Glycomol: A pervasive tool for structure predication of natural saponin products basing on MS data.

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Therapeutic SHPRH-146aa encoded by circ-SHPRH dynamically upregulates P21 to inhibit CDKs in neuroblastoma.

Recent research has underscored the significance of circular RNAs (circRNAs) in various cancers, including neuroblastoma (NB). Specifically, circ-SHPRH, a unique circRNA, has been revealed to inhibit tumor growth by sequestering miRNAs or producing the SHPRH-146aa protein. To explore circ-SHPRH's involvement in NB and its potential application in gene therapy, this study examined circ-SHPRH expression in 94 NB tissues and cell lines (SK-N-BE(2), SH-SY5Y) using real-time PCR and fluorescence in situ hybridization (FISH). Functional assays encompassing both overexpression and knockdown experiments in NB cell lines, as well as in vivo investigations, were conducted. RNA-seq analysis revealed a correlation between circ-SHPRH and the pathway of P21 (CDKN1A), a pivotal cell cycle regulator. Validation through PCR and other techniques confirmed that circ-SHPRH upregulated P21 expression. Furthermore, the regulatory role of circ-SHPRH in the P21-CDK pathway was corroborated through SHPRH-146aa expression analysis. Notably, adenovirus-mediated circ-SHPRH overexpression effectively curbed NB tumor growth in NSG mice, while combining circ-SHPRH with everolimus exhibited potential for NB treatment. This study elucidates the remarkable significance of circ-SHPRH in NB and its prospective utility in gene therapy, thereby paving the way for innovative therapeutic approaches.

Impairment in acquisition of conditioned fear in people with depressive symptoms.

Background: Depression is one of the primary global public health issues, and there has been a dramatic increase in depression levels among young people over the past decade. The neuroplasticity theory of depression postulates that a malfunction in neural plasticity, which is responsible for learning, memory, and adaptive behavior, is the primary source of the disorder's clinical manifestations. Nevertheless, the impact of depression symptoms on associative learning remains underexplored. Methods: We used the differential fear conditioning paradigm to investigate the effects of depressive symptoms on fear acquisition and extinction learning. Skin conductance response (SCR) is an objective evaluation indicator, and ratings of nervousness, likeability, and unconditioned stimuli (US) expectancy are subjective evaluation indicators. In addition, we used associability generated by a computational reinforcement learning model to characterize the skin conductance response. Results: The findings indicate that individuals with depressive symptoms exhibited significant impairment in fear acquisition learning compared to those without depressive symptoms based on the results of the skin conductance response. Moreover, in the discrimination fear learning task, the skin conductance response was positively correlated with associability, as estimated by the hybrid model in the group without depressive symptoms. Additionally, the likeability rating scores improved post-extinction learning in the group without depressive symptoms, and no such increase was observed in the group with depressive symptoms. Conclusion: The study highlights that individuals with pronounced depressive symptoms exhibit impaired fear acquisition and extinction learning, suggesting a possible deficit in associative learning. Employing the hybrid model to analyze the learning process offers a deeper insight into the associative learning processes of humans, thus allowing for improved comprehension and treatment of these mental health problems.

Case report: The effect of second-line vebreltinib treatment on a patient with advanced NSCLC harboring the MET exon 14 skipping mutation after tepotinib treatment.

Background: Highly selective type Ib mesenchymal-epithelial transition gene (MET) tyrosine kinase inhibitors (TKIs) are the standard-of-care (SOC) therapy for previously untreated non-small cell lung cancer (NSCLC) harboring MET exon 14 (METex14) skipping mutations. However, there are rare reports describing effective regimens for patients who fail SOC without identifying resistant mutations or tissue transformation. Case report: We report the first case of a 74-year-old woman with lung adenocarcinoma (cT1cNxM0) harboring METex14 splice region mutation, which was identified by a next-generation sequencing (NGS)-based assay. The patient was administered two treatments, including first-line tepotinib and second-line vebreltinib. The patient achieved progression-free survival (PFS) of 7.6 months, and then disease progression of tepotinib was observed. A re-biopsy was performed for NGS, which revealed the same mutations as before, with no new gene mutations detected. The woman received subsequent vebreltinib therapy and experienced durable clinical benefits. In the first 6.8 months, chest computed tomography demonstrated stable disease. Then, she achieved partial response (PR). The durable PR lasted for more than 13 months, and the PFS is currently over 20 months, exceeding the prior treatment. Conclusion: This case highlights the importance of considering re-biopsy and reanalysis of genetic profiles in NSCLC patients harboring METex14 skipping mutations after progressive disease in MET TKI treatment. This raises the possibility that vebreltinib may have long-term survival benefits for patients without mutations conferring resistance (funded by Beijing Pearl Biotechnology Co., Ltd; ClinicalTrials.gov number, NCT04258033).

An Artificial Neural Network Based on Oxide Synaptic Transistor for Accurate and Robust Image Recognition.

Synaptic transistors with low-temperature, solution-processed dielectric films have demonstrated programmable conductance, and therefore potential applications in hardware artificial neural networks for recognizing noisy images. Here, we engineered AlOx/InOx synaptic transistors via a solution process to instantiate neural networks. The transistors show long-term potentiation under appropriate gate voltage pulses. The artificial neural network, consisting of one input layer and one output layer, was constructed using 9 × 3 synaptic transistors. By programming the calculated weight, the hardware network can recognize 3 × 3 pixel images of characters z, v and n with a high accuracy of 85%, even with 40% noise. This work demonstrates that metal-oxide transistors, which exhibit significant long-term potentiation of conductance, can be used for the accurate recognition of noisy images.

Role of estrogen in sex differences in memory, emotion and neuropsychiatric disorders.

Estrogen regulates a wide range of neuronal functions in the brain, such as dendritic spine formation, remodeling of synaptic plasticity, cognition, neurotransmission, and neurodevelopment. Estrogen interacts with intracellular estrogen receptors (ERs) and membrane-bound ERs to produce its effect via genomic and non-genomic pathways. Any alterations in these pathways affect the number, size, and shape of dendritic spines in neurons associated with psychiatric diseases. Increasing evidence suggests that estrogen fluctuation causes changes in dendritic spine density, morphology, and synapse numbers of excitatory and inhibitory neurons differently in males and females. In this review, we discuss the role of estrogen hormone in rodents and humans based on sex differences. First, we explain estrogen role in learning and memory and show that a high estrogen level alleviates the deficits in learning and memory. Secondly, we point out that estrogen produces a striking difference in emotional memories in men and women, which leads them to display sex-specific differences in underlying neuronal signaling. Lastly, we discuss that fluctuations in estrogen levels in men and women are related to neuropsychiatric disorders, including schizophrenia, autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder (BPD), major depressive disorder (MDD), substance use disorder (SUD), and anxiety disorders.

Electron deficient Bi3+δ serves as N2 absorption sites and inhibits carriers recombination to enhance N2 photo-fixation in BiOBr/TiO2 S-scheme heterojunction.

Efficient carriers separation and multiple nitrogen (N2) activation sites are essential for N2 photo-fixation. Here, we found that the BiOBr/TiO2 (BBTO) displayed an attractive reversible photochromism (white → grey) due to the generation of electron deficient Bi3+δ, which was produced by the hole trapping of Bi3+ under light irradiation. Interestingly, more Bi3+δ were detected in the BBTO heterojunction than in pure BiOBr, attributing that the hole trapping was promoted by the built-in electric field in the Step scheme (S-scheme) heterojunction. In the BBTO, the electron deficient Bi3+δ enhanced carriers separation and served as the reactive active site to adsorb more N2. Consequently, the BBTO possessed an excellent N2 photo-fixation activity (191 µmol gcat-1 h-1), which was 7.7 and 18 times higher than that of pure BiOBr (24.8 µmol gcat-1 h-1) and TiO2 (10.6 µmol gcat-1 h-1), respectively. Therefore, this work provides a new perspective for enhancing N2 photo-fixation by the electron deficient photocatalysts with S-scheme heterojunction.

The olfactory working memory capacity paradigm: A more sensitive and robust method of assessing cognitive function in male 5XFAD mice.

The olfactory working memory capacity (OWMC) paradigm is able to detect cognitive deficits in 5XFAD mice (an animal model of Alzheimer's disease [TG]) as early as 3 months of age, while other behavioral paradigms detect cognitive deficits only at 4-5 months of age. Therefore, we aimed to demonstrate that the OWMC paradigm is more sensitive and consistent in the early detection of declines in cognitive function than other commonly used behavioral paradigms. The prefrontal cortex (PFC), retrosplenial cortex (RSC), subiculum (SUB), and amygdala (AMY) of 5XFAD mice were harvested and subjected to immunostaining to detect the expression of ß-amyloid (Aß). Additionally, we compared the performance of 3-month-old male 5XFAD mice on common behavioral paradigms for assessing cognitive function (i.e., the open field [OF] test, novel object recognition [NOR] test, novel object location [NOL] test, Y-maze, and Morris water maze [MWM]) with that on the OWMC task. In the testing phase of the OWMC task, we varied the delay periods to evaluate the working memory capacity (WMC) of wild-type (WT) mice. Significant amyloid plaque deposition was observed in the PFC, RSC, SUB, and AMY of 3-month-old male 5XFAD mice. However, aside from the OWMC task, the other behavioral tests failed to detect cognitive deficits in 5XFAD mice. Additionally, to demonstrate the efficacy of the OWMC task in assessing WMC, we varied the retention delay periods; we found that the WMC of WT mice decreased with longer delay periods. The OWMC task is a sensitive and robust behavioral assay for detecting changes in cognitive function.

Effect of Hashimoto's thyroiditis on the dual-energy CT quantitative parameters and performance in diagnosing metastatic cervical lymph nodes in patients with papillary thyroid cancer.

BACKGROUND: To evaluate the effect of Hashimoto's thyroiditis (HT) on dual-energy computed tomography (DECT) quantitative parameters of cervical lymph nodes (LNs) in patients with papillary thyroid cancer (PTC), and its effect on the diagnostic performance and threshold of DECT in preoperatively identifying metastatic cervical LNs. METHODS: A total of 479 LNs from 233 PTC patients were classified into four groups: HT+/LN+, HT+/LN-, HT-/LN + and HT-/LN - group. DECT quantitative parameters including iodine concentration (IC), normalized IC (NIC), effective atomic number (Zeff), and slope of the spectral Hounsfield unit curve (λHU) in the arterial phase (AP) and venous phase were compared. Receiver operating characteristic curve analyses were performed to evaluate DECT parameters' diagnostic performance in differentiating metastatic from nonmetastatic LNs in the HT - and HT + groups. RESULTS: The HT+/LN + group exhibited lower values of DECT parameters than the HT-/LN + group (all p < 0.05). Conversely, the HT+/LN - group exhibited higher values of DECT parameters than the HT-/LN - group (all p < 0.05). In the HT + group, if an AP-IC of 1.850 mg/mL was used as the threshold value, then the optimal diagnostic performance (area under the curve, 0.757; sensitivity, 69.4%; specificity, 71.0%) could be obtained. The optimal threshold value of AP-IC in the HT - group was 2.050 mg/mL. In contrast, in the HT - group, AP-NIC demonstrated the highest area under the curve of 0.988, when an optimal threshold of 0.243 was used. The optimal threshold value of AP-NIC was 0.188 in the HT + group. CONCLUSIONS: HT affected DECT quantitative parameters of LNs and subsequent the diagnostic thresholds. When using DECT to diagnose metastatic LNs in patients with PTC, whether HT is coexistent should be clarified considering the different diagnostic thresholds.

Added value of arterial enhancement fraction derived from dual-energy computed tomography for preoperative diagnosis of cervical lymph node metastasis in papillary thyroid cancer: initial results.

OBJECTIVES: To explore the added value of arterial enhancement fraction (AEF) derived from dual-energy computed tomography CT (DECT) to conventional image features for diagnosing cervical lymph node (LN) metastasis in papillary thyroid cancer (PTC). METHODS: A total of 273 cervical LNs (153 non-metastatic and 120 metastatic) were recruited from 92 patients with PTC. Qualitative image features of LNs were assessed. Both single-energy CT (SECT)-derived AEF (AEFS) and DECT-derived AEF (AEFD) were calculated. Correlation between AEFD and AEFS was determined using Pearson's correlation coefficient. Multivariate logistic regression analysis with the forward variable selection method was used to build three models (conventional features, conventional features + AEFS, and conventional features + AEFD). Diagnostic performances were evaluated using receiver operating characteristic (ROC) curve analyses. RESULTS: Abnormal enhancement, calcification, and cystic change were chosen to build model 1 and the model provided moderate diagnostic performance with an area under the ROC curve (AUC) of 0.675. Metastatic LNs demonstrated both significantly higher AEFD (1.14 vs 0.48; p < 0.001) and AEFS (1.08 vs 0.38; p < 0.001) than non-metastatic LNs. AEFD correlated well with AEFS (r = 0.802; p < 0.001), and exhibited comparable performance with AEFS (AUC, 0.867 vs 0.852; p = 0.628). Combining CT image features with AEFS (model 2) and AEFD (model 3) could significantly improve diagnostic performances (AUC, 0.865 vs 0.675; AUC, 0.883 vs 0.675; both p < 0.001). CONCLUSIONS: AEFD correlated well with AEFS, and exhibited comparable performance with AEFS. Integrating qualitative CT image features with both AEFS and AEFD could further improve the ability in diagnosing cervical LN metastasis in PTC. CLINICAL RELEVANCE STATEMENT: Arterial enhancement fraction (AEF) values, especially AEF derived from dual-energy computed tomography, can help to diagnose cervical lymph node metastasis in patients with papillary thyroid cancer, and complement conventional CT image features for improved clinical decision making. KEY POINTS: • Metastatic cervical lymph nodes (LNs) demonstrated significantly higher arterial enhancement fraction (AEF) derived from dual-energy computed tomography (DECT) and single-energy CT (SECT)-derived AEF (AEFS) than non-metastatic LNs in patients with papillary thyroid cancer. • DECT-derived AEF (AEFD) correlated significantly with AEFS, and exhibited comparable performance with AEFS. • Integrating qualitative CT images features with both AEFS and AEFD could further improve the differential ability.

The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a stress-associated complex and debilitating psychiatric disorder due to an imbalance of neurotransmitters in response to traumatic events or fear. PTSD is characterized by re-experiencing, avoidance behavior, hyperarousal, negative emotions, insomnia, personality changes, and memory problems following exposure to severe trauma. However, the biological mechanisms and symptomatology underlying this disorder are still largely unknown or poorly understood. Considerable evidence shows that PTSD results from a dysfunction in highly conserved brain systems involved in regulating stress, anxiety, fear, and reward circuitry. This review provides a contemporary update about PTSD, including new data from the clinical and preclinical literature on stress, PTSD, and fear memory consolidation and extinction processes. First, we present an overview of well-established laboratory models of PTSD and discuss their clinical translational value for finding various treatments for PTSD. We then highlight the research progress on the neural circuits of fear and extinction-related behavior, including the prefrontal cortex, hippocampus, and amygdala. We further describe different molecular mechanisms, including GABAergic, glutamatergic, cholinergic, and neurotropic signaling, responsible for the structural and functional changes during fear acquisition and fear extinction processes in PTSD.

Differential regulation of hippocampal transcriptome by circulating estrogen.

Estrogen (E2) modulates the synaptic structure and plasticity in the hippocampus. Previous studies showed that E2 fluctuations during various phases of the menstrual cycle produce subtle neurosynaptic changes that impact women's behavior, emotion, and cognitive functions. In this study, we explored the transcriptome of the hippocampus via RNA-seq (RNA-sequencing) between proestrus (PE) and diestrus (DE) stages in young female rats to determine the effect of E2 of PE and DE stages on hippocampal gene expression. We identified 238 genes (at 1.5-fold-change selection criteria, FDR adjusted p-value < 0.05) as differentially expressed genes (DEGs) that responded to E2 between PE and DE stages. Functional analysis based on Gene Ontology (GO) revealed that a higher E2 level corresponded to an increase in gene transcription among most of the DEGs, suggesting biological mechanisms operating differentially in the hippocampus of female rats between PE and DE stages in the estrus cycle; while analysis with Kyoto Encyclopedia of Genes and Genomes database (KEGG) found that the DEGs involving neuroactive ligand-receptor interaction, antigen processing, cell adhesion molecules, and presentation were upregulated in PE stage, whereas DEGs in pathways relating to bile secretion, coagulation cascades, osteoclast differentiation, cysteine and methionine metabolism were upregulated in DE stage of the estrus cycle. The high-fold expression of DEGs was confirmed by a follow-up quantitative real-time PCR. Our findings in this current study have provided fundamental information for further dissection of neuro-molecular mechanisms in the hippocampus in response to E2 fluctuation and its relationship with disorders.

2D/2D MgO/g-C3N4 S-scheme heterogeneous tight with Mg-N bonds for efficient photo-Fenton degradation: Enhancing both oxygen vacancy and charge migration.

Construction of S-scheme heterojunction is an efficient strategy to enhance photocatalytic efficiency. Besides the retained redox ability, the wide work function gap and intimate interface contact are essential for efficient degradation. Nontoxic magnesium oxide (MgO) with two dimensional (2D) structures and high work function is a potential material for S-scheme photocatalysts. Herein, MgO was used to in-situ grown on graphitic carbon nitride (g-C3N4) for constructing the strongly connected MgO/g-C3N4 S-scheme photocatalyst with tight Mg-N bonds. Meanwhile, the presence of Mg-N bonds induces the formation of oxygen vacancy in MgO, which enhances the Fenton-like degradation. Furthermore, the Mg-N bond promotes the charge migration between MgO and g-C3N4. Consisting of the enhanced Fenton-like process and photocatalysis, the MgO/g-C3N4 shows a higher photo-Fenton degradation activity (80.01%) for degradation of organic pollutants (Rhodamine B, 100 mg L-1) in water, than g-C3N4 (28.46%) and MgO (55.64%). Therefore, the interfacial chemical bonds in heterojunction photocatalysts provide an efficient strategy for further enhancing the photocatalysis of S-scheme photocatalysts.

Corrigendum: Case Report: Durable response to immuno-chemotherapy in a case of ROS1 fusion-positive advanced lung adenocarcinoma: A case report.

[This corrects the article DOI: 10.3389/fphar.2022.898623.].

Diminished activation of excitatory neurons in the prelimbic cortex leads to impaired working memory capacity in mice.

BACKGROUND: Working memory capacity impairment is an early sign of Alzheimer's disease, but the underlying mechanisms remain unclear. Clarifying how working memory capacity is affected will help us better understand the pathological mechanism of Alzheimer's disease. We used the olfactory working memory capacity paradigm to evaluate memory capacity in 3-month-old 5XFAD (an animal model of Alzheimer's disease) mice. Immunofluorescence staining of the prefrontal cortex was performed to detect the number of FOS-positive neurons, calmodulin-dependent protein kinase II-positive neurons, and glutamate decarboxylase-positive neurons in the prelimbic cortex and infralimbic cortex. A chemogenetic method was then used to modulate the inhibition and activation of excitatory neurons in the prelimbic cortex of wild-type and 5XFAD mice and to measure the memory capacity of mice. RESULTS: Working memory capacity was significantly diminished in 5XFAD mice compared to littermate wild-type mice. Neuronal activation of the prelimbic cortex, but not the infralimbic cortex, was attenuated in 5XFAD mice performing the olfactory working memory capacity task. Subsequently, the FOS-positive neurons were co-localized with both calmodulin-dependent protein kinase II-positive neurons and glutamate decarboxylase-positive neurons. The results showed that the activation of excitatory neurons in the prelimbic cortex was correlated with working memory capacity in mice. Our results further demonstrate that the chemogenetic inhibition of prelimbic cortex excitatory neurons resulted in reduced working memory capacity in wild-type mice, while the chemogenetic activation of prelimbic cortex excitatory neurons improved the working memory capacity of 5XFAD mice. CONCLUSION: The diminished activation of prelimbic cortex excitatory neurons in 5XFAD mice during task performance is associated with reduced working memory capacity, and activation modulation of excitatory neurons by chemogenetic methods can improve memory capacity impairment in 5XFAD mice. These findings may provide a new direction for exploring Alzheimer's disease therapeutic approaches.

TAF1D promotes proliferation by transcriptionally activating G2/M phase-related genes in MYCN-amplified neuroblastoma.

High-risk neuroblastoma (HR-NB) is an aggressive childhood cancer that responds poorly to currently available therapies and is associated with only about a 50% 5-year survival rate. MYCN amplification is a critical driver of these aggressive tumors, but so far there have not been any approved treatments to effectively treat HR-NB by targeting MYCN or its downstream effectors. Thus, the identification of novel molecular targets and therapeutic strategies to treat children diagnosed with HR-NB represents an urgent unmet medical need. Here, we conducted a targeted siRNA screening and identified TATA box-binding protein-associated factor RNA polymerase I subunit D, TAF1D, as a critical regulator of the cell cycle and proliferation in HR-NB cells. Analysis of three independent primary NB cohorts determined that high TAF1D expression correlated with MYCN-amplified, high-risk disease and poor clinical outcomes. TAF1D knockdown more robustly inhibited cell proliferation in MYCN-amplified NB cells compared with MYCN-non-amplified NB cells, as well as suppressed colony formation and inhibited tumor growth in a xenograft mouse model of MYCN-amplified NB. RNA-seq analysis revealed that TAF1D knockdown downregulates the expression of genes associated with the G2/M transition, including the master cell-cycle regulator, cell-cycle-dependent kinase 1 (CDK1), resulting in cell-cycle arrest at G2/M. Our findings demonstrate that TAF1D is a key oncogenic regulator of MYCN-amplified HR-NB and suggest that therapeutic targeting of TAF1D may be a viable strategy to treat HR-NB patients by blocking cell-cycle progression and the proliferation of tumor cells.

Charge Trapping and Emission Properties in CAAC-IGZO Transistor: A First-Principles Calculations.

The c-axis aligned crystalline indium-gallium-zinc-oxide field-effect transistor (CAAC-IGZO FET), exhibiting an extremely low off-state leakage current (~10-22 A/µm), has promised to be an ideal candidate for Dynamic Random Access Memory (DRAM) applications. However, the instabilities leaded by the drift of the threshold voltage in various stress seriously affect the device application. To better develop high performance CAAC-IGZO FET for DRAM applications, it's essential to uncover the deep physical process of charge transport mechanism in CAAC-IGZO FET. In this work, by combining the first-principles calculations and nonradiative multiphonon theory, the charge trapping and emission properties in CAAC-IGZO FET have been systematically investigated. It is found that under positive bias stress, hydrogen interstitial in Al2O3 gate dielectric is probable effective electron trap center, which has the transition level (ε (+1/-1) = 0.52 eV) above Fermi level. But it has a high capture barrier about 1.4 eV and low capture rate. Under negative bias stress, oxygen vacancy in Al2O3 gate dielectric and CAAC-IGZO active layer are probable effective electron emission centers whose transition level ε (+2/0) distributed at -0.73~-0.98 eV and 0.69 eV below Fermi level. They have a relatively low emission barrier of about 0.5 eV and 0.25 eV and high emission rate. To overcome the instability in CAAC-IGZO FET, some approaches can be taken to control the hydrogen concentration in Al2O3 dielectric layer and the concentration of the oxygen vacancy. This work can help to understand the mechanisms of instability of CAAC-IGZO transistor caused by the charge capture/emission process.

Influence of sex, age and thyroid function indices on dual-energy computed tomography-derived quantitative parameters of thyroid in patients with or without Hashimoto's thyroiditis.

PURPOSE: To study the influence of sex, age and thyroid function indices on dual-energy computed tomography (DECT)-derived quantitative parameters of thyroid in patients with or without Hashimoto's thyroiditis (HT). MATERIAL AND METHODS: A total of 198 consecutive patients who underwent DECT scan of neck due to unilateral thyroid lesions were retrospectively enrolled. Iodine concentration (IC), total iodine content (TIC) and volume of normal thyroid lobe were calculated. Influences of sex, age and thyroid function indices on DECT-derived parameters in overall study population, subgroup patients with, and those without HT were assessed using Mann-Whitney U test, Student's T-test, and Spearman correlation analyses, respectively, as appropriate. RESULTS: HT group showed significantly lower IC and TIC, while higher volume than No-HT group (all p < 0.001). The volume was larger in male than that in female in overall study population and No-HT group (p = 0.047 and 0.010, respectively). There was no significant difference in any DECT-derived parameters between low (≤ 35 years) and high (> 35 years) age group in all three groups (all p > 0.05). TPOAb and TgAb correlated positively with IC and TIC, and negatively with volume in overall study population (all p < 0.05). TPOAb and TgAb also correlated positively with IC in HT group (p = 0.002 and 0.007, respectively). CONCLUSION: DECT-derived parameters of thyroid differed significantly between patients with and without HT. Sex and thyroid function indices could affect the DECT-derived parameters. Aforementioned physiological factors should be considered when analyzing the DECT-derived parameters of thyroid.