Zero-shot stance detection based on cross-domain feature enhancement by contrastive learning

Zero-shot stance detection is challenging because it requires detecting the stance of previously unseen targets in the inference phase. The ability to learn transferable target-invariant features is critical for zero-shot stance detection. In this work, we propose a stance detection approach that can efficiently adapt to unseen targets, the core of which is to capture target-invariant syntactic expression patterns as transferable knowledge. Specifically, we first augment the data by masking the topic words of sentences, and then feed the augmented data to an unsupervised contrastive learning module to capture transferable features. Then, to fit a specific target, we encode the raw texts as target-specific features. Finally, we adopt an attention mechanism, which combines syntactic expression patterns with target-specific features to obtain enhanced features for predicting previously unseen targets. Experiments demonstrate that our model outperforms competitive baselines on four benchmark datasets

Fusion of EML4 and ALK is associated with development of lung adenocarcinomas lacking EGFR and KRAS mutations and is correlated with ALK expression

<p>Abstract</p> <p>Background</p> <p>The anaplastic lymphoma kinase (<it>ALK</it>) gene is frequently involved in translocations that lead to gene fusions in a variety of human malignancies, including lymphoma and lung cancer. Fusion partners of <it>ALK </it>include <it>NPM</it>, <it>EML4</it>, <it>TPM3</it>, <it>ATIC</it>, <it>TFG</it>, <it>CARS</it>, and <it>CLTC</it>. Characterization of ALK fusion patterns and their resulting clinicopathological profiles could be of great benefit in better understanding the biology of lung cancer.</p> <p>Results</p> <p>RACE-coupled PCR sequencing was used to assess <it>ALK </it>fusions in a cohort of 103 non-small cell lung carcinoma (NSCLC) patients. Within this cohort, the <it>EML4</it>-<it>ALK </it>fusion gene was identified in 12 tumors (11.6%). Further analysis revealed that <it>EML4</it>-<it>ALK </it>was present at a frequency of 16.13% (10/62) in patients with adenocarcinomas, 19.23% (10/52) in never-smokers, and 42.80% (9/21) in patients with adenocarcinomas lacking <it>EGFR </it>and <it>KRAS </it>mutations. The <it>EML4</it>-<it>ALK </it>fusion was associated with non-smokers (<it>P </it>= 0.03), younger age of onset (<it>P </it>= 0.03), and adenocarcinomas without <it>EGFR</it>/<it>KRAS </it>mutations (<it>P </it>= 0.04). A trend towards improved survival was observed for patients with the <it>EML4</it>-<it>ALK </it>fusion, although it was not statistically significant (<it>P </it>= 0.20). Concurrent deletion in <it>EGFR </it>exon 19 and fusion of <it>EML4</it>-<it>ALK </it>was identified for the first time in a Chinese female patient with an adenocarcinoma. Analysis of ALK expression revealed that ALK mRNA levels were higher in tumors positive for the <it>EML</it>-<it>ALK </it>fusion than in negative tumors (normalized intensity of 21.99 vs. 0.45, respectively; <it>P </it>= 0.0018). However, expression of EML4 did not differ between the groups.</p> <p>Conclusions</p> <p>The <it>EML4</it>-<it>ALK </it>fusion gene was present at a high frequency in Chinese NSCLC patients, particularly in those with adenocarcinomas lacking <it>EGFR</it>/<it>KRAS </it>mutations. The <it>EML4</it>-<it>ALK </it>fusion appears to be tightly associated with ALK mRNA expression levels. RACE-coupled PCR sequencing is a highly sensitive method that could be used clinically for the identification of <it>EML4</it>-<it>ALK</it>-positive patients.</p

Evidence based on Mendelian randomization and colocalization analysis strengthens causal relationships between structural changes in specific brain regions and risk of amyotrophic lateral sclerosis

BackgroundAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the degeneration of motor neurons in the brain and spinal cord with a poor prognosis. Previous studies have observed cognitive decline and changes in brain morphometry in ALS patients. However, it remains unclear whether the brain structural alterations contribute to the risk of ALS. In this study, we conducted a bidirectional two-sample Mendelian randomization (MR) and colocalization analysis to investigate this causal relationship.MethodsSummary data of genome-wide association study were obtained for ALS and the brain structures, including surface area (SA), thickness and volume of subcortical structures. Inverse-variance weighted (IVW) method was used as the main estimate approach. Sensitivity analysis was conducted detect heterogeneity and pleiotropy. Colocalization analysis was performed to calculate the posterior probability of causal variation and identify the common genes.ResultsIn the forward MR analysis, we found positive associations between the SA in four cortical regions (lingual, parahippocampal, pericalcarine, and middle temporal) and the risk of ALS. Additionally, decreased thickness in nine cortical regions (caudal anterior cingulate, frontal pole, fusiform, inferior temporal, lateral occipital, lateral orbitofrontal, pars orbitalis, pars triangularis, and pericalcarine) was significantly associated with a higher risk of ALS. In the reverse MR analysis, genetically predicted ALS was associated with reduced thickness in the bankssts and increased thickness in the caudal middle frontal, inferior parietal, medial orbitofrontal, and superior temporal regions. Colocalization analysis revealed the presence of shared causal variants between the two traits.ConclusionOur results suggest that altered brain morphometry in individuals with high ALS risk may be genetically mediated. The causal associations of widespread multifocal extra-motor atrophy in frontal and temporal lobes with ALS risk support the notion of a continuum between ALS and frontotemporal dementia. These findings enhance our understanding of the cortical structural patterns in ALS and shed light on potentially viable therapeutic targets

Building osteogenic microenvironments with a double-network composite hydrogel for bone repair

The critical factor determining the in vivo effect of bone repair materials is the microenvironment, which greatly depends on their abilities to promote vascularization and bone formation. However, implant materials are far from ideal candidates for guiding bone regeneration due to their deficient angiogenic and osteogenic microenvironments. Herein, a double-network composite hydrogel combining vascular endothelial growth factor (VEGF)-mimetic peptide with hydroxyapatite (HA) precursor was developed to build an osteogenic microenvironment for bone repair. The hydrogel was prepared by mixing acrylated β-cyclodextrins and octacalcium phosphate (OCP), an HA precursor, with gelatin solution, followed by ultraviolet photo-crosslinking. To improve the angiogenic potential of the hydrogel, QK, a VEGF-mimicking peptide, was loaded in acrylated β-cyclodextrins. The QK-loaded hydrogel promoted tube formation of human umbilical vein endothelial cells and upregulated the expression of angiogenesis-related genes, such as Flt1 , Kdr , and VEGF , in bone marrow mesenchymal stem cells. Moreover, QK could recruit bone marrow mesenchymal stem cells. Furthermore, OCP in the composite hydrogel could be transformed into HA and release calcium ions facilitating bone regeneration. The double-network composite hydrogel integrated QK and OCP showed obvious osteoinductive activity. The results of animal experiments showed that the composite hydrogel enhanced bone regeneration in skull defects of rats, due to perfect synergistic effects of QK and OCP on vascularized bone regeneration. In summary, improving the angiogenic and osteogenic microenvironments by our double-network composite hydrogel shows promising prospects for bone repair

Coping strategies following the diagnosis of a fetal anomaly: A scoping review

IntroductionMany women experience severe emotional distress (such as grief, depression, and anxiety) following a diagnosis of fetal anomaly. The ability to cope with stressful events and regulate emotions across diverse situations may play a primary role in psychological wellbeing. This study aims to present coping strategies after disclosing a fetal anomaly to pregnant women.MethodsThis is a scoping review based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) extension for scoping reviews (PRISMA-ScR). Electronic databases, including Web of Science (WOS, BCI, KJD, MEDLINE, RSCI, SCIELO), CINAHL, and EBSCO PsycARTICLES, were used to search for primary studies from the inception of each database to 2021. The keywords were determined by existing literature and included: “fetal anomaly,” “fetal abnormality,” “fetal anomaly,” “fetal abnormality” AND “cope,” “coping,” “deal,” “manage,” “adapt*,” “emotion* regulate*,” with the use of Boolean operators AND/OR. A total of 16 articles were reviewed, followed by advancing scoping review methodology of Arksey and O'Malley's framework.ResultsIn this review, we identified 52 coping strategies using five questionnaires in seven quantitative studies and one mixed-method study. The relationship between coping strategies and mental distress was explored. However, the results were inconsistent and incomparable. We synthesized four coping categories from qualitative studies and presented them in an intersection.ConclusionThis scoping review identified the coping strategies of women with a diagnosis of a fetal anomaly during pregnancy. The relationship between coping strategies and mental distress was uncertain and needs more exploration. We considered an appropriate measurement should be necessary for the research of coping in women diagnosed with fetal anomaly pregnancy