bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epidemiological analysis of rubella-confirmed cases from measles-suspected cases in Ethiopia: threat for congenital rubella syndrome
Authors: Gemechu Diriba Sufa , Worku Yoseph , Edae Zewdu Assefa , Feyisa Yohannis Dugasa , Watere Shambel Habebe , Woyessa Abyot Bekele , Dukessa Abebe , Gerema Urge 
Published: February 2022

Abstract
Rubella is a highly contagious mild viral illness. It is a leading cause of congenital rubella syndrome (CRS). Routine data of rubella do not exist in Ethiopia. However, laboratory-based conformation of rubella cases from measles negative samples were collected from a measles surveillance system. The current study was to analyse the epidemiological distribution of rubella cases from measles-suspected cases in Ethiopia from 2011 to 2015. National-based secondary data analysis of rubella through measles-based surveillances was carried out. Measles-suspected cases were investigated using the case investigation form, and a serum sample collected and sent to the Ethiopian laboratory for conformation. Samples tested for measles immunoglobulin M (IgM) were tested for rubella. The investigation results were entered into an electronic database using SPSS version 25 for analysis. Out of 11749 samples tested for rubella IgM from 2011 to 2015, 2295 (19.5%) were positive for rubella IgM and 51% of rubella-positive cases were female. Five per cent of all cases were female aged between 15 and 49. Cases were confirmed from all regions, two administrative towns and seasonal variations were observed with peaks in the first and fourth seasonal periods of the years. As fear of congenital abnormality (CRS), the Ethiopian government should focus on rubella syndrome surveillance with the aim of starting a rubella vaccine.
Pulmonary atresia with intact ventricular septum in the setting of D-transposition of the great arteries associated with hypoplastic left ventricle and severe mitral regurgitation
Authors: Suzuki Kota , Mitsushita Norie , Ikai Akio 
Published: February 2022

AbstractWe report the first successful Glenn procedure for pulmonary atresia with intact ventricular septum in the setting of D-transposition of the great arteries. This case was complicated by hypoplastic left ventricle and severe mitral regurgitation. Partial closure of the mitral valve at the time of Blalock-Taussig shunting resulted in improvement of heart failure.
Unusual intramural course in an anomalous left coronary artery from the opposite coronary sinus
Authors: Giusti Giuliano , Villano Mariantonia , Pozzi Marco 
Published: February 2022

AbstractWe report a case of a patient with an anomalous left coronary artery originating from the opposite coronary sinus with evidence of intramural course at the level of the septal commissure and no slit-like deformation of the coronary ostium, acute take-off, or proximal vessel narrowing. According to previous publications, patients with anomalous coronary artery and intramural segments identified at surgery had coronary CT findings of acute take-off angle or proximal vessel narrowing; slit-like orifice; and elliptical cross-sectional shape. Although further investigation is required, we suggest that the intramural course may not be ruled out based on the absence of slit-like ostium, acute take-off, or proximal vessel narrowing.
SASSY21: A 3‐D Seismic Structural Model of the Lithosphere and Underlying Mantle Beneath Southeast Asia From Multi‐Scale Adjoint Waveform Tomography
Authors: Wehner Deborah , Blom Nienke , Rawlinson Nicholas , Daryono  , Böhm Christian , Miller Meghan S. , Supendi Pepen , Widiyantoro Sri 
Published: February 2022

AbstractWe present the first continental‐scale seismic model of the lithosphere and underlying mantle beneath Southeast Asia obtained from adjoint waveform tomography (often referred to as full‐waveform inversion or FWI), using seismic data filtered at periods from 20 to 150 s. Based on >3,000 hr of analyzed waveform data gathered from ∼13,000 unique source‐receiver pairs, we image isotropicP‐wave velocity, radially anisotropicS‐wave velocity and density via an iterative non‐linear inversion that begins from a 1‐D reference model. At each iteration, the full 3‐D wavefield is determined through an anelastic Earth, accommodating effects of topography, bathymetry and ocean load. Our data selection aims to maximize sensitivity to deep structure by accounting for body wave arrivals separately.SASSY21, our final model after 87 iterations across seven period bands, is able to explain true‐amplitude data from events and receivers not included in the inversion. The trade‐off between inversion parameters is estimated through an analysis of the Hessian‐vector product.SASSY21reveals detailed anomalies down to the mantle transition zone, including multiple subduction zones. The most prominent feature is the (Indo‐)Australian plate descending beneath Indonesia, which is imaged as one continuous slab along the 180° curvature of the Banda Arc. The tomography confirms the existence of a hole in the slab beneath Mount Tambora and locates a highS‐wave velocity zone beneath northern Borneo that may be associated with subduction termination in the mid‐late Miocene. A previously undiscovered feature beneath the east coast of Borneo is also revealed, which may be a signature of post‐subduction processes, delamination or underthrusting from the formation of Sulawesi.
Phosphorylated NFS1 weakens oxaliplatin-based chemosensitivity of colorectal cancer by preventing PANoptosis
Authors: Lin Jin-Fei , Hu Pei-Shan , Wang Yi-Yu , Tan Yue-Tao , Yu Kai , Liao Kun , Wu Qi-Nian , Li Ting , Meng Qi , Lin Jun-Zhong , Liu Ze-Xian , Pu Heng-Ying , Ju Huai-Qiang , Xu Rui-Hua , Qiu Miao-Zhen 
Published: February 2022

AbstractMetabolic enzymes have an indispensable role in metabolic reprogramming, and their aberrant expression or activity has been associated with chemosensitivity. Hence, targeting metabolic enzymes remains an attractive approach for treating tumors. However, the influence and regulation of cysteine desulfurase (NFS1), a rate-limiting enzyme in iron–sulfur (Fe–S) cluster biogenesis, in colorectal cancer (CRC) remain elusive. Here, using an in vivo metabolic enzyme gene-based clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 library screen, we revealed that loss of NFS1 significantly enhanced the sensitivity of CRC cells to oxaliplatin. In vitro and in vivo results showed that NFS1 deficiency synergizing with oxaliplatin triggered PANoptosis (apoptosis, necroptosis, pyroptosis, and ferroptosis) by increasing the intracellular levels of reactive oxygen species (ROS). Furthermore, oxaliplatin-based oxidative stress enhanced the phosphorylation level of serine residues of NFS1, which prevented PANoptosis in an S293 phosphorylation-dependent manner during oxaliplatin treatment. In addition, high expression of NFS1, transcriptionally regulated by MYC, was found in tumor tissues and was associated with poor survival and hyposensitivity to chemotherapy in patients with CRC. Overall, the findings of this study provided insights into the underlying mechanisms of NFS1 in oxaliplatin sensitivity and identified NFS1 inhibition as a promising strategy for improving the outcome of platinum-based chemotherapy in the treatment of CRC.
CD19-targeted BiTE expression by an oncolytic vaccinia virus significantly augments therapeutic efficacy against B-cell lymphoma
Authors: Lei Wen , Ye Qian , Hao Yuanyuan , Chen Jie , Huang Yu , Yang Liu , Wang Shibing , Qian Wenbin 
Published: February 2022

AbstractImmunotherapy with CD19-targeting bispecific T-cell engagers (CD19BiTEs) has demonstrated highly effective killing of cancer cells in patients with precursor acute lymphoblastic leukemia and non-Hodgkin’s lymphomas. However, there are some drawbacks to this therapy, such as toxicity, short half-life in the serum, and immunosuppressive tumor microenvironment that could limit the use of CD19BiTEs in the clinic. Here, we generate an oncolytic vaccinia virus (OVV) encoding a CD19-specific BiTE (OVV-CD19BiTE). We demonstrate that OVV-CD19BiTE’s ability to replicate and induce oncolysis was similar to that of its parental counterpart. Supernatants from OVV-CD19BiTE-infected cells could induce activation and proliferation of human T cells, and the bystander effect of the virus was also demonstrated. In vivo study showed that OVV-CD19BiTE selectively replicated within tumor tissue, and contributed to a more significantly increased percentage of CD3, CD8, and naïve CD8 T subpopulations within tumors in contrast to blinatumomab. More importantly, treatment with OVV-CD19BiTE both in vitro and in vivo resulted in potent antitumor activity in comparison with control OVV or blinatumomab, a first-in-class BiTE, thereby resulting in long-term tumor remissions without relapse. The study provides strong evidence for the therapeutic benefits of CD19-targeting BiTE expression by OVV, and suggests the feasibility of testing the approach in clinical trials.
Dichotomy in hypoxia-induced mitochondrial fission in placental mesenchymal cells during development and preeclampsia: consequences for trophoblast mitochondrial homeostasis
Authors: Gillmore Taylor , Farrell Abby , Alahari Sruthi , Sallais Julien , Kurt Merve , Park Chanho , Ausman Jonathan , Litvack Michael , Post Martin , Caniggia Isabella 
Published: February 2022

AbstractDynamic changes in physiologic oxygen are required for proper placenta development; yet, when low-oxygen levels persist, placental development is halted, culminating in preeclampsia (PE), a serious complication of pregnancy. Considering mitochondria’s function is intimately linked to oxygen changes, we investigated the impact of oxygen on mitochondrial dynamics in placental mesenchymal stromal cells (pMSCs) that are vital for proper placental development. Transmission electron microscopy, proximity ligation assays for mitochondrial VDAC1 and endoplasmic reticulum IP3R, and immunoanalyses of p-DRP1 and OPA1, demonstrate that low-oxygen conditions in early 1st trimester and PE promote mitochondrial fission in pMSCs. Increased mitochondrial fission of mesenchymal cells was confirmed in whole PE placental tissue sections. Inhibition of DRP1 oligomerization with MDiVi-1 shows that low oxygen-induced mitochondrial fission is a direct consequence of DRP1 activation, likely via HIF1. Mitophagy, a downstream event prompted by mitochondrial fission, is a prominent outcome in PE, but not 1st trimester pMSCs. We also investigated whether mesenchymal–epithelial interactions affect mitochondrial dynamics of trophoblasts in PE placentae. Exposure of trophoblastic JEG3 cells to exosomes of preeclamptic pMSCs caused heightened mitochondrial fission in the cells via a sphingomyelin-dependent mechanism that was restored by MDiVi-1. Our data uncovered dichotomous regulation of mitochondrial fission and health in human placental mesenchymal cells under physiologic and pathologic hypoxic conditions and its impact on neighboring trophoblast cells.
Identification of Nanog as a novel inhibitor of Rad51
Authors: Xin Ying , Wang Juanjuan , Wu Yahong , Li Qianqian , Dong Mingyang , Liu Chang , He Qijia , Wang Ruifeng , Wang Dian , Jiang Sen , Xiao Wei , Tian Yang , Zhang Weiwei 
Published: February 2022

AbstractTo develop inhibitors targeting DNA damage repair pathways is important to improve the effectiveness of chemo- and radiotherapy for cancer patients. Rad51 mediates homologous recombination (HR) repair of DNA damages. It is widely overexpressed in human cancers and overwhelms chemo- and radiotherapy-generated DNA damages through enhancing HR repair signaling, preventing damage-caused cancer cell death. Therefore, to identify inhibitors of Rad51 is important to achieve effective treatment of cancers. Transcription factor Nanog is a core regulator of embryonic stem (ES) cells for its indispensable role in stemness maintenance. In this study, we identified Nanog as a novel inhibitor of Rad51. It interacts with Rad51 and inhibits Rad51-mediated HR repair of DNA damage through its C/CD2 domain. Moreover, Rad51 inhibition can be achieved by nanoscale material- or cell-penetrating peptide (CPP)-mediated direct delivery of Nanog-C/CD2 peptides into somatic cancer cells. Furthermore, we revealed that Nanog suppresses the binding of Rad51 to single-stranded DNAs to stall the HR repair signaling. This study provides explanation for the high γH2AX level in unperturbed ES cells and early embryos, and suggests Nanog-C/CD2 as a promising drug candidate applied to Rad51-related basic research and therapeutic application studies.
miR-204-5p is sponged by TUG1 to aggravate neuron damage induced by focal cerebral ischemia and reperfusion injury through upregulating COX2
Authors: Xiang Pu , Hu Jian , Wang Hong , Luo Ying , Gu Chao , Tan Xiaodan , Tu Yujun , Guo Wenjia , Chen Lin , Gao Lin , Chen Rongchun , Yang Junqing 
Published: February 2022

AbstractStudies have reported that miR-204-5p is involved in multiple biological processes. However, little is known about the expression and mechanism of miR-204-5p in cerebral ischemia and reperfusion injury. This study found that miR-204-5p expression was significantly downregulated in the blood of patients with ischemic stroke, MCAO/R rat brains, and OGD/R neurons. Overexpression of miR-204-5p markedly reduced infarct volume and neurological impairment and alleviated the inflammatory response in vivo. miR-204-5p promoted neuronal viability and reduced apoptotic cells in vitro. Mechanically, miR-204-5p was negatively regulated by the expression lncRNA TUG1 upstream and down-regulated COX2 expression downstream. Therefore, the TUG1/miR-204-5p/COX2 axis was involved in ischemia and reperfusion-induced neuronal damage. This finding may provide a novel strategy for the treatment of cerebral ischemia and reperfusion injury.
Targeting the Erk1/2 and autophagy signaling easily improved the neurobalst differentiation and cognitive function after young transient forebrain ischemia compared to old gerbils
Authors: Wang Fuxing , Xia Zihao , Sheng Peng , Ren Yu , Liu Jiajia , Ding Lidong , Yan Bing Chun 
Published: February 2022

AbstractThe hippocampal neurogenesis occurs constitutively throughout adulthood in mammalian species, but declines with age. In this study, we overtly found that the neuroblast proliferation and differentiation in the subgranular zone and the maturation into fully functional and integrated neurons in the granule-cell layer in young gerbils following cerebral ischemia/reperfusion was much more than those in old gerbils. The neurological function and cognitive and memory-function rehabilitation in the young gerbils improved faster than those in the old one. These results demonstrated that, during long term after cerebral ischemia/reperfusion, the ability of neurogenesis and recovery of nerve function in young animals were significantly higher than that in the old animals. We found that, after 14- and 28-day cerebral ischemia/reperfusion, the phosphorylation of MEK1/2, ERK1/2, p90RSK, and MSK1/2 protein levels in the hippocampus of young gerbils was significantly much higher than that of old gerbils. The levels of autophagy-related proteins, including Beclin-1, Atg3, Atg5, and LC3 in the hippocampus were effectively maintained and elevated at 28 days after cerebral ischemia/reperfusion in the young gerbils compared with those in the old gerbils. These results indicated that an increase or maintenance of the phosphorylation of ERK1/2 signal pathway and autophagy-related proteins was closely associated with the neuroblast proliferation and differentiation and the process of maturation into neurons. Further, we proved that neuroblast proliferation and differentiation in the dentate gyrus and cognitive function were significantly reversed in young cerebral ischemic gerbils by administering the ERK inhibitor (U0126) and autophagy inhibitor (3MA). In brief, following experimental young ischemic stroke, the long-term promotion of the neurogenesis in the young gerbil’s hippocampal dentate gyrus by upregulating the phosphorylation of ERK signaling pathway and maintaining autophagy-related protein levels, it overtly improved the neurological function and cognitive and memory function.
Myoglobin promotes macrophage polarization to M1 type and pyroptosis via the RIG-I/Caspase1/GSDMD signaling pathway in CS-AKI
Authors: Li Ning , Chen Jiale , Geng Chenhao , Wang Xinyue , Wang Yuru , Sun Na , Wang Pengtao , Han Lu , Li Zizheng , Fan Haojun , Hou Shike , Gong Yanhua 
Published: February 2022

AbstractCrush syndrome (CS) is a life-threatening illness in traffic accidents and earthquakes. Crush syndrome-induced acute kidney injury (CS-AKI) is considered to be mainly due to myoglobin (Mb) circulation and deposition after skeletal muscle ruptures and releases. Macrophages are the primary immune cells that fight foreign substances and play critical roles in regulating the body’s natural immune response. However, what effect does myoglobin have on macrophages and the mechanisms involved in the CS-AKI remain unclear. This study aims to look into how myoglobin affects macrophages of the CS-AKI model. C57BL/6 mice were used to construct the CS-AKI model by digital crush platform. Biochemical analysis and renal histology confirmed the successful establishment of the CS-AKI mouse model. Ferrous myoglobin was used to treat Raw264.7 macrophages to mimic the CS-AKI cell model in vitro. The macrophage polarization toward M1 type and activation of RIG-I as myoglobin sensor were verified by real-time quantitative PCR (qPCR), Western blotting (WB), and immunofluorescence (IF). Macrophage pyroptosis was observed under light microscopy. The interaction between RIG-I and caspase1 was subsequently explored by co-immunoprecipitation (Co-IP) and IF. Small interfering RNA (siRIG-I) and pyroptosis inhibitor dimethyl fumarate (DMF) were used to verify the role of macrophage polarization and pyroptosis in CS-AKI. In the kidney tissue of CS-AKI mice, macrophage infiltration and M1 type were found. We also detected that in the cell model of CS-AKI in vitro, ferrous myoglobin treatment promoted macrophages polarization to M1. Meanwhile, we observed pyroptosis, and myoglobin activated the RIG-I/Caspase1/GSDMD signaling pathway. In addition, pyroptosis inhibitor DMF not only alleviated kidney injury of CS-AKI mice but also inhibited macrophage polarization to M1 phenotype and pyroptosis via the RIG-I/Caspase1/GSDMD signaling pathway. Our research found that myoglobin promotes macrophage polarization to M1 type and pyroptosis via the RIG-I/Caspase1/GSDMD signaling pathway in CS-AKI.
Population-scale dietary interests during the COVID-19 pandemic
Authors: Gligorić Kristina , Chiolero Arnaud , Kıcıman Emre , White Ryen W. , West Robert 
Published: February 2022

AbstractThe SARS-CoV-2 virus has altered people’s lives around the world. Here we document population-wide shifts in dietary interests in 18 countries in 2020, as revealed through time series of Google search volumes. We find that during the first wave of the COVID-19 pandemic there was an overall surge in food interest, larger and longer-lasting than the surge during typical end-of-year holidays in Western countries. The shock of decreased mobility manifested as a drastic increase in interest in consuming food at home and a corresponding decrease in consuming food outside of home. The largest (up to threefold) increases occurred for calorie-dense carbohydrate-based foods such as pastries, bakery products, bread, and pies. The observed shifts in dietary interests have the potential to globally affect food consumption and health outcomes. These findings can inform governmental and organizational decisions regarding measures to mitigate the effects of the COVID-19 pandemic on diet and nutrition.
LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer
Authors: Murray Christopher W. , Brady Jennifer J. , Han Mingqi , Cai Hongchen , Tsai Min K. , Pierce Sarah E. , Cheng Ran , Demeter Janos , Feldser David M. , Jackson Peter K. , Shackelford David B. , Winslow Monte M. 
Published: February 2022

AbstractLKB1is among the most frequently altered tumor suppressors in lung adenocarcinoma. Inactivation ofLkb1accelerates the growth and progression of oncogenic KRAS-driven lung tumors in mouse models. However, the molecular mechanisms by which LKB1 constrains lung tumorigenesis and whether the cancer state that stems fromLkb1deficiency can be reverted remains unknown. To identify the processes governed by LKB1 in vivo, we generated an allele which enablesLkb1inactivation at tumor initiation and subsequentLkb1restoration in established tumors. Restoration ofLkb1in oncogenic KRAS-driven lung tumors suppressed proliferation and led to tumor stasis.Lkb1restoration activated targets of C/EBP transcription factors and drove neoplastic cells from a progenitor-like state to a less proliferative alveolar type II cell-like state. We show that C/EBP transcription factors govern a subset of genes that are induced by LKB1 and depend upon NKX2-1. We also demonstrate that a defining factor of the alveolar type II lineage, C/EBPα, constrains oncogenic KRAS-driven lung tumor growth in vivo. Thus, this key tumor suppressor regulates lineage-specific transcription factors, thereby constraining lung tumor development through enforced differentiation.
Humoral immune responses to COVID-19 vaccination in people living with HIV receiving suppressive antiretroviral therapy
Authors: Brumme Zabrina L. , Mwimanzi Francis , Lapointe Hope R. , Cheung Peter K. , Sang Yurou , Duncan Maggie C. , Yaseen Fatima , Agafitei Olga , Ennis Siobhan , Ng Kurtis , Basra Simran , Lim Li Yi , Kalikawe Rebecca , Speckmaier Sarah , Moran-Garcia Nadia , Young Landon , Ali Hesham , Ganase Bruce , Umviligihozo Gisele , Omondi F. Harrison , Atkinson Kieran , Sudderuddin Hanwei , Toy Junine , Sereda Paul , Burns Laura , Costiniuk Cecilia T. , Cooper Curtis , Anis Aslam H. , Leung Victor , Holmes Daniel , DeMarco Mari L. , Simons Janet , Hedgcock Malcolm , Romney Marc G. , Barrios Rolando , Guillemi Silvia , Brumme Chanson J. , Pantophlet Ralph , Montaner Julio S. G. , Niikura Masahiro , Harris Marianne , Hull Mark , Brockman Mark A. 
Published: February 2022

AbstractHumoral responses to COVID-19 vaccines in people living with HIV (PLWH) remain incompletely characterized. We measured circulating antibodies against the SARS-CoV-2 spike protein receptor-binding domain (RBD), ACE2 displacement and viral neutralization activities one month following the first and second COVID-19 vaccine doses, and again 3 months following the second dose, in 100 adult PLWH and 152 controls. All PLWH were receiving suppressive antiretroviral therapy, with median CD4+ T-cell counts of 710 (IQR 525–935) cells/mm3, though nadir CD4+ T-cell counts ranged as low as <10 cells/mm3. After adjustment for sociodemographic, health and vaccine-related variables, HIV infection was associated with lower anti-RBD antibody concentrations and ACE2 displacement activity after one vaccine dose. Following two doses however, HIV was not significantly associated with the magnitude of any humoral response after multivariable adjustment. Rather, older age, a higher burden of chronic health conditions, and dual ChAdOx1 vaccination were associated with lower responses after two vaccine doses. No significant correlation was observed between recent or nadir CD4+ T-cell counts and responses to two vaccine doses in PLWH. These results indicate that PLWH with well-controlled viral loads and CD4+ T-cell counts in a healthy range generally mount strong initial humoral responses to dual COVID-19 vaccination. Factors including age, co-morbidities, vaccine brand, response durability and the rise of new SARS-CoV-2 variants will influence when PLWH will benefit from additional doses. Further studies of PLWH who are not receiving antiretroviral treatment or who have low CD4+ T-cell counts are needed, as are longer-term assessments of response durability.