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Abstract Lung cancer has emerged as a major global public health concern. With growing public interest in lung cancer, online searches for related information have surged. However, a comprehensive evaluation of the credibility, quality, and value of lung cancer-related videos on digital media platforms remains unexamined. This study aimed to assess the informational quality and content of lung cancer-related videos on Douyin and Bilibili. A total of 200 lung cancer-related videos that met the criteria were selected from Douyin and Bilibili for evaluation and analysis. The first step involved recording and analyzing the basic information provided in the videos. Subsequently, the source and type of content for each video were identified. All videos’ educational content and quality were then evaluated using JAMA, GQS, and Modified DISCERN. Douyin videos were found to be more popular in terms of likes, comments, favorites, and shares, whereas Bilibili videos were longer in duration (P

BackgroundPrevious research has linked systemic inflammatory markers and the Dietary Inflammatory Index (DII) with depression. However, the relationship between DII and these markers, and their impact on mortality risk among depressed adults, remains underexplored. This study aims to explore the association between DII and systemic inflammatory markers and their mediating effect on mortality risk in adults with depression.MethodsThis study analyzed data from 4,981 adults with depression in the National Health and Nutrition Examination Survey (NHANES). This study quantified dietary inflammatory potential with the DII and systemic inflammation with the Systemic Immune-Inflammation Index (SII) and Systemic Inflammation Response Index (SIRI). Cox proportional hazards regression and inverse probability weighting evaluated the impact of DII, SII, and SIRI on mortality risk in depressed adults, as well as their mediating effects. Multiple linear regression analyzed the associations between DII and SII/SIRI. Restricted cubic spline analysis explored the non-linear relationship between DII and mortality risk.ResultsIn adjusted regression models, DII, SII, and SIRI were significantly associated with all-cause mortality risk in depressed adults, with hazard ratios (HRs) (95% CIs) from 1.333 to 1.497 (1.051–1.233, 1.689–1.832). DII was linearly related to SII, with βs (95% CIs) from 0.001 to 0.121 (0.001–0.017, 0.001–0.224). SII significantly mediated the DII-mortality risk link, especially in males (8.07%). The DII-mortality relationship was linear (Pnon-linear = 0.174), with a beneficial threshold at 1.62.ConclusionDII and SII are associated with increased all-cause mortality risk in depressed adults. The DII-related mortality risk in depression can be partially mediated by SII, with a more pronounced effect in males.

Abstract Objective This study endeavors to examine the feasibility of predicting the clinical outcomes of patients suffering from peripheral artery disease (PAD) who undergo endovascular intervention, by employing the Syngo iFlow technology. Methods Retrospectively enrolling 76 patients from December 2021 to May 2023, yielding a total of 77 affected limbs, this study employs clinical outcomes (improvement or otherwise) as the gold standard. Two physicians conducted visual assessments on both DSA and iFlow images to gauge patient improvement and assessed inter-observer consistency for each image modality. The Time to Peak (TTP) of regions of interest (ROI) at the femoral head, knee joint, and ankle joint was measured. Differences in pre- and post-procedure TTP were juxtaposed, and statistically significant parameter cutoff values were identified via ROC analysis. Employing these cutoffs for TTP classification, multivariate logistic regression and the C-statistic were utilized to assess the predictive value of distinct parameters for clinical success. Results Endovascular procedure exhibited technical and clinical success rates of 82.58 and 75.32%, respectively. Diagnostic performance of iFlow image visual assessment surpassed that of DSA images. Inter-observer agreement for iFlow and DSA image evaluations was equivalent (κ = 0.48 vs 0.50). Post-classification using cutoff values, multivariate logistic regression demonstrated the statistical significance of ankle joint TTP in post-procedure iFlow images of the endovascular procedure for clinical success evaluation (OR 7.21; 95% CI 1.68, 35.21; P = 0.010), with a C-statistic of 0.612. Conclusion Syngo iFlow color-encoded imagery holds practical value in assessing the technical success of post-endovascular procedures, offering comprehensive lower limb arterial perfusion visualization. Its quantifiable parameters exhibit promising potential for prognosticating clinical success.

ObjectivePrior research underscores the significance of paraspinal muscles in maintaining spinal stability. This study aims to investigate the predictive value of paraspinal muscle parameters for the occurrence of new vertebral compression fractures (NVCF) following percutaneous vertebroplasty (PVP) or percutaneous kyphoplasty (PKP) in patients with osteoporotic vertebral compression fractures (OVCF).MethodsRetrospectively collected data from October 2019 to February 2021 (internal validation, n = 235) and March 2021 to November 2021 (external validation, n = 105) for patients with OVCF treated with PVP/PKP at our institution. They were randomly divided into training (188 cases) and validation groups (47 cases) at an 8:2 ratio. Lasso regression and multivariable logistic regression identified independent risk factors in the training set, and a Nomogram model was developed. Accuracy was assessed using receiver operating characteristic curves (ROC), calibration was evaluated with calibration curves and the Hosmer-Lemeshow test, and clinical utility was analyzed using decision curve analysis (DCA) and clinical impact curve (CIC).ResultsSurgical approach, spinal computed tomography (CT) values, and multifidus skeletal muscle index (SMI) are independent predictors of postoperative NVCF in OVCF patients. A Nomogram model, based on the identified predictors, was developed and uploaded online. Internal validation results showed area under the curve (AUC) values of 0.801, 0.664, and 0.832 for the training set, validation set, and external validation, respectively. Hosmer-Lemeshow goodness-of-fit tests (χ2 = 7.311–14.474, p = 0.070–0.504) and calibration curves indicated good consistency between observed and predicted values. DCA and CIC demonstrated clinical net benefit within risk thresholds of 0.06–0.84, 0.12–0.23, and 0.01–0.27. At specificity 1.00–0.80, the partial AUC (0.106) exceeded that at sensitivity 1.00–0.80 (0.062).ConclusionCompared to the spinal CT value, the multifidus SMI has certain potential in predicting the occurrence of NVCF. Additionally, the Nomogram model of this study has a greater negative predictive value.

IntroductionDown syndrome (DS) is the most common genetic condition that causes intellectual disability in humans. The molecular mechanisms behind the DS phenotype remain unclear. Therefore, in this study, we present new findings on its molecular mechanisms through single-cell RNA sequencing.MethodsInduced pluripotent stem cells (iPSCs) from the patients with DS and the normal control (NC) patients were differentiated into iPSCs-derived neural stem cells (NSCs). Single-cell RNA sequencing was performed to achieve a comprehensive single-cell level differentiation roadmap for DS-iPSCs. Biological experiments were also performed to validate the findings.Results and DiscussionThe results demonstrated that iPSCs can differentiate into NSCs in both DS and NC samples. Furthermore, 19,422 cells were obtained from iPSC samples (8,500 cells for DS and 10,922 cells for the NC) and 16,506 cells from NSC samples (7,182 cells for DS and 9,324 cells for the NC), which had differentiated from the iPSCs. A cluster of DS-iPSCs, named DS-iPSCs-not differentiated (DSi-PSCs-ND), which had abnormal expression patterns compared with NC-iPSCs, were demonstrated to be unable to differentiate into DS-NSCs. Further analysis of the differentially expressed genes revealed that inhibitor of differentiation family (ID family) members, which exhibited abnormal expression patterns throughout the differentiation process from DS-iPSCs to DS-NSCs, may potentially have contributed to the neural differentiation of DS-iPSCs. Moreover, abnormal differentiation fate was observed in DS-NSCs, which resulted in the increased differentiation of glial cells, such as astrocytes, but decreased differentiation into neuronal cells. Furthermore, functional analysis demonstrated that DS-NSCs and DS-NPCs had disorders in axon and visual system development. The present study provided a new insight into the pathogenesis of DS.

Hematopoietic stem cells (HSCs) are stem cells that can differentiate into various blood cells and have long-term self-renewal capacity. At present, HSC transplantation is an effective therapeutic means for many malignant hematological diseases, such as aplastic hematological diseases and autoimmune diseases. The hematopoietic microenvironment affects the proliferation, differentiation, and homeostasis of HSCs. The regulatory effect of the hematopoietic microenvironment on HSCs is complex and has not been thoroughly studied yet. In this study, we focused on mononuclear cells (MNCs), which provided an important microenvironment for HSCs and established a methodological system for identifying cellular composition by means of multiple technologies and methods. First, single-cell RNA sequencing (scRNA-seq) technology was used to investigate the cellular composition of cells originating from different microenvironments during different stages of hematopoiesis, including mouse fetal liver mononuclear cells (FL-MNCs), bone marrow mononuclear cells (BM-MNCs), and in vitro-cultured fetal liver stromal cells. Second, bioinformatics analysis showed a higher proportion and stronger proliferation of the HSCs in FL-MNCs than those in BM-MNCs. On the other hand, macrophages in in vitro-cultured fetal liver stromal cells were enriched to about 76%. Differential gene expression analysis and Gene Ontology (GO) functional enrichment analysis demonstrated that fetal liver macrophages have strong cell migration and actin skeleton formation capabilities, allowing them to participate in the hematopoietic homeostasis through endocytosis and exocytosis. Last, various validation experiments such as quantitative real-time PCR (qRT-PCR), ELISA, and confocal image assays were performed on randomly selected target genes or proteins secreted by fetal liver macrophages to further demonstrate the potential relationship between HSCs and the cells inhabiting their microenvironment. This system, which integrates multiple methods, could be used to better understand the fate of these specific cells by determining regulation mechanism of both HSCs and macrophages and could also be extended to studies in other cellular models.

Dopa-responsive dystonia (DRD), also known as Segawa syndrome, is a rare neurotransmitter disease. The decrease in dopamine caused by tyrosine hydroxylase (TH) gene mutation may lead to dystonia, tremor and severe encephalopathy in children. Although the disease caused by recessive genetic mutation of the tyrosine hydroxylase (TH) gene is rare, we found that the clinical manifestations of seven children with tyrosine hydroxylase gene mutations are similar to dopa-responsive dystonia. To explore the clinical manifestations and possible pathogenesis of the disease, we analyzed the clinical data of seven patients. Next-generation sequencing showed that the TH gene mutation in three children was a reported homozygous mutation (c.698G>A). At the same time, two new mutations of the TH gene were found in other children: c.316_317insCGT, and c.832G>A (p.Ala278Thr). We collected venous blood from four patients with Segawa syndrome and their parents for real-time quantitative polymerase chain reaction analysis of TH gene expression. We predicted the structure and function of proteins on the missense mutation iterative thread assembly refinement (I-TASSER) server and studied the conservation of protein mutation sites. Combined with molecular biology experiments and related literature analysis, the qPCR results of two patients showed that the expression of the TH gene was lower than that in 10 normal controls, and the expression of the TH gene of one mother was lower than the average expression level. We speculated that mutation in the TH gene may clinically manifest by affecting the production of dopamine and catecholamine downstream, which enriches the gene pool of Segawa syndrome. At the same time, the application of levodopa is helpful to the study, diagnosis and treatment of Segawa syndrome.

Epilepsy of infancy with migrating focal seizures (EIMFS) is a kind of epileptic encephalopathy with high genetic heterogeneity. The most common pathogenic gene for EIMFS is potassium sodium-activated channel subfamily T member 1 (KCNT1). Using Sendai virus-mediated reprogramming, we established an induced pluripotent stem cell (iPSC) line from the peripheral blood mononuclear cells (PBMCs) of a five-month-old Chinese girl with heterozygous missense mutation (c.2800 G>A) in the KCNT1 gene. The iPSCs were stable during amplification, expressed pluripotent genes, maintained a normal karyotype, and showed characteristics of the three germs layers in an in vitro differentiation assay.

Background: The chromodomain helicase DNA-binding protein 2 (CHD2) gene, is an ATPase and part of the CHD family of chromatin remodelers. Mutations in the CHD2 gene are inherited in an autosomal-dominant manner and can lead to intellectual disability, epilepsy, and autism. We investigated the clinical characteristics of CHD2-related conditions and their possible pathogenesis.Methods: We collected and analysed the clinical data of patients that were identified as having CHD2 mutations. Genetic testing was performed using targeted sequencing or whole-exome sequencing. We analysed the expression of CHD2 and repressor element 1-silencing transcription factor (REST) in blood samples using quantitative PCR and the conservation of the mutations. The CHD2 mutations we identified were compared with the known mutations reported in the CHD2-related literature.Results: Eight patients with CHD2 gene mutations were analysed. Six mutations were identified; four were unreported previously (c.670C>T; c.4012A>C; c.2416dup; c.1727–1728insAT), and two were known mutations: c.5035C>T (two cases) and c.4173dup (two cases). Among these mutations, seven were de novo mutations, and one could not be determined because the parents refused genetic testing. The clinical manifestations included mild or severe intellectual disability, epilepsy, and behavioural abnormalities. Quantitative PCR showed that the CHD2 gene expression levels among the patients, parents, and the controls were not significantly different. The levels of REST gene expression in the patients were significantly higher than those of the controls; thus, mutation of the CHD2 gene led to an increase in the expression level of the REST gene. The mutations reported were all located in conserved positions in different species. Among the various medications administered for treatment, valproate showed the best results for the treatment of epilepsy caused by CHD2 gene mutation.Conclusion: Mutation in CHD2 did not lead to a significant decrease in its expression level, indicating that the clinical phenotype was unrelated to its expression level, and the mutant protein may retain some function. Most of the mutations relatively stable. In addition, the clinical manifestations from the same mutation in the CHD2 gene were different among the known cases; this may be related to the regulation of REST or other regulatory factors.

RNA editing is a co- or post-transcriptional modification through which some cells can make discrete changes to specific nucleotide sequences within an RNA molecule after transcription. Previous studies found that RNA editing may be critically involved in cancer and aging. However, the function of RNA editing in human early embryo development is still unclear. In this study, through analyzing single cell RNA sequencing data, 36.7% RNA editing sites were found to have a have differential editing ratio among early embryo developmental stages, and there was a great reprogramming of RNA editing rates at the 8-cell stage, at which most of the differentially edited RNA editing sites (99.2%) had a decreased RNA editing rate. In addition, RNA editing was more likely to occur on RNA splicing sites during human early embryo development. Furthermore, long non-coding RNA (lncRNA) editing sites were found more likely to be on RNA splicing sites (odds ratio = 2.19, P = 1.37×10-8), while mRNA editing sites were less likely (odds ratio = 0.22, P = 8.38×10-46). Besides, we found that the RNA editing rate on lncRNA had a significantly higher correlation coefficient with the percentage spliced index (PSI) of lncRNA exons (R = 0.75, P = 4.90×10-16), which indicated that RNA editing may regulate lncRNA splicing during human early embryo development. Finally, functional analysis revealed that those RNA editing-regulated lncRNAs were enriched in signal transduction, the regulation of transcript expression, and the transmembrane transport of mitochondrial calcium ion. Overall, our study might provide a new insight into the mechanism of RNA editing on lncRNAs in human developmental biology and common birth defects.

The gene encoding collagen like tail subunit of asymmetric acetylcholinesterase (COLQ) is responsible for the transcription of three strands of collagen of acetylcholinesterase, which is attached to the endplate of neuromuscular junctions. Mutations in the COLQ gene are inherited in an autosomal-recessive manner and can lead to type V congenital myasthenia syndrome (CMS), which manifests as decreased muscle strength at birth or shortly after birth, respiratory failure, restricted eye movements, drooping of eyelids, and difficulty swallowing. Here we reported three variants within COLQ in two unrelated children with CMS. An intronic variant (c.393+1G>A) and a novel missense variant (p.Q381P) were identified as compound heterozygous in a 13-month-old boy, with the parents being carriers of each. An intragenic deletion including exons 14 and 15 was found in a homozygous state in a 12-year-old boy. We studied the relative expression of the COLQ and AChE gene in the probands' families, performed three-dimensional protein structural analysis, and analyzed the conservation of the missense mutation c.1142A>C (p.Q381P). The splicing mutation c.393+1G>A was found to affect the normal splicing of COLQ exon 5, resulting in a 27-bp deletion. The missense mutation c.1142A>C (p.Q381P) was located in a conserved position in different species. We found that homozygous deletion of COLQ exons 14–15 resulted in a 241-bp deletion, which decreased the number of amino acids and caused a frameshift translation. COLQ expression was significantly lower in the probands than in the probands' parents and siblings, while AChE expression was significantly higher. Moreover, the mutations were found to cause significant differences in the predicted three-dimensional structure of the protein. The splicing mutation c.393+1G>A, missense mutation c.1A>C (p.Q381P), and COLQ exon 14–15 deletion could cause CMS.

β654-thalassemia is a prominent Chinese subtype of b-thalassemia, representing 17% of all cases of β-thalassemia in China. The molecular mechanism underlying this subtype involves the IVS-2-654 C→T mutation leading to aberrant β-globin RNA splicing. This results in an additional 73-nucleotide exon between exons 2 and 3 and leads to a severe thalassemia syndrome. Herein, we explored a CRISPR/Cas9 genome editing approach to eliminate the additional 73- nucleotide by targeting both the IVS-2-654 C→T and a cryptic acceptor splice site at IVS-2-579 in order to correct aberrant b-globin RNA splicing and ameliorate the clinical β-thalassemia syndrome in β654 mice. Gene-edited mice were generated by microinjection of sgRNA and Cas9 mRNA into one-cell embryos of β654 or control mice: 83.3% of live-born mice were gene-edited, 70% of which produced correctly spliced RNA. No off-target events were observed. The clinical symptoms, including hematologic parameters and tissue pathology of all of the edited β654 founders and their offspring were significantly improved compared to those of the non-edited β654 mice, consistent with the restoration of wild-type b-globin RNA expression. Notably, the survival rate of gene-edited heterozygous β654 mice increased significantly, and liveborn homozygous β654 mice were observed. Our study demonstrated a new and effective gene-editing approach that may provide groundwork for the exploration of β654-thalassemia therapy in the future.

Down's syndrome (DS) is one of the most commonly known disorders with multiple congenital disabilities. Besides severe cognitive impairment and intellectual disability, individuals with DS also exhibit additional phenotypes of variable penetrance and severity, with one or more comorbid conditions, including Alzheimer's disease, congenital heart disease, or leukemia. Various vital genes and regulatory networks had been studied to reveal the pathogenesis of the disease. Nevertheless, very few studies have examined alternative splicing. Alternative splicing (AS) is a regulatory mechanism of gene expression when making one multi-exon protein-coding gene produce more than one unique mature mRNA. We employed the GeneChip Human Transcriptome Array 2.0 (HTA 2.0) for the global gene analysis with hiPSCs from DS and healthy individuals. Examining differentially expressed genes (DEGs) in these groups and focusing on specific transcripts with AS, 466 up-regulated and 722 down-regulated genes with AS events were identified. These genes were significantly enriched in biological processes, such as cell adhesion, cardiac muscle contraction, and immune response, through gene ontology (GO) analysis of DEGs. Candidate genes, such as FN1 were further explored for potentially playing a key role in DS. This study provides important insights into the potential role that AS plays in DS.

Mental retardation, X-linked 21/34 (MRX21/34), is a rare intellectual disability disease caused by mutations in the IL1RAPL1 (Interleukin-1 Receptor Accessory Protein-Like 1) gene. Using Sendai virus-mediated reprogramming, we established an induced pluripotent stem cell (iPSC) line from PBMCs collected from a ten-year-old boy with MRX21/34. The iPSCs showed stable amplification, expressed pluripotent genes, displayed a normal karyotype, and had characteristics of trilineage differentiation potential in an in vitro differentiation assay.

Allan–Herndon–Dudley syndrome (AHDS) is a rare, X-chromosome-linked inherited disorder that affects brain development and is caused by a mutation in SLC16A2. Herein, we generated an induced pluripotent stem cell (iPSC) line from the peripheral blood mononuclear cells of a one-year-old male infant with AHDS using Sendai-virus-mediated reprogramming. These iPSCs exhibited stable amplification, expressed pluripotent markers, and differentiated spontaneously into three germ layers in vitro. Additionally, this iPSC line was found to maintain a normal karyotype and retain the pathogenic mutation in SLC16A2, facilitating the study of disease mechanisms and development of new therapies of AHDS.

Mediator complex subunit 12 (MED12)-related disorders are recessive-X-linked intellectual disabilities present primarily in male patients. We came across a female patient with a heterozygous mutation (c.1249-1G > C) related to MED12-related syndrome. MED12 expression was significantly lower than that in her parents, and another X chromosome was inactive. We established an induced pluripotent stem cell (iPSC) line from peripheral blood mononuclear cells (PBMCs) of a 1-year old Chinese girl with a heterozygous mutation (c.1249-1G > C) in MED12. PBMCs were reprogrammed using nonintegrative Sendai viral vectors. The iPSCs showed stable amplification, pluripotency-related gene expression, trilineage differentiation potential, and a normal karyotype.

Although β-thalassemia is one of the most common human genetic diseases, there is still no effective treatment other than bone marrow transplantation. Induced pluripotent stem cells have been considered good candidates for the future repair or replacement of malfunctioning organs. As a basis for developing transgenic induced pluripotent stem cell therapies for thalassemia, β654 induced pluripotent stem cells from a β654 -thalassemia mouse transduced with the normal human β-globin gene, and the induced pluripotent stem cells with an erythroid-expressing reporter GFP were used to produce chimeric mice. Using these chimera models, we investigated changes in various pathological indices including hematologic parameters and tissue pathology. Our data showed that when the chimerism of β654 induced pluripotent stem cells with the normal human β-globin gene in β654 mice is over 30%, the pathology of anemia appeared to be reversed, while chimerism ranging from 8% to 16% provided little improvement in the typical β-thalassemia phenotype. Effective alleviation of thalassemia-related phenotypes was observed when chimerism with the induced pluripotent stem cells owning the erythroid-expressing reporter GFP in β654 mouse was greater than 10%. Thus, 10% or more expression of the exogenous normal β-globin gene reduces the degree of anemia in our β-thalassemia mouse model, whereas treatment with β654 induced pluripotent stem cells which had the normal human β-globin gene had stable therapeutic effects but in a more dose-dependent manner.

Background β-thalassemia is one of the most common genetic diseases in the world and requires extensive therapy. Lentiviral-mediated gene therapy has been successfully exploited in the treatment of β-thalassemia and showed promise in clinical application. Using a human β-globin transgenic mouse line in a β-thalassemia diseased model generated with a lentiviral-mediated approach, we investigate the stable therapeutic effect on a common thalassemia syndrome.Design and Methods Human β-globin gene lentiviral vector was constr ucted, followed by subzonal microinjection into single-cell embryos of βIVS-2-654-thalassemia mice to generate a transgenic line. Human β-globin gene expression was examined with RT-PCR, Western-blotting and ELISA. The hematologic parameters and tissue pathology were investigated over time in founder mice and their off-spring.Results Transgenic mice with stable expression of the lentivirus carrying human β-globin gene were obtained. A marked improvement in red blood cell indices and a dramatic reduction in red blood cell anisocytosis, poikilocytosis and target cells were observed. Nucleated cell proportion was greatly decreased in bone marrow, and splenomegaly with extramedullary hematopoiesis was ameliorated. Iron deposition in liver was also reduced. There was a two-fold increase in the survival rate of the βIVS-2-654 mice carrying human β-globin transgene. Significantly, the germline integration of the lentiviral construct was obtained and stable hematologic phenotype correction was observed over the next two generations of the transgenic mice.Conclusions The generation of human β-globin transgenic mice in a βIVS-2-654-thalassemia mouse mediated with lentiviral vectors provides a useful model and offers an attractive means to investigate the transgenic stable therapeutic effect in β-thalassemia.

BACKGROUND: The investigation of UV-induced fluorescence imaging coupled with machine learning was conducted to non-destructively detect the total volatile basic nitrogen (TVB-N) of frozen-whole-round tilapia (FWRT) during freezing and thawing. The UV-induced fluorescence images of FWRT at the wavelength of 365 nm were acquired by self-developed fluorescence image acquisition system. In total, 169 color and texture features based on RGB, hue-saturation-intensity and L*a*b* color spaces and gray level co-occurrence matrix were extracted, respectively. Successive projections algorithm (SPA) was employed to select the optimal 16 features to achieve feature dimension reduction modeling. With full and extracted features as input, the models of partial least squares regression (PLSR), least-squares support vector machine (LSSVM) and convolutional neural network (CNN) were established for TVB-N prediction. RESULTS: Results indicated that the full features-based CNN performed better than SPA based prediction models (SPA-PLSR and SPA-LSSVM). The CNN model was determined to be the optimal with an RP2 value of 0.9779, RMSEP value of 1.1502 x 10-2 g N kg-1 and RPD value of 6.721 for TVB-N content predictiin. CONCLUSION: The CNN method based on UV fluorescence imaging technology has potential for quality and safety detection of FWRT. [ABSTRACT FROM AUTHOR]

Using a biopsychosocial framework, our study examines the biological, psychological, and sociocultural factors associated with depression among a crosssectional sample of undergraduate international students (N = 712) attending 28 U.S. colleges and universities. Consistent with hypotheses, regression analysis reveals that self-esteem, life satisfaction, and coping self-efficacy are negatively associated with depressive symptoms, and that ethnic minority status, perceived discrimination, and financial concerns are positively associated with depressive symptoms. Contrary to predictions, age, optimism, friendships, and school belonging are not significant predictors, and perseverance predicted increases depression in this sample. The novel findings highlight adaptation issues among international undergraduate students and suggest preventive measures and interventions against depression for university administrators and counselors. [ABSTRACT FROM AUTHOR]