Clinical Treatment Strategies Research Articles

Juvenile Behçet syndrome: a contemporary view and differential diagnosis in pediatric practice.

This review aims to provide a comprehensive and contemporary overview of juvenile Behçet syndrome (jBS), highlighting its clinical manifestations, diagnostic challenges, and treatment strategies. Behçet syndrome, with its intricate etiopathogenesis and diverse clinical phenotypes, is more aptly classified as a syndrome than a single disease. Its heterogeneous nature requires a broad diagnostic approach and sophisticated differential diagnosis capabilities. The relatively rare occurrence of Behçet syndrome, combined with incomplete clinical presentations and overlapping differential diagnoses, presents significant diagnostic challenges, particularly in pediatric cases. Nevertheless, substantial progress has been made in treatment, especially in managing inflammatory components and preventing complications. Juvenile patients, given their developmental stage, require distinct therapeutic strategies compared to adults, with careful consideration of treatment side effects on growth and psychosocial development. To ensure early identification of jBS, it is imperative to refine and develop diagnostic criteria specifically tailored to pediatric populations. With a deeper understanding of the disease mechanisms, treatment protocols should be designed to address the developmental, psychosocial, and individual needs of patients, aiming to minimize long-term side effects. Additionally, comprehensive studies considering age, sex, and ethnic differences are necessary to fill gaps in the literature and resolve existing inconsistencies.

Key regulators of vascular calcification in chronic kidney disease: Hyperphosphatemia, BMP2, and RUNX2

Vascular calcification is quite common in patients with end-stage chronic kidney disease and is a major trigger for cardiovascular complications in these patients. These complications significantly impact the survival rate and long-term prognosis of individuals with chronic kidney disease. Numerous studies have demonstrated that the development of vascular calcification involves various pathophysiological mechanisms, with the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) being of utmost importance. High phosphate levels, bone morphogenetic protein 2 (BMP2), and runt-related transcription factor 2 (RUNX2) play crucial roles in the osteogenic transdifferentiation process of VSMCs. This article primarily reviews the molecular mechanisms by which high phosphate, BMP2, and RUNX2 regulate vascular calcification secondary to chronic kidney disease, and discusses the complex interactions among these factors and their impact on the progression of vascular calcification. The insights provided here aim to offer new perspectives for future research on the phenotypic switching and osteogenic transdifferentiation of VSMCs, as well as to aid in optimizing clinical treatment strategies for this condition, bearing significant clinical and scientific implications.

Red Blood Cell Transfusion for Incidence of Retinopathy of Prematurity: Prospective Multicenter Cohort Study

Abstract Background Retinopathy of prematurity (ROP) is a leading cause of visual impairment and blindness in preterm infants. Objective This study sought to investigate the association between red blood cell (RBC) transfusion and ROP in very preterm infants (VPIs) to inform clinical strategies for ROP prevention and treatment. Methods We designed a prospective multicenter cohort study that included VPIs and follow-up data from January 2017 to December 2022 at 3 neonatal clinical medicine centers. They were categorized into a transfusion group (infants who received an RBC transfusion within 4 wk) and a nontransfusion group. The relationship between RBC transfusion and ROP incidence was assessed using binary logistic regression, with subgroup analyses based on gestational age, birth weight, sex, and sepsis status. Inverse probability of treatment weighting and propensity score matching were applied to account for all potential confounding factors that could affect ROP development, followed by sensitivity analysis. Results The study included 832 VPIs, including 327 in the nontransfusion group and 505 in the transfusion group. The transfusion group had a lower average birth weight and gestational age and a greater incidence of ROP, ≥stage 2 ROP, and severe ROP. Logistic regression analysis revealed that the transfusion group had a significantly greater risk of ROP (adjusted odds ratio [aOR] 1.70, 95% CI 1.14‐2.53, P=.009) and ≥stage 2 ROP (aOR 1.68, 95% CI 1.02‐2.78, P=.04) but not severe ROP (aOR 1.75, 95% CI 0.61‐5.02, P=.30). The trend analysis also revealed an increased risk of ROP with an increasing number of transfusions and a larger volume of blood transfused (P for trend<.001). Subgroup analyses confirmed a consistent trend, with the transfusion group at a higher risk for ROP across all subgroups. Inverse probability of treatment weighting and propensity score matching analyses supported the initial findings. Conclusions For VPIs, RBC transfusion significantly increases the risk of ROP, and the risk increases with an increasing number of transfusions and volume of blood transfused.

Tracheal Tumors: Clinical Practice Guidelines for Palliative Treatment and Follow-Up

A substantial portion of patients with advanced cancer cannot be cured, regardless of the therapeutic methods employed. Hence, rational palliative causal treatment becomes crucial. Representative studies specifically addressing the exclusive palliative treatment of patients diagnosed with tracheal cancers have not been identified. In most studies, patients treated palliatively constituted a subset of the overall evaluated group. A thorough literature review was conducted, focusing on three types of palliative treatment: palliative radiotherapy, palliative surgical procedures, and systemic treatment for advanced disease. This review uniquely fills a significant gap in the existing literature by providing the first comprehensive and updated clinical practice guidelines specifically focused on the palliative treatment of tracheal tumors. The proposed guidelines emphasize the unique clinical challenges and treatment strategies pertinent to palliative care in tracheal tumors, which are not adequately covered in existing guidelines for other thoracic malignancies.

Clinical characteristics of pyoderma gangrenosum: Case series and literature review.

Pyoderma gangrenosum (PG) is a neutrophilic skin disease characterized by recurrent painful cutaneous ulcers, often accompanied by inflammatory bowel disease, joint pain, and other systemic damage. This disease is relatively rare in clinical practice and its diagnosis and treatment are often delayed, leading to secondary infections in the skin lesions, prolonged disease course, and increased disease burden on patients. This study retrospectively analyzed the clinical characteristics and treatment strategies of patients with PG admitted to our hospital and conducted a literature review, in order to improve the understanding of the disease among clinical doctors, enable patients to receive better diagnosis and treatment, and ultimately improve patient prognosis. Clinical data of patients diagnosed with PG and hospitalized in Beijing Chaoyang Hospital, Capital Medical University from January 2014 to December 2022 were retrospectively collected. The clinical manifestations, treatment strategies, efficacy, and disease outcomes were analyzed. A total of 14 patients, including 8 males and 6 females, aged 14 to 66 years, were included. Skin lesion types: 13 cases were ulcer-type, 1 case was pustule combined with ulcer-type, and the lower limbs were the most commonly affected areas. All the 14 patients presented with comorbidities. All patients were treated with glucocorticoids, with a daily dose equivalent to 20 to 100 mg prednisone and a median dose of 40 mg. Among them, 3 patients were treated with minocycline in combination, 1 patient was treated with mycophenolate mofetil 0.5 twice daily in combination, 1 patient was treated with cyclophosphamide 0.1 once daily in combination, and 1 patient was treated with thalidomide 0.1 every night in combination. PG is a relatively rare immune-related skin disease. Our small sample data analysis found that male PG is not uncommon in the Chinese population. Systemic glucocorticoids can quickly control the symptoms of PG in most patients with PG. In patients with poor efficacy or limited use of glucocorticoids, immunosuppressive drugs or novel targeted drugs such as biologics or small-molecule drugs should be used in combination as early as possible. Skin lesion care focuses on preventing infection, avoiding surgical debridement, and emphasizing pain management and the symptomatic treatment of comorbidities.

Transcriptome sequencing analysis reveals the molecular regulatory mechanism of myocardial hypertrophy induced by angiotensin II

The pathogenesis of myocardial hypertrophy remains incompletely understood, highlighting the critical need for in-depth investigation into its pathogenesis and pathophysiology to develop innovative strategies for preventing and treating heart diseases. In this study, a model of angiotensin II (Ang II)-induced myocardial hypertrophy was established using subcutaneous administration with a micropump. Echocardiography, wheat germ agglutinin staining, and western blot analysis were used to evaluate the myocardial hypertrophy model after 5, 10, and 15 days of Ang II treatment. RNA-seq was employed to analyze the differential expression profile of mRNA, followed by bioinformatics analysis. Subsequently, the anti-inflammatory drug meloxicam was utilized to explore its impact on cardiac hypertrophy in mice. The findings demonstrated that mice developed myocardial hypertrophy following subcutaneous administration of Ang II. Transcriptomic analysis revealed significant changes in gene expression in the myocardium induced by Ang II, with the most pronounced differences observed at day 10. Functional analysis and verification of differentially expressed genes indicated that Ang II triggered an inflammatory response in the myocardium, leading to up-regulation of genes associated with fibrosis and apoptosis while decreasing energy metabolism; alterations were also observed in genes related to oxidative stress and calcium ion binding. Treatment with meloxicam improved Ang II-induced myocardial hypertrophy. This study not only elucidated the molecular regulatory mechanism underlying mouse myocardial hypertrophy at a transcriptional level but also provided new insights into clinical prevention and treatment strategies for cardiac diseases such as dilated cardiomyopathy and heart failure.

Immune responses of pulpodentinal complex during caries progression

Caries is an infectious disease in which the invasion of pathogens and their metabolites can activate the recognition and defense system of the pulpodentinal complex. In-depth understanding of the immune responses mediated by the pulpodentinal complex will help to estimate the real state of the dental pulp during the progression of caries and to take reasonable clinical treatment strategies, which can be more targeted and less invasive. Based on the physiology of the pulpodentinal complex, the present article introduce its immunocompetence and mechanism, reactive changes, clinical intervention and its significance during the caries progression, as to improve diagnostics as well as treatment strategies for caries.

Case Analysis of Hypokalemia Induced by Irbesartan-Hydrochlorothiazide: A Case Study

Irbesartan-hydrochlorothiazide is a commonly used antihypertensive drug, but potential adverse reactions such as hypokalemia should not be overlooked. This study analyzes a case of hypokalemia induced by irbesartan-hydrochlorothiazide, exploring the drug’s association with hypokalemia and clinical treatment strategies. The patient experienced symptoms of muscle weakness and palpitations after taking irbesartan-hydrochlorothiazide and was diagnosed with hypokalemia through laboratory tests. Reviewing the patient’s medication history and disease progression, it was hypothesized that the drug’s potassium-wasting effect was the direct cause of the hypokalemia. After discontinuing the medication and initiating potassium supplementation, the patient’s potassium levels returned to normal, and symptoms significantly improved, further confirming the link between hypokalemia and the medication. This case suggests that clinicians should consider the risk of hypokalemia when treating hypertension, especially in patients with chronic kidney disease, the elderly, or those at risk for electrolyte disturbances. For patients who have already developed hypokalemia, potassium supplementation and adjustment of the treatment regimen are recommended to prevent further deterioration. Timely discontinuation of potential causative drugs is also advised. In summary, ensuring medication safety and preventing potential complications has significant clinical importance in recognizing and managing hypokalemia induced by irbesartan-hydrochlorothiazide. Future research should focus on optimizing treatment protocols and developing more effective strategies for preventing and managing related adverse reactions to improve patient quality of life.

Cytomegalovirus Retinitis: Clinical Manifestations, Diagnosis and Treatment

Cytomegalovirus (CMV) retinitis is the most common eye disease associated with CMV infection in immunocompromised individuals. The CMVR may initially be asymptomatic; however, relatively mild vitreous inflammation at the onset may be an important differential point from other diseases in HIV patients. Fundus photography, CD4 T-cell count, and telemedicine could be used to screen and monitor the high-risk population, particularly in resource-limited regions. Retinitis generally starts in the peripheral retina and advances toward the posterior pole, which could develop to the characteristic “pizza pie” appearance marked by central retinal necrosis and intraretinal hemorrhage. CMVR causes vision loss if left untreated, and early antiviral therapy significantly reduces the risk of vision loss. Alongside traditional antiviral treatments, immunotherapies including CMV-specific adoptive T-cell therapy and CMV immunoglobulin (CMVIG) are emerging as promising treatment options due to their favorable tolerability and reduced mortality. This review comprehensively examines CMV retinitis, encompassing the clinical features, differential diagnosis, laboratory tests, and updated treatment strategies to inform clinical management.

Interaction of major facilitator superfamily domain containing 2A with the blood-brain barrier.

The functional and structural integrity of the blood-brain barrier is crucial in maintaining homeostasis in the brain microenvironment; however, the molecular mechanisms underlying the formation and function of the blood-brain barrier remain poorly understood. The major facilitator superfamily domain containing 2A has been identified as a key regulator of blood-brain barrier function. It plays a critical role in promoting and maintaining the formation and functional stability of the blood-brain barrier, in addition to the transport of lipids, such as docosahexaenoic acid, across the blood-brain barrier. Furthermore, an increasing number of studies have suggested that major facilitator superfamily domain containing 2A is involved in the molecular mechanisms of blood-brain barrier dysfunction in a variety of neurological diseases; however, little is known regarding the mechanisms by which major facilitator superfamily domain containing 2A affects the blood-brain barrier. This paper provides a comprehensive and systematic review of the close relationship between major facilitator superfamily domain containing 2A proteins and the blood-brain barrier, including their basic structures and functions, cross-linking between major facilitator superfamily domain containing 2A and the blood-brain barrier, and the in-depth studies on lipid transport and the regulation of blood-brain barrier permeability. This comprehensive systematic review contributes to an in-depth understanding of the important role of major facilitator superfamily domain containing 2A proteins in maintaining the structure and function of the blood-brain barrier and the research progress to date. This will not only help to elucidate the pathogenesis of neurological diseases, improve the accuracy of laboratory diagnosis, and optimize clinical treatment strategies, but it may also play an important role in prognostic monitoring. In addition, the effects of major facilitator superfamily domain containing 2A on blood-brain barrier leakage in various diseases and the research progress on cross-blood-brain barrier drug delivery are summarized. This review may contribute to the development of new approaches for the treatment of neurological diseases.

Unraveling the role of bisphenol A in osteosarcoma biology: insights into prognosis and immune microenvironment modulation

BackgroundBisphenol A (BPA) is a common environmental pollutant, and its specific mechanisms in cancer development and its impact on the tumor immune microenvironment are not yet fully understood.MethodsTranscriptome data from osteosarcoma (OS) patients were downloaded from the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database. BPA-related genes were identified through the Comparative Toxicogenomics Database (CTD), yielding 177 genes. Differentially expressed genes were analyzed using the GSE162454 dataset from the Tumor Immune Single Cell Hub 2 (TISCH2). We constructed the prognostic model using univariate Cox regression and LASSO analysis. The model was validated using the GSE16091 dataset. GO, KEGG, and GSEA analyses were performed to investigate the mechanisms of BPA-related genes.ResultsA total of 15 BPA-related genes were identified as differentially expressed in OS. Univariate Cox regression and LASSO analysis identified four key prognostic genes (FOLR1, MYC, ESRRA, VEGFA). The prognostic model exhibited strong predictive performance with area under the curve (AUC) values of 0.89, 0.6, and 0.79 for predicting 1-, 2-, and 3-year survival, respectively. External validation using the GSE16091 dataset confirmed the model's high accuracy with AUC values exceeding 0.88. Our results indicated that the prognosis of the high-risk population is generally poorer, which may be associated with alterations in the tumor immune microenvironment. In the high-risk group, immune cells showed predominantly low expression levels, while immune checkpoint genes were significantly overexpressed, along with markedly elevated tumor purity. These findings revealed a correlation between upregulation of BPA-related genes and formation of an immunosuppressive microenvironment, leading to unfavorable patient outcomes.ConclusionOur study highlighted the significant association of BPA with OS biology, particularly in its potential role in modulating the tumor immune microenvironment. We offered a fresh insight into the influence of BPA on cancer development, thus providing valuable insights for future clinical interventions and treatment strategies.

Role of myeloid cells in mediating the effects of lipids on ulcerative colitis.

To evaluate the causal relationship between lipids and ulcerative colitis (UC) through Mendelian Randomization (MR), and to further investigate the involvement of immune cells in mediating this process. Utilizing summary statistics from genome-wide association studies (GWAS) of individuals with European ancestry, we analyzed the causal link between 179 lipid types and UC (2,569 UC cases and 453,779 controls) through Two-sample Mendelian randomization (2SMR) and Bayesian-weighted MR (BWMR). Based on this, a mediation screening of 731 immune cell phenotypes was conducted to identify exposure and mediator factors. Lastly, the role and proportion of immune cells in mediating the causal effects of lipids on UC were assessed via reverse MR (RMR) and two-step MR. The results of MR showed that there was a causal relationship between the six genetically predicted lipid types and UC (P <0.05), and the four immune cell phenotypes were identified as mediators of the association between lipids and UC. Notably, Phosphatidylcholine (PC) (16:0_0:0) served as the exposure factor, and myeloid cells CD11b on CD33+ HLA DR+ CD14dim acted as the mediator. Mediation analysis showed that CD11b on CD33+ HLA DR+ CD14dim had a mediation effect of -0.0205 between PC (16:0_0:0) and UC, with the mediation effect ratio at 15.38%. Our findings elucidate the causal effect of lipids on UC and identify the significant mediating role of myeloid cells CD11b on CD33+ HLA DR+ CD14dim in regulating UC through PC (16:0_0:0), offering new pathways and strategies for UC clinical treatment.

Synthetic lumbar MRI can aid in diagnosis and treatment strategies based on self-pix networks

CT and MR tools are commonly used to diagnose lumbar fractures (LF). However, numerous limitations have been found in practice. The aims of this study were to innovate and develop a spinal disease-specific neural network and to evaluate whether synthetic MRI of the LF affected clinical diagnosis and treatment strategies. A total of 675 LF patients who met the inclusion and exclusion criteria were included in the study. For each participant, two mid-sagittal CT and T2-weighted MR images were selected; 1350 pairs of LF images were also included. A new Self-pix based on Pix2pix and Self-Attention was constructed. A total of 1350 pairs of CT and MR images, which were randomly divided into a training group (1147 pairs) and a test group (203 pairs), were fed into Pix2pix and Self-pix. The quantitative evaluation included PSNR and SSIM (PSNR1 and SSIM1: real MR images and Pix2pix-generated MR images; PSNR2 and SSIM2: real MR images and Self-pix-generated MR images). The qualitative evaluation, including accurate diagnosis of acute fractures and accurate selection of treatment strategies based on Self-pix-generated MRI, was performed by three spine surgeons. In the LF group, PSNR1 and PSNR2 were 10.884 and 11.021 (p < 0.001), and SSIM1 and SSIM2 were 0.766 and 0.771 (p < 0.001), respectively. In the ROI group, PSNR1 and PSNR2 were 12.350 and 12.670 (p = 0.004), and SSIM1 and SSIM2 were 0.816 and 0.832 (p = 0.005), respectively. According to the qualitative evaluation, Self-pix-generated MRI showed no significant difference from real MRI in identifying acute fractures (p = 0.689), with a good sensitivity of 84.36% and specificity of 96.65%. No difference in treatment strategy was found between the Self-pix-generated MRI group and the real MRI group (p = 0.135). In this study, a disease-specific GAN named Self-pix was developed, which demonstrated better image generation performance compared to traditional GAN. The spine surgeon could accurately diagnose LF and select treatment strategies based on Self-pix-generated T2 MR images.

Lyme Disease and Papilledema: A Retrospective Study on Clinical Characteristics and Outcomes.

Describe the clinical characteristics, treatment strategies, and outcome data of children with papilledema associated with Lyme disease at a large tertiary care pediatric hospital. Retrospective cohort study of children 1-18 years old who received care at our institution between 1995 and 2019 with concurrent diagnoses of papilledema and Lyme disease. Data were abstracted from records and prospective family surveys. Among 44 children included (median age 9.7 years), 66% (29/44) had additional cranial neuropathies, and 78% (32/41) had cerebrospinal fluid pleocytosis. All children were treated with antibiotics (39% oral, 55% intravenous, 7% both); 61% (27/44) were also treated with oral acetazolamide. Symptoms fully resolved in 86% (30/35) of children with follow-up data. Proportion recovered did not significantly differ by antibiotic administration route or presence/absence of cerebrospinal fluid pleocytosis. Papilledema in Lyme disease may occur with or without cerebrospinal fluid pleocytosis. Most children recover without residual deficits following treatment, although exceptions exist.

A novel molecular classification based on efferocytosis-related genes for predicting clinical outcome and treatment response in acute myeloid leukemia.

Previous studies have shown that macrophage-mediated efferocytosis is involved in immunosuppression in acute myeloid leukemia (AML). However, the regulatory role of efferocytosis in AML remains unclear and needs further elucidation. We first identified the key efferocytosis-related genes (ERGs) based on the expression matrix. Efferocytosis-related molecular subtypes were obtained by consensus clustering algorithm. Differences in immune landscape and biological processes among molecular subtypes were further evaluated. The efferocytosis score model was constructed to quantify molecular subtypes and evaluate its value in prognosis prediction and treatment decision-making in AML. Three distinct efferocytosis-related molecular subtypes were identified and divided into immune activation, immune desert, and immunosuppression subtypes based on the characteristics of the immune landscape. We evaluated the differences in clinical and biological features among different molecular subtypes, and the construction of an efferocytosis score model can effectively quantify the subtypes. A low efferocytosis score is associated with immune activation and reduced mutation frequency, and patients have a better prognosis. A high efferocytosis score reflects immune exhaustion, increased activity of tumor marker pathways, and poor prognosis. The prognostic predictive value of the efferocytosis score model was confirmed in six AML cohorts. Patients exhibiting high efferocytosis scores may derive therapeutic benefits from anti-PD-1 immunotherapy, whereas those with low efferocytosis scores tend to exhibit greater sensitivity towards chemotherapy. Analysis of treatment data in ex vivo AML cells revealed a group of drugs with significant differences in sensitivity between different efferocytosis score groups. Finally, we validated model gene expression in a clinical cohort. This study reveals that efferocytosis plays a non-negligible role in shaping the diversity and complexity of the AML immune microenvironment. Assessing the individual efferocytosis-related molecular subtype in individuals will help to enhance our understanding of the characterization of the AML immune landscape and guide the establishment of more effective clinical treatment strategies.

Focal adhesion kinase regulates tendon cell mechanoresponse and physiological tendon development.

Tendons enable locomotion by transmitting high tensile mechanical forces between muscle and bone via their dense extracellular matrix (ECM). The application of extrinsic mechanical stimuli via muscle contraction is necessary to regulate healthy tendon function. Specifically, applied physiological levels of mechanical loading elicit an anabolic tendon cell response, while decreased mechanical loading evokes a degradative tendon state. Although the tendon response to mechanical stimuli has implications in disease pathogenesis and clinical treatment strategies, the cell signaling mechanisms by which tendon cells sense and respond to mechanical stimuli within the native tendon ECM remain largely unknown. Therefore, we explored the role of cell-ECM adhesions in regulating tendon cell mechanotransduction by perturbing the genetic expression and signaling activity of focal adhesion kinase (FAK) through both invitro and invivo approaches. We determined that FAK regulates tendon cell spreading behavior and focal adhesion morphology, nuclear deformation in response to applied mechanical strain, and mechanosensitive gene expression. In addition, our data reveal that FAK signaling plays an essential role in invivo tendon development and postnatal growth, as FAK-knockout mouse tendons demonstrated reduced tendon size, altered mechanical properties, differences in cellular composition, and reduced maturity of the deposited ECM. These data provide a foundational understanding of the role of FAK signaling as a critical regulator of insitu tendon cell mechanotransduction. Importantly, an increased understanding of tendon cell mechanotransductive mechanisms may inform clinical practice as well as lead to the discovery of diagnostic and/or therapeutic molecular targets.

Pseudomonas aeruginosa exotoxin A as a novel allergen induced Non-TH2 inflammation in a murine model of steroid-insensitive asthma

BackgroundDespite the immediate in vivo occurrence of anaphylactic and allergic reactions following treatment with Pseudomonas aeruginosa exotoxin A (PEA)-based immunotoxins, the immunological role of PEA in asthma pathogenesis remains unclear. ObjectiveThis study investigated the allergenic potential of PEA and the specific type of asthma induced. MethodsRecombinant PEA (rPEA) lacking domain Ia (to eliminate non-specific cytotoxicity) was expressed, purified, and employed to detect serum PEA-specific IgE levels in asthmatic patients. Competitive ELISA assays were used to assess rPEA's IgE binding capacity and allergenicity. Additionally, rPEA-challenged C57BL/6 mice were subjected to inflammatory endotyping and therapeutic assays to characterize the allergic nature of PEA. ResultsPEA-specific IgE was identified in 17 (14.2 %) of 120 asthma patients. The rPEA-sensitized and challenged mice had increased PEA-specific immunoglobulins (such as IgE, IgG1 and IgG2a) and developed asthma-like phenotypes with airway hyperresponsiveness, severe airway inflammation, and airway remodeling. Lungs from these mice displayed significant increases in neutrophils and IL-17A+ cells. Innate lymphoid cells (ILCs) produced type 2 cytokines (IL-4, IL-5, and IL-13), whereas Th cells did not. Nonetheless, airway inflammation, rather than hyperresponsiveness, was elicited in non-sensitized mice upon challenge with rPEA. Importantly, rPEA-induced asthmatic mice were unresponsive to dexamethasone treatment. ConclusionPEA is a novel allergen that sensitizes asthmatic patients. Furthermore, mice developed steroid-resistant asthma, characterized by an atypical cytokine profile associated with non-TH2 inflammation, only after being sensitized and challenged with rPEA. These findings suggest a potentially significant role for PEA in asthma development, warranting consideration in clinical diagnosis and treatment strategies.

795. REVIEW OF CLINICAL CHARACTERISTICS AND PROGNOSIS OF MULTIPLE PRIMARY ESOPHAGEAL SQUAMOUS CELL CARCINOMA

Abstract Background Multiple Primary Esophageal Squamous Cell Carcinoma (MPESCC) is a rare and highly aggressive type of tumor, classified into Synchronous Multiple Primary Esophageal Squamous Cell Carcinoma (S-MPESCC) and Metachronous Multiple Primary Esophageal Squamous Cell Carcinoma (M-MPESCC). MPESCC has garnered increasing attention in recent years due to its complex pathogenesis, poor prognosis, and unclear treatment protocols. Compared to solitary esophageal squamous cell carcinoma (SESCC), patients with MPESCC typically show higher rates of lymph node and distant metastasis, leading to a poorer prognosis. This review aims to summarize the clinical characteristics, common treatment methods, and prognosis of MPESCC by analyzing existing literature, providing references for clinical practice. Methods The clinical characteristics of MPESCC patients differ significantly from those of SESCC patients, relevant literature was collected for meta-analysis of the following data of the patients: Gender and Age, Medical History, Pathological Features, Lymph Node and Distant Metastasis, Tumor Distribution. Treatment Methods include Surgical Treatment, Radiotherapy and Chemotherapy. Postoperative recurrence and metastasis are also included in the statistics. Results Tumors in MPESCC patients exhibit significant differences in pathological staging and grading, which makes treatment more challenging. Patients with MPESCC have significantly higher rates of lymph node and distant metastasis compared to those with SESCC. MPESCC tumors can appear in multiple locations within the esophagus, with pathological characteristics that may vary between sites. Surgery remains the primary treatment method for MPESCC. Due to the high risk of recurrence and metastasis in MPESCC patients, regular endoscopic and imaging examinations are necessary postoperatively to detect and address any recurrent or new tumors early. Conclusion MPESCC is a complex type of esophageal cancer with a poor prognosis. It’s clinical characteristics and treatment strategies differ significantly from those of SESCC. Multidisciplinary comprehensive treatment and close postoperative follow-up are crucial for improving the prognosis of patients with MPESCC. Further research is needed to optimize treatment protocols and enhance patient survival rates.

295P Long-term clinical outcomes and treatment strategy considerations by ER expression level in breast cancer

295P Long-term clinical outcomes and treatment strategy considerations by ER expression level in breast cancer

Finite Element Analysis of Mechanical Ocular Sequelae from Badminton Shuttlecock Projectile Impact

PurposeWith the growing popularity of badminton worldwide, the incidence of badminton-related ocular injuries is expected to rise. The high velocity of shuttlecocks renders ocular traumas particularly devastating, especially with the possibility of permanent vision loss. This study investigated the mechanism behind ocular complications though simulation analyses of mechanical stresses and pressures upon shuttlecock impact. DesignComputational simulation study ParticipantsNone MethodsA 3-dimensional human eye model was reconstructed based on the physiological and biomechanical properties of various ocular tissues. FEA simulations involved a frontal collision with a shuttlecock projectile at 128.7 km/h (80 mph). Intraocular pressure changes and tissue stress were mapped and quantified in the following ocular structures: the limbus, ciliary body, zonular fibers, ora serrata, retina, and optic nerve head. Main Outcome MeasuresIntraocular pressure and tissue stress ResultsUpon shuttlecock impact, compressive force was transferred to the anterior pole of the cornea, propagating posteriorly to the optic nerve head. Deflection of forces anteriorly contributed to refractory oscillations of compressive and tensile stress of ocular tissue. Initial impact led to a momentary (< 1 ms) spike in intraocular pressure 5.66 MPa (42.5 x 103 mmHg) that radially distributed for a very brief instance (< 1 ms) of pressure at the trabecular meshwork of the iridocorneal angle of 1.25 MPa (9.4 x 103 mmHg). The lens had a maximal posterior displacement of 1.5 mm with peak zonular fiber tensile strain of 52%. The limbus, ciliary body, and ora serrata had a peak tensile stress of 5.16 MPa, 1.90 MPa, and 0.62 MPa, respectively. Compressive force from the sclera concentrated at the optic nerve head for a peak stress of 5.97 MPa while peak pressure from vitreous humor was 7.99 MPa. ConclusionShuttlecock impact led to a very brief, substantial rise in pressure and stress significant for tissue damage and subsequent complications, such as secondary glaucoma, angle recession, lens subluxation, hyphema, or retinal dialysis. Our findings offer valuable mechanistic insights into how ocular structures are affected by shuttlecock projectile impact to inform clinical assessments and treatment strategies, while highlighting the importance of protective eyewear in racket sports.