bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sexual Dimorphism in Facial Fluctuating Asymmetry among Hausa Population of Nigeria
Authors: Taura Magaji Garba , Adamu Lawan , Danborno Barnabas 
Published: November 2023

The aim of the study was to investigate the sex differences in three fluctuating asymmetry (FA) indices, and to determine the side dominance in facial features among Hausas of Kano State Nigeria. A total of 283 participants comprising 147 males and 136 females of age range 18–25 years were randomly selected. Photometric method was used to capture the face. Three indices of asymmetry used include signed asymmetry (SA), absolute asymmetry (AA) and composite asymmetry (CA). Independent sample t test was used to test for sex differences in the variables and one sample t test was used to determine fluctuating asymmetry. The result showed that females tend to have statistically significant mean value in orbital width. For zygon to gnathion facial distance, a statistically significant higher mean value was observed in males. For the three indices of fluctuating asymmetry above, no significant sexual dimorphism in signed FA index was observed. However, males tend to have leftward FA in orbital width and zygon to gnathion distance. In absolute and composite FA, a significant sexual dimorphism was noticed only in zygon to gnathion distance, with females having higher mean value in AA and males having higher mean value in CA respectively. The facial parameters exhibited fluctuating type of asymmetry. In conclusion, there were no sex differences in the FA indices. However, left warded type of FA was exhibited in males of Hausa origin.Support or Funding InformationNoneSexual dimorphism in signed asymmetry (SA) of the paired facial dimensionsimage
One sample t test and normality test for evaluation of fluctuating asymmetry of facial dimensions

One sample t – test

Sex
Variables
Mean
SEM
t

Male
ps‐pi1
−0.11
0.12
−0.93*

ex‐en1
0.06
0.16
0.37*

zy‐gn1
−0.02
0.34
−0.07*

Female
Ps‐Pi1
0.08
0.12
0.63*

ex‐en1
0.08
0.16
0.53*

zy‐gnl
0.19
0.42
0.46*

P>0.05.
SEM: standard error of mean,
Shapiro‐Wilk test P > 0.05
Comparison Analysis of Metopism Prevalence in Sexes and Various Populations
Authors: Bliss Kaitlyn N , Russell Michelle L , Koons Aaron W , Mangus Kelsey R , Zdilla Matthew J 
Published: November 2023

The metopic suture (MS) is a cranial suture located at the junction between the two primary intramembranous nuclei of the developing frontal bone. The MS first becomes evident at the end of the second month of fetal life and typically closes in infancy or early childhood. For reasons that remain unclear, the MS may persist into adulthood‐ a condition commonly referred to as metopism. The prevalence of metopism is significant from both a developmental and clinical perspective. Alone, persistent metopic sutures may mimic midline fractures; however, metopism may also be related to several craniofacial defects including frontal sinus anomalies, cleft lip, and cleft palate. This study analyzed 505 crania from varied populations. Of the 505 crania studied, 13 crania demonstrated metopism (1.01%). Out of the total population, 0.99% observed were European (Anglo‐American, Swedish, German, Irish, Finnish, European, Spaniard, Etruscan, Sclavonian, and Celtic), 0.40% were East Asian (Japanese and Chinese), 0.40% were Egyptian, 0.20% were Bengali, and 0.60% were from other populations. Within the total population, 0.99% were males with metopism and 1.60% were females.Support or Funding InformationWV Research Challenge Fund [HEPC.dsr.14.13]
Student Generated Structure Lists: Bringing Self‐Directed Learning into the Anatomy Laboratory
Authors: Dunham Stacey M 
Published: November 2023

Self‐directed learning (SDL) opportunities are a necessary component of medical education and identified as an approach to developing lifelong learning skills. The anatomy laboratory is one place that SDL can be incorporated in the medical curriculum. This study examined the content generated by a group of approximately 40 first year medical students in a yearlong human gross anatomy course. Students were required to generate their own anatomy structure list based on the instructions provided in the class dissector. Structure lists were to indicate the anatomical structures to be identified in the day's dissection. This required students to thoughtfully and carefully review the dissection instructions for the lab procedure prior to attending the laboratory session. Rather than simply list the structures, students were asked to classify structures into primary, secondary, and tertiary groups and provide an explanation for their chosen organizing principle. Organizing principals used by students included: size based divisions, clinical relevance, body systems, and locations. While some students consistently exhibited principles of self‐directed learning in the work submitted, the lack of a grade based assignment led other students to submit work of limited value in preparing for the dissection.Support or Funding InformationThis study was not funded.
Glutamic acid 446 and Arginine 447 in heat shock protein 70 (hsp70) are critical for regulating superoxide dismutase‐2 (SOD2) function
Authors: Afolayan Adeleye James , Teng Ru Jeng , Konduri Girija Garnesh 
Published: November 2023

BackgroundStress‐inducible hsp70 interacts with SOD2 after synthesis to transfer the enzyme to the mitochondria for subsequent activation. However, the amino acid residues in hsp70 that are critical for SOD2 interactions remain unknown.Methods and resultsWe map the SOD2‐binding site in hsp70 by making a series of hsp70 mutants (GST‐tagged 1–400, 393–537 and 537–641) and tested for their ability to bind SOD2. The GST‐tagged hsp70 mutants and EGFP‐tagged wild type SOD2 were co‐expressed in HEK293T cells. Using pull down assays, we showed that SOD2 preferentially bound to the hsp70 mutant corresponding to amino acid 393–537 region in hsp70 (Fig. 1). SOD2 did not bind to the other regions tested. This exclusivity suggests that SOD2 associates with the 393hsp70537 domain. To better define the binding site, nine overlapping decoy peptides (p1–p9) were made spanning the entire length of the 393hsp70537 region, where SOD2 is suspected to bind to hsp70. The peptides were screened to determine which one could inhibit SOD2/hsp70 interactions. Out of the nine decoy peptides tested, p4 (YSDNOPGVLIQVYEGERAMT: amino acid residues 423–443) and p5 (GERAMTRDNNLLGRFELSGIP; amino acid residues 439–459) significantly disrupted SOD2 association with hsp70 in endothelial cell lysates (Fig 2A). Since GERAMT is common to both p4 and p5 peptides, we speculated that this sequence may represent the minimal portion responsible for disrupting SOD2 interactions with hsp70. To test this hypothesis, we added the GERAMT peptide alone or GERAMT‐less P4 and P5 peptides (Δp4 and Δp5) individually to aliquots of cell lysates. Colorimetry analysis revealed that GERAMT‐treated lysates had ~3‐fold decrease in SOD2 activity compared to the GERAMT‐less peptides (Fig 2B). Small peptides containing the GERAMT sequence decreased the activity of SOD2 in vitro and in vivo. To determine the amino acid residues in hsp70 that are critical for SOD2 interactions, we substituted each amino acid residue for alanine (A) in the GERAMT‐binding site in a step‐wise fashion and tested the effects of mutations on SOD2‐hsp70 interactions. Substitutions of alanine for glutamic acid (E446A) and arginine (R447A) inhibited the ability of hsp70 to bind SOD2 and decreased SOD2 activity, more than other substitutions (Fig 3).ConclusionsTogether, these findings indicate that the GERAMT sequence is critical for the chaperone‐mediated regulation of SOD2 antioxidant function and that E446 and R447 cooperate with other residues in the GERAMT‐binding site for proper hsp70 chaperone functions.Support or Funding InformationFunding supports from Department of Pediatrics and Children's Research institute (CRI) at the Medical College of Wisconsin and 1K08HL133379‐01 (Adeleye Afolayan)
Investigating the regulation of recA in the emerging pathogen Acinetobacter baumannii
Authors: Ching Carly , Gozzi Kevin , Heinemann Bjorn , Godoy Veronica G 
Published: November 2023

Acinetobacter baumannii (Ab) is an emerging multidrug‐resistant, opportunistic pathogen. Ab survives desiccation, remaining on hospital surfaces affecting immunocompromised individuals. Ab antibiotic resistance acquisition has been linked to its DNA damage response (DDR). DDR genes, including error‐prone DNA polymerases, are involved in DNA damage and desiccation induced mutagenesis. In Escherichia coli, RecA, the cells' main recombinase, binds single stranded DNA, the signal of DNA damage, forming the nucleoprotein filament (RecA*), which is endowed with co‐protease activity. RecA* promotes cleavage and inactivation of LexA, the global DDR repressor, resulting in expression of DDR genes. In Ab, this well‐known circuitry does not exist in part because Ab lacks a functional LexA. We have shown that conserved DDR genes in Ab form two phenotypic subpopulations in response to DNA damage: one with low and another with high expression. The DDR in Ab is dependent on RecA. Thus, we are focused on understanding the mechanism underlying recA regulation to begin to understand the regulatory network that underlies this bimodality.We have found that the recA gene contains a cis‐acting element in its 5′ untranslated region (UTR). In‐vitro transcription demonstrated that this 5′UTR contains secondary structure. A plasmid‐borne reporter was constructed that contains the cis‐regulatory element driving a fluorescent reporter. Mutants of the cis‐regulatory element that deletes putative regulatory sequences or predicted in silico secondary structure were constructed using site‐directed mutagenesis. Using fluorescent microscopy of the reporter strains, we have shown that the cis‐acting regulatory element and its structure are important for bimodal expression of recA, while the promoter contains elements for DNA Damage sensing. Furthermore, we found that the recA 5′UTR modulates transcript levels and subsequently RecA in the cell. Disrupting the structure of the 5′UTR results in a significant decrease of UV survival and antibiotic resistance acquisition. This provides evidence that in Ab, two levels of regulation mediate recA. Remarkably, the Ab promoter and UTR sequence is capable of responding not only in Ab but also in other bacterial species as observed through similar fluorescent reporters induced with DNA damaging agents. Bimodal DDR gene expression may provide a strategy for survival and plasticity in an ever‐changing environment. These findings may also provide insight into the evolution of other highly antibiotic resistant bacteria lacking conserved DDR gene networksSupport or Funding InformationNIH Grant (GM088230) to VG
The Epsilon Subunit of DNA Polymerase III in the Bacterial Response to Quinolones
Authors: Whatley Zakiya , Sy Nene , DiDomenico Sarah , Finck Amanda 
Published: November 2023

Quinolones are widely prescribed, broad‐spectrum antibacterial drugs. Despite their widespread use, the molecular mechanisms of quinolone cytotoxicity are not clearly understood. Quinolones target topoisomerases, preventing the resealing of otherwise transient DNA breaks. Poisoned topoisomerase, or stabilized cleavage complexes, are not sufficient for cell death. The goal of this study is to determine how stabilized cleavage complexes are converted into irreversible double strand DNA breaks (DSBs) that accumulate and drive quinolone cytotoxicity.Previous studies identified an unexpected connection between dnaQ and quinolone‐induced DNA damage in Escherichia coli. The ɛ subunit of DNA polymerase III, encoded by dnaQ, is an exonuclease providing the 3′ ‐> 5′ proofreading activity of the core. The absence of ɛ causes higher mutation rates, slow growth, constitutive SOS, and a defective SOS response following quinolone treatment. We found that these phenotypes are separable, which implies that ɛ has multiple, separable roles, aside from proofreading.We explore the role of ɛ‐β interaction in quinolone‐induced DSB generation. Using two different types of cell lysis in conjunction with pulsed‐field gel electrophoresis, we distinguished between latent breaks at the cleavage complex and overt chromosomal breaks due to additional processing. We provide evidence that supports the replication run‐off model of DSB generation, whereby a stronger ɛ‐β interaction causes the replicase to physically interact with stabilized cleavage complexes rather than stalling or disassembling.Support or Funding InformationGettysburg College Research & Professional Development Grant & Howard Hughes Medical Institute ‐ Cross‐Disciplinary Sciences Institute at Gettysburg College
The role of CCCTC binding factor (CTCF) in epithelial to mesenchymal transition (EMT)
Authors: Bhattacharya Atrayee , Hur Junguk , Dhasarathy Archana 
Published: November 2023

The process of Epithelial to Mesenchymal transition (EMT) plays a major role in cancer metastasis. TGF‐β or EGF signaling pathways can trigger EMT, which involves a cell state transition from an attached, epithelial state to a migratory, mesenchymal phenotype. In addition, massive reorganization of chromatin occurs during EMT, coupled with significant gene expression changes. However, the underlying cause for what triggers these chromatin structure changes remains unknown. The well‐studied transcription factor CTCF is known to regulate the 3D structure of chromatin, and reorganize the genome. Recently, it was shown in Drosophila cells that CTCF recruits Smad proteins to their gene targets following addition of TGF‐β. EMT master regulatory protein SNAIL is among the key targets of Smad proteins. Therefore, we hypothesized that CTCF plays a role in TGF‐β‐induced EMT, both at the transcriptional level, and at the genome architectural level, leading to acquisition of an invasive phenotype.To test our hypothesis, we induced EMT in normal murine mammary gland (NMuMG) cells followed by chromatin immunoprecipitation (ChIP), to determine CTCF enrichment at the SNAIL promoter. We found TGF‐β, but not EGF, dependent enrichment of CTCF at the promoter and upstream regions of SNAIL relative to the control‐untreated cells. Correspondingly, we noted a TGF‐β dependent increase in expression of SNAIL mRNA, which is diminished when coupled with siRNA knockdown of CTCF. Further, CTCF is associated with the promoter and upstream regions of the SNAIL gene in metastatic cancer cell lines with high endogenous SNAIL expression. Taken together, we propose a role for CTCF in direct transcriptional regulation of genes involved in EMT. We are currently investigating the functional role of CTCF in EMT.Support or Funding InformationThis work was supported by award 5P20GM104360 from the National Institutes of Health to AD.
The Role of mRNA Degradation in Dynamic Nitrogen Environments in Saccharomyces cerevisiae
Authors: Rodriguez‐Tirado Carla Sofia , Gresham David , Abdul‐Rahman Farah 
Published: November 2023

Studying the reprogramming of gene expression is fundamental to understanding cellular growth, development and stem cell differentiation. In Saccharomyces cerevisiae cells undergo reprogramming of gene expression when they are grown in nitrogen‐poor conditions and then switched to nitrogen‐rich conditions. This is controlled by the nitrogen catabolite repression (NCR) response. In a previous study, NCR transcripts were shown to undergo accelerated degradation when the cells where switched from growth on proline in a nitrogen‐poor environment to growth in a nitrogen‐rich environment upon the addition of glutamine. This study aims to determine the benefit of accelerated mRNA degradation in dynamic nitrogen environments by studying the effects of mutants of NCR repressors during this transition. We suspect that knocking out the repressors will stop the accelerated degradation once glutamine is added. This will in turn affect the growth rates and cause the mutants to have longer lag phase, a period where there is no detectable change in the growth. The general amino acid permease (GAP1) was used in representation of NCR transcripts to study the effects. This gene encodes a permease that senses the presence of amino acids substrates to regulate localization to the plasma membrane when needed. We identified mutants where GAP1 is stabilized in a nitrogen‐rich environment by using knock‐outs (KO) of the NCR repressor genes Ure2, Dal80 and Gzf3. The Ure2KO mutant showed depression of GAP1 in nitrogen‐rich conditions, but it caused a growth defect when the cells were grown in nitrogen‐poor conditions. In addition, we tested the effect of the GAP1 5′ untranslated region (UTR) mutant on growth dynamics because it has been shown to stabilize the GAP1 transcript during the transition from nitrogen‐poor environment to a nitrogen‐rich environment. A T‐test was performed to see if there was any difference between the growth rates of the wildtype and the 5′UTR deletion. Turns out that there was no significant difference between them before (p value=0.13) and after the glutamine addition (p value= 0.15), despite there being a notable distinction between the slopes. When the graphs for the nitrogen up shift were generated a lag phase was detected and it appeared to be an hour longer in the mutant. Which indicates that accelerated degradation is an important process in dynamic nitrogen environments.Support or Funding InformationNIH‐MARC Program undergraduate fellowship (5T34GM00781‐37)
Carbohydrate‐linked cisplatin analogue: reactivity studies with RNA and DNA
Authors: Gamage Supuni Duneeshya Thalalla , Muthunayake Nisansala , Sonousi Amr , Crich David , Chow Christine 
Published: November 2023

With the discovery of cisplatin in the 1960s, it has been widely studied as a precursor for anticancer drug development. Despite its effectiveness against certain cancers, clinical usage of cisplatin is restricted by a number of side effects and resistance. In the past decade, scientists have been exploring biologically important ligands such as sugar derivatives in the hope of overcoming such challenges. Attachment of a sugar moiety could facilitate lower accumulation of platinum drugs in the body as well as enhance cellular uptake. In this study, a carbohydrate‐linked cisplatin analogue, cis‐dichloro[(2‐β‐D‐glucopyranosidyl)propane‐1,3‐diamine]platinum (1) has been studied. The aim is to evaluate the binding targets and mechanism of action compared to cisplatin. Compound 1 was synthesized and a reactivity study was carried out with deoxy‐/ribonucleosides and nucleic acids using high performance liquid chromatography (HPLC), liquid chromatography mass spectrometry (LC‐MS), and matrix‐assisted laser‐desorption ionization mass spectrometry (MALDI‐MS). A study was done to analyze the effects of compound 1 on DNA duplex structure by measuring the bending angles. Further probing studies on ribosomal RNA showed compound 1 localization on rRNA. Overall, this work allows us to compare ligand binding and subsequent effects on nucleic acids through a series of chemical and biochemical techniques.Support or Funding InformationWayne State University‐Faculty Schaap Fellowship
Effect of bleaching products on the collagen of teeth
Authors: Cavallaro Christina , Schiliro Chelsea , Keenan Kelly 
Published: November 2023

Americans spend an estimated 1.4 billion dollars on over‐the‐counter bleaching products which whiten teeth. The active ingredient is hydrogen peroxide which can damage proteins. The dentin contains an estimated 90% of its protein in the form of collagen and the effect of bleaching on collagen has not been determined. In this project, the non‐collagen proteins from teeth were extracted with EDTA and the remains of the teeth were dialyzed against water and then pulverized with liquid nitrogen. The resulting powder was re‐suspended and treated with pepsin to produce fragments. The protein level of these fragments was tested using the Lowry assay and individual fragments were separated using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS‐PAGE). Individual fragments were removed and hydrolyzed to produce amino acids which were separated and identified using reverse phase high performance liquid chromatography. This was done on untreated teeth as well as teeth that had received either one or three rounds of tooth whitening with an over‐the‐counter product.Support or Funding InformationThe authors wish to thank the NAMS and Provost Travel Funds and the Provost Opportunity funds.
Elucidation of molecular signaling battles between the eukaryotic host and a bacterial pathogen
Authors: Orth Kim , de Souza Santos Marcela , Salomon Dor 
Published: November 2023

The marine bacterium Vibrio parahaemolyticus is the worldwide leading cause of seafood‐borne acute gastroenteritis. For decades, this pathogen has been studied exclusively as an extracellular bacterium. However, recent results have revealed the pathogen's ability to invade and replicate within host cells. Microbial killing by host cells is largely a function of phagocytosis followed by generation of reactive oxygen species (ROS) to kill the engulfed microbes. The phagocytic NADPH oxidase (NOX2) complex, which is composed of at least five proteins, generates these superoxides at the site of engulfment, which activates proteolytic enzymes that mediate killing and immune signaling. The GTPase Rac1/2 is essential for the function of the complex as its activation, localization to the membrane, and binding to p67 activates the complex. To maintain its existence inside a eukaryotic cell, the pathogen manipulates the intracellular host cell environment to suit its needs and survive. We have discovered a novel posttranslational mechanism that prevents the localization of Rac to the membrane, thereby, disabling the ability of the host to produce ROS and cripple the invading bacteria.Support or Funding InformationNIHAID, NIHGMS, Welch Foundation, Once Upon a Time..., HHMI