bluuebunny/crossref_metadata_2025_split huggingface dataset:
TFAP2B overexpression contributes to tumor growth and progression of thyroid cancer through the COX-2 signaling pathway
Authors: Fu Xiaoyan , Zhang Huayong , Chen Zhipeng , Yang Zhongyuan , Shi Dingbo , Liu Tianrun , Chen Weichao , Yao Fan , Su Xuan , Deng Wuguo , Chen Miao , Yang Ankui 
Published: May 2019

AbstractThyroid cancer is commonly seen in the clinic with a rapidly increasing incidence globally. COX-2 overexpression correlates with the pathologic type of thyroid carcinoma, and it has been suggested that COX-2 overexpression is associated with a poor prognosis. However, little is known about its upstream regulatory mechanism. Bioinformatics suggested that transcription factor AP-2 beta (TFAP2B) might specifically bind to the COX-2 promoter, which was confirmed by biotin-labeled COX-2 promoter pulldown and luciferase reporter assays. We performed western blot and immunohistochemical staining to detect the expression of TFAP2B/COX-2 in thyroid cancer tissues (T) and the matched adjacent noncarcinoma tissues (ANT), and investigated the relationship between TFAP2B/COX-2 expression and clinical pathological factors in thyroid cancer patients. Afterward, MTS, colony formation, cell-apoptosis assay, transwell-invasion and scratch assays were performed to examine the proliferation, apoptosis, invasion, and migration of thyroid cancer cells with TFAP2B knocked down or overexpressed. The mouse xenograft experiment was performed to study in vivo the proliferation of thyroid cancer cells with TFAP2B knocked down or overexpressed. We found that TFAP2B bound to the promoter of COX-2 to activate its expression. Western blot and immunohistochemistry showed that TFAP2B/COX-2 was highly expressed in thyroid cancer, and high TFAP2B and COX-2 expression was associated with aggressive clinicopathological features in thyroid cancer. TFAP2B mediated thyroid cancer cell proliferation, apoptosis, invasion, and migration via the COX-2 signaling pathway in vitro and in vivo. TFAP2B bound to the promoter of COX-2 to activate its expression, indicating that TFAP2B is a critical regulatory molecule in the COX-2 signaling pathway that promoted tumor progression in thyroid cancer.
Strategies by which WWOX-deficient metastatic cancer cells utilize to survive via dodging, compromising, and causing damage to WWOX-positive normal microenvironment
Authors: Chou Pei-Yi , Lai Feng-Jie , Chen Yu-An , Sie Yong-Da , Kuo Hsiang-Ling , Su Wan-Pei , Wu Chia-Yun , Liu Tsung-Yun , Wen Kuang-Yu , Hsu Li-Jin , Sze Chun-I , Chang Nan-Shan 
Published: May 2019

AbstractProapoptotic tumor suppressor WWOX is upregulated in the early stage of cancer initiation, which probably provides limitation to cancer growth and progression. Later, WWOX protein is reduced to enhance cancer cell growth, migration, invasiveness and metastasis. To understand how WWOX works in controlling cancer progression, here we demonstrate that apoptotic stress mediated by ectopic WWOX stimulated cancer cells to secrete basic fibroblast growth factor (bFGF) in order to support capillary microtubule formation. This event may occur in the cancer initiation stage. Later, when WWOX loss occurs in cancer cells, hyaluronidase production is then increased in the cancer cells to facilitate metastasis. We determined that inhibition of membrane hyaluronidase Tyr216-phosphorylated Hyal-2 by antibody suppresses cancer growth in vivo. WWOX-negative (WWOX-) cells dodged WWOX+cells in the microenvironment by migrating individually backward to avoid physical contacts and yet significantly upregulating the redox activity of WWOX+parental cells or other WWOX+cell types for causing apoptosis. Upon detecting the presence of WWOX+cells from a distance, WWOX- cells exhibit activation of MIF, Hyal-2, Eph, and Wnt pathways, which converges to MEK/ERK signaling and enables WWOX- cells to evade WWOX+cells. Inhibition of each pathway by antibody or specific chemicals enables WWOX- cells to merge with WWOX+cells. In addition, exogenous TGF-β assists WWOX- cells to migrate collectively forward and merge with WWOX+cells. Metastatic WWOX- cancer cells frequently secrete high levels of TGF-β, which conceivably assists them to merge with WWOX+cells in target organs and secure a new home base in the WWOX+microenvironment. Together, loss of WWOX allows cancer cells to develop strategies to dodge, compromise and even kill WWOX-positive cells in microenvironment.
Experimental limit on an exotic parity-odd spin- and velocity-dependent interaction using an optically polarized vapor
Authors: Kim Young Jin , Chu Ping-Han , Savukov Igor , Newman Shaun 
Published: May 2019

AbstractExotic spin-dependent interactions between fermions have recently attracted attention in relation to theories beyond the Standard Model. The exotic interactions can be mediated by hypothetical fundamental bosons which may explain several unsolved mysteries in physics. Here we expand this area of research by probing an exotic parity-odd spin- and velocity-dependent interaction between the axial-vector electron coupling and the vector nucleon coupling for polarized electrons. This experiment utilizes a high-sensitivity atomic magnetometer, based on an optically polarized vapor that is a source of polarized electrons, and a solid-state mass containing unpolarized nucleons. The atomic magnetometer can detect an effective magnetic field induced by the exotic interaction between unpolarized nucleons and polarized electrons. We set an experimental limit on the electron-nucleon coupling $$g_{\mathrm{A}}^{\mathrm{e}}g_{\mathrm{V}}^{\mathrm{N}} \, < \, 10^{ - 30}$$

g

A

e

g

V

N

<

1

0

-
30

at the mediator boson mass below 10−4 eV, significantly improving the current limit by up to 17 orders of magnitude.
Tissue-specific alteration of gene expression and function by RU486 and the GeneSwitch system
Authors: Robles-Murguia Maricela , Hunt Liam C. , Finkelstein David , Fan Yiping , Demontis Fabio 
Published: May 2019

AbstractThe GeneSwitch (GS) is a modified Gal4/UAS system, whereby transgene expression is induced in Drosophila by adding the drug RU486 to food. The GS system is routinely used in Drosophila aging and behavioral studies to avoid confounding effects related to genetic background mutations. Here, we report transcriptional and functional defects that are induced by RU486 in a stock- and tissue-dependent manner, such as defects in flight and mitochondrial gene expression. In addition to including proper controls, our findings suggest that context-specific side effects induced by RU486 should be considered in the experimental design and when interpreting the observed phenotypes.
Role of Bcl2-associated Athanogene 3 in Turnover of Gap Junction Protein, Connexin 43, in Neonatal Cardiomyocytes
Authors: Ghasemi Tahrir Farzaneh , Gupta Manish , Myers Valerie , Gordon Jennifer , Cheung Joseph Y. , Feldman Arthur M. , Khalili Kamel 
Published: May 2019

AbstractAny pathological stress that impairs expression, turnover and phosphorylation of connexin 43 (Cx43), one of the major proteins of gap junctions, can adversely impact myocardial cell behavior, thus leading to the development of cardiac arrhythmias and heart failure. Our results in primary neonatal rat ventricular cardiomyocytes (NRVCs) show that impairment of the autophagy-lysosome pathway dysregulates degradation of Cx43, either by inhibiting lysosomal activity or suppressing the level of Bcl2-associated athanogene 3 (BAG3), a stress-induced pleiotropic protein that is involved in protein quality control (PQC) via the autophagy pathway. Inhibition of lysosomal activity leads to the accumulation of Cx43 aggregates and suppression of BAG3 significantly diminished turnover of Cx43. In addition, knock-down of BAG3 reduced the levels of Cx43 by dysregulating Cx43 protein stability. Under stress conditions, expression of BAG3 affected the state of Cx43 phosphorylation and its degradation. Furthermore, we found that BAG3 co-localized with the cytoskeleton protein, α-Tubulin, and depolymerization of α-Tubulin led to the intracellular accumulation of Cx43. These observations ascribe a novel function for BAG3 that involves control of Cx43 turnover under normal and stress conditions and potentially for optimizing communication of cardiac muscle cells through gap junctions.
The role of cysteine and sulfide in the interplay between microbial Hg(ii) uptake and sulfur metabolism
Authors: Thomas Sara A , Catty Patrice , Hazemann Jean-Louis , Michaud-Soret Isabelle , Gaillard Jean-François 
Published: May 2019

AbstractBiogenic thiols, such as cysteine, have been used to control the speciation of Hg(ii) in bacterial exposure experiments. However, the extracellular biodegradation of excess cysteine leads to the formation of Hg(ii)–sulfide species, convoluting the interpretation of Hg(ii) uptake results. Herein, we test the hypothesis that Hg(ii)–sulfide species formation is a critical step during bacterial Hg(ii) uptake in the presence of excess cysteine. An Escherichia coli (E. coli) wild-type and mutant strain lacking the decR gene that regulates cysteine degradation to sulfide were exposed to 50 and 500 nM Hg with 0 to 2 mM cysteine. The decR mutant released ∼4 times less sulfide from cysteine degradation compared to the wild-type for all tested cysteine concentrations during a 3 hour exposure period. We show with thermodynamic calculations that the predicted concentration of Hg(ii)–cysteine species remaining in the exposure medium (as opposed to forming HgS(s)) is a good proxy for the measured concentration of dissolved Hg(ii) (i.e., not cell-bound). Likewise, the measured cell-bound Hg(ii) correlates with thermodynamic calculations for HgS(s) formation in the presence of cysteine. High resolution X-ray absorption near edge structure (HR-XANES) spectra confirm the existence of cell-associated HgS(s) at 500 nM total Hg and suggest the formation of Hg–S clusters at 50 nM total Hg. Our results indicate that a speciation change to Hg(ii)–sulfide controls Hg(ii) cell-association in the presence of excess cysteine.
As a downstream target of the AKT pathway, NPTX1 inhibits proliferation and promotes apoptosis in hepatocellular carcinoma
Authors: Zhao Yue , Yu Yaqi , Zhao Wenxiu , You Song , Feng Min , Xie Chengrong , Chi Xiaoqin , Zhang Yi , Wang Xiaomin 
Published: May 2019

Abstract
Hepatocellular carcinoma (HCC) is correlated with a poor prognosis and high mortality worldwide. Neuronal pentraxin 1 (NPTX1) has been reported to play an oncogenic role in several types of tumors. However, its expression and function in HCC is not yet fully understood. In the present study, we aimed to investigate the clinicopathological significance of NPTX1 in HCC and the underlying mechanisms. We observed that the expression of NPTX1 was decreased significantly in HCC and was associated with tumor size and metastasis in patients. Gain-of-function approaches revealed that NPTX1 suppressed the growth ability of HCC cells and contributed to mitochondria- related apoptosis. Furthermore, mechanistic investigations showed that the AKT (AKT serine/threonine kinase) pathway can regulate the effects of NPTX1 in HCC cells. After blocking the AKT pathway, the action of NPTX1 was greatly increased. In summary, we demonstrated that NPTX1 inhibited growth and promoted apoptosis in HCC via an AKT-mediated signaling mechanism. These findings indicate that NPTX1 is a potential clinical therapeutic target.
The association of genetic variants in FGFR2 with osteoporosis susceptibility in Chinese Han population
Authors: Yang Yang , Fei Mengxue , Zhou Xinying , Li Yuejun , Jin Dadi 
Published: May 2019

Abstract
Objective: The present study was conducted for exploring the influence of fibroblast growth factor 2 receptor (FGFR2) gene polymorphisms on osteoporosis occurrence risk in the Chinese population.
Methods: Polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP) was conducted for the genotyping of polymorphism in 145 osteoporosis patients and 123 controls. The status of Hardy–Weinberg equilibrium was detected in the control group. Genotype and allele frequency comparison of polymorphism between the two groups was performed by χ2 test, odds ratio (OR) with 95% confidence interval (95% CI) was used for the result expression about the association of FGFR2 polymorphisms with osteoporosis. Furthermore, the results were adjusted by clinical features via logistic regression analysis.
Results: AA genotype and A allele of rs2420946 were significantly associated with the increased risk of osteoporosis development adjusted by clinical features (OR = 2.238, 95% CI = 1.055–4.746; OR = 1.482, 95% CI = 1.042–2.019). Similarly, CC genotype and C allele frequencies of rs1219648 were detected the significant difference between the case and control groups (P&lt;0.01); moreover, it was still significant by the adjustion of clinical features, which indicated that rs1219648 was significantly associated with the risk of osteoporosis occurrence (OR = 2.900, 95% CI = 1.341–6.271; OR = 1.602, 95% CI = 1.126–2.279). Haplotype T-A-C-T also obviously increased the occurrence risk of osteoporosis (OR = 1.844, 95% CI = 1.180–2.884). Besides, the significant interaction of FGFR2 polymorphisms with drinking status in osteoporosis was also found (P&lt;0.05), especially rs2981579.
Conclusion: FGFR2 rs2420946 and rs1219648 polymorphisms may be the risk factor of osteoporosis in Chinese population. Furthermore, the interaction of FGFR2 polymorphisms with drinking may play an important role in osteoporosis etiology.
LncRNA PACER is down-regulated in osteoarthritis and regulates chondrocyte apoptosis and lncRNA HOTAIR expression
Authors: Jiang Mingwei , Liu Jie , Luo Tao , Chen Qiu , Lu Ming , Meng Deqiang 
Published: May 2019

Abstract
LncRNA PACER is a chondrocyte inflammation-associated long non-coding RNA (lncRNA), and chondrocyte inflammation is involved in osteoarthritis (OA). We observed that plasma PACER was down-regulated, while plasma HOTAIR was up-regulated in OA patients. Altered plasma levels of PACER and HOTAIR distinguished OA patients from healthy controls. PACER and HOTAIR were inversely correlated in both OA patients and healthy controls. PACER overexpression mediated the down-regulation of HOTAIR, while HOTAIR overexpression did not significantly affect PACER. PACER overexpression led to inhibited, while HOTAIR overexpression led to promoted apoptosis of chondrocyte. HOTAIR overexpression attenuated the effects of PACER overexpression. Therefore, lncRNA PACER is down-regulated in OA and regulates chondrocyte apoptosis by down-regulating lncRNA HOTAIR.
Associations of leptin and leptin receptor genetic variants with coronary artery disease: a meta-analysis
Authors: Xiao Peilin , Shi Jianli , Liu Xiaoli 
Published: May 2019

Abstract
Background: Some pilot studies already tried to investigate potential associations of leptin (LEP) and LEP receptor (LEPR) variants with coronary artery disease (CAD). However, the results of these studies were not consistent. Thus, we performed the present meta-analysis to explore associations between LEP/LEPR variants and CAD in a larger pooled population.
Methods: Systematic literature research of PubMed, Web of Science, Embase and CNKI was performed to identify eligible case–control studies on associations between LEP/LEPR variants and CAD. The initial search was conducted in September 2018 and the latest update was performed in December 2018. Q test and I2 statistic were employed to assess between-study heterogeneities. If probability value(P-value) of Q test was less than 0.1 or I2 was greater than 50%, random-effect models (REMs) would be used to pool the data. Otherwise, fixed-effect models (FEMs) would be applied for synthetic analyses.
Results: A total of ten studies published between 2006 and 2018 were eligible for analyses (1989 cases and 2601 controls). Pooled analyses suggested that LEP rs7799039 variant was significantly associated with CAD under over-dominant model (P=0.0007, odds ratio (OR) = 1.36, 95% confidence interval (CI): 1.14–1.63, I2 = 41%, FEM) in overall population, and this significant finding was further confirmed in East Asians in subsequent subgroup analyses. However, no positive findings were observed for LEPR rs1137100 and rs1137101 variants in overall and subgroup analyses.
Conclusions: Our meta-analysis suggested that LEP rs7799039 variant might affect individual susceptibility to CAD.
Longitudinal Growth in Single Word Intelligibility Among Children With Cerebral Palsy From 24 to 96 Months of Age: Predicting Later Outcomes From Early Speech Production
Authors: Hustad Katherine C. , Sakash Ashley , Natzke Phoebe E. M. , Broman Aimee Teo , Rathouz Paul J. 
Published: May 2019

Purpose
Children with cerebral palsy (CP) are at risk for significant communication problems. Reduced speech intelligibility is common, even for those who do not have speech motor deficits. Development of intelligibility has not been comprehensively quantified in children with CP; as a result, we are currently unable to predict later speech outcomes. Such information would advance treatment decision making. We sought to examine growth in speech intelligibility among children with CP using a prospective longitudinal design, with a focus on age of crossing target intelligibility thresholds, age of greatest intelligibility growth, and how well intelligibility at 36 months predicted intelligibility at 96 months.

Method

Sixty-nine children with CP were followed longitudinally between 24 and 96 months of age. A total of 566 time points were examined across children (
M
= 8.2 time points per child,
SD
= 2.6). We fitted a nonlinear random effects model for longitudinal observations and then used the fitted model trajectories to generate descriptive analyses of growth. We used results of the model to generate a set of simulations, which we analyzed to determine how well 36-month intelligibility data predicted 96-month data.

Results
Half of children crossed 25% and 50% intelligibility thresholds at 36 and 49 months of age, respectively. Slightly more than half of children did not reach 75% intelligibility by 96 months of age. Age of crossing 25%, 50%, and 75% intelligibility thresholds was highly negatively correlated with intelligibly at 96 months. Children had the steepest intelligibility growth at 36 months, followed by 48 and 60 months. Intelligibility at 36 months was highly predictive of intelligibility at 96 months.

Conclusions
The developmental window from 3 to 5 years constitutes a time of rapid growth in speech intelligibility in children with CP. Children who cross intelligibility thresholds of 25%, 50%, and 75% at earlier ages have better outcomes when they are older; early performance is highly predictive of later speech intelligibility outcomes. Children with CP as a group have delayed speech intelligibility development but are still growing through 96 months of age.
Effects of a Family Literacy Program for Latino Parents: Evidence From a Single-Subject Design
Authors: Mesa Carol , Restrepo M. Adelaida 
Published: May 2019

Purpose

This study investigated the effects of a family literacy program on Latino parents' language practices at home and their children's oral language skills. The study examined the extent to which (a) the program called
Family Reading Intervention for Language and Literacy in Spanish
was effective at teaching low-income, low-education Latino parents 3 language strategies (i.e., comments, high-level questions, and recasts) for reading aloud and (b) parent implementation of the target strategies influenced children's language skills.

Method
Five Latino mothers and their Spanish-speaking preschool children participated in a multiple-baseline, single-subject design across participants. Program initiation was staggered across the mothers after obtaining a stable baseline. Data on parent and child outcomes were collected across 3 experimental conditions: baseline, intervention, and follow-up. This study employed visual data analysis (e.g., level, trend, variability) to examine the program effects on parent and child outcomes.

Results
The program had an important effect on parental use of comments and high-level questions, but less impact on recasts. In addition, the program had a notable effect on the children's use of different words and conversational turns, less effect on inferences, and no effect on the mean length of utterance in words.

Conclusion
Family Reading Intervention for Language and Literacy in Spanish is an effective program to extend and enrich the reading practices that low-income children from a culturally and linguistically diverse background experience at home. The results have implications for family literacy programs aimed at minority Spanish-speaking families.
Outcomes of Self-Esophageal Dilation for Head and Neck Cancer Patients
Authors: Sinha Uttam K. , Swanson Mark S. , Villegas Brenda Capobres , Ouyoung Laishyang Melody , Kokot Niels 
Published: May 2019

Introduction
Dysphagia is common following treatment for head and neck cancers, and self-esophageal dilation is a safe and effective treatment method. Prior studies on self-dilation have reported only qualitative results and included heterogeneous populations with dysphagia. The objective of this study is to quantitatively assess the safety and efficacy of a self-esophageal dilation program for patients with oropharyngeal squamous cell cancer with treatment-induced dysphagia.

Materials and Methods

This is a retrospective review of patients with oropharyngeal squamous cell cancer treated at the University of Southern California from 2009 to 2013 with dysphagia following radiation treatment that persisted after swallow therapy. The treatment program consisted of swallow therapy in conjunction with weekly self-esophageal dilation at home with increasing size bougie dilators. Oral intake was monitored using the Functional Oral Intake Scale (
Crary, Mann, & Groher, 2005
), Modified Barium Swallow Impairment Profile Pharyngoesophageal opening score, and Penetration–Aspiration Scale (
Rosenbek, Robbins, Roecker, Coyle, & Wood, 1996
) pre- and posttreatment.

Results

Thirty-three patients met study criteria and completed the program. Twenty-five patients required nutrition via a gastrostomy tube prior to starting therapy, and 84% (21/25) of these patients were able to have the feeding tube removed. Median Functional Oral Intake Scale (
Crary et al., 2005
) predilation was 1 (range: 1–5), and postdilation was 6 (range: 3–6,
p
< .05). In addition, there was improvement of the Modified Barium Swallow Impairment Profile Pharyngoesophageal opening score from 2 to 1 after treatment (
p
< .05). No complications were encountered.

Discussion
Home self-dilation with concurrent swallowing therapy is a safe and feasible procedure to be used in motivated patients with dysphagia following head and neck cancer treatment.
Much Ado About Fried Chicken: Abetting Aspiration or Respecting Autonomy?
Authors: Chin Laurence Tan Lean , Lim Yu Jun , Choo Wan Ling 
Published: May 2019

PurposePalliative care is a philosophy of care that encompasses holistic, patient-centric care involving patients and their family members and loved ones. Palliative care patients often have complex needs. A common challenge in managing patients near their end of life is the complexity of navigating clinical decisions and finding achievable and realistic goals of care that are in line with the values and wishes of patients. This often results in differing opinions and conflicts within the multidisciplinary team.ConclusionThis article describes a tool derived from the biopsychosocial model and the 4-quadrant ethical model. The authors describe the use of this tool in managing a patient who wishes to have fried chicken despite aspiration risk and how this tool was used to encourage discussions and reduce conflict and distress within the multidisciplinary team.