intramural Research Program of NIAID, NIH Intramural Research Program of NIAID, NIH

Novel sonic hedgehog gene variant in a patient with hyponatremia, microsomia, and midline defects; phenotype description in association with a variant of unknown significance [c.755_757del p.(Phe252del)] and an approach to salt-wasting in SHH-related adrenal disorders

To contribute a novel sonic hedgehog (SHH) gene variant in association with a novel-meagerly described phenotype and discuss SHH signaling pathway pathology. We present a 5-year-old boy with excessive hyponatremia and natriuresis, microform holoprosencephaly and microsomia, with morphologically intact hypothalamic-pituitary-adrenal (HPA) axis, and hypoaldosteronism, yet without hyperreninemia, hyperkalemia, dehydration episodes, or glucocorticoid insufficiency. Extensive workup excluded common causes of salt-wasting and revealed a novel variant of unknown significance on the sonic hedgehog (SHH) gene; NM_000193.4:c.755_757del (p.Phe252del), in heterozygosity. Salt-wasting in children is predominantly caused by central nervous system lesions, renal tubular dysfunction, or adrenal insufficiency. The SHH protein is a signaling molecule, essential in embryogenesis-including HPA axis differentiation. Inactivating SHH variants disrupt the signaling pathway, leading to dysplasia or dysfunction of target organs. What's new: • We analyze the patient's phenotype in the light of this novel variant • Patient's isolated aldosterone deficiency possibly implies a selective signaling defect affecting the development of adrenal zona glomerulosa • Unexplained hyporeninemia and hypokalemia in the context of hypoaldosteronism raise questions on SHH signaling pathophysiology.

Lack of Herpes Virus Entry Mediator Signals in Thymocytes Impairs Conventional CD8 T Cell Selection and Promotes Memory-like CD8 T Cell Development.

Thymocytes having diverse Ag specificities are selected in response to self-MHC-peptide expressed in thymic epithelial cells, which contributes to the formation of a T cell repertoire. However, it is not well understood whether additional signals from epithelial cells are required to drive positive selection. In this study, we found that one of the TNFR superfamily members, herpes virus entry mediator (HVEM), when expressed on thymocytes provides signals for positive selection. HVEM deficiency in double-positive (DP) thymocytes impaired positive selection of CD8 thymocytes. HVEM-deficient thymocytes in OT-1 TCR transgenic mice exhibited significant defects in positive selection and impaired CD69 upregulation of selected thymocytes. HVEM ligands (lymphotoxin-like, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes, and B and T lymphocyte attenuator) were expressed in cortical thymic epithelial cells. Weak TCR ligation combined with HVEM signals enhanced ERK activation in DP thymocytes developed invitro. Insufficient signals for positive selection in HVEM-deficient DP thymocytes led to the development of innate memory-like CD8 T cells expressing high levels of CD122, along with the increased development of PLZF+ NKT cells. These results suggest that thymocytes receive activation signals through HVEM during positive selection. Thus, our findings provide evidence that the threshold of thymocyte positive selection is set by signals from TCR in association with HVEM.

Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons.

Presynaptic inputs determine the pattern of activation of postsynaptic neurons in a neural circuit. Molecular and genetic pathways that regulate the selective formation of subsets of presynaptic inputs are largely unknown, despite significant understanding of the general process of synaptogenesis. In this study, we have begun to identify such factors using the spinal monosynaptic stretch reflex circuit as a model system. In this neuronal circuit, Ia proprioceptive afferents establish monosynaptic connections with spinal motor neurons that project to the same muscle (termed homonymous connections) or muscles with related or synergistic function. However, monosynaptic connections are not formed with motor neurons innervating muscles with antagonistic functions. The ETS transcription factor ER81 (also known as ETV1) is expressed by all proprioceptive afferents, but only a small set of motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional mouse genetic techniques to eliminate Er81 expression selectively from motor neurons. We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive afferents conveying information from homonymous and synergistic muscles, with no change observed in the connectivity pattern from antagonistic proprioceptive afferents. In summary, these findings suggest a role for ER81 in defined motor neuron pools to control the assembly of specific presynaptic inputs and thereby influence the profile of activation of these motor neurons.

Mechanisms of continual efferocytosis by macrophages and its role in mitigating atherosclerosis.

Atherosclerotic cardiovascular disease is the leading cause of death worldwide. Rupture-prone atheromas that give rise to myocardial infarction and stroke are characterized by the presence of a necrotic core and a thin fibrous cap. During homeostasis, cellular debris and apoptotic cells are cleared quickly through a process termed "efferocytosis". However, clearance of apoptotic cells is significantly compromised in many chronic inflammatory diseases, including atherosclerosis. Emerging evidence suggests that impairments in efferocytosis drive necrotic core formation and contribute significantly to plaque vulnerability. Recently, it has been appreciated that successive rounds of efferocytosis, termed "continual efferocytosis", is mechanistically distinct from single efferocytosis and relies heavily on the metabolism and handling of apoptotic cell-derived cargo. In vivo, selective defects in continual efferocytosis drive secondary necrosis, impair inflammation resolution, and worsen atherosclerosis. This Mini Review focuses on our current understanding of the cellular and molecular mechanisms of continual efferocytosis and how dysregulations in this process mediate nonresolving inflammation. We will also discuss possible strategies to enhance efferocytosis when it fails.

Numerical simulation of lead-free vacancy ordered Cs2PtI6 based perovskite solar cell using SCAPS-1D.

In recent years, vacancy-ordered halide double perovskites have emerged as promising non-toxic and stable alternatives for their lead-based counterparts in optoelectronic applications. In particular, vacancy ordered Cs2PtI6 has emerged as a star material because of its high absorption coefficient, band gap of 1.37 eV, and long minority carrier lifetime. Despite substantial experimental research on this new class of material, theoretical simulations of their device properties remain scarce. In this work, a novel n-i-p device architecture (FTO/SnO2/Cs2PtI6/MoO3/C) is theoretically investigated using a solar cell capacitance simulator (SCAPS-1D). Theoretical investigations are carried out in order to optimize the device performance structure by varying the perovskite and selective charge transport layer thickness, absorber and interface defect density, operating temperature, back contact, series and shunt resistance, respectively. The optimized device showed an impressive power conversion efficiency (PCE) of 23.52% at 300 K, which is higher than the previously reported values. Subsequent analysis of the device's spectral response indicated that it possessed 98.9% quantum efficiency (QE) and was visibly active. These findings will provide theoretical guidelines for enhancing the performance of Cs2PtI6-based photovoltaic solar cells (PSCs) and pave the way for the widespread implementation of environmentally benign and stable perovskites.

Recent Progress of Surface Passivation Molecules for Perovskite Solar Cell Applications

Due to the solution processable nature, the prepared perovskite films are polycrystalline with considerable number of defects. These defects, especially defects at interface accelerate the carrier recombination and reduce the carrier collection. Besides, the surface defects also affect the long-term stability of the perovskite solar cells (PVSCs). To solve this problem, surface passivation molecules are introduced at selective interface (the interface between perovskite and carrier selective layer). This review summarizes recent progress of small molecules used in PVSCs. Firstly, different types of defect states in perovskite films are introduced and their effects on device performance are discussed. Subsequently, surface passivation molecules are divided into four categories, and the interaction between the functional groups of the surface passivation molecules and selective defect states in perovskite films are highlighted. Finally, we look into the prospects and challenges in design noble small molecules for PVSCs applications.

Atomic site-targeted doping in Ti2FeNiSb2 double half-Heusler alloys: zT improvement via selective band engineering and point defect scattering

Ti2FeNiSb2 is a promising double half-Heusler thermoelectric compound with intrinsically low thermal conductivity due to low phonon group velocity. Since it is introduced in 2019, many efforts have been focused on further reducing its thermal conductivity via doping. However, the effects of doping on its electronic transport properties have been neglected. Here, we investigate the effects of doping Co and Bi at the Fe- and Sb-sites, respectively, in Ti2FeNiSb2 for the first time. Changes in band parameters due to atomic site-targeted doping are estimated by the Single Parabolic Band model. Bypassing the trade-off relation between the Seebeck coefficient and electrical conductivity is observed when doping Co at Fe-sites. The physics behind the bypass is explained in terms of temperature-dependent reduced chemical potential and non-degenerate mobility. As a result, peak figure of merit zT values of ∼0.69 in Ti2Fe0.9Co0.1NiSb2 is achieved, which is approximately six times higher than that of the pristine Ti2FeNiSb2. The thermoelectric performance of Ti2FeNiSb2 can be improved by selective band engineering to bypass the Seebeck coefficient-electrical conductivity trade-off relation from atomic-site targeted doping.

Connecting children with birth defects to health and social service programs: A collaboration between the Texas Birth Defects Registry and agency social workers.

Timely referral to services for children born with birth defects can improve health outcomes. Birth defects surveillance registries may be a valuable data source for connecting children to health and social service programs. Population-based, state-wide data from the Texas Birth Defects Registry (TBDR) at the Texas Department of State Health Services (DSHS) were used to connect children 9-18 months old, born with select birth defects with DSHS social workers. The social workers reviewed developmental milestones and referred children and their families to various health and social service programs. We tabulated the proportions of children meeting milestones and referral characteristics by referral program type and type of birth defect. Social workers reached 67% (909/1,362) of identified families. Over half of children (54%, 488/909) were not meeting the developmental milestones for their age. Social workers provided over 3,000 program referrals, including referring 21% (194/909) of children to Early Childhood Intervention (ECI) and 28% (257/909) to case management. Our results illustrate a method of leveraging a birth defects surveillance system for referral services. Given the large number of referrals made, our findings suggest that birth defects registries can be a valuable source of data for referring children to programs.

OR06-4 Women With Obesity Display Defects in Follicular Recruitment, Selection, and Dominance Alongside Luteal Phase Dysfunction During Natural Ovulatory Cycles

Abstract Although obesity is closely associated with reproductive dysfunction, many women with obesity remain eumenorrheic. The degree to which obesity affects menstrual cycle characteristics in this population is limited to endocrine assessments with few data available on how endocrine aberrations align with defects in antral follicle development.We have previously shown alterations in the distribution of recruitable (2-5mm) versus selectable (6-9mm) follicles in those with obesity that were associated with decreased gonadotropin and progesterone production despite normal menstrual cycle length. The objectives of the present study were to further contrast follicular growth and endocrine dynamics between obese and non-obese eumenorrheic women with the goal of determining any alterations in distinct events in folliculogenesis. 21 non-obese (total percent body fat <35%) and 21 obese (total percent body fat ≥35%) reproductive age females with regular menstrual cycles (21-35d) were evaluated by serial ovarian transvaginal ultrasonography and venipuncture every-other-day for one complete inter-ovulatory interval (IOI). The number and diameters of all follicles ≥2mm at each visit were documented offline using the Grid Method. Growth profiles of individual follicles which grew to ≥7mm were assessed using the Identity Method to characterize antral follicle recruitment, selection, and ovulation. Clinical, morphologic, and endocrine features were compared across groups using t-tests and mixed models. Women with obesity exhibited fewer recruitment events versus non-obese women (1±0.6 vs. 2±0.9; p=0.010). They also had fewer selectable follicles (4±3 vs. 8±6 follicles/participant, p=0.022) which grew faster but remained static longer and regressed slower (all growth rates, p<0.05) compared to their non-obese counterparts. Anti-Mullerian hormone levels were lower in the obese versus non-obese group (4.40±3.01 vs. 5.94±2.49ng/mL, p=0.023). Of the selectable follicles, fewer progressed to ≥10mm in the obese versus non-obese group (1±0.7 vs. 2±0.8 follicles, p=0.030) with ultimately fewer anovulatory follicles achieving dominance (0±0.7 vs. 1±0.9 follicle, p=0.029). Ovulatory follicles in the obese group were selected at smaller diameters (7.5±1.6 vs. 9.5±1.9mm, p=0.001) versus their non-obese counterparts. However, the kinetics of dominant follicle growth were similar between groups. Post-ovulation, progesterone concentrations across the luteal phase were lower in women with obesity (4.95±3.34 vs. 7.85±5.74ng/mL, p=0.001) and the prevalence of luteal phase defects (LPDs) higher versus non-obese women, defined by either integrated (76 vs. 29%, p=0.002) or maximum (71 vs. 24%, p=0.002) progesterone levels. Eumenorrheic women with obesity display evidence of suppressed follicle dynamics as evidenced by fewer recruitment events, selectable follicles, and anovulatory dominant follicles. LPDs are more prevalent in women with obesity during natural ovulatory cycles which may underlie subfertility in this population. A smaller size at selection suggests premature responsiveness to luteinizing hormone which may result in suboptimal luteinization. Further studies are needed to elucidate the degree to which these defects impact fertility and fecundity in our increasingly obese demographic. Presentation: Saturday, June 11, 2022 12:15 p.m. - 12:30 p.m.