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Often there is the need of moving endodontically treated teeth. Orthodontic movement may have no effect on the prognosis of teeth with root canal treatment (RCT). To verify this subject, we evaluated the effect of orthodontic movement on the prognosis of RCT teeth using cone-beam computed tomography (CBCT) and further explored the influence of orthodontic movement on the prognosis of RCT teeth with and without apical periodontitis (AP). This retrospective study was conducted by evaluating 169 RCT teeth of 100 patients who had undergone fixed orthodontic treatment. AP was assessed and classified using the CBCT periapical index. Univariate analysis of RCT outcome was performed for the total RCT group, RCT without AP group and RCT with AP group. Multivariate logistic regression was performed for the total RCT group and RCT without AP group, respectively, but not for the RCT with AP group. Variables related to the prognosis of RCT were included, such as age, gender, tooth position, RCT quality, coronal restoration quality, periodontal condition, orthodontic traction distance, and orthodontic rotation angle. The orthodontic traction distance and rotation angle were not significantly correlated to the RCT outcomes, regardless of the presence of AP. Among the total RCT group, teeth with unqualified RCT (odds ratio = 3.42, P =.004) and inadequate coronal restoration (odds ratio = 4.40, P =.031) had a lower success rate. Of the 97 RCT teeth without AP, unqualified RCT was a risk factor for treatment failure (odds ratio = 3.55, P =.041). Of the 72 RCT teeth with AP, the univariate analysis showed that RCT quality were significantly related to the outcome (P =.042). Orthodontic movement had no effect on the prognosis of RCT teeth regardless of the presence of AP. [ABSTRACT FROM AUTHOR]

This study investigates the biomass and carbon fixation rate of Chlorella sp. by the main valuable elements in converter steel slag in F/2 seawater medium. The results indicate that Ca, Mg, P, Si, Fe, and Mn can increase the biomass and carbon fixation rate of Chlorella sp. , while Cu, Zn, Cr, and Al can decrease the biomass and carbon fixation rate of Chlorella sp.. Three machine learning methods known as Back Propagation neural network (BPNN), decision tree (DT), and random forest (RF) were applied to construct the prediction model for the carbon fixation rate of Chlorella sp. based on real-life experimental data obtained from single factor experiments. The overall results exhibited that the BPNN model is better than the DT model and RF model to predict the carbon fixation rate of Chlorella sp.. Finally, the maximum carbon fixation rate for Chlorella sp. predicted by BPNN model is 50.86 mg/(L·d), which was 2.46 times that of the control group, under the optimum conditions of Ca 5.77 g/L, Mg 4.74 g/L, P 1.27 g/L, Si 6.31×10−1 g/L, Fe 6.50×10−4 g/L, Mn 5.00×10−5 g/L, Cu 2.51×10−6 g/L, Zn 4.98×10−6 g/L, Cr 0 g/L, and Al 0 g/L in F/2 seawater medium. [ABSTRACT FROM AUTHOR]

Glioma is the most prevailing main malignant neoplasm of the central nervous system with a miserable prognosis. Temozolomide is the first-line chemotherapy drug for glioma, but its drug resistance reduces temozolomide's clinical efficacy and becomes the principal cause of the failure of glioma chemotherapy. Polyphyllin I (PPI), an active component in Rhizoma Paridis, demonstrates favorable therapeutic actions in diverse malignant neoplasms. Its effect on temozolomide-resistant glioma, however, has not yet been characterized. Here, we demonstrated that polyphyllin I inhibited the proliferation of temozolomide-resistant glioma cell in a concentration-dependent manner. Further, we found that polyphyllin I had a direct effect on temozolomide-resistant glioma tumor cells and promote reactive oxygen species (ROS)-dependent apoptosis and autophagy via mitogen-activated protein kinase (MAPK)-signaling (p38-JNK) pathway. Mechanistically, we showed that polyphyllin I downregulate the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway, indicating that polyphyllin I may be an expected therapeutic strategy for patients with temozolomide-resistant gliomas. [ABSTRACT FROM AUTHOR]

• Most studies (13/20) supported unhealthy food environments as a risk factor of CVD. • Healthy food environments were positively linked with CVD in 3 out of 7 studies. • The relationship between comprehensive food environments and CVD was inconsistent. • Future studies should examine food environments and CVD in developing countries. Cardiovascular disease (CVD) is the leading cause of death worldwide, particularly affecting low- and middle-income countries. Food environments may be linked with the risk of CVD; however, current study findings regarding their relationship are inconsistent. A systematic review of their associations is needed to guide interventions to improve cardiovascular health. This systematic review aimed to comprehensively assess the relationship between food environments and CVD outcomes, including incidence, hospitalization, mortality, and recurrence rates. According to PRISMA guidelines, a systematic search was conducted until 28th March 2024, using eight databases, including PubMed, Embase, Ovid, CINAHL, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI), and Wanfang Data. The review quality was assessed according to the Agency for Healthcare Research and Quality (AHRQ) and Newcastle-Ottawa Scale (NOS). The included studies were categorized based on their exposure factors into unhealthy, healthy, and comprehensive food environments, encompassing facilities that offer healthy and unhealthy foods. The findings were narratively synthesized according to this classification. A total of 23 studies, encompassing 13 cross-sectional studies and 10 cohort-longitudinal studies, were included in this review. Among the 20 studies on unhealthy food environments, 13 found a positive association with CVD outcomes. Of the seven studies on healthy food environments, 3 found a negative association with CVD outcomes. Additionally, 4 out of 8 studies on comprehensive food environments found a significant but inconsistent association with CVD outcomes. This study suggested that unhealthy food environments are probably associated with CVD outcomes. At the same time, there is currently no conclusive evidence to indicate a relationship between healthy food environments or comprehensive food environments and CVD outcomes. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) is restricted due to its severe cardiotoxicity. There is still a lack of viable and effective drugs to prevent or treat DOX-induced cardiotoxicity(DIC). Vericiguat is widely used to treat heart failure with reduced ejection fraction. However, it is not clear whether vericiguat can improve DIC. In the present study, we constructed a DIC model using mice and neonatal rat cardiomyocytes and found that vericiguat ameliorated DOX-induced cardiac insufficiency in mice, restored DOX-induced mitochondrial dysfunction in neonatal rat cardiomyocytes, and inhibited the expression of inflammatory factors. Further studies showed that vericiguat improved mitochondrial dysfunction and reduced mtDNA leakage into the cytoplasm by up-regulating PRKG1, which activated PINK1 and then inhibited the STING/IRF3 pathway to alleviate DIC. These findings demonstrate for the first time that vericiguat has therapeutic potential for the treatment of DIC. The model illustrated that DOX inhibited PRKG1, PINK1 and PARKIN expression in the heart and activated STING/INF3 signaling pathway, leading to myocardial inflammation and cardiac dysfunction. Vericiguat alleviated myocardial inflammation and cardiac dysfunction by activating PRKG1, promoting PINK1 and PARKIN expression, inhibiting STING/INF3 signaling pathway, and improving mitochondrial function [Display omitted]. [ABSTRACT FROM AUTHOR]

Microbiota and feeding modes influence the susceptibility of premature newborns to necrotizing enterocolitis (NEC) through mechanisms that remain unknown. Here, we show that microbiota colonization facilitated by breastmilk feeding promotes NOD-like receptor family CARD domain containing 5 (Nlrc5) gene expression in mouse intestinal epithelial cells (IECs). Notably, inducible knockout of the Nlrc5 gene in IECs predisposes neonatal mice to NEC-like injury in the small intestine upon viral inflammation in an NK1.1+ cell-dependent manner. By contrast, formula feeding enhances neonatal gut colonization with environment-derived tilivalline-producing Klebsiella spp. Remarkably, tilivalline disrupts microbiota-activated STAT1 signaling that controls Nlrc5 gene expression in IECs through a PPAR-γ-mediated mechanism. Consequently, this dysregulation hinders the resistance of neonatal intestinal epithelium to self-NK1.1+ cell cytotoxicity upon virus infection/colonization, promoting NEC development. Together, we discover the underappreciated role of intestinal microbiota colonization in shaping a disease tolerance program to viral inflammation and elucidate the mechanisms impacting NEC development in neonates. [Display omitted] • Breastmilk-fed gut microbiota sparks STAT1 to shift IECs into an NLRC5highTAP1high state • Formula feeding enhances tilivalline (TV)-producing Klebsiella spp. colonization • TV confers IECs with an NLRC5lowTAP1low state via PPAR-γ-mediated STAT1 inhibition • NLRC5lowTAP1low IECs are killed by self-NK cells upon viral inflammation, leading to NEC Subramanian, Geng, and colleagues discover that formula-feeding facilitates neonatal gut colonization with environment-derived tilivalline-producing Klebsiella spp., which impedes STAT1-NLRC5 axis maturation in intestinal epithelial cells through tilivalline-induced PPAR-γ activation. This dysregulation causes the epithelium to lose resistance to autologous NK cell cytotoxicity, leading to necrotizing enterocolitis (NEC) during virus colonization/infection. [ABSTRACT FROM AUTHOR]

South Asia and Southeast Asia are the regions with relatively high and increased disease burden of oral cancer. The purpose of this study was to analyze the scientometric characteristics of oral cancer research in these regions. There are 8 countries from South Asia and 11 countries from Southeast Asia. All the articles on oral cancer from these countries were retrieved in the Scopus database. A total of 5660 articles originated from South Asia (n = 4718) and Southeast Asia (n = 942). India (n = 4302; 91.2%) was the country publishing most articles on oral cancer in South Asia, and Malaysia (n = 355; 37.7%) was first in Southeast Asia. Tobacco smoking, alcohol consumption, and areca nut as risk factors were common keywords, attention should be paid to them while developing polices for oral cancer control. In India, the most topic including distinctive keywords was diagnostics (sensitivity/specificity, saliva, and predictive value), followed by molecular biology (antioxidants, lipid peroxidation, and glutathione), experimental in vivo (hamster and cheek pouch), and risk factor (smokeless tobacco). In Malaysia, the most topic containing keywords was molecular biology followed by epidemiology and drug research. This study for the first time reported the scientometric characteristics of oral cancer research in South Asia (India) and Southeast Asia (Malaysia). It is essential to improve the public awareness of risk factors control to reduce the oral cancer burden, especially in low-and middle-income countries. [ABSTRACT FROM AUTHOR]

Quantitative in vitro research was conducted on the learning process of a dynamic navigation system. This study provides guidance for the promotion and application of dynamic navigation technology in the endodontic apical surgery field. Standardized models were designed and 3D printed to form the approach operation of endodontic apical surgery. 6 clinicians with no experience in dynamic navigation performed the operation. The distance deviation tolerance was set as 0.6 mm, and the angle deviation tolerance was set as 5°. Fifteen mm deep approach operation was completed using dynamic navigation. Each operator performed 10 consecutive exercises on the models. The positioning deviation and operation time of each operator for each practice were recorded. Based on this, the learning curve of the dynamic navigation of every operator was mapped. The learning difficulty of dynamic navigation was evaluated. The learning curves of all operators reached a stable level after the 7th practice, which can ensure that the distance and angle deviations are maintained within the deviation tolerances (0.6 mm, 5°). Operators with no experience in dynamic navigation technology need practice to master dynamic navigation operations. For this navigation system, operators with no operational experience can master dynamic navigation operations after 7 exercises. [ABSTRACT FROM AUTHOR]

We aimed to evaluate clinical characteristics and quantitative CT imaging features for the prediction of liver metastases (LMs) in patients with pancreatic neuroendocrine tumors (PNETs). Patients diagnosed with pathologically confirmed PNETs were included, 133 patients were in the training group, 22 patients in the prospective internal validation group, and 28 patients in the external validation group. Clinical information and quantitative features were collected. The independent variables for predicting LMs were confirmed through the implementation of univariate and multivariate logistic analyses. The diagnostic performance was evaluated by conducting receiver operating characteristic curves for predicting LMs in the training and validation groups. PNETs with LMs demonstrated significantly larger diameter and lower arterial/portal tumor-parenchymal enhancement ratio, arterial/portal absolute enhancement value (AAE/PAE value) (p < 0.05). After multivariate analyses, A high level of tumor marker (odds ratio (OR): 5.32; 95% CI, 1.54–18.35), maximum diameter larger than 24.6 mm (OR: 7.46; 95% CI, 1.70–32.72), and AAE value ≤ 51 HU (OR: 4.99; 95% CI, 0.93–26.95) were independent positive predictors of LMs in patients with PNETs, with area under curve (AUC) of 0.852 (95%CI, 0.781–0.907). The AUCs for prospective internal and external validation groups were 0.883 (95% CI, 0.686–0.977) and 0.789 (95% CI, 0.602–0.916), respectively. Tumor marker, maximum diameter and absolute enhancement value in arterial phase were independent predictors with good predictive performance for the prediction of LMs in patients with PNETs. Combining clinical and quantitative features may facilitate the attainment of good predictive precision in predicting LMs. [ABSTRACT FROM AUTHOR]

• PAFAH1B1, also known as LIS1, is associated with type I lissencephaly in humans, which is a severe developmental brain disorder believed to result from abnormal neuronal migration. • The aim of this present study is to elucidate the phenotypic presentations and molecular genetic characteristics of PAFAH1B1-related epilepsy in a Chinese cohort. • Notably, the clinical presentation in patients with PAFAH1B1 gene variants exhibits heterogeneity, and this heterogeneity is associated with the specific type of variant. PAFAH1B1, also known as LIS1, is associated with type I lissencephaly in humans, which is a severe developmental brain disorder believed to result from abnormal neuronal migration. Our objective was to characterize the genotypes and phenotypes of PAFAH1B1-related epilepsy. We conducted a comprehensive analysis of the medical histories, magnetic resonance imaging findings, and video-electroencephalogram recordings of 11 patients with PAFAH1B1 variants at the Neurology Department of Beijing Children's Hospital from June 2017 to November 2022. The age of onset of epilepsy ranged from 2 months to 4 years, with a median onset age of 5 months. Among these 11 patients (comprising 6 boys and 5 girls), all were diagnosed with lissencephaly type 1. Predominantly, generalized tonic-clonic and spasm seizures characterized PAFAH1B1-related epilepsy. Additionally, 10 out of the 11 patients exhibited severe developmental disorders. All patients exhibited de novo variants, with three individuals displaying 17p13.3 deletions linked to haploinsufficiency of PAFAH1B1. Four variants were previously unreported. Notably, three patients with 17p13.3 deletions displayed developmental delay and drug resistant epilepsy, whereas the single patient with mild developmental delay, Intelligence Quotient (IQ) 57 and well-controlled seizures had a splicing-site variant. The severity of the phenotype in patients with PAFAH1B1 variants ranged from drug-responsive seizures to severe epileptic encephalopathy. These observations underscore the clinical heterogeneity of PAFAH1B1-related disorders, with most patients exhibiting developmental disorders. Moreover, the severity of epilepsy appears to be linked to genetic variations. [ABSTRACT FROM AUTHOR]