Polypoidal choroidal vasculopathy(PCV)is one of the important subtypes of neovascular age-related macular degeneration(nARMD), which causes severe vision loss. It is necessary to distinguish PCV from other nARMD subtypes to guide the clinical treatment plans and predict disease outcomes. In recent years, artificial intelligence(AI)has been widely used in the diagnosis and research of ophthalmic diseases. By utilizing machine learning or deep learning combined with examination images in disease classification, lesion segmentation, and quantitative assessment, etc. This article reviews the recent applications of AI in the differential diagnosis of PCV through various examination images, the segmentation and quantification of biomarkers, as well as the prediction of genotype, response to anti-vascular endothelial growth factor(VEGF)therapy, and the short-term risk of vitreous hemorrhage. It summarizes the difficulties and challenges in clinical practice of AI and looks forward to the advantages and development trends of AI in PCV applications in the future. The article aims to provide more information for further research and application, thereby improving the diagnostic rate of PCV, optimizing treatment plans, and improving patients' visual prognosis.

Polypoidal choroidal vasculopathy(PCV)is one of the important subtypes of neovascular age-related macular degeneration(nARMD), which causes severe vision loss. It is necessary to distinguish PCV from other nARMD subtypes to guide the clinical treatment plans and predict disease outcomes. In recent years, artificial intelligence(AI)has been widely used in the diagnosis and research of ophthalmic diseases. By utilizing machine learning or deep learning combined with examination images in disease classification, lesion segmentation, and quantitative assessment, etc. This article reviews the recent applications of AI in the differential diagnosis of PCV through various examination images, the segmentation and quantification of biomarkers, as well as the prediction of genotype, response to anti-vascular endothelial growth factor(VEGF)therapy, and the short-term risk of vitreous hemorrhage. It summarizes the difficulties and challenges in clinical practice of AI and looks forward to the advantages and development trends of AI in PCV applications in the future. The article aims to provide more information for further research and application, thereby improving the diagnostic rate of PCV, optimizing treatment plans, and improving patients' visual prognosis.

ObjectivePatients with hepatic glycogen storage disease（GSD）have recurrent episodes of hypoglycemia. This study aimed to investigate and analyze blood glucose and biochemical indicators in pediatric patients with hepatic GSD， thus provide data support for hypoglycemia prevention and its clinical management. MethodsA cross-sectional field study was conducted among patients with hepatic GSD treated in the Department of Pediatrics of Guangdong Provincial People's Hospital on July 14， 2024. We collected the peripheral blood samples of the patients and their healthy family controls on site， then analyzed and compared their blood glucose and biochemical indicators. ResultsOf the 44 patients with hepatic GSD， there were 34 males and 10 females， including GSD Ib（n =14）， GSD Ia（n=15）， GSD Ⅲ（n=2）， GSD Ⅵ（n=7）and GSD Ⅸ（n=6）. The average age was 7.60（5.08-11.98）years. All patients were on uncooked cornstarch（UCCS）therapy. Of the patients， 77.3%（34/44）had hepatomegaly， 61.4%（27/44）had recurrent hypoglycemia， 61.4%（27/44）had blood glucose ≤ 3.9 mmol/L， 18.2%（8/44）had blood glucose ≤ 2.8 mmol/L， and none of the 8 cases was GSD Ib. The lowest blood glucose level was 1.19 mmol/L and no episodes of hypoglycemia occurred. Of the family control subjects， 65.9%（29/44）had blood glucose ≤ 3.9 mmol/L. There was no significant difference in hypoglycemia prevalence between hepatic GSD group and control group（P=0.658）. The hepatic GSD patients had hyperlactacemia， hyperuricemia and hypercholesterolemia prevalence rates of 65.9%， 45.5% and 9.1%， respectively， as compared with 18.2%， 43.2% and 15.9%， respectively， for the family control subjects. No significant difference was found in the prevalence rates of hyperuricemia and hypercholesterolemia between the two groups（P=0.830 and P=0.334， respectively）. ConclusionsAsymptomatic hypoglycemia is common in patients with hepatic GSD， especially in non-GSD-Ib patients. It is necessary to optimize the diet management of UCCS， conduct dynamic blood glucose monitoring and follow a light diet， so as to decrease hyperuricemia and hypercholesterolemia， avoid and reduce the serious adverse reactions and complications caused by severe hypoglycemia.

Objective To compare the benefits and drawbacks of primary patch expansion versus pericardial tube right ventricular-pulmonary artery connection in patients diagnosed with pulmonary atresia with ventricular septal defect (PA/VSD). Methods A retrospective study was conducted on patients diagnosed with PA/VSD who underwent primary right ventricular-pulmonary artery connection surgery at our center between 2010 and 2020. Patients were categorized into two groups based on the type of right ventricular-pulmonary artery connection: a pericardial tube group and a patch expansion group. Clinical data and imaging findings were compared between the two groups. Results A total of 51 patients were included in the study, comprising 31 males and 20 females, with a median age of 12.57 (4.57, 49.67) months. The pericardial tube group included 19 patients with a median age of 17.17 (7.33, 49.67) months, while the patch expansion group consisted of 32 patients with a median age of 8.58 (3.57, 52.72) months. In both groups, the diameter of pulmonary artery, McGoon index, and Nakata index significantly increased after treatment (P<0.001). However, the pericardial tube group exhibited a longer extracorporeal circulation time (P<0.001). The reoperation rate was notably high, with 74.51% of patients requiring further surgical intervention, including 26 (81.25%) patients in the patch expansion group and 12 (63.16%) patients in the pericardial tube group. No statistical differences were observed in long-term cure rates or mortality between the two groups (P＞0.005). Conclusion In patients with PA/VSD, both patch expansion and pericardial tube right ventricular-pulmonary artery connection serve as effective initial palliative treatment strategies that promote pulmonary vessel development and provide a favorable foundation for subsequent radical operations. However, compared to the pericardial tube approach, the patch expansion technique is simpler to perform and preserves some intrinsic potential for pulmonary artery development, making it the preferred procedure.

ObjectiveNeuroinflammation plays a crucial role in both the onset and progression of ischemic stroke, exerting a significant impact on the recovery of the central nervous system. Excessive neuroinflammation can lead to secondary neuronal damage, further exacerbating brain injury and impairing functional recovery. As a result, effectively modulating and reducing neuroinflammation in the brain has become a key therapeutic strategy for improving outcomes in ischemic stroke patients. Among various approaches, targeting immune regulation to control inflammation has gained increasing attention. This study aims to investigate the role of in vitro induced regulatory T cells (Treg cells) in suppressing neuroinflammation after ischemic stroke, as well as their potential therapeutic effects. By exploring the mechanisms through which Tregs exert their immunomodulatory functions, this research is expected to provide new insights into stroke treatment strategies. MethodsNaive CD4⁺ T cells were isolated from mouse spleens using a negative selection method to ensure high purity, and then they were induced in vitro to differentiate into Treg cells by adding specific cytokines. The anti-inflammatory effects and therapeutic potential of Treg cells transplantation in a mouse model of ischemic stroke was evaluated. In the middle cerebral artery occlusion (MCAO) model, after Treg cells transplantation, their ability to successfully migrate to the infarcted brain region and their impact on neuroinflammation levels were examined. To further investigate the role of Treg cells in stroke recovery, the changes in cytokine expression and their effects on immune cell interactions was analyzed. Additionally, infarct size and behavioral scores were measured to assess the neuroprotective effects of Treg cells. By integrating multiple indicators, the comprehensive evaluation of potential benefits of Treg cells in the treatment of ischemic stroke was performed. ResultsTreg cells significantly regulated the expression levels of both pro-inflammatory and anti-inflammatory cytokines in vitro and in vivo, effectively balancing the immune response and suppressing excessive inflammation. Additionally, Treg cells inhibited the activation and activity of inflammatory cells, thereby reducing neuroinflammation. In the MCAO mouse model, Treg cells were observed to accumulate in the infarcted brain region, where they significantly reduced the infarct size, demonstrating their neuroprotective effects. Furthermore, Treg cell therapy notably improved behavioral scores, suggesting its role in promoting functional recovery, and increased the survival rate of ischemic stroke mice, highlighting its potential as a promising therapeutic strategy for stroke treatment. ConclusionIn vitro induced Treg cells can effectively suppress neuroinflammation caused by ischemic stroke, demonstrating promising clinical application potential. By regulating the balance between pro-inflammatory and anti-inflammatory cytokines, Treg cells can inhibit immune responses in the nervous system, thereby reducing neuronal damage. Additionally, they can modulate the immune microenvironment, suppress the activation of inflammatory cells, and promote tissue repair. The therapeutic effects of Treg cells also include enhancing post-stroke recovery, improving behavioral outcomes, and increasing the survival rate of ischemic stroke mice. With their ability to suppress neuroinflammation, Treg cell therapy provides a novel and effective strategy for the treatment of ischemic stroke, offering broad application prospects in clinical immunotherapy and regenerative medicine.

Background With the large-scale production and application of carbon black nanoparticles (CBNPs), occupational and general exposure is obviously increasing. Related studies have shown that exposure to CBNPs can induce oxidative stress, inflammation, and DNA damage. Objective To establish a CBNPs-induced malignant transformation (C-BEAS-2B) model of human lung epithelial cells (BEAS-2B) and explore the role and mechanism of circCCDC138 in the malignant transformation process. Methods At 0, 10, 20, 40 and 80 μg·mL⁻¹ CBNPs concentrations, cell viability was detected by CCK8 assay. BEAS-2B cells were exposed to 20 mg·mL⁻¹ CBNPs for three months, and a malignant transformation model of BEAS-2B induced by CBNPs was constructed. The migration and invasion abilities of the cells were detected by cell scratch and Transwell assays. The expressions of circ-CCDC138 in BEAS-2B and C-BEAS-2B were detected by qRT-PCR, and its stability was verified by a digestive resistance test. A cell model with interference or overexpression of circCCDC138 was constructed, and the expression of circCCDC138 in the cells was detected by quantitative reverse transcription-PCR. The cell cycle and apoptosis were determined by flow cytometry. Western blot was used to analyze the expression of p53 protein. Results The CBNPs used in the experiment were spherical particles with a chain-like structure. In the 20 μg·mL⁻¹ CBNPs group, the reduction in the viability of BEAS-2B cells was relatively small (10%). Compared with the control cells, the 20 μg·mL⁻¹ CBNPs group showed more obvious cell migration and invasion at 24 h and 48 h, indicating that the exposure to CBNPs induced early malignant transformation of BEAS-2B cells (P<0.01). The circCCDC138 expression in C-BEAS-2B was upregulated in a time-dependent manner after exposure to CBNPs. Compared with the C-BEAS-2B cells, the C-BEAS-2B cells over-expressing circCCDC138 exhibited arrested S phase progression (36.9%) and apoptosis resistance (P<0.01), along with down regulation of p53 protein expression in the cells (P<0.01), while the C-BEAS-2B cells interfering with circCCDC138 showed the opposite results (P<0.01). Conclusion BEAS-2B cells exposed to CBNPs (20 μg·mL⁻¹) have significantly enhanced migration and invasion abilities, showing early malignant transformation characteristics. In addition, circCCDC138 is highly expressed in C-BEAS-2B cells with RNase R digestive resistance and increases in a time-dependent manner with CBNPs exposure. More importantly, circCCDC138 may promote the induction of malignant transformation of cells by inhibiting p53 protein expression.

Objective To analyze the monitoring status of occupational hazard factors in key industry workplaces in a city of the Pearl River Delta area from 2019 to 2023. Methods A total of 1 548 enterprises in 12 key industries of the city were selected as the research subjects using the judgmental sampling method. Their monitoring data for dust, chemical factors, and noise, along with the occupational health management status of the enterprises were analyzed. Results Among the 1 548 enterprises, large and medium-sized enterprises accounted for 2.7% and 13.4%, while small and micro enterprises accounted for 83.9%. A total of 474 enterprises exceeded the national limit in the detection of occupational hazard factors, with an exceedance rate of 30.6%. The rates of workers exposed to occupational hazard factors, dust, chemical factors, and noise were 29.4%, 6.9%, 21.0%, and 13.0%, respectively, all showing a downward trend year by year (all P<0.05). The training rates for occupational health among enterprise managers, responsible persons, and workers were 84.1%, 84.2%, and 91.2%, respectively. The detection rates for abnormal occupational health examinations among workers exposed to dust, chemical factors, and noise were 0.2%, 0.3%, and 0.5%, respectively. The setting rates of warning signs and warning instructions among enterprises for dust, chemical toxins, and noise were 87.3%, 91.1%, and 89.5%, respectively. The setting rates for dust, toxic chemical, and noise control facilities were 72.4%, 75.4%, and 46.0%, with effectiveness rates of 70.5%, 56.6%, and 55.2%, respectively. The distribution rates of personal protective dust masks, gas masks, and noise earplugs/earmuffs were 91.9%, 83.8%, and 86.4%, with wearing rates of 80.8%, 70.5%, and 76.4%, respectively. The detection rates of exceeding national limits for dust, chemical factors, and noise in the work site of occupational hazard factors were15.2%, 1.0%, and 21.6%, respectively. The detection rates of exceeding national limits for dust, chemical factors, and noise in the workplace of occupational hazard factors were 2.4%, 2.5%, and 12.3%, respectively. The exceedance rate for noise in work site showed an upward trend year by year (P<0.01). Conclusion Occupational disease prevention and control work in the key industries of this city needs strengthening. It is essential to further enhance the regular monitoring and preventive measures of occupational hazard factors in enterprises, improve protective measures, strengthen the use of personal protective equipment, and enhance occupational health training and supervision, to effectively reduce the risk of occupational diseases and protect workers' occupational health rights.

[摘 要] 目的：探索预后营养指数（PNI）在接受诱导化疗联合免疫（化免）序贯放疗的局部晚期食管鳞状细胞癌（ESCC）中的疗效预测价值及预后影响。方法: 回顾性分析浙江省肿瘤医院2019年5月至2023年8月期间收治的126例行诱导化免序贯放疗的局部晚期ESCC患者的临床资料。绘制受试者工作特征曲线（ROC曲线），确定患者诱导化免前1周内、放疗前1周内、放疗开始后4 ± 1周的PNI最佳临界值并对患者进行分组。采用Kaplan-Meier法绘制生存曲线，并用Log-Rank法比较组间患者的总生存期（OS）及无进展生存期（PFS），采用Cox回归分析探讨诱导化免序贯放疗的局部晚期ESCC患者的预后影响因素。结果: 共纳入126例局部晚期ESCC患者，男性118例，女性8例，中位年龄65岁（44~78岁）。运用ROC曲线确认的患者诱导化免前、放疗前和放疗中PNI最佳临界值为46.2、48.3和37.9。放疗前PNI ≥ 48.3组中位OS、PFS分别为47.3、28.2个月，放疗前PNI < 48.3组中位OS、PFS分别为18.7、15.2个月（P < 0.01，P < 0.05）。放疗中PNI ≥ 37.9组中位OS未达到，中位PFS为25.7个月，放疗中PNI < 37.9组中位OS、PFS分别为17.0、12.5个月（P < 0.01，P < 0.05）。诱导化免后PNI升高组中位OS未达到，中位PFS为28.4个月；PNI降低组中位OS、PFS分别为20.4、16.0个月（P < 0.01，P < 0.05）。多因素分析显示，放疗中PNI[HR = 2.292，95% CI（1.264,4.159），P < 0.05]、诱导化免后PNI变化[HR = 2.120, 95% CI（1.007, 4.463），P < 0.05]为影响OS因素。结论: 放疗中PNI、诱导化免后PNI变化与患者治疗疗效及预后有一定相关性，可作为预测ESCC化免序贯放疗获益的重要指标。

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.