Shape-Regulated Photothermal-Catalytic Tumor Therapy Using Polydopamine@Pt Nanozymes with the Elicitation of an Immune Response.

Recently, nanozyme-based photothermal-catalytic therapy has emerged as a promising strategy for antitumor treatment. Extensive research has focused on optimizing the catalytic activity and photothermal conversion performance of nanozymes through size, morphology, and surface property regulations. However, the biological effects of nanozymes, such as cellular uptake and cytotoxicity, resulting from their physicochemical properties, remain largely unexplored. In this study, two types of polydopamine/platinum (PDA@Pt) nanozymes, flower-like (FPDA@Pt) and mesoporous spherical-like (MPDA@Pt), to comprehensively compare their enzyme-mimicking activity, photothermal conversion capacity, and antitumor efficiency are designed. These findings revealed that FPDA@Pt exhibited superior peroxidase-like activity and higher photothermal conversion efficiency compared to MPDA@Pt. This led to enhanced production of reactive oxygen species (ROS) and increased heat generation at tumor sites. Importantly, it is observed thatthe flower-like structure of FPDA@Pt facilitated enhanced cellular uptake, leading to an increased accumulation of nanozymes within tumor cells. Furthermore, the light irradiation on tumors also triggered a series of anti-tumor immune responses, further enhancing the therapeutic efficacy. This work provides a possible design orientation for nanozyme-based photothermal-catalytic tumor therapy, highlighting the importance of considering the physicochemical properties of nanozymes to optimize their therapeutic potential in antitumor strategies.

Translation and validation of 17-item Wound-QoL questionnaire in a Chinese population.

We aimed to translate the 17-item questionnaire to measure the quality of life of patients with chronic wounds (Wound-QoL-17) and verify its reliability and validity in the Chinese population. The standard Chinese version of the Wound-QoL-17 was determined through translation, back translation, and cultural adaptation. A total of 121 patients with chronic wounds from the wound center of a tertiary hospital in Beijing were recruited. Through a questionnaire and physical examination, we tested the criterion-related validity, known group validity, structural validity, internal consistency coefficient (Cronbach's alpha), and test-retest correlation. A new structure of four factors was extracted by exploratory factor analysis, and the cumulative contribution rate was 72.23%. The total score and that of the four factors, which were significantly correlated with the EuroQol Five Dimensions Questionnaire (EQ-5D) and the Short Form-36 Health Survey (SF-36) (P < 0.05), also showed statistically significant differences between patients with different pain grades, with or without wound odour, and between different groups of patients reporting wound changes in the past 2 weeks. Cronbach's alpha was between 0.779 and 0.906, while the test-retest reliability was between 0.532 and 0.802. We concluded that the Chinese Wound-QoL-17 has good reliability and validity and is suitable for evaluating the quality of life of patients with chronic wounds.

Routine replacement versus replacement as clinical indicated of peripheral intravenous catheters: A multisite randomised controlled trial.

AIMS AND OBJECTIVES: To compare the safety of replacing peripheral intravenous catheter as clinically indicated versus routine replacement on patient outcomes in the Chinese context. BACKGROUND: Some evidence from developed countries recommend replacing peripheral intravenous catheter as clinically indicated; however, there is limited evidence from developing countries. DESIGN: A multisite randomised controlled trial. METHODS: The 3050 participants from three hospitals in China were randomly assigned to clinically indicated or routine replacement groups. Patients in the clinically indicated group had the catheters kept in situ until any of the following clinical signs appeared: phlebitis, infiltration, occlusion, displacement, local infection and diagnosed catheter-related bloodstream infection. Patients in the routine replacement group had their peripheral intravenous catheters replaced every 96 hours. The outcomes of phlebitis, infiltration, occlusion, displacement; catheter-related bloodstream infection, all-cause bloodstream infection, and local infection were compared. CONSORT checklist was used to guide the reporting of this RCT. RESULTS: The risk of phlebitis, phlebitis per 1000 catheter days, occlusion, dislodgement, all bloodstream infections, local infection and mortality between the two groups were not significantly different. The risk of infiltration was increased in the clinically indicated group (HR 1.29). There was no catheter-related bloodstream infection reported in either group. Patients' first peripheral intravenous catheter dwelling time and cumulative indwelling time of all peripheral intravenous catheters in the clinically indicated group were significantly longer than the routine replacement group. There was no statistical significant difference in survival times from phlebitis between the two groups. CONCLUSIONS: In the Chinese context, removing peripheral catheters as clinical indicated did not increase the risk of phlebitis, occlusion, catheter displacement and catheter infection; however, there was an increased infiltration incidence. RELEVANCE TO CLINICAL PRACTICE: In developing countries, removing peripheral catheters as clinical indicated is feasible, but more frequent observations of infiltration are highly recommended.

SBF2-AS1: An oncogenic lncRNA in small-cell lung cancer.

The long noncoding RNAs (lncRNAs) SBF2 antisense RNA 1 (SBF2-AS1) was found to act as an oncogenic lncRNA in non-small-cell lung cancer (NSCLC), but the role of SBF2-AS1 in small-cell lung cancer (SCLC) was still unclear. The purpose of this study was to provide the clinical significance and biological function of SBF2-AS1 in SCLC. In our results, SBF2-AS1 was found to be upregulated in SCLC tissues compared with NSCLC tissues or adjacent normal lung tissues. Besides, SBF2-AS1 expression was also elevated in SCLC cell lines compared with the normal bronchial epithelial cell line or NSCLC lines. Moreover, high expression of SBF2-AS1 was associated with clinical stage, tumor size, lymph node metastasis and distant metastasis in SCLC patients. Survival analysis showed SCLC patients with high expression of SBF2-AS1 had shorter overall survival than patients with low expression of SBF2-AS1, and high expression of SBF2-AS1 acted as an independent poor prognostic factor for overall survival in SCLC patients. The study in vitro suggested inhibition of SBF2-AS1 obviously depressed cell proliferation, migration, and invasion in SCLC. In conclusion, SBF2-AS1 acts as a novel oncogenic lncRNA in SCLC.

Characterization of ginsenoside compound K metabolites in rat urine and feces by ultra-performance liquid chromatography with electrospray ionization quadrupole time-of-flight tandem mass spectrometry.

Ginsenoside compound K (CK) is an active metabolite of ginsenoside and has been shown to have ameliorative property in various diseases. However, the detailed in vivo metabolism of this compound has rarely been reported. In the present study, a method using liquid chromatography quadrupole time-of-flight tandem mass spectrometry together with multiple data processing techniques, including extracted ion chromatogram, multiple mass defect filter and MS/MS scanning, was developed to detect and characterize the metabolites of CK in rat urine and feces. After oral administration of CK at a dose of 50 mg/kg, urine and feces were collected for a period of time and subjected to a series of pretreatment. A total of 12 metabolites were tentatively or conclusively identified, comprising 11 phase I metabolites and a phase II metabolite. Metabolic pathways of CK has been proposed, including oxidation, deglycosylation, deglycosylation with sequential oxidation and dehydrogenation and deglycosylation with sequential glucuronidation. Relative quantitative analyses suggested that deglycosylation was the main metabolic pathway. The result could offer insights for better understanding of the mechanism of its pharmacological activities.

Zinc alpha2 glycoprotein protects against obesity-induced hepatic steatosis.

BACKGROUND/AIM: Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, impaired insulin sensitivity, and chronic low-grade inflammation. Our previous studies indicated that zinc alpha2 glycoprotein (ZAG) alleviates palmitate (PA)-induced intracellular lipid accumulation in hepatocytes. This study is to further characterize the roles of ZAG on the development of hepatic steatosis, insulin resistance (IR), and inflammation. METHODS: ZAG protein levels in the livers of NAFLD patients, high-fat diet (HFD)-induced or genetically (ob/ob) induced obese mice, and in PA-treated hepatocytes were determined by western blotting. C57BL/6J mice injected with an adenovirus expressing ZAG were fed HFD for indicated time to induce hepatic steatosis, IR, and inflammation, and then biomedical, histological, and metabolic analyses were conducted to identify pathologic alterations in these mice. The molecular mechanisms underlying ZAG-regulated hepatic steatosis were further explored and verified in mice and hepatocytes. RESULTS: ZAG expression was decreased in NAFLD patient liver biopsy samples, obese mice livers, and PA-treated hepatocytes. Simultaneously, ZAG overexpression alleviated intracellular lipid accumulation via upregulating adiponectin and lipolytic genes (FXR, PPARα, etc.) while downregulating lipogenic genes (SREBP-1c, LXR, etc.) in obese mice as well as in cultured hepatocytes. ZAG improved insulin sensitivity and glucose tolerance via activation of IRS/AKT signaling. Moreover, ZAG significantly inhibited NF-ĸB/JNK signaling and thus resulting in suppression of obesity-associated inflammatory response in hepatocytes. CONCLUSIONS: Our results revealed that ZAG could protect against NAFLD by ameliorating hepatic steatosis, IR, and inflammation.

Genetic determinants of myocardial dysfunction.

Heart failure (HF) is a major killer with high morbidity and mortality and nearly 37.7 million people are affected by HF globally, making this a global epidemic. HF is a complex pathophysiological syndrome in which the mechanical function of heart for pumping blood is compromised. Cardiac structural and functional abnormalities culminate in decreased cardiac output along with increased intracardiac pressures under resting or stress conditions, leading to HF. Besides the acquired risk factors, the independent role of hereditary and genetic factors in the development, progression and prognosis of HF remains to be established. One of the most common causes of HF is cardiomyopathy and dilated cardiomyopathy and hypertrophic cardiomyopathy are the major forms, transmitted by autosomal dominant inheritance and often result from mutations in single or multiple genes, which predominantly code for proteins present in the cardiac sarcomere. Other inherited forms of cardiomyopathies that can trigger HF are metabolic and mitochondrial cardiomyopathies that result from mutations in proteins involved in fat or carbohydrate metabolism or mitochondrial biogenesis, affecting cardiomyocyte energy balance. Because of the inherent complications in the aetiology of HF, only a small number of genome-wide association studies (GWAS) could be conducted to identify SNPs in genes that are causally related to HF. Recent attempts to conduct GWAS in a focused approach on the HF risk factors led to identification of more SNPs. Initial attempts for gene therapy using adeno-associated viral vectors have not been successful, but more studies are needed to understand the pathophysiological and genetic basis of HF.

Gastric cancer: somatic genetics as a guide to therapy.

Gastric cancer is the leading cause of cancer-related mortality across the world, with poor prognosis and a median overall survival of ≤12 months for advanced stage gastric cancer. Environmental, genetic and other predisposing factors contribute to the development of gastric cancer and a predominant factor was found to be infection of Helicobacter pylori Advances in understanding the deranged signalling pathways that are critical for normal cellular homeostasis helped in the development of novel drugs that target specific proteins and pathways to curtail the growth of gastric cancer. Genetic studies revealed several single nucleotide polymorphisms, chromosomal aberrations and epigenetic alterations that likely play a major role in elevating the susceptibility to develop gastric cancer. Methylation pattern of specific genes may likely prove to be a valid biomarker for early detection of gastric cancer, but much progress is needed to establish specific markers. Important developments have been made in targeting human epidermal growth factor receptor-2 and vascular endothelial growth factor receptor 2 for treating advanced gastro-oesophageal junction cancer, using specific monoclonal antibodies. Lack of efficacy with regard to targeting other signalling pathways including mesenchymal-epithelial transition/hepatocyte growth factor and mammalian target of rapamycin is probably due to suboptimal patient selection for these clinical trials, which is probably due to the lack of appropriate biomarkers, to decide on responsive patient population. Besides the development of antagonists for the cell growth-related signalling pathways, advances are also being made to tackle gastric cancer by immunotherapies, targeting immune check-points, which may hold promise for better treatment options in future.

Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents.

Dicer participates in heterochromatin formation in fission yeast and plants. However, whether it has a similar role in mammals remains controversial. Here we showed that the human Dicer protein interacts with SIRT7, an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm. Dicer knockdown led to an increase of chromatin-associated SIRT7 and simultaneously a decrease of cytoplasmic SIRT7, while its overexpression induced SIRT7 reduction in the chromatin-associated fraction and increment in the cytoplasm. Furthermore, DNA damaging agents promoted Dicer expression, leading to decreased level of chromatin-associated SIRT7 and increased level of H3K18Ac, which can be alleviated by Dicer knockdown. Taken together with that H3K18Ac was exclusively associated with the chromatin, our findings suggest that Dicer induction by DNA damaging treatments prevents H3K18Ac deacetylation, probably by trapping more SIRT7 in the cytoplasm.

Dicer regulates non-homologous end joining and is associated with chemosensitivity in colon cancer patients.

DNA double-strand break (DSB) repair is an important mechanism underlying chemotherapy resistance in human cancers. Dicer participates in DSB repair by facilitating homologous recombination. However, whether Dicer is involved in non-homologous end joining (NHEJ) remains unknown. Here, we addressed whether Dicer regulates NHEJ and chemosensitivity in colon cancer cells. Using our recently developed NHEJ assay, we found that DSB introduction by I-SceI cleavage leads to Dicer upregulation. Dicer knockdown increased SIRT7 binding and decreased the level of H3K18Ac (acetylated lysine 18 of histone H3) at DSB sites, thereby repressing the recruitment of NHEJ factors to DSB sites and inhibiting NHEJ. Dicer overexpression reduced SIRT7 binding and increased the level of H3K18Ac at DSB sites, promoting the recruitment of NHEJ factors to DSBs and moderately enhancing NHEJ. Dicer knockdown and overexpression increased and decreased, respectively, the chemosensitivity of colon cancer cells. Dicer protein expression in colon cancer tissues of patients was directly correlated with chemoresistance. Our findings revealed a function of Dicer in NHEJ-mediated DSB repair and the association of Dicer expression with chemoresistance in colon cancer patients.

Pilose antler peptide potentiates osteoblast differentiation and inhibits osteoclastogenesis via manipulating the NF-κB pathway.

Bones are inflexible yet ever-changing metabolic organs, and bone homeostasis is maintained through two delicately regulated processes: bone construction and bone reabsorption. An imbalance in bone metabolism is linked to most orthopedic diseases, including osteoporosis and rheumatoid arthritis. Importantly, tumor necrosis factor-α (TNF-α) blocks osteoblast differentiation and stimulates osteoclast formation, resulting in delayed deposition of new bone and accelerated bone resorption, especially in rheumatoid arthritis patients with inflammatory conditions. Pilose antler peptide (PAP) isolated and purified from deer antlers has been shown to have beneficial effects on chronic inflammation. In the present study, we studied the impact of PAP on osteoblast differentiation and evaluated the regulatory mechanism, with particular emphasis on the effect of PAP on TNF-α-mediated NF-κB signaling. Mouse primary osteoblast cells were activated with bone morphogenetic protein-2 (BMP-2) for osteoblast differentiation. A significant stimulatory effect of PAP in osteoblastogenesis was observed using ALP activity and Alizarin Red S staining assays. Meanwhile, PAP significantly rescued TNF-α-induced impairment of osteoblast formation as well as mineralization. Furthermore, we found a similar trend upon analyzing osteoblast-specific gene expression. PAP significantly rescued TNF-α-mediated decrease in expression of osteoblast-specific genes. A molecular mechanism assay indicated that PAP significantly inhibited TNF-α-mediated stimulation of NF-κB signaling activity, as well as nuclear translocation of its subunit p65. Moreover, over-expression of p65 reversed the stimulatory effects of PAP on osteoblast differentiation. Furthermore, we also identified that PAP dose dependently inhibit osteoclastogenesis, and this effect might be achieved via suppressing NF-κB activity. In summary, this study shows that PAP promotes osteoblast differentiation and blocks TNF-α-mediated suppression of osteoblastogenesis in vitro via the NF-κB/p65 pathway, as well as inhibits osteoclastsogenesis in vitro. Therefore, PAP, a novel drug with both antiresorptive and osteoanabolic activity, shows therapeutic potential as an alternative treatment for osteolytic diseases, including rheumatoid arthritis and osteoporosis.

hsCRP and ET-1 expressions in patients with no-reflow phenomenon after Percutaneous Coronary Intervention.

OBJECTIVE: To explore hsCRP and ET-1 expressions in patients with no-reflow phenomenon after percutaneous coronary intervention (PCI). METHODS: A total of 136 patients with single coronary artery disease receiving PCI were divided into a reflow group and a no-reflow group to compare the level use of ET-1 alone with combined level of ET-1 and hs-CRP in PCI regarding sensitivity, specificity, positive and negative predictive values and accuracy for postoperative no-reflow. The study was conducted between 2014-2016 at our hospital. RESULTS: Postoperative levels of ET-1 and hs-CRP in no-reflow group were significantly higher than those of reflow group (P<0.05). ET-1 level of reflow group peaked three hours after PCI and then declined. Serum level of hs-CRP decreased most obviously within three hours after PCI in reflow group and three hours - three days after PCI in no-reflow group. Left ventricular end-diastolic diameters of both groups after PCI were apparently lower than those before PCI, without significant inter-group difference (P>0.05). Left ventricular end-systolic diameters and left ventricular ejection fractions of both groups evidently increased after PCI, without significant inter-group differences either (P>0.05). Corrected TIMI frame count (CTFC) and wall motion score index of reflow group after PCI were significantly lower than those of no-reflow group (P<0.05). ET-1 level was positively correlated with CTFC (P<0.05). Multivariate linear regression showed hs-CRP was negatively correlated with the serum level (P<0.05) (r=-0.34). CONCLUSION: hsCRP and ET-1 levels significantly increased in patients with no-reflow phenomenon.

Viral metagenomics analysis of picobirnavirus-positive feces from children with sporadic diarrhea in China.

Picobirnaviruses (PBVs) infect humans and a wide range of animals and may cause diarrhea. The aim of this study was to investigate PBV infection and its association with diarrhea. Here, seven PBV RT-PCR-positive fecal samples from diarrheic children and four fecal samples from healthy children as controls were analyzed by viral metagenomics. The results indicated that all the seven diarrheic fecal samples contain high titers of PBV sequences, while three of the controls were negative, and one had low titers of PBV. Three of the diarrheic fecal samples were also positive for other viruses, including anellovirus, human gyrovirus, human parechovirus, and porcine stool-associated circular virus. PBV sequences from the seven patients were assembled, generating seven large contigs with the complete ORF of RNA-dependent RNA polymerase (RdRp). Phylogenetic analysis of the amino acid sequences of RdRp indicated that the seven PBVs in the present study belonged to three different genogroups. Our data suggest that PBV might have been the cause of diarrhea in these seven children.

[Preventive Effect of Fangshuan Capsule on PCI-induced Myocardial Damage and Vascular Endo- thelial Injury in Patients with Unstable Angina Pectoris].

Objective To observe the prevention of Fangshuan Capsule (FC) on percutaneous coronary intervention (PCI) induced myocardial damage and vascular endothelial injury in patients with un- stable angina pectoris (UAP). Methods Totally 100 UAP patients undergoing PCI were assigned to the control group and the treatment group by random digit table, 50 in each group. All patients received routine Western medicine therapy. Those in the treatment group additionally took FC, 6 pills each time, three times per day for at least 2 days before PCI operation. The therapeutic course for each group was 2 weeks. The clinical therapeutic effect was observed in the two groups. Heart rate (HR), systolic blood pressure (SBP) , changes of myocardial oxygen consumption ( HR x SBP, kPa/min) were compared. The levels of serum troponin I (cTn 1), creatinine kinase-MB (CK-MB) , myoglobin (MYO) , endothelin (ET), and nitric oxide (NO) were measured before PCI, and 6, 12, 24 h, 3 and 7 days after PCI. Results The markedly effective rate of Chinese medical syndromes was 54% (17/50) and the total effective rate was 94% (47/50) in the treatment group, obviously higher than those of the control group [26% (13/50) and 88% (44/50) ; P <0. 01]. Compared with before treatment in the same group, HR, SBP, myocardial oxygen consumption, and plasma ET level were reduced, plasma NO level was elevated in two groups after treatment (P <0.05, P <0. 01). cTnl concentration increased at 6, 12, 24 h, and day 3 (P <0. 05, P <0. 01 ) ; CK-MB concentration was elevated at 6, 12, and 24 h (P <0. 05, P <0. 01) ; MYO concentration increased at 6 and 12 h (P < 0. 01) in the control group after treatment. cTnl concentration increased at 12 and 24 h (P <0. 05, P <0. 01); CK-MB concentration was elevated at 6 and 12 h (P <0. 05) ; MYO concentration increased at 6 h (P <0. 01) in the treatment group after treatment. Compared with the control group at the same time point, HR, myocardial oxygen consumption, and plasma ET level decreased (P <0. 05); cTnl decreased at 6, 12, and 24 h (P <0. 05); CK-MB concentration decreased at 12 h (P <0. 05); MYO concentration decreased at 6 and 12 h (P <0. 05) in the treatment group after treatment. Conclusion FC could effectively improve scores of Chinese medical syndromes after PCI surgery, reduce myocardial oxygen consumption, attenuate myocar- dial damage and vascular endothelial injury in UAP patients after PCI.

Subarachnoid extension of intracerebral hemorrhage and 90-day outcomes in INTERACT2.

BACKGROUND AND PURPOSE: The prognostic significance of subarachnoid extension of intracerebral hemorrhage was determined in the INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2) study. METHODS: INTERACT2 was an open randomized controlled trial of early intensive compared with guideline-recommended blood pressure lowering in patients with elevated systolic blood pressure within 6 hours of intracerebral hemorrhage. Independent predictors of death or major disability (scores 3-6 on the modified Rankin Scale) at 90 days were analyzed in logistic regression models. RESULTS: Of 2582 participants, 192 (7%) had subarachnoid extension, which was associated with larger hematoma volumes (P<0.0001) and higher National Institute of Health Stroke Scale score (P<0.0001). Subarachnoid extension predicted death or major disability at 90 days (71% versus 53%; unadjusted odds ratio, 2.25; 95% confidence interval, 1.63-3.10; P<0.0001). The association remained significant after adjusting for age, region, lipid-lowering therapy, systolic blood pressure, glucose, location of hematoma, intraventricular extension, and randomized treatment (odds ratio, 2.17; 95% confidence interval, 1.50-3.14; P<0.0001), but not after further adjustment for baseline hematoma volume (P=0.62). CONCLUSIONS: Subarachnoid extension of intracerebral hemorrhage is associated with poor prognosis, which is determined by a larger volume of the underlying intraparenchymal hematoma. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00716079.

Association between continuous positive airway pressure and changes in serum leptin in patients with obstructive sleep apnoea: a meta-analysis.

PURPOSE: The role of leptin in the development of obstructive sleep apnoea (OSA) has been identified. However, the effects of OSA treatment using continuous positive airway pressure (CPAP) on serum leptin levels remain controversial. To address this issue, a meta-analysis was conducted to evaluate the effects of CPAP therapy on serum leptin levels in OSA. METHODS: A comprehensive literature search was performed to identify studies that focused on the effects of CPAP therapy (treatment duration, ≥4 weeks) on the serum leptin levels of OSA patients. Standardised mean difference (SMD) was used to analyse the summary estimates for CPAP therapy. RESULTS: Fifteen studies involving 427 patients were included in the meta-analysis. Results indicate that the overall SMD of the leptin levels before and after CPAP therapy was 0.137 (95% confidence interval (CI) 0.002 to 0.272); test for overall effect z=1.99 (P=0.046). Sources of heterogeneity were not found by subgroup and meta-regression analyses. Subgroup analyses showed that differences in OSA severity, baseline body mass index, compliance, CPAP duration and leptin assay did not affect the effectiveness of CPAP therapy. CONCLUSIONS: The evidence for the use of CPAP therapy on decrease of leptin levels in OSA patients is low, and stronger evidence is needed.

Effects of perspective taking on attention bias to body-related information among junior high school students with body image disturbance.

Using lexical judgment tasks, the present study explored whether perspective taking affected attention bias to body-related information among junior high school students with body image disturbance. Experiment 1 examined the junior high school students' attention bias to body schema-related words; the results showed the body image disturbance group responded significantly more quickly to negative body schema-related words than positive words, whereas the control group did not show a significant difference between positive and negative words. In Experiment 2, participants were asked to judge whether the positive or negative body schema-related words were suitable to describe themselves, when adopting their own perspective or that of another person. The results showed that reaction times to negative words were significantly shorter than to positive words when adopting a self-perspective. When taking another's perspective, there was no significant difference of reaction time between positive and negative words. This result demonstrated that perspective taking reduced attention bias to negative body schema-related information among junior high school students with body image disturbance. The present research suggests that guiding adolescents to view themselves from different perspectives can help them form a more accurate and objective body image.

Cerium-Luteolin Nanocomplexes in Managing Inflammation-Related Diseases by Antioxidant and Immunoregulation.

Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the antioxidant defense system, plays a pivotal role in inflammation-related diseases. Excessive ROS levels can induce cellular damage and impair normal physiological functions, triggering the release of inflammatory mediators and exacerbating the inflammatory response, ultimately leading to irreversible tissue damage. In this study, we synthesized cerium ion-luteolin nanocomplexes (CeLutNCs) by coordinating Ce ions with the natural product luteolin, aiming to develop a therapeutic agent with excellent antioxidant and immunoregulation properties for ROS-related inflammation treatment. In vitro experiments demonstrated that the prepared CeLutNCs effectively scavenged excess ROS, prevented cell apoptosis, down-regulated levels of important inflammatory cytokines, regulated the response of inflammatory macrophages, and suppressed the activation of the nuclear factor-κ-gene binding (NF-κB) pathway. In an acute kidney injury (AKI) animal model, CeLutNCs exhibited significant efficacy in improving kidney function, repairing damaged renal tissue, and reducing oxidative stress, inflammatory response, and cellular apoptosis. Moreover, the therapeutic potential of CeLutNCs in an acute lung injury (ALI) model was confirmed through the assessment of inflammatory responses and histopathological studies. This study emphasizes the effectiveness of these metal-natural product coordination nanocomplexes as a promising therapeutic approach for preventing AKI and other diseases associated with oxidative stress.

Identification of ID1 and miR-150 interaction and effects on proliferation and apoptosis in ovine granulosa cells.

Granulosa cells (GCs) proliferation and apoptosis play a significantly role in follicular development and atresia. ID1 and miR-150 are involved in cell apoptosis and follicular atresia, but the interaction and function of ID1 and miR-150 in GCs are unclear. This study focuses on ID1 and miR-150 in terms of the interaction and effects on proliferation and apoptosis in ovine granulosa cells. Our findings revealed that ID1 decreased the promoter activity and expression level of oar-miR-150. However, the expression of ID1 was downregulated by miR-150, and ID1 was identified as a target gene of oar-miR-150. miR-150 mimic inhibited proliferation and upregulated apoptosis rate in ovine GCs, while the results of miR-150 inhibitor were opposite. Overexpression of ID1 significantly inhibited ovine GCs proliferation and cell cycle-related genes (CDK1, CDK2, CDK4, CCND2, CDC20, and PCNA) expression, whereas knockdown of ID1 promoted cell proliferation and those genes expression. Overexpression of ID1 significantly downregulated mitochondrial membrane potential and Bcl-2 expression in ovine GCs, and upregulated the expression of pro-apoptosis genes Bax, Caspase-3, and Caspase-9, whereas the results of ID1 knockdown were reversed. Collectively, these findings indicate the interaction and the vital role of ID1 and miR-150 on proliferation and apoptosis in ovine granulosa cells, which may suggest a novel target for ovine follicular development and atresia.

Chronic disease diagnosis model based on convolutional neural network and ensemble learning method.

Introduction: Chronic diseases have become one of the main causes of premature death all around the world in recent years. The diagnosis of chronic diseases is time-consuming and costly. Therefore, timely diagnosis and prediction of chronic diseases are very necessary. Methods: In this paper, a new method for chronic disease diagnosis is proposed by combining convolutional neural network (CNN) and ensemble learning. This method utilizes random forest (RF) as the base classifier to improve classification performance and diagnostic accuracy, and then combines AdaBoost to successfully replace the Softmax layer of CNN to generate multiple accurate base classifiers while determining their optimal attributes, achieving high-quality classification and prediction of chronic diseases. Results: To verify the effectiveness of the proposed method, real-world Electronic Medical Records dataset (C-EMRs) was used for experimental analysis. The results show that compared with other traditional machine learning methods such as CNN, K-Nearest Neighbor, and RF, the proposed method can effectively improve the accuracy of diagnosis and reduce the occurrence of missed diagnosis and misdiagnosis. Conclusions: This study will provide effective information for the diagnosis of chronic diseases, assist doctors in making clinical decisions, develop targeted intervention measures, and reduce the probability of misdiagnosis.