Autologous blood patch pleurodesis (ABPP) was first proposed in 1987. Now it is mainly used to treat intractable pneumothorax and persistent air leakage after pneumonectomy, and also used to treat pneumothorax in children and other rare secondary pneumothorax. Persistent air leakage and pneumothorax of various causes are essentially alveolar pleural fistula. It can usually be treated by closed thoracic drainage, continuous negative pressure suction and surgery. Pleurodesis is a safe and effective alternative to surgery for patients who have failed conventional conservative treatment and can not receive operations. Compared with other pleurodesis adhesives, autologous blood (ABPP) is safer and more effective, and it is simple, painless, cheap and easy to be accepted by patients. But in the domestic and foreign researches in recent years, many details of ABPP treatment have not been standardized. For further research and popularization of ABPP, this article reviews the detailed regulations, efficacy and safety of this technology.

[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。

The lung collaterals form a network that branches from the lung meridian, traversing the lung system and extending across the body′s surface. Lung collateral disease refers to the structural alterations or dysfunction in these collaterals caused by external or internal pathogens. Research into the structural and physiological functions of children′s lung collaterals, as well as the pathogenesis and syndrome differentiation for treating lung collateral diseases in children, holds significant value in guiding the prevention and treatment of pediatric respiratory conditions. Drawing on the theory of collateral disease, the clinical insights of both historical and contemporary physicians, and modern research findings—while considering the unique physiological and pathological characteristics of children′s respiratory systems—this study provides a foundational summary of the morphology and spatial distribution of children′s lung collaterals. The characteristics of these collaterals are highlighted as thin, sparse, short, narrow, brittle, and tender. From this structural understanding, the unique physiological functions of children′s lung collaterals are analyzed. The study further explores the interactions between pathogenic factors and lung collaterals, elucidating the pathogenesis and progression of children′s lung collateral diseases. It proposes treatment principles centered on "seeking treatment in the collaterals and employing the method of unblocking collaterals, "which align with the unique features of pediatric lung collaterals. Common treatment approaches, and relevant prescriptions for managing these diseases are summarized. This paper lays the foundation for a theoretical system encompassing the structure, function, pathogenesis, and syndrome differentiation for treating children′s lung collateral diseases. It offers valuable insights for the clinical diagnosis and management of pediatric respiratory diseases linked to collateral dysfunction and serves as a reference for the systematic development of a broader theoretical framework for children′s collateral diseases.

It is considered that the fundamental pathogenesis of pediatric pertussis lies in the dysfunction of lung qi， and it is advocated to treat the disease with the method of regulating qi and relieving cough. Clinically， the disease is divided into three stages for syndrome differentiation and treatment， initial coughing stage， spasmodic coughing stage， and prolonged coughing stage. In the initial coughing stage， the pathogenesis involves invasion by external pathogens and failure of lung qi to disperse； the treatment principle is to release the exterior， expel pathogens， ventilate the lungs， and relieve cough. For cold patterns， modified San'ao Decoction （三拗汤） is prescribed； for heat type， a self-formulated Qingqi Xuanfei Decoction （清气宣肺汤） is used. In the spasmodic coughing stage， the pathogenesis is the congealing of phlegm and fire with impaired lung purification； the treatment focuses on eliminating phlegm， dredging the meridians， purging the lungs， and relieving cough. Mild cases are treated with a self-formulated Tongluo Xiefei Decoction （通络泻肺汤）， while severe cases are treated with a modified combination of Maxing Shigan Decoction （麻杏石甘汤） and Qianjin Weijing Decoction （千金苇茎汤）. In the prolonged coughing stage， the pathogenesis involves the depletion of qi and yin and latent pathogens in a weakened lung； the treatment aims to tonify qi， nourish yin， moisten the lungs， and eliminate residual pathogens. For lung yin deficiency， modified Shashen Maidong Decoction （沙参麦冬汤） is used； for lung-spleen qi deficiency， a self-formulated Jianpi Gufei Decoction （健脾固肺汤） is prescribed.

[摘 要] 目的：探究长链非编码RNA葡萄糖醛酸酶β假基因11（GUSBP11）调节miR-339-5p/小鼠双分钟同源物2（MDM2）轴对胃癌细胞AGS增殖、迁移和侵袭的影响。方法：收集2023年12月至2024年6月期间在广州中医药大学附属佛山中医院手术治疗的25例胃癌患者的癌旁组织及癌组织。常规培养胃癌细胞AGS和正常胃黏膜上皮细胞GES-1，用转染试剂将对照质粒和敲减质粒转染AGS细胞，分为Ctrl组、sh-NC、sh-GUSBP11、sh-GUSBP11 + anti-NC、sh-GUSBP11 + anti-miR-339-5p。qPCR法检测胃癌组织及各组细胞中GUSBP11、miR-339-5p和MDM2 mRNA的表达；双萤光素酶报告基因实验检测GUSBP11或MDM2与miR-339-5p间的靶向关系；EdU法检、Transwell小室实验、划痕愈合实验和WB法分别检测各组AGS的增殖、迁移和侵袭能力和细胞中CDK1、MMP-2、MMP-9蛋白的表达；AGS细胞移植瘤实验检测敲减GUSBP11对移植瘤生长的影响。结果：胃癌组织和细胞中GUSBP11、MDM2 mRNA均呈高表达（均P < 0.05），miR-339-5p呈低表达（P < 0.05）。GUSBP11与miR-339-5p和MDM2与miR-339-5p间存在靶向关系。在AGS细胞中敲减GUSBP11可明显抑制MDM2蛋白、促进miR-339-5p的表达而抑制miR-339-5p则可促进MDM2蛋白表达。敲减GUSBP11可抑制AGS细胞的增殖、迁移和侵袭能力而抑制miR-339-5p则可逆转此作用。敲减GUSBP11可明显抑制CDK1、MMP-2和MMP-9蛋白的表达而抑制miR-339-5p则可逆转此作用。敲减GUSBP11可明显抑制AGS细胞移植瘤的生长。结论：GUSBP11在胃癌组织和细胞中呈高表达，敲减GUSBP11表达可能通过调控miR-339-5p/MDM2轴抑制胃癌细胞的恶性生物学行为。

Objective To investigate the clinical features，laboratory findings，and prognosis of patients with autoimmune encephalitis positive for leucine rich glioma inactivated 1（LGI1）antibody. Methods We reviewed the clinical data of 11 patients with anti-LGI1 encephalitis hospitalized in Fu Yang People's Hospital from October 2019 to December 2024. Results All the 11 patients（100%）had cognitive function involvement，9（81.8%）had epileptic seizures，5（45.5%）had mental and behavioral abnormalities，4（36.4%）had sleep disorders，3（27.3%）had autonomic nervous dysfunction，2（18.2%）had faciobrachial dystonic seizures（FBDS），2（18.2%）had facial numbness，and 1（9.1%）had phantosmia and pruritus in both eyes and the neck. LGI1 antibody was positive in the serum of all the cases（100%）and present in the cerebrospinal fluid of 8 cases（72.3%）. Seven cases（63.6%）had hyponatremia，and 5 cases（45.5%）also had hypophosphatemia，hypocalcemia，and hypomagnesemia in addition to blood sodium lower than 134 mmol/L. Intracranial abnormalities were detected in 7 cases（63.6%）on magnetic resonance imaging. Electroencephalogram abnormalities were recorded in 6 cases（54.5%）. After immunosuppressive treatment，2 cases（18.2%）had recurrent symptoms，and 2 cases（18.2%）had residual mild memory impairment. In terms of prognosis，the modified Rankin Scale scores were generally favorable. Conclusion Anti-LGI1 encephalitis manifests as convulsions，FBDS，memory decline，mental and behavioral abnormalities，autonomic nervous dysfunction，sleep disorders，hyponatremia，and multiple electrolyte disorders such as hypomagnesemia，hypocalcemia，and hypophosphatemia when blood sodium is below 134 mmol/L. The prognosis with immunosuppressive treatment is favorable，but recurrent symptoms may occur.

Objective To understand the sleep status in patients with Parkinson's disease (PD), and to explore its relationship with dyskinesia and negative emotions. Methods A total of 308 patients with PD who met the inclusion and exclusion criteria in the hospital from September 2022 to May 2024 were selected as the research subjects. The scores of sleep status [Pittsburgh Sleep Quality Index (PSQI)], dyskinesia [Simplified Fugl-Meyer Motor Assessment (FMA)] and negative emotions [Beck Anxiety Inventory (BAI), Beck Depression Inventory-II (BDI-II)] were analyzed, and the PSQI score was compared among patients with different demographic characteristics. Pearson correlation analysis was performed to analyze the correlation of sleep with dyskinesia and negative emotions in patients with PD. Results The total score of PSQI scale was (6.16±0.97) points in 308 PD patients, of which 208 cases (67.53%) were complicated with sleep disorders. The proportions of female, 61-75 years old, technical secondary school or below, disease course of 4 years and above, Hoehn-Yahr stage IV and unmarried status in the sleep disorder group were higher than those in the non-sleep disorder group (P<0.05). Compared with the non-sleep disorder group, the FMA score in the sleep disorder group was lower (P<0.05) while the BAI score and BDI-II score were higher (P<0.05). Pearson correlation analysis revealed that PSQI was negatively correlated with FMA (r=-0.489, P<0.05), and was positively correlated with BAI and BDI-II (r=0.476, 0.502, P<0.05). Conclusion The incidence rate of sleep disorders in PD patients is high. PSQI is negatively correlated with FMA, and is positively correlated with BAI and BDI-II.

Objective To evaluate the predictive ability and clinical application value of artificial intelligence (AI) systems in the benign and malignant differentiation and pathological type of pulmonary nodules, and to summarize clinical application experience. Methods A retrospective analysis was conducted on the clinical data of patients with pulmonary nodules admitted to the Department of Thoracic Surgery, Second Hospital of Lanzhou University, from February 2016 to February 2025. Firstly, pulmonary nodules were divided into benign and non-benign groups, and the discriminative abilities of AI systems and clinicians were compared. Subsequently, lung nodules reported as precursor glandular lesions (PGL), microinvasive adenocarcinoma (MIA), and invasive adenocarcinoma (IAC) in postoperative pathological results were analyzed, comparing the efficacy of AI systems and clinicians in predicting the pathological type of pulmonary nodules. Results In the analysis of benign/non-benign pulmonary nodules, clinical data from a total of 638 patients with pulmonary nodules were included, of which there were 257 males (10 patients and 1 patient of double and triple primary lesions, respectively) and 381 females (18 patients and 1 patient of double and triple primary lesions, respectively), with a median age of 55.0 (47.0, 61.0) years. Different lesions in the same patient were analyzed as independent samples. Univariate analysis of the two groups of variables showed that, except for nodule location, the differences in the remaining variables were statistically significant (P<0.05). Multivariate logistic regression analysis showed that age, nodule type (subsolid pulmonary nodule), average density, spicule sign, and vascular convergence sign were independent influencing factors for non-benign pulmonary nodules, among which age, nodule type (subsolid pulmonary nodule), spicule sign, and vascular convergence sign were positively correlated with non-benign pulmonary nodules, while average density was negatively correlated with the occurrence of non-benign pulmonary nodules. The area under the receiver operating characteristic curve (AUC) of the malignancy risk value given by the AI system in predicting non-benign pulmonary nodules was 0.811, slightly lower than the 0.898 predicted by clinicians. In the PGL/MIA/IAC analysis, clinical data from a total of 411 patients with pulmonary nodules were included, of which there were 149 males (8 patients of double primary lesions) and 262 females (17 patients of double primary lesions), with a median age of 56.0 (50.0, 61.0) years. Different lesions in the same patient were analyzed as independent samples. Univariate analysis results showed that, except for gender, nodule location, and vascular convergence sign, the differences in the remaining variables among the three groups of PGL, MIA, and IAC patients were statistically significant (P<0.05). Multinomial multivariate logistic regression analysis showed that the differences between the parameters in the PGL group and the MIA group were not statistically significant (P>0.05), and the maximum diameter and average density of the nodules were statistically different between the PGL and IAC groups (P<0.05), and were positively correlated with the occurrence of IAC as independent risk factors. The average AUC value, accuracy, recall rate, and F1 score of the AI system in predicting lung nodule pathological type were 0.807, 74.3%, 73.2%, and 68.5%, respectively, all better than the clinical physicians’ prediction of lung nodule pathological type indicators (0.782, 70.9%, 66.2%, and 63.7% respectively). The AUC value of the AI system in predicting IAC was 0.853, and the sensitivity, specificity, and optimal cutoff value were 0.643, 0.943, and 50.0%, respectively. Conclusion This AI system has demonstrated high clinical value in predicting the benign and malignant nature and pathological type of lung nodules, especially in predicting lung nodule pathological type, its ability has surpassed that of clinical physicians. With the optimization of algorithms and the adequate integration of multimodal data, it can better assist clinical physicians in formulating individualized diagnostic and treatment plans for patients with lung nodules.

To investigate and analyze the distribution characteristics and genetic variation of mitochondrial encephalomyopathy (ME) in children in Hainan province.

Brain cancer remains among the most lethal malignancies worldwide, with approximately 321,476 new cases and 248,305 deaths reported globally in 2022. The treatment of malignant brain tumors presents substantial clinical challenges, primarily due to their resistance to standard therapeutic approaches. Despite decades of intensive research, effective treatment strategies for brain cancer are still lacking. Nuclear receptors (NRs), a superfamily of ligand-activated transcription factors, regulate a broad range of physiological processes including metabolism, immunity, stress response, reproduction, and cellular differentiation. Increasing evidence highlights the involvement of NRs in oncogenesis, with several members demonstrating altered expression and function in brain tumors. Aberrations in NR signaling, encompassing receptors such as androgen receptors, estrogen receptors, estrogen-related receptors, glucocorticoid receptors, NR subfamily 4 group A, NR subfamily 1 group D member 2, NR subfamily 5 group A member 2, NR subfamily 2 group C member 2, liver X receptors, peroxisome-proliferator activated receptors, progesterone receptors, retinoic acid receptors, NR subfamily 2 group E member 1, thyroid hormone receptors, vitamin D receptors, and retinoid X receptors, have been implicated in promoting hallmark malignant phenotypes, including enhanced survival, proliferation, invasion, migration, metastasis, and resistance to therapy. This review aims to explore the roles of key NRs in brain cancer, with an emphasis on their prognostic significance, and to evaluate the therapeutic potential of targeting these receptors using selective agonists or antagonists.
Humans ; Brain Neoplasms/drug therapy* ; Receptors, Cytoplasmic and Nuclear/metabolism* ; Animals ; Signal Transduction/physiology*