bluuebunny/crossref_metadata_2025_split huggingface dataset:
Efficacy and safety of telbivudine to prevent mother‐to‐child transmission of hepatitis B virus in middle‐ and late‐stage pregnancy with high viral loads
Authors: Xu Jing , Tao Lin lin , Ma Li xian 
Published: August 2019

AbstractObjectiveTo observe the efficacy and safety of telbivudine on mother‐infant blockade in pregnant women with hepatitis B virus (HBV) DNA.MethodsA total of 141 pregnant women between 24 and 28 weeks of gestation and chronic HBV carriers with HBV DNA ≥106 copies/mL were enrolled, 105 in the treatment group and 36 in the control group. The treatment group was given telbivudine 600 mg/d oral, and the control group did not use antiviral drugs. Hepatitis B immunoglobulin 200 IU intramuscular injection and hepatitis B vaccine (HBVac) 10 μg subcutaneous injection were given to the infants in both groups within 12 hours after birth, and 10 μg of HBVac was subcutaneously injected when the infants were 1‐month and 6‐month old. Safety endpoints including HBV DNA quantification, liver function, CK were observed before treatment, 4 weeks after treatment, before delivery, and 24 weeks after delivery.ResultsThere was no difference in HBV DNA levels between the two groups before treatment and 6 months after delivery (P > .05). The HBV DNA level in the treatment group was significantly lower than that in the control group before delivery (P < .05). Between the two groups, the HBV positive rate was statistically different between the two groups (P < .05), and the difference of serum HBsAg of infants had statistical significance (P < .05), but the safety of the telbivudine group was not significantly different from that of the control group (P > .05).ConclusionThe application of telbivudine antiviral therapy in the middle and late stage of pregnancy of HBV high‐load pregnant women can significantly reduce the HBV DNA level before delivery, reduce the mother‐to‐child transmission rate of HBV, and have excellent security.
Raman spectroscopic evidence of impurity‐induced structural distortion in SmB6
Authors: Nguyen Thi Huyen , Nguyen Thi Minh Hien , Kang Boyoun , Cho Beongki , Han Mancheon , Choi Hyoung Joon , Kong Mihye , Lee Yongjae , Yang In‐Sang 
Published: August 2019

AbstractImpurity‐induced structural distortion in SmB6 is suggested by Raman spectroscopy study on impurity‐controlled samples. Significant differences in the Raman spectra of single crystals SmB6(6N), synthesized with 99.9999%‐pure boron, and SmB6(3N), synthesized with 99.9%‐pure boron, are detected. While no noticeable differences are detected in the X‐ray diffraction of SmB6(3N) and SmB6(6N), all the Raman phonon modes of the T2g, Eg, and A1g of SmB6(3N) are clearly broader and shift to higher wavenumbers than those of SmB6(6N), and the T2g and Eg modes of SmB6(3N) show doublet features. Based on the high‐pressure Raman measurements and phonon calculation in uniaxial compression model, we argue that small amount of impurities in SmB6(3N) is enough to induce anisotropic distortion in the B6 octahedra, leading to peculiar behaviors in Raman spectrum of SmB6(3N). Our results may present a clue for understanding the current puzzles about SmB6 of various origins with different impurities.
Raman spectroscopy of zinc oxide nanoplatelets modified with ruthenium (II) complexes
Authors: Ristić‐Djurović Jasna L. , Fernández‐Izquierdo Leunam , Hadžić Branka , Jiménez‐Hernández Linnavel , Díaz‐García Alicia M. , Mitrić Jelena , Babić Biljana , Romčević Maja , Ćirković Saša , Romčević Nebojša 
Published: August 2019

AbstractWe analyzed and compared the unmodified and three modified zinc oxide nanoplatelet materials. The three components used in zinc oxide modification were the 4,4apos;‐bipyridine and two ruthenium (II) complexes, namely, the trans‐[Ru (bpy)(bpyCOO)Cl2]2– and cis‐[Ru (bpy)(bpyCOO)Cl2]2–. The obtained results revealed that after modification, ZnO nanoplatelets became smaller and embedded in the materials used for the modification. When ZnO was modified with either of the two ruthenium (II) complexes, the interaction between them led to a higher activity of ZnO. The metal‐to‐ligand charge transfer that was also detected in the two cases of ZnO nanoplatelets modified with the ruthenium (II) complexes caused significant alteration of the Raman spectrum and consequent changes of the optical properties. Various forms of ruthenium (II) complexes were used in several published studies related to dye‐sensitized solar cells and biomedicine. The biomedical applications include, for example, the ATP (adenosine‐5apos;‐triphosphate) detection, interaction with human serum albumin, DNA analysis, and cancer detection and treatment. The properties of the ZnO nanoplatelets modified with the two ruthenium (II) complexes presented here indicate that it may be worth exploring if the studied materials are applicable in the dye sensitized solar cells and biomedicine. Possible advantage of our results is that they were obtained at room temperature.
Characterizing and evaluating the impacts of national land restoration initiatives on ecosystem services in Ethiopia
Authors: Abera Wuletawu , Tamene Lulseged , Tibebe Degefie , Adimassu Zenebe , Kassa Habtemariam , Hailu Habtamu , Mekonnen Kindu , Desta Gizaw , Sommer Rolf , Verchot Louis 
Published: August 2019

AbstractLand restoration is considered to be the remedy for 21st century global challenges of land degradation. As a result, various land restoration and conservation efforts are underway at different scales. Ethiopia is one of the countries with huge investments in land restoration. Tremendous land management practices have been implemented across the country since the 1970s. However, the spatial distribution of the interventions has not been documented, and there is no systematic, quantitative evidence on whether land restoration efforts have achieved the restoration of desired ecosystem services. Therefore, we carried out a meta‐analysis of peer‐reviewed scientific literature related to land restoration efforts and their impacts in Ethiopia. Results show that most of the large‐scale projects have been implemented in the highlands, specifically in Tigray and Amhara regions covering about 24 agroecological zones, and land restoration impact studies are mostly focused in the highlands but restricted in about 11 agroecological zones. The highest mean effect on agricultural productivity is obtained from the combination of bunds and biological interventions followed by conservation agriculture practices with 170% and 18% increases, respectively. However, bunds alone, biological intervention alone, and terracing (fanya juu) reveal negative effects on productivity. The mean effect of all land restoration interventions on soil organic carbon is positive, the highest effect being from “bunds + biological” (139%) followed by exclosure (90%). Reduced soil erosion and runoff are the dominant impacts of all interventions. The results can be used to improve existing guidelines to better match land restoration options with specific desired ecosystem functions and services. Although the focus of this study was on the evaluation of the impacts of land restoration efforts on selected ecosystem services, impacts on livelihood and national socioeconomy have not been examined. Thus, strengthening socioeconomic studies at national scale to assess the sustainability of land restoration initiatives is an essential next step.
Assessment of biomass utilization potential of Caragana korshinskii and its effect on carbon sequestration on the Northern Shaanxi Loess Plateau, China
Authors: Liu Weiguo , Yu Zhen , Zhu Qiuan , Zhou Xiaolu , Peng Changhui 
Published: August 2019

AbstractBiomass has been promoted as a promising energy resource to mitigate global climate change. To evaluate the contribution of biomass utilization to climate change mitigation under the “Grain for Green” program in Northern Shaanxi, China, a soil carbon dynamic model and a life cycle assessment model were integrated to examine the benefits of using Caragana korshinskii Kom. as an energy crop. We found that the annual dry biomass output is maintained at 0.7 Tg during the simulation period (2020–2097). Due to the compensatory effect of biomass regrowth, the global warming potential of biomass‐derived CO2 emissions is approximately 0.045; therefore, the total annual biogenic CO2 emission is 57,211 ± 6,168 Mg CO2 eq. The total annual life cycle CO2 emissions approach 867,072 Mg CO2 eq yr−1. Under the scenario of no biomass removal, final carbon storage ranges from 15.7 to 19.3 TgC, and the highest carbon sequestration rate is 0.47 TgC yr−1. In comparison with the no biomass removal scenario, the carbon sequestration rate (close to 0 MgC yr−1) in the biomass utilization scenario indicates a carbon loss; however, a portion of the carbon loss (31.39–62.09%) can be offset by carbon emission reductions from the substitution of fossil fuels.
Downregulation of CPA4 inhibits non small–cell lung cancer growth by suppressing the AKT/c‐MYC pathway
Authors: Fu Yangyang , Su Lihuang , Cai Mengsi , Yao Boyang , Xiao Sisi , He Qinlian , Xu Le , Yang Lehe , Zhao Chengguang , Wan Tingting , Shao Lianyou , Wang Liangxing , Huang Xiaoying 
Published: August 2019

AbstractCarboxypeptidase A4 (CPA4) is a member of the metallocarboxypeptidase family. A previous study indicated that CPA4 may participate in the modulation of peptide hormone activity and hormone‐regulated tissue growth and differentiation. However, the role of CPA4 in lung tumorigenesis remains unclear. Our study revealed that CPA4 expression was higher in both lung cancer cells and tumor tissues. We performed 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assays, colony‐formation assays, and Cellomics ArrayScan Infinity analysis to demonstrate that CPA4 knockdown inhibited non small–cell lung cancer (NSCLC) cell proliferation. Conversely, ectopic expression of CPA4 enhanced lung cancer cell proliferation. Consistent with these observations, we generated xenograft tumor models to confirm that CPA4 downregulation suppressed NSCLC cell growth. Mechanistically, we revealed that CPA4 downregulation may induce apoptosis and G1‐S arrest by suppressing the protein kinase B/c‐MYC pathway. These results suggest that CPA4 has an oncogenic effect on lung cancer growth. Taken together, we identified a novel gene in lung cancer that might provide a basis for new therapeutic targets.
Inhibition of mutant Kras and p53‐driven pancreatic carcinogenesis by atorvastatin: Mainly via targeting of the farnesylated DNAJA1 in chaperoning mutant p53
Authors: Xu Dandan , Tong Xin , Sun Leyu , Li Haonan , Jones Ryan D. , Liao Jie , Yang Guang‐Yu 
Published: August 2019

AbstractRecent studies have indicated that using statins to inhibit the mevalonate pathway induces mutant p53 degradation by impairing the interaction of mutant p53 with DnaJ subfamily A member 1 (DNAJA1). However, the role of the C‐terminus of DNAJA1 with a CAAX box for farnesylation in the binding, folding, and translocation of client proteins such as mutant p53 is not known. In the present study, we used a genetically engineered mouse model of pancreatic carcinoma and showed that atorvastatin significantly increased animal survival and inhibited pancreatic carcinogenesis. There was a dramatic decrease in mutant p53 protein accumulation in the pancreatic acini, pancreas intraepithelial neoplasia lesions, and adenocarcinoma. Supplementation with farnesyl pyrophosphate, a substrate for protein farnesylation, rescued atorvastatin‐induced mutant p53 degradation in pancreatic cancer cells. Tipifarnib, a farnesyltransferase inhibitor, mirrored atorvastatin's effects on mutant p53, degraded mutant p53 in a dose‐dependent manner, and converted farnesylated DNAJA1 into unfarnesylated DNAJA1. Farnesyltransferase gene knockdown also significantly promoted mutant p53 degradation. Coimmunoprecipitation either by an anti‐DNAJA1 or p53 antibody confirmed the direct interaction of mutant p53 and DNAJA1 and higher doses of atorvastatin treatments converted more farnesylated DNAJA1 into unfarnesylated DNAJA1 with much less mutant p53 pulled down by DNAJA1. Strikingly, C394S mutant DNAJA1, in which the cysteine of the CAAX box was mutated to serine, was no longer able to be farnesylated and lost the ability to maintain mutant p53 stabilization. Our results show that farnesylated DNAJA1 is a crucial chaperone in maintaining mutant p53 stabilization and targeting farnesylated DNAJA1 by atorvastatin will be critical for inhibiting p53 mutant cancer.
Clinical implications of sarcomere and nonsarcomere gene variants in patients with left ventricular noncompaction cardiomyopathy
Authors: Li Shijie , Zhang Ce , Liu Nana , Bai Hui , Hou Cuihong , Pu Jielin 
Published: August 2019

AbstractBackgroundRobust data regarding genotype–phenotype correlations in left ventricular noncompaction cardiomyopathy (LVNC) are lacking.MethodsAbout 72 cardiomyopathy‐related genes were comprehensively screened in a cohort of LVNC patients using targeted sequencing. Baseline and follow‐up data were collected. The primary endpoint was a composite of death and heart transplantation.ResultsA total of 83 unrelated adult patients were included in analyses. Following stringent classification according to the American College of Medical Genetics and Genomics (ACMG) guidelines, 36 pathogenic variants of 14 genes were detected in 32 patients. Among them, 12 patients carried at least one nonsarcomere variant (NSV). At baseline, NSV carriers had a higher frequency of atrial fibrillation, but lower left ventricular ejection fraction, than did noncarriers. During a median follow‐up of 4.2 years, NSV carriers experienced a higher rate of the primary endpoint compared with noncarriers. There was no significant difference in the rate between carriers of sarcomere variant (SV) and noncarriers, as well as between carriers of SV and NSV. The presence of NSV was associated with an increased risk of the primary endpoint independent of age, sex, and cardiac function (hazard ratio: 3.61, 95% confidence interval: 1.42–9.19, p = .002).ConclusionNSV may act as a genetic modifier and worsen the clinical phenotype in patients with LVNC.
Novel IFT140 variants cause spermatogenic dysfunction in humans
Authors: Wang Xiong , Sha Yan‐wei , Wang Wen‐ting , Cui Yuan‐qing , Chen Jie , Yan Wei , Hou Xiao‐tao , Mei Li‐bin , Yu Cui‐cui , Wang Jiahui 
Published: August 2019

AbstractBackgroundThe intraflagellar transport protein 140 homolog (IFT140) is involved in the process of intraflagellar transport (IFT), a process that is essential for the formation and maintenance of most eukaryotic cilia and flagella. Variants IFT140 have been reported to account for ciliopathy but association with male fertility has never been described in humans. Here we report the identification of two novel variants of IFT140 which caused spermatogenic dysfunction and male infertility.MethodsWhole‐exome sequencing was performed in a 27‐year‐old infertile man presented with severe oligozoospermia, asthenozoospermia, and teratozoospermia (OAT) without other physical abnormality. Sanger sequencing was used to verify gene variants in the patient, his healthy brother, and their parents. Morphology and protein expression in the patient's sperm were examined by transmission electron microscopy (TEM) and immunofluorescence staining. Function of gene variants was predicted by online databases.ResultsCompound heterozygous variants of IFT140: exon16: c.1837G > A: p.Asp613Asn and exon31: c.4247G > A: p.Ser1416Asn were identified in the patient, both of which showed autosomal recessive inheritance in his family, and had extremely low allele frequency in the population. Morphological abnormalities of the head, nucleus, and tails and the absence of IFT140 from the neck and mid‐piece of the patient's spermatozoa were observed. Mutation Taster database predicted a high probability of damage‐causing by both variations.ConclusionThis study for the first time reported IFT140 variants that cause infertility in humans.
Novel SZT2 mutations in three patients with developmental and epileptic encephalopathies
Authors: Sun Xiaomin , Zhong Xuefei , Li Tingsong 
Published: August 2019

AbstractBackgroundThe seizure threshold 2 (SZT2) gene encodes a large, highly conserved protein that lowers seizure threshold and may also enhance epileptogenesis. In this study, three patients diagnosed with SZT2‐related developmental and epileptic encephalopathies (DEEs) were reviewed aiming to expand knowledge of the genotype and phenotype of SZT2 mutations.MethodsTargeted next‐generation sequencing was performed to identify pathogenic mutations in 205 cases with DEEs of unknown etiology. Detailed clinical and genetic data were collected from SZT2‐associated patients.ResultsFour novel mutations were found (c.1626 + 1G>A, c.5772dupA, c.4209C > A, c.7307_7308insG) in three patients. All the variants were inherited from their parents. Two patients were siblings and harbored the same mutations and presented developmental delay prior to the onset of seizures. All the individuals were diagnosed as DEEs, drug refractory epilepsy, and experienced status epilepticus (SE); one patient died of SE. One subject showed subependymal nodules as similar as those of tuberous sclerosis complex (TSC) in cranial magnetic resonance imaging (MRI).ConclusionOur results expand the genotype and phenotypes of SZT2‐related DEEs, suggesting that SZT2 mutations play a role in developmental delay and epileptic encephalopathy, with high susceptibility to SE and relatively specific MRI findings.
Radiographic patterns of muscle involvement in the idiopathic inflammatory myopathies
Authors: Day Jessica A. , Bajic Nicholas , Gentili Sheridan , Patel Sandy , Limaye Vidya 
Published: August 2019

AbstractIntroductionThis study assesses the burden, distribution, and evolution of muscle inflammation and damage on MRI among subtypes of idiopathic inflammatory myopathy (IIM).MethodsMusculoskeletal MRIs performed in 66 patients with IIM and 10 patients with non‐IIM between 2009 and 2016 were retrospectively graded for muscle edema, fatty replacement (FR), and atrophy.ResultsImmune‐mediated necrotizing myopathy (IMNM) patients had severe and extensive lower limb muscle edema, FR, and atrophy. The pelvic muscles and adductors were significantly more affected than in patients with dermatomyositis and polymyositis. Inclusion body myositis (IBM) was characterized by marked anterior thigh involvement, which stabilized or progressed at follow‐up imaging. Atrophy and FR grades improved over time in some non‐IBM IIM patients.DiscussionPatients with IMNM and IBM have characteristic patterns of muscle MRI abnormalities that may allow them to be differentiated radiologically from other IIM subtypes. Muscle damage in non‐IBM IIM may be reversible.
Real‐world experience using hydroxyurea in children with sickle cell disease in Lilongwe, Malawi
Authors: Mvalo Tisungane , Topazian Hillary M. , Kamthunzi Portia , Chen Jane S. , Kambalame Isobel , Mafunga Pilirani , Mumba Noel , Chiume Msandeni , Paseli Khadija , Tegha Gerald , Kumwenda Wiza , Heimlich J. Brett , Ellis Graham , Key Nigel , Gopal Satish , Hoffman Irving , Ataga Kenneth I. , Westmoreland Kate D. 
Published: August 2019

AbstractIntroductionSickle cell disease (SCD) is among the most common inherited hematologic diseases in sub‐Saharan Africa (SSA). Historically, hydroxyurea administration in SSA has been restricted due to limited region‐specific evidence for safety and efficacy.MethodsWe conducted a prospective observational cohort study of pediatric patients with SCD in Malawi. From January 2015 to November 2017, hydroxyurea at doses of 10–20 mg/kg/day was administered to children with clinically severe disease (targeted use policy). From December 2017 to July 2018, hydroxyurea was prescribed to all patients (universal use policy).ResultsOf 187 patients with SCD, seven (3.7%) died and 23 (12.3%) were lost to follow‐up. The majority (135, 72.2%) were prescribed hydroxyurea, 59 (43.7%) under the targeted use policy and 76 (56.3%) under the universal use policy. There were no documented severe toxicities. Under the targeted use policy, children with SCD demonstrated absolute decreases in the rates of hospitalization (−4.1 per 1000 person‐days; −7.2, −1.0; P = .004), fevers (−4.2 per 1000 person‐days; −7.2, −1.1; P = .002), transfusions (−2.3 per 1000 person‐days; 95% confidence interval: −4.9, 0.3; P = .06), and annual school absenteeism (−51.2 per person‐year; −60.1, −42.3; P < .0001) within 6 months of hydroxyurea commencement.ConclusionWe successfully implemented universal administration of hydroxyurea to children with SCD at a tertiary hospital in Malawi. Similar to recently reported trials, hydroxyurea was safe and effective during routine programmatic experience, with clinical benefits particularly among high‐risk children. This highlights the importance of continued widespread scale‐up of hydroxyurea within SCD programs across SSA.
Treatment patterns of prostate cancer with bone metastasis in Beijing: A real‐world study using data from an administrative claims database
Authors: Cheng Yinchu , Zhuo Lin , Pan Yuting , Wang Shengfeng , Zong Jihong , Sun Wentao , Gao Shuangqing , Lu Jian , Zhan Siyan 
Published: August 2019

AbstractPurposeTo explore treatment patterns among patients with prostate cancer and bone metastasis and to compare clinical outcomes following use of different hormone therapies including combined androgen blockade (CAB), nonsteroidal antiandrogen (NSAA) monotherapy, and castration monotherapy.MethodsWe conducted a population‐based cohort study using data from the Urban Employee Basic Medical Insurance database (2011‐2014) in Beijing. We identified 475 patients with newly diagnosed bone metastatic prostate cancer with at least one prescription for hormone therapy and described their treatment patterns over a median follow‐up of 20.7 months. Cox proportional hazards model was used to compare time to chemotherapy initiation between patients starting on different hormone therapies.ResultsHormone therapy and/or bisphosphonate therapy with zoledronic acid were the initial treatments in the majority of patients (87.8%); chemotherapy, radiotherapy, and surgery were usually given later in the treatment pathway. CAB was the most common hormone treatment (73.7%). For time to chemotherapy initiation, hazard ratios (95% confidence intervals) were 2.43 (1.08‐5.44) for NSAA alone vs CAB and 1.29 (0.78‐2.13) for castration alone vs CAB.ConclusionsOur findings show that while a wide range of therapies are used to treat patients with prostate cancer and bone metastasis in Beijing, hormone therapy and bisphosphonate therapy are the most commonly prescribed, and use of CAB was seen to be advantageous in delaying time to chemotherapy initiation over NSAA monotherapy. Future studies should explore longer‐term treatment patterns, including use of newly approved treatments.