bluuebunny/crossref_metadata_2025_split huggingface dataset:
Models for malaria control optimization—a systematic review
Authors: Ngwafor Randolph , Pokharel Sunil , Aguas Ricardo , White Lisa , Shretta Rima 
Published: October 2024

Abstract
Background
Despite advances made in curbing the global malaria burden since the 2000s, progress has stalled, in part due to a plateauing of the financing available to implement needed interventions. In 2020, approximately 3.3 billion USD was invested globally for malaria interventions, falling short of the targeted 6.8 billion USD set by the GTS, increasing the financial gap between desirable and actual investment. Models for malaria control optimization are used to disentangle the most efficient interventions or packages of interventions for inherently constrained budgets. This systematic review aimed to identify and characterise models for malaria control optimization for resource allocation in limited resource settings and assess their strengths and limitations.

Methods
Following the Prospective Register of Systematic Reviews and Preferred reporting Items for Systematic Reviews and Meta-Analysis guidelines, a comprehensive search across PubMed and Embase databases was performed of peer-reviewed literature published from inception until June 2024. The following keywords were used: optimization model; malaria; control interventions; elimination interventions. Editorials, commentaries, opinion papers, conference abstracts, media reports, letters, bulletins, pre-prints, grey literature, non-English language studies, systematic reviews and meta-analyses were excluded from the search.

Results
The search yielded 2950 records, of which 15 met the inclusion criteria. The studies were carried out mainly in countries in Africa (53.3%), such as Ghana, Nigeria, Tanzania, Uganda, and countries in Asia (26.7%), such as Thailand and Myanmar. The most used interventions for analyses were insecticide-treated bed nets (93.3%), IRS (80.0%), Seasonal Malaria Chemoprevention (33.3%) and Case management (33.3%). The methods used for estimating health benefits were compartmental models (40.0%), individual-based models (40.0%), static models (13.0%) and linear regression model (7%). Data used in the analysis were validated country-specific data (60.0%) or non-country-specific data (40.0%) and were analysed at national only (40.0%), national and subnational levels (46.7%), or subnational only levels (13.3%).

Conclusion
This review identified available optimization models for malaria resource allocation. The findings highlighted the need for country-specific analysis for malaria control optimization, the use of country-specific epidemiological and cost data in performing modelling analyses, performing cost sensitivity analyses and defining the perspective for the analysis, with an emphasis on subnational tailoring for data collection and analysis for more accurate and good quality results. It is critical that the future modelling efforts account for fairness and target at risk malaria populations that are hard-to-reach to maximize impact.
Trial registration: PROSPERO Registration number: CRD42023436966
Proteasome inhibition suppresses the induction of lipocalin-2 upon systemic lipopolysaccharide challenge in mice
Authors: Bae Jin-Sil , Heo Ji-Eun , Ryu Kwon-Yul 
Published: October 2024

AbstractLipocalin-2 (Lcn2), a protein secreted by immune-activated cells, including reactive astrocytes, is detrimental to the brain and induces neurodegeneration. We previously showed that Lcn2 levels are reduced in primary mouse astrocytes after treatment with the proteasome inhibitor bortezomib (BTZ). However, it remains unknown whether a decrease in Lcn2 levels after BTZ treatment can also be observed in vivo and whether it reduces neurotoxicity during lipopolysaccharide (LPS)-induced systemic inflammation in vivo. To answer these questions, we performed LPS challenge experiments by intraperitoneal injection in mice and found that Lcn2 levels were significantly increased in the brain, recapitulating in vitro experiments using astrocytes. Co-administration of LPS and BTZ reduced the Lcn2 levels compared to the levels in LPS-treated controls. Upon LPS challenge, the expression levels of glial marker genes were upregulated in the mouse brain. Of note, this upregulation was hampered by the co-administration of BTZ. Taken together, our results suggested that BTZ can reduce LPS-induced Lcn2 levels and may alleviate LPS-induced neuroinflammation and neurotoxicity in mice.
Utilising primary care electronic health records to deliver the ALABAMA randomised controlled trial of penicillin allergy assessment
Authors: Ahmed Shadia , Fielding Joanne , Porter Catherine E. , Armitage Kelsey F. , Wanat Marta , Bates Chris , Engonidou Lazarina , West Robert M. , Yu Ly-Mee , Galal Ushma , Howard Philip , Butler Christopher C. , Savic Sinisa , Boards Jenny , Tonkin-Crine Sarah , Parry John , Pavitt Sue A. , Sandoe Jonathan T. ,   on behalf of ALABAMA research team
Published: October 2024

Abstract
Background
Use of electronic health records (EHR) to provide real-world data for research is established, but using EHR to deliver randomised controlled trials (RCTs) more efficiently is less developed. The Allergy AntiBiotics And Microbial resistAnce (ALABAMA) RCT evaluated a penicillin allergy assessment pathway versus usual clinical care in a UK primary care setting. The aim of this paper is to describe how EHRs were used to facilitate efficient delivery of a large-scale randomised trial of a complex intervention embracing efficient participant identification, supporting minimising GP workload, providing accurate post-intervention EHR updates of allergy status, and facilitating participant follow up and outcome data collection. The generalisability of the EHR approach and health economic implications of EHR in clinical trials will be reported in the main ALABAMA trial cost-effectiveness analysis.

Methods
A descriptive account of the adaptation of functionality within SystmOne used to deliver/facilitate multiple trial processes from participant identification to outcome data collection.

Results
An ALABAMA organisation group within SystmOne was established which allowed sharing of trial functions/materials developed centrally by the research team. The ‘ALABAMA unit’ within SystmOne was also created and provided a secure efficient environment to access participants’ EHR data. Processes of referring consented participants, allocating them to a trial arm, and assigning specific functions to the intervention arm were developed by adapting tools such as templates, reports, and protocols which were already available in SystmOne as well as pathways to facilitate allergy de-labelling processes and data retrieval for trial outcome analysis.

Conclusions
ALABAMA is one of the first RCTs to utilise SystmOne EHR functionality and data across the RCT delivery, demonstrating feasibility and applicability to other primary care RCTs.

Trial registration
ClinicalTrials.gov: NCT04108637, registered 05/03/2019. ISRCTN: ISRCTN20579216.
Host diversity of Aedes albopictus in relation to invasion history: a meta-analysis of blood-feeding studies
Authors: Garamszegi László Zsolt 
Published: October 2024

Abstract
Background
The invasive mosquito Aedes albopictus is a major concern for human and animal health given its high potential to spread over large geographical distances, adapt to various habitats and food sources, and act as a vector for pathogens. It is crucial to understand how this species establishes ecological relationships at different locations, as it determines its role in transmission of diseases.

Methods
Based on published blood meal surveys, a meta-analysis was performed to investigate how host diversity changes along the process of invasion at a large scale. For 48 independent localities, the Shannon diversity index was calculated and was then assessed against several moderator variables describing invasion status, habitat type, methodology, survey year and the year of introduction for invasive populations.

Results
Diet diversity was higher in the invasive than in the native populations when the strong habitat effects were held constant. Furthermore, the year of introduction also had a significant role, as invasive populations that had been established earlier had wider diet diversity than more recent populations.

Conclusions
Invasive Ae. albopictus has considerable ecological flexibility. The species’ ability to adapt to various food sources goes hand in hand with its successful worldwide dispersion, which has strong implications for its role in pathogen transmission.

Graphical Abstract
Spatio-temporal distribution and international context of bovine viral diarrhoea virus genetic diversity in France
Authors: Lescoat Claire , Perrotte Delphine , Barry Séverine , Oden Élise , Herbet Valentin , Beaunée Gaël , Tabouret Marc , Benoit Fabienne , Pitel Pierre-Hugues , Duquesne Véronique , Bailly Xavier , Thézé Julien , Kouokam Guy 
Published: October 2024

AbstractBovine viral diarrhoea (BVD) is one of the most economically damaging livestock enzootic diseases in the world. BVD aetiological agents are three pestiviruses (BVDV-1, -2 and HoBi-like pestivirus), which exhibit high genetic diversity and complex transmission cycles. This considerably hampers the management of the disease, which is why eradication plans have been implemented in several countries. In France, a national plan has been in place since 2019. Our understanding of its impact on the distribution of BVDV genotypes is limited by the availability of French genetic data. Here, we conducted a molecular epidemiology study to refine our knowledge of BVDV genetic diversity in France, characterise its international relationships, and analyse national spatio-temporal genotypic distribution. We collated 1037 BVDV-positive samples throughout France between 2011 and 2023, with a greater sampling effort in two major cattle production areas. We developed a high-throughput sequencing protocol which we used to complete the 5’UTR genotyping of this collection. We show that two main BVDV-1 genotypes, 1e and 1b, account for 88% of genotyped sequences. We also identified seven other BVDV-1 genotypes occurring at low frequencies and three BVDV-2 samples (genotype 2c). Phylogenetic analyses indicate different worldwide distribution patterns between the two main BVDV-1 genotypes. Their relative frequencies present no major changes in France since the 1990s and few variations at the national scale. We also found some degree of local spatial structuring in western France. Overall, our results demonstrate the potential of large-scale sequence-based surveillance to monitor changes in the epidemiological situation of enzootic diseases.
Stem CH4 emissions from the reclaimed forests: magnitude, drivers, and contribution
Authors: Ge Mengyu , Tan Min , Liu Yang 
Published: October 2024

Abstract
Background
Trees in natural forests are a major contributor to atmospheric methane (CH4), yet these emissions have never been investigated in reclaimed forests. Our study aimed to assess the magnitude, seasonality, drivers, and contributions of tree CH4 emissions to ecosystem CH4 flux in the reclaimed forests. We measured CH4 emissions from different emission pathways, including the stems of trees (Populus euramericana, Metasequoia glyptostroboides, and Camphora officinarum), shoots of herbs (Carex breviculmis and Carex dispalata), and soils in the two reclaimed forests with reclamation periods of 12 and 5 years. We identified factors controlling seasonal tree CH4 emissions and measured tree morphological variables (diameter at breast height, wood density, and lenticel density) to determine species differences in emissions.

Results
CH4 emissions from trees in the 12-year-old reclaimed forest were significantly higher than those in the 5-year-old forest. Seasonal variations in tree CH4 emissions were primarily driven by growth stage and soil parameters, including soil CH4 flux, temperature, and moisture.

Conclusion
In the reclaimed forests, tree-mediated CH4 emissions could be an important contributor to ecosystem CH4 flux, with contributions varying by season. As these forests mature and become ecologically restored, they may significantly impact regional and global CH4 emissions.
Factors Influencing Measurement of Dynamic Elastic Modulus from Disk-Shaped Concrete Specimen
Authors: Kim Min Suk , Son Jeong Jin , Chung Chul-Woo , Lee Chang Joon 
Published: October 2024

AbstractThe decrease in dynamic elastic modulus is a primary indicator of quantitative damage in concrete. To quantitatively assess depth-by-depth damage within a concrete structure, cylindrical specimens obtained through coring can be cut into disk specimens to measure the dynamic elastic modulus of concrete at each depth. To minimize external damage during coring, it is essential to extract cylinders with the smallest possible diameter. In addition, for higher resolution in depth-based damage assessment, creating disk specimens with the smallest possible thickness is necessary. However, there is no information available in the literature on experimental limitation of smallest possible diameter and thickness for dynamic elastic modulus of disk-shaped specimens. This study evaluated whether the dynamic modulus measured from various sizes of concrete disk specimens provided sufficient reliability compared to reference values obtained from cylinders. Moreover, the study examined how the presence of coarse aggregate and variation in the water–cement ratio significantly influenced the dynamic modulus measurement. In addition, test results from impulse excitation technique (IET) and impact resonance (IR) were compared to find a more reliable test method for dynamic elastic modulus of disk specimen. The experimental findings revealed that as the thickness-to-radius ratio of the disk specimens decreased, measured data variation increased. Mortar specimens without coarse aggregates showed less variability compared to concrete specimens, and the variation in dynamic modulus measured by IR was lower than that measured by IET.
Deletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury by reducing accumulation of reparative macrophage and production of HGF
Authors: Tanabe Mina , Hosono Kanako , Yamashita Atsushi , Ito Yoshiya , Majima Masataka , Narumiya Shuh , Kusano Chika , Amano Hideki 
Published: October 2024

Abstract
Background
Acetaminophen (APAP)-induced liver injury is the most common cause of acute liver failure. Macrophages are key players in liver restoration following APAP-induced liver injury. Thromboxane A2 (TXA2) and its receptor, thromboxane prostanoid (TP) receptor, have been shown to be involved in tissue repair. However, whether TP signaling plays a role in liver repair after APAP hepatotoxicity by affecting macrophage function remains unclear.

Methods
Male TP knockout (TP−/−) and C57BL/6 wild-type (WT) mice were treated with APAP (300 mg/kg). In addition, macrophage-specific TP-knockout (TP△mac) and control WT mice were treated with APAP. We explored changes in liver inflammation, liver repair, and macrophage accumulation in mice treated with APAP.

Results
Compared with WT mice, TP−/− mice showed aggravated liver injury as indicated by increased levels of alanine transaminase (ALT) and necrotic area as well as delayed liver repair as indicated by decreased expression of proliferating cell nuclear antigen (PCNA). Macrophage deletion exacerbated APAP-induced liver injury and impaired liver repair. Transplantation of TP-deficient bone marrow (BM) cells to WT or TP−/− mice aggravated APAP hepatotoxicity with suppressed accumulation of macrophages, while transplantation of WT-BM cells to WT or TP−/− mice attenuated APAP-induced liver injury with accumulation of macrophages in the injured regions. Macrophage-specific TP−/− mice exacerbated liver injury and delayed liver repair, which was associated with increased pro-inflammatory macrophages and decreased reparative macrophages and hepatocyte growth factor (HGF) expression. In vitro, TP signaling facilitated macrophage polarization to a reparative phenotype. Transfer of cultured BM-derived macrophages from control mice to macrophage-specific TP−/− mice attenuated APAP-induced liver injury and promoted liver repair. HGF treatment mitigated APAP-induced inflammation and promoted liver repair after APAP-induced liver injury.

Conclusions
Deletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury, which is associated with reduced accumulation of reparative macrophages and the hepatotrophic factor HGF. Specific activation of TP signaling in macrophages may be a potential therapeutic target for liver repair and regeneration after APAP hepatotoxicity.
Evaluation of Aedes aegypti control intervention with pyriproxyfen by lcWGS in Manacapuru, Amazonas, Brazil
Authors: Leles Lorena Ferreira de Oliveira , Niz Alvarez Marcus Vinicius , Cortés Jose Joaquin Carvajal , Alonso Diego Peres , Ribolla Paulo Eduardo Martins , Luz Sérgio Luiz Bessa 
Published: October 2024

Background
Ae. aegypti mosquitoes are considered a global threat to public health due to its ability to transmit arboviruses such as yellow fever, dengue, Zika and Chikungunya to humans. The lack of effective arboviral vaccines and etiological treatments make vector control strategies fundamental in interrupting the transmission cycle of these pathogens. This study evaluated Ae. aegypti mosquito populations pre- and post-intervention period with disseminating stations of the larvicide pyriproxyfen to understand its potential influence on the genetic structure and population diversity of these vectors.

Methodology/Principal findings
This study was conducted in Manacapuru city, Amazonas, Brazil, where 1,000 pyriproxyfen dissemination stations were deployed and monitored from FEB/2014 to FEB/2015 (pre-intervention) and AUG/2015 to JAN/2016 (post-intervention). Low-coverage whole genome sequencing of 36 individuals was performed, revealing significant stratification between pre- and post-intervention groups (pairwise FST estimate of 0.1126; p-value < 0.033). Tajima’s D estimates were -3.25 and -3.07 (both p-value < 0.01) for pre- and post-intervention groups, respectively. Molecular diversity estimates (Theta(S) and Theta(Pi)) also showed divergences between pre- and post-intervention groups. PCA and K-means analysis showed clustering for SNP frequency matrix and SNP genotype matrix, respectively, being both mainly represented by the first principal component. PCA and K-means clustering also showed significant results that corroborate the impact of pyriproxyfen intervention on genetic structure populations of Ae. aegypti mosquitoes.

Conclusions/Significance
The results revealed a bottleneck effect and reduced mosquito populations during intervention, followed by reintroduction from adjacent and unaffected populations by this vector. We highlighted that low-coverage whole genome sequencing can contribute to genetic and structure population data, and also generate important information to aid in genomic and epidemiological surveillance.
Involvement of INS15 in the development and pathogenicity of the zoonotic pathogen Cryptosporidium parvum
Authors: He Wei , Cui Hao , Li Na , Guo Yaqiong , Zeng Songrong , Feng Yaoyu , Xiao Lihua , Xu Rui 
Published: October 2024

Background
Cryptosporidium parvum is a common protozoan pathogen responsible for moderate to severe diarrhea in humans and animals. The C. parvum genome contains 22 genes encoding insulinase-like M16 proteases (INS) with diverse structures and sequences, suggesting that members of the protein family may have distinct biological functions in the life cycle of parasites. Here, we investigated the role of INS15 and INS16, two proteases encoded by neighboring genes with high sequence identity, in the growth and development of C. parvum in vivo and in vitro.

Methodology/Principal findings
INS15 and INS16 genes were tagged and knocked out using CRISPR/Cas9 technology in C. parvum IIdA20G1-HLJ isolate. The expression of INS15 and INS16 was determined by immunofluorescence analysis and immunoelectron microscopy. The effect of depletion of INS15 and INS16 on parasite growth and pathogenicity were assessed on HCT-8 cells and in interferon-γ knockout mice. Endogenous tagging showed that INS15 and INS16 expressed in the oocyst, trophozoite, meront and female gametes. INS15 also expressed in male gamonts, while INS16 was not detected in the male gamonts. Although depletion of the INS15 or INS16 gene affected late development of C. parvum in vitro, only depletion of INS15 significantly reduced parasite burden in infected mice. Mice infected with the INS15-depleted strain had reduced clinical signs, body weight, intestinal villus length to crypt height ratio, and survival time compared to infected with the tagging mutant.

Conclusions/Significance
The results of this study indicate that INS15 is mainly involved in the late development of C. parvum. Depletion of this gene attenuates the pathogenicity of this important zoonotic parasite.
High blood eosinophils predict the risk of COPD exacerbation: A systematic review and meta-analysis
Authors: Chen Fangying , Yang Mei , Wang Hao , Liu Lian , Shen Yongchun , Chen Lei 
Published: October 2024

Background
The association between blood eosinophils and COPD exacerbation has been controversial. This study aims to investigate whether high blood eosinophils predict the risk of COPD exacerbation across different thresholds and subgroups.

Methods
PubMed, Embase and Web of science were searched for randomized controlled trial (RCT) and observational studies regarding the relationship between blood eosinophils and COPD exacerbation. Pooled risk ratio (RR) for COPD exacerbation was calculated using the Mantel-Haenszel method with a random-effects model.

Results
A total of 21 studies (1 RCT and 20 observational studies) with 79868 participants were included. Thresholds of high blood eosinophils including absolute counts (200, 300 and 400 cell/μL) and percentages (2%, 3% and 4%) were analyzed respectively. Pooled analyses suggested that high blood eosinophils were significantly associated with increased risk of COPD exacerbation when using the thresholds of 300 cells/μL (RR 1.21, 95%CI 1.12–1.30, P <0.001, 16 studies), 400 cells/μL (RR 1.79, 95%CI 1.41–2.28, P <0.001, 3 studies), 2% (RR 1.26, 95%CI 1.02–1.55, P = 0.030, 10 studies) and 4% (RR 1.44, 95%CI 1.05–1.96, P = 0.022, 4 studies), but not 200 cells/μL and 3% (P>0.05). Moreover, high blood eosinophils contributed to moderate-severe exacerbation of COPD by the cutoffs of 300 cells/μL (RR 1.30, 95%CI 1.16–1.45, P<0.001, 11 studies) and 2% (RR 1.33, 95%CI 1.02–1.76, P = 0.037, 8 studies). In subgroup analyses, the pooled results further showed a significant association between high blood eosinophils (especially over 300 cells/μL) and risk of COPD exacerbation among patients from Europe and Asia, and whether with stable or exacerbation phase at baseline, and regardless of the follow-up time (≤ or > 1year).

Conclusions
This study demonstrates that high blood eosinophils (over 300 cells/μL or 2%) could predict the risk of moderate-severe exacerbation of COPD in specific subgroups. However, large sample-sized, prospective, and well-designed studies are required to validate the present findings.