Open Access Publishing Fund

Permanent URI for this collection

https://hdl.handle.net/1805/6519

The IUPUI Open Access Fund underwrites reasonable publication charges for articles published in fee-based, peer-reviewed journals that are openly accessible. This fund addresses changes in scholarly communications while increasing the impact of and access to scholarship created by IUPUI faculty. Learn more at: https://library.indianapolis.iu.edu/digitalscholarship/oa/fund-oa

Annual reports on the progress of the fund are available from: https://scholarworks.indianapolis.iu.edu/handle/1805/11935

Browse

Now showing 1 - 10 of 294

The 1st International Joint Mini-Symposium on Advanced Coatings between Indiana University-Purdue University Indianapolis and Changwon National University: Preface
(2014) Zhang, Jing; Jung, Yeon-Gil
The 1st international joint mini-symposium on advanced coatings between Indiana University-Purdue University Indianapolis (IUPUI) and Changwon National University (CNU) was held on March 18-20, 2014 in Indianapolis, Indiana, USA. Research papers presented in the symposium are included in this proceeding. The symposium covered recent development in advanced coatings and related functional materials. The symposium offered the students and researchers from both universities a valuable opportunity to share a wide spectrum of new knowledge of advanced coatings and related functional materials. The research topics presented in the symposium included thermal barrier coatings, bio-related coatings, nano-materials and materials for energy conversion. The symposium enabled face-to-face discussions and developed genuine friendship, which promoted international collaboration and exchange program for researcher as well as students to carry out science work together. J.Z. would like to thank the support provided by the US Department of Energy (Grant No. DE-FE0008868, program manager Richard Dunst) and International Development Fund by the IUPUI Office of Vice Chancellor for Research. Y.G.J. acknowledges the support provided by the National Research Foundation of Korea (NRF) grant funded by the Korean Government (MSIP) (No. 2011-0030058) and the Human Resources Development Program (No. 20134030200220) of the Korea Institute of Energy Technology Evaluation and Planning (KETEP) grant funded by the Korean Government Ministry of Trade, Industry and Energy.
A Perceptual Evaluation of Music Real-Time Communication Applications
(IEEE, 2023-04-28) Goot, Dana Kemack; Chaubey, Harshit; Hsu, Timothy Y.; Deal , William Scott; Music and Arts Technology, School of Engineering and Technology
Music Real-time Communication applications (M-RTC) enable music making (musiking) for musicians simultaneously across geographic distance. When used for musiking, M-RTC such as Zoom and JackTrip, require satisfactorily received acoustical perception of the transmitted music to the end user; however, degradation of audio can be a deterrent to using M-RTC for the musician. Specific to the audio quality of M-RTC, we evaluate the quality of the audio, or the Quality of Experience (QoE), of five network music conferencing applications through quantitative perceptual analysis to determine if the results are commensurate with data analysis. The ITU-R BS.1534-3 MUlti Stimulus test with Hidden Reference and Anchor (MUSHRA) analysis is used to evaluate the perceived audio quality of the transmitted audio files in our study and to detect differences between the transmitted audio files and the hidden reference file. A comparison of the signal-to-noise ratio (SNR) and total harmonic distortion (THD) analysis to the MUSHRA analysis shows that the objective metrics may indicate that SNR and THD are factors in perceptual evaluation and may play a role in perceived audio quality; however, the SNR and THD scores do not directly correspond to the MUSHRA analysis and do not adequately represent the preferences of the individual listener. Since the benefits of improved M-RTC continue to be face-to-face communication, face-to-face musiking, reduction in travel costs, and depletion of travel time, further testing with statistical analysis of a larger sample size can provide the additional statistical power necessary to make conclusions to that end.
Acquired Factor X Deficiency without Amyloidosis Presenting with Massive Hematuria: A Case Report and Review of the Literature
(MDPI, 2023-05-15) Menakuru, Sasmith R.; Dhillon, Vijaypal S.; Salih, Ahmed; Beirat, Amir F.; Medicine, School of Medicine
Acquired factor X deficiency is a rare diagnosis, especially without the association of other co-existing conditions such as amyloidosis. The authors report the case of a 34-year-old male with severe frank hematuria found to have markedly prolonged prothrombin time and activated partial thromboplastin time. A mixing study showed correction utilizing normal plasma and a coagulation panel testing revealed decreased factor X activity. The patient was treated with multiple blood transfusions, fresh frozen plasma, high-dose pulse steroids, and rituximab. The patient’s condition improved during his 21-day hospital stay and was followed up every 2 weeks for 3 months. The patient’s factor X level recovered after two weeks of discharge with no other hemorrhagic episodes.
ACVR2B antagonism as a countermeasure to multi‐organ perturbations in metastatic colorectal cancer cachexia
(Wiley, 2020-12) Huot, Joshua R.; Pin, Fabrizio; Narasimhan, Ashok; Novinger, Leah J.; Keith, Austin S.; Zimmers, Teresa A.; Willis, Monte S.; Bonetto, Andrea; Surgery, School of Medicine
Background: Advanced colorectal cancer (CRC) is often accompanied by the development of liver metastases, as well as cachexia, a multi-organ co-morbidity primarily affecting skeletal (SKM) and cardiac muscles. Activin receptor type 2B (ACVR2B) signalling is known to cause SKM wasting, and its inhibition restores SKM mass and prolongs survival in cancer. Using a recently generated mouse model, here we tested whether ACVR2B blockade could preserve multiple organs, including skeletal and cardiac muscle, in the presence of metastatic CRC. Methods: NSG male mice (8 weeks old) were injected intrasplenically with HCT116 human CRC cells (mHCT116), while sham-operated animals received saline (n = 5-10 per group). Sham and tumour-bearing mice received weekly injections of ACVR2B/Fc, a synthetic peptide inhibitor of ACVR2B. Results: mHCT116 hosts displayed losses in fat mass ( - 79%, P < 0.0001), bone mass ( - 39%, P < 0.05), and SKM mass (quadriceps: - 22%, P < 0.001), in line with reduced muscle cross-sectional area ( - 24%, P < 0.01) and plantarflexion force ( - 28%, P < 0.05). Further, despite only moderately affected heart size, cardiac function was significantly impaired (ejection fraction %: - 16%, P < 0.0001; fractional shortening %: - 25%, P < 0.0001) in the mHCT116 hosts. Conversely, ACVR2B/Fc preserved fat mass ( + 238%, P < 0.001), bone mass ( + 124%, P < 0.0001), SKM mass (quadriceps: + 31%, P < 0.0001), size (cross-sectional area: + 43%, P < 0.0001) and plantarflexion force ( + 28%, P < 0.05) in tumour hosts. Cardiac function was also completely preserved in tumour hosts receiving ACVR2B/Fc (ejection fraction %: + 19%, P < 0.0001), despite no effect on heart size. RNA sequencing analysis of heart muscle revealed rescue of genes related to cardiac development and contraction in tumour hosts treated with ACVR2B/Fc. Conclusions: Our metastatic CRC model recapitulates the multi-systemic derangements of cachexia by displaying loss of fat, bone, and SKM along with decreased muscle strength in mHCT116 hosts. Additionally, with evidence of severe cardiac dysfunction, our data support the development of cardiac cachexia in the occurrence of metastatic CRC. Notably, ACVR2B antagonism preserved adipose tissue, bone, and SKM, whereas muscle and cardiac functions were completely maintained upon treatment. Altogether, our observations implicate ACVR2B signalling in the development of multi-organ perturbations in metastatic CRC and further dictate that ACVR2B represents a promising therapeutic target to preserve body composition and functionality in cancer cachexia.
Adipose-derived Stem Cell Conditioned Media Extends Survival time of a mouse model of Amyotrophic Lateral Sclerosis
(Nature Publishing Group, 2015-11-20) Fontanilla, Christine V.; Gu, Huiying; Liu, Qingpeng; Zhu, Timothy Z.; Johnstone, Brian H.; March, Keith L.; Pascuzzi, Robert M.; Farlow, Martin R.; Du, Yansheng; Department of Neurology, IU School of Medicine
Adipose stromal cells (ASC) secrete various trophic factors that assist in the protection of neurons in a variety of neuronal death models. In this study, we tested the effects of human ASC conditional medium (ASC-CM) in human amyotrophic lateral sclerosis (ALS) transgenic mouse model expressing mutant superoxide dismutase (SOD1(G93A)). Treating symptomatic SOD1(G93A) mice with ASC-CM significantly increased post-onset survival time and lifespan. Moreover, SOD1(G93A) mice given ASC-CM treatment showed high motor neuron counts, less activation of microglia and astrocytes at an early symptomatic stage in the spinal cords under immunohistochemical analysis. SOD1(G93A) mice treated with ASC-CM for 7 days showed reduced levels of phosphorylated p38 (pp38) in the spinal cord, a mitogen-activated protein kinase that is involved in both inflammation and neuronal death. Additionally, the levels of α-II spectrin in spinal cords were also inhibited in SOD1(G93A) mice treated with ASC-CM for 3 days. Interestingly, nerve growth factor (NGF), a neurotrophic factor found in ASC-CM, played a significant role in the protection of neurodegeneration inSOD1(G93A) mouse. These results indicate that ASC-CM has the potential to develop into a novel and effective therapeutic treatment for ALS.
Adolescent Health-Risk Behavior and Community Disorder
(2013-11) Wiehe, Sarah E.; Kwan, Mei-Po; Wilson, Jeffrey S.; Fortenberry, J. Dennis
Background Various forms of community disorder are associated with health outcomes but little is known about how dynamic context where an adolescent spends time relates to her health-related behaviors. Objective Assess whether exposure to contexts associated with crime (as a marker of community disorder) correlates with self-reported health-related behaviors among adolescent girls. Methods Girls (N = 52), aged 14–17, were recruited from a single geographic urban area and monitored for 1 week using a GPS-enabled cell phone. Adolescents completed an audio computer-assisted self-administered interview survey on substance use (cigarette, alcohol, or marijuana use) and sexual intercourse in the last 30 days. In addition to recorded home and school address, phones transmitted location data every 5 minutes (path points). Using ArcGIS, we defined community disorder as aggregated point-level Unified Crime Report data within a 200-meter Euclidian buffer from home, school and each path point. Using Stata, we analyzed how exposures to areas of higher crime prevalence differed among girls who reported each behavior or not. Results Participants lived and spent time in areas with variable crime prevalence within 200 meters of their home, school and path points. Significant differences in exposure occurred based on home location among girls who reported any substance use or not (p 0.04) and sexual intercourse or not (p 0.01). Differences in exposure by school and path points were only significant among girls reporting any substance use or not (p 0.03 and 0.02, respectively). Exposure also varied by school/non-school day as well as time of day. Conclusions Adolescent travel patterns are not random. Furthermore, the crime context where an adolescent spends time relates to her health-related behavior. These data may guide policy relating to crime control and inform time- and space-specific interventions to improve adolescent health.
An Adolescent with a Rare De Novo Distal Trisomy 6p and Distal Monosomy 6q Chromosomal Combination
(Hindawi, 2020-08-31) Peterman, Leia A.; Vance, Gail H.; Conboy, Erin E.; Anderson, Katelynn; Weaver, David D.; Medical and Molecular Genetics, School of Medicine
We report on a 12-year-old female with both a partial duplication and deletion involving chromosome 6. The duplication involves 6p25.3p24.3 (7.585 Mb) while the deletion includes 6q27q27 (6.244 Mb). This chromosomal abnormality is also described as distal trisomy 6p and distal monosomy 6q. The patient has a Chiari II malformation, hydrocephalus, agenesis of the corpus callosum, microcephaly, bilateral renal duplicated collecting system, scoliosis, and myelomeningocele associated with a neurogenic bladder and bladder reflux. Additional features have included seizures, feeding dysfunction, failure to thrive, sleep apnea, global developmental delay, intellectual disability, and absent speech. To our knowledge, our report is just the sixth case in the literature with concomitant distal 6p duplication and distal 6q deletion. Although a majority of chromosomal duplication-deletion cases have resulted from a parental pericentric inversion, the parents of our case have normal chromosomes. This is the first reported de novo case of distal 6p duplication and distal 6q deletion. Alternate explanations for the origin of the patient's chromosome abnormalities include parental gonadal mosaicism, nonallelic homologous recombination, or potentially intrachromosomal transposition of the telomeres of chromosome 6. Nonpaternity was considered but ruled out by whole exome sequencing analysis.
Advanced glycation end (AGE) product modification of laminin downregulates Kir4.1 in retinal Müller cells
(PLOS, 2018-02-23) Thompson, Kayla; Chen, Jonathan; Luo, Qianyi; Xiao, Yucheng; Cummins, Theodore R.; Bhatwadekar, Ashay D.; Ophthalmology, School of Medicine
Diabetic retinopathy (DR) is a major cause of adult blindness. Retinal Müller cells maintain water homeostasis and potassium concentration via inwardly rectifying Kir4.1 channels. Accumulation of advanced glycation end products (AGEs) is a major pathologic event in DR. While diabetes leads to a decrease in the Kir4.1 channels, it remains unknown whether AGEs-linked to the basement membrane (BM) affect normal Kir4.1 channels. For this study, we hypothesized that AGE-modification of laminin is detrimental to Kir4.1 channels, therefore, disrupting Müller cell function. The AGE-modified laminin-coated substrates were prepared by incubating Petri-dishes with laminin and methylglyoxal for seven days. The rat Müller cells (rMC-1) were propagated on AGE-modified laminin, and Kir4.1 expression and function were evaluated. Quantification of AGEs using ELISA revealed a dose-dependent increase in methylglyoxal-hydro-imidazolone adducts. The rMC-1 propagated on AGE-modified laminin demonstrated a decrease in Kir4.1 levels in immunofluorescence and western blot studies and a decrease in the Kir4.1 channel function. Kir4.1 decrease on AGE-modified laminin resulted in a disorganization of an actin cytoskeleton and disruption of α-dystroglycan-syntrophin-dystrophin complexes. Our studies suggest that AGE-modification of laminin is detrimental to Kir4.1 channels. By studying the role of AGEs in Kir4.1 channels we have identified a novel mechanism of Müller cell dysfunction and its subsequent involvement in DR.
The adverse childhood experiences questionnaire: Two decades of research on childhood trauma as a primary cause of adult mental illness, addiction, and medical diseases
(Taylor & Francis, 2019-01-01) Zarse, Emily M.; Neff, Mallory R.; Yoder, Rachel; Hulvershorn, Leslie; Chambers, Joanna E.; Chambers, R. Andrew; Psychiatry, School of Medicine
Objective. In 1998, Felitti and colleagues published the first study of the Adverse Childhood Experiences-Questionnaire (ACE-Q), a 10-item scale used to correlate childhood maltreatment and adverse rearing contexts with adult health outcomes. This paper qualitatively reviews nearly two decades of research utilizing the ACE-Q, highlighting its contribution to our understanding of the causal roots of common, interlinked comorbidities of the brain and body.Methods. An OVID/PubMed search was conducted for English language articles published before 2016, containing the phrase “Adverse Childhood Experiences” in which the ACE-Q was utilized. Source review included a manual search of bibliographies, resulting in 134 articles, including 44 based on the original ACE-Q study population.Results. ACE-Q research has demonstrated that exposures to adverse childhood experiences converge dose-dependently to potently increase the risk for a wide array of causally interlinked mental illnesses, addictions, and multi-organ medical diseases. The intergenerational transmission of this disease burden via disrupted parenting and insecure rearing contexts is apparent throughout this literature. However, the ACE-Q does not tease out genetic or fetal drug exposure components of this transmission.Conclusions. Adverse childhood experiences and rearing may generate a public health burden that could rival or exceed all other root causes. Translating this information to health-care reform will require strengthening brain-behavioral health as core public and preventative health-care missions. Greater integration of mental health and addiction services for parents should be accompanied by more research into brain mechanisms impacted by different forms and interactions between adverse childhood experiences.
Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum
(Nature Publishing group, 2018-04-03) Muñoz, Braulio; Fritz, Brandon M.; Yin, Fuqin; Atwood, Brady K.; Psychiatry, School of Medicine
Drugs of abuse, including alcohol, ablate the expression of specific forms of long-term synaptic depression (LTD) at glutamatergic synapses in dorsal striatum (DS), a brain region involved in goal-directed and habitual behaviors. This loss of LTD is associated with altered DS-dependent behavior. Given the role of the µ-opioid receptor (MOR) in behavioral responding for alcohol, we explored the impact of alcohol on various forms of MOR-mediated synaptic depression that we find are differentially expressed at specific DS synapses. Corticostriatal MOR-mediated LTD (mOP-LTD) in the dorsolateral striatum occurs exclusively at inputs from anterior insular cortex and is selectively disrupted by in vivo alcohol exposure. Alcohol has no effect on corticostriatal mOP-LTD in dorsomedial striatum, thalamostriatal MOR-mediated short-term depression, or mOP-LTD of cholinergic interneuron-driven glutamate release. Disrupted mOP-LTD at anterior insular cortex–dorsolateral striatum synapses may therefore be a key mechanism of alcohol-induced neuroadaptations involved in the development of alcohol use disorders., µ-opioid receptors (MOR) are known to modulate the reward effects of drugs of abuse, and MOR activation induces long-term depression (LTD) at striatal synapses. Here the authors show that alcohol exposure disrupts MOR-induced LTD only at specific cortical inputs to the striatum.

Browse

Browsing Open Access Publishing Fund by Title

Results Per Page

Sort Options