Antifungal Potential and Mechanism of Bacillus velezensis HeN-7 Isolated from Tobacco Leaves on Bipolaris sorokiniana.

Wheat leaf blight caused by Bipolaris sorokiniana is a widespread fungal disease that poses a serious risk to wheat. Biological control without causing environmental pollution is one of the safest and most effective method to control plant diseases. The antagonistic bacterial strain HeN-7 (identified as Bacillus velezensis) was isolated from tobacco leaves cultivated in Henan province, China. The results of different concentrations of cell-free supernatant (CFS) from HeN-7 culture against B. sorokiniana mycelia showed that 20% HeN-7 CFS (v/v) reached the maximum inhibition rate of 96%. In the potted plants control assay, B. velezensis HeN-7 CFS exhibited remarkable biocontrol activity on the wheat infected with B. sorokiniana, the best pot control efficacy was 65% at 20% CFS. The research on the mechanism of action demonstrated that HeN-7 CFS induced the membrane lipid peroxidation in B. sorokiniana, leading to the disruption of cell membrane integrity and resulting in the leakage of cell contents; in addition, the intracellular mitochondrial membrane potential in mycelium dissipated and reactive oxygen species accumulated, thereby inhibiting the growth of B. sorokiniana. These results indicate that B. velezensis HeN-7 is a promising candidate as a biological control agent against Bipolaris sorokiniana infection.

Functional activities of three Rehmannia glutinosa enzymes: Elucidation of the Rehmannia glutinosa salidroside biosynthesis pathway in Saccharomyces cerevisiae.

Rehmannia glutinosa produces many phenylethanoid glycoside (PhG) compounds, including salidroside, which not only possesses various biological activities but also is a core precursor of some medicinal PhGs, so it is very important to elucidate the species' salidroside biosynthesis pathway to enhance the production of salidroside and its derivations. Although some plant copper-containing amine oxidases (CuAOs), phenylacetaldehyde reductases (PARs) and UDP-glucose glucosyltransferases (UGTs) are thought to be vital catalytic enzymes involved in the downstream salidroside biosynthesis pathways, to date, none of these proteins or the associated genes in R. glutinosa have been characterized. To verify a postulated R. glutinosa salidroside biosynthetic pathway starting from tyrosine, this study identified and characterized a set of R. glutinosa genes encoding RgCuAO, RgPAR and RgUGT enzymes for salidroside biosynthesis. The functional activities of these proteins were tested in vitro by heterologous expression of these genes in Escherichia coli, confirming these catalytic abilities in these corresponding reaction steps of the biosynthetic pathway. Importantly, four enzyme-encoding genes (including the previously reported RgTyDC2 encoding tyrosine decarboxylase and the RgCuAO1, RgPAR1 and RgUGT2 genes) were cointegrated into Saccharomyces cerevisiae to reconstitute the R. glutinosa salidroside biosynthetic pathway, achieving an engineered strain that produced salidroside and validating these enzymes' catalytic functions. This study elucidates the complete R. glutinosa salidroside biosynthesis pathway from tyrosine metabolism in S. cerevisiae, establishing a basic platform for the efficient production of salidroside and its derivatives.

Predictive role and molecular biological function of proline-rich small repeat protein SPRR3 in the diagnosis of lung adenocarcinoma.

The fascinating role of SPRR3 in various malignant tumors has prompted extensive research to unravel its expression patterns and prognostic significance. To comprehensively investigate SPRR3, we leveraged multiple datasets containing invaluable biomedical information, specifically focusing on the comparative analysis of SPRR3 gene expression levels across different cancer types. Meticulous examination of lung adenocarcinoma allowed us to delve deeper into the correlation between SPRR3 expression and its molecular biological functions. Our comprehensive analysis encompassed 33 malignant tumors, and the results unveiled significant differential expression of SPRR3 across a range of malignancies. Moreover, this aberrant expression of SPRR3 was observed to be closely associated with poorer prognosis in these malignant tumors. Notably, our investigation also unearthed a compelling link between SPRR3 and immune infiltrating cells in lung adenocarcinoma. The utilization of receiver operating characteristic (ROC) curves and survival curves in our study illustrated the immense potential of SPRR3 as a highly accurate predictor of cancer. These findings further emphasize the possibility of SPRR3 serving as a promising diagnostic and prognostic biomarker for a diverse array of cancers.

Clinicopathologic and prognostic implications of HOXA gene and its associated long-noncoding RNAs expression in non-small cell carcinoma: A meta-analysis.

BACKGROUND: We conducted an investigation into the correlation between HOXA and associated long-noncoding RNAs, along with their clinicopathologic and prognostic features in non-small cell lung cancer (NSCLC). METHODS: A comprehensive search across multiple electronic databases, including PubMed and the Web of Science, was conducted to identify relevant studies. The association between HOXA, clinicopathologic parameters, and prognosis was assessed using relative risk (RR) and hazard ratio (HR) with a 95% confidence interval (CI). Data compilation was performed using STATA 12.0 software. RESULTS: A total of 11 trials involving 2058 patients with NSCLC were included in our study. Significant correlations were observed between HOXA-AS2 and TNM stage (III-IV) (RR=2.173, 95% CI: 1.386-5.437, P< 0.05) and HOTTIP and age (≥60-year-old) (RR=2.628, 95% CI: 1.185-5.829, P< 0.05) and non-smoking (RR=0.387, 95% CI: 0.156-0.959, P< 0.05). The combined results indicated a significant association between HOXA5 and increased overall survival (HR = 0.69, 95% CI = 0.57-0.84, P < .001). Additionally, HOXA-AS2, HOXA11 and HOTTIP were identified as potential independent predictors for poorer OS (HOXA-AS2: HR =3.48, 95% CI = 1.95 to 6.21, P < 0.05; HOXA11: HR=1.39, 95%CI = 1.08 to 1.79, P < 0.05; HOTTIP: HR=2.44, 95%CI = 1.10 to 5.42, P < 0.05). The prognostic significance of HOXA1, HOXA3 and HOXA4 was uncertain (HOXA1: HR=1.40, 95% CI =0.28 to 7.06, P > 0.05; HOXA3: HR=1.20, 95% CI = 0.96 to 1.50, P > 0.05; HOXA4: HR=0.97, 95% CI = 0.77 to 1.23, P > 0.05). CONCLUSIONS: The HOXA gene family has some potential to emerge as a novel prognostic factor for NSCLC and is correlated with some clinicopathological parameters such as the TNM stage, age and smoking. However, further meticulously designed prospective studies are warranted to substantiate these findings.

Prime Editing of Vascular Endothelial Growth Factor Receptor 2 Attenuates Angiogenesis In Vitro.

Vascular endothelial growth factor receptor (VEGFR)-2 is a key switch for angiogenesis, which is observed in various human diseases. In this study, a novel system for advanced prime editing (PE), termed PE6h, is developed, consisting of dual lentiviral vectors: (1) a clustered regularly interspaced palindromic repeat-associated protein 9 (H840A) nickase fused with reverse transcriptase and an enhanced PE guide RNA and (2) a dominant negative (DN) MutL homolog 1 gene with nicking guide RNA. PE6h was used to edit VEGFR2 (c.18315T>A, 50.8%) to generate a premature stop codon (TAG from AAG), resulting in the production of DN-VEGFR2 (787 aa) in human retinal microvascular endothelial cells (HRECs). DN-VEGFR2 impeded VEGF-induced phosphorylation of VEGFR2, Akt, and extracellular signal-regulated kinase-1/2 and tube formation in PE6h-edited HRECs in vitro. Overall, our results highlight the potential of PE6h to inhibit angiogenesis in vivo.

Mechanism Insights into Allylic Hydroxylation versus Epoxidation of Propene Catalyzed by Model Catalyst Iron Phthalocyanine in the Presence of Hydrogen Peroxide.

High-valent metal-oxo species are key reactive intermediates in many biological and biological oxidation reactions. Herein, allylic hydroxylation (C-H) versus epoxidation (C═C) reactions of propene with a model catalyst iron phthalocyanine (FePc) in the presence of hydrogen peroxide were investigated contrastively, aiming to probe the active intermediates, structure-activity relationship, and reaction pathways. Our results showed that H2O2 as an oxygen-donor reagent can be easily decomposed on FePc to produce key active intermediates O═FePc and O═FePc═O with the energy barriers of 19.57 and 23.89 kcal/mol, respectively. In the selective oxidation of propene, O═FePc has a small preference for C═C epoxidation over C-H hydroxylation while O═FePc═O has a small preference for C-H hydroxylation. Since the electron-withdrawing O axial ligand in O═FePc═O further increases the radical character (Fe-O·) and Fe-O bond length of the iron-oxo moiety, O═FePc═O has better catalytic performance in both C═C epoxidation and C-H hydroxylation than O═FePc. Furthermore, in the whole reaction processes, the dual-hydrogen bonds between the two terminal H atoms of the alkene and allylic groups of propene and oxygen atom of the iron-oxo moiety would lead to the reaction toward C═C epoxidation while the single-hydrogen bond between the terminal H atom of the allylic group and the oxygen atom of the iron-oxo moiety would lead to the reaction toward C-H hydroxylation, implying that the weakly interacting hydrogen bonds affecting oxidation pathways also play a very important role in the regioselectivity of C═C epoxidation and C-H hydroxylation.

From crisis to cure: harnessing the potential of mycobacteriophages in the battle against tuberculosis.

Tuberculosis (TB) is a serious and fatal disease caused by Mycobacterium tuberculosis (Mtb). The World Health Organization reported an estimated 1.30 million TB-related deaths in 2022. The escalating prevalence of Mtb strains classified as being multi-, extensively, extremely, or totally drug resistant, coupled with the decreasing efficacies of conventional therapies, necessitates the development of novel treatments. As viruses that infect Mycobacterium spp., mycobacteriophages may represent a strategy to combat and eradicate drug-resistant TB. More exploration is needed to provide a comprehensive understanding of mycobacteriophages and their genome structure, which could pave the way toward a definitive treatment for TB. This review focuses on the properties of mycobacteriophages, their potential in diagnosing and treating TB, the benefits and drawbacks of their application, and their use in human health. Specifically, we summarize recent research on mycobacteriophages targeted against Mtb infection and newly developed mycobacteriophage-based tools to diagnose and treat diseases caused by Mycobacterium spp. We underscore the urgent need for innovative approaches and highlight the potential of mycobacteriophages as a promising avenue for developing effective diagnosis and treatment to combat drug-resistant Mycobacterium strains.

Diagnostic performance of Node-RADS score for mesorectal lymph node metastasis in rectal cancer.

PURPOSE: To explore the diagnostic performance of the Node-RADS scoring system on preoperative assessment of mesorectal lymph node metastasis (LNM) status in rectal cancer, in comparison with the ESGAR category and size of lymph node (LN). METHODS: Preoperative clinical and MRI data of 154 rectal adenocarcinoma patients treated with radical resection surgery were retrospectively analyzed. The differences in the clinical, pathological and imaging characteristics between the pN- and pN + groups were surveyed. The correlations of Node-RADS score and ESGAR category to pN stage, LNM number and lymph node ratio (LNR) were investigated. The performances on assessing pathological LNM were compared among individual approaches. A nomogram combined the imaging and clinical features was also established and evaluated. RESULTS: Significant differences in CEA, tumor maximum diameter, tumor location, LN short-axis diameter, Node-RADS score and ESGAR category were found between the pN- and pN + groups. Node-RADS correlated significantly with pN stage, LNM number, and LNR (r = 0.665, 0.685, and 0.675, p < 0.001). Node-RADS had the highest AUC (0.862) for predicting pN + status, surpassing ESGAR (AUC = 0.797, p = 0.040) and LN size (AUC = 0.762, p = 0.015). The nomogram had the best diagnostic performance (AUC = 0.901), significantly outperforming Node-RADS alone (p = 0.037). CONCLUSIONS: The Node-RADS scoring system is comparable to the ESGAR category and surpasses short-axis diameter in preoperatively predicting LNM in rectal cancer. Integrating imaging and clinical features will lead to an enhancement in diagnostic performance. Moreover, a clear relationship was demonstrated between the Node-RADS score and the quantity-dependent pathological characteristics of LNM.

Dapagliflozin improves skeletal muscle insulin sensitivity through SIRT1 activation induced by nutrient deprivation state.

Lipid peroxidation and mitochondrial damage impair insulin sensitivity in skeletal muscle. Sirtuin-1 (SIRT1) protects mitochondria and activates under energy restriction. Dapagliflozin (Dapa) is an antihyperglycaemic agent that belongs to the sodium-glucose cotransporter-2 (SGLT2) inhibitors. Evidence shows that Dapa can induce nutrient deprivation effects, providing additional metabolic benefits. This study investigates whether Dapa can trigger nutrient deprivation to activate SIRT1 and enhance insulin sensitivity in skeletal muscle. We treated diet-induced obese (DIO) mice with Dapa and measured metabolic parameters, lipid accumulation, oxidative stress, mitochondrial function, and glucose utilization in skeletal muscle. ß-hydroxybutyric acid (ß-HB) was intervened in C2C12 myotubes. The role of SIRT1 was verified by RNA interference. We found that Dapa treatment induced nutrient deprivation state and reduced lipid deposition and oxidative stress, improved mitochondrial function and glucose tolerance in skeletal muscle. The same positive effects were observed after ß-HB intervening for C2C12 myotubes, and the promoting effects on glucose utilization were diminished by SIRT1 RNA interference. Thus, Dapa promotes a nutrient deprivation state and enhances skeletal muscle insulin sensitivity via SIRT1 activation. In this study, we identified a novel hypoglycemic mechanism of Dapa and the potential mechanistic targets.

Enhancing predictive validity of motoric cognitive risk syndrome for incident dementia and all-cause mortality with handgrip strength: insights from a prospective cohort study.

Background: This study aimed to assess whether integrating handgrip strength (HGS) into the concept of motoric cognitive risk (MCR) would enhance its predictive validity for incident dementia and all-cause mortality. Methods: A cohort of 5, 899 adults from the Health and Retirement Study underwent assessments of gait speed, subjective cognitive complaints, and HGS were involved. Over a 10-year follow-up, biennial cognitive tests and mortality data were collected. Cox proportional hazard analyses assessed the predictive power of MCR alone and MCR plus HGS for incident dementia and all-cause mortality. Results: Patients with MCR and impaired HGS (MCR-HGS) showed the highest adjusted hazard ratios (AHR) for dementia (2.33; 95% CI, 1.49-3.65) and mortality (1.52; 95% CI, 1.07-2.17). Even patients with MCR and normal HGS (MCR-non-HGS) experienced a 1.77-fold increased risk of incident dementia; however, this association was not significant when adjusted for socioeconomic status, lifestyle factors, and medical conditions. Nevertheless, all MCR groups demonstrated increased risks of all-cause mortality. The inclusion of HGS in the MCR models significantly improved predictive discrimination for both incident dementia and all-cause mortality, as indicated by improvements in the C-statistic, integrated discrimination improvement (IDI) and net reclassification indices (NRI). Conclusion: Our study underscores the incremental predictive value of adding HGS to the MCR concept for estimating risks of adverse health outcomes among older adults. A modified MCR, incorporating HGS, could serve as an effective screening tool during national health examinations for identifying individuals at risk of dementia and mortality.

Prognostic value of lung immune prognostic index in non-small cell lung cancer patients receiving immune checkpoint inhibitors: a meta-analysis.

Background and Purpose: Until now, it has been difficult to accurately predict the efficacy of immunotherapy in patients with non-small cell lung cancer (NSCLC). A novel indicator, the lung immune prognostic index (LIPI), has shown relatively high prognostic value in patients with solid cancer. Therefore, this study aimed to further identify the association between LIPI and the survival of patients with NSCLC who receive immune checkpoint inhibitors (ICIs). Methods: Several electronic databases were searched for available publications up to April 23, 2023. Immunotherapy outcomes included overall survival (OS), progression-free survival (PFS), and hazard ratios (HRs) with 95% confidence intervals (CIs). Subgroup analysis based on the study design and comparison of the LIPI was conducted. Results: In this meta-analysis, 21 studies with 9,010 patients were included in this meta-analysis. The pooled results demonstrated that elevated LIPI was significantly associated with poor OS (HR = 2.50, 95% CI:2.09-2.99, p < 0.001) and PFS (HR = 1.77, 95% CI:1.64-1.91, p < 0.001). Subgroup analyses stratified by study design (retrospective vs. prospective) and comparison of LIPI (1 vs. 0, 2 vs. 0, 1-2 vs. 0, 2 vs. 1 vs. 0, 2 vs. 0-1 and 2 vs. 1) showed similar results. Conclusion: LIPI could serve as a novel and reliable prognostic factor in NSCLC treated with ICIs, and elevated LIPI predicts worse prognosis.

Exploitation of enhanced prime editing for blocking aberrant angiogenesis.

INTRODUCTION: Aberrant angiogenesis plays an important part in the development of a variety of human diseases including proliferative diabetic retinopathy, with which there are still numerous patients remaining a therapeutically challenging condition. Prime editing (PE) is a versatile gene editing approach, which offers a novel opportunity to genetically correct challenging disorders. OBJECTIVES: The goal of this study was to create a dominant-negative (DN) vascular endothelial growth factor receptor (VEGFR) 2 by editing genomic DNA with an advanced PE system to block aberrant retinal angiogenesis in a mouse model of oxygen-induced retinopathy. METHODS: An advanced PE system (referred to as PE6x) was established within two lentiviral vectors, with one carrying an enhanced PE guide RNA and a canonical Cas9 nickase fused with an optimized reversal transcriptase, and the other conveying a nicking guide RNA and a DN-MLH1 to improve PE efficiency. Dual non-integrating lentiviruses (NILVs) produced with the two lentiviral PE6x vectors were then employed to create a mutation of VEGFR2 T17967A by editing the Mus musculus VEGFR2 locus in vitro and in vivo, leading to generation of a premature stop codon (TAG, K796stop) to produce DN-VEGFR2, to interfere with the wild type VEGFR2 which is essential for angiogenesis. RESULTS: NILVs targeting VEGFR2 delivered into cultured murine vascular endothelial cells led to 51.06 % VEGFR2 T17967A in the genome analyzed by next generation sequencing and the production of DN-VEGFR2, which was found to hamper VEGF-induced VEGFR2 phosphorylation, as demonstrated by Western blot analysis. Intravitreally injection of the dual NILVs into postnatal day 12 mice in a model of oxygen-induced retinopathy, led to production of retinal DN-VEGFR2 in postnatal day 17 mice which blocked retinal VEGFR2 expression and activation as well as abnormal retinal angiogenesis without interfering with retinal structure and function, as assessed by electroretinography, optical coherence tomography, fundus fluorescein angiography and histology. CONCLUSION: DN-VEGFR2 resulted from editing genomic VEGFR2 using the PE6x system can be harnessed to treat intraocular pathological angiogenesis.

Intermittent protein restriction before but not after the onset of diabetic kidney disease attenuates disease progression in mice.

Background: High dietary protein intake exacerbates proteinuria in individuals with diabetic kidney disease (DKD). However, studies on the impacts of low protein diet (LPD) on DKD have yielded conflicting results. Furthermore, patient compliance to continuous protein restriction is challenging. Objective: The current study aims to investigate the effects of intermittent protein restriction (IPR) on disease progression of DKD. Methods: Diabetic KK-Ay mice were used in this study. For the IPR treatment, three consecutive days of LPD were followed by four consecutive days of normal protein diet (NPD) within each week. For early intervention, mice received IPR before DKD onset. For late intervention, mice received IPR after DKD onset. In both experiments, age-matched mice fed continuous NPD served as the control group. Kidney morphology, structure and function of mice in different groups were examined. Results: Intermittent protein restriction before DKD onset ameliorated pathological changes in kidney, including nephromegaly, glomerular hyperfiltration, tubular injuries and proteinuria, without improving glycemic control. Meanwhile, IPR initiated after DKD onset showed no renoprotective effects despite improved glucose homeostasis. Conclusion: Intermittent protein restriction before rather than after DKD onset protects kidneys, and the impacts of IPR on the kidneys are independent of glycemic control. IPR shows promise as an effective strategy for managing DKD and improving patient compliance.

Establishment of the Diagnostic Signature of Ferroptosis Genes in Multiple Sclerosis.

Ferroptosis is a novel form of membrane-dependent cell death that differs from other cell death modalities such as necrosis, apoptosis, and autophagy. Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system primarily affecting brain and spinal cord neurons. Although the pathogenesis of these two conditions may seem unrelated, recent studies have indicated a connection between ferroptosis and multiple sclerosis. In fact, ferroptosis plays a significant role in the development of MS, as evidenced by the presence of elevated iron levels and iron metabolism abnormalities in the brains, spinal cords, and other neurons of MS patients. These abnormalities disrupt iron homeostasis within cells, leading to the occurrence of ferroptosis. However, there is currently a lack of research on the diagnostic value of ferroptosis-related genes in multiple sclerosis. In this study, we employed bioinformatics methods to identify ferroptosis-related genes (ATM, GSK3B, HMGCR, KLF2, MAPK1, NFE2L1, NRAS, PCBP1, PIK3CA, RPL8, VDAC3) associated with the diagnosis of multiple sclerosis and constructed a diagnostic model. The results demonstrated that the diagnostic model accurately identified the patients' condition. Subsequently, subgroup analysis was performed based on the expression levels of ferroptosis-related genes, dividing patients into high and low expression groups. The results showed differences in immune function and immune cell infiltration between the two groups. Our study not only confirms the correlation between ferroptosis and multiple sclerosis but also demonstrates the diagnostic value of ferroptosis-related genes in the disease. This provides guidance for clinical practice and direction for further mechanistic research.

Diagnostic performance of Node Reporting and Data System (Node-RADS) for assessing mesorectal lymph node in rectal cancer by CT.

BACKGROUND: To compare the diagnostic performance of the Node-RADS scoring system and lymph node (LN) size in preoperative LN assessment for rectal cancer (RC), and to investigate whether the selection of size as the primary criterion whereas morphology as the secondary criterion for LNs can be considered the preferred method for clinical assessment. METHODS: Preoperative CT data of 146 RC patients treated with radical resection surgery were retrospectively analyzed. The Node-RADS score and short-axis diameter of size-prioritized LNs and the morphology-prioritized LNs were obtained. The correlations of Node-RADS score to the pN stage, LNM number and lymph node ratio (LNR) were investigated. The performances on assessing pathological lymph node metastasis were compared between Node-RADS score and short-axis diameter. A nomogram combined the Node-RADS score and clinical features was also evaluated. RESULTS: Node-RADS score showed significant correlation with pN stage, LNM number and LNR (Node-RADS of size-prioritized LN: r = 0.600, 0.592, and 0.606; Node-RADS of morphology-prioritized LN: r = 0.547, 0.538, and 0.527; Node-RADSmax: r = 0.612, 0.604, and 0.610; all p < 0.001). For size-prioritized LN, Node-RADS achieved an AUC of 0.826, significantly superior to short-axis diameter (0.826 vs. 0.743, p = 0.009). For morphology-prioritized LN, Node-RADS exhibited an AUC of 0.758, slightly better than short-axis diameter (0.758 vs. 0.718, p = 0.098). The Node-RADS score of size-prioritized LN was significantly better than that of morphology-prioritized LN (0.826 vs. 0.758, p = 0.038). The nomogram achieved the best diagnostic performance (AUC = 0.861) than all the other assessment methods (p < 0.05). CONCLUSIONS: The Node-RADS scoring system outperforms the short-axis diameter in predicting lymph node metastasis in RC. Size-prioritized LN demonstrates superior predictive efficacy compared to morphology-prioritized LN. The nomogram combined the Node-RADS score of size-prioritized LN with clinical features exhibits the best diagnostic performance. Moreover, a clear relationship was demonstrated between the Node-RADS score and the quantity-dependent pathological characteristics of LNM.

Correlation between vertebral bone mineral density and multi-level virtual non-calcium imaging parameters from dual-layer spectral detector computed tomography.

Background: Virtual non-calcium (VNCa) imaging based on dual-energy computed tomography (CT) plays an increasingly important role in diagnosing spinal diseases. However, the utility of VNCa technology in the measurement of vertebral bone mineral density (BMD) is limited, especially the VNCa CT value at multiple calcium suppression levels and the slope of VNCa curve. This retrospective cross-sectional study aimed to explore the correlation between vertebral BMD and new VNCa parameters from dual-layer spectral detector CT. Methods: The dual-layer spectral detector CT and quantitative CT (QCT) data of 4 hydroxyapatite (HAP) inserts and 667 vertebrae of 234 patients (132 male and 102 female) who visited a university teaching hospital between April and May 2023 were retrospectively analyzed. The BMD values of 3 vertebrae (T12, L1, and L2) and inserts were measured using QCT, defined as QCT-BMD. The VNCa CT values and the slope λ of the VNCa attenuation curve of vertebrae and inserts were recorded. The correlations between VNCa parameters (VNCa CT value, slope λ) and QCT-BMD were analyzed. Results: For the vertebrae, the correlation coefficient ranged from -0.904 to 0.712 (all P<0.05). As the calcium suppression index (CaSI) increased, the correlation degree exhibited a decrease first and then increased, with the best correlation (r=-0.904, P<0.001) observed at the index of 25%. In contrast, the correlation coefficient for the inserts remained relatively stable (r=-0.899 to -1, all P<0.05). For the vertebrae, the values of 3 slopes λ (λ1, λ2, and λ3) derived from the VNCa attenuation curve were 6.50±1.99, 3.75±1.15, and 2.04±0.62, respectively. Regarding the inserts, the λ1, λ2, and λ3 values were 11.56 [interquartile range (IQR): 2.40-22.62], 6.68 (IQR: 1.39-13.49), and 3.63 (IQR: 0.75-7.8), respectively. For the vertebrae, all 3 correlation coefficients between 3 slopes λ and QCT-BMD were 0.956 (all P<0.05). For the inserts, the 3 correlation coefficients were 0.996, 0.998, and 1 (all P<0.05), respectively. Conclusions: A promising correlation was detected between VNCa CT parameters and QCT-BMD in vertebrae, warranting further investigation to explore the possibility of VNCa imaging to assess BMD.

A nomogram combining CT-based radiomic features with clinical features for the differentiation of benign and malignant cystic pulmonary nodules.

BACKGROUND: Currently, the differentiation between benign and malignant cystic pulmonary nodules poses a significant challenge for clinicians. The objective of this retrospective study was to construct a predictive model for determining the likelihood of malignancy in patients with cystic pulmonary nodules. METHODS: The current study involved 129 patients diagnosed with cystic pulmonary nodules between January 2017 and June 2023 at the Neijiang First People's Hospital. The study gathered the clinical data, preoperative imaging features of chest CT, and postoperative histopathological results for both cohorts. Univariate and multivariate logistic regression analyses were employed to identify independent risk factors, from which a prediction model and nomogram were developed. In addition, The model's performance was assessed through receiver operating characteristic (ROC) curve analysis, calibration curve analysis, and decision curve analysis (DCA). RESULTS: A cohort of 129 patients presenting with cystic pulmonary nodules, consisting of 92 malignant and 37 benign lesions, was examined. Logistic data analysis identified a cystic airspace with a mural nodule, spiculation, mural morphology, and the number of cystic cavities as significant independent predictors for discriminating between benign and malignant cystic lung nodules. The nomogram prediction model demonstrated a high level of predictive accuracy, as evidenced by an area under the ROC curve (AUC) of 0.874 (95% CI: 0.804-0.944). Furthermore, the calibration curve of the model displayed satisfactory calibration. DCA proved that the prediction model was useful for clinical application. CONCLUSION: In summary, the risk prediction model for benign and malignant cystic pulmonary nodules has the potential to assist clinicians in the diagnosis of such nodules and enhance clinical decision-making processes.

Export priority technique for Uni-portal thoracoscopic left upper lobectomy.

BACKGROUND: Further explore the safety and feasibility of Uni-portal video assisted thoracoscopic (UVATS) left upper lobectomy by optimizing the treatment of incisions and blood vessels. METHODS: We conducted a retrospective analysis of data from 32 patients who underwent UVATS left upper lobectomy and systematic mediastinal lymph node dissection utilizing the Export priority technique between January 2021 and December 2022. We documented perioperative indicators, including surgical time, intraoperative blood loss, the number of lymph nodes dissected, and postoperative pathological staging. RESULTS: All surgeries were conducted utilizing the Export priority technique in UVATS. The mean surgical duration was (98.93 ± 14.98) minutes, with an average intraoperative blood loss of (79.53 ± 37.96) ml. The mean count of dissected lymph nodes was (13.96 ± 2.69). The length of hospital Stay averaged (5.62 ± 1.81) days. On the first postoperative day, the thoracic drainage volume was (101.87 ± 49.46) ml. The mean duration of postoperative thoracic tube insertion was (3.1 ± 1.84) days. No occurrences of postoperative hoarseness, pulmonary infection, or complications such as bronchopleural fistula were observed. CONCLUSION: The application of the Export priority technique improves the safety and feasibility of UVATS left upper lobectomy.

Comparative Analysis of the Anti-Inflammatory Effects of Liraglutide and Dulaglutide.

Inflammation plays a pathophysiological role in atherosclerosis and its clinical consequences. In addition to glycemic control, glucagon-like peptide-1 receptor agonists (GLP-1RAs) are of wide concern for cardioprotective effects. The structure, half-life, homology, and clinical efficacy of GLP-1RAs exhibit remarkable disparity. Several studies have compared the disparities in anti-inflammatory effects between daily and weekly GLP-1RAs. This study aimed to compare the similarities and differences between liraglutide and dulaglutide in terms of inhibiting atherosclerotic inflammation and improving co-cultured endothelial cell function. The expression of inflammation markers was examined by immunofluorescence, Western blotting, and real-time PCR. The tube-forming ability of endothelial cells was tested on Matrigel. The results verify that 10/50/100 nmol/L liraglutide and 100 nmol/L dulaglutide markedly suppressed the expression of inflammatory factors in LPS-induced atherosclerosis after 24 and 72 hours, respectively. Moreover, they promoted the polarization of M1 macrophages toward the M2 phenotype and improved the function of co-cultured endothelial cells. Both liraglutide and dulaglutide ameliorate atherosclerosis development. The difference between the two resided in the extended intervention duration required to observe the effect of dulaglutide, and liraglutide demonstrated a superior dose-dependent manner. We provide a potential strategy to understand the dynamics of drug action and possible timing administration.