bluuebunny/crossref_metadata_2025_split huggingface dataset:
Barrels of Monkeys: Effects of Long‐term Ethanol Storage on Volar Fat Pad Morphology
Authors: Kingston Amanda Kathryn 
Published: June 2021

Museum fluid collections preserve tissues from endangered and protected species for study. Tissues are often fixed in 10% buffered formalin to halt metabolic activities and transferred to a solution of ethanol for long term storage. This process, however, forces water from the tissues and has been shown to alter the morphology of preserved specimens in ways that may influence the biological interpretation of results. The degree to which fluid preservation alters morphology is linked to multiple biological and methodological factors and should therefore be examined prior to functional analysis. This study was conducted as part of an evaluation of mammalian volar pad morphology and comprises two analyses. In the first, a sample of rats (Rattus norvegicus) is utilized to evaluate longitudinal changes in the dimensions of the volar pads across fixation in 10% buffered formalin and preservation in 70% ethanol for one year. In the second, a cross‐sectional sample of fresh primate volar pads from varying species is compared to a corresponding sample from museum specimens fixed in 10% buffered formalin and preserved in 70% ethanol. No significant changes to the measured dimensions of the volar pads are present across stages of fixation and preservation, nor are significant differences evident between fresh and preserved specimen groups. These findings are likely related to the anhydrous nature of the volar fat pads and their confined position between major joints.Support or Funding InformationThis work was funded by NSF Doctoral Dissertation Improvement Grant #1128861.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Neurovasculature of the Upper Extremity in the Aye‐aye, Daubentonia madagascariensis
Authors: Avakian Melody , Townsend K.E. Beth , Smith Heather F. 
Published: June 2021

The aye‐aye, Daubentonia madagascariensis, is an arboreal lemuroid primate and is the sole representative of its genus. The aye‐aye has unique anatomical characteristics including a thin, long, flexible third digit, unique dental anatomy, a single pair of inguinal mammary glands, greater brain size than those of other strepsirrhines, and large mobile ears that separate it from other lemuroids and make it an interesting organism to study from an anatomical, developmental, and evolutionary standpoint. The aye‐aye also has a distinctive method of obtaining its food from trees known as percussive foraging, which entails tapping on wood with its long middle finger, listening to the resulting sounds to determine the locations of cavities that may contain larvae, and then scooping out the larvae with its specialized third digit. The bony and muscular anatomy of the brachium, antebrachium, and manus of the aye‐aye has been previously studied and described in detail. However, there have been no studies that have described and depicted the complete neurovasculature of the forelimb of the aye‐aye, including the important brachial plexus. Given the unique anatomy and behavioral forelimb adaptations of this species, understanding the various nerves and blood vessels in relation to the musculature will provide a more complete picture of aye‐aye functional morphology and comparative anatomy.This study identifies and describes the neurovasculature of the forelimb of the aye‐aye with emphasis placed on the musculature and neurovasculature on the hand. The forelimbs from one female Daubentonia madagascariensis were dissected, photographed, and described in detail. In this specimen, we confirmed that the anatomy of the forelimb muscles was generally consistent with previous descriptions, although we observed a few minor variations. The brachial plexus was found to originate from the C5‐T2 roots, a feature that has also been observed in other lemurs and rhesus monkeys. The large deltoid and brachioradialis muscles observed in this specimen may serve to support the frequent use of head‐first descent, which requires a robust shoulder girdle and specific alterations in hand and body position that allow the forelimbs to undergo increased compressive forces. Future studies will analyze the development of the muscles of the arm and hand, along with the vasculature that migrated with them, and also compare them to the developmental patterns of related primates which can give insight into the aye‐aye's specialized adaptations.Support or Funding InformationThis research was supported by a Midwestern University Kenneth A. Suarez summer research fellowship to MA.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
NGF and VEGF expressions on crushed sciatic nerve treated with laser therapy and latex protein
Authors: Dias Fernando Jose , Fazan Valéria Paula Sassoli , Iyomasa Mamie Mizusaki , Borie Eduardo , Coutinho‐Netto Joaquim , Watanabe Ii‐sei 
Published: June 2021

Lesions that affect peripheral nerves still is a challenge in medical sciences. In this context, previous studies employing low‐level laser therapy (LLLT) and natural latex protein (Hevea brasiliensis, F1) revealed promising results in nerve regeneration.The aim of this study was to analyze the effects of LLLT associated with F1 protein applied in sciatic nerve crush injury (15 kgf, 10 min.) in male rats. The animals (♂, 250 g) were allocated in 6 groups (n=5): C ‐ Control; E ‐ exposed nerve without injury; I ‐ injured nerve without treatment; L ‐ injured nerve treated with LLLT (15 J/cm2, 780 nm); F1 ‐ injured nerve treated with F1 application (0.1%); and L&F1 ‐ injured nerve treated with the LLLT and F1 protein. After 4 and 8 weeks of nerve injury the animals were euthanized by anesthetic overdose and cardiac perfusion (glutaraldehyde 2.5%, PBS 0.1, pH 7.4), the sciatic nerve samples were collected and processed. Quantitative morphological parameters (myelin and capillary density) and immunohistochemical reactions (peroxidase) for nerve growth factor (NGF) and vascular endothelium growth factor (VEGF) were performed and analyzed.After 4 weeks in the injured groups (I, L, F1 and L&F1) was observed a significant reduction in myelin density. After 8 weeks the treated groups showed improvements compared to the previous period, the F1 and L&F1 groups presented values similar to the non‐injured groups (C and E). Capillary density was significantly higher in the F1 and L&F1 groups after 8 weeks of nerve damage. NGF was present in the injured groups (I, L, F1, L&F1) after 4 weeks, the group I showed the highest and the F1 group revealed the lowest positive expressions. VEGF was present in all study groups, showing more intense expressions in the injured groups, especially after 4 weeks of lesion in the F1 and L&F1 groups. After 8 weeks all the groups reduced the marking intensity.It was concluded that the nerve injury crushing results in a reduction in myelin density. NGF is mainly expressed when nerve tissue is injured. The treatments were effective in the improvements of the morphological parameters analyzed. The F1 protein presented the best quantitative results and an increase in vascular density when applied alone or in association with LLLT. In addition, the less intense NGF expression after 4 weeks associated with morphological improvement in group F1 suggests the acceleration of sciatic nerve recovery.Support or Funding InformationFunding: FAPESP 2014/07253‐4This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
High Resolution X‐ray Micro‐Tomography of the Posterior Ampullary Nerve
Authors: LABROUSSE Marc , BLANCHOT Delphine , DUBERNARD Xavier , SETTEMBRE Nicla , AVISSE Claude , DEVY Jerôme , RENARD Yohann 
Published: June 2021

IntroductionThe posterior ampullary (singular) nerve runs from the posterior ampulla to the saccular nerve (forming the inferior vestibular nerve) through the singular canal of Morgagni in temporal bone. Posterior ampullary neurectomy can be proposed in a few chronically disabling benign paroxysmal positional vertigo. The purpose of this study is to investigate the surgical anatomy of the posterior ampullary nerve using 3D reconstructions high resolution X‐ray micro‐tomography.Materials and Methods10 human petrous parts of temporal bones were fixed with Winckler's solution. CT images were acquired with a CT scanner (Skyscan 1076, Bruker, Kontich, Belgium). The camera was continuously rotated by 180° and the following parameters were used for acquisition: 50 kV, 0.5 mm Al filter, 200 A source current, 35 m isotropic resolution, 180 ms exposure time, and 0.7° rotation step. The projections were reconstructed with a filtered backprojection algorithm in Skyscan software (NRecon, Skyscan). Reconstructed images were analyzed with ORS Visual software (v1.5, Montreal) which allowed multiple display and post‐processing possibilities (3D VR; orthogonal/curved multiplanar reformation).Results and DiscussionThree‐dimensional and multiplanar studies of the singular canal of Morgagni morphology were possible with appropriate thresholding. The topographical correlations between the posterior ampullary nerve, posterior semicircular canal and the round window were evaluated. The level of the nerve in comparison with the round window may vary. Three types of positions are described. Type 1 is the lowest position: the nerve is located under the inferior part of the scala tympani. Type 3 is the highest position: the nerve is located higher than the superior part of the round window (this type goes straight from the internal auditory canal to the posterior ampulla). Type 2 is an intermediate form. Difficulty level in singular neurectomy depends on the course of the singular nerve. Type 1 is the easiest to operate on with the lowest risk, whereas type 2 and particularly type 3 are riskier in terms of damage to the round window membrane.Conclusion3D reconstructions using high resolution X‐ray micro‐tomography aid comprehension of posterior ampullary nerve complex anatomy. Transtympanal posterior ampullary neurectomy can be performed only in selective cases.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Elucidating the Role of α3‐containing Nicotinic Acetylcholine Receptors (nAChRs) in Anxiety Behavior
Authors: Smith Ciearra B. , Tapper Andrew R. , Gardner Paul D. 
Published: June 2021

More than 260 million people suffer from anxiety disorder, thus it is important to understand the molecular mechanisms underlying anxiety disorder in order to develop more treatments. Studies showed that nicotinic acetylcholine receptors (nAChRs) play a role in anxiety‐related behaviors. nAChRs are ligand‐gated cation channels that bind the endogenous neurotransmitter acetylcholine for activation. There are eleven mammalian neuronal nAChR subunits, α2‐α7, α9, α10 and β2‐β4, which are encoded by the CHRNA2‐CHRNA7, CHRNA9, CHRNA10, and CHRNB2‐B4 genes. These subunits co‐assemble to form functional homopentamers or heteropentamers consisting of various combinations of alpha and beta subunits. nAChRs are highly expressed in the habenulo‐interpeduncular pathway, a brain circuit that is involved with negative emotional state. Although knockout studies identified nAChRs as key players in anxiety‐related behaviors, little is known regarding the physiological relevance of α3‐containing nAChRs in anxiogenic behaviors due to α3 nAChR subunit knockout mice being inviable shortly after birth. I plan to test the physiological role of α3‐containing nAChRs in anxiety‐related behaviors by knocking down α3 nAChR subunits in the medial habenula (MHb) or interpeduncular nucleus (IPN) of 6‐week old mice and subsequently testing for anxiogenic behaviors. Here, I present approximately 45% and 80% knockdown of Chrna3 mRNA expression in Neuro‐2A (N2A) cells by lentiCRISPRv2‐sgRNA20 and shRNA 8843, respectively. Chrna3 mRNA levels were measured by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR). Thus, both CRISPR and shRNA approaches produced significant reduction of Chrna3 mRNA expression and can be applied in vivo to knockdown α3 nAChR subunit expression. My findings may identify α3‐containing nAChRs as novel targets for anxiety disorder therapies.Support or Funding InformationNIH Award Number: DA035371This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effect of Alaskan low bush cranberry on alpha‐synuclein overexpression in a transgenic model of C. elegans
Authors: Lu Brianna , Maulik Malabika , Bult‐Ito Abel 
Published: June 2021

Parkinson's Disease is the second most prevalent neurodegenerative disorder affecting more than 10 million worldwide (Tanner and Goldman 1996). The disease is characterized by a loss of dopaminergic neurons and aggregation of α‐synuclein proteins in the brain, resulting in impaired motor function and cognition that worsens with age. This study aims to observes the effects of Alaska low‐bush cranberry (Vaccinium vitis‐idaea) extracts on the α‐synuclein overexpression in a popular transgenic model, Caenorhabditis elegans. We tested the hypothesis that the low‐bush cranberry extracts would aid in reducing protein aggregation, and increase overall motility and lifespan of the OW13 C. elegans expressing human α‐synuclein proteins by using fluorescent imaging and microscopy. Preliminary results from our study finds that the certain doses of this botanical extract reduces the protein expression significantly (p<0.05). This study encourages further research on such endemic natural compounds as potential treatment for Parkinson's disease and identifying associated molecular mechanisms for the same.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Neuroprotective effects of estrogen on Alzheimer induced SH‐SY5Y neuroblastoma cells and N38 hypothalamic neuronal cells
Authors: Almathhur Rayan , Yakubov Rakshim , Donkor Issac , Suh Catherina , Chakraborty Sanjoy , Chakraborty Tandra R. 
Published: June 2021

Alzheimer's disease is a neurodegenerative disease characterized by neuronal cell damage and death, neurofibrillary tangle formation and cerebral plaques formed by beta amyloid peptides. Previous studies have shown that the hippocampus, a region of brain related to cognition and memory is mainly affected by Alzheimer's disease. This study is designed to induce Alzheimer's disease by treating SH‐SY5Y neuroblastoma cells and N38 hypothalamic neuronal cells with synthetic beta‐amyloid plaques under in vitro conditions. In the current study, we wanted to determine whether hypothalamus; a region involved in feeding, sleep, reproduction and energy balance is affected similarly as well. Hypothalamic cells were treated with beta‐amyloid1‐42 to induce neurofibrillary tangles and plaque formation. The cell viability, toxicity and proliferation were determined using different bioassays like cell count, MTT and lactate dehydrogenase assay. Preliminary results indicated a significant loss in mitochondrial function when exposed to beta‐amyloid. Cell damage and cellular toxicity were further analyzed by lactate dehydrogenase (LDH). Further, western blotting was done to determine the changes associated with biomarkers like P53 and Tau protein. Taking together the biochemical and molecular data the neuroprotective effect of estrogen on beta amyloid plaque formation will be analyzed.Support or Funding InformationAdelphi UniversityThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Radial Glia and Cell Heterogeneity Across The Lizard Central Nervous System: Distal Spinal Cord Rupture Does Not Induce a System‐Wide Response
Authors: McDonald Rebecca Paula , Donato Sarah Vita , Austin Laura , Vickaryous Matthew Kenneth 
Published: June 2021

Radial glia are resident neural stem/progenitor cells of the central nervous system of many non‐mammalian species. Radial glia are capable of spontaneously generating new neurons, and are considered to be crucial for both brain development and injury‐mediated regeneration. Recently, radial glia have also been identified in the tail spinal cord of the lizard Eublepharis macularius (the leopard gecko), a species capable of tail spinal cord regeneration. Here, we investigated whether similar populations of radial glia were present within the body spinal cord (bSC) and brain. Using a bromodeoxyuridine pulse‐chase strategy, we determined that label‐retaining cells were found throughout the bSC and the forebrain following a 20‐week chase. Next, we established that populations of cells lining the central canal (of the bSC) and ventricular system (of the brain) express a panel of radial glia markers, including the transcription factor SOX2 and the intermediate filaments GFAP and Vimentin. However, Vimentin expression was conspicuously absent from the diencephalon (except for the hypothalamic eminence), as well as the midbrain and hindbrain. Further, cell populations lining the central canal of the bSC include both radial glia and cells with a neuronal phenotype (as evidenced by expression of the neuronal marker HuCD). An identical diversity of cell types is also reported for in the regeneration‐competent tail spinal cord. Finally, we determined that constitutive proliferation by cells lining the central canal (of the bSC) and the ventricular system (of the forebrain) are essentially unaltered in response to distal central nervous system injury (tail spinal cord rupture as a result of tail loss). Combined, our data demonstrates that radial glia are present throughout the central nervous system of the gecko, that the bSC is essentially identical to that of the tail, and that the bSC and forebrain are resilient to distal spinal cord injuries.Support or Funding InformationNatural Sciences and Engineering Research Council Discovery Grant 400358 (MKV), Canadian Foundation for Innovation Leaders Opportunity Fund 25371(MKV)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Defects in base excision repair and homologous recombination, but not nucleotide excision repair, lead to altered cell cycle phase distributions in Saccharomyces cerevisiae
Authors: Oviedo Alejandro , Valencia Sarah , DeForge Taylor R. , Fitzgerald O'taveon R. , Lewis L. Kevin 
Published: June 2021

The DNA within cells is constantly subjected to chemical modifications resulting from exposure to endogenous and exogenous DNA damaging agents. Damaged or oxidized bases are primarily repaired by the base excision repair (BER) pathway, crosslinks induced by ultraviolet (UV) light and many bulky lesions are repaired by nucleotide excision repair (NER), mismatches are resolved by the mismatch repair system (MMR), and double‐strand breaks in DNA are repaired by either the homologous recombination (HR) pathway or the nonhomologous end‐joining (NHEJ) pathway. Inactivation of NER genes such as RAD2, RAD7 or RAD14 leads to extreme UV sensitivity in yeast cells. Mutants with defects in BER genes OGG1 or UNG1 are defective in repair of oxidized guanines and the removal of uracil bases from DNA, respectively. Yeast rad52 mutants are deficient in HR and are hypersensitive to ionizing radiation and chemicals that induce double‐strand breaks.Our laboratory has previously observed that rad52 haploid and diploid mutant cell cultures have high levels of distended large‐budded G2 phase cells and long cell cycle transit times (see poster by C. England et al.). This work also demonstrated that the high G2 phase cell phenotype of rad52 cells was abolished when any of seven known DNA damage checkpoint genes were co‐inactivated. The current project has extended these studies and asked whether defects in other DNA repair pathways also lead to accumulation of G2 phase cells and increases in doubling times. Initial studies revealed that log phase cultures of mutants deficient in NER (rad2, rad7 and rad14) or MMR (msh2, msh3 and msh6) do not have high levels of large‐budded cells. By contrast, such cells were strongly elevated in mutant cultures defective in the BER pathway (ogg1 and ung1 cells). Recent experiments are attempting to determine the fraction of these large‐budded cells that are G2 vs. M phase cells via DAPI staining and whether they are specifically associated with activation of the DNA damage checkpoint system. Cell cultures containing mutants defective in other DNA repair processes, such as Rad6‐mediated postreplication repair, translesion synthesis and nuclease processing of DNA ends, are also being analyzed using phase contrast and fluorescence microscopy to identify unusual cell morphology and cell cycle phase characteristics.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Heterochromatin proteins influence the choice of DNA repair in euchromatin domains
Authors: Forsburg Susan , Jensen Amanda , Jones Chance , Li Ting‐Ting , Yuan Ji‐Ping 
Published: June 2021

In most eukaryotes including the fission yeast, constitutive heterochromatin in pericentromere and telomere domains is marked by methylation of histone H3K9, which provides a binding platform for specialized proteins including heterochromatin protein 1 (HP1). These proteins contribute to transcriptional silencing, cohesion, and kinetochore recruitment. We showed previously that loss of heterochromatin leads to genome rearrangement in the pericentromere repeats that is exacerbated by replication fork destabilization (e.g., Li et al (2013) Cell Rep. 3:638). This indicates that heterochromatin and fork stability make unique contributions to maintain a repetitive domain and resist recombination.Evidence from mammalian systems has implicated heterochromatin proteins in transient response to induced DNA double strand breaks in euchromatin domains. Unexpectedly, we observed that mutants lacking the histone methyltransferase Clr4, or chromodomain proteins Chp1 or Swi6 show evidence of genome instability in euchromatin even in the absence of exogenous damage. Using molecular and cytological approaches, we have investigated the role of these proteins in maintaining euchromatin genome stability in otherwise unperturbed cells, as well as in response to distinct forms of genome stress. We determined that a subset of heterochromatin‐associated proteins contribute to the choice of repair pathway in euchromatin domains by modulating resection of DNA ends. Thus, H3K9 histone methylation and its associated proteins are not limited to heterochromatin domains and influence chromosome stability broadly throughout the genome.Support or Funding InformationSupport by NIH R35 GM118109This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.