The development and validation of a nomogram-based risk prediction model for mortality among older adults.

Objective: This research aims to construct and authenticate a comprehensive predictive model for all-cause mortality, based on a multifaceted array of risk factors. Methods: The derivation cohort for this study was the Chinese Longitudinal Healthy Longevity Survey (CLHLS), while the Healthy Ageing and Biomarkers Cohort Study (HABCS) and the China Health and Retirement Longitudinal Study (CHARLS) were used as validation cohorts. Risk factors were filtered using lasso regression, and predictive factors were determined using net reclassification improvement. Cox proportional hazards models were employed to establish the mortality risk prediction equations, and the model's fit was evaluated using a discrimination concordance index (C-index). To evaluate the internal consistency of discrimination and calibration, a 10x10 cross-validation technique was employed. Calibration plots were generated to compare predicted probabilities with observed probabilities. The prediction ability of the equations was demonstrated using nomogram. Results: The CLHLS (mean age 88.08, n = 37074) recorded 28158 deaths (179683 person-years) throughout the course of an 8-20 year follow-up period. Additionally, there were 1384 deaths in the HABCS (mean age 86.74, n = 2552), and 1221 deaths in the CHARLS (mean age 72.48, n = 4794). The final all-cause mortality model incorporated demographic characteristics like age, sex, and current marital status, as well as functional status indicators including cognitive function and activities of daily living. Additionally, lifestyle factors like past smoking condition and leisure activities including housework, television viewing or radio listening, and gardening work were included. The C-index for the derivation cohort was 0.728 (95% CI: 0.724-0.732), while the external validation results for the CHARS and HABCS cohorts were 0.761 (95% CI: 0.749-0.773) and 0.713 (95% CI: 0.697-0.729), respectively. Conclusion: This study introduces a reliable, validated, and acceptable mortality risk predictor for older adults in China. These predictive factors have potential applications in public health policy and clinical practice.

Plasma neuron specific enolase (NSE), tumour necrosis factor-alpha (TNF-α) and soluble IL-2 receptor alpha (sIL-2Rα) levels in children with developmental delay (DD): Use of combined ROC curves to increase their diagnostic value.

BACKGROUND: Developmental delay (DD) occurs when children fail to reach developmental milestones in comparison to peers of the same age range. However, there are no valuable biomarkers for the early diagnosis of DD. Since there is no specific marker for screening the disease, we evaluated plasma NSE, TNF-α and sIL2-Rα as potential markers for this purpose. METHODS: In this cross-sectional randomized case-control study, a total of 174 DD patients and 49 matched elderly controls aged between 2 months and 60 months were recruited. A sensitive enzyme-linked immunosorbent assay and an immunoradiometric assay were used to evaluate the levels of plasma IL-1, IL-6, IL-8, IL-10, sIL2-Rα, TNF-α, and NSE. Statistical analyses using t test, χ2, ANOVA, ROC curves and binary logistic regression models were performed. RESULTS: In comparison to the control group, the DD group had greater levels of NSE, TNF-α, and sIL2-Rα(p < 0.05). In the binary logistic regression analysis of DD, NSE had an odds ratio (OR) of 1.783 (95 % CI 1.297 to 2.451, p = 0.000), indicating that NSE was an independent risk factor for DD. The plasma TNF-α level was positively correlated with plasma NSE and sIL2-Rα levels in the DD group (r = 0.366 and 0.433, respectively), and the DQ score and plasma sIL2-Rα level in the DD group were positively correlated. The ROC curve revealed that the respective areas under the NSE, TNF-α, and sIL2-Rα ROC curves were 0.9797, 0.9365, and 0.8533, respectively. Moreover, a significant increase in AUC was observed using combined ROC curve analysis. CONCLUSIONS: Children with DD have significantly altered plasma concentrations of sIL2-Rα, NSE, and TNF-α. NSE, TNF-α and sIL2-Rα can be used as DD blood biomarkers. This information may be helpful in early diagnosis and intervention.

[Traditional Chinese therapy in the treatment of ICU-acquired weakness: a Meta-analysis].

OBJECTIVE: To systematically assess the efficacy of traditional Chinese therapy in the treatment of ICU-acquired weakness (ICU-AW). METHODS: PubMed, Cochrane Library, Embase, Web of Science, CNKI, Wanfang, VIP were retrieved by computer and were used to collect a randomized controlled trials (RCT) of traditional Chinese therapy for ICU-AW. The retrieval time was from databases establishment to December 2021. After 2 researchers independently screened the literature, extracted data and evaluated the risk of bias included in the study, and RevMan 5.4 software was used for Meta-analysis. RESULTS: 334 articles were selected, totally 13 clinical studies and 982 patients were included, including 562 in the trial group and 420 in the control group. Meta-analysis results showed that traditional Chinese therapy could improve clinical efficacy of ICU-AW patients [relative risk (RR) = 1.35, 95% confidence interval (95%CI) was 1.20 to 1.52, P < 0.000 01], improve the muscle strength [Medical Research Council score (MRC score); standardized mean difference (SMD) = 1.00, 95%CI was 0.67 to 1.33, P < 0.000 01], improve daily life ability [modified Barthel index score (MBI score); SMD = 1.67, 95%CI was 1.20 to 2.14, P < 0.000 01], shorten mechanical ventilation time (SMD = -1.47, 95%CI was -1.84 to -1.09, P < 0.000 01), reduce the length of intensive care unit (ICU) stay [mean difference (MD) = -3.28, 95%CI was -3.89 to -2.68, P < 0.000 01], reduce the total hospitalization time (MD = -4.71, 95%CI was -5.90 to -3.53, P < 0.000 01), reduce tumor necrosis factor-α (TNF-α; MD = -4.55, 95%CI was -6.39 to -2.70, P < 0.000 01) and interleukin-6 (IL-6; MD = -5.07, 95%CI was -6.36 to -3.77, P < 0.000 01). There was no obvious advantage in reducing the severity of the disease [acute physiology and chronic health evaluation II (APACHE II; SMD = -0.45, 95%CI was -0.92 to 0.03, P = 0.07). CONCLUSIONS: Based on the current research, traditional Chinese therapy can improve the clinical efficacy of ICU-AW, improve muscle strength and daily life ability, shorten mechanical ventilation, the length of ICU stay and total hospitalization time, reduce TNF-α and IL-6. But traditional Chinese therapy can not reduce the overall disease severity.

Shengjie Tongyu Decoction Regulates Cardiomyocyte Autophagy Through Modulating ROS-PI3K/Akt/mTOR Axis by LncRNA H19 in Diabetic Cardiomyopathy.

Context: Diabetic cardiomyopathy (DCM) is particularly dangerous in diabetes mellitus (DM). The Shengjie Tongyu decoction (SJTYD) is a well-known, traditional Chinese medicinal formulation that practitioners use to treat myocardial diseases in China; however, its role in DCM remain unclear. Objective: The study intended to investigate: (1) SJTYD's role in the treatment of DCM and its underlying mechanisms, (2) the association of autophagy with DCM, and (3) the involvement of mammalian target of rapamycin (mTOR) signaling in the regulation of DCM. Design: The research team performed an animal study. Setting: The study took place in the Department of Endocrinology in the No. 2 ward-Traditional and Complementary Medicine(TCM) of the China-Japan Friendship Hospital in Beijing, China. Animals: The animals were 60 C57/BL6 mice weighing 200-250 g. Intervention: To determine the role of SJTYD in treating DCM, the research team established a mouse model of DM using streptozotocin (STZ). The team randomly divided the mice into three groups with 20 mice each: (1) a negative control group, which didn't receive injections of STZ or treatment with SJTYD; (2) a model group, the Model group, which received injections of STZ but didn't receive treatment with SJTYD; and (3) an SJTYD group, which received injections of STZ and treatment with SJTYD. Outcome Measures: The research team: (1) conducted a differential analysis to identify the differentially expressed genes; (2) performed deep sequencing of the long noncoding RNAs (lncRNAs) expressed in cardiomyocytes from the control, Model, and SJTYD groups ; (3) performed a bioinformatics analysis; (4) used the ultrasonic and pathological, transmission electron microscopy (TEM) test as well as a Western blot to evaluate cardiac function, myocardial-injury areas, and autophagy in vivo; (5) transfected primary cardiomyocytes treated them with lncRNA H19 and SJTY 3-MA to establish SJTYD subgroups in which the H19 protected against DCM and the 3-MA inhibited autophagy; and (6) carried out immunofluorescence staining and Western blot to test the phosphorylated levels of phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT)/ mammalian target of rapamycin (mTOR) as well as autophagy levels in vitro. Results: The bioinformatics analysis indicated that SJTYD significantly modulated lncRNA H19 as well as the mTOR pathway. The vevo2100's results indicated the SJTYD reversed the cardiac-dysfunction parameters in DCM. The Masson' staining, TEM, and Western blot demonstrated that the SJTYD could suppress the myocardial-injury areas as well as the numbers of autophagosomes and the expression proteins of autophagy in vivo. The SJTYD promoted the phosphorylated-levels of PI3K, AKT, and mTOR and decreased the levels of autophagy proteins. LC3A-II and Beclin-1; lncRNA H19 amplified the SJTYD's role; and 3-MA reversed those effects, as tested using immunofluorescence and Western blot in primary cardiomyocytes. Conclusions: The SJTYD can protect against diabetic myocardial injury by inhibiting cardiomyocyte autophagy through the activation of lncRNA H19, reactive oxygen species (ROS), and the PI3K/Akt/mTOR signaling pathway. SJTYD may be an effective strategy to ameliorate diabetic myocardial injuries.

Distribution of thrombus predicts severe reperfusion pulmonary edema after pulmonary endarterectomy.

OBJECTIVES: Patients underwent pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH). This study aimed to investigate the effect of thrombus distribution on the occurrence of severe reperfusion pulmonary edema (RPE) and identify specific parameters for predicting severe RPE. METHODS: Patients with CTEPH who underwent PEA surgery were retrospectively analyzed. The thrombus in pulmonary arteries were evaluated through computed tomography pulmonary angiography. Based on presence of prolonged artificial ventilation, extracorporeal membrane oxygenation required, or perioperative death due to RPE, the patients were divided into the severe RPE and without severe RPE groups. MAIN RESULTS: Among the 77 patients (29 women), 16 (20.8%) patients developed severe RPE. The right major pulmonary artery (RPA) (0.64[0.58, 0.73] vs 0.58[0.49, 0.64]; p = 0.008) and pulmonary artery trunk (PAT) thrombus ratios (0.48[0.44, 0.61] vs 0.42[0.39, 0.50]; p = 0.009) (the PAT ratio is expressed as the sum of the right middle lobe clot burden and right lower lobe clot burden divided by the total clot burden multiplied by 100) of the severe RPE group was significantly higher than that of the without severe RPE group. Receiver operator characteristics curve identified a PAT ratio of 43.4% as the threshold with areas under the curve = 0.71(95%CI 0.582; 0.841) for the development of severe RPE (sensitivity 0.875, specificity 0.541). The logistic regression analysis demonstrated that age, period from symptom onset to PEA, NT-pro BNP, preoperative mPAP, preoperative PVR, RPA ratio, and PAT ratio were associated with the development of severe RPE. Multivariable logistic regression analysis revealed PAT ratio (odds ratio = 10.2; 95% confidence interval 1.87, 55.53, P = 0.007) and period from symptom onset to PEA (OR = 1.01; 95% CI = 1.00-1.02, P = 0.015) as independent risk factors for the development of severe RPE. CONCLUSIONS: The thrombus distribution could be a key factor in the severity of RPE. PAT ratio and medical history could predict the development of severe RPE.

Prevalence and characteristics of anxiety in patients with unconfirmed pulmonary nodules.

This study focuses on the prevalence and characteristics of anxiety in patients with pulmonary nodules that was assessed by Hamilton Anxiety Scale (HAMA) scores. A total of 890 patients were enrolled in this study, including incidence of absence of anxiety n = 343 (38.54%), mild or probable anxiety n = 459 (51.57%) and moderate or definite anxiety n = 79 (8.88%) and obvious anxiety n = 9 (1.01%), respectively. According to the definition of anxiety, 88 (9.89%) patients were enrolled in anxiety group. The incidence of anxiety in females was significantly higher than male (11.98% vs. 7.20%, p = 0.018), patients with respiratory symptoms were significantly higher than without respiratory symptoms (13.33% vs. 8.50%, p = 0.029) and diameter of pulmonary nodules >8 mm is significantly higher than ≤8 mm (13.35% vs. 7.10%, p = 0.002). Regression analysis showed that female (OR = 0.548, 95% CI: 0.340-0.884), family history of malignant tumour (OR = 1.691, 95% CI: 1.067-2.678), respiratory symptoms (OR = 1.713, 95% CI: 1.073-2.733) and diameter >8 mm (OR = 2.135, 95% CI: 1.350-3.375) were independent risk factors of anxiety. Further analysis of 88 patients with anxiety showed the sum of psychic anxiety was significantly higher than somatic anxiety (16.66 ± 2.46 vs. 0.97 ± 1.10, p < 0.0001). Hence, vast majority of patients with unconfirmed pulmonary nodules suffered various severity of anxiety and manifested as psychic anxiety. And gender, respiratory symptoms, family history of malignant tumour and diameter of pulmonary nodules were independent influencing factors of anxiety. Effective strategies urgently need exploring and providing for improving the mental health.

Circ_0000253 promotes the progression of osteosarcoma via the miR-1236-3p/SP1 axis.

OBJECTIVE: Circular RNAs (circRNAs) play important roles in modulating tumour progression. This study investigated the role of circ_0000253 in osteosarcoma (OS). METHODS: We downloaded the chip dataset GSE140256 from the Gene Expression Omnibus database and the circRNAs differentially expressed in OS tissue and normal tissue samples were analysed. Quantitative real-time PCR (qRT-PCR) was carried out to examine circ_0000253 expression in OS tissues and cells. Cell counting kit-8, BrdU and flow cytometry assays were performed to verify the effects of circ_0000253 on OS cell growth and apoptosis. Bioinformatics analysis was conducted to predict, and RNA immunoprecipitation assay and dual-luciferase reporter gene assay were performed to verify the targeted relationships of miR-1236-3p with circ_0000253 and Sp1 transcription factor (SP1) mRNA 3'UTR. The effects of miR-1236-3p and circ_0000253 on SP1 expression in OS cells were detected through Western blot. KEY FINDINGS: Circ_0000253 was upregulated in OS tissues and cell lines. Circ_0000253 overexpression facilitated OS cell growth and suppressed apoptosis, whereas knocking down circ_0000253 inhibited OS cell growth and facilitated apoptosis. Circ_0000253 targeted miR-1236-3p directly and negatively modulated its expression. SP1 was miR-1236-3p's target gene and positively regulated by circ_0000253. CONCLUSION: Circ_0000253 promotes OS cell proliferation and suppresses cell apoptosis via regulating the miR-1236-3p/SP1 molecular axis.

Different reaction mechanisms of SO4•- and •OH with organic compound interpreted at molecular orbital level in Co(II)/peroxymonosulfate catalytic activation system.

Hydroxyl radical (•OH) and sulfate radical (SO4•-) produced in advanced oxidation processes (AOPs) have been widely studied for organic contaminants degradation, however, the different radical characteristics and reaction mechanisms on organics degradation are still needed. In this study, a homogeneous Co(II)/peroxymonosulfate activation system was established for caffeine (CAF) degradation, and pH was controlled to regulate the radicals production. The different attack routes driven by SO4•- and •OH were deeply explored by transformation products (TPs) identification and theoretical calculations. Specifically, a method on dynamic electronic structure analysis of reactants (R), transition state (TS) and intermediates (IMs) during reaction was proposed, which was applied to elucidate the underlying mechanism of CAF oxidation by •OH and SO4•- at the molecular orbital level. In total, SO4•- is kinetically more likely to attack CAF than •OH due to its higher oxidation potential and electrophilicity index. Single electron transfer reaction (SET) is only favorable for SO4•-due to its higher electron affinity than •OH, while only •OH can react with CAF via hydrogen atom abstraction (HAA) route. Radical adduct formation (RAF) is the most favorable route for both •OH and SO4•- attack according to both kinetics and thermodynamics results. These findings can significantly promote the understanding on the degradation mechanism of organic pollutants driven by •OH and SO4•- in AOPs.

Whole exome sequencing facilitated the diagnosis in four Chinese pediatric cases of Joubert syndrome related disorders.

OBJECTIVES: Joubert syndrome is a spectrum of rare genetic disorders, mainly characterized by a distinctive cerebellar and brain stem malformation called the "molar tooth sign" (MTS), hypotonia, and intellectual disability/developmental delay. METHODS: In this study, 4 pediatric cases with developmental delay and oculomotor abnormities were recruited, and submitted to a clinical evaluation and magnetic resonance imaging (MRI) examination. Afterwards, genetic detection with whole exome sequencing (WES) was conducted on the 4 patients. RESULTS: Imaging results demonstrated cerebellar dysplasia in all probands, yet the MTS findings varied in severity. WES detected diagnostic variations in all four probands, which were distributed in four genes, namely CC2D2A, NPHP1, AHI1, and C5orf42. Two variants were novelly identified, which were the CC2D2A: c.2444delC (p.P815fs*2) and the AIH1: exon (15-17) del. In silico analysis supported the pathogenicity of the variations in this study. CONCLUSIONS: Our findings expanded the mutation spectrum of Joubert syndrome related disorders, and provided solid evidence to the affected families for further genetic counseling and pregnancy guidance.

LncRNA H19 inhibits ER stress induced apoptosis and improves diabetic cardiomyopathy by regulating PI3K/AKT/mTOR axis.

OBJECTIVE: Extensive studies have shown that ERS may be implicated in the pathogenesis of DCM. We explored the therapeutic effects of lncRNAH19 on DCM and its effect on ERS-associated cardiomyocyte apoptosis. METHODS: C57/BL-6j mice were randomly divided into 3 groups: non-DM group (controls), DM group (DCM), and lncRNAH19 overexpression group (DCM+H19 group). The effect of H19 on cardiac function was detected. The effect of H19 on cardiomyocyte apoptosis and cardiac fibrosis in DM was examined. Differentially expressed genes (DEGs) and activated pathways were examined by bioinformatics analysis. STRING database was applied to construct a PPI network using Cytoscape software. The expression of p-PERK, p-IRE1, ATF6, CHOP, cleaved caspase-3, -9, -12 and BAX proteins in cardiac tissue was used to determine the ERS-associated apoptotic indicators. We established the HG-stimulated inflammatory cell model. The expression of p-PERK and CHOP in HL-1 cells following HG was determined by immunofluorescence labeling. The effects of H19 on ERS and PI3K/AKT/mTOR pathway were also detected. RESULTS: H19 improved left ventricular dysfunction in DM. H19 could reduce cardiomyocytes apoptosis and improve fibrosis in vivo. H19 could reduce the expression of p-PERK, p-IRE1α, ATF6, CHOP, cleaved caspase-3, cleaved caspase-9, cleaved caspase-12, and BAX proteins in cardiac tissues. Furthermore, H19 repressed oxidative stress, ERS and apoptosis in vitro. Moreover, the effect of H19 on ERS-associated apoptosis might be rescued by LY294002 (the specific inhibitor for PI3K and AKT). CONCLUSION: H19 attenuates DCM in DM and ROS, ERS-induced cardiomyocyte apoptosis, which is associated with the activation of PI3K/AKT/mTOR signaling pathway.

Evaluation of two automated treatment planning techniques for multiple brain metastases using a single isocenter.

Two automated treatment planning techniques were evaluated for multiple brain metastases using a single isocenter. One technique is knowledge-based planning (KBP) using a stereotactic radiosurgery (SRS) model in Eclipse treatment planning system (TPS); and the other is the Multiple Brain Mets (MBM) SRS technique in Brainlab Elements TPS. Eighteen plans each with 3-10 lesions were used for the study. Plan evaluation metrics included the planning target volume (PTV) coverage, conformity index (CI), total monitor units (MUs), plan optimization time, brain V12 Gy, V8 Gy, and V5 Gy. Both the KBP and MBM planning techniques produced comparable plans to the manually generated clinical plans in terms of PTV coverage and CI. For irregularly shaped lesions, the KBP plans provided more conformal dose distribution to the PTV than the MBM plans. The KBP plans took significantly longer time to plan but have fewer MUs than the MBM plans. The MBM plans spared normal brain tissues better than the KBP plans in terms of V5 Gy.

Gu-Ben-Zhi-Ke-Zhong-Yao Alleviated PM2.5-Induced Lung Injury via HMGB1/NF-κB Axis.

Background: Inhalation of particles with a diameter of less than 2.5 µm (PM2.5) among air pollutants may cause lung damage. Gu-Ben-Zhi-Ke-Zhong-Yao (GBZK) is a traditional Chinese medicine prescription that has a beneficial effect on the treatment of chronic obstructive pulmonary disease (COPD). However, the effect of GBZK on PM2.5-induced lung injury remains to be elucidated. Methods: We constructed a mice lung injury model through PM2.5 stimulation and simultaneously performed GBZK gavage treatment. After 4 weeks, the lung tissues of the mice were collected for pathological staining to analyze the degree of damage. The activities of myeloperoxidase (MPO), malondialdehyde (MDA), and oxidative stress-related factors (superoxide dismutase, SOD; glutathione peroxidase, GSH-Px) were detected by commercial kit in lung tissue. Furthermore, the number of neutrophils and related inflammatory factors (interleukin-1, IL-1ß; tumor necrosis factor α, TNF-α; interleukin-6, IL-6) in bronchoalveolar lavage fluid (BALF) and serum were collected and tested to evaluate the effect of GBZK on inflammation. Masson staining was used to detect the level of lung fibrosis in mice. The activation of HMGB1 (high-mobility group protein 1) and NFκBp65 (nucleus factor kappa B) in lung tissue was evaluated by immunohistochemistry and western blot. Results: The result revealed that PM2.5 induces lung damage, and GBZK gavage treatment could reduce the degree of injury in a concentration-dependent manner in mice. After GBZK treatment, the MPO activity, MDA content, and oxidative stress level in the lung tissues of mice decreased. And after GBZK treatment, the expression levels of inflammatory cytokines in BALF and blood were decreased. GBZK treatment also improved pulmonary fibrosis in mice. In addition, we also found that GBZK prevented the up-regulation of the HMGB1/NF-κB axis in the lungs of mice. Conclusion: These results indicated that GBZK might protect mice from PM2.5-induced lung injury by inhibiting the HMGB1/NFκB pathway, thus repressing inflammation and pulmonary fibrosis.

18F-FDG PET/CT Findings in a Woman With Kaposiform Hemangioendothelioma in the Sacrum.

ABSTRACT: Kaposiform hemangioendothelioma is a rare vascular tumor with borderline malignancy and is typically diagnosed in infancy or early childhood. It most commonly affects cutaneous tissues, whereas the subtype with only primary bone involvement is extremely rare. Herein, we report a case of Kaposiform hemangioendothelioma involving the sacrum in a 37-year-old woman, with intense 18F-FDG accumulation in the lytic lesion on PET/CT. This case indicates that Kaposiform hemangioendothelioma with the primary bone involvement should be taken into consideration as a rare differential diagnosis for lytic lesions with increased 18F-FDG uptake on PET/CT.

Integrated MicroRNA-mRNA Analyses of Distinct Expression Profiles in Hyperoxia-Induced Bronchopulmonary Dysplasia in Neonatal Mice.

OBJECTIVE: Bronchopulmonary dysplasia (BPD) is a common chronic lung disease of preterm neonates; the underlying pathogenesis is not fully understood. Recent studies suggested microRNAs (miRNAs) may be involved in BPD. STUDY DESIGN: miRNA and mRNA microarrays were performed to analyze the expression profiles of miRNA and mRNA in BPD and control lung tissues after oxygen and air exposure on day 21. Bioinformatics methods, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), were performed to predict the potential functions of differentially expressed genes. Then, miRNA-mRNA regulatory network was constructed by protein-protein interaction (PPI) data and TarBase data. RESULTS: Our results showed that a total of 192 differentially expressed miRNAs (74 downregulated and 118 upregulated) and 1,225 differentially expressed mRNAs (479 downregulated and 746 upregulated) were identified between BPD mice and normoxia-control mice. GO and KEGG analysis showed that for downregulated genes, the top significant enriched GO terms and KEGG pathways were both mainly related to immune and inflammation processes; for upregulated genes, the top significant enriched GO terms and KEGG pathways were both mainly related to extracellular matrix (ECM) remodeling. PPI network and miRNA-mRNA regulatory network construction revealed that the key genes and pathways associated with inflammation and immune regulation. CONCLUSION: Our findings revealed the integrated miRNA-mRNA data of distinct expression profiles in hyperoxia-induced BPD mice, and may provide some clues of the potential biomarkers for BPD, and provide novel insights into the development of new promising biomarkers for the treatment of BPD. KEY POINTS: · Integrated advanced bioinformatics methods may offer a better way to understand the molecular expression profiles involved in BPD.. · ECM remodeling, inflammation, and immune regulation may be essential to BPD.. · The miRNA-mRNA regulatory network construction may contribute to develop new biomarkers for the treatment of BPD..

A prospective randomized controlled study on mouse nerve growth factor in the treatment of global developmental delay in children. / é¼ ç¥žç»ç”Ÿé•¿å› å­æ²»ç–—å ¨é¢æ€§å‘è‚²è¿Ÿç¼“çš„å‰çž»æ€§éšæœºå¯¹ç §ç ”ç©¶.

OBJECTIVES: To study the clinical effect of mouse nerve growth factor (mNGF) in the treatment of children with global developmental delay (GDD). METHODS: A prospective clinical trial was conducted in 60 children with GDD who were treated in the First Affiliated Hospital of Anhui Medical University between July 2016 and July 2017. These children were randomly divided into two groups: conventional rehabilitation treatment and mNGF treatment group (n=30 each). The children in the conventional rehabilitation treatment group were given neurodevelopmental therapy, and those in the mNGF treatment group were given mNGF treatment in addition to the treatment in the control group. The evaluation results of the Gesell Developmental Scale were compared between the two groups before and after treatment. RESULTS: Before treatment and after 1.5 months of treatment, there was no significant difference in the developmental quotient (DQ) of each functional area of the Gesell Developmental Scale between the mNGF treatment and conventional rehabilitation treatment groups (P>0.05). After 3 months of treatment, the mNGF treatment group had significantly higher DQs of gross motor, fine motor, and personal-social interaction than the conventional rehabilitation treatment group (P˂0.05). The incidence rate of transient injection site pain after injection of mNGF was 7% (2/30), and there was no epilepsy or other serious adverse reactions. CONCLUSIONS: In children with GDD, routine rehabilitation training combined with mNGF therapy can significantly improve their cognitive, motor, and social abilities.

Oxygen defective titanate nanotubes induced by iron deposition for enhanced peroxymonosulfate activation and acetaminophen degradation: Mechanisms, water chemistry effects, and theoretical calculation.

The large consumption of acetaminophen (APAP) worldwide and unsatisfactory treatment efficiencies by conventional wastewater treatment processes give rise to the seeking of new technology for its effective removal. Herein, we proposed a facile one-step hydrothermal method to synthesize defective iron deposited titanate nanotubes (Fe/TNTs) for peroxymonosulfate (PMS) activation and APAP degradation. The retarded first-order reaction rate of APAP degradation by Fe/TNTs was 5.1 times higher than that of neat TNTs. Characterizations indicated iron deposition effectively induced oxygen vacancies and Ti3+, facilitating the electrical conductivity and PMS binding affinity of Fe/TNTs. Besides, oxygen vacancies could act as an electron mediator through PMS activation by iron. Moreover, the formation of Fe-O-Ti bond facilitated the synergistic redox coupling between Fe and Ti, further enhancing the PMS activation. SO4•- was the major radical, causing C-N bond cleavage and decreasing the overall toxicity. In contrast, APAP degradation by neat TNTs-PMS system mainly works through nonradical reaction. The Fe/TNTs activated PMS showed desired APAP removal under mild water chemistry conditions and good reusability. This work is expected to expand the potential application of titanate nanomaterials for PMS activation, and shed light on facile synthesis of oxygen defective materials for sulfate-radical-based advanced oxidation processes.

Clinical value of serum Ape1/Ref-1 combined with TGF-ß1 monitoring in predicting the occurrence of radiation pneumonitis (RP) in non-small cell lung cancer patients.

BACKGROUND: The aim of the present study was to explore the predictive value of serum apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ape1/Ref-1) combined with transforming growth factor ß1 (TGF-ß1) levels in the occurrence of radiation pneumonitis (RP) in patients with non-small cell lung cancer (NSCLS). METHODS: Eighty-one patients with NSCLS who were admitted from August 2017 to July 2019 were enrolled in the present study. All patients were treated with concurrent radiotherapy and chemotherapy. Serum Ape1/Ref-1 and TGF-ß1 levels were measured before treatment and 12 weeks after treatment. Patients with radiation-induced lung injury were assessed and divided into the RP group (lung injury ≥2) and non-RP (NRP) group (grade <2). The levels of serum Ape1/Ref-1 and TGF-ß1 before and after treatment between the 2 groups were compared. The relationship between clinical characteristics, serum Ape1/Ref-1, TGF-ß1 levels, and the occurrence of RP were then analyzed, and the relationship between serum Ape1/Ref-1, TGF-ß1 levels, and their predictive value for the occurrence of RP was also assessed. RESULTS: The incidence of RP in 81 patients was 30.86%. After treatment, the serum Ape1/Ref-1 and TGF-ß1 levels of the 2 groups were significantly higher than those before treatment (P<0.05). Furthermore, after treatment, the levels of serum Ape1/Ref-1 and TGF-ß1 in the RP group were significantly higher than those of the NRP group (P<0.05). Multivariate logistic regression analysis showed that V20, Ape1/Ref-1, and TGF-ß1 were associated with the occurrence of RP (P<0.05). The levels of serum Ape1/Ref-1 were positively correlated with TGF-ß1 (r=0.734, P<0.05). Finally, the area under the curve of RP occurrence, which was predicted by the levels of serum Ape1/Ref-1, TGF-ß1, and the combination of both were 0.779, 0.69, and 0.842, respectively. CONCLUSIONS: The occurrence of RP in NSCLS patients is closely related to the levels of serum Ape1/Ref-1 and TGF-ß1, and the combination of both has important predictive values for the occurrence of RP.

Silencing of MicroRNA-503 in Rat Mesenchymal Stem Cells Exerts Potent Antitumorigenic Effects in Lung Cancer Cells.

PURPOSE: Mesenchymal stem cells (MSCs) are largely studied for their potential clinical use. Recently, there has been gained further interest in the relationship between MSCs and tumorigenesis. MSCs are reported to both promote and abrogate tumor growth. The present study was designed to investigate whether miRNAs are involved in the interactions between MSCs and tumor cells in the tumor microenvironment. MATERIALS AND METHODS: Rat bone marrow-derived MSCs (rMSCs) were cultured with or without tumor-conditioned medium (TCM) to observe the effect upon MSCs by TCM. Microarrays and real-time PCR were performed between the two groups. A series of experiments were used to reveal the functional significance of microRNA-503 (miR-503) in rMSCs. Furthermore, the antitumorigenic effect of silencing of miR-503 in rMSCs (miR-503-i-rMSCs) in vivo was measured. RESULTS: We found that rMSCs in vitro exhibited tumor-promoting properties in TCM, and the microRNA profiles of rMSCs were significantly altered in TCM. However, miR-503-i-rMSCs can decrease the angiogenesis and growth of A549 cells. We also demonstrated in an in vivo tumor model that miR-503-i-rMSCs inhibited A549 tumor angiogenesis and significantly abrogated tumor initiation and growth. CD133 assays in peripheral blood and A549 xenografts further validated that miR-503-i-rMSCs, rather than rMSCs, exerted an antitumorigenic action in the A549 tumor model. CONCLUSION: Our results suggest that miR-503-i-rMSCs are capable of tumor suppression. Further studies are required to develop clinical therapies based on the inhibition of the tumor-promoting properties and potentiation of the anti-tumor properties of MSCs.