Welcome to the SUNY Open Access Repository

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  The Effect of Biofeedback Training on Accommodation During MFCL Wear in Young Adults

  Patel, Sweta (2025)

  "Purpose: Myopia currently affects 22.9% of the global population and it is estimated that 50% of the world population will be myopia by 2050. Multifocal contact lenses (MFCLs) are effective in reducing myopia progression, but with variable efficacies. One potential reason could be reduced accommodation through the MFCLs. This is due to the near add in the MFCLs superimposing peripheral myopic defocus or reducing peripheral hyperopic defocus, which then leads to a relaxation of accommodation. The drawback, however, is that if myopes reduce accommodation when reading through the MFCLs, it may reduce peripheral myopic defocus and ultimately, reduce the treatment effect of MFCLs. Recent studies show that auditory biofeedback training can help improve accommodation through the MFCLs in young myopes both immediately after the training and one week later, which may ultimately improve the efficacy of MFCLs. In this study, we evaluated, in young adults, the time course of biofeedback training in increasing accommodative response during MFCL wear and if weekly repetition of the biofeedback training and increased training duration could lead to longer lasting results. Methods: This was a prospective study with 4 weekly visits. Twenty-seven young myopes with normal accommodation and binocularity were fit with Biofinity single vision (SV) and MF (+2.00 Add center distance) CLs over both eyes and randomized to 3 groups: (1) Group 1 – single training, (2) Group 2 – regular repeated training, and (3) Group 3 – extended repeated training. During Visit 1 for all 3 groups, accommodation was measured first through the SVCLs, then through the MFCLs before and after an auditory biofeedback training at four different dioptric distances: 2.5D, 3D, and 4D. During Visits 2 and 3 for group 1, accommodation through the MFCLs was measured without the biofeedback training. During Visits 2 and 3 for group 2, accommodation was measured before and after auditory biofeedback training. During Visits 2 and 3 for group 3, accommodation was measured before and after an extended auditory biofeedback training (twice the duration). Visit 4 for all groups consisted of measuring accommodation through the MFCLs without auditory biofeedback training. Results: Analysis of the data confirmed that accommodative responses were reduced in MFCLs compared to SVCLs. One session of auditory biofeedback training was also shown to increase the accommodative responses in MFCLs at the 2.5 D, 3 D, and 4D distances and the effect of the training lasted for at least one week as supported from the data pooled together of all subjects. In subjects who received the training in the first session, effects of the training lasted for the entire month. However, increasing the number of trainings (as performed for Group 2 subjects) or the duration of the training (as performed for Group 3 subjects) did not significantly further increase the efficacy of the biofeedback training. Conclusion: Biofeedback training could potentially be used as an adjunct treatment for slowing down myopia progression when coupled with MFCL wear. Since one training of auditory biofeedback training showed success in increasing accommodative responses, it may be worthwhile to determine what changes can be made in the execution of the training to yield the best results. While this study was performed on young adults, future directions may include performing a similar study design on myopic children due to the greater accommodative capabilities of children in comparison to adults. "
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  Artificial Intelligence and Machine Learning for Future Terahertz Wireless Networks: Design, Development, and Conceptualization

  Primus, Ryan (SUNY Polytechnic Institute, 2025-05-10)

  This thesis explores the integration of artificial intelligence (AI) and machine learning (ML) techniques into future terahertz (THz) wireless communication networks, focusing on system design, optimization, and deployment. We first address one of the major impediments to THz communications: the severe impact of phase noise (PN) compounded by additive white Gaussian noise (AWGN). By developing an in-house PN model based on empirical measurements, we synthetically generated a large dataset to train several regression models. Among these, the AdaBoost Regressor (ABR) demonstrated superior performance, achieving high predictive accuracy in estimating bit error rates (BER) across diverse system configurations. Building upon the predictive capabilities of the regression model, we integrated the Differential Evolution (DE) optimization algorithm to automate waveform parameter selection for minimized BER, revealing critical insights into the nonlinear relationship between PN, bandwidth, and AWGN. Our findings demonstrated that while increasing bandwidth exacerbates AWGN, it can simultaneously mitigate the detrimental effects of PN, a relationship that cannot be captured analytically and thus necessitates a data-driven approach. In parallel, we developed a large language model (LLM)-based expert system hosted on OpenAI’s platform to accelerate not only undergraduate research on the SUNY Poly ACES v testbed, but AI predictive capabilites for future THz networks. By combining the k-nearest neighbors regressor (kNN), which predicts real-world THz link performance, with natural language interfaces, students can now access predictive tools and receive experimental advice conversationally. This approach bridges the gap between complex system modeling and intuitive experimental operation, paving the way for a new era of AI-assisted wireless systems. While this work focuses on specific waveform optimization within a single testbed, it serves as an early building block toward AI-driven, self-optimizing THz networks that will form the backbone of ultra-high-speed, adaptive wireless systems in the coming decade. Overall, this work contributes a novel, modular framework for THz waveform optimization and educational facilitation, highlighting how AI-driven methods can address core challenges in high-frequency wireless communications while fostering human-in-the-loop innovation. Our methodology paves the way for the intelligent, adaptive frameworks that will shape the evolution of THz communications, setting the stage for the fully autonomous wireless networks of the future.
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  Effect of phospholipid transfer protein and apolipoprotein M in sphingosine-1-phosphate and chylomicron metabolism

  Jones, Quiana

  Phospholipid transfer protein (PLTP) is a monomeric protein primarily responsible for the transfer of hydrophobic molecules, including phospholipids, cholesterol, triglycerides from apolipoprotein B containing particles to high-density lipoprotein (HDL). Shingosine-1-phoshate is a lipid mediator which acts on five unique receptors expressed in various tissues. Both PLTP and S1P have been implicated in cardio-related disease. Germline PLTP KO studies reveal plasma S1P decreases without affected apoM, a major carrier of S1P which is bound to HDL particles. From this data, we hypothesize that PLTP could be a carrier for S1P in circulation and that its carrier function is independent of the apoM-S1P axis. We, therefore, developed single apoM and inducible PLTP KO lines as well as a double PLTP/apoM KO mice model and compared plasma changes for S1P. Our theory was that if our hypothesis was correct, double PLTP/apoM KO should decrease plasma S1P more than single KO models suggesting an additive or synergetic effect. We observed that single apoM KO reduced plasma S1P roughly 50% and single PLTP KO reduced plasma S1P roughly 40%; however, double KO did not reduce plasma S1P more than 50%. In addition, we found that PLTP KO also reduced plasma HDL, suggesting that the S1P reduction observed in this inducible KO model was due to HDL reduction in circulation. Further, we found that KO of albumin, which has long been thought to be a non-apoM-related S1P carrier, had no effect on S1P levels suggesting that although PLTP may not be an independent carrier of S1P, neither is albumin. Our focus on HDL in this set of experiments also lead us to studying apoM more closely. A previous report detailed that apoM deficiency led to decreased circulating triglyceride (TG) levels. In the liver, very low-density lipoproteins (VLDL) are produced; however, in the small intestine chylomicron (CM) are produced. CM production only happens postprandially or after 26 fat loading. These two particles are mostly responsible for the circulation of TG and both contain apolipoprotein B (apoB) – VLDL has apoB-100 and CM has apoB-48 as their main structural proteins. After confirming the previously observed apoM deficiency phenotype, we measured small intestinal as well as liver proteins related to the formation and secretion of apoB-containing particles. Although the liver and the small intestine have a similar set of proteins responsible for apoB-containing particle secretion, we found that in the small intestine but not the liver of apoM KO mice, levels of microsomal triglyceride transfer protein (MTP) and Sar1B are decreased. Both these proteins are necessary components in the formation and secretion. In addition to this, we found accumulation of lipids confirmed by Oil Red O Staining in small intestinal cells of apoM KO mice. To confirm this observation, we conducted electron microscopy of the intestinal cells using apoM KO mice which showed increased ER lipid accumulation as well as increased cytosolic lipid droplet accumulation as compared to WT mice. We also observed dysfunction in the transport of vesicles from the ER to the Golgi in apoM KO mice as compared to WT mice. Coat protein complex II are the group of proteins responsible for this transfer, one of which is Sar1B. Other proteins in this complex include Sec12, 23, 24, 13, and 31. We measured protein levels of Sec 12, 23, and 24 and found they were significantly decreased in the small intestine of apoM KO mice but not in the liver. In addition to this, we measure the mRNA levels of Sar1B and MTP in both the liver and small intestines of WT and apoM KO mice. There was no difference between the two tissues in terms of mRNA for these proteins which indicates that the effect of apoM deficiency is at the protein level. Together, our data suggests a novel role of apoM in postprandial TG metabolism. Using apoM as a target may give a method to explore the role of dietary fat intake in lipid metabolism.
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  microRNAs in Retinal Development and Müller glia Reprogramming

  Kang, Seoyoung (2025)

  "Retinal diseases lead to visual impairments with loss of neurons and often cause blindness. Since the mammalian retina has no regenerative capability, one of attractive strategies is cell replacement, achieved by reprogramming endogenous mature cells. There are attractive molecules that regulate gene expression and are elementary during retinal development (retinogenesis), and also can induce reprogramming in mouse Müller glia (MG). MG, predominant glia in the retina, are known to have regenerative capacity naturally in fish, unlike mammalian. Recent studies demonstrated that microRNAs (miRNAs) play an important role in the embryonic phase of retinogenesis, and the set of miRNAs can induce mouse MG reprogramming into neuronal-like cells that express neuronal markers and have neuronal morphologies. The miRNAs were, however, poorly understood in the postnatal processes of retinogenesis. Furthermore, the questions include which cell types can be generated and, most importantly whether these neuronal cells are mature and functional were not answered yet. Therefore, the aims of this study were to 1) analyze the effects of loss of miRNAs in the late retinal progenitor cells (RPCs) during postnatal retinal development, to 2) evaluate the reprogramming efficiency of the RPC-miRNA miR-25 with regard to the generation of functional neurons. Aim 2 included the establishment of an improved cell culture protocol together with calcium imaging in order to investigate the functionality and maturation state of these newly generated neuronal-like cells. Aims one and two included the establishment of luciferase reporter assays to identify a possible underlying mechanism. Loss of miRNAs in late RPCs is caused by a genetic knock-out of the enzyme Dicer, required for the formation of mature, functional miRNA and Ascl1CreER:tdTomato strain (RPC reporter mouse). The tissue was examined at different timepoints and evaluated histologically. For MG reprogramming, RPC-miRNA miR-25 was overexpressed using artificially made miRNAs called mimics, in mouse primary MG. Cells were monitored and evaluated over the time course of three weeks. miRNA target gene analyses were performed to identify potential underlying mechanisms. Our data showed that loss of miRNAs in late RPC reduced populations of bipolar cells, rod photoreceptors, MG and increased an amacrine cell population. We found that miR-25 directly target amacrine cell mRNAs, Elavl3, a gene that encodes for HuC, a protein expressed in amacrine cells. Using the RPC-miRNA miR-25 to reprogram young primary MG led to a conversion of the cells to more immature cells. We show for the first time that one miRNA alone, namely miR-25, was sufficient to successfully reprogram primary MG into progenitor cells that subsequently differentiate into functional neurons. This cell conversion might be partly due to the inhibition of the neuronal repressor Rest, a direct target of miR-25. Furthermore, we found that miRNA molecules were taken up efficiently by all glia, however, not all glia were reprogrammed. This suggests that the competence state of the glia might play a role in reprogramming. Taken together, late RPC-miRNAs are essential for the proper development of late-born cells and miRNA loss leads to reduced bipolar cells, photoreceptors, and MG populations but an increase in amacrine cells. The reduced bipolar cell number might be partly due to a competent shift of the progenitors towards amacrine cell generation. Furthermore, the RPC-miRNA miR-25 alone is sufficient to successfully reprogram primary MG into progenitor cells that subsequently differentiate into functional neurons. The neuronal repressor Rest might be one of the primary key players in this process. Since miRNA molecules were taken up efficiently, remained at least 4 weeks after transfection, and no toxicity was detected, miR-25 might be a promising tool for in vivo MG reprogramming. "
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  The influence of video prompting with embedded safety checks to teach child passenger safety restraint skills

  Zonneveld, Kimberley L. M.; Rasuratnam, Niruba; Vladescu, Jason C. (Wiley, 2025-04-08)

  Motor vehicle collisions are among the leading causes of unintended injury-related deaths among children under the age of 14. The primary cause of these deaths is the improper use of child passenger safety restraints (CPSRs). Correctly installed CPSRs can decrease the risk of fatal injury by 45% to 95%. To date, no studies have used video prompting with embedded safety checks to teach correct CPSR installation and harnessing in the absence of researcher-delivered instruction and feedback. We used a concurrent multiple-baseline-across-participants design to evaluate the efficacy of a video-prompting procedure with embedded safety checks to teach four prospective parents and caregivers CPSR installation and harnessing skills. All participants learned to perform these skills, and these effects maintained for 4 weeks. Furthermore, this training improved all participants' performance of an untrained installation position, vehicle, and harnessing skill, and these effects were largely maintained for 4 weeks.

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