bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Platform for Mechanical Assembly Education Using the Microsoft Kinect
Authors: Chang Yizhe , Aziz El-Sayed , Zhang Zhou , Zhang Mingshao , Esche Sven , Chassapis Constantin 
Published: January 2017

Mechanical assembly activities involve multiple factors including humans, mechanical parts, tools and assembly environments. In order to simulate assembly processes by computers for educational purposes, all these factors should be considered. Virtual reality (VR) technology, which aims to integrate natural human motion into real-world scenarios, provides an ideal simulation medium. Novel VR devices such as 3D glasses, motion-tracking gloves, haptic sensors, etc. are able to fulfill fundamental assembly simulation needs. However, most of these implementations focus on assembly simulations for computer-aided design, which are geared toward professionals rather than students, thus leading to complicated assembly procedures not suitable for students. Furthermore, the costs of these novel VR devices and specifically designed VR platforms represent an untenable financial burden for most educational institutions.
In this paper, a virtual platform for mechanical assembly education based on the Microsoft Kinect sensor and Garry’s Mod (GMod) is presented. With the help of the Kinect’s body tracking function and voice recognition technology in conjunction with the graphics and physics simulation capabilities of GMod, a low-cost VR platform that enables educators to author their own assembly simulations was implemented. This platform utilizes the Kinect as the sole input device. Students can use voice commands to navigate their avatars inside of a GMod powered virtual laboratory as well as use their body’s motions to integrate pre-defined mechanical parts into assemblies. Under this platform, assembly procedures involving the picking, placing and attaching of parts can be performed collaboratively by multiple users. In addition, the platform allows collaborative learning without the need for the learners to be co-located. A pilot study for this platform showed that, with the instructor’s assistance, mechanical engineering undergraduate students are able to complete basic assembly operations.
Design and Analysis of an Example Lathe Spindle
Authors: Vyasa Rupal , Echempati Raghu 
Published: January 2017

This paper discusses the modeling and analysis of an example medium speed medium precision lathe spindle. This and few other similar topics have been assigned as term projects in an introductory senior undergraduate/graduate level finite element analysis course taught at Kettering University. The experiences and the general feedback from the students of the class show satisfactory organization of the course material that includes modeling and analysis of real life examples.
With reference to the specific topic on design of machine tool spindles, it is not a new area, however, it is generally taught at the graduate and research levels. Use of modern computational tools to perform iterative design and analysis calculations of such spindles make the senior undergraduate and/or graduate master students aware of the implications of modeling a real life system using the 1D and 3D finite beam elements and to validate those results by a CAE tool. Final course projects such as this serve as a good learning tool to the graduating engineers. Sample results obtained from various CAE tools such as UG-NX 7.5 are presented in the paper and discussed.
Monophosphoryl Lipid A Enhances Efficacy of a Francisella tularensis LVS-Catanionic Nanoparticle Subunit Vaccine against F. tularensis Schu S4 Challenge by Augmenting both Humoral and Cellular Immunity
Authors: Richard Katharina , Mann Barbara J. , Qin Aiping , Barry Eileen M. , Ernst Robert K. , Vogel Stefanie N. 
Published: January 2017

ABSTRACT

Francisella tularensis
, a bacterial biothreat agent, has no approved vaccine in the United States. Previously, we showed that incorporating lysates from partially attenuated
F. tularensis
LVS or fully virulent
F. tularensis
Schu S4 strains into catanionic surfactant vesicle (V) nanoparticles (LVS-V and Schu S4-V, respectively) protected fully against
F. tularensis
LVS intraperitoneal (i.p.) challenge in mice. However, we achieved only partial protection against
F. tularensis
Schu S4 intranasal (i.n.) challenge, even when employing heterologous prime-boost immunization strategies. We now extend these findings to show that both LVS-V and Schu S4-V immunization (i.p./i.p.) elicited similarly high titers of anti-
F. tularensis
IgG and that the titers could be further increased by adding monophosphoryl lipid A (MPL), a nontoxic Toll-like receptor 4 (TLR4) adjuvant that is included in several U.S. FDA-approved vaccines. LVS-V+MPL immune sera also detected more
F. tularensis
antigens than LVS-V immune sera and, after passive transfer to naive mice, significantly delayed the time to death against
F. tularensis
Schu S4 subcutaneous (s.c.) but not i.n. challenge. Active immunization with LVS-V+MPL (i.p./i.p.) also increased the frequency of gamma interferon (IFN-γ)-secreting activated helper T cells, IFN-γ production, and the ability of splenocytes to control intramacrophage
F. tularensis
LVS replication
ex vivo
. Active LVS-V+MPL immunization via heterologous routes (i.p./i.n.) significantly elevated IgA and IgG levels in bronchoalveolar lavage fluid and significantly enhanced protection against i.n.
F. tularensis
Schu S4 challenge (to ∼60%). These data represent a significant step in the development of a subunit vaccine against the highly virulent type A strains.
Evaluation of Alere i RSV for Rapid Detection of Respiratory Syncytial Virus in Children Hospitalized with Acute Respiratory Tract Infection
Authors: Peters Rebecca Marie , Schnee Sarah Valerie , Tabatabai Julia , Schnitzler Paul , Pfeil Johannes 
Published: January 2017

ABSTRACT
Alere i RSV is a novel rapid test which applies a nicking enzyme amplification reaction to detect respiratory syncytial virus in point-of-care settings. In this study, we evaluated the Alere i RSV assay by using frozen nasopharyngeal swab samples that were collected in viral transport medium from children hospitalized with acute respiratory tract infection during the 2015-2016 winter season. Alere i RSV assay results were compared to those for Altona RealStar RSV real-time reverse transcription-PCR (RT-PCR). We found that the overall sensitivity and specificity of the Alere i RSV test was 100% (95% confidence intervals [CI], 93% to 100%) and 97% (95% CI, 89% to 100%), respectively. Positive samples were identified within 5 to 7 min from sample collection. Overall, the Alere i RSV test performed well compared to the RT-PCR assay and has the potential to facilitate the detection of RSV in point-of-care settings.
Melanin or a Melanin-Like Substance Interacts with the N-Terminal Portion of Prion Protein and Inhibits Abnormal Prion Protein Formation in Prion-Infected Cells
Authors: Hamanaka Taichi , Nishizawa Keiko , Sakasegawa Yuji , Oguma Ayumi , Teruya Kenta , Kurahashi Hiroshi , Hara Hideyuki , Sakaguchi Suehiro , Doh-ura Katsumi 
Published: January 2017

ABSTRACTPrion diseases are progressive fatal neurodegenerative illnesses caused by the accumulation of transmissible abnormal prion protein (PrP). To find treatments for prion diseases, we searched for substances from natural resources that inhibit abnormal PrP formation in prion-infected cells. We found that high-molecular-weight components from insect cuticle extracts reduced abnormal PrP levels. The chemical nature of these components was consistent with that of melanin. In fact, synthetic melanin produced from tyrosine or 3-hydroxy-l-tyrosine inhibited abnormal PrP formation. Melanin did not modify cellular or cell surface PrP levels, nor did it modify lipid raft or cellular cholesterol levels. Neither did it enhance autophagy or lysosomal function. Melanin was capable of interacting with PrP at two N-terminal domains. Specifically, it strongly interacted with the PrP region of amino acids 23 to 50 including a positively charged amino acid cluster and weakly interacted with the PrP octarepeat peptide region of residues 51 to 90. However, thein vitroandin vivodata were inconsistent with those of prion-infected cells. Abnormal PrP formation in protein misfolding cyclic amplification was not inhibited by melanin. Survival after prion infection was not significantly altered in albino mice or exogenously melanin-injected mice compared with that of control mice. These data suggest that melanin, a main determinant of skin color, is not likely to modify prion disease pathogenesis, even though racial differences in the incidence of human prion diseases have been reported. Thus, the findings identify an interaction between melanin and the N terminus of PrP, but the pathophysiological roles of the PrP-melanin interaction remain unclear.IMPORTANCEThe N-terminal region of PrP is reportedly important for neuroprotection, neurotoxicity, and abnormal PrP formation, as this region is bound by many factors, such as metal ions, lipids, nucleic acids, antiprion compounds, and several proteins, including abnormal PrP in prion disease and the Aβ oligomer in Alzheimer's disease. In the present study, melanin, a main determinant of skin color, was newly found to interact with this N-terminal region and inhibits abnormal PrP formation in prion-infected cells. However, the data for prion infection in mice lacking melanin production suggest that melanin is not associated with the prion disease mechanism, although the incidence of prion disease is reportedly much higher in white people than in black people. Thus, the roles of the PrP-melanin interaction remain to be further elucidated, but melanin might be a useful competitive tool for evaluating the functions of other ligands at the N-terminal region.
Expression of
Ifnlr1
on Intestinal Epithelial Cells Is Critical to the Antiviral Effects of Interferon Lambda against Norovirus and Reovirus
Authors: Baldridge Megan T. , Lee Sanghyun , Brown Judy J. , McAllister Nicole , Urbanek Kelly , Dermody Terence S. , Nice Timothy J. , Virgin Herbert W. 
Published: January 2017

ABSTRACT

Lambda interferon (IFN-λ) has potent antiviral effects against multiple enteric viral pathogens, including norovirus and rotavirus, in both preventing and curing infection. Because the intestine includes a diverse array of cell types, however, the cell(s) upon which IFN-λ acts to exert its antiviral effects is unclear. Here, we sought to identify IFN-λ-responsive cells by generation of mice with lineage-specific deletion of the receptor for IFN-λ,
Ifnlr1
. We found that expression of IFNLR1 on intestinal epithelial cells (IECs) in the small intestine and colon is required for enteric IFN-λ antiviral activity. IEC
Ifnlr1
expression also determines the efficacy of IFN-λ in resolving persistent murine norovirus (MNoV) infection and regulates fecal shedding and viral titers in tissue. Thus, the expression of
Ifnlr1
by IECs is necessary for the response to both endogenous and exogenous IFN-λ. We further demonstrate that IEC
Ifnlr1
expression is required for the sterilizing innate immune effects of IFN-λ by extending these findings in
Rag1
-deficient mice. Finally, we assessed whether our findings pertained to multiple viral pathogens by infecting mice specifically lacking IEC
Ifnlr1
expression with reovirus. These mice phenocopied
Ifnlr1
-null animals, exhibiting increased intestinal tissue titers and enhanced reovirus fecal shedding. Thus, IECs are the critical cell type responding to IFN-λ to control multiple enteric viruses. This is the first genetic evidence that supports an essential role for IECs in IFN-λ-mediated control of enteric viral infection, and these findings provide insight into the mechanism of IFN-λ-mediated antiviral activity.

IMPORTANCE
Human noroviruses (HNoVs) are the leading cause of epidemic gastroenteritis worldwide. Type III interferons (IFN-λ) control enteric viral infections in the gut and have been shown to cure mouse norovirus, a small-animal model for HNoVs. Using a genetic approach with conditional knockout mice, we identified IECs as the dominant IFN-λ-responsive cells in control of enteric virus infection
in vivo
. Upon murine norovirus or reovirus infection,
Ifnlr1
depletion in IECs largely recapitulated the phenotype seen in
Ifnlr1
−/−
mice of higher intestinal tissue viral titers and increased viral shedding in the stool. Moreover, IFN-λ-mediated sterilizing immunity against murine norovirus requires the capacity of IECs to respond to IFN-λ. These findings clarify the mechanism of action of this cytokine and emphasize the therapeutic potential of IFN-λ for treating mucosal viral infections.
Exosome-Mediated Intercellular Communication between Hepatitis C Virus-Infected Hepatocytes and Hepatic Stellate Cells
Authors: Devhare Pradip B. , Sasaki Reina , Shrivastava Shubham , Di Bisceglie Adrian M. , Ray Ranjit , Ray Ratna B. 
Published: January 2017

ABSTRACT
Fibrogenic pathways in the liver are principally regulated by activation of hepatic stellate cells (HSC). Fibrosis is associated with chronic hepatitis C virus (HCV) infection, although the mechanism is poorly understood. HSC comprise the major population of nonparenchymal cells in the liver. Since HCV does not replicate in HSC, we hypothesized that exosomes secreted from HCV-infected hepatocytes activate HSC. Primary or immortalized human hepatic stellate (LX2) cells were exposed to exosomes derived from HCV-infected hepatocytes (HCV-exo), and the expression of fibrosis-related genes was examined. Our results demonstrated that HCV-exo internalized to HSC and increased the expression of profibrotic markers. Further analysis suggested that HCV-exo carry miR-19a and target SOCS3 in HSC, which in turn activates the STAT3-mediated transforming growth factor β (TGF-β) signaling pathway and enhances fibrosis marker genes. The higher expression of miR-19a in exosomes was also observed from HCV-infected hepatocytes and in sera of chronic HCV patients with fibrosis compared to healthy volunteers and non-HCV-related liver disease patients with fibrosis. Together, our results demonstrated that miR-19a carried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 axis. Our results implicated a novel mechanism of exosome-mediated intercellular communication in the activation of HSC for liver fibrosis in HCV infection.

IMPORTANCE
HCV-associated liver fibrosis is a critical step for end-stage liver disease progression. However, the molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are underexplored. Here, we provide a role for miR-19a carried through the exosomes in intercellular communication between HCV-infected hepatocytes and HSC in fibrogenic activation. Furthermore, we demonstrate the role of exosomal miR-19a in activation of the STAT3–TGF-β pathway in HSC. This study contributes to the understanding of intercellular communication in the pathogenesis of liver disease during HCV infection.
Role of Litopenaeus vannamei Yin Yang 1 in the Regulation of the White Spot Syndrome Virus Immediate Early Gene
ie1
Authors: Huang Ping-Han , Huang Ting-Yi , Cai Pei-Si , Chang Li-Kwan 
Published: January 2017

ABSTRACT

Yin Yang 1 (YY1) is a multifunctional zinc finger transcription factor that regulates many key cellular processes. In this study, we report the cloning of YY1 from
Litopenaeus vannamei
shrimp (LvYY1). This study shows that LvYY1 is ubiquitously expressed in shrimp tissues, and knockdown of LvYY1 expression by double-stranded RNA (dsRNA) injection in white spot syndrome virus (WSSV)-infected shrimp reduced both mRNA levels of the WSSV immediate early gene
ie1
as well as overall copy numbers of the WSSV genome. The cumulative mortality rate of infected shrimp also declined with LvYY1 dsRNA injection. Using an insect cell model, we observed that LvYY1 activates
ie1
expression, and a mutation introduced into the
ie1
promoter subsequently repressed this capability. Moreover, reporter assay results suggested that LvYY1 is involved in basal transcriptional regulation via an interaction with
L. vannamei
TATA-binding protein (LvTBP). Electrophoretic mobility shift assay (EMSA) results further indicated that LvYY1 binds to a YY1-binding site in the region between positions −119 and −126 in the
ie1
promoter. Chromatin immunoprecipitation analysis also confirmed that LvYY1 binds to the
ie1
promoter in WSSV-infected shrimp. Taken together, these results indicate that WSSV uses host LvYY1 to enhance
ie1
expression via a YY1-binding site and the TATA box in the
ie1
promoter, thereby facilitating lytic activation and viral replication.

IMPORTANCE
WSSV has long been a scourge of the shrimp industry and remains a serious global threat. Thus, there is a pressing need to understand how the interactions between WSSV and its host drive infection, lytic development, pathogenesis, and mortality. Our successful cloning of
L. vannamei
YY1 (LvYY1) led to the elucidation of a critical virus-host interaction between LvYY1 and the WSSV immediate early gene
ie1
. We observed that LvYY1 regulates
ie1
expression via a consensus YY1-binding site and TATA box. LvYY1 was also found to interact with
L. vannamei
TATA-binding protein (LvTBP), which may have an effect on basal transcription. Knockdown of LvYY1 expression inhibited
ie1
transcription and subsequently reduced viral DNA replication and decreased cumulative mortality rates of WSSV-infected shrimp. These findings are expected to contribute to future studies involving WSSV-host interactions.
A Cytoplasmic RNA Virus Alters the Function of the Cell Splicing Protein SRSF2
Authors: Rivera-Serrano Efraín E. , Fritch Ethan J. , Scholl Elizabeth H. , Sherry Barbara 
Published: January 2017

ABSTRACT
To replicate efficiently, viruses must create favorable cell conditions and overcome cell antiviral responses. We previously reported that the reovirus protein μ2 from strain T1L, but not strain T3D, represses one antiviral response: alpha/beta interferon signaling. We report here that T1L, but not T3D, μ2 localizes to nuclear speckles, where it forms a complex with the mRNA splicing factor SRSF2 and alters its subnuclear localization. Reovirus replicates in cytoplasmic viral factories, and there is no evidence that reovirus genomic or messenger RNAs are spliced, suggesting that T1L μ2 might target splicing of cell RNAs. Indeed, RNA sequencing revealed that reovirus T1L, but not T3D, infection alters the splicing of transcripts for host genes involved in mRNA posttranscriptional modifications. Moreover, depletion of SRSF2 enhanced reovirus replication and cytopathic effect, suggesting that T1L μ2 modulation of splicing benefits the virus. This provides the first report of viral antagonism of the splicing factor SRSF2 and identifies the viral protein that determines strain-specific differences in cell RNA splicing.

IMPORTANCE
Efficient viral replication requires that the virus create favorable cell conditions. Many viruses accomplish this by repressing specific antiviral responses. We demonstrate here that some mammalian reoviruses, RNA viruses that replicate strictly in the cytoplasm, express a protein variant that localizes to nuclear speckles, where it targets a cell mRNA splicing factor. Infection with a reovirus strain that targets this splicing factor alters splicing of cell mRNAs involved in the maturation of many other cell mRNAs. Depletion of this cell splicing factor enhances reovirus replication and cytopathic effect. Our results provide the first evidence of viral antagonism of this splicing factor and suggest that downstream consequences to the cell are global and benefit the virus.
Fungal Ligninolytic Enzymes and Their Applications
Authors: Mäkelä Miia R. , Bredeweg Erin L. , Magnuson Jon K. , Baker Scott E. , de Vries Ronald P. , Hildén Kristiina 
Published: January 2017

ABSTRACT

The global push toward an efficient and economical biobased economy has driven research to develop more cost-effective applications for the entirety of plant biomass, including lignocellulosic crops. As discussed elsewhere (Karlsson M, Atanasova L, Funck Jensen D, Zeilinger S, in Heitman J et al. [ed],
Tuberculosis and the Tubercle Bacillus
, 2nd ed, in press), significant progress has been made in the use of polysaccharide fractions from lignocellulose, cellulose, and various hemicellulose types. However, developing processes for use of the lignin fraction has been more challenging. In this chapter, we discuss characteristics of lignolytic enzymes and the fungi that produce them as well as potential and current uses of lignin-derived products.
Fungal Cell Cycle: A Unicellular versus Multicellular Comparison
Authors: Dörter Ilkay , Momany Michelle 
Published: January 2017

ABSTRACT

All cells must accurately replicate DNA and partition it to daughter cells. The basic cell cycle machinery is highly conserved among eukaryotes. Most of the mechanisms that control the cell cycle were worked out in fungal cells, taking advantage of their powerful genetics and rapid duplication times. Here we describe the cell cycles of the unicellular budding yeast
Saccharomyces cerevisiae
and the multicellular filamentous fungus
Aspergillus nidulans
. We compare and contrast morphological landmarks of G1, S, G2, and M phases, molecular mechanisms that drive cell cycle progression, and checkpoints in these model unicellular and multicellular fungal systems.
Amyloid Prions in Fungi
Authors: Saupe Sven J. , Jarosz Daniel F. , True Heather L. 
Published: January 2017

ABSTRACT
Prions are infectious protein polymers that have been found to cause fatal diseases in mammals. Prions have also been identified in fungi (yeast and filamentous fungi), where they behave as cytoplasmic non-Mendelian genetic elements. Fungal prions correspond in most cases to fibrillary β-sheet-rich protein aggregates termed amyloids. Fungal prion models and, in particular, yeast prions were instrumental in the description of fundamental aspects of prion structure and propagation. These models established the “protein-only” nature of prions, the physical basis of strain variation, and the role of a variety of chaperones in prion propagation and amyloid aggregate handling. Yeast and fungal prions do not necessarily correspond to harmful entities but can have adaptive roles in these organisms.
Gastrointestinal Tuberculosis
Authors: Choi Eric H. , Coyle Walter J. 
Published: January 2017

ABSTRACTGastrointestinal tuberculosis (TB) is a fascinating disease which can be observed both in the clinical context of active pulmonary disease and as a primary infection with no pulmonary involvement. It represents a significant clinical challenge because of the resurgence of TB as well as the diagnostic challenges it poses. A high clinical suspicion remains the most powerful tool in an era of medicine when reliance on diagnostic technology increases. Antimicrobial therapy is the mainstay of therapy, but surgical and endoscopic interventions are frequently required for intestinal TB. Gastrointestinal TB is truly the “great mimic” and continues to require the astute clinical acumen of skillful clinicians to diagnose and treat.
Tuberculous Otomastoiditis
Authors: Hand Jonathan M. , Pankey George A. 
Published: January 2017

ABSTRACT

Tuberculous otitis media and mastoiditis, or tuberculous otomastoiditis, is a rare but well-described infectious process occasionally affecting individuals in the United States but more frequently seen in countries where tuberculosis is endemic. Infection may be primary and occur through mucus aspirated through the Eustachian tube. Alternatively, organisms may secondarily infect the nasopharynx when expectorated from the lungs and, less frequently, may be hematogenously spread. Chronic otorrhea and hearing loss are common symptoms, and extensive perforation of the tympanic membranes and facial nerve paralysis are routinely described. Diagnosis is made by direct culture of
Mycobacterium tuberculosis
, although more recently, molecular techniques have been used. Successful treatment of tuberculous otomastoiditis routinely involves surgical intervention combined with prolonged antituberculosis therapy.