bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of the Stop Transmission of Polio (STOP) program in developing countries: the experience of Kenya
Authors: Tesfaye Brook , K. Makam Jeevan , Sergon Kibet , Onuekwusi Iheoma , Muitherero Charles , Sowe Alieu 
Published: July 2020

Abstract
Background
In 1988, the 41st World Health Assembly (WHA) marked the launch of the Global Polio Eradication Initiative (GPEI) for the eradication of polio. A key component of the GPEI has been the development and deployment of a skilled workforce to implement eradication activities. In 1989, the Stop Transmission of Polio (STOP) was initiated to address skilled human resource gaps and strengthen poliovirus surveillance. This paper describes the role of the STOP 52 team in technical capacity building and health system strengthening in the implementation of polio eradication strategies in Kenya following the outbreak of Circulating Vaccine-derived Poliovirus type 2 (cVDPV2).

Methods
Overview of the STOP program, deployment, and the modality of support are described. Descriptive analysis was conducted using data collected by the STOP 52 team during integrated supportive supervisory visits conducted from July 2018 to September 2019. Analyses were carried out using Epi-Info statistical software (Version 7.0) and maps were developed using Quantum Geographic Information System (Q-GIS) (version 3.12.0).

Results
The STOP 52 team supportively supervised 870 health facilities on Expanded Program on Immunization (EPI), and Acute Flaccid Paralysis (AFP) and other Vaccine-Preventable Diseases (VPDs) surveillance in 16 (34.1%) of the 47 counties during the study period. AFP surveillance was conducted in all health facilities supervised leading to the detection and investigation of 11 unreported AFP cases. The STOP 52 team, as part of the outbreak response, provided technical support to five successive rounds of polio Supplementary Immunization Activities (SIAs) conducted during the study period. Moreover, in addressing programmatic data needs, the STOP 52 Data Manager played a valuable role in enhancing the quality and use of data for evidence-based planning and decision-making. The STOP 52 team contributed to the development of operational plans, guidelines and training manuals, and participated in the delivery of various Training of Trainers (TOT) and On-the-Job Training (OJT) on EPI, AFP and other VPDs surveillance including data management.

Conclusion
The STOP 52 team has contributed to polio eradication efforts in Kenya by enhancing AFP and other VPDs surveillance, supporting polio SIAs, strengthening EPI, use of quality EPI, AFP and other VPDs data, and capacity building of Frontline Health Workers (FLWs). The use of Open Data Kit (ODK) technology during supportive supervision, and AFP and other VPDs surveillance was found to be advantageous. A national STOP program should be modeled to produce a homegrown workforce to ensure the availability of more sustainable technical support for polio eradication efforts in Kenya and possibly other polio-affected countries.
Applying equity-centered principles in an interprofessional global health course: a mixed methods study
Authors: Stallwood Lisa , Adu Prince A. , Tairyan Kate , Astle Barbara , Yassi Annalee 
Published: July 2020

Abstract
Background
Medical students, practitioners and other health professionals are commonly unprepared to address the many complex issues that emerge while conducting research in the Global South. As a response to identified deficiencies in global health education, a hybrid online/face-to-face multi-institutional credit course was developed based on the equity-centered principles advanced by the Canadian Coalition for Global Health Research (CCGHR), namely Authentic partnering, Inclusion, Shared benefits, Commitment to the future, Responsiveness to causes of inequities, and Humility. This study aimed to analyze the extent to which the course was effective in fortifying attitudes consistent with the CCGHR principles; identify successes and challenges; and assess how a course such as this can fill an identified gap.

Methods
This interprofessional course was offered to 25 graduate and postgraduate students in various health professions and public health. Faculty were drawn from medicine, public health, nursing and social sciences from four universities in Western Canada. A pre-post retrospective survey, key informant interviews and participant observation were used to gather data for this study.

Results
Findings showed that student attitudes regarding global health research and practice significantly evolved towards views consistent with the principles articulated. The multiple instructors and hybrid course format created both opportunities and challenges; the interprofessional nature of the cohort was considered a strong asset, as was the fact that many students came from the Global South. Some students suggested that the course could be further strengthened by concretely partnering with institutions in the Global South rather than offered solely to learners registered in universities in the Global North.

Conclusions
While weaknesses were identified, results support the conclusion that a course focused on the CCGHR principles could be useful in preparing the next generation of global health researchers and practitioners to mitigate historical limitations in this field. Longitudinal follow-up is warranted to provide more definitive conclusions.
Inequalities in caesarean section in Burundi: evidence from the Burundi Demographic and Health Surveys (2010–2016)
Authors: Yaya Sanni , Zegeye Betregiorgis , Idriss-Wheeler Dina , Shibre Gebretsadik 
Published: July 2020

Abstract
Background
Despite caesarean section (CS) being a lifesaving intervention, there is a noticeable gap in providing this service, when necessary, between different population groups within a country. In Burundi, there is little information about CS coverage inequality and the change in provision of this service over time. Using a high-quality equity analysis approach, we aimed to document both magnitude and change of inequality in CS coverage in Burundi over 7 years to investigate disparities.

Methods
For this study, data were extracted from the 2010 and 2016 Burundi Demographic and Health Surveys (BDHS) and analyzed through the recently updated Health Equity Assessment Toolkit (HEAT) of the World Health Organization. CS delivery was disaggregated by four equity stratifiers, namely education, wealth, residence and sub-national region. For each equity stratifier, relative and absolute summary measures were calculated. We built a 95% uncertainty interval around the point estimate to determine statistical significance.

Main findings
Disparity in CS was present in both survey years and increased over time. The disparity systematically favored wealthy women (SII = 10.53, 95% UI; 8.97, 12.10), women who were more educated (PAR = 8.89, 95% UI; 8.51, 9.26), women living in urban areas (D = 12.32, 95% UI; 9.00, 15.63) and some regions such as Bujumbura (PAR = 11.27, 95% UI; 10.52, 12.02).

Conclusions
Burundi had not recorded any progress in ensuring equity regarding CS coverage between 2010 and 2016. It is important to launch interventions that promote justified use of CS among all subpopulations and discourage overuse among high income, more educated women and urban dwellers.
FAM20B-catalyzed glycosaminoglycans control murine tooth number by restricting FGFR2b signaling
Authors: Wu Jingyi , Tian Ye , Han Lu , Liu Chao , Sun Tianyu , Li Ling , Yu Yanlei , Lamichhane Bikash , D’Souza Rena N. , Millar Sarah E. , Krumlauf Robb , Ornitz David M. , Feng Jian Q. , Klein Ophir , Zhao Hu , Zhang Fuming , Linhardt Robert J. , Wang Xiaofang 
Published: July 2020

AbstractBackgroundThe formation of supernumerary teeth is an excellent model for studying the molecular mechanisms that control stem/progenitor cell homeostasis needed to generate a renewable source of replacement cells and tissues. Although multiple growth factors and transcriptional factors have been associated with supernumerary tooth formation, the regulatory inputs of extracellular matrix in this regenerative process remains poorly understood.ResultsIn this study, we present evidence that disrupting glycosaminoglycans (GAGs) in the dental epithelium of mice by inactivating FAM20B, a xylose kinase essential for GAG assembly, leads to supernumerary tooth formation in a pattern reminiscent of replacement teeth. The dental epithelial GAGs confine murine tooth number by restricting the homeostasis of Sox2(+) dental epithelial stem/progenitor cells in a non-autonomous manner. FAM20B-catalyzed GAGs regulate the cell fate of dental lamina by restricting FGFR2b signaling at the initial stage of tooth development to maintain a subtle balance between the renewal and differentiation of Sox2(+) cells. At the later cap stage, WNT signaling functions as a relay cue to facilitate the supernumerary tooth formation.ConclusionsThe novel mechanism we have characterized through which GAGs control the tooth number in mice may also be more broadly relevant for potentiating signaling interactions in other tissues during development and tissue homeostasis.
Seropositivity and associated intrinsic and extrinsic factors for Rift Valley fever virus occurrence in pastoral herds of Nigeria: a cross sectional survey
Authors: Alhaji Nma Bida , Aminu Jibrin , Lawan Mohammed Kabiru , Babalobi Olutayo Olajide , Ghali-Mohammed Ibrahim , Odetokun Ismail Ayoade 
Published: July 2020

Abstract
Background
Rift Valley fever (RVF) is a vector-borne emerging zoonotic disease of animals and humans, characterized by socioeconomic losses to livestock farmers and global public health threat. The study determined RVFV seroprevalence in cattle, assessed pastoralists’ knowledge about RVF, and factors that influence its occurrence in pastoral cattle herds of Nigeria. A cross-sectional study was conducted in pastoral herds of North-central Nigeria from 2017 to 2018. Data were collected using serology and questionnaire tools. Descriptive statistics were used to analyze the obtained data. Categorical variables were presented as proportions and their associations determined by Chi-square tests. Associations of risk factors were analyzed by univariable and multivariable logistic regressions analyses at 95% confidence level.

Results
The overall IgM seropositivity of RVFV in pastoral cattle herds was 5.6%. This was higher in nomadic herds (7.4%) than in agro-pastoral herds (3.8%). All animal demographic characteristics of age, sex and breeds were not significantly (p > 0.05) associated with RVFV occurrence in pastoral herds. All the 403 pastoralists selected participated in the study, with the majorities of them being male, married and have no formal education. Majority of the pastoralists had low knowledge levels about zoonotic RVFV infection. All identified socio-ecological factors significantly (p < 0.05) influenced RVFV occurrence in herds. Mosquitoes availability in cattle environment (OR = 7.81; 95% CI: 4.85, 12.37), presence of rivers and streams at grazing fields (OR = 10.80; 95% CI: 6.77, 17.34), high rainfall (OR = 4.30; 95% CI: 2.74, 6.59), irrigated rice fields (OR = 5.14; 95% CI: 3.21, 7.79), bushy vegetation (OR = 6.11; 95% CI: 3.96, 9.43), animal movement (OR = 2.2; 95% CI: 1.45, 3.25), and seasons (OR = 2.34; 95% CI: 1.55, 3.51) were more likely to influenced RVFV occurrence in cattle herds.

Conclusions
Results of this study had illustrated recent circulation of RVFV in pastoral cattle herds in Nigeria and needs urgent interventions. The surveyed pastoralists had low knowledge level about RVF while the socio-ecological factors significantly influenced RVFV occurrence in herds. To address these gaps, pastoralists should be educated on clinical manifestations and modes of transmission of the disease in animals and humans, and mitigation measures. Adequate knowledge about RVF epidemiology will assure food security and public health.
The sputum microbiome is distinct between COPD and health, independent of smoking history
Authors: Haldar Koirobi , George Leena , Wang Zhang , Mistry Vijay , Ramsheh Mohammadali Yavari , Free Robert C. , John Catherine , Reeve Nicola F. , Miller Bruce E. , Tal-Singer Ruth , Webb Adam J. , Brookes Anthony J. , Tobin Martin D. , Singh Dave , Donaldson Gavin C. , Wedzicha Jadwiga A. , Brown James R. , Barer Michael R. , Brightling Christopher E. 
Published: July 2020

Abstract
Background
Airway bacterial dysbiosis is a feature of chronic obstructive pulmonary disease (COPD). However, there is limited comparative data of the lung microbiome between healthy smokers, non-smokers and COPD.

Methods
We compared the 16S rRNA gene-based sputum microbiome generated from pair-ended Illumina sequencing of 124 healthy subjects (28 smokers and 96 non-smokers with normal lung function), with single stable samples from 218 COPD subjects collected from three UK clinical centres as part of the COPDMAP consortium.

Results
In healthy subjects Firmicutes, Bacteroidetes and Actinobacteria were the major phyla constituting 88% of the total reads, and Streptococcus, Veillonella, Prevotella, Actinomyces and Rothia were the dominant genera. Haemophilus formed only 3% of the healthy microbiome. In contrast, Proteobacteria was the most dominant phylum accounting for 50% of the microbiome in COPD subjects, with Haemophilus and Moraxella at genus level contributing 25 and 3% respectively. There were no differences in the microbiome profile within healthy and COPD subgroups when stratified based on smoking history. Principal coordinate analysis on operational taxonomic units showed two distinct clusters, representative of healthy and COPD subjects (PERMANOVA, p = 0·001).

Conclusion
The healthy and COPD sputum microbiomes are distinct and independent of smoking history. Our results underline the important role for Gammaproteobacteria in COPD.
An unlabelled probe-based real time PCR and modified semi-nested PCR as molecular tools for analysis of chloroquine resistant Plasmodium vivax isolates from Afghanistan
Authors: Mosawi Sayed Hussain , Dalimi Abdolhossein , Safi Najibullah , Fotouhi-Ardakani Reza , Ghaffarifar Fatemeh , Sadraei Javid 
Published: July 2020

Abstract
Background
Plasmodium vivax resistance to chloroquine (CQ) has been reported from many endemic regions in the world. Plasmodium vivax is responsible for 95% of malaria cases in Afghanistan and CQ is the first-line treatment given for vivax malaria. The pvmdr-1 and pvcrt-o (K10 insertion) genes are possible markers for CQ-resistance in P. vivax isolates. There have been no studies done on the presence or absence of molecular markers for CQ-resistance P. vivax in Afghanistan. The present work aimed to evaluate the frequency of mutations in the pvmdr-1 and K10 insertion in the pvcrt-o genes of P. vivax.

Methods
Plasmodium vivax isolates were collected from Laghman, Baghlan and Khost provinces. For investigation of polymorphisms of desired regions in pvmdr-1 and pvcrt-o genes, sequencing was applied on the PCR products. A new asymmetric qPCR and melting analysis assay based on unlabelled probe developed for scanning of K10 insertion in pvcrt-o gene.

Results
The analysis of sequencing data of the pvmdr-1 gene showed wild type Y976 and K997 and mutant M958 and L1076 in 33 isolates from three provinces. Of the 36 samples evaluated for K10 insertion in pvcrt-o, 2/18(11%), 0/10(0%) and 0/8(0%) isolates from Laghman, Baghlan and Khost province, respectively, possessed K10 insertion, confirmed by either sequencing and unlabelled probes.

Conclusion
Two samples with K10 insertion and 33 samples with pvmdr1 polymorphism, indicating on the possibility of CQ resistance in P. vivax populations in Afghanistan. Furthermore, unlabelled probes are simple and inexpensive alternative tools for screening of P. vivax mutations.
The skeletal muscles of mice infected with Plasmodium berghei and Plasmodium chabaudi reveal a crosstalk between lipid mediators and gene expression
Authors: Marrelli Mauro Toledo , Wang Zhiying , Huang Jian , Brotto Marco 
Published: July 2020

Abstract
Background
Malaria is one of the most prevalent infectious disease in the world with 3.2 billion humans at risk. Malaria causes splenomegaly and damage in other organs including skeletal muscles. Skeletal muscles comprise nearly 50% of the human body and are largely responsible for the regulation and modulation of overall metabolism. It is essential to understand how malaria damages muscles in order to develop effective preventive measures and/or treatments. Using a pre-clinical animal model, the potential molecular mechanisms of Plasmodium infection affecting skeletal muscles of mice were investigated.

Methods
Mouse Signal Transduction Pathway Finder PCR Array was used to monitor gene expression changes of 10 essential signalling pathways in skeletal muscles from mice infected with Plasmodium berghei and Plasmodium chabaudi. Then, a new targeted-lipidomic approach using liquid chromatography with tandem mass spectrometry (LC–MS/MS) to profile 158 lipid signalling mediators (LMs), mostly eicosanoids derived from arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), was applied. Finally, 16 key LMs directly associated with inflammation, oxidative stress, and tissue healing in skeletal muscles, were quantified.

Results
The results showed that the expression of key genes altered by Plasmodium infection is associated with inflammation, oxidative stress, and atrophy. In support to gene profiling results, lipidomics revealed higher concentrations of LMs in skeletal muscles directly related to inflammatory responses, while on the levels of LMs crucial in resolving inflammation and tissue repair reduced significantly.

Conclusion
The results provide new insights into the molecular mechanisms of malaria-induced muscle damage and revealed a potential mechanism modulating inflammation in malarial muscles. These pre-clinical studies should help with future clinical studies in humans aimed at monitoring of disease progression and development of specific interventions for the prevention and mitigation of long-term chronic effects on skeletal muscle function.
Down regulating PHGDH affects the lactate production of sertoli cells in varicocele
Authors: Guo Wen-bin , Huang Zhen-hui , Yang Cheng , Lv Xian-yuan , Xia Hui , Tian Hu , Yang Jian-kun , Zhou Qi-zhao , Chen Ming-kun , Xue Kang-yi , Liu Cun-dong 
Published: July 2020

AbstractBackgroundAlthough varicocele is considered to be one of the leading causes of male infertility, the precise mechanism underlying how varicocele leads to male infertility is not completely understood. We found the lactate concentration on the varicocele side of the patients was decreased compare with peripheral venous blood. In the testicles, the lactate produced by the sertoli cells through the glycolysis pathway provides most of the energy needed for spermatogenesis, the reduction of lactate will affect spermatogenesis. The objective of this study was to investigate the mechanism of this abnormal energy metabolism phenomenon in varicocele.MethodsIn this study, we collected the testicular tissue from patients with varicocele, the glycolysis related proteins PHGDH was identified by iTRAQ proteomics technology. Experimental rat varicocele model was constructed according to our new clip technique, the mRNA and protein expression levels of PHGDH were examined with qRT-PCR and Western blotting. We constructed a sertoli cell of PHGDH down-regulation model, and then detected the glucose consumption, LDH activities and lactate production in the sertoli cells. Western blot was conducted to investigate the effects of PHGDH on the expression of phosphoserine phosphatase (PSPH) and Pyruvate kinase M2 (PKM2). Flow cytometry was used to detect the cell apoptosis and cell cycle in sertoli cells.ResultsThe results showed that testicular protein PHGDH was down-regulated in patients with varicocele and in experimental rat varicocele model. Down-regulation of PHGDH in sertoli cells significantly decreased the glucose consumption, LDH activities and lactate production in the sertoli cells, indicating that the low expression of PHGDH ultimately led to a decrease in lactate production by affecting the glycolysis. The Western blot results showed that the down-regulation of PHGDH significantly reduced the expression of pathway protein PSPH and PKM2, leading to the reduction of lactate production. Moreover, PHGDH knockdown can promote apoptosis and inhibit cell cycle to affect cell growth.ConclusionsOverall, we conformed that varicocele lead to the decreasing of testis lactate production. Down-regulation of PHGDH in sertoli cells may mediate the process of abnormal glucose metabolism. Our study provide new insight into the mechanisms underlying metabolism-associated male infertility and suggests a novel therapeutic target for male infertility.
The deubiquitinase USP22 regulates PD-L1 degradation in human cancer cells
Authors: Wang Yu , Sun Qingguo , Mu Ning , Sun Xiaoyang , Wang Yingying , Fan Songqing , Su Ling , Liu Xiangguo 
Published: July 2020

Abstract
Background
Many cancers evade immune surveillance by overexpressing PD-L1. PD-L1 interacted with its receptor PD-1, resulting in reduction of T cell proliferation and activation and thereafter cancer cell death mediated by T-lymphocyte. Understanding the mechanisms that regulate PD-L1 was of vital importance for immune checkpoint blockade therapy (ICBT).

Methods
Human non-small cell lung cancer cells and 293FT cells were used to investigate the function of USP22 upon PD-L1 and CSN5 by WB, Immunoprecipitation, Immunofluorescence and Flow cytometry analysis. B16-F10 cells were used to explore the role of USP22 on tumorigenesis and T cell cytotoxicity. The relationship between USP22 and PD-L1 expression was investigated by Immunohistochemistry analysis in human non-small cell lung cancer samples.

Results
Our data showed that USP22 interacted with PD-L1 and promoted its stability. USP22 deubiquitinated PD-L1 and inhibited its proteasome degradation. Moreover, USP22 also interacted with CSN5 and stabilized CSN5 through deubiquitination. Either USP22 or CSN5 could facilitate the interaction of PD-L1 with the other one. Furthermore, USP22 removed K6, K11, K27, K29, K33 and K63-linked ubiquitin chain of both CSN5 and PD-L1. In addition, USP22 depletion inhibited tumorigenesis and promoted T cell cytotoxicity. Besides, USP22 expression positively correlated with PD-L1 expression in human non-small cell lung cancer samples.

Conclusions
Here, we suggested that USP22 is a new regulator for PD-L1. On the one hand, USP22 could directly regulate PD-L1 stability through deubiquitination. On the other hand, USP22 regulated PD-L1 protein level through USP22-CSN5-PD-L1 axis. In addition, USP22 depletion inhibited tumorigenesis and promoted T cell cytotoxicity. Besides, USP22 expression positively correlated with PD-L1 expression in human non-small cell lung cancer samples. Together, we identified a new regulator of PD-L1 and characterized the important role of USP22 in PD-L1 mediated immune evasion. Targeting USP22 might be a new solution to ICBT.

Graphical abstract