Is Genetic Drift to Blame for Testicular Dysgenesis Syndrome in Semliki Chimpanzees (Pan Troglodytes Schweinfurthii)?
Schöpfer:
Rich, Alicia M., Hunt, Kevin D., Breeden, Scott K. OMS-4, Wasserman, Michael D., Kaestle, Frederika, and Deimel, Caroline
Related Url Tesim:
Full Text available at the following URL: https://onlinelibrary.wiley.com/doi/abs/10.1111/jmp.12352
Beschreibung:
Background We present 3 likely cases of testicular dysgenesis syndrome (TDS) within a community of chimpanzees (<em>Pan troglodytes schweinfurthii</em>). We tested whether genetic drift may be the culprit, as a genetic cause has been suspected to account for TDS among other wildlife. Methods: We successfully sequenced a 367?bp segment spanning the first hypervariable region within the D?loop of the mitochondrial genome for 78 DNA samples. Results: We found 24 polymorphic sequence sites consisting of 7 singletons and 17 parsimony informative sites. This sample contained 9 haplotypes with a diversity index of 0.78 (SD = 0.03). All tests against the null hypothesis of neutral polymorphisms were non?significant (<em>P</em> > .10). The mismatch distribution of pairwise differences does not fit a Poisson's curve (raggedness index = 0.166; SSD = 0.12; <em>P</em> = 1). Conclusions: Thus, we found no significant signs of genetic isolation, population expansion, or genetic bottleneck. Alternative causes of TDS and how they might pertain to this population are discussed.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Identifikator:
https://doi.org/10.1111/jmp.12352
Ressourcentyp:
Article
Stichwort:
Primatology, Testicular Dysgenesis Syndrome, and Chimpanzees
Choe, David, MacLean, A. G., and Delery, Elizabeth
Related Url Tesim:
available from the library catalog: https://marianunivindianapolis.on.worldcat.org/oclc/9462337632 and Available from the publisher: https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2022.36.S1.L6382
Beschreibung:
Klotho is a regulatory anti-aging protein that is significantly expressed in the choroid plexus, plays an important role in regulating the immune response in the CNS, and diminishes with age. It is known that a decline of klotho expression has been linked to significant neuroinflammation, oxidative damage in the neural parenchyma, and decline in neurocognitive functions. As the choroid plexus is a known reservoir for latent Human Immunodeficiency Virus (HIV) infection, the relationship between HIV and klotho expression could be a cause of the neurocognitive dysfunction that accompanies HIV infections. The objective of this project was to observe levels of klotho expression in the choroid plexus in a Simian Immunodeficiency Virus (SIV) model of HIV infection, as well as to determine a pattern of age-related decline in klotho expression. To carry out the study, Choroid plexus samples of Rhesus macaques of various ages and SIV-infection status were studied. The tissues were stained using immunohistochemistry for polyclonal klotho, structural proteins (vimentin), and nuclei (DAPI), and imaged at varying magnifications of 4x, 10x, and 40x. The images obtained were then analyzed using the fluorescent imaging software Fiji. The epithelial cells of the choroid plexus were measured for their fluorescence intensity to measure their relative klotho expression levels. Although klotho expression was varied in the uninfected Rhesus macaques, there was an overall decreasing trend with the advancement of age. In SIV-infected Rhesus macaques, the choroid plexus had significantly less klotho expression than the uninfected control group regardless of age (p=0.01). Analysis of the uninfected data shows that there was a decreasing pattern of klotho expression in Rhesus macaques. The variability of klotho levels in the uninfected individuals can be attributed to genetic variations between individuals. However, SIV infection significantly reduced klotho expression in the choroid plexus in comparison to uninfected individuals. This decrease in klotho expression was regardless of age. The exact mechanism in which SIV diminishes klotho expression is unknown and additional studies are warranted to examine this phenomenon.
Publisher Note: This is the full abstract presented at the Experimental Biology meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Herausgeber:
Federation of American Societies for Experimental Biology (FASEB)
immune response, regulatory anti-aging protein, Simian Immunodeficiency Virus (SIV) model of HIV infection, and latent Human Immunodeficiency Virus (HIV) infection
Loss of the Nutrient Sensor TAS1R3 Leads to Reduced Bone Resorption
Schöpfer:
Arthur, Jon, Shively, Stephen R, Wauson, Eric M, Shor, Ryann, Newby, Jordan B, Davis, Hannah M, Plattes, Maggie M, Eaton, Michael S., Weinstein, Nicholas, Nathan, Justin, Foster, Hanna E, Ward, Taylor D, Broege, Aaron, Lowery, Jonathan W. Ph.D., Plotkin, Lilian I, and Dewar, Brian J
Related Url Tesim:
Full Text Available at the following address: https://link.springer.com/article/10.1007/s13105-017-0596-7
Beschreibung:
The taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient status. TAS1R member 3 (TAS1R3) is a bi-functional protein that recognizes amino acids such as L-glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. It was recently reported that deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass but the underlying cellular mechanism leading to this phenotype remains unclear. Here, we independently corroborate the increased thickness of cortical bone in femurs of 20-week-old male Tas1R3 mutant mice and confirm that Tas1R3 is expressed in the bone environment. Tas1R3 is expressed in undifferentiated bone marrow stromal cells (BMSCs) in vitro and its expression is maintained during BMP2-induced osteogenic differentiation. However, levels of the bone formation marker procollagen type I N-terminal propeptide (PINP) are unchanged in the serum of 20-week-old Tas1R3 mutant mice as compared to controls. In contrast, levels of the bone resorption marker collagen type I C-telopeptide are reduced greater than 60% in Tas1R3 mutant mice. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and their expression levels positively correlate with differentiation status. Collectively, these findings suggest that high bone mass in Tas1R3 mutant mice is due to uncoupled bone remodeling with reduced osteoclast function and provide rationale for future experiments examining the cell-type-dependent role for TAS1R family members in nutrient sensing in postnatal bone remodeling.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Identifikator:
10.1007/s13105-017-0596-7
Ressourcentyp:
Article
Stichwort:
Taste receptor, Osteoclast, TAS1R3, Bone, TAS1R1, Osteoblast, and TAS1R2
Malnutrition Screening and Treatment in Pediatric Oncology: A systematic review
Schöpfer:
Runco, D.V., Bishop, Chris, and Franke, Jessica
Related Url Tesim:
Available from vthe publisher: https://www.researchsquare.com/article/rs-1499120/v1
Beschreibung:
Purpose: Malnutrition and cachexia during pediatric cancer treatment worsen toxicity and quality-of-life. Clinical practice varies with lack of standard malnutrition definition and nutrition interventions. This systematic review highlights available malnutrition screening and intervention data in childhood cancer and the need for standardizing assessment and treatment. Methods:
Ovid Medline, CINAHL, and Cochrane Library were searched for studies containing malnutrition as the primary outcome with anthropometric, radiographic, or biochemical measurements. Secondary outcomes included validated nutritional assessment or screening tools. Two authors reviewed full manuscripts for inclusion. Narrative analysis was chosen over statistical analysis due to study heterogeneity. Results: The search yielded 234 articles and 17 articles identified from external sources. Nine met inclusion criteria with six nutritional intervention studies (examining appetite stimulants, nutrition supplementation, and proactive feeding tubes) and three nutritional screening studies (algorithms or nutrition support teams) each with variable measures and outcomes. Both laboratory evaluations (albumin, prealbumin, total protein) and body measurement (weight loss, mid-upper arm circumference) were used. Studies demonstrated improved weight, without difference between formula or appetite stimulant used. Screening studies yielded mixed results on preventing weight loss, weight gain, and survival. Conclusion: Our review demonstrated a paucity of evidence for malnutrition screening and intervention in pediatric cancer treatment. While a variety of malnutrition outcomes, interventions, and screening tools exist, nutritional interventions increased weight and decreased complications. Screening tools decreased malnutrition risk and may improve weight gain. Potential age- and disease-specific nutritional benefits and toxicities also exist, further highlighting the benefit of standardizing malnutrition definitions, screening, and interventions. This is a preprint submission.
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http://rightsstatements.org/vocab/InC/1.0/
Lizenz:
https://creativecommons.org/licenses/by/4.0/
Sprache:
English
Herausgeber:
Research Square
Identifikator:
DOI: https://doi.org/10.21203/rs.3.rs-1499120/v1
Ressourcentyp:
Article
Stichwort:
cancer cachexia, nutrition, malnutrition, and pediatric
Malnutrition Screening and Treatment in Pediatric Oncology: A systematic review
Schöpfer:
Runco, D.V., Bishop, Chris, and Franke, Jessica
Beschreibung:
Pediatric cancer is the leading cause of non-accidental childhood death in the United States[34]. 80% of children experience malnutrition during cancer treatment[34]. Malnutrition effects with cancer treatment: increases toxicities (neuropathy, infections, physical function, quality of life)[10]. Exacerbates dietary and metabolic changes[5,30]. Malnutrition is variable in diagnosis and interventions. Standard screening and treatment are not widely agreed upon in pediatrics[25]. Adult cancer cachexia is more studied and standardized [29]. Nutritional needs are more static in adults, while protein and caloric needs change and evolve for the growing child [4]. This systematic review aims to: summarize evidence-based studies of screening and nutritional intervention for children with cancer; highlight the need for standardizing malnutrition assessment and treatment.
Erklärung der Rechte:
http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Ressourcentyp:
Poster
Stichwort:
Malnutrition Screening, nutritional intervention , and Pediatric cancer
The Metabolic Bone Disease X-linked Hypophosphatemia: Case Presentation, Pathophysiology and Pharmacology
Schöpfer:
Vincze, Jon, Hum, Julia, Conaway, Kory, Skinner, Brian, Tucker, Katherine, and Lowery, Jonathan
Related Url Tesim:
Available from the publisher: https://www.mdpi.com/2075-1729/11/6/563 and Available from PubMed Central: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8232744/
Beschreibung:
The authors present a stereotypical case presentation of X-linked hypophosphatemia (XLH) and provide a review of the pathophysiology and related pharmacology of this condition, primarily focusing on the FDA-approved medication burosumab. XLH is a renal phosphate wasting disorder caused by loss of function mutations in the PHEX gene (phosphate-regulating gene with homologies to endopeptidases on the X chromosome). Typical biochemical findings include elevated serum levels of bioactive/intact fibroblast growth factor 23 (FGF23) which lead to (i) low serum phosphate levels, (ii) increased fractional excretion of phosphate, and (iii) inappropriately low or normal 1,25-dihydroxyvitamin D (1,25-vitD). XLH is the most common form of heritable rickets and short stature in patients with XLH is due to chronic hypophosphatemia. Additionally, patients with XLH experience joint pain and osteoarthritis from skeletal deformities, fractures, enthesopathy, spinal stenosis, and hearing loss. Historically, treatment for XLH was limited to oral phosphate supplementation, active vitamin D supplementation, and surgical intervention for cases of severe bowed legs. In 2018, the United States Food and Drug Administration (FDA) approved burosumab for the treatment of XLH and this medication has demonstrated substantial benefit compared with conventional therapy. Burosumab binds circulating intact FGF23 and blocks its biological effects in target tissues, resulting in increased serum inorganic phosphate (Pi) concentrations and increased conversion of inactive vitamin D to active 1,25-vitD.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Herausgeber:
MDPI
Identifikator:
PMID: 34203792 and DOI: 10.3390/life11060563
Ressourcentyp:
Article
Stichwort:
burosumab, Crysvita®, KRN23, metabolic bone disease, and X-linked hypophosphatemia
A method to switch from oral dopamine agonists to rotigotine in patients with restless legs syndrome and mild augmentation.
Schöpfer:
Winkelman, John W., Schoerning, Laura, Platt, Samuel, Mei, Leslie A, and Mackie, Susan E
Related Url Tesim:
Article available at the following URL: https://www.ncbi.nlm.nih.gov/pubmed/27810181
Beschreibung:
BACKGROUND: We examined the short- and long-term efficacy and tolerability of a cross-titration algorithm from oral dopamine agonists to the rotigotine transdermal patch in patients dissatisfied with their restless legs syndrome (RLS) treatment, predominantly with mild augmentation. METHODS: Patients with RLS (n?=?20) were recruited at a single site. The cross-titration consisted of decreasing oral dopaminergic agents (ropinirole by 1?mg or pramipexole by 0.25?mg) and increasing rotigotine by 1?mg every two days. Efficacy and adverse events (AEs) were assessed at one, three, six and 12 months after the switch. RESULTS: Patients had moderate-severe RLS symptoms at the baseline (mean international restless legs syndrome (IRLS) score 19.4?±?5.5); 85% had augmentation and 45% reported afternoon RLS symptoms. The baseline mean pramipexole equivalent dose was 0.6?±?0.3?mg. At Week 5, 85% (17/20) had successfully switched from their oral dopamine agonist to rotigotine (mean dose 2.5?±?0.6?mg; change in IRLS score: -6.7?±?8.4, p?=?0.002); 14 patients were CGI-I responders (much or very much improved). Three patients withdrew due to lack of efficacy. Twelve months after cross-titration, 10 patients continued on rotigotine, of whom four required either higher doses of rotigotine or supplemental RLS medication compared with their optimal Week 5 dose; five patients withdrew due to AEs and two due to lack of efficacy. CONCLUSION: A cross-titration to rotigotine was efficacious after five weeks in 70% of patients dissatisfied with RLS treatment, most of whom had mild augmentation. At one year following the medication switch, 50% had discontinued rotigotine due to lack of continued efficacy or side effects.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Identifikator:
10.1016/j.sleep.2016.05.004
Ressourcentyp:
Article
Stichwort:
Thiophenes, Severity of Illness Index, Administration, Restless Legs Syndrome, Transdermal Patch, Dopamine Agonists, Time Factors, Tetrahydronaphthalenes, Benzothiazoles, and Drug Synergism
Mitigation of stomach dehiscence risk during gastrostomy tube changes - a retrospective analysis of patient outcomes.
Schöpfer:
Smith, David A and Blocher-Smith, Ethan Charles OMS III
Related Url Tesim:
Full Text Available at the following address: https://pubmed.ncbi.nlm.nih.gov/27670959/
Beschreibung:
INTRODUCTION: Stomach dehiscence from the abdominal wall is a serious and potentially life-threatening complication of gastrostomy tube changes. This retrospective study evaluates gastric aspiration as an inexpensive and safe alternative to endoscopic or radiographic confirmation. METHODS: From August 1998 to June 2016, 682 patients (301 female, 381 male) underwent 1713 gastrostomy tube changes in the medical setting, with an average age of 7.59years and an average site age of 3.43years. The most common diagnoses were GERD (304), aspiration (168), and failure to thrive (143). RESULTS: All newly inserted tubes were aspirated to visually inspect for gastric fluid. This procedure as a confirmatory test for intragastric placement was found to have a positive predictive value of 99.5% and negative predictive value of 77.8%, with a sensitivity of 99.8% and specificity of 63.6%. In cases with successful aspiration of gastric fluid, 75.5% of changes resulted in no complications, with intraperitoneal insertion or leak in only 0.48% of cases. CONCLUSIONS: Positive gastric aspirate is a strong predictor of proper G-tube placement with high sensitivity, eliminating the requirement of specialized equipment and the cost associated with endoscopic or radiographic guidance, and has a comparable or superior risk profile. LEVELS OF EVIDENCE: Study of diagnostic test level II.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Identifikator:
10.1016/j.jpedsurg.2016.09.004
Ressourcentyp:
Conference Proceeding
Stichwort:
Intubation, Gastrostomy, Enteral Nutrition, Retrospective Studies, Stomach Diseases, and Gastrointestinal
Mouse Model of Marfan Syndrome Accelerates Aneurysmal Formation through Well-Characterized TGF-? Signaling Pathways
Schöpfer:
Turek, JW, Qian, L, Westergaard, NM, Cavanaugh, Nicholas B., and Dyle, MC
Beschreibung:
Marfan syndrome (MFS) represents a genetic disorder with ranging clinical presentation, most notably ascending aortic aneurysms. There has been extensive research to elucidate the mechanistic biochemistry of this disease. In this regard, the abundance of TGF-? from a mutation in fibrillin-1 is the suggested etiology. Many important signaling pathways downstream of TGF-? have been well-characterized. Our laboratory has previously demonstrated a unique murine model of MFS resulting in the accelerated formation of ascending aortic aneurysms. This study aims to characterize the relevance of this model to known signaling mechanisms in MFS.
Muscle-derived factors influencing bone metabolism
Schöpfer:
Zysik, Victoria S., Gries, Kevin, Jobe, Tyler K., Leeds, Benjamin P., Lowery, Jonathan W., and Griffin, Nicole
Related Url Tesim:
Available for request from the library catalog: https://marianunivindianapolis.on.worldcat.org/oclc/9415331686, Available from PubMed: https://pubmed.ncbi.nlm.nih.gov/34756782/, and Available from the publisher: https://www.sciencedirect.com/science/article/abs/pii/S108495212100272X?via%3Dihub
Beschreibung:
A significant amount of attention has been brought to the endocrine-like function of skeletal muscle on various tissues, particularly with bone. Several lines of investigation indicate that the physiology of both bone and muscle systems may be regulated by a given stimulus, such as exercise, aging, and inactivity. Moreover, emerging evidence indicates that bone is heavily influenced by soluble factors derived from skeletal muscle (i.e., muscle-to-bone communication). The purpose of this review is to discuss the regulation of bone remodeling (formation and/or resorption) through skeletal muscle-derived cytokines (hereafter myokines) including the anti-inflammatory cytokine METRNL and pro-inflammatory cytokines (e.g., TNF-α, IL-6, FGF-2 and others). Our goal is to highlight possible therapeutic opportunities to improve muscle and bone health in aging.
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http://rightsstatements.org/vocab/InC/1.0/
Sprache:
English
Herausgeber:
Elsevier
Identifikator:
PMID: 34756782 and DOI: 10.1016/j.semcdb.2021.10.009
Ressourcentyp:
Article
Stichwort:
anti-inflammatory cytokine METRNL, bone remodeling, muscle-to-bone communication, myokine, skeletal muscle-derived cytokines, and crosstalk