bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accurate stochastic reconstruction of heterogeneous microstructures by limited x‐ray tomographic projections
Authors: LI HECHAO , KAIRA SHASHANK , MERTENS JAMES , CHAWLA NIKHILESH , JIAO YANG 
Published: July 2016

SummaryAn accurate knowledge of the complex microstructure of a heterogeneous material is crucial for its performance prediction, prognosis and optimization. X‐ray tomography has provided a nondestructive means for microstructure characterization in 3D and 4D (i.e. structural evolution over time), in which a material is typically reconstructed from a large number of tomographic projections using filtered‐back‐projection (FBP) method or algebraic reconstruction techniques (ART). Here, we present in detail a stochastic optimization procedure that enables one to accurately reconstruct material microstructure from a small number of absorption contrast x‐ray tomographic projections. This discrete tomography reconstruction procedure is in contrast to the commonly used FBP and ART, which usually requires thousands of projections for accurate microstructure rendition. The utility of our stochastic procedure is first demonstrated by reconstructing a wide class of two‐phase heterogeneous materials including sandstone and hard‐particle packing from simulated limited‐angle projections in both cone‐beam and parallel beam projection geometry. It is then applied to reconstruct tailored Sn‐sphere‐clay‐matrix systems from limited‐angle cone‐beam data obtained via a lab‐scale tomography facility at Arizona State University and parallel‐beam synchrotron data obtained at Advanced Photon Source, Argonne National Laboratory. In addition, we examine the information content of tomography data by successively incorporating larger number of projections and quantifying the accuracy of the reconstructions. We show that only a small number of projections (e.g. 20–40, depending on the complexity of the microstructure of interest and desired resolution) are necessary for accurate material reconstructions via our stochastic procedure, which indicates its high efficiency in using limited structural information. The ramifications of the stochastic reconstruction procedure in 4D materials science are also discussed.
The clinical value of controlled attenuation parameter for the noninvasive assessment of liver steatosis
Authors: Ferraioli Giovanna , Tinelli Carmine , De Silvestri Annalisa , Lissandrin Raffaella , Above Elisabetta , Dellafiore Carolina , Poma Gianluigi , Di Gregorio Marta , Maiocchi Laura , Maserati Renato , Filice Carlo 
Published: July 2016

AbstractBackground & AimsUltrasound is the imaging modality most widely utilized in the general population for diagnostic purposes. Controlled attenuation parameter is a novel noninvasive method for assessing steatosis. Our aim was to investigate whether the clinical value of controlled attenuation parameter in patients referred for abdominal ultrasound examinations is affected by liver fibrosis.MethodsConsecutive patients referred for abdominal ultrasound examinations were enrolled. Controlled attenuation parameter and liver stiffness were assessed with the FibroScan (Echosens, France). Liver fibrosis was staged according to published cutoffs of liver stiffness measurements. Pearson's or Spearman's rank correlation coefficient was used to test the association between two study variables. Optimal cutoff of controlled attenuation parameter for diagnosing liver steatosis (S≥2) was 256 dB/m. The diagnostic performance and accuracy of dichotomized controlled attenuation parameter, ultrasound and body mass index were analysed using the imperfect gold standard methodology.ResultsA total of 726 subjects (464 males and 262 females) were studied. Five hundred and eight‐nine (81.1%) patients were affected by chronic viral hepatitis. Correlation of controlled attenuation parameter with ultrasound score was 0.48 and 0.57 in patients with and without chronic viral hepatitis respectively. In patients with chronic viral hepatitis, ultrasound, dichotomized controlled attenuation parameter and body mass index showed performance of 58.2%, 82.3% and 46.7%, respectively, whereas in patients without chronic viral hepatitis, the performance was 86.4%, 68.6% and 48.6% respectively.ConclusionsIn patients with chronic viral hepatitis and advanced liver fibrosis, controlled attenuation parameter performs better than ultrasound for assessing liver steatosis, whereas in patients without viral hepatitis and with nonsignificant liver disease ultrasound shows the best performance.
Integrated low‐intensity biofeedback therapy in fecal incontinence: evidence that “good” in‐home anal sphincter exercise practice makes perfect
Authors: Vasant D. H. , Solanki K. , Balakrishnan S. , Radhakrishnan N. V. 
Published: July 2016

AbstractBackgroundBiofeedback therapy (BFT) is an established treatment for fecal incontinence (FI), with access often being restricted to tertiary centers due to resources and the perceived requirement for high‐intensity regimes. However, the optimal regime remains unknown. We evaluated outcomes from our low‐intensity integrated BFT program in a secondary care center.MethodsOutcomes of our BFT service for FI were evaluated retrospectively. Response was defined by ≥50% improvement in FI frequency from baseline or complete continence. Responders were compared to non‐responders for factors including symptoms, manometry data, sphincter exercise technique and duration of practice, and the number and frequency of sessions. Where patients dropped out, outcomes and the reason for dropout were obtained retrospectively.Key ResultsFecal incontinence patients (n=205, median 62 years, 72% female) attended a median (IQR) 3 (2) BFT sessions with 55 (36) days between visits. Overall, 146/205 (71%) responded with 97/205 (47%) achieving continence. Fecal incontinence frequency improved dramatically in completed cases (P=0.000). While non‐response was associated with males (P=0.03) and dropout (P=0.000), “good” anal sphincter exercise technique (P=0.008) and longer in‐home practice (P=0.007) and more sessions (P=0.04) were associated with response. Dropout rate was 80/205 (39%), with the reason for dropout being obtained in 80%.Conclusions & InferencesDespite low‐intensity BFT, comparable outcomes to data from tertiary centers were achieved. Our data emphasize the importance of technique and in‐home practice of anal sphincter exercises. Customizing BFT intensity based on predictive factors and encouraging in‐home practice may optimize outcomes, reduce dropout rates, and rationalize resources.
Taxonomic similarity, more than contact opportunity, explains novel plant–pathogen associations between native and alien taxa
Authors: Bufford Jennifer L. , Hulme Philip E. , Sikes Benjamin A. , Cooper Jerry A. , Johnston Peter R. , Duncan Richard P. 
Published: July 2016

Summary

Novel associations between plants and pathogens can have serious impacts on managed and natural ecosystems world‐wide. The introduction of alien plants increases the potential for biogeographically novel plant–pathogen associations to arise when pathogens are transmitted from native to alien plant species and vice versa.

We quantified biogeographically novel associations recorded in New Zealand over the last 150 yr between plant pathogens (fungi, oomycetes and plasmodiophorids) and vascular plants. We examined the extent to which taxonomic similarity, pathogen traits, contact opportunity and sampling effort could explain the number of novel associates for host and pathogen species.

Novel associations were common; approximately one‐third of surveyed plants and pathogens were recorded with at least one biogeographically novel associate. Native plants had more alien pathogens than vice versa. Taxonomic similarity between the native and alien flora and the total number of recorded associations (a measure of sampling effort) best explained the number of novel associates among species.

The frequency of novel associations and the importance of sampling effort as an explanatory variable emphasize the need for effective monitoring and risk assessment tools to mitigate the potential environmental and economic impact of novel pathogen associations.
Characterization of Anaplasma marginale subsp. centrale Strains by Use of
msp1aS
Genotyping Reveals a Wildlife Reservoir
Authors: Khumalo Zamantungwa T. H. , Catanese Helen N. , Liesching Nicole , Hove Paidashe , Collins Nicola E. , Chaisi Mamohale E. , Gebremedhin Assefaw H. , Oosthuizen Marinda C. , Brayton Kelly A. 
Published: July 2016

ABSTRACT

Bovine anaplasmosis caused by the intraerythrocytic rickettsial pathogen
Anaplasma marginale
is endemic in South Africa.
Anaplasma marginale
subspecies
centrale
also infects cattle; however, it causes a milder form of anaplasmosis and is used as a live vaccine against
A. marginale
. There has been less interest in the epidemiology of
A. marginale
subsp.
centrale
, and, as a result, there are few reports detecting natural infections of this organism. When detected in cattle, it is often assumed that it is due to vaccination, and in most cases, it is reported as coinfection with
A. marginale
without characterization of the strain. A total of 380 blood samples from wild ruminant species and cattle collected from biobanks, national parks, and other regions of South Africa were used in duplex real-time PCR assays to simultaneously detect
A. marginale
and
A. marginale
subsp.
centrale.
PCR results indicated high occurrence of
A. marginale
subsp.
centrale
infections, ranging from 25 to 100% in national parks. Samples positive for
A. marginale
subsp.
centrale
were further characterized using the
msp1aS
gene, a homolog of
msp1
α of
A. marginale
, which contains repeats at the 5′ ends that are useful for genotyping strains. A total of 47 Msp1aS repeats were identified, which corresponded to 32
A. marginale
subsp.
centrale
genotypes detected in cattle, buffalo, and wildebeest. RepeatAnalyzer was used to examine strain diversity. Our results demonstrate a diversity of
A. marginale
subsp.
centrale
strains from cattle and wildlife hosts from South Africa and indicate the utility of
msp1aS
as a genotypic marker for
A. marginale
subsp.
centrale
strain diversity.
First Evaluation of GenoType MTBDR
plus
2.0 Performed Directly on Respiratory Specimens in Central America
Authors: Lanzas Fedora , Ioerger Thomas R. , Shah Harita , Acosta William , Karakousis Petros C. 
Published: July 2016

ABSTRACT

The turnaround times for conventional methods used to detect
Mycobacterium tuberculosis
in sputum samples and to obtain drug susceptibility information are long in many developing countries, including Panama, leading to delays in appropriate treatment initiation and continued transmission in the community. We evaluated the performance of a molecular line probe assay, the Genotype MTBDR
plus
version 2.0 assay, in detecting
M. tuberculosis
complex directly in respiratory specimens from smear-positive tuberculosis cases from four different regions in Panama, as well as the most frequent mutations in genes conferring resistance to isoniazid (
katG
and
inhA
) and rifampin (
rpoB
). Our results were confirmed with the nitrate reductase assay and genomic sequencing.
M. tuberculosis
complex was detected by the Genotype MTBDR
plus
2.0 assay with 100% sensitivity and specificity. The sensitivity and specificity for rifampin resistance were 100% and 100%, respectively, and those for isoniazid resistance were 90.7% and 100%. Isoniazid monoresistance was detected in 5.2% of new cases. Genotype MTBDR
plus
2.0 is highly accurate in detecting
M. tuberculosis
complex in respiratory specimens and is able to discriminate isoniazid-monoresistant cases from multidrug-resistant cases within 2 days.
Human Cathelicidin Compensates for the Role of Apolipoproteins in Hepatitis C Virus Infectious Particle Formation
Authors: Puig-Basagoiti Francesc , Fukuhara Takasuke , Tamura Tomokazu , Ono Chikako , Uemura Kentaro , Kawachi Yukako , Yamamoto Satomi , Mori Hiroyuki , Kurihara Takeshi , Okamoto Toru , Aizaki Hideki , Matsuura Yoshiharu 
Published: July 2016

ABSTRACT
Exchangeable apolipoproteins (ApoA, -C, and -E) have been shown to redundantly participate in the formation of infectious hepatitis C virus (HCV) particles during the assembly process, although their precise role in the viral life cycle is not well understood. Recently, it was shown that the exogenous expression of only short sequences containing amphipathic α-helices from various apolipoproteins is sufficient to restore the formation of infectious HCV particles in ApoB and ApoE double-gene-knockout Huh7 (BE-KO) cells. In this study, through the expression of a small library of human secretory proteins containing amphipathic α-helix structures, we identified the human cathelicidin antimicrobial peptide (CAMP), the only known member of the cathelicidin family of antimicrobial peptides (AMPs) in humans and expressed mainly in bone marrow and leukocytes. We showed that CAMP is able to rescue HCV infectious particle formation in BE-KO cells. In addition, we revealed that the LL-37 domain in CAMP containing amphipathic α-helices is crucial for the compensation of infectivity in BE-KO cells, and the expression of CAMP in nonhepatic 293T cells expressing claudin 1 and microRNA miR-122 confers complete propagation of HCV. These results suggest the possibility of extrahepatic propagation of HCV in cells with low-level or no expression of apolipoproteins but expressing secretory proteins containing amphipathic α-helices such as CAMP.

IMPORTANCE
Various exchangeable apolipoproteins play a pivotal role in the formation of infectious HCV during the assembly of viral particles, and amphipathic α-helix motifs in the apolipoproteins have been shown to be a key factor. To the best of our knowledge, we have identified for the first time the human cathelicidin CAMP as a cellular protein that can compensate for the role of apolipoproteins in the life cycle of HCV. We have also identified the domain in CAMP that contains amphipathic α-helices crucial for compensation and show that the expression of CAMP in nonhepatic cells expressing claudin 1 and miR-122 confers complete propagation of HCV. We speculate that low levels of HCV propagation might be possible in extrahepatic tissues expressing secretory proteins containing amphipathic α-helices without the expression of apolipoproteins.
Analysis of Major Histocompatibility Complex-Bound HIV Peptides Identified from Various Cell Types Reveals Common Nested Peptides and Novel T Cell Responses
Authors: Rucevic Marijana , Kourjian Georgio , Boucau Julie , Blatnik Renata , Garcia Bertran Wilfredo , Berberich Matthew J. , Walker Bruce D. , Riemer Angelika B. , Le Gall Sylvie 
Published: July 2016

ABSTRACTDespite the critical role of epitope presentation for immune recognition, we still lack a comprehensive definition of HIV peptides presented by HIV-infected cells. Here we identified 107 major histocompatibility complex (MHC)-bound HIV peptides directly from the surface of live HIV-transfected 293T cells, HIV-infected B cells, and primary CD4 T cells expressing a variety of HLAs. The majority of peptides were 8 to 12 amino acids (aa) long and mostly derived from Gag and Pol. The analysis of the total MHC-peptidome and of HLA-A02-bound peptides identified new noncanonical HIV peptides of up to 16 aa that could not be predicted by HLA anchor scanning and revealed an heterogeneous surface peptidome. Nested sets of surface HIV peptides included optimal and extended HIV epitopes and peptides partly overlapping or distinct from known epitopes, revealing new immune responses in HIV-infected persons. Surprisingly, in all three cell types, a majority of Gag peptides derived from p15 rather than from the most immunogenic p24. The cytosolic degradation of peptide precursors in corresponding cells confirmed the generation of identified surface-nested peptides. Cytosolic degradation revealed peptides commonly produced in all cell types and displayed by various HLAs, peptides commonly produced in all cell types and selectively displayed by specific HLAs, and peptides produced in only one cell type. Importantly, we identified areas of proteins leading to common presentations of noncanonical peptides by several cell types with distinct HLAs. These peptides may benefit the design of immunogens, focusing T cell responses on relevant markers of HIV infection in the context of HLA diversity.IMPORTANCEThe recognition of HIV-infected cells by immune T cells relies on the presentation of HIV-derived peptides by diverse HLA molecules at the surface of cells. The landscape of HIV peptides displayed by HIV-infected cells is not well defined. Considering the diversity of HLA molecules in the human population, it is critical for vaccine design to identify HIV peptides that may be displayed despite the HLA diversity. We identified 107 HIV peptides directly from the surface of three cell types infected with HIV. They corresponded to nested sets of HIV peptides of canonical and novel noncanonical lengths not predictable by the presence of HLA anchors. Importantly, we identified areas of HIV proteins leading to presentation of noncanonical peptides by several cell types with distinct HLAs. Including such peptides in vaccine immunogen may help to focus immune responses on common markers of HIV infection in the context of HLA diversity.
Characterization of Viral Populations by Using Circular Sequencing
Authors: Whitfield Zachary J. , Andino Raul 
Published: July 2016

ABSTRACT
With the enormous sizes viral populations reach, many variants are at too low a frequency to be detected by conventional next-generation sequencing (NGS) methods. Circular sequencing (CirSeq) is a method by which the error rate of next-generation sequencing is decreased so that even low-frequency viral variants can be accurately detected. The ability to visualize almost the entire genetic makeup of a viral swarm has implications for epidemiology, viral evolution, and vaccine design. Here we discuss experimental planning, analysis, and recent insights using CirSeq.
Herpes Simplex Virus 1 Interaction with Myeloid CellsIn Vivo
Authors: Shivkumar Maitreyi , Lawler Clara , Milho Ricardo , Stevenson Philip G. 
Published: July 2016

ABSTRACTHerpes simplex virus 1 (HSV-1) enters mice via olfactory epithelial cells and then colonizes the trigeminal ganglia (TG). Most TG nerve endings are subepithelial, so this colonization implies subepithelial viral spread, where myeloid cells provide an important line of defense. The outcome of infection of myeloid cells by HSV-1in vitrodepends on their differentiation state; the outcomein vivois unknown. Epithelial HSV-1 commonly infected myeloid cells, and Cre-Lox virus marking showed nose and lung infections passing through LysM-positive (LysM+) and CD11c+cells. In contrast, subcapsular sinus macrophages (SSMs) exposed to lymph-borne HSV-1 were permissive only when type I interferon (IFN-I) signaling was blocked; normally, their infection was suppressed. Thus, the outcome of myeloid cell infection helped to determine the HSV-1 distribution: subepithelial myeloid cells provided a route of spread from the olfactory epithelium to TG neurons, while SSMs blocked systemic spread.IMPORTANCEHerpes simplex virus 1 (HSV-1) infects most people and can cause severe disease. This reflects its persistence in nerve cells that connect to the mouth, nose, eye, and face. Established infection seems impossible to clear. Therefore, we must understand how it starts. This is difficult in humans, but mice show HSV-1 entry via the nose and then spread to its preferred nerve cells. We show that this spread proceeds in part via myeloid cells, which normally function in host defense. Myeloid infection was productive in some settings but was efficiently suppressed by interferon in others. Therefore, interferon acting on myeloid cells can stop HSV-1 spread, and enhancing this defense offers a way to improve infection control.
Molecular Determinants Directing HIV-1 Gag Assembly to Virus-Containing Compartments in Primary Macrophages
Authors: Inlora Jingga , Chukkapalli Vineela , Bedi Sukhmani , Ono Akira 
Published: July 2016

ABSTRACT

The subcellular sites of HIV-1 assembly, determined by the localization of the structural protein Gag, vary in a cell-type-dependent manner. In T cells and transformed cell lines used as model systems, HIV-1 assembles at the plasma membrane (PM). The binding and localization of HIV-1 Gag to the PM are mediated by the interaction between the matrix (MA) domain, specifically the highly basic region, and a PM-specific acidic phospholipid, phosphatidylinositol-4,5-bisphosphate [PI(4,5)P
2
]. In primary macrophages, prominent accumulation of assembling or assembled particles is found in the virus-containing compartments (VCCs), which largely consist of convoluted invaginations of the PM. To elucidate the molecular mechanism of HIV-1 Gag targeting to the VCCs, we examined the impact of overexpression of polyphosphoinositide 5-phosphatase IV (5ptaseIV), which depletes cellular PI(4,5)P
2
, in primary macrophages. We found that the VCC localization and virus release of HIV-1 are severely impaired upon 5ptaseIV overexpression, suggesting an important role for the MA-PI(4,5)P
2
interaction in HIV-1 assembly in primary macrophages. However, our analysis of HIV-1 Gag derivatives with MA changes showed that this interaction contributes to Gag membrane binding but is dispensable for specific targeting of Gag to the VCCs
per se
. We further determined that deletion of the NC domain abolishes VCC-specific localization of HIV-1 Gag. Notably, HIV-1 Gag localized efficiently to the VCCs when the NC domain was replaced with a leucine zipper dimerization motif that promotes Gag multimerization. Altogether, our data revealed that targeting of HIV-1 Gag to the VCCs requires NC-dependent multimerization.

IMPORTANCE
In T cells and model cell lines, HIV-1 Gag localizes to the PM in a manner dependent on the MA-PI(4,5)P
2
interaction. On the other hand, in primary macrophages, HIV-1 Gag localizes to convoluted intracellular membrane structures termed virus-containing compartments (VCCs). Although these compartments have been known for decades, and despite the implication of viruses in VCCs being involved in virus reservoir maintenance and spread, the viral determinant(s) that promotes Gag targeting to VCCs is unknown. In this study, we found that the MA-PI(4,5)P
2
interaction facilitates efficient Gag membrane binding in macrophages but is not essential for Gag targeting to VCCs. Rather, our results revealed that NC-dependent multimerization promotes VCC targeting. Our findings highlight the differential roles played by MA and NC in HIV-1 Gag membrane binding and targeting and suggest a multimerization-dependent mechanism for Gag trafficking in primary macrophages similar to that for Gag localization to uropods in polarized T cells.