Diagnostic efficacy of the contrast-enhanced ultrasound thyroid imaging reporting and data system classification for benign and malignant thyroid nodules.

Background: The contrasted-enhanced ultrasound thyroid imaging reporting and data system (CEUS TI-RADS) is the first international risk stratification system for thyroid nodules based on conventional ultrasound (US) and CEUS. This study aimed to evaluate the diagnostic efficacy of CEUS TI-RADS for benign and malignant thyroid nodules and to assess the related interobserver agreement. Methods: The study recruited 433 patients who underwent thyroid US and CEUS between January 2019 and June 2023 at the Affiliated Hospital of Guangdong Medical University. A retrospective analysis of 467 thyroid nodules confirmed by fine-needle aspiration (FNA) and/or surgery was performed. Further, a CEUS TI-RADS classification was assigned to each thyroid nodule based on the CEUS TI-RADS scoring criteria for the US and CEUS features of the nodule. The nodules were grouped based on their sizes as follows: size ≤1 cm, group A; size >1 and ≤4 cm, group B; and size >4 cm, group C. Multivariate logistic regression was used to analyze independent risk factors for malignant thyroid nodules. Pathological assessment was the reference standard for establishing the sensitivity (SEN), specificity (SPE), accuracy (ACC), positive predictive value (PPV), and negative predictive value (NPV) of CEUS TI-RADS in diagnosing malignant thyroid nodules. The area under the curve (AUC) in the receiver operating characteristic (ROC) curve analysis was used to compare the diagnostic efficacy of the scoring system in predicting malignancy in three groups of nodules. The intragroup correlation coefficient (ICC) was adopted to assess the interobserver agreement of the CEUS TI-RADS score. Results: Out of the 467 thyroid nodules, 262 were malignant and 205 were benign. Logistic regression analysis revealed that the independent risk factors for malignant thyroid nodules included punctate echogenic foci (P<0.001), taller-than-wide shape (P=0.015), extrathyroidal invasion (P=0.020), irregular margins/lobulation (P=0.036), hypoechoicity on US (P=0.038), and hypoenhancement on CEUS (P<0.001). The AUC for the CEUS TI-RADS in diagnosing malignant thyroid nodules was 0.898 for all nodules, 0.795 for group A, 0.949 for group B, and 0.801 for group C, with the optimal cutoff values of the CEUS TI-RADS being 5 points, 6 points, 5 points, and 5 points, respectively. Among these groups of nodules, group B had the highest AUC, with the SEN, SPE, ACC, PPV, and NPV for diagnosing malignant nodules being 95.9%, 88.1%, 92.8%, 92.6%, and 93.2%, respectively. The ICC of the CEUS TI-RADS classification between senior and junior physicians was 0.862 (P<0.001). Conclusions: In summary, CEUS TI-RADS demonstrated significant efficacy in distinguishing thyroid nodules. Nonetheless, there were variations in its capacity to detect malignant nodules across diverse sizes, and it demonstrate optimal performance in 1- to 4-cm nodules. These findings may serve as important insights for clinical diagnoses.

Andrographolide sulfonate downregulation of TLR3-TRIF and amelioration of airway inflammation caused by respiratory syncytial virus infection.

Background: Andrographolide sulfonate (Andro-S), a traditional Chinese medicine, is commonly used to treat pediatric respiratory tract infections in China. However, its therapeutic effects in infections caused by respiratory syncytial virus (RSV) have not been reported. We thus aimed to investigate the therapeutic effects of Andro-S using a mouse model of RSV infection-induced airway inflammation. Methods: Immunocompromised (cyclophosphamide-treated) BALB/c mice were intranasally infected with RSV and treated with intranasal or intraperitoneal Andro-S once daily for five consecutive days, starting on the day of infection. Histopathological changes in the lung were evaluated using hematoxylin and eosin staining. Total inflammatory cell counts and macrophage, lymphocyte, neutrophil, and eosinophil counts in the bronchoalveolar lavage fluid (BALF) were microscopically determined. Interferon-γ (IFN-γ) levels in the BALF were detected using enzyme-linked immunosorbent assay (ELISA). The messenger RNA levels of RSV nucleoprotein (N) and Toll-like receptors (TLRs) 1-9 in lung tissues were determined with quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of RSV N, RSV fusion protein (F), TLR2, TLR3, and TIR domain-containing adapter-inducing interferon-ß (TRIF) were detected via Western blot analysis. Results: RSV infection caused lung inflammation, manifesting as bronchiolitis, alveolitis, and perivascular inflammation; increased the number of inflammatory cells; and elevated IFN-γ levels in the BALF. Lung inflammation was positively correlated with pulmonary RSV N levels in infected mice. Intranasal Andro-S significantly downregulated RSV N, RSV F, TLR3, and TRIF protein expression in the lung and ameliorated lung inflammation in infected animals. However, intraperitoneal Andro-S showed no effects on lung inflammation caused by RSV infection. Conclusions: Intranasal Andro-S inhibits RSV replication and ameliorates RSV infection-induced lung inflammation by downregulating TLR3 and TRIF. Therefore, intranasal administration may be a suitable drug delivery method for treating RSV infection.

Synergistic delivery of hADSC-Exos and antioxidants has inhibitory effects on UVB-induced skin photoaging.

Ultraviolet B (UVB) light exposure accelerates skin photoaging. Human adipose-derived stem cell exosomes (hADSC-Exos) and some antioxidants may have anti-photoaging effects. However, it is unknown whether the combination of hADSC-Exos and antioxidants plays a synergistic role in anti-photoaging. In cellular and 3D skin models, we showed that vitamin E (VE) and hADSC-Exos were optimal anti-photoaging combinations. In vivo, VE and hADSC-Exos increased skin tightening and elasticity in UVB-induced photoaging mice Combined treatment with VE and hADSC-Exos inhibited SIRT1/NF-κB pathway. These findings contribute to the understanding of hADSC-Exos in conjunction with other antioxidants, thereby providing valuable insights for the future pharmaceutical and cosmetic industries.

Sunitinib alleviates hepatic ischemia reperfusion injury by inhibiting the JAK2/STAT pathway and promoting the M2 polarization of macrophages.

BACKGROUND: Hepatic ischemia reperfusion injury (IRI) is a common liver surgery complication. This study aims to explore the effect and potential mechanism of Sunitinib - a multi-target tyrosine kinase inhibitor - on hepatic IRI. METHODS: We established a hepatic IRI model using C57BL/6 mice, and integrated 40 mg/kg of Sunitinib, solely or combined with 100 µg/kg of coumermycin A1 (C-A1), in the treatment strategy. H&E staining, TUNEL assay, and detection of serum ALT and AST activities were used to assess liver damage. Further, ELISA kits and Western Blots were utilized to determine IL-1ß, TNF-α, IL-6, CXCL10, and CXCL2 levels. Primary macrophages, once isolated, were cultured in vitro with either 2 nM of Sunitinib, or Sunitinib in conjunction with 1 µM of C-A1, to gauge their influence on macrophage polarization. qPCR and Western blot were conducted to examine the level of p-STAT1/STAT1, p-STAT3/STAT3, p-JAK2/JAK2, and M1/M2 polarization markers. To quantify immune cell infiltration, we applied Immunofluorescence. RESULTS: Sunitinib pretreatment significantly alleviated liver injury and reduced p-STAT1/STAT1, p-STAT3/STAT3, p-JAK2/JAK2 levels. In vitro, Sunitinib treatment curbed M1 polarization induced by LPS + IFN-γ and bolstered M2 polarization triggered by IL-4. C-A1 application upregulated JAK2/STAT pathway phosphorylation and promoted LPS + IFN-γ-induced M1 polarization, which was reversed by Sunitinib treatment. In IL-4-stimulated macrophages, application of C-A1 activated the JAK2/STAT pathway and decreased M2-type macrophages, which was reversed by Sunitinib treatment either. CONCLUSION: Sunitinib is capable of guiding the polarization of macrophages toward an M2-type phenotype via the inhibition of the JAK2/STAT pathway, thereby exerting a protective effect on hepatic IRI.

Experiences of Exercise-Related Worry Among Chinese Childhood Cancer Survivors and Their Carers: A Qualitative Study.

BACKGROUND: The low levels of physical activity in childhood cancer survivors have increasingly garnered attention from nursing scholars. Exercise-related worry is a prominent barrier, yet the understanding of such experiences among childhood cancer survivors and their primary caregivers remains scarce. OBJECTIVE: The aim of this study was to further understand the factors contributing to exercise-related worry from the perspective of childhood cancer survivors and their primary caregivers. METHODS: In this qualitative study, we conducted face-to-face semistructured interviews with childhood cancer survivors (n = 20) and carers (n = 20) in 2 hospitals in China. The interviews were analyzed according to thematic analysis. RESULTS: Two main themes and 8 subthemes emerged: (1) internal factors: changes in the perception of physical activity (threat perception from the disease, active avoidance of stressful events, lack of safety due to past experiences), and (2) external factors: weak support system (limited peer support, family strength, feeling abandoned by the tumor team, reintegration into school, external environmental constraints). In summary, exercise-related worry is from internal factors and can be influenced by external factors. CONCLUSION: There are various factors contributing to the concerns of exercise in childhood cancer survivors, which may be a key factor for their significantly lower levels of physical activity compared to guideline recommendations. IMPLICATIONS FOR PRACTICE: The findings of this study call for healthcare professionals to provide additional assistance for childhood cancer survivors with exercise-related worry and establish personalized mechanisms for supporting physical activity in pediatric cancer survivors within the Chinese healthcare system.

Electron-injection-engineering induced dual-phase MoO2.8F0.2/MoO2.4F0.6 heterostructure for magnesium storage.

Rechargeable magnesium batteries (RMBs) have received increased attention due to their high volumetric capacity and safety. Nevertheless, the sluggish diffusion kinetics of highly polarized Mg2+ in host lattices severely hinders the development of RMBs. Herein, we report an electron injection strategy for modulating the Mo 4d-orbital splitting manner and first fabricate a dual-phase MoO2.8F0.2/MoO2.4F0.6 heterostructure to accelerate Mg2+ diffusion. The electron injection strategy triggers weak Jahn-Teller distortion in MoO6 octahedra and reorganization of the Mo 4d-orbital, leading to a partial phase transition from orthorhombic phase MoO2.8F0.2 to cubic phase MoO2.4F0.6. As a result, the designed heterostructure generates a built-in electric field, simultaneously improving its electronic conductivity and ionic diffusivity by at least one order of magnitude compared to MoO2.8F0.2 and MoO2.4F0.6. Importantly, the assembled MoO2.8F0.2/MoO2.4F0.6//Mg full cell exhibits a remarkable reversible capacity of 172.5 mAh g-1 at 0.1 A g-1, pushing forward the orbital-scale manipulation for high-performance RMBs.

Microplastics exposure disrupts nephrogenesis and induces renal toxicity in human iPSC-derived kidney organoids.

Microplastics (MPs) have emerged as a pervasive environmental pollutant of global concern. Their detection within the human placenta and fetal organs has prompted apprehension regarding the potential hazards of MPs during early organogenesis. The kidney, a vital multifunctional organ, is susceptible to damage from MPs in adulthood. However, the precise adverse effects of MP exposure on human nephrogenesis remain ambiguous due to the absence of a suitable model. Here, we explore the potential impact of MPs on early kidney development utilizing human kidney organoids in vitro. Human kidney organoids were subjected to polystyrene-MPs (PS-MPs, 1 µm) during the nephron progenitor cell (NPC) stage, a critical phase in early kidney development and patterning. We delineate the effects of PS-MPs on various stages of nephrogenesis, including NPC, renal vesicle, and comma-shaped body, through sequential examination of kidney organoids. PS-MPs were observed to adhere to the surface of cells during the NPC stage and accumulate within glomerulus-like structures within kidney organoids. Moreover, both short- and long-term exposure to PS-MPs resulted in diminished organoid size and aberrant nephron structure. PS-MP exposure heightened reactive oxygen species (ROS) production, leading to NPC apoptosis during early kidney development. Increased apoptosis, diminished cell viability, and NPC reduction likely contribute to the observed organoid size reduction under PS-MP treatment. Transcriptomic analysis at both NPC and endpoint stages revealed downregulation of Notch signaling, resulting in compromised proximal and distal tubular structures, thereby disrupting normal nephron patterning following PS-MP exposure. Our findings highlight the significant disruptive impact of PS-MPs on human kidney development, offering new insights into the mechanisms underlying PS-MP-induced nephron toxicity.

Przewaquinone A inhibits Angiotensin II-induced endothelial diastolic dysfunction activation of AMPK.

BACKGROUND: Endothelial dysfunction (ED), characterized by markedly reduced nitric oxide (NO) bioavailability, vasoconstriction, and a shift toward a proinflammatory and prothrombotic state, is an important contributor to hypertension, atherosclerosis, and other cardiovascular diseases. Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) is widely involved in cardiovascular development. Przewaquinone A (PA), a lipophilic diterpene quinone extracted from Salvia przewalskii Maxim, inhibits vascular contraction. PURPOSE: Herein, the goal was to explore the protective effect of PA on ED in vivo and in vitro, as well as the underlying mechanisms. METHODS: A human umbilical vein endothelial cell (HUVEC) model of ED induced by angiotensin II (AngII) was used for in vitro observations. Levels of AMPK, endothelial nitric oxide synthase (eNOS), vascular cell adhesion molecule-1 (VCAM-1), nitric oxide (NO), and endothelin-1 (ET-1) were detected by western blotting and ELISA. A mouse model of hypertension was established by continuous infusion of AngII (1000 ng/kg/min) for 4 weeks using osmotic pumps. Following PA and/or valsartan administration, NO and ET-1 levels were measured. The levels of AMPK signaling-related proteins in the thoracic aorta were evaluated by immunohistochemistry. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were measured using the tail cuff method. Isolated aortic vascular tone measurements were used to evaluate the vasodilatory function in mice. Molecular docking, molecular dynamics, and surface plasmon resonance imaging (SPRi) were used to confirm AMPK and PA interactions. RESULTS: PA inhibited AngII-induced vasoconstriction and vascular adhesion as well as activated AMPK signaling in a dose-dependent manner. Moreover, PA markedly suppressed blood pressure, activated vasodilation in mice following AngII stimulation, and promoted the activation of AMPK signaling. Furthermore, molecular simulations and SPRi revealed that PA directly targeted AMPK. AMPK inhibition partly abolished the protective effects of PA against endothelial dysfunction. CONCLUSION: PA activates AMPK and ameliorates endothelial dysfunction during hypertension.

Tranexamic acid efficacy in geriatric hip fractures: impact of nutritional status on blood loss, transfusion rates, and safety.

BACKGROUND: Tranexamic acid (TXA) is a widely employed intervention in orthopedic surgeries to minimize blood loss and the need for postoperative transfusions. This study focuses on assessing the efficacy and safety of TXA specifically in undernourished older adults undergoing hip fracture procedures. METHODS: A total of 216 patients were classified into two groups based on the Geriatric Nutritional Risk Index: undernourished and normal. In total, 82 patients received intravenous TXA at a dosage of 15 mg/kg before incision, with an additional 1 g administered intravenously over a 3-hour period postoperatively. Postoperative hemoglobin (Hb) drop, blood transfusion rate, and the incidence of deep venous thrombosis (DVT) were assessed in each group according to the presence or absence of TXA. Additionally, demographic factors including age, sex, body mass index, and serum albumin were investigated. RESULTS: 51.9% patients were identified as undernourished, experiencing progressive anemia (Hb: 10.9 ± 1.5 g/dL) and hypoalbuminemia (serum albumin: 31.9 ± 8 g/L). In comparison with the normal group, undernourished individuals were more likely to sustain femoral neck fractures (undernutrition vs. normal: 56.2 vs. 42.3%) and less likely to incur trochanteric fractures (undernutrition vs. normal: 43.8 vs. 57.7%) (P = 0.043). TXA administration significantly reduced the transfusion rate (P = 0.014) and Hb drop (P = 0.001) in the normal nutritional group, while its impact on the undernourished group remained less pronounced. There was no significant association between TXA administration and the rate of DVT complications, irrespective of the nutritional status. CONCLUSIONS: Undernutrition not only diminishes muscle strength and gait function, leading to various types of hip fractures, but it may also hinder the efficacy of TXA in reducing blood transfusion rates and blood loss.

Pan-cancer analysis and experimental validation reveal FAM72D as a potential novel biomarker and therapeutic target in lung adenocarcinoma.

BACKGROUND: Cancers, particularly lung adenocarcinoma (LUAD), represent a major global health concern. However, the role of FAM72D in various cancers, including LUAD, remains poorly understood. METHODS: We utilized databases such as The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression Project (GTEx) and online tools to investigate the correlation between FAM72D expression and its prognostic, diagnostic, and mutational significance, as well as its impact on immune cell infiltration across multiple cancers. Additionally, we developed LUAD cell lines overexpressing FAM72D to confirm its oncogenic role. RESULTS: FAM72D expression was elevated in cancerous tissues compared to noncancerous tissues, with diagnostic and prognostic implications in many cancers, including LUAD. Moreover, associations were identified between FAM72D expression and diverse immune subtypes, alongside factors such as microsatellite instability, neoantigens, and tumour mutational burden across pan-cancers. Additionally, FAM72D was associated with immune infiltration and various immune checkpoint-related genes in LUAD. In vitro experiments demonstrated that FAM72D promoted cell proliferation, colony formation, and migration, while inhibiting apoptosis in LUAD cells. CONCLUSIONS: Our study establishes associations between FAM72D expression and diagnosis, prognosis, and tumour immunity across multiple cancers, as well as its oncogenic effects in LUAD. FAM72D shows promise as a biomarker and therapeutic target in LUAD.

Engineered in vivo and in vitro tumor model recapitulates vasculogenic mimicry signatures in melanoma.

Vasculogenic mimicry (VM) describes a process by which tumor cells formed a novel microcirculation pattern in an endothelial cell-free manner. Clinically, VM is associated with aggressive phenotype and poor patient survival. However, the current models for investigating VM include 2D monolayer cultures, Matrigel-based cultures, and animal models, each of which has limitations. Matrigel-based models often exhibit batch-to-batch variations, while in vivo tumor models currently produce insufficient amounts of VM. There is currently no suitable tumor model to discover new therapeutic targets against VM. Herein, we establish an extracellular matrix (ECM)-based engineered tumor model in vivo and in vitro. In this study, we demonstrate that matrix proteins enhanced the VM formation in the engineered xenograft model. Furthermore, we also investigated the role of collagen/fibronectin (FN) in melanoma progression and VM formation. Compared with cells cultured on TCPS plates, the B16F10 cells cultured on collagen/FN coated plates showed increased proliferation and stemness, and significantly enhanced invasion and formation of VM networks. Molecular mechanism analysis showed that Integrin/VE-cadherin/EphA2/PI3K/MMP-2 signaling pathways are responsible for VM formation. Our results indicate that collagen/FN matrix plays an important role in VM formation in melanoma, suggesting that ECM protein is a potential therapeutic target for anti-VM therapy for melanoma.

A novel GNAS mutation in pseudohypoparathyroidism type 1a with articular flexion deformity: A case report.

Pseudohypoparathyroidism (PHP) type 1a (PHP 1a) is a rare hereditary disorder characterized by target organ resistance to hormonal signaling and the Albright hereditary osteodystrophy (AHO) phenotype, which features round facial features, short fingers, subcutaneous calcifications, short stature, obesity, and intellectual disability. Progressive osseous heteroplasia (POH) is another rare disorder characterized by heterotopic ossification (HO) that progressively affects skin, subcutaneous tissues, and deep skeletal muscle. PHP 1a is inherited maternally due to a GNAS mutation, while pure POH is inherited paternally. This case study presented a Chinese boy with congenital hypothyroidism, tonic-clonic seizures, hypoparathyroidism, AHO, POH, and joint fixation deformity. Sequencing analysis of GNAS-Gsα revealed a heterozygous C.432+2T>C(P.?) variant (NM_000516.7) affecting the canonical splice donor site of intron 5 in the boy and his mother, indicating maternal inheritance of a GNAS mutation. The patient was diagnosed with POH overlap syndrome (POH/PHP 1a). Following calcium and calcitriol supplementation, he experienced a reduction in seizures, and surgery was performed to correct the joint fixation deformity caused by HO. This case report provided valuable insights into the genotype-phenotype correlations of POH overlap syndrome and underscored the significance of genetic testing in diagnosing rare diseases.

Microrna-605-3p Inhibited the Growth and Chemoresistance of Osteosarcoma Cells via Negatively Modulating RAF1.

BACKGROUND: Osteosarcoma (OS) is the leading cancer-associated mortality in childhood and adolescence. Increasing evidence has demonstrated the key function of microRNAs (miRNAs) in OS development and chemoresistance. Among them, miRNA-605-3p acted as an important tumor suppressor and was frequently down-regulated in multiple cancers. However, the function of miR-650-3p in OS has not been reported. OBJECTIVE: The aim of this work is to explore the novel role of miR-605-3p in osteosarcoma and its possible involvement in OS chemotherapy resistance. METHOD: The expression levels of miR-605-3p in OS tissues and cells were assessed by reverse transcription quantitative PCR (RT-qPCR). The relevance of miR-605-3p with the prognosis of OS patients was determined by the Kaplan-Meier analysis. Additionally, the influence of miR-605-3p on OS cell growth was analyzed using the cell counting kit-8, colony formation assay, and flow cytometry. The mRNA and protein expression of RAF1 were detected by RT-qPCR and western blot. The binding of miR-605-3p with the 3'-UTR of RAF1 was confirmed by dual-luciferase reporter assay. RESULTS: Our results showed that miR-605-3p was markedly decreased in OS tissues and cells. A lower level of miR-605-3p was strongly correlated with lymph node metastasis and poor 5-year overall survival rate of OS patients. In vitro assay found that miR-605-3p suppressed OS cell proliferation and promoted cell apoptosis. Mechanistically, the proto-oncogene RAF1 was seen as a target of miR-605-3p and strongly suppressed by miR-605-3p in OS cells. Restoration of RAF1 markedly eliminated the inhibitory effect of miR-605-3p on OS progression, suggesting RAF1 as a key mediator of miR-605-3p. Consistent with the decreased level of RAF1, miR-605-3p suppressed the activation of both MEK and ERK in OS cells, which are the targets of RAF1. Moreover, lower levels of miR-605-3p were found in chemoresistant OS patients, and downregulated miR-605-3p increased the resistance of OS cells to therapeutic agents. CONCLUSION: Our data revealed that miR-605-3p serves as a tumor suppressor gene by regulating RAF1 and increasing the chemosensitivity of OS cells, which provided the novel working mechanism of miR-605-3p in OS. Engineering stable nanovesicles that could efficiently deliver miR-605-3p with therapeutic activity into tumors could be a promising therapeutic approach for the treatment of OS.

Strain-Temperature Dual Sensor Based on Deep Learning Strategy for Human-Computer Interaction Systems.

Thermoelectric (TE) hydrogels, mimicking human skin, possessing temperature and strain sensing capabilities, are well-suited for human-machine interaction interfaces and wearable devices. In this study, a TE hydrogel with high toughness and temperature responsiveness was created using the Hofmeister effect and TE current effect, achieved through the cross-linking of PVA/PAA/carboxymethyl cellulose triple networks. The Hofmeister effect, facilitated by Na+ and SO42- ions coordination, notably increased the hydrogel's tensile strength (800 kPa). Introduction of Fe2+/Fe3+ as redox pairs conferred a high Seebeck coefficient (2.3 mV K-1), thereby enhancing temperature responsiveness. Using this dual-responsive sensor, successful demonstration of a feedback mechanism combining deep learning with a robotic hand was accomplished (with a recognition accuracy of 95.30%), alongside temperature warnings at various levels. It is expected to replace manual work through the control of the manipulator in some high-temperature and high-risk scenarios, thereby improving the safety factor, underscoring the vast potential of TE hydrogel sensors in motion monitoring and human-machine interaction applications.

A Simple Prognostic Scoring System for Hepatocellular Carcinoma Treated with DEB-TACE.

Objective: To develop a simple and effective prognostic scoring system to predict the efficacy of drug-eluting bead-transcatheter arterial chemoembolization (DEB-TACE) in the treatment of hepatocellular carcinoma (HCC). Methods: Data were retrospectively collected from 230 patients with HCC who received DEB-TACE treatment at six medical centers between January 2019 and December 2022. We developed a predictive score based on independent risk factors for overall survival (OS), validated the model using a validation cohort, and compared its prognostic accuracy with commonly used HCC staging systems. Results: The number of tumors, albumin-bilirubin levels, alpha-fetoprotein levels, and portal vein thrombus grade were identified as independent factors influencing OS. Based on these factors, we established the DEB-TACE treatment of HCC (DTH) scoring system. The DTH score correlated well with OS, which decreased as the DTH score increased. According to the DTH score, patients were categorized into three risk groups: low-risk (DTH-A, 0-4 points), medium-risk (DTH-B, 5-6 points), and high-risk (DTH-A, 7 points). The OS of each risk group was 18.73±0.62 months, 12.73±0.10 months, and 6.93±0.19 months, respectively (p<0.001). The external cohort validation confirmed the accuracy of the DTH score, demonstrating superior predictive performance compared to other commonly used HCC scoring systems. Conclusion: The DTH-HCC scoring system effectively predicts the outcomes of HCC patients undergoing DEB-TACE as initial treatment. This model can aid in the initial planning and decision-making process for DEB-TACE treatment in HCC patients.

Best evidence summary of sleep protection in premature infants in the neonatal intensive care unit: a narrative review.

Background and Objective: Sleep influences the interaction between infants and their environment, as well as the achievement of crucial milestones in motor and language development. This is particularly significant for preterm infants in vulnerable positions. However, prematurely born infants in the neonatal intensive care unit (NICU) are exposed to various stimuli such as noise and light, which disrupt their normal sleep patterns. This study assesses and consolidates the existing evidence on non-pharmacological strategies for protecting and promoting sleep in preterm infants. By providing an evidence-based data repository, it offers a valuable reference for clinical interventions. Methods: We conducted computer-based searches using various databases and resources, including UpToDate, BMJ Best Practice, Guidelines International Network (GIN), National Institute for Health and Clinical Excellence (NICE), Scottish Intercollegiate Guidelines Network (SIGN), National Guideline Clearinghouse (NGC), Registered Nurses Association of Ontario (RNAO), Joanna Briggs Institute (JBI), World Health Organization (WHO), Cochrane Library, Web of Science, PubMed, China National Knowledge Infrastructure (CNKI), Wanfang Data, and China Biology Medicine disc (CBM). The search period spanned from January 2014 to May 2024. Key Content and Findings: We have included a total of 22 articles in our review, comprising two guidelines, 11 systematic reviews, 1 evidence summary, 1 technical report, 2 practice recommendations, and 5 randomized controlled trials. The evidence was synthesized from eight domains: sleep team construction, risk factor assessment, sleep assessment tools, positional management, noise control, light management, sensory stimulation, and hospital-home transition sleep management, resulting in 27 pieces of evidence. Conclusions: This study summarizes the optimal evidence for the management of sleep in premature infants, providing empirical support for standardizing the management of sleep in premature infants. It is recommended that healthcare professionals judiciously apply the best evidence while considering the clinical context, thus promoting safe sleep for premature infants.

Development and evaluation of interpretable machine learning regressors for predicting femoral neck bone mineral density in elderly men using NHANES data.

Osteoporotic femoral neck fractures (OFNFs) pose a significant orthopedic challenge in the elderly population, accounting for up to 40% of all osteoporotic fractures and leading to considerable health deterioration and increased mortality. In addressing the critical need for early identification of osteoporosis through routine screening of femoral neck bone mineral density (FNBMD), this study developed a user-friendly prediction model aimed at men aged 50 years and older, a demographic often overlooked in osteoporosis screening. Utilizing data from the National Health and Nutrition Examination Survey (NHANES), the study involved outlier detection and handling, missing value imputation via the K nearest neighbor (KNN) algorithm, and data normalization and encoding. The dataset was split into training and test sets with a 7:3 ratio, followed by feature screening through the least absolute shrinkage and selection operator (LASSO) and the Boruta algorithm. Eight different machine learning algorithms were then employed to construct predictive models, with their performance evaluated through a comprehensive metric suite. The random forest regressor (RFR) emerged as the most effective model, characterized by key predictors such as age, body mass index (BMI), poverty income ratio (PIR), serum calcium, and race, achieving a coefficient of determination (R²) of 0.218 and maintaining robustness in sensitivity analyses. Notably, excluding race from the model resulted in sustained high performance, underscoring the model's adaptability. Interpretations using Shapley additive explanations (SHAP) highlighted the influence of each feature on FNBMD. These findings indicate that our predictive model effectively aids in the early detection of osteoporosis, potentially reducing the incidence of OFNFs in this high-risk population.

Hemispherical Retina Emulated by Plasmonic Optoelectronic Memristors with All-Optical Modulation for Neuromorphic Stereo Vision.

Binocular stereo vision relies on imaging disparity between two hemispherical retinas, which is essential to acquire image information in three dimensional environment. Therefore, retinomorphic electronics with structural and functional similarities to biological eyes are always highly desired to develop stereo vision perception system. In this work, a hemispherical optoelectronic memristor array based on Ag-TiO2 nanoclusters/sodium alginate film is developed to realize binocular stereo vision. All-optical modulation induced by plasmonic thermal effect and optical excitation in Ag-TiO2 nanoclusters is exploited to realize in-pixel image sensing and storage. Wide field of view (FOV) and spatial angle detection are experimentally demonstrated owing to the device arrangement and incident-angle-dependent characteristics in hemispherical geometry. Furthermore, depth perception and motion detection based on binocular disparity have been realized by constructing two retinomorphic memristive arrays. The results demonstrated in this work provide a promising strategy to develop all-optically controlled memristor and promote the future development of binocular vision system with in-sensor architecture.

Sinomenine ameliorates bleomycin-induced pulmonary fibrosis by inhibiting the differentiation of fibroblast into myofibroblast.

Idiopathic pulmonary fibrosis (IPF) represents a severe interstitial lung disease characterized by limited therapeutic interventions. Recent study has suggested that sinomenine (SIN), an alkaloid derived from the roots of Sinomenium acutum, demonstrates efficacy in interrupting aerobic glycolysis, a predominant metabolic pathway in myofibroblasts. However, its pharmacological potential in the context of pulmonary fibrosis remains inadequately explored. In the present study, we established a bleomycin (BLM)-induced pulmonary fibrosis mouse model and subjected the mice to a one-week regimen of SIN treatment to assess its efficacy. Additionally, a TGF-ß1-induced primary lung fibroblast model was employed to investigate the molecular mechanism underlying the effects of SIN. Our observations revealed robust anti-pulmonary fibrosis properties associated with SIN treatment, as evidenced by reduced extracellular matrix deposition, diminished hydroxyproline contents, improved Ashcroft scores, and enhanced lung function parameters. Furthermore, SIN administration significantly impeded TGF-ß1-induced fibroblast-to-myofibroblast differentiation. Mechanistically, SIN exerted its beneficial effects by mitigating aerobic glycolysis, achieved through the inhibition of the expression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (Pfkfb3). Notably, the protective effects of SIN on fibroblasts were reversed upon ectopic overexpression of Pfkfb3. In conclusion, our data underscore the potential of SIN to attenuate fibroblast-to-myofibroblast differentiation by modulating Pfkfb3-associated aerobic glycolysis and SIN emerges as a promising anti-fibrotic agent for pulmonary fibrosis in clinical practice.

Logistic regression modeling of cytokines for cerebrospinal fluid evaluation in primary central nervous system lymphoma.

BACKGROUND: The diagnostic utility of cerebrospinal fluid (CSF) cytology encounters impediments stemming from variability in cell collection techniques and pathologists' morphological acumen, resulting in wide-ranging CSF positivity rates for primary central nervous system lymphomas (PCNSL). Such disparity impacts patient evaluation, treatment stratagem, and prognostication. Thus, this study endeavors to explore liquid biomarkers complementary to CSF cytology or immunophenotype analysis in the diagnosis of CSF involvement. METHODS: 398 newly diagnosed PCNSL patients were categorized into CSF involvement and non-involvement groups based on CSF cytology and immunophenotype analysis. Binary logistic regression analysis was performed on 338 patients to investigate factors predicting CSF involvement and to develop a joint prediction model. An additional cohort of 60 PCNSL patients was recruited for model validation. Statistical analyses included the Mann-Whitney U test for comparing various CSF parameters between two groups. ROC curve analyses were performed for each biomarker to identify PCNSL CSF involvement. RESULTS: The cytokine IL-10 level in CSF has emerged as the most promising biomarker for CSF evaluation, boasting an ROC AUC of 0.922. C-TNFα and soluble C-IL2R demonstrate efficacy in quantifying tumor burden within the CSF. Logistic regression identified C-IL10lg (OR = 30.103, P < 0.001), C-TNC (OR = 1.126, P < 0.001), C-IL2Rlg (OR = 3.743, P = 0.029) as independent predictors for CSF involvement, contributing to a joint predictive model with an AUC of 0.935, sensitivity of 74.1 %, and specificity of 93.0 %. Validation of the model in an independent cohort confirmed its effectiveness, achieving an AUC of 0.9713. CONCLUSIONS: The identification of these feasible biomarkers and the development of an accurate prediction model may facilitate the precise evaluation of CSF status in PCNSL, offering significant advancements in patient management.