13 research outputs found
An overview of direct somatic reprogramming: The ins and outs of iPSCs
No full textStem cells are classified into embryonic stem cells and adult stem cells. An evolving alternative to conventional stem cell therapies is induced pluripotent stem cells (iPSCs), which have a multi-lineage potential comparable to conventionally acquired embryonic stem cells with the additional benefits of being less immunoreactive and avoiding many of the ethical concerns raised with the use of embryonic material. The ability to generate iPSCs from somatic cells provides tremendous promise for regenerative medicine. The breakthrough of iPSCs has raised the possibility that patient-specific iPSCs can provide autologous cells for cell therapy without the concern for immune rejection. iPSCs are also relevant tools for modeling human diseases and drugs screening. However, there are still several hurdles to overcome before iPSCs can be used for translational purposes. Here, we review the recent advances in somatic reprogramming and the challenges that must be overcome to move this strategy closer to clinical application
Implementing COOL: comparative welfare effects of different labeling schemes
No full textCountry-of-origin labeling (COOL) is being implemented in different forms and degrees in the United States and other countries across the world. The first implementation of mandatory country of origin labeling (MCOOL) in the United States was for seafood in 2005. This is an example of partial MCOOL because it exempts the foodservice sector and excludes processed seafood from labeling. Using a conceptual framework, we analyze the welfare impacts of partial MCOOL when compared to no, voluntary, and total mandatory COOL, taking into account imperfect competition in the downstream markets, information asymmetry, and diversion of low-quality product to the unlabeled market. The model is general enough to apply to any incomplete regulation for which the perceived low-quality product is required to be labeled, such as the labeling of genetically modified food in the European Union. Our results show that when consumers have a strong enough preference for domestic relative to imported product, regulators can overestimate the gain in consumer welfare from partial mandatory labeling if they ignore the diversion of lower quality imports to the unlabeled sector. We show that if the preference for domestic product is large enough, total MCOOL benefits the home market the most overall, including domestic consumers and producers, but not the imperfectly competitive downstream agents. However, if total MCOOL is too costly to implement, partial MCOOL is the second-best solution, but only if consumers falsely believe the unlabeled product to be of higher quality than it truly is. Our results suggest more research is needed to determine the extent to which consumers value the information provided by MCOOL and to enable regulators to consider the welfare impact of diversion in evaluating incomplete mandatory labeling regulations
How COOL is U.S. Shrimp trade?
No full textWe investigate the economic impact of partial implementation of COOL on U.S. shrimp trade by developing a conceptual model that encompasses horizontal and vertical product differentiation. Horizontal differentiation is characterized by explicitly accounting for differences in shrimp processing – fresh or frozen versus peeled, canned, or breaded. Vertical differentiation in the conceptual model is captured by two scenarios – presence and absence of COOL – on trade between major shrimp exporters and United States. COOL implementation results in quality disclosure through origin labeling and additional costs of labeling on fresh and frozen shrimp sold at retail while processed shrimp products are excluded from labeling. The conceptual model indicates a change in product mix with COOL implementation: the relative share of processed shrimp increases when compared to unprocessed shrimp. Empirically testing the hypothesis using an econometric model shows there is no change in the product mix in the two scenarios. The results however change depending on the choice of variable used to proxy quality
High efficiency IBC solar cells with poly-Si implanted passivating contacts
No full textCrystalline silicon (c-Si) interdigitated back contacted (IBC) solar cell with poly-Si passivating contacts is one of the most promising approaches to achieve high conversion efficiency solar cells. The fabrication of IBC silicon-based solar cells provided by poly-Si passivating contacts is investigated in this thesis. The passivating poly-Si contacts structure used in this work is based on an ultra-thin layer of t-SiOX with optimized poly-Si thicknesses of 250 nm and the implantation parameters of Phosphorous and Boron doping with 6e15 and 5e15 ions/cm2 respectively, at a fixed implantation energy of 20 keV. The influence of the post-implantation annealing conditions is discussed with experimental results, obtained on symmetrical test structures with thermal SiOx/doped poly-Si on each side. The bestobtained passivation result for n+ -poly-Si contact was 728 mV at annealing conditions of 1050°C for 1 minute, while for the p+ poly-Si contact at the same annealing conditions 699 mV is obtained. To enhance the passivation, PECVD deposited SiNX capping layer and annealing in forming gas as hydrogenation processes are carried out. Then, FBC solar cells are fabricated to evaluate the electrical performances, in terms of passivation and carrier transport, of the poly-Si contacts structures, which are prepared with different annealing conditions, in terms of temperature and time. The results obtained from the FBC cells show that increasing the annealing temperature leads to an increase in the passivation thus the VOC. The best-obtained VOC was 706mV for the wafer annealed at 1050°C for 1 minute. To enhance the optical properties of the IBC cells, the surface is textured and the influence of doping dose on passivation of the front surface field (FSF) is evaluated. Four different passivation stack layers SiNX, AlOX/SiNX, a-Si/SiNX, and double SiNy /SiNX are evaluated for FSF implanted with dose of 1e14 ions/cm2. The best-obtained passivation result is from FSF sample passivated with a-Si/SiNX. It shows excellent passivation property with iVOC of 714 mV and a J0 of 7.5 fA/cm2. while the other stacks show lower passivation of iVOC 708 mV for the AlOX/SiNX sample and iVoc=686 mV for the SiNy /SiNX sample. The influence of FGA on the FSF passivation quality is also evaluated. The results show that the sample passivated with a-Si/SiNX experienced a sharp decrease of 35 mV in the iVOC after FGA due to the low thermal stability of the a-Si:H. On the other hand, other FSF samples with passivation stacks of SiNX, AlOX/SiNX, and SiNX /SiNX show a positive influence upon the FGA on their passivation quality as a result of the extra hydrogen diffusion during the FGA which saturates more defects on the c-Si surface. The implantation of the optimized thermal SiOx/ doped poly-Si structure and FSF with a-Si/SiNX passivating layer into the IBC solar cells leads to high-efficiency IBC solar cells. The record cell has a conversion efficiency of 21.04% and 22.15% after the post metallization annealing, VOC of 681 mV, and FF of 78,9 with Jsc of 37.5 mA/cm
Quantifying navigational difficulty for visually impaired users in indoor spaces with AccessQuotient
No full textThis is an open access article under the CC BY license.Navigating unfamiliar indoor spaces is particularly challenging for blind or visually impaired (BVI) individuals due to complex layouts and inadequate signage. To address this, we introduce AccessQuotient - a metric that quantifies navigational difficulty in built environments for BVI users. Based on a simplified mathematical model and validated through a small-scale user study, AccessQuotient predicts both the likelihood of mistake-free traversal and expected navigation errors. This exploratory model aims to establish a foundation for further research rather than provide definitive assessments. By quantifying spatial complexity, AccessQuotient supports designers and planners in evaluating and improving indoor accessibility. © 2025 Copyright held by the owner/author(s).National Science Foundation, NSF, (2409227, 2340870, 2345057); National Science Foundation, NSFThis work was supported in part by U.S. National Science Foundation awards #2409227, #2340870, #2345057
Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-Derived Parietal Bone Through Downregulation of Fgf23
No full textCraniofacial development is a program exquisitely orchestrated by tissue contributions and regulation of genes expression. The basic helix–loop–helix (bHLH) transcription factor Twist1 expressed in the skeletal mesenchyme is a key regulator of craniofacial development playing an important role during osteoskeletogenesis. This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. We show that Twist1 haplonsufficiency as well Twist1-sh-mediated silencing selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived bones. Transcriptomic profiling, gain-and loss-of-function experiments revealed that Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived bone through a sharp downregulation of the bone-derived hormone Fgf23 that is upregulated exclusively in wild-type parietal bone
Image_3_Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-Derived Parietal Bone Through Downregulation of Fgf23.TIF
No full textCraniofacial development is a program exquisitely orchestrated by tissue contributions and regulation of genes expression. The basic helix–loop–helix (bHLH) transcription factor Twist1 expressed in the skeletal mesenchyme is a key regulator of craniofacial development playing an important role during osteoskeletogenesis. This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. We show that Twist1 haplonsufficiency as well Twist1-sh-mediated silencing selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived bones. Transcriptomic profiling, gain-and loss-of-function experiments revealed that Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived bone through a sharp downregulation of the bone-derived hormone Fgf23 that is upregulated exclusively in wild-type parietal bone.</p
Image_2_Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-Derived Parietal Bone Through Downregulation of Fgf23.TIF
No full textCraniofacial development is a program exquisitely orchestrated by tissue contributions and regulation of genes expression. The basic helix–loop–helix (bHLH) transcription factor Twist1 expressed in the skeletal mesenchyme is a key regulator of craniofacial development playing an important role during osteoskeletogenesis. This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. We show that Twist1 haplonsufficiency as well Twist1-sh-mediated silencing selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived bones. Transcriptomic profiling, gain-and loss-of-function experiments revealed that Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived bone through a sharp downregulation of the bone-derived hormone Fgf23 that is upregulated exclusively in wild-type parietal bone.</p
Image_1_Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-Derived Parietal Bone Through Downregulation of Fgf23.TIF
No full textCraniofacial development is a program exquisitely orchestrated by tissue contributions and regulation of genes expression. The basic helix–loop–helix (bHLH) transcription factor Twist1 expressed in the skeletal mesenchyme is a key regulator of craniofacial development playing an important role during osteoskeletogenesis. This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. We show that Twist1 haplonsufficiency as well Twist1-sh-mediated silencing selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived bones. Transcriptomic profiling, gain-and loss-of-function experiments revealed that Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived bone through a sharp downregulation of the bone-derived hormone Fgf23 that is upregulated exclusively in wild-type parietal bone.</p
Table_1_Twist1-Haploinsufficiency Selectively Enhances the Osteoskeletal Capacity of Mesoderm-Derived Parietal Bone Through Downregulation of Fgf23.docx
No full textCraniofacial development is a program exquisitely orchestrated by tissue contributions and regulation of genes expression. The basic helix–loop–helix (bHLH) transcription factor Twist1 expressed in the skeletal mesenchyme is a key regulator of craniofacial development playing an important role during osteoskeletogenesis. This study investigates the postnatal impact of Twist1 haploinsufficiency on the osteoskeletal ability and regeneration on two calvarial bones arising from tissues of different embryonic origin: the neural crest-derived frontal and the mesoderm-derived parietal bones. We show that Twist1 haplonsufficiency as well Twist1-sh-mediated silencing selectively enhanced osteogenic and tissue regeneration ability of mesoderm-derived bones. Transcriptomic profiling, gain-and loss-of-function experiments revealed that Twist1 haplonsufficiency triggers its selective activity on mesoderm-derived bone through a sharp downregulation of the bone-derived hormone Fgf23 that is upregulated exclusively in wild-type parietal bone.</p
