bluuebunny/crossref_metadata_2025_split huggingface dataset:
Implementing standard antenatal care interventions: health system cost at primary health facilities in Tanzania
Authors: Chamani Amisa Tindamanyile , Mori Amani Thomas , Robberstad Bjarne 
Published: December 2021

AbstractBackgroundSince 2002, Tanzania has been implementing the focused Antenatal Care (ANC) model that recommended four antenatal care visits. In 2016, the World Health Organization (WHO) reintroduced the standard ANC model with more interventions including a minimum of eight contacts. However, cost-implications of these changes to the health system are unknown, particularly in countries like Tanzania, that failed to optimally implement the simpler focused ANC model. We compared the health system cost of providing ANC under the focused and the standard models at primary health facilities in Tanzania.MethodsWe used a micro-costing approach to identify and quantify resources used to implement the focused ANC model at six primary health facilities in Tanzania from July 2018 to June 2019. We also used the standard ANC implementation manual to identify and quantify additional resources required. We used basic salary and allowances to value personnel time while the Medical Store Department price catalogue and local market prices were used for other resources. Costs were collected in Tanzanian shillings and converted to 2018 US$.ResultsThe health system cost of providing ANC services at six facilities (2 health centres and 4 dispensaries) was US$185,282 under the focused model. We estimated that the cost would increase by about 90% at health centres and 97% at dispensaries to US$358,290 by introducing the standard model. Personnel cost accounted for more than one third of the total cost, and more than two additional nurses are required per facility for the standard model. The costs per pregnancy increased from about US$33 to US$63 at health centres and from about US$37 to US$72 at dispensaries.ConclusionIntroduction of a standard ANC model at primary health facilities in Tanzania may double resources requirement compared to current practice. Resources availability has been one of the challenges to effective implementation of the current focused ANC model. More research is required, to consider whether the additional costs are reasonable compared to the additional value for maternal and child health.
Virus infection induced pulmonary fibrosis
Authors: Huang Wei Jie , Tang Xiao Xiao 
Published: December 2021

AbstractPulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the relationship between virus infection and pulmonary fibrosis is getting more and more attention, especially after the outbreak of SARS-CoV-2 in 2019, however, the mechanisms underlying the virus-induced pulmonary fibrosis are not fully understood. Here, we review the relationship between pulmonary fibrosis and several viruses such as Human T-cell leukemia virus (HTLV), Human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Epstein–Barr virus (EBV), Murine γ-herpesvirus 68 (MHV-68), Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome (MERS)-CoV, Severe acute respiratory syndrome (SARS)-CoV and SARS-CoV-2 as well as the mechanisms underlying the virus infection induced pulmonary fibrosis. This may shed new light on the potential targets for anti-fibrotic therapy to treat pulmonary fibrosis induced by viruses including SARS-CoV-2.
Relations of physical signs to genotype, lipid and inflammatory markers, coronary stenosis or calcification, and outcomes in patients with heterozygous familial hypercholesterolemia
Authors: Liu Ming-Ming , Peng Jia , Guo Yuan-Lin , Zhu Cheng-Gang , Wu Na-Qiong , Xu Rui-Xia , Dong Qian , Li Jian-Jun 
Published: December 2021

Abstract
Background
Although the presence of physical signs [tendon xanthomas and/or corneal arcus (TX/CA)], are associated with the risk of coronary artery disease in patients with heterozygous familial hypercholesterolemia (HeFH), their relationship with genotypes and clinical characteristics has not been fully determined. This study aimed to examine the association of TX/CA with genetic mutation, lipid- and inflammation-related markers, the severity of coronary stenosis or calcification, and cardiovascular events (CVEs) in patients with HeFH.

Methods
LDLR, APOB, and PCSK9 genes were screened in 523 HeFH patients, and patients with TX/CA (n = 50) were 1:4 propensity score-matched to patients without TX/CA (n = 200) to adjust for age and sex. Laboratory markers (proprotein convertase subtilisin/kexin type 9 [PCSK9], lipoprotein(a) and high-sensitivity C-reactive protein [hsCRP]), computed tomography angiography, coronary angiography, and follow-up for CVEs were performed.

Results
Patients with physical signs had significantly higher low-density lipoprotein cholesterol levels; higher PCSK9 or hsCRP concentrations; more LDLR positive mutations; and higher prevalence of high tertiles of Gensini, SYNTAX and Jeopardy scores as well as coronary artery calcium scores than did those without. Over an average follow-up of 3.7 years, the incidence of CVEs was significantly higher in patients with TX/CA (log-rank p < 0.001). Patients with physical signs and mutation positivity had threefold higher risks of CVEs (adjusted hazard ratio 3.34, 95% confidence interval 1.04–10.72, p = 0.024).

Conclusions
Physical signs were associated with genotypes and phenotypes, and worse outcomes in patients with HeFH, suggesting that these signs may help in risk stratification in these patients.
Down-regulation of circular RNA CDC14A peripherally ameliorates brain injury in acute phase of ischemic stroke
Authors: Zuo Lei , Xie Jian , Liu Yun , Leng Shuo , Zhang Zhijun , Yan Fuling 
Published: December 2021

Abstract
Background
Inflammation is integral to the pathophysiology of ischemic stroke and a prime target for the development of new stroke therapies. The aim of the present study is to seek out the regulatory mechanism of circCDC14A in neuroinflammatory injury in tMCAO mice.

Methods
The expression level of circCDC14A in peri-infarct cortex and plasma of mice were detected by qPCR. The localization of circCDC14A in peripheral blood cells and peri-infarct cortex of tMCAO mice were explored by in situ hybridization and immunofluorescence colocalization staining. Lentivirus were microinjected into lateral ventricular of brain or injected into tail vein to interfere with the expression of circCDC14A, thus their effects on behavior, morphology, and molecular biology of tMCAO mice were analyzed.

Results
The expression of circCDC14A in plasma and peri-infarct cortex of tMCAO mice significantly increased, and circCDC14A was mainly localized in neutrophils peripherally while in astrocytes in peri-infarct cortex centrally. Tail vein injection of lentivirus to interfere with the expression of circCDC14A significantly reduced the infarct volume (P < 0.01) at 72 h after reperfusion and density of activated astrocytes in peri-infarct cortex at 3 days, 5 days and 7 days after tMCAO modeling (all P < 0.0001). Moreover, mNSS (P < 0.0001) and survival rate (P < 0.001) were significantly improved within 7 days in si-circCDC14A group compared to circCon group. Additionally, morphology analysis showed the volume and surface area of each activated astrocytes significantly decreased (P < 0.0001). Quantification analysis measured the percentage of N2 phenotype among infiltrated neutrophils in brain sections and found N2 ratio was significantly higher in si-circCDC14A group compared to circCon group (P < 0.001).

Conclusion
Knocking down the expression of circCDC14A in peripheral blood cells relieved astrocytes activation in peri-infarct cortex, thereby relieved brain damage in the acute phase of ischemic stroke.
Expression of plasma IFN signaling-related miRNAs during acute SARS-CoV-2 infection and its association with RBD-IgG antibody response
Authors: Wu Jing , Liu Xingxiang , Shao Jianguo , Zhang Yuanyuan , Lu Renfei , Xue Hong , Xu Yunfang , Wang Lijuan , Zhou Hui , Yu Lugang , Yue Ming , Dong Chen 
Published: December 2021

Abstract
Background
Coronavirus disease 2019 (COVID-19) is a huge challenge worldwide. Although previous studies have suggested that type I interferon (IFN-I) could inhibit the virus replication, the expression characteristics of IFN-I signaling-related miRNAs (ISR-miRNAs) during acute severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and its relationship with receptor-binding domain (RBD) IgG antibody response at the recovery phase remain unclear.

Methods
Expression profiles of 12 plasma ISR-miRNAs in COVID-19 patients and healthy controls were analyzed using RT-qPCR. The level of RBD-IgG antibody was determined using the competitive ELISA. Spearman correlation was done to measure the associations of plasma ISR-miRNAs with clinical characteristics during acute SARS-CoV-2 infection and RBD-IgG antibody response at the recovery phase.

Results
Compared with the healthy controls, COVID-19 patients exhibited higher levels of miR-29b-3p (Z = 3.15, P = 0.002) and miR-1246 (Z = 4.98, P < 0.001). However, the expression of miR-186-5p and miR-15a-5p were significantly decreased. As the results shown, miR-30b-5p was negatively correlated with CD4 + T cell counts (r = − 0.41, P = 0.027) and marginally positively correlated with fasting plasma glucose in COVID-19 patients (r = 0.37, P = 0.052). The competitive ELISA analysis showed the plasma level of miR-497-5p at the acute phase was positively correlated with RBD-IgG antibody response (r = 0.48, P = 0.038).

Conclusions
Our present results suggested that the expression level of ISR-miRNAs was not only associated with acute SARS-CoV-2 infection but also with RBD-IgG antibody response at the recovery phase of COVID-19. Future studies should be performed to explore the biological significance of ISR-miRNAs in SARS-CoV-2 infection.
Prostate deformation during hypofractionated radiotherapy: an analysis of implanted fiducial marker displacement
Authors: Knybel Lukas , Cvek Jakub , Blazek Tomas , Binarova Andrea , Parackova Tereza , Resova Kamila 
Published: December 2021

Abstract
Background
To report prostate deformation during treatment, based on an analysis of fiducial marker positional differences in a large sample.

Material and methods
This study included 144 patients treated with prostate stereotactic body radiation therapy after implantation in each of 4 gold fiducial markers (FMs), which were located and numbered consistently. The center of mass of the FMs was recorded for every pair of X-ray images taken during treatment. The distance between each pair of fiducials in the live X-ray images is calculated and compared with the respective distances as determined in the CT volume. The RBE is the difference between these distances. Mean RBE and intrafraction and interfraction RBE were evaluated. The intrafraction and intefraction RBE variability were defined as the standard deviation, respectively, of all RBE during 1 treatment fraction and of the mean daily RBE over the whole treatment course.

Results
We analyzed 720 treatment fractions comprising 24,453 orthogonal X-ray image acquisitions. We observed a trend to higher RBE related to FM4 (apex) during treatment. The fiducial marker in the prostate apex could not be used in 16% of observations, in which RBE was > 2.5 mm. The mean RBEavg was 0.93 ± 0.39 mm (range 0.32–1.79 mm) over the 5 fractions. The RBEavg was significantly lower for the first and second fraction compared with the others (P < .001). The interfraction variability of RBEavg was 0.26 ± 0.16 mm (range 0.04–0.74 mm). The mean intrafraction variability of all FMs was 0.45 ± 0.25 mm. The highest Pearson correlation coefficient was observed between FM2 and FM3 (middle left and right prostate) (R = 0.78; P < .001). Every combination with FM4 yielded lower coefficients (range 0.66–0.71; P < .001), indicating different deformation of the prostate apex.

Conclusions
Ideally, prostate deformation is generally small, but it is very sensitive to rectal and bladder filling. We observed RBE up to 11.3 mm. The overall correlation between FMs was affected by shifts of individual fiducials, indicating that the prostate is not a “rigid” organ. Systematic change of RBE average between subsequent fractions indicates a systematic change in prostate shape.
Thoracolumbar flexion dysfunction and thoracolumbar compression fracture in postmenopausal women: a single-center retrospective study
Authors: Zheng Zhirong , Liu Chao , Zhang Zhen , Hu Wenhao , Gao Meng , Jia Chengqi , Zhang Xuesong 
Published: December 2021

Abstract
Objective
To investigate whether thoracolumbar flexion dysfunctions increase the risk of thoracolumbar compression fractures in postmenopausal women.

Methods
The records of postmenopausal women with thoracolumbar vertebral compression fractures and without vertebral compression fractures were surveyed. Demographic data, clinical data, and quantitative computed tomography (QCT) findings were compared between the groups. Chi-squared tests, unpaired t-tests, Spearman, and Mann–Whitney U were used to assess the group characteristics and proportions. The relationship between the risk of fracture and the difference of Cobb’s angle of thoracolumbar segment (DCTL) was evaluated by logistic regression. DCTL was calculated by subtracting thoracolumbar Cobb’s angles (TLCobb’s) from thoracolumbar hyperflexion Cobb’s angles (TLHCobb’s). Quantitative computed tomography (QCT) values and spinal osteoarthritis (OA) of postmenopausal women in the two groups were compared.

Results
102 of 312 were enrolled to the study group of postmenopausal women with the fracture, and 210 of 312 were enrolled to the control group of postmenopausal women without the fracture. There were significant differences in QCT values and spinal OA including disc narrowing (DSN) and osteophytes (OPH) between the two groups (p < 0.001 for all four). The risk of thoracolumbar compression fractures in the postmenopausal women with DCTL ≤ 8.7° was 9.95 times higher (95% CI 5.31–18.64) than that with > 8.7° after adjusting for age, BMI, and QCT values.

Conclusion
Low DCTL may be a risk factor of thoracolumbar compression fractures in postmenopausal women, and a DCTL ≤ 8.7° can be a threshold value of thoracolumbar compression fractures.
Discoidin domain receptor 2 activation of p38 mitogen-activated protein kinase as an important pathway for osteonectin-regulating osteoblast mineralization
Authors: Zhu Yun-Sen , Zhang Jiang-Nan , Mo Ting-Ting , Jiang Chang , Ma Ru-Chao , Chen Liang 
Published: December 2021

Abstract
Objective
The present study aimed to determine the role of the discoidin domain receptor 2 (DDR2) in the osteonectin (ON) regulation of osteoblast mineralization through the activation of p38 mitogen-activated protein kinase (MAPK).

Methods
Four groups were established: the ON group, the inhibitor group, the Ddr2-small interfering ribonucleic acid (siRNA) group, and the control group. Osteoblasts from the parietal bones of neonatal Sprague–Dawley rats were isolated and cultured. In the ON group, 1 µg/mL ON was added to the osteoblasts. The gene expressions of collagen 1 (Col 1) and Ddr2 were detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In the inhibitor group, the osteoblasts were added to WRG-28 (a specific DDR2 inhibitor), and in the Ddr2-siRNA group, the osteoblasts were transfected with Ddr2-siRNA. The gene and protein expressions of DDR2, bone sialoprotein, osteocalcin, osteopontin, and p38 MAPK were determined using RT-qPCR and western blot analysis. Alizarin red staining and transmission electron microscopy were used to detect mineralization.

Results
The results showed that ON enhanced the osteoblast Col 1 and Ddr2 gene expressions, while the use of a Ddr2-siRNA/DDR2-blocker decreased the OPN, BSP, OCN, and P38 gene and protein expressions and reduced osteoblast cellular activity and mineralized nodules.

Conclusion
The present study demonstrated that DDR2 activation of p38 MAPK is an important approach to ON-regulating osteoblast mineralization.
Modelling the disappearance of coarse woody debris, following a land clearing event
Authors: Pringle Matthew J. , Bray Steven G. , Carter John O. 
Published: December 2021

Abstract
Background
Land clearing generates coarse woody debris (CWD), much of which ultimately becomes atmospheric CO2. Schemes for greenhouse gas accounting must consider the contribution from land clearing, but the timing of the contribution will have large uncertainty, due to a paucity of knowledge about the rate of CWD disappearance. To better understand above-ground CWD disappearance following a land clearing event—through the actions of microorganisms, invertebrates, wildfire, or deliberate burning—we combined statistical modelling with an archive of semi-quantitative observations (units of CWD %), made within Queensland, Australia.

Results
Using a generalised additive mixed-effects model (median absolute error = 14.7%), we found that CWD disappearance was strongly influenced by the: (i) number of years elapsed since clearing; (ii) clearing method; (iii) bioregion (effectively a climate-by-tree species interaction); and (iv) the number of times burned. Years-since-clearing had a strongly non-linear effect on the rate of CWD disappearance. The data suggested that disappearance was reverse-sigmoidal, with little change in CWD apparent for the first three years after clearing. In typical conditions for Queensland, the model predicted that it will take 38 years for 95% of CWD to disappear, following a land clearing event; however, accounting for uncertainty in the data and model, this value could be as few as 5 years, or > 100 years. In contrast, due to an assumption about the propensity of land managers to burn CWD, the official method used to assess Australia’s greenhouse gas emissions predicted that 95% of CWD will disappear in < 1 year.

Conclusions
In Queensland, the CWD generated by land clearing typically takes 38 years to disappear. This ultimately implies that a key assumption of Australia’s official greenhouse gas reporting—i.e. that 98% of CWD is burned soon after a clearing event—does not adequately account for delayed CO2 emissions.
Basal lamina changes in neurodegenerative disorders
Authors: Nguyen Benjamin , Bix Gregory , Yao Yao 
Published: December 2021

Abstract
Background
Neurodegenerative disorders are a group of age-associated diseases characterized by progressive degeneration of the structure and function of the CNS. Two key pathological features of these disorders are blood-brain barrier (BBB) breakdown and protein aggregation.

Main body
The BBB is composed of various cell types and a non-cellular component---the basal lamina (BL). Although how different cells affect the BBB is well studied, the roles of the BL in BBB maintenance and function remain largely unknown. In addition, located in the perivascular space, the BL is also speculated to regulate protein clearance via the meningeal lymphatic/glymphatic system. Recent studies from our laboratory and others have shown that the BL actively regulates BBB integrity and meningeal lymphatic/glymphatic function in both physiological and pathological conditions, suggesting that it may play an important role in the pathogenesis and/or progression of neurodegenerative disorders. In this review, we focus on changes of the BL and its major components during aging and in neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). First, we introduce the vascular and lymphatic systems in the CNS. Next, we discuss the BL and its major components under homeostatic conditions, and summarize their changes during aging and in AD, PD, and ALS in both rodents and humans. The functional significance of these alterations and potential therapeutic targets are also reviewed. Finally, key challenges in the field and future directions are discussed.

Conclusions
Understanding BL changes and the functional significance of these changes in neurodegenerative disorders will fill the gap of knowledge in the field. Our goal is to provide a clear and concise review of the complex relationship between the BL and neurodegenerative disorders to stimulate new hypotheses and further research in this field.
WDR26 and MTF2 are therapeutic targets in multiple myeloma
Authors: Sun Fumou , Cheng Yan , Riordan Jesse D. , Dupuy Adam , Dubois Wendy , Pisano Michael , Dong Jing , Mock Beverly , Zhan Fenghuang , Hari Parameswaran , Janz Siegfried 
Published: December 2021

AbstractUnbiased genetic forward screening using retroviral insertional mutagenesis in a genetically engineered mouse model of human multiple myeloma may further our understanding of the genetic pathways that govern neoplastic plasma cell development. To evaluate this hypothesis, we performed a tumor induction study in MYC-transgenic mice infected as neonates with the Moloney-derived murine leukemia virus, MOL4070LTR. Next-generation DNA sequencing of proviral genomic integration sites yielded rank-ordered candidate tumor progression genes that accelerated plasma cell neoplasia in mice. Rigorous clinical and biological validation of these genes led to the discovery of two novel myeloma genes: WDR26 (WD repeat-containing protein 26) and MTF2 (metal response element binding transcription factor 2). WDR26, a core component of the carboxy-terminal to LisH (CTLH) complex, is overexpressed or mutated in solid cancers. MTF2, an ancillary subunit of the polycomb repressive complex 2 (PRC2), is a close functional relative of PHD finger protein 19 (PHF19) which is currently emerging as an important driver of myeloma. These findings underline the utility of genetic forward screens in mice for uncovering novel blood cancer genes and suggest that WDR26-CTLH and MTF2-PRC2 are promising molecular targets for new approaches to myeloma treatment and prevention.
Enterobacter hormaechei in the intestines of housefly larvae promotes host growth by inhibiting harmful intestinal bacteria
Authors: Zhang Qian , Wang Shumin , Zhang Xinyu , Zhang Kexin , Liu Wenjuan , Zhang Ruiling , Zhang Zhong 
Published: December 2021

Abstract
Background
As a pervasive insect that transmits a variety of pathogens to humans and animals, the housefly has abundant and diverse microbial communities in its intestines. These gut microbes play an important role in the biology of insects and form a symbiotic relationship with the host insect. Alterations in the structure of the gut microbial community would affect larval development. Therefore, it is important to understand the mechanism regulating the influence of specific bacteria on the development of housefly larvae.

Methods
For this study we selected the intestinal symbiotic bacterium Enterobacter hormaechei, which is beneficial to the growth and development of housefly larvae, and used it as a probiotic supplement in larval feed. 16S rRNA gene sequencing technology was used to explore the effect of E. hormaechei on the intestinal flora of housefly larvae, and plate confrontation experiments were performed to study the interaction between E. hormaechei and intestinal microorganisms.

Results
The composition of the gut microflora of the larvae changed after the larvae were fed E. hormaechei, with the abundance of Pseudochrobactrum, Enterobacter and Vagococcus increasing and that of Klebsiella and Bacillus decreasing. Analysis of the structure and interaction of larval intestinal flora revealed that E. hormaechei inhibited the growth of harmful bacteria, such as Pseudomonas aeruginosa, Providencia stuartii and Providencia vermicola, and promoted the reproduction of beneficial bacteria.

Conclusions
Our study has explored the influence of specific beneficial bacteria on the intestinal flora of houseflies. The results of this study reveal the important role played by specific beneficial bacteria on the development of housefly larvae and provide insight for the development of sustained biological agents for housefly control through interference of gut microbiota.

Graphical abstract