Spatial Transcriptomics: A Powerful Tool in Disease Understanding and Drug Discovery.

Recent advancements in modern science have provided robust tools for drug discovery. The rapid development of transcriptome sequencing technologies has given rise to single-cell transcriptomics and single-nucleus transcriptomics, increasing the accuracy of sequencing and accelerating the drug discovery process. With the evolution of single-cell transcriptomics, spatial transcriptomics (ST) technology has emerged as a derivative approach. Spatial transcriptomics has emerged as a hot topic in the field of omics research in recent years; it not only provides information on gene expression levels but also offers spatial information on gene expression. This technology has shown tremendous potential in research on disease understanding and drug discovery. In this article, we introduce the analytical strategies of spatial transcriptomics and review its applications in novel target discovery and drug mechanism unravelling. Moreover, we discuss the current challenges and issues in this research field that need to be addressed. In conclusion, spatial transcriptomics offers a new perspective for drug discovery.

Scutellarin activates IDH1 to exert antitumor effects in hepatocellular carcinoma progression.

Isochlorate dehydrogenase 1 (IDH1) is an important metabolic enzyme for the production of α-ketoglutarate (α-KG), which has antitumor effects and is considered to have potential antitumor effects. The activation of IDH1 as a pathway for the development of anticancer drugs has not been attempted. We demonstrated that IDH1 can limit glycolysis in hepatocellular carcinoma (HCC) cells to activate the tumor immune microenvironment. In addition, through proteomic microarray analysis, we identified a natural small molecule, scutellarin (Scu), which activates IDH1 and inhibits the growth of HCC cells. By selectively modifying Cys297, Scu promotes IDH1 active dimer formation and increases α-KG production, leading to ubiquitination and degradation of HIF1a. The loss of HIF1a further leads to the inhibition of glycolysis in HCC cells. The activation of IDH1 by Scu can significantly increase the level of α-KG in tumor tissue, downregulate the HIF1a signaling pathway, and activate the tumor immune microenvironment in vivo. This study demonstrated the inhibitory effect of IDH1-α-KG-HIF1a on the growth of HCC cells and evaluated the inhibitory effect of Scu, the first IDH1 small molecule agonist, which provides a reference for cancer immunotherapy involving activated IDH1.

Incidence, prevalence, and mortality of schizophrenia from 2016 to 2020 in Shandong, China.

The epidemiology of schizophrenia has been reported in many countries. However, due to the limitations of those studies, the findings cannot be generalized to other parts of the world, especially in China. In this study, the incidence, prevalence, and mortality of schizophrenia in Shandong, China were calculated using data from the National Severe Mental Disorder Registration System collected between 2016 and 2020 and census data from 2010 to 2020. The overall incidence decreased from 9.61 per 100,000 in 2016 to 4.40 per 100,000 in 2020, the aggregate prevalence was approximately 3.20 per 1000, and the overall mortality ranged from 6.17 per 100,000 to 7.71 per 100,000. The evidence from this study indicated that the incidence, prevalence, and mortality of schizophrenia were higher in rural areas than in urban areas. Females had higher incidence, prevalence, and mortality than males. This study provided epidemiological information on schizophrenia and opened avenues for future research.

Competition-cooperation mechanism between Escherichia coli and Staphylococcus aureus based on systems mapping.

Introduction: Interspecies interactions are a crucial driving force of species evolution. The genes of each coexisting species play a pivotal role in shaping the structure and function within the community, but how to identify them at the genome-wide level has always been challenging. Methods: In this study, we embed the Lotka-Volterra ordinary differential equations in the theory of community ecology into the systems mapping model, so that this model can not only describe how the quantitative trait loci (QTL) of a species directly affects its own phenotype, but also describe the QTL of the species how to indirectly affect the phenotype of its interacting species, and how QTL from different species affects community behavior through epistatic interactions. Results: By designing and implementing a co-culture experiment for 100 pairs of Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus), we mapped 244 significant QTL combinations in the interaction process of the two bacteria using this model, including 69 QTLs from E. coli and 59 QTLs from S. aureus, respectively. Through gene annotation, we obtained 57 genes in E. coli, among which the genes with higher frequency were ypdC, nrfC, yphH, acrE, dcuS, rpnE, and ptsA, while we obtained 43 genes in S. aureus, among which the genes with higher frequency were ebh, SAOUHSC_00172, capF, gdpP, orfX, bsaA, and phnE1. Discussion: By dividing the overall growth into independent growth and interactive growth, we could estimate how QTLs modulate interspecific competition and cooperation. Based on the quantitative genetic model, we can obtain the direct genetic effect, indirect genetic effect, and genome-genome epistatic effect related to interspecific interaction genes, and then further mine the hub genes in the QTL networks, which will be particularly useful for inferring and predicting the genetic mechanisms of community dynamics and evolution. Systems mapping can provide a tool for studying the mechanism of competition and cooperation among bacteria in co-culture, and this framework can lay the foundation for a more comprehensive and systematic study of species interactions.

Development of youth tennis players: A study based on the ranking history of top ATP/WTA players worldwide and China.

BACKGROUND: The top 100 ATP/WTA ranking points are a crucial indicator of entry into the high-level world of tennis players, and the number of players from a nation in this ranking reflects the overall level of their tennis. However, the growth time series characteristics of elite tennis athletes are unclear. OBJECTIVE: This study aims to examine the historical career ranking changes of elite players and provide valuable insights for aspiring young players looking to achieve success in the sport. At the same time, it is of great significance for the efficient and sustainable cultivation of Chinese tennis players. METHODS: Data on the rankings of 202 players were analyzed, Spearman and Pearson correlations were employed to investigate the association between ranking and time-use patterns. The variance test was utilized to compare disparities in time characteristics of the ranking, with a statistical significance level of p<0.05. RESULTS: There was a significant correlation between the time of entering the professional tournament ranking system and the ranking, top 100 time, top 100 age, and age of starting tennis. Top 50 ATP players are earlier than those ranked 51-100. There was a significant difference between the age of starting tennis and the time to top 10 among the ATP and WTA players. Chinese female players showed no significant differences compared to their global Top 10 counterparts in terms of time-to-success characteristics. CONCLUSION: The elite tennis players who achieve success typically start playing and competing in the sport at a young age, with professional competition often commencing around 18 years of age. Notably, these players frequently attain high rankings before reaching the age of 20. Furthermore, top 10 ATP male players tend to start tennis at an earlier age and require a shorter time to achieve a top 10 ranking compared with WTA female players.

Age-related differences in clinical and laboratory characteristics of childhood-onset systemic lupus erythematosus: Pre-puberal-onset SLE is prone to delayed diagnosis.

OBJECTIVE: This study aimed to analyze age-specific characteristics of childhood-onset systemic lupus erythematosus (cSLE) at a health center in China. METHODS: The children with SLE were grouped based on age at disease-onset: pre-pubertal (≤7 years), peri-pubertal (8-13 years), and adolescence (14-18 years). The retrospective study included patients with cSLE diagnosed at the Beijing Children's Hospital between 2013 and 2021. RESULTS: A total of 675 females and 178 males were eligible for inclusion in this study. Among them, 160 patients were diagnosed during pre-puberty, 635 during peri-puberty, and 58 during adolescence. The female-to-male ratio of pre-pubertal, peri-pubertal, and adolescent diagnosis was 3.5: 1, 3.6: 1, and 7.28:1, respectively. The median time from onset to diagnosis during the pre-puberal period was 3.0 (IQR 1.0-24.0 months), which was longer than that during the peri-puberal period (1.4; IQR 0.7-4) months and adolescence (1.0; IQR 0.4-2) months (p = <.0001). The proportion of LN in patients diagnosed during the peri-puberal period (304, 46.6%) and during adolescence (27, 47.9%) was higher than that of patients diagnosed during the pre-puberal period (59, 36.9%) (p = .044). 46 (28.8%), 233 (36.7%), and 32 (55.2%) of children diagnosed during the pre-pubertal period, peri-pubertal period, and adolescence, respectively, suffered from leukopenia. CONCLUSION: The proportion of renal involvement and leukopenia in the pre-pubertal group was lower than that of the pubertal group and adolescent group. More importantly, the younger the age of the patient, the more likely the diagnosis to be delayed.

Janus kinase inhibitor, tofacitinib, in refractory juvenile dermatomyositis: a retrospective multi-central study in China.

OBJECTIVES: Juvenile dermatomyositis (JDM) is a chronic autoimmune disease. Some patients remain in an active state even though they were administrated with a combination of corticosteroid and methotrexate. Existing research has suggested that interferon and Janus kinase played an important role in pathogenesis. Existing research has suggested the efficacy of JAK inhibitors (JAKi). Our retrospective study aimed to investigate the efficacy of tofacitinib in refractory JDM patients. METHODS: A total of eighty-eight patients in China who had been diagnosed with JDM and subjected to tofacitinib therapy for over 3 months were retrospectively analyzed. Skin and muscle manifestations were assessed using the Cutaneous Assessment Tool-binary method (CAT-BM), Childhood Myositis Assessment Scale (CMAS), and kinase. Pulmonary function was assessed using a high-resolution CT (computerized tomography) scan and pulmonary symptoms. All patients were subjected to regular follow-up, and core measures were assessed every 3 months after initiation. Furthermore, the data were analyzed using the Wilcoxon single test, Mann-Whitney U test, and chi-square test. RESULTS: Compared with the baseline data, skin and muscle manifestations were found significantly improved during the respective follow-up visit. At the most recent follow-up, nearly 50% of patients achieved a clinical complete response and six patients received tofacitinib monotherapy. Sixty percent of patients suffering from interstitial lung disease well recovered on high-resolution CT. Seventy-five percent of patients showed a reduction in the size or number of calcinosis, and 25% of patients showed completely resolved calcinosis. CONCLUSION: In this study, the result suggested that tofacitinib therapy exerted a certain effect on skin manifestations, muscle manifestations, interstitial lung disease (ILD), calcinosis, as well as downgrade of medication. In-depth research should be conducted to focus on the correlation between the pathogenesis of JDM and JAKi.

Programmed Cell Death Protein 2-like Promotes Inflammation and Oxidative Stress in Vascular Endothelial Cells.

Programmed cell death protein 2-like (PDCD2L) is a shuttle protein of the nucleus and cytoplasm and is related to the ribosome biogenesis. However, there are few reports on the relationship between PDCD2L and inflammation, and the exact relationship between PDCD2L and inflammation has not been determined in vascular endothelial cells yet. Accordingly, we focus on exploring the relationship between PDCD2L and inflammation and its potential mechanisms. Our research findings suggested that PDCD2L is a proinflammatory target. The result showed that, by interfering with the expression of PDCD2L, LPS-induced inflammation of vascular endothelial cells can be reduced, such as IL-6 and IL-1ß, as well as the adhesion factor ICAM1. Meanwhile, overexpression of PDCD2L can further increase LPS-induced inflammation levels, ICAM1, and ROS production, reduce CAT, GSH/GSSG levels, and increase SOD levels. Therefore, we determined that PDCD2L has a regulatory effect on inflammation and oxidative stress of vascular endothelial cells, and its regulatory mechanism may be related to inflammatory transcription factors STAT1, NF-κB regulation, transport of inflammatory messenger mRNA, and ribosome biogenesis. Then, we screened that andrographolide (Andro) can bind to PDCD2L, thus inhibiting inflammation and endothelial cell adhesion caused by the overexpression of PDCD2L. This study reveals that PDCD2L is a potential anti-inflammatory therapeutic target, providing new exploration for the development of anti-inflammatory drugs.

Effects of triclosan exposure on stem cells from human exfoliated deciduous teeth (SHED) fate.

Triclosan (TCS), a widely used broad-spectrum antibacterial agent and preservative, is commonly found in products and environments. Widespread human exposure to TCS has drawn increasing attention from researchers concerning its toxicological effect. However, minimal studies have focused on the impact of TCS exposure on human stem cells. Therefore, the aim of the present study was to evaluate the effects of TCS exposure on stem cells from human exfoliated deciduous teeth (SHED) and its molecular mechanisms. A series of experimental methods were conducted to assess cell viability, morphology, proliferation, differentiation, senescence, apoptosis, mitochondrial function, and oxidative stress after SHED exposure to TCS. Furthermore, transcriptome analysis was applied to investigate the response of SHED to different concentrations of TCS exposure and to explore the molecular mechanisms. We demonstrated that TCS has a dose-dependent proliferation and differentiation inhibition of SHED, while promoting cellular senescence, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and oxidative stress, as well as significantly induces apoptosis and autophagy flux inhibition at high concentrations. Interestingly, no significant morphological changes in SHED were observed after TCS exposure. Transcriptome analysis of normal and TCS-induced SHED suggested that SHED may use different strategies to counteract stress from different concentrations of TCS and showed significant differences. We discovered that TCS mediates cellular injury of SHED by enhancing the expression of PTEN, thereby inhibiting the phosphorylation levels of PI3K and AKT as well as mTOR expression. Collectively, our findings provide a new understanding of the toxic effects of TCS on human stem cell fate, which is important for determining the risk posed by TCS to human health.

Lipid profiles in patients with juvenile idiopathic arthritis: a systematic literature review and meta-analysis.

OBJECTIVE: The purpose of this study was to comprehensively evaluate the lipid profiles in patients with juvenile idiopathic arthritis (JIA). METHODS: The literature and relevant reviews were searched for published clinical studies on the relationship between JIA and blood lipid levels. The Newcastle-Ottawa scale (NOS) was applied to evaluate the risk and methodological value of the included case‒control and cohort studies. Standardized mean differences (SMDs) and 95% confidence intervals were derived for all variables with adequate unprocessed data. This meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines. RESULTS: In total, 16 studies were incorporated through screening. The analysis findings revealed that the levels of very low-density lipoprotein cholesterol [SMD=-0.411, 95% CI (-0.774~-0.048), P = 0.026], high-density lipoprotein cholesterol [SMD=-0.528, 95% CI (-0.976~-0.079), P = 0.021], and apolipoprotein A1 [SMD=-1.050, 95% CI (-1.452~-0.647), P = 0.000] in JIA patients were statistically lower than those observed in healthy controls. The level of low-density lipoprotein cholesterol [SMD = 0.202, 95% CI (0.003 ~ 0.400), P = 0.046] was significantly higher in JIA patients than in healthy controls. In JIA patients, body mass index [SMD=-0.189, 95% CI (-0.690 ~ 0.311), P = 0.459], high-density lipoprotein [SMD =-1.235, 95% CI (-2.845 ~ 0.374), P = 0.133), low-density lipoprotein [SMD = 0.616, 95% CI (-0.813 ~ 2.046), P = 0.398), triglycerides (SMD = 0.278, 95% CI (-0.182 ~ 0.738), P = 0.236], total cholesterol [SMD=-0.073, 95% CI (-0.438 ~ 0.293), P = 0.696] and apolipoprotein B levels [SMD = 0.226, 95% CI (-0.133 ~ 0.585), P = 0.217] were not significantly different from those in healthy controls. CONCLUSIONS: The outcomes of this meta-analysis suggest that dyslipidemia is common in JIA patients compared to healthy controls. Patients with JIA have a significantly increased risk of atherosclerosis and cardiovascular disease later in life.

Organ-on-a-chip meets artificial intelligence in drug evaluation.

Drug evaluation has always been an important area of research in the pharmaceutical industry. However, animal welfare protection and other shortcomings of traditional drug development models pose obstacles and challenges to drug evaluation. Organ-on-a-chip (OoC) technology, which simulates human organs on a chip of the physiological environment and functionality, and with high fidelity reproduction organ-level of physiology or pathophysiology, exhibits great promise for innovating the drug development pipeline. Meanwhile, the advancement in artificial intelligence (AI) provides more improvements for the design and data processing of OoCs. Here, we review the current progress that has been made to generate OoC platforms, and how human single and multi-OoCs have been used in applications, including drug testing, disease modeling, and personalized medicine. Moreover, we discuss issues facing the field, such as large data processing and reproducibility, and point to the integration of OoCs and AI in data analysis and automation, which is of great benefit in future drug evaluation. Finally, we look forward to the opportunities and challenges faced by the coupling of OoCs and AI. In summary, advancements in OoCs development, and future combinations with AI, will eventually break the current state of drug evaluation.

MiR-34a targets SIRT1 to reduce p53 deacetylation and promote sevoflurane inhalation anesthesia-induced neuronal autophagy and apoptosis in neonatal mice.

This study is to investigate the function of miR-34a and interactions between miR-34a, SIRT1, and p53 in sevoflurane-induced neuronal apoptosis and autophagy in neonatal mice. A mouse model was established by inhalation anesthesia with sevoflurane and injected with genetic reagents, followed by tests of learning and memory abilities and histological staining of the hippocampus. CCK-8 and AnnexinV/PI staining respectively measured the survival and apoptosis rates of primary hippocampal neurons cultured with sevoflurane. The expression levels of miR-34a, SIRT1, p53, Ac-p53, and autophagy- or apoptosis-related proteins were measured. Sevoflurane impaired the learning and memory abilities of mice, increased TUNEL-positive cells in their hippocampus, and hindered the survival of hippocampal neurons. Sevoflurane increased miR-34a, Bax, cleaved caspase-3, and the ratio of LC3-II/LC3-I and reduced SIRT1 and p62. MiR-34a overexpression promoted sevoflurane-induced neural damage, whereas SIRT1 inhibition or p53 upregulation counteracted the neuroprotection of miR-34a knockdown. SIRT1 was a target of miR-34a and promoted p53 deacetylation. MiR-34a promotes sevoflurane-stimulated neuronal apoptosis and autophagy in neonatal mice by inhibiting SIRT1 expression and subsequent p53 deacetylation.

Association between furosemide administration and clinical outcomes in patients with sepsis-associated acute kidney injury receiving renal replacement therapy: a retrospective observational cohort study based on MIMIC-IV database.

OBJECTIVE: To investigate the association between furosemide administration and clinical outcomes in patients with sepsis-associated acute kidney injury (SAKI) receiving renal replacement therapy (RRT). DESIGN: A retrospective observational cohort study. SETTING: The data were collected from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, which contains clinical data from more than 380 000 patients admitted to the intensive care units (ICUs) of the Beth Israel Deaconess Medical Center from 2008 to 2019. PARTICIPANTS: All adult patients with SAKI receiving RRT were enrolled. Data for each patient within the first 24 hours of ICU admission were extracted from the MIMIC-IV database. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was in-hospital mortality, and the secondary outcome was the length of hospital stay, length of ICU stay, RRT-free time and ventilator-free time. Logistic regression was used to investigate the association between furosemide administration and in-hospital mortality. Subgroup analysis was employed to explore the potential sources of heterogeneity. RESULTS: A total of 1663 patients with SAKI receiving RRT were enrolled in the study, of whom 991 patients (59.6%) were retrospectively allocated to the Furosemide group and 672 (40.4%) patients to the non-furosemide group. Univariate and multivariate logistic regression showed that furosemide administration was associated with reduced in-hospital mortality, respectively ((OR 0.77; 95% CI 0.63 to 0.93; p=0.008 < 0.05), (OR 0.59; 95% CI 0.46 to 0.75; p<0.001)). The association remained robust to different ways of adjusting for baseline confounding (all p<0.05). Subgroup analysis suggested that AKI-stage may be a source of heterogeneity. Patients in the furosemide group also had longer RRT-free time (p<0.001) and longer ventilator-free time (p<0.001) than those in the non-furosemide group. CONCLUSIONS: Furosemide is associated with decreased in-hospital mortality, longer RRT-free time and ventilator-free time in patients with SAKI receiving RRT.

A systematic review and meta-analysis of environmental factors associated with juvenile idiopathic arthritis.

OBJECTIVES: Juvenile idiopathic arthritis (JIA) is the most common pediatric rheumatic disease, thought to be influenced by both genetics and the environment. Identifying environmental factors associated with disease risk will improve knowledge of disease mechanisms and ultimately benefit patients. This review aimed to collate and synthesize the current evidence of environmental factors associated with JIA. METHODS: MEDLINE (Ovid), EMBASE (Ovid), Cumulative Index of Nursing and Related Health Literature (EBSCOhost), science network (WOS, Clarivate Analytics), Chinese National Knowledge Infrastructure, and Chinese Biological Medical Database were systematically searched. Study quality was rated using the Newcastle-Ottawa Scale. Pooled estimates for each environmental factor were generated using a random-effects, inverse-variance method, where possible. The remaining environmental factors were synthesized in narrative form. RESULTS: This review includes environmental factors from 23 studies (6 cohorts and 17 case-control studies). Cesarean section delivery was associated with increased JIA risk (pooled relative risk [RR] 1.103, 95% CI 1.033-1.177). Conversely, maternal smoking of more than 20 cigarettes/day (pooled RR 0.650, 95% CI 0.431-0.981) and gestational smoking (pooled RR0.634, 95% CI 0.452-0.890) were associated with decreased JIA risk. CONCLUSION: This review identifies several environmental factors associated with JIA and demonstrates the huge breadth of environmental research. We also highlight the challenges of combining data collected over this period due to limited study comparability, evolution in healthcare and social practices, and changing environment, which warrant consideration when planning future studies.

Association Between Sunlight Exposure and Mental Health: Evidence from a Special Population Without Sunlight in Work.

Purpose: In recent years, mental health problems have become the most serious social problems worldwide. Past studies have proposed that some links exist between sunlight and mental health; however, relevant studies examining low-dose sunlight exposure populations are lacking. We conducted a study among a group of operating room nurses (ORNs) who work long hours in operating rooms and have limited sunlight exposure. We aim to add to and refine previous researches on the association between mental health and sunlight exposure in community population. Patients and Methods: A total of 787 ORNs were interviewed and analyzed. Mental health, sunlight exposure duration, sociodemographic and work-related variables, and chronic diseases were evaluated. The Kessler 10 scale (K10) was used to assess participants' mental health status, and their sunlight exposure duration was assessed using their self-reports. Multiple linear regression analysis was adopted to examine the association between sunlight exposure and mental health. Results: The average K10 score of ORNs was 25.41. ORNs exhibit poorer mental health than other populations. Poor mental health was negatively associated with greater sunlight exposure hours per day (ß=-0.378) and sleep regularity (ß=-3.341). Poor mental health was positively associated with chronic disease (ß=3.514). Conclusion: This study indicated that the positive association between sunlight exposure and mental health existed. Appropriate enhancement of sunlight exposure will be beneficial to mental health. Hospitals, related organizations and individuals should pay greater attention to ORNs' mental health and sunlight exposure conditions. More policy recommendations as well as building structure recommendations should be proposed.

Targeted Energy Metabolomics Combined with Spatial Metabolomics Study on the Efficacy of Guhong Injection Against Cerebral Ischemia Reperfusion.

Optimizing the metabolic phenotype to improve cerebral function is critical for treatment of cerebral ischemia-reperfusion (I/R) injury. Guhong injection (GHI), which comprised safflower extract and aceglutamide, is widely prescribed in Chinese medicine for the treatment of cerebrovascular diseases. In this study, a combination of LC-QQQ-MS and MALDI-MSI were utilized to explore tissue-specific metabolic alterations in the brain of I/R, as well as to evaluate the therapeutic effect of GHI. Pharmacological evaluation demonstrated that GHI can significantly improve infarction rate, neurological deficit, cerebral blood flow, and neuronal damage in I/R rats. Based on LC-QQQ-MS, 23 energy metabolites were found to be significantly altered in the I/R group compared to the sham group (P < 0.05). After GHI treatment, 12 metabolites, including G6P, TPP, NAD, citrate, succinate, malate, ATP, GTP, GDP, ADP, NADP, and FMN showed a significant tendency of returning to baseline values (P < 0.05). Based on MALDI-MSI, 4 metabolites in glycolysis and TCA, 4 metabolites in nucleic acid metabolism, 4 amino acid metabolites, and 6 metabolites were discovered and compared between the different groups in the four special regions of cortex, hippocampus, hypothalamus, and striatum. Parts of these were found to have significant changes after I/R in the special brain region, and were regulated by GHI. The study provides comprehensive and detailed information for specific metabolic reprogramming of brain tissue in rats with I/R, and the therapeutic effect of GHI. Schema describing the discovery strategies of integrated LC-MS and MALDI-MSI to identify cerebral ischemia reperfusion metabolic reprogramming and GHI therapeutic effects.

Paraneoplastic pemphigus misdiagnosed as juvenile dermatomyositis: A case report.

Paraneoplastic pemphigus (PNP) is a rare autoimmune skin disease closely related to tumors, characterized by a maculopapular rash with mucosal pain, bronchiole occlusion, and respiratory failure may occur over time, even resulting in death. We report a rare case of a child with autoimmune PNP misdiagnosed as juvenile dermatomyositis (JDM), and summarize the key points of differentiation of clinical manifestations and auxiliary examinations of PNP and JDM. When the diagnosis is not clear because the patient has features not typical of JDM, then skin biopsy and other diagnostic studies should be considered prior to any immunosuppressive therapy, as this could potentially obscure and delay the diagnosis of malignancy.

Clinical Presentation and Treatment of Juvenile Idiopathic Arthritis Combined with Lung Disease: A Narrative Review.

Juvenile idiopathic Arthritis (JIA) is a common rheumatic disorder in children that can cause multiple systems to be affected simultaneously, leading to severe clinical symptoms and a high mortality rate in those with pulmonary involvement. Pleurisy is the most common manifestation of pulmonary involvement. At the same time, other conditions, such as pneumonia, interstitial lung disease, occlusive bronchiectasis, and alveolar protein deposition, have been increasingly reported in recent years. This review aims to provide an overview of the clinical manifestations of JIA lung damage and the current treatment options to assist in identifying and treating JIA lung involvement.