bluuebunny/crossref_metadata_2025_split huggingface dataset:
Poverty and Education: Attainments and Challenges for Tribal Communities
Authors: Rupavath Ramdas 
Published: October 2021

Various educational policies and government initiatives at the national level in India have aimed at improving the literacy rate of the tribal communities. However, even after 73 years of independence, the literacy levels of the tribal people have not risen to the desired levels. On top, there is the issue of high dropout rates (Ministry of Tribal Affairs, Statistics Division, Government of India, 2013, Statistical Profile of Scheduled Tribes in India, https://tribal.nic.in/ST/StatisticalProfileofSTs2013.pdf ; 70.9%, according to a recent study) among the Tribals (Rupavath, 2016a, Review Pub Administration Management, 4, p. 183). In such a situation, it is important to find out why tribal communities are still lagging behind in the education sector. This study will deal with the various aspects of access to education for the tribal communities. It will also try to examine the linkage between poverty and education. This is considered important since literacy can mean much more than mere bookish knowledge. A literate person can be expected to have more awareness about matters of importance to him or her. On the employment front, a literate person can have wider livelihood options—and not be confined to pursue occupations which largely entail manual labour. At the same time, a literate person would know more about his or her legitimate entitlements and be in a better position to avail of these. It is one thing for the government to reserve vacancies for candidates belonging to the deprived sections of society. It is equally important for more persons hailing from these sections to know about these and utilize these. Education can be a means for such persons to optimally utilize the opportunities available to them. It is a proven fact that students learn better and retain more when they are active participants in the teaching–learning process. For the purpose of this study, two districts—Anantapur and Vishakhapatnam (in Andhra Pradesh), and Hyderabad district (in Telangana)—have been selected for a detailed examination. The study will include not only the availability of infrastructure but also participation of the tribal students in the classroom discussions. The study will utilize both purposive and random sampling methods.
Type 1 interferon to prevent leukemia relapse after allogeneic transplantation
Authors: Magenau John M. , Peltier Dan , Riwes Mary , Pawarode Attaphol , Parkin Brian , Braun Thomas , Anand Sarah , Ghosh Monalisa , Maciejewski John , Yanik Gregory , Choi Sung Won , Talpaz Moshe , Reddy Pavan 
Published: October 2021

Abstract
A potent graft-versus-leukemia (GVL) response is crucial in preventing relapse, the major impediment to successful allogeneic hematopoietic cell transplantation (HCT). In preclinical studies, type 1 interferon (IFN-α) enhanced cross-presentation of leukemia-specific antigens by CD8α dendritic cells (DCs) and amplified GVL. This observation was translated into a proof-of-concept phase 1/2 clinical trial with long-acting IFN-α (pegylated IFN-α [pegIFNα]) in patients undergoing HCT for high-risk acute myeloid leukemia (AML). Patients with treatment-resistant AML not in remission or those with poor-risk leukemia were administered 4 dosages of pegIFNα every 14 days beginning at day −1 before HCT. Dose selection was established by adaptive design that continuously assessed the probability of dose-limiting toxicities throughout the trial. Efficacy was evaluated by determining the 6-month incidence of relapse at the maximum tolerated dose (MTD). Thirty-six patients (median age, 60 years) received pegIFNα treatment. Grade 3 or greater severe adverse events occurred in 25% of patients, establishing 180 μg as the MTD. In phase 2, the incidence of relapse was 39% at 6 months, which was sustained through 1-year post-HCT. The incidence of transplant-related mortality was 13%, and severe grade III-IV acute graft-versus-host disease (GVHD) occurred in 11%. Paired blood samples from donors and recipients after HCT revealed elevated levels of type 1 IFN with cellular response, the persistence of cross-presenting DCs, and circulating leukemia antigen-specific T cells. These data suggest that prophylactic administration of pegIFNα is feasible in the peri-HCT period. In high-risk AML, increased toxicity was not observed with preliminary evidence for reduction in leukemia relapse after HCT. This trial was registered at www.clinicaltrials.gov as #NCT02328755.
Multiple breath washout: measuring early manifestations of lung pathology
Authors: Stanojevic Sanja , Bowerman Cole , Robinson Paul 
Published: October 2021

The multiple breath washout (MBW) test measures the efficiency of gas mixing in the lungs and has gained significant interest over the past 20 years. MBW outcomes detect early lung function impairment and peripheral airway pathology, through its main outcome measure lung clearance index (LCI). LCI measures the number of lung turnovers required to washout an inert tracer gas. MBW is performed during normal (tidal) breathing, making it particularly suitable for young children or those who have trouble performing forced manoeuvres. Additionally, research in chronic respiratory disease populations has shown that MBW can detect acute clinically relevant changes before conventional lung function tests, such as spirometry, thus enabling early intervention. The development of technical standards for MBW and commercial devices have allowed MBW to be implemented in clinical research and potentially routine clinical practice. Although studies have summarised clinimetric properties of MBW indices, additional research is required to establish the clinical utility of MBW and, if possible, shorten testing time. Sensitive, feasible measures of early lung function decline will play an important role in early intervention for people living with respiratory diseases.Educational aimTo describe the multiple breath washout test, its applications to lung pathology and respiratory disease, as well as directions for future research.
Rickettsia burneti and Brucella melitensis co-infection: a case report and literature review
Authors: Song Jiangqin , Hu Xiaorong , Li Xiaolong , Chen Youping , Yan Xiangyuan , Zhu Weifang , Ding Yan , Zhou Junyang 
Published: October 2021

AbstractRickettsia is the pathogen of Q fever, Brucella ovis is the pathogen of brucellosis, and both of them are Gram-negative bacteria which are parasitic in cells. The mixed infection of rickettsia and Brucella ovis is rarely reported in clinic. Early diagnosis and treatment are of great significance to the treatment and prognosis of brucellosis and Q fever. Here, we report a case of co-infection Rickettsia burneti and Brucella melitensis. The patient is a 49-year-old sheepherder, who was hospitalized with left forearm trauma. Three days after admission, the patient developed fever of 39.0°C, accompanied by sweating, fatigue, poor appetite and headache. Indirect immunofluorescence (IFA) was used to detect Rickettsia burneti IgM. After 72 hours of blood culture incubation, bacterial growth was detected in aerobic bottles, Gram-negative bacilli were found in culture medium smear, the colony was identified as Brucella melitensis by mass spectrometry. Patients were treated with doxycycline (100 mg bid, po) and rifampicin (600 mg qd, po) for 4 weeks. After treatment, the symptoms disappeared quickly, and there was no sign of recurrence or chronic infection. Q fever and Brucella may exist in high-risk practitioners, so we should routinely detect these two pathogens to prevent missed diagnosis.
The essential roles of OsFtsH2 in developing the chloroplast of rice
Authors: Wu Qingfei , Han Tiantian , Yang Li , Wang Qiang , Zhao Yingxian , Jiang Dean , Ruan Xiao 
Published: October 2021

AbstractBackgroundFilamentation temperature-sensitive H (FtsH) is an ATP-dependent zinc metalloprotease with ATPase activity, proteolysis activity and molecular chaperone-like activity. For now, a total of nine FtsH proteins have been encoded in rice, but their functions have not revealed in detail. In order to investigate the molecular mechanism ofOsFtsH2here, severalosftsh2knockout mutants were successfully generated by the CRISPR/Cas9 gene editing technology.ResultsAll the mutants exhibited a phenotype of striking albino leaf and could not survive through the stage of three leaves. OsFtsH2 was located in the chloroplast and preferentially expressed in green tissues. In addition,osftsh2mutants could not form normal chloroplasts and had lost photosynthetic autotrophic capacity. RNA sequencing analysis indicated that many biological processes such as photosynthesis-related pathways and plant hormone signal transduction were significantly affected inosftsh2mutants.ConclusionsOverall, the results suggested OsFtsH2 to be essential for chloroplast development in rice.
Comparative characterization and osteogenic / adipogenic differentiation of mesenchymal stem cells derived from male rat hair follicles and bone marrow
Authors: Zaki Abdel Kader A. , Almundarij Tariq I. , Abo-Aziza Faten A. M. 
Published: October 2021

AbstractClinical applications of cell therapy and tissue regeneration under different conditions need a multiplicity of adult stem cell sources. Up to date, little is available on the comparative isolation, characterization, proliferation, rapid amplification, and osteogenic/adipogenic differentiation of rat mesenchymal stem cells (MSCs) isolated from living bulge cells of the hair follicle (HF) and bone marrow (BM) from the same animal. This work hopes to use HF-MSCs as an additional adult stem cell source for research and application. After reaching 80% confluence, the cell counting, viability %, and yields of HF-MSCs and BM-MSCs were nearly similar. The viability % was 91.41 ± 2.98 and 93.11 ± 3.06 while the cells yield of initial seeding was 33.15 ± 2.76 and 34.22 ± 3.99 and of second passage was 28.76 ± 1.01 and 29.56 ± 3.11 for HF-MSCs and BM-MSCs respectively. Clusters of differentiation (CDs) analysis revealed that HF-MSCs were positively expressed CD34, CD73 and CD200 and negatively expressed CD45. BM-MSCs were positively expressed CD73 and CD200 and negatively expressed of CD34 and CD45. The proliferation of HF-MSCs and BM-MSCs was determined by means of incorporation of Brd-U, population doubling time (PDT) assays and the quantity of formazan release. The percentage of Brd-U positive cells and PDT were relatively similar in both types of cells. The proliferation, as expressed by the quantity of formazan assay in confluent cells, revealed that the quantity of release by BM-MSCs was slightly higher than HF-MSCs. Adipogenic differentiated BM-MSCs showed moderate accumulation of oil red-O stained lipid droplets when compared to that of HF-MSCs which exhibited high stain. The total lipid concentration was significantly higher in adipogenic differentiated HF-MSCs than BM-MSCs (P < 0.05). It was found that activity of bone alkaline phosphatase and calcium concentration were significantly higher (P < 0.01 andP < 0.05 respectively) in osteogenic differentiated BM-MSCs than that of HF-MSCs. The present findings demonstrate that the HF-MSCs are very similar in most tested characteristics to BM-MSCs with the exception of differentiation. Additionally; no issues have been reported during the collection of HF-MSCs. Therefore, the HF may represent a suitable and accessible source for adult stem cells and can be considered an ideal cell source for adipogenesis research.
Positive feedback between retinoic acid and 2-phospho-L-ascorbic acid trisodium salt during somatic cell reprogramming
Authors: Zhang Mengdan , Li Qian , Yang Tingting , Meng Fei , Lai Xiaowei , Liang Lining , Li Changpeng , Sun Hao , Sun Jiaqi , Zheng Hui 
Published: October 2021

AbstractRetinoic acid (RA) and 2-phospho-L-ascorbic acid trisodium salt (AscPNa) promote the reprogramming of mouse embryonic fibroblasts to induced pluripotent stem cells. In the current studies, the lower abilities of RA and AscPNa to promote reprogramming in the presence of each other suggested that they may share downstream pathways at least partially. The hypothesis was further supported by the RNA-seq analysis which demonstrated a high-level overlap between RA-activated and AscPNa activated genes during reprogramming. In addition, RA upregulated Glut1/3, facilitated the membrane transportation of dehydroascorbic acid, the oxidized form of L-ascorbic acid, and subsequently maintained intracellular L-ascorbic acid at higher level and for longer time. On the other hand, AscPNa facilitated the mesenchymal-epithelial transition during reprogramming, downregulated key mesenchymal transcriptional factors like Zeb1 and Twist1, subsequently suppressed the expression of Cyp26a1/b1 which mediates the metabolism of RA, and sustained the intracellular level of RA. Furthermore, the different abilities of RA and AscPNa to induce mesenchymal-epithelial transition, pluripotency, and neuronal differentiation explain their complex contribution to reprogramming when used individually or in combination. Therefore, the current studies identified a positive feedback between RA and AscPNa, or possibility between vitamin A and C, and further explored their contributions to reprogramming.
Cardiac cell type-specific responses to injury and contributions to heart regeneration
Authors: Zhang Weijia , Liang Jinxiu , Han Peidong 
Published: October 2021

AbstractHeart disease is the leading cause of mortality worldwide. Due to the limited proliferation rate of mature cardiomyocytes, adult mammalian hearts are unable to regenerate damaged cardiac muscle following injury. Instead, injured area is replaced by fibrotic scar tissue, which may lead to irreversible cardiac remodeling and organ failure. In contrast, adult zebrafish and neonatal mammalian possess the capacity for heart regeneration and have been widely used as experimental models. Recent studies have shown that multiple types of cells within the heart can respond to injury with the activation of distinct signaling pathways. Determining the specific contributions of each cell type is essential for our understanding of the regeneration network organization throughout the heart. In this review, we provide an overview of the distinct functions and coordinated cell behaviors of several major cell types including cardiomyocytes, endocardial cells, epicardial cells, fibroblasts, and immune cells. The topic focuses on their specific responses and cellular plasticity after injury, and potential therapeutic applications.
Overexpression of HOXA9 upregulates NF-κB signaling to promote human hematopoiesis and alter the hematopoietic differentiation potentials
Authors: Zeng Jiahui , Yi Danying , Sun Wencui , Liu Yuanlin , Chang Jing , Zhu Lijiao , Zhang Yonggang , Pan Xu , Dong Yong , Zhou Ya , Lai Mowen , Bian Guohui , Zhou Qiongxiu , Liu Jiaxin , Chen Bo , Ma Feng 
Published: October 2021

Abstract
Background
The HOX genes are master regulators of embryogenesis that are also involved in hematopoiesis. HOXA9 belongs to a cluster of HOX genes that play extensively studied roles in hematopoiesis and leukemogenesis.

Methods
We established HOXA9-inducible human embryonic stem cells (HOXA9/hESCs) with normal pluripotency and potential for hematopoiesis, which could be used to analyze gene function with high accuracy. HOXA9/hESCs co-cultured with aorta–gonad–mesonephros-derived stromal cells (AGM-S3) were induced to overexpress HOXA9 with doxycycline (DOX) at various times after hematopoiesis started and then subjected to flow cytometry.

Results
Induction of HOXA9 from Day 4 (D4) or later notably promoted hematopoiesis and also increased the production of CD34+ cells and derived populations. The potential for myelogenesis was significantly elevated while the potential for erythrogenesis was significantly reduced. At D14, a significant promotion of S phase was observed in green fluorescent protein positive (GFP+) cells overexpressing HOXA9. NF-κB signaling was also up-regulated at D14 following induction of HOXA9 on D4. All of these effects could be counteracted by addition of an NF-κB inhibitor or siRNA against NFKB1 along with DOX.

Conclusions
Overexpression of HOXA9 starting at D4 or later during hematopoiesis significantly promoted hematopoiesis and the production of myeloid progenitors while reduced the production of erythroid progenitors, indicating that HOXA9 plays a key role in hematopoiesis and differentiation of hematopoietic lineages.
From wound response to repair – lessons from C. elegans
Authors: Ma Yicong , Xie Jing , Wijaya Chandra Sugiarto , Xu Suhong 
Published: October 2021

AbstractAs a result of evolution, the ability to repair wounds allows organisms to combat environment insults. Although the general process of wound healing at the tissue level has been described for decades, the detailed molecular mechanisms regarding the early wound response and rapid wound repair at the cellular level remain little understood.Caenorhabditis elegansis a model organism widely used in the field of development, neuroscience, programmed cell death etc. The nematode skin is composed of a large epidermis associated with a transparent extracellular cuticle, which likely has a robust capacity for epidermal repair. Yet, until the last decades, relatively few studies had directly analyzed the wound response and repair process. Here we review recent findings in howC. elegansepidermis responds to wounding and initiates early actin-polymerization-based wound closure as well as later membrane repair. We also discussed some remained outstanding questions for future study.
Evolutionary insights into heart regeneration
Authors: Xiong Jing-Wei 
Published: October 2021

AbstractSome lower vertebrates such as zebrafish and axolotl have incredible cardiac regenerative potential while mammals have very limited ones. Comparative studies among species have revealed that cardiomyocyte polyploidy, endothermy, and injury-induced activation of certain transcriptional factors including AP1 complexes are critical for cardiomyocyte proliferation and heart regeneration during animal evolution. Gaining insights into these evolutionarily conserved mechanisms will likely lead to achieving heart regeneration in non-regenerative mammals including humans.
RhoA/Rock activation represents a new mechanism for inactivating Wnt/β-catenin signaling in the aging-associated bone loss
Authors: Shi Wei , Xu Chengyun , Gong Ying , Wang Jirong , Ren Qianlei , Yan Ziyi , Mei Liu , Tang Chao , Ji Xing , Hu Xinhua , Qv Meiyu , Hussain Musaddique , Zeng Ling-Hui , Wu Ximei 
Published: October 2021

AbstractThe Wnt/β-catenin signaling pathway appears to be particularly important for bone homeostasis, whereas nuclear accumulation of β-catenin requires the activation of Rac1, a member of the Rho small GTPase family. The aim of the present study was to investigate the role of RhoA/Rho kinase (Rock)-mediated Wnt/β-catenin signaling in the regulation of aging-associated bone loss. We find that Lrp5/6-dependent and Lrp5/6-independent RhoA/Rock activation by Wnt3a activates Jak1/2 to directly phosphorylate Gsk3β at Tyr216, resulting in Gsk3β activation and subsequent β-catenin destabilization. In line with these molecular events, RhoA loss- or gain-of-function in mouse embryonic limb bud ectoderms interacts genetically with Dkk1 gain-of-function to rescue the severe limb truncation phenotypes or to phenocopy the deletion of β-catenin, respectively. Likewise, RhoA loss-of-function in pre-osteoblasts robustly increases bone formation while gain-of-function decreases it. Importantly, high RhoA/Rock activity closely correlates with Jak and Gsk3β activities but inversely correlates with β-catenin signaling activity in bone marrow mesenchymal stromal cells from elderly male humans and mice, whereas systemic inhibition of Rock therefore activates the β-catenin signaling to antagonize aging-associated bone loss. Taken together, these results identify RhoA/Rock-dependent Gsk3β activation and subsequent β-catenin destabilization as a hitherto uncharacterized mechanism controlling limb outgrowth and bone homeostasis.
miRNA in cardiac development and regeneration
Authors: Ouyang Zhaohui , Wei Ke 
Published: October 2021

AbstractIschemic heart disease is one of the main causes of morbidity and mortality in the world. In adult mammalian hearts, most cardiomyocytes are terminally differentiated and have extremely limited capacity of proliferation, making it impossible to regenerate the heart after injuries such as myocardial infarction. MicroRNAs (miRNAs), a class of non-coding single-stranded RNA, which are involved in mRNA silencing and the regulation of post-transcriptional gene expression, have been shown to play a crucial role in cardiac development and cardiomyocyte proliferation. Muscle specific miRNAs such as miR-1 are key regulators of cardiomyocyte maturation and growth, while miR-199-3p and other miRNAs display potent activity to induce proliferation of cardiomyocytes. Given their small size and relative pleiotropic effects, miRNAs have gained significant attraction as promising therapeutic targets or tools in cardiac regeneration. Increasing number of studies demonstrated that overexpression or inhibition of specific miRNAs could induce cardiomyocyte proliferation and cardiac regeneration. Some common targets of pro-proliferation miRNAs, such as the Hippo-Yap signaling pathway, were identified in multiple species, highlighting the power of miRNAs as probes to dissect core regulators of biological processes. A number of miRNAs have been shown to improve heart function after myocardial infarction in mice, and one trial in swine also demonstrated promising outcomes. However, technical difficulties, especially in delivery methods, and adverse effects, such as uncontrolled proliferation, remain. In this review, we summarize the recent progress in miRNA research in cardiac development and regeneration, examine the mechanisms of miRNA regulating cardiomyocyte proliferation, and discuss its potential as a new strategy for cardiac regeneration therapy.
Forkhead box family transcription factors as versatile regulators for cellular reprogramming to pluripotency
Authors: Fu Meijun , Chen Huan , Cai Zepo , Yang Yihang , Feng Ziyu , Zeng Mengying , Chen Lijun , Qin Yue , Cai Baomei , Zhu Pinghui , Zhou Chunhua , Yu Shengyong , Guo Jing , Liu Jing , Cao Shangtao , Pei Duanqing 
Published: October 2021

AbstractForkhead box (Fox) transcription factors play important roles in mammalian development and disease. However, their function in mouse somatic cell reprogramming remains unclear. Here, we report that FoxD subfamily and FoxG1 accelerate induced pluripotent stem cells (iPSCs) generation from mouse fibroblasts as early as day4 while FoxA and FoxO subfamily impede this process obviously. More importantly, FoxD3, FoxD4 and FoxG1 can replace Oct4 respectively and generate iPSCs with germline transmission together with Sox2 and Klf4. On the contrary, FoxO6 almost totally blocks reprogramming through inhibiting cell proliferation, suppressing the expression of pluripotent genes and hindering the process of mesenchymal to epithelial transition (MET). Thus, our study uncovers unexpected roles of Fox transcription factors in reprogramming and offers new insights into cell fate transition.