bluuebunny/crossref_metadata_2025_split huggingface dataset:
The association between iodine intake and semen quality among fertile men in China
Authors: Sun Yu , Chen Chen , Liu Gordon G. , Wang Meijiao , Shi Cuige , Yu Ge , Lv Fang , Wang Ning , Zhang Shucheng 
Published: April 2020

Abstract
Background
Iodine intake is essential in the production of thyroid hormone but very few foods are rich in it. Iodine deficiency or excess iodine level may both lead to thyroid disorders, which further affects human fertility function. The objective of this study is to investigate the relationship between iodine intake and seminal parameters among fertile men in China.

Methods
A total of 1098 couples were recruited by trained physicians at different family planning service stations in 2015. Semen and iodine samples were obtained from male respondents. A questionnaire survey inquired about demographic information from couples. The main outcome variables of semen quality were semen volume, semen concentration, semen motility, and sperm count, and time to pregnancy. Urinary iodine concentration (UIC) was used to measure iodine levels for male respondents. Ordinary least squared regressions and logistic regressions were performed to estimate the association between iodine intake level and semen quality parameters.

Results
Male respondents with deficient or excess iodine levels had a 5% higher semen volume relative to those with optimal iodine intake (p < 0.1). Suboptimal iodine intake was negatively associated with semen concentration and semen counts (p < 0.01). Longer time of pregnancy was observed in iodine deficiency and excess group than those in the optimal group (p < 0.01).

Conclusion
In general, iodine deficiency and excess were both associated with decreasing semen quality parameters in male respondents.
The effect of the necrotic area on the biomechanics of the femoral head - a finite element study
Authors: Wen Pengfei , Zhang Yumin , Hao Linjie , Yue Ju’an , Wang Jun , Wang Tao , Song Wei , Guo Wanshou , Ma Tao 
Published: April 2020

AbstractBackgroundFemoral head collapse is the key to the progress of osteonecrosis of the femoral head (ONFH), but the causes of collapse are not completely clear. The better understanding of the progress of femoral head collapse will guide the treatment strategy for ONFH patients. The purpose of this study was to evaluate the biomechanical influence of necrosis area on the collapse of the femoral head by finite element analysis.MethodsCT and MRI data from the hip joint of a healthy volunteer were collected to establish a finite element (FE) model of a normal hip. Subsequently, five categories of osteonecrosis FE models were established by using the normal model and computer software according to China-Japan Friendship Hospital (CJFH) classification for ONFH. The CJFH system includes five types based on the size and location of necrosis lesions in the femoral head (type M, C, L1, L2, and L3) and the stage of ONFH. The collapse indices of each model were analyzed by FE method, including the displacement, peak von Mises stress and stress index of the simulated necrotic area as well as the lateral pillar contact area of the femoral head to acetabular.Results(1) The displacement increments in the simulated necrotic areas of type M, C, L1, L2, and L3 models were 3.75 μm, 8.24 μm, 8.47 μm, 18.42 μm, and 20.44 μm respectively; the peak von Mises stress decrements were 1.50 MPa, 3.74 MPa, 3.73 MPa, 4.91 MPa, and 4.92 MPa respectively; and the stress indices were 0.04, 0.08, 0.08, 0.27, and 0.27 respectively. (2) The displacement increments in the lateral pillar contact areas of five type models were significantly different (P < 0.001) and increased in sequence as follows: 1.93 ± 0.15 μm, 5.74 ± 0.92 μm, 5.84 ± 1.42 μm, 14.50 ± 3.00 μm, and 16.43 ± 3.05 μm. The peak von Mises stress decrements were also significantly different (P < 0.001) and increased in sequence as follows: 0.52 ± 0.30 MPa, 0.55 ± 0.12 MPa, 0.67 ± 0.33 MPa, 4.17 ± 0.59 MPa, and 4.19 ± 0.60 MPa. (3) The collapse indices including the displacement increments and peak von Mises stress decrements of type L2 and L3 models were markedly higher than those of type M, C, and L1 models (P < 0.001).ConclusionsThe collapse indices of the femoral heads of type L2 and L3 FE models were significantly higher than those of type M, C, and L1. Different areas of necrosis result in varied impact on the femoral head collapse.
AKT2 deficiency impairs formation of the BCR signalosome
Authors: Du Zuochen , Yang Di , Zhang Yongjie , Xuan Xingtian , Li Han , Hu Leling , Ruan Changshun , Li Liling , Chen Anwei , Deng Liang , Chen Yan , Xie Jingwen , Westerberg Lisa S. , Huang Lu , Liu Chaohong 
Published: April 2020

Abstract
Background
AKT2 is one of the key molecules that involves in the insulin-induced signaling and the development of cancer. In B cells, the function of AKT2 is unclear.

Methods
In this study, we used AKT2 knockout mice model to study the role of AKT2 in BCR signaling and B cell differentiation.

Results
AKT2 promotes the early activation of B cells by enhancing the BCR signaling and actin remodeling. B cells from AKT2 KO mice exhibited defective spreading and BCR clustering upon stimulation in vitro. Disruption of Btk-mediated signaling caused the impaired differentiation of germinal center B cells, and the serum levels of both sepecific IgM and IgG were decreased in the immunized AKT2 KO mice. In addition, the actin remodeling was affected due to the decreased level of the activation of WASP, the actin polymerization regulator, in AKT2 KO mice as well. As a crucial regulator of both BCR signaling and actin remodeling during early activation of B cells, the phosphorylation of CD19 was decreased in the AKT2 absent B cells, while the transcription level was normal.

Conclusions
AKT2 involves in the humoral responses, and promotes the BCR signaling and actin remodeling to enhance the activation of B cells via regulating CD19 phosphorylation.
Loss of mural cell-derived laminin aggravates hemorrhagic brain injury
Authors: Gautam Jyoti , Xu Lingling , Nirwane Abhijit , Nguyen Benjamin , Yao Yao 
Published: April 2020

AbstractBackgroundMural cells synthesize and deposit laminin to the basement membrane. To investigate the function of mural cell-derived laminin, we generated a mutant mouse line lacking mural cell-derived laminin (termed PKO). In a previous study, we showed that the PKO mice were grossly normal under homeostatic condition, but developed blood-brain barrier (BBB) breakdown with advanced age (> 8 months), suggesting that these mutants are intrinsically weak. Based on these findings, we hypothesized that PKO mice have exacerbated injuries in pathological conditions.MethodsUsing collagenase-induced intracerebral hemorrhage (ICH) as an injury model, we examined various stroke outcomes, including hematoma volume, neurological function, neuronal death, BBB integrity, paracellular/transcellular transport, inflammatory cell infiltration, and brain water content, in PKO mice and their wildtype littermates at young age (6–8 weeks). In addition, transmission electron microscopy (TEM) analysis and an in vitro ICH model were used to investigate the underlying molecular mechanisms.ResultsCompared to age-matched wildtype littermates, PKO mice display aggravated stroke outcomes, including larger hematoma size, worse neurological function, increased neuronal cell death, enhanced BBB permeability, increased transcytosis, and elevated inflammatory cell infiltration. These mutants also exhibit high baseline brain water content independent of aquaporin-4 (AQP4). In addition, mural cell-derived laminin significantly reduced caveolin-1 without affecting tight junction proteins in the in vitro ICH model.ConclusionsThese results suggest that mural cell-derived laminin attenuates BBB damage in ICH via decreasing caveolin-1 and thus transcytosis, regulates brain water homeostasis, and plays a beneficial role in ICH.
Mechanistic insights into pH-dependent H2 photoproduction in bisulfite-treated Chlamydomonas cells
Authors: Wei Lanzhen , Fan Baoqiang , Yi Jing , Xie Tianqun , Liu Kun , Ma Weimin 
Published: April 2020

Abstract
Background
Bisulfite addition is an important H2 photoproduction strategy that removes O2 and activates hydrogenase. The pH values of cell cultures can change the ratio of bisulfite to sulfite, which may affect H2 photoproduction. However, little is known regarding the pH effect of bisulfite addition on H2 photoproduction and relevant underlying mechanism.

Results
Here, changes in H2 photoproduction with different initial extracellular pH values showed a parabolic distribution and a pH of 8.0 is an optimal value for H2 photoproduction in Chlamydomonas reinhardtii cells treated with bisulfite. Compared to the growth pH (pH 7.3), increased photoproduction of H2 at this optimal pH was primarily caused by a relatively high residual activity of photosystem II (PSII), which provides a relatively plentiful source of electrons for H2 photoproduction. Such increased H2 photoproduction was most likely a result of decreased the ratio of bisulfite to sulfite, consistent with the result that the toxicity of bisulfite on PSII was much more than that of sulfite. This possibility was corroborated by the result that treatment with a combination of 7 mM bisulfite and 6 mM sulfite further enhanced H2 photoproduction compared with 13 mM bisulfite alone.

Conclusions
Collectively, our findings provide novel mechanistic insights into pH-dependent H2 photoproduction in C. reinhardtii cells treated with bisulfite, and demonstrate that sulfite addition is another important strategy for H2 photoproduction, just like bisulfite addition.
Characteristic features of the SERA multigene family in the malaria parasite
Authors: Arisue Nobuko , Palacpac Nirianne M. Q. , Tougan Takahiro , Horii Toshihiro 
Published: April 2020

AbstractSerine repeat antigen (SERA) is conserved among species of the genusPlasmodium.Seragenes form a multigene family and are generally tandemly clustered on a single chromosome. Although allPlasmodiumspecies encode multipleseragenes, the number varies between species. Among species, the members share similar sequences and gene organization. SERA possess a central papain-like cysteine protease domain, however, in some members, the active site cysteine residue is substituted with a serine. Recent studies implicate this gene family in a number of aspects in parasite biology and induction of protective immune response. This review summarizes the current understanding on this important gene family in severalPlasmodiumspecies. ThePlasmodium falciparum(Pf)-serafamily, for example, consists of nine gene members. Unlike other multigene families inPlasmodiumspecies,Pf-seragenes do not exhibit antigenic variation.Pf-sera5nucleotide diversity is also low. Moreover, althoughPf-sera5is highly transcribed during the blood stage of malaria infection, and a large amount is released into the host blood following schizont rupture, in malaria endemic countries the sero-positive rates for Pf-SERA5 are low, likely due to Pf-SERA5 binding of host proteins to avoid immune recognition. As an antigen, the N-terminal 47 kDa domain of Pf-SERA5 is a promising vaccine candidate currently undergoing clinical trials. Pf-SERA5 and Pf-SERA6, as well asP. berghei(Pb)-SERA3, and Pb-SERA5, have been investigated for their roles in parasite egress. TwoP. yoeliiSERA, which have a serine residue at the protease active center, are implicated in parasite virulence. Overall, these studies provide insight that during the evolution of thePlasmodiumparasite, theseragene family members have increased by gene duplication, and acquired various functions that enable the parasite to survive and successfully maintain infection in the host.
Hypoxic preconditioning of human urine-derived stem cell-laden small intestinal submucosa enhances wound healing potential
Authors: Zhang Xiu-Ru , Huang Yi-Zhou , Gao Hong-Wei , Jiang Yan-Lin , Hu Jun-Gen , Pi Jin-Kui , Chen An-Jing , Zhang Yi , Zhou Li , Xie Hui-Qi 
Published: April 2020

AbstractBackgroundUrine-derived stem cells (USCs) are a valuable stem cell source for tissue engineering because they can be harvested non-invasively. Small intestine submucosa (SIS) has been used as scaffolds for soft tissue repair in the clinic. However, the feasibility and efficacy of a combination of USCs and SIS for skin wound healing has not been reported. In this study, we created a tissue-engineered skin graft, termed the SIS+USC composite, and hypothesized that hypoxic preconditioning would improve its wound healing potential.MethodsUSCs were seeded on SIS membranes to fabricate the SIS+USC composites, which were then cultured in normoxia (21% O2) or preconditioned in hypoxia (1% O2) for 24 h, respectively. The viability and morphology of USCs, the expression of genes related to wound angiogenesis and reepithelialization, and the secretion of growth factors were determined in vitro. The wound healing ability of the SIS+USC composites was evaluated in a mouse full-thickness skin wound model.ResultsUSCs showed good cell viability and morphology in both normoxia and hypoxic preconditioning groups. In vitro, hypoxic preconditioning enhanced not only the expression of genes related to wound angiogenesis (VEGFandAng-2) and reepithelialization (bFGFandEGF) but also the secretion of growth factors (VEGF, EGF, and bFGF). In vivo, hypoxic preconditioning significantly improved the wound healing potential of the SIS+USC composites. It enhanced wound angiogenesis at the early stage of wound healing, promoted reepithelialization, and improved the deposition and remodeling of collagen fibers at the late stage of wound healing.ConclusionsTaken together, this study shows that hypoxic preconditioning provides an easy and efficient strategy to enhance the wound healing potential of the SIS+USC composite.
Pregnancy-associated cardiac dysfunction and the regulatory role of microRNAs
Authors: Aryan Laila , Medzikovic Lejla , Umar Soban , Eghbali Mansoureh 
Published: April 2020

AbstractMany crucial cardiovascular adaptations occur in the body during pregnancy to ensure successful gestation. Maladaptation of the cardiovascular system during pregnancy can lead to complications that promote cardiac dysfunction and may lead to heart failure (HF). About 12% of pregnancy-related deaths in the USA have been attributed to HF and the detrimental effects of cardiovascular complications on the heart can be long-lasting, pre-disposing the mother to HF later in life. Indeed, cardiovascular complications such as gestational diabetes mellitus, preeclampsia, gestational hypertension, and peripartum cardiomyopathy have been shown to induce cardiac metabolic dysfunction, oxidative stress, fibrosis, apoptosis, and diastolic and systolic dysfunction in the hearts of pregnant women, all of which are hallmarks of HF. The exact etiology and cardiac pathophysiology of pregnancy-related complications is not yet fully deciphered. Furthermore, diagnosis of cardiac dysfunction in pregnancy is often made only after clinical symptoms are already present, thus necessitating the need for novel diagnostic and prognostic biomarkers. Mounting data demonstrates an altered expression of maternal circulating miRNAs during pregnancy affected by cardiovascular complications. Throughout the past decade, miRNAs have become of growing interest as modulators and biomarkers of pathophysiology, diagnosis, and prognosis in cardiac dysfunction. While the association between pregnancy-related cardiovascular complications and cardiac dysfunction or HF is becoming increasingly evident, the roles of miRNA-mediated regulation herein remain poorly understood. Therefore, this review will summarize current reports on pregnancy-related cardiovascular complications that may lead to cardiac dysfunction and HF during and after pregnancy in previously healthy women, with a focus on the pathophysiological role of miRNAs.
Nonalcoholic fatty liver disease experiences accumulation of hepatic liquid crystal associated with increasing lipophagy
Authors: Wang Liyang , Xu MengMeng , Jones Odell D. , Li Zhongguang , Liang Yu , Yu Qiuxia , Li Jiali , Wu Yajun , Lei Xinjuan , He Boling , Yue Huimin , Xiao Liqin , Zhou Rong , Zhang Wei , Zhou Xin , Zhang Yuhui , Bryant Joseph L. , Ma Jianjie , Liu Yingli , Xu Xuehong 
Published: April 2020

Abstract
Background
In the past 30 years, incidences of non-alcoholic fatty liver disease (NAFLD) has risen by 30%. However, there is still no clear mechanism or accurate method of anticipating liver failure. Here we reveal the phase transitions of liquid crystalline qualities in hepatic lipid droplets (HLDs) as a novel method of anticipating prognosis.

Methods
NAFLD was induced by feeding C57BL/6J mice on a high-fat (HiF) diet. These NAFLD livers were then evaluated under polarized microscopy, X-ray diffraction and small-angle scattering, lipid component chromatography analysis and protein expression analysis. Optically active HLDs from mouse model and patient samples were both then confirmed to have liquid crystal characteristics. Liver MAP1LC3A expression was then evaluated to determine the role of autophagy in liquid crystal HLD (LC-HLD) formation.

Results
Unlike the normal diet cohort, HiF diet mice developed NAFLD livers containing HLDs exhibiting Maltese cross birefringence, phase transition, and fluidity signature to liquid crystals. These LC-HLDs transitioned to anisotropic crystal at 0 °C and remain crystalline. Temperature increase to 42 °C causes both liquid crystal and crystal HLDs to convert to isotropic droplet form. These isotropic HLDs successfully transition to anisotropic LC with fast temperature decrease and anisotropic crystal with slow temperature decrease. These findings were duplicated in patient liver. Patient LC-HLDs with no inner optical activity were discovered, hinting at lipid saturation as the mechanism through which HLD acquire LC characteristics. Downregulation of MAP1LC3A in conjunction with increased LC-HLD also implicated autophagy in NAFLD LC-HLD formation.

Conclusions
Increasing concentrations of amphiphilic lipids in HLDs favors organization into alternating hydrophilic and hydrophobic layers, which present as LC-HLDs. Thus, evaluating the extent of liquid crystallization with phase transition in HLDs of NAFLD patients may reveal disease severity and predict impending liver damage.
Alternative donor peripheral blood stem cell transplantation for the treatment of high-risk refractory and/or relapsed childhood acute leukemia: a randomized trial
Authors: Zhang Binglei , Zhou Jian , Yu Fengkuan , Lv Tianxin , Fang Baijun , Fan Dandan , Ji Zhenyu , Song Yongping 
Published: April 2020

AbstractBackgroundThe high-risk refractory and/or relapsed (R/R) childhood acute leukemia prognosis is poor, and allogeneic stem cell transplantation (allo-HSCT) is the most prudent treatment modality. However, there are limited matched sibling donors (MSDs), and alternative donors (ADs) are the main source for allo-HSCT. Thus, we evaluated the clinical efficacy of AD peripheral allo-HSCT for treating high-risk R/R childhood acute leukemia.MethodsWe assessed 111 children who underwent allo-HSCT at the Affiliated Cancer Hospital of Zhengzhou University between October 2006 and July 2019. The patients were divided in the MSD and AD groups, and their clinical characteristics, complications, and survival rates were compared.ResultsThe cumulative incidences of Epstein–Barr virus and cytomegalovirus infections were significantly higher in the AD than in the MSD group (P < 0.001); however, the recurrence and mortality rates were significantly higher in the MSD than in the AD group (P < 0.05). Furthermore, the 5-year disease-free (DFS) (65.2% vs. 43.3%,P = 0.033) and overall survival (OS) rates (71.6% vs. 53.8%,P = 0.053) were significantly higher in the AD than in the MSD group. In the AD group, the grade II–IV acute graft-versus-host disease (aGVHD), donor-recipient ABO compatibility, conditioning regimen, and CMV infection affected the 5-year OS. The grade II–IV aGVHD also affected the 5-year DFS; however, only the donor-recipient ABO compatibility affected the 5-year DFS. The donor MSD (HR: 2.035, 95% confidence interval [CI] 1.057–3.920,P = 0.034) and the grade II–IV aGVHD (HR: 2.914, 95% CI 1.261–6.736,P = 0.012) affected the 5-year DFS of childhood acute leukemia after allo-HSCT, and the grade II–IV aGVHD (HR: 3.016, 95% CI 1.217–7.473,P = 0.017) affected the 5-year OS. Moreover, the donor source (HR: 2.836, 95% CI 1.179–6.823,P = 0.020) and grade II–IV aGVHD (HR: 3.731, 95% CI 1.332–10.454,P = 0.012) were independent predictors of the 5-year DFS, while the latter (HR: 3.524, 95% CI 1.310–10.988,P = 0.030) was an independent predictor of the 5-year OS.ConclusionsAD-PBSCT was effective for high-risk R/R childhood leukemia and may have better clinical outcomes than MSD-PBSCT; thus, it can be used as first-line treatment for high-risk R/R childhood leukemia.
Characterization and functional analysis of SIAH1 during skin and hair follicle development in the angora rabbit (Oryctolagus cuniculus)
Authors: Zhou Tong , Chen Yang , Zhao Bohao , Hu Shuaishuai , Li Jiali , Liu Ming , Liang Shuang , Bao Zhiyuan , Wu Xinsheng 
Published: April 2020

AbstractBackgroundSeven in absentia homolog 1 (SIAH1) is an E3 ubiquitin ligase containing a RING-finger domain and a key regulator of normal development. Skin and hair follicle development is a complex and special process of morphogenesis involving multiple signaling pathways.SIAH1is enriched in the Wnt signaling pathway and potentially related to hair follicle cycle and skin development. This study aims to provide evidence for the role ofSIAH1in skin and hair development.ResultsFull-length cloning and analysis ofSIAH1was conducted to better understand its function. Phylogenetically, the sequence of SIAH1 in the rabbit shares the greatest homology withHome sapiens,Pongo abeliiandMus mulatta.Based on the rabbit hair follicle synchronization model, we found that the expression level ofSIAH1in the regressive period of the rabbit hair cycle is significantly lower than in the active growth and rest periods. In addition, the mRNA expression levels of skin and hair follicle development-related genes changed significantly whenSIAH1was overexpressed and silenced. AfterSIAH1overexpression, the expression levels ofWNT2,LEF1andFGF2decreased, and those ofSFRP2andDKK1increased (P < 0.05). After interference ofSIAH1, the expression levels ofWNT2,LEF1andFGF2increased (P < 0.05), andSFRP2andDKK1decreased.ConclusionsSIAH1can affect skin and hair follicle development and exert an inhibitory effect. These results could provide foundamental insights into the role ofSIAH1as a target gene in rabbit skin and hair follicle development.