bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lattice reduced and complete convex bodies
Authors: Codenotti Giulia , Freyer Ansgar 
Published: September 2024

AbstractThe purpose of this paper is to study convex bodies for which there exists no convex body of the same lattice width. Such bodies will be called ‘lattice reduced’, and they occur naturally in the study of the flatness constant in integer programming, as well as other problems related to lattice width. We show that any simplex that realizes the flatness constant must be lattice reduced and prove structural properties of general lattice reduced convex bodies: they are polytopes with at most vertices and their lattice width is attained by at least independent directions. Strongly related to lattice reduced bodies are the ‘lattice complete bodies’, which are convex bodies for which there exists no such that has the same lattice diameter as . Similar structural results are obtained for lattice complete bodies. Moreover, various construction methods for lattice reduced and complete convex bodies are presented.
Integrated care for adults with chronic musculoskeletal disorders: a scoping review protocol
Authors: Chala Mulugeta Bayisa , Elliott Jacobi , Baker G. Ross , Walton David M. , Steele Micheline , Schabrun Siobhan 
Published: September 2024

Objective:
The objective of this scoping review is to describe the current evidence exploring integrated care for people with chronic musculoskeletal disorders.

Introduction:
The integrated model of care is an emerging approach to delivering person-centered care. Integrated care supports the management of people with major chronic health conditions; however, the evidence behind its use to support people with chronic musculoskeletal disorders is scant. This scoping review will synthesize how integrated care is conceptualized, delivered, and evaluated for people with chronic musculoskeletal disorders. The review will also synthesize the attributes, components, elements, goals, frequently evaluated outcomes, theories/frameworks, and facilitators and barriers to delivering this model among people with musculoskeletal disorders.

Inclusion criteria:
Studies conducted on the delivery and/or evaluation of integrated care for people with chronic musculoskeletal disorders in any health care setting (eg, primary, secondary, tertiary) and/or geographical location (countries, cultures) will be considered.

Methods:
The review will follow the JBI scoping review methodology. Databases such as MEDLINE (Ovid), CINAHL (EBSCOhost), Scopus, Embase (Ovid), PsycINFO (Ovid), the JBI EBP Database, PEDRO, Cochrane Central Register of Controlled Trials (CENTRAL), Google Scholar, and Web of Science, as well as sources of gray literature, will be thoroughly searched. Papers published in all languages will be considered. Two reviewers will independently review the selected articles and extract data using a data extraction tool developed for this scoping review. The analysis will involve numerical and descriptive summaries of the selected articles and will be presented using graphs and tables, in line with Preferred Reported Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR).
Lipopolysaccharide accelerates peristalsis by stimulating glucagon‐like peptide‐1 release from L cells in the rat proximal colon
Authors: Nakamori Hiroyuki , Niimi Atsuko , Mitsui Retsu , Hashitani Hikaru 
Published: September 2024

AbstractUpon epithelial barrier dysfunction, lipopolysaccharide (LPS) stimulates glucagon‐like peptide‐1 (GLP‐1) secretion from enteroendocrine L cells by activating Toll‐like receptor 4 (TLR4). Because GLP‐1 accelerates peristalsis in the proximal colon, the present study aimed to explore whether LPS facilitates colonic peristalsis by stimulating L cell‐derived GLP‐1 release. In isolated segments of rat proximal colon that were serosally perfused with physiological salt solution and luminally perfused with 0.9% saline, peristaltic wall motion was video recorded and converted into spatio‐temporal maps. Fluorescence immunohistochemistry was also carried out. Intraluminal administration of LPS (100 or 1 µg mL−1 but not 100 ng mL−1) increased the frequency of oro‐aboral propagating peristaltic contractions. The LPS‐induced acceleration of colonic peristalsis was blocked by TAK‐242 (the TLR4 antagonist), exendin‐3 (the GLP‐1 receptor antagonist) or BIBN4096 (the calcitonin gene‐related peptide receptor antagonist). GLP‐1‐positive epithelial cells co‐expressed TLR4 immunoreactivity. In aspirin‐pretreated preparations where epithelial barrier function had been impaired, a lower dose of LPS (100 ng mL−1) became capable of accelerating peristalsis. By contrast, luminally applied dimethyl sulphoxide, a reactive oxygen species scavenger that protects epithelial integrity, attenuated the prokinetic effects of a higher dose of LPS (100 µg mL−1). In colonic segments of a stress rat model leading to a leaky gut, LPS induced more pronounced prokinetic effects. Colonic L cells may well sense luminal LPS via TLR4 triggering the release of GLP‐1 that stimulates calcitonin gene‐related peptide‐containing neurons. The resultant acceleration of peristalsis would facilitate excretion of Gram‐negative bacteria from the intestine, and thus L cells may have a protective role against intestinal bacterial infections.
imageKey points
Colonic epithelial cells form a barrier against bacterial invasion but also may contribute more actively to the exclusion of luminal pathogen by stimulating colonic motility.
Luminal lipopolysaccharide (LPS) accelerated colonic peristalsis by stimulating calcitonin gene‐related peptide‐containing neurons.
The prokinetic effect of LPS was mediated by the secretion of glucagon‐like peptide‐1 from enteroendocrine L cells in which Toll‐like receptor 4 was expressed.
The LPS‐mediated acceleration of peristalsis depended on epithelial barrier integrity.
L cells have a defensive role against Gram‐negative bacterial infections by facilitating faecal excretion, and could be a potential therapeutic target for gastrointestinal infections.
Expanding the Realms of Sport Psychology in Esports: An Epilogue
Authors: Swettenham Laura , Leis Oliver , Birch Phil , Price David 
Published: September 2024

In this epilogue to the special issue, we provide a summary of four case studies in esports. Specifically, we draw attention to (1) interventions with teams and esports athletes, (2) coach support and development, and (3) practitioner development. We explore these areas in relation to the case studies presented in the special issue, providing a structured analysis and discussion of the experiences shared in these case studies and shedding light on how sport psychology is applied in esports. Lastly, we offer future research and practice opportunities for those intending to practice or currently practicing in the realm of esports.
Gentamicin and clindamycin antibiotic-eluting depot technology eradicates
S. aureus
in an implant-associated osteomyelitis pig model without systemic antibiotics
Authors: Henriksen Nicole L. , Serrano-Chávez Elizabeth , Fuglsang-Madsen Albert , Jensen Louise K. , Gottlieb Hans , Bue Mats , Andresen Thomas L. , Henriksen Jonas R. , Hansen Anders E. 
Published: September 2024

ABSTRACT

The therapeutic challenges of orthopedic device-related infections and emerging antimicrobial resistance have attracted attention to drug delivery technologies. This study evaluates the preclinical efficacy of local single- and dual-antibiotic therapy against implant-associated osteomyelitis (IAO) using a drug-eluting depot technology, CarboCell, that provides sustained release of high-dose antibiotics and allows for strategic
in situ
placement in relation to infectious lesions. Clindamycin and gentamicin were formulated in CarboCell compositions. One-stage-revision of tibial
Staphylococcus aureus
IAO was conducted in 19 pigs. Pigs were treated locally with CarboCell containing either gentamicin alone for 1 week or a co-formulation of gentamicin and clindamycin for 1 or 3 weeks. Bone, soft tissue, and antibiotic depots were collected for microbiology, histology, and HPLC analyses. Supporting
in vivo
release studies of CarboCell formulations were performed on mice. Both single- and dual-antibiotic CarboCell formulations were developed and capable of eradicating the infectious bacteria in bone and preventing colonization of implants inserted at revision. Eradication in soft tissue was observed in all pigs after 3 weeks and in 6/9 pigs after 1 week of treatment. Neutrophil counts in bone tissue were below the infection cut-off in all pigs receiving the dual-antibiotic therapies, but above in all pigs receiving the single-antibiotic therapy. Histological signs of active bone reorganization and healing were observed at 3 weeks. In conclusion, all CarboCell formulations demonstrated strong therapeutic activity against IAO, eradicating
S. aureus
in bone tissue and preventing colonization of implants even without the addition of systemic antibiotic therapy.
Sporadic phage defense in epidemic
Vibrio cholerae
mediated by the toxin-antitoxin system DarTG is countered by a phage-encoded antitoxin mimic
Authors: Patel Kishen M. , Seed Kimberley D. 
Published: September 2024

ABSTRACT

Bacteria and their viral predators (phages) are constantly evolving to subvert one another. Many bacterial immune systems that inhibit phages are encoded on mobile genetic elements that can be horizontally transmitted to diverse bacteria. Despite the pervasive appearance of immune systems in bacteria, it is not often known if these immune systems function against phages that the host encounters in nature. Additionally, there are limited examples demonstrating how these phages counter-adapt to such immune systems. Here, we identify clinical isolates of the global pathogen
Vibrio cholerae
harboring a novel genetic element encoding the bacterial immune system DarTG and reveal the immune system’s impact on the co-circulating lytic phage ICP1. We show that DarTG inhibits ICP1 genome replication, thus preventing ICP1 plaquing. We further characterize the conflict between DarTG-mediated defense and ICP1 by identifying an ICP1-encoded protein that counters DarTG and allows ICP1 progeny production. Finally, we identify this protein, AdfB, as a functional antitoxin that abrogates the toxin DarT likely through direct interactions. Following the detection of the DarTG system in clinical
V. cholerae
isolates, we observed a rise in ICP1 isolates with the functional antitoxin. These data highlight the use of surveillance of
V. cholerae
and its lytic phages to understand the co-evolutionary arms race between bacteria and their phages in nature.

IMPORTANCE

The global bacterial pathogen
Vibrio cholerae
causes an estimated 1 to 4 million cases of cholera each year. Thus, studying the factors that influence its persistence as a pathogen is of great importance. One such influence is the lytic phage ICP1, as once infected by ICP1,
V. cholerae
is destroyed. To date, we have observed that the phage ICP1 shapes
V. cholerae
evolution through the flux of anti-phage bacterial immune systems. Here, we probe clinical
V. cholerae
isolates for novel anti-phage immune systems that can inhibit ICP1 and discover the toxin-antitoxin system DarTG as a potent inhibitor. Our results underscore the importance of
V. cholerae
and ICP1 surveillance to elaborate novel means by which
V. cholerae
can persist in both the human host and aquatic reservoir in the face of ICP1.
SIRT7 remodels the cytoskeleton
via
RAC1 to enhance host resistance to
Mycobacterium tuberculosis
Authors: Li Fuxiang , Zhang Ximeng , Xu Jinjin , Zhang Yue , Li Guo , Yang Xirui , Deng Guofang , Dai Youchao , Liu Baohua , Kosan Christian , Chen Xinchun , Cai Yi 
Published: September 2024

ABSTRACT

Phagocytosis of
Mycobacterium tuberculosis
(
Mtb
) followed by its integration into the matured lysosome is critical in the host defense against tuberculosis. How
Mtb
escapes this immune attack remains elusive. In this study, we unveiled a novel regulatory mechanism by which SIRT7 regulates cytoskeletal remodeling by modulating RAC1 activation. We discovered that SIRT7 expression was significantly reduced in CD14
+
monocytes of TB patients.
Mtb
infection diminished SIRT7 expression by macrophages at both the mRNA and protein levels. SIRT7 deficiency impaired actin cytoskeleton-dependent macrophage phagocytosis, LC3II expression, and bactericidal activity. In a murine tuberculosis model, SIRT7 deficiency detrimentally impacted host resistance to
Mtb
, while
Sirt7
overexpression significantly increased the host defense against
Mtb
, as determined by bacterial burden and inflammatory–histopathological damage in the lung. Mechanistically, we demonstrated that SIRT7 limits
Mtb
infection by directly interacting with and activating RAC1, through which cytoskeletal remodeling is modulated. Therefore, we concluded that SIRT7, in its role regulating cytoskeletal remodeling through RAC1, is critical for host responses during
Mtb
infection and proposes a potential target for tuberculosis treatment.

IMPORTANCE

Tuberculosis (TB), caused by
Mycobacterium tuberculosis
(
Mtb
), remains a significant global health issue. Critical to macrophages’ defense against
Mtb
is phagocytosis, governed by the actin cytoskeleton. Previous research has revealed that
Mtb
manipulates and disrupts the host’s actin network, though the specific mechanisms have been elusive. Our study identifies a pivotal role for SIRT7 in this context:
Mtb
infection leads to reduced SIRT7 expression, which, in turn, diminishes RAC1 activation and consequently impairs actin-dependent phagocytosis. The significance of our research is that SIRT7 directly engages with and activates Rac Family Small GTPase 1 (RAC1), thus promoting effective phagocytosis and the elimination of
Mtb
. This insight into the dynamic between host and pathogen in TB not only broadens our understanding but also opens new avenues for therapeutic development.
Gut microbiota-derived butyrate improved acute leptospirosis in hamster
via
promoting macrophage ROS mediated by HDAC3 inhibition
Authors: Chen Xi , Xie Xufeng , Sun Ni , Liu Xin , Liu Jiuxi , Zhang Wenlong , Cao Yongguo 
Published: September 2024

ABSTRACT

Leptospirosis is a re-emerging worldwide zoonotic disease. Infected patients and animals often exhibit intestinal symptoms. Mounting evidence suggests that host immune responses to bacterial infection are closely associated with intestinal homeostasis. Our previous research has shown that the gut microbiota can protect the host from acute leptospirosis, while the specific bacterial metabolic mediators participating in the pathogenesis remain to be identified. Short-chain fatty acids (SCFAs) are metabolites produced mainly by the gut microbiota that play a role in immune regulation. However, whether SCFAs are the key to protecting the host against leptospirosis and the underlying regulatory mechanisms are unknown. In this study, our results showed that the SCFA butyrate is involved in ameliorating leptospirosis. The depletion of SCFAs by antibiotic cocktail treatment reduced survival time after
Leptospira
infection while supplementation with butyrate but not acetate or propionate significantly amelioration of leptospirosis.
In vitro
experiments showed that butyrate treatment enhanced the intracellular bactericidal activity mediated by reactive oxygen species (ROS) production. Mechanistically, butyrate functions as a histone deacetylase 3 inhibitor (HDAC3i) to promote ROS production
via
monocarboxylate transporter (MCT). The protection of butyrate against acute leptospirosis mediated by ROS was also proven
in vivo
. Collectively, our data provide evidence that the butyrate-MCT-HDAC3i-ROS signaling axis is a potential therapeutic target for acute leptospirosis. Our work not only interprets the microbial metabolite signaling involved in transkingdom interactions between the host and gut microbiota but also provides a possible target for developing a prevention strategy for acute leptospirosis.

IMPORTANCE

Leptospirosis is a worldwide zoonotic disease caused by
Leptospira
. An estimated 1 million people are infected with leptospirosis each year. Studies have shown that healthy gut microbiota can protect the host against leptospirosis but the mechanism is not clear. This work elucidated the mechanism of gut microbiota protecting the host against acute leptospirosis. Here, we find that butyrate, a metabolite of gut microbiota, can improve the survival rate of hamsters with leptospirosis by promoting the bactericidal activity of macrophages. Mechanistically, butyrate upregulates reactive oxygen species (ROS) levels after macrophage infection with
Leptospira
by inhibiting HDAC3. This work confirms the therapeutic potential of butyrate in preventing acute leptospirosis and provides evidence for the benefits of the macrophage-HDAC3i-ROS axis.
Reconceptualizing transcriptional slippage in plant RNA viruses
Authors: Valli Adrian A. , Domingo-Calap María Luisa , González de Prádena Alfonso , García Juan Antonio , Cui Hongguang , Desbiez Cécile , López-Moya Juan José 
Published: September 2024

ABSTRACT

RNA viruses have evolved sophisticated strategies to exploit the limited encoded information within their typically compact genomes. One of them, named transcriptional slippage (TS), is characterized by the appearance of indels in nascent viral RNAs, leading to changes in the open reading frame (ORF). Although members of unrelated viral families express key proteins via TS, the available information about this phenomenon is still limited. In potyvirids (members of the
Potyviridae
family), TS has been defined by the insertion of an additional A at A
n
motifs (
n
≥ 6) in newly synthesized transcripts at a low frequency, modulated by nucleotides flanking the A-rich motif. Here, by using diverse experimental approaches and a collection of plant/virus combinations, we discover cases not following this definition. In summary, we observe (i) a high rate of single-nucleotide deletions at slippage motifs, (ii) overlapping ORFs acceded by slippage at an U
8
stretch, and (iii) changes in slippage rates induced by factors not related to cognate viruses. Moreover, a survey of whole-genome sequences from potyvirids shows a widespread occurrence of species-specific A
n
/U
n
(
n
≥ 6) motifs. Even though many of them, but not all, lead to the production of truncated proteins rather than access to overlapping ORFs, these results suggest that slippage motifs appear more frequently than expected and play relevant roles during virus evolution. Considering the potential of this phenomenon to expand the viral proteome by acceding to overlapping ORFs and/or producing truncated proteins, a re-evaluation of TS significance during infections of RNA viruses is required.

IMPORTANCE
Transcriptional slippage (TS) is used by RNA viruses as another strategy to maximize the coding information in their genomes. This phenomenon is based on a peculiar feature of viral replicases: they may produce indels in a small fraction of newly synthesized viral RNAs when transcribing certain motifs and then produce alternative proteins due to a change of the reading frame or truncated products by premature termination. Here, using plant-infecting RNA viruses as models, we discover cases expanding on previously established features of plant virus TS, prompting us to reconsider and redefine this expression strategy. An interesting conclusion from our study is that TS might be more relevant during RNA virus evolution and infection processes than previously assumed.
Lactobacillus johnsonii
is a dominant
Lactobacillus
in the murine oral mucosa and has chitinase activity that compromises fungal cell wall integrity
Authors: Vazquez-Munoz Roberto , Thompson Angela , Sobue Takanori , Dongari-Bagtzoglou Anna 
Published: September 2024

ABSTRACT

The oral microbiome is a critical determinant of health and disease, as interactions between oral microorganisms can influence their physiology and the development or severity of oral infections. Lactobacilli have a widely recognized antagonistic relationship with
Candida albicans
and may exhibit probiotic properties that limit oral fungal infection. We previously reported that
Lactobacillus johnsonii
strain MT4, an oral strain isolated from C57BL/6 mice, can induce global changes in the murine oral microbiome and has anti-
Candida
activity
in vitro
. To build on this information, we analyzed its abundance on the mouse oral mucosa, tested its impact on the severity and progression of oropharyngeal candidiasis (OPC) in a mouse model, and further explored the mechanism of antifungal activity
in vitro
. Our findings reveal that
L. johnsonii
MT4 is a dominant cultivable
Lactobacillus
in the oral mucosa of C57BL/6 mice. Strain MT4 has chitinase activity against
C. albicans
, which damages the cell wall and compromises fungal metabolic activity. Oral inoculation with strain MT4 causes a reduction in the
Candida
-induced rise in the abundance of oral enterococci and oral mucosal damage. This research underscores the potential of
L. johnsonii
strain MT4 as a novel probiotic agent in the prevention or management of OPC, and it contributes to a better understanding of the role of oral bacterial microbiota role in the pathogenesis of fungal infections.

IMPORTANCE

The interactions between the opportunistic pathogen
Candida albicans
and resident oral bacteria are particularly crucial in maintaining oral health. Emerging antifungal drug-resistant strains, slow-paced drug discovery, and the risk of side effects can compromise the effectiveness of current treatments available for oropharyngeal candidiasis. This study advances the search for alternative microbiome-targeted therapies in oral fungal infections. We report that
Lactobacillus johnsonii
strain MT4 prevents the
Candida
-induced bloom of dysbiotic oral enterococci and reduces oral mucosal lesions in an oropharyngeal candidiasis murine model. We also show that this strain directly compromises the cell wall and reduces fungal metabolic activity, partly due to its chitinase activity.
Draft genome sequence of
Bacillus cereus
sequence type 2255 isolated from powdered infant formula
Authors: Patil Sonali , Wong Catherine W.Y. , Zhang Richard , Zhang Annika , Zhou Xinyi , Zhang Wei 
Published: September 2024

ABSTRACT

The draft genome sequence of a
Bacillus cereus
strain, DFPST-SP1, isolated from powdered infant formula in the United States is reported. The 5,216,828-bp draft genome comprises 46 contigs with 66.4× coverage and 36% GC content and was typed as sequence type 2255.