Statins are widely used to treat hyperlipidemia and atherosclerotic cardiovascular diseases (ACVD) by significantly lowering low-density lipoprotein cholesterol (LDL-C) levels. However, their use has been associated with an increased risk of type 2 diabetes (T2D), a paradox given their lipid-lowering benefits. This study investigates the role of LDL receptors (LDLR) and proprotein convertase subtilisin/kexin type 9 (PCSK9) in the diabetogenic effects of atorvastatin on pancreatic β-cells. Using the MIN6 pancreatic β-cell line, we assessed the impact of atorvastatin on LDL-C uptake, PCSK9 expression, glucose-stimulated insulin release (GSIR), and cell proliferation. Cellular cholesterol assays, EdU labeling, Dil-LDL uptake, western blot analysis, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and ELISA, were employed to measure relevant biomarkers and cellular responses. Male C57BL/6j mice were treated with atorvastatin to validate in vitro findings. Atorvastatin enhances LDL-C uptake by upregulating LDLR on the cell surface, without causing excess cholesterol accumulation. Additionally, atorvastatin suppresses PCSK9 expression, which is crucial for LDLR degradation. Interestingly, atorvastatin, combined with exogenous LDL-C, impairs glucose-stimulated insulin release (GSIR) but promotes cell proliferation, highlighting a potential mechanism for statin-associated diabetes. Oral administration of atorvastatin in mice reduced plasma PCSK9 and insulin levels, supporting the in vitro findings. These results indicate that while atorvastatin effectively lowers circulating cholesterol, it may adversely affect pancreatic β-cell function by modulating LDLR and LDL-C uptake, thereby increasing the risk of T2D. This study highlights the importance of further research to develop strategies mitigating the diabetogenic effects of statins while maintaining their cardiovascular benefits.

INTRODUCTION:Electronic cigarettes (E-cigs) are in a controversial state. Although E-cig aerosol generally contains fewer harmful substances than smoke from burned traditional cigarettes, aerosol along with other compounds of the E-cigs may also affect lung functions and promote the development of lung-related diseases. We investigated the effects of E-cig on the pulmonary functions of male C57BL/6 mice and reveal the potential underlying mechanisms. METHODS:A total of 60 male C57BL/6 mice were randomly divided into four groups. They were exposed to fresh-air, traditional cigarette smoke, E-cig vapor with 12 mg/mL of nicotine, and E-cig with no nicotine for 8 weeks. Lung functions were evaluated by using quantitative analysis of the whole body plethysmograph, FlexiVent system, lung tissue histological and morphometric analysis, and RT-PCR analysis of mRNA expression of inflammation-related genes. In addition, the effects of nicotine and acrolein on the survival rate and DNA damage were investigated using cultured human alveolar basal epithelial cells. RESULTS:Exposure to E-cig vapor led to significant changes in lung functions and structures including the rupture of the alveolar cavity and enlarged alveolar space. The pathological changes were also accompanied by increased expression of interleukin-6 and tumor necrosis factor-α. CONCLUSIONS:The findings of the present study indicate that the safety of E-cig should be further evaluated. IMPLICATIONS:Some people currently believe that using nicotine-free E-cigs is a safe way to smoke. However, our research shows that E-cigs can cause lung damage regardless of whether they contain nicotine.

目的 编制医护人员低血糖症知信行问卷并对其进行信效度检验.方法 以知信行理论为框架,通过文献回顾和德尔菲专家函询形成初始问卷,对西安市某三级甲等医院1215名医护人员进行调查,进一步检验问卷的信效度,形成正式问卷.结果 最终形成的问卷包括知识、态度、行为3个维度共23个条目,探索性因子分析显示3个公因子的累计方差贡献率为61.501％.问卷总内容效度为0.890,总Cronbachα系数为0.882,各维度的Cronbachα系数为0.769～0.934.总问卷折半信度为0.872,各维度的折半信度为0.788～0.916.验证性因子分析显示各适配值良好,提示该问卷拟合度良好.结论 医护人员低血糖症知信行问卷具有良好的信效度,可作为评价医护人员低血糖症知信行现状的研究工具.

Statins are the most effective lipid-lowering drugs ever developed, and numerous patients with cardiovascular disease (CVD) have obtained remarkable benefits from statin therapy. However, issues with statin resistance and intolerance cannot be ignored in clinical practice. Additionally, adverse effects, such as an increased risk of new-onset diabetes and muscle symptoms, may limit the utilization of statins. Therefore, the development of new lipid-lowering agents is necessary to reduce CVD risk in patients who are unable to receive statin therapy. Among these new lipid-lowering strategies, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) is an effective way to enhance clearance of LDL-C from the circulation by impeding the degradation of LDL receptor (LDLR) in hepatocytes. Interestingly, given that upregulation of LDLR is an effective method for lowering lipid levels, the question arises as to whether other LDLR-mediated genes could serve as potential therapeutic targets for CVD. As an E3-ubiquitin ligase, inducible degrader of LDLR (IDOL) can cause ubiquitination and degradation of LDLR in lysosome and is a novel regulator of LDLR expression similar to PCSK9. Although there are no approved drugs for targeting the IDOL-LDLR pathway, recent studies demonstrate that IDOL could serve as a potential therapeutic target for hyperlipidemia. Herein, we have summarized these novel studies to present the pathological role of IDOL in CVD, further assessing its pharmacological effects for lipid-lowering therapy.

Secreted frizzled-related protein 4 (SFRP4) is a member of the SFRP family that contains a cysteine-rich domain homologous to the putative Wnt-binding site of frizzled proteins. In the present report, the effects of SFRP4 on murine brown adipocyte differentiation were evaluated, which exhibited an intrinsic capacity to differentiate with high efficiency. Brown preadipocytes were isolated from the scapular region of brown adipose tissue, which showed that the overexpression of recombinant active SFRP4 protein at three concentrations (1, 10 and 100 ng/ml) significantly increased the expression of adipocyte differentiation-associated genes (C/EBPα, C/EBPβ, UCP-1, PRDM16, PGC1α and GLUT4) in a dose-dependent manner compared with the control group. Secondly, adiponectin protein expression was significantly inhibited in a dose-independent manner, while leptin was increased in brown adipocytes by incubation with the high concentration (100 ng/ml) of SFRP4. Thirdly, the role of interleukin-1β (IL-1β) was investigated in brown adipocytes and discovered that IL-1β cannot induce SFRP4 mRNA expression in brown adipocytes, similar to human islet cells. These data suggested that SFRP4-treated brown adipocytes represent a valuable in vitro model for the study of adipogenesis and indicated that SFRP4 served various functions during brown adipocyte differentiation.

目的 了解陕西西安地区2型糖尿病患者血清中载脂蛋白A1、载脂蛋白B含量的差异,并进一步探讨两者与2型糖尿病患者血管病变的相关关系. 方法 选择2016-03 ～2018-03在我科住院的150例2型糖尿病患者为研究组,其中78例合并血管病变、72例无血管病变,同期我院健康体检的115例同龄健康人为对照组.全自动生化仪上测定所有受试者血清载脂蛋白A1、载脂蛋白B含量. 结果 2型糖尿病患者载脂蛋白A1水平与健康对照组间差异无统计学意义(P≥0.05),载脂蛋白B水平明显高于健康对照组且差异有统计学意义(P＜0.05)、ApoA1/ApoB明显低于健康对照组且差异有统计学意义(P＜0.05);在2型糖尿病患者中,有血管并发症者中ApoA1、ApoA1/ApoB明显低于无血管并发症者且差异有统计学意义(P＜0.05),而有血管并发症者ApoB明显高于无血管并发症者且差异有统计学意义(P＜0.05). 结论 2型糖尿病与血脂关系密切,载脂蛋白代谢紊乱是导致糖尿病患者血管并发症的重要因素之一,临床治疗中不应忽视对血脂异常的治疗,这对预防2型糖尿病及其血管并发症具有重要意义.

Objective To investigate the effects of transcription factor 2(TCF2) overexpression on insulin resistance in HepG2 cells. Methods HepG2 cells were treated with high concentration of insulin(1×10-8mol/L) for 24 hours to induce insulin resistance (IR). Cells were divided into four groups:control group,IR group,IR+vector group and IR+TCF2 overexpression group. RT-qPCR and Western blot were performed to detect the expres-sion of TCF2. Glucose consumption and glycogen synthesis were assayed by glucose oxidase method and anthrone method respectively. Cell viability was evaluated by MTT assay. The activities of hexokinase and pyruvate kinase were detected by colorimetry. The protein level of IRS-1 and GLUT4 was detected by Western blot.Results Com-pared with control group,the decreased glucose consumption was observed in IR group(P＜0.05),indicating that insulin-resistance model was established successfully. The mRNA and protein expression of TCF2 was remarkably down-regulated in IR group as compared with control group. Compared with IR group,overexpression of TCF2 sig-nificantly improved glucose consumption, liver glycogen content, and the activities of hexokinase and pyruvate kinase (P＜0.05). Moreover,TCF2 overexpression up-regulated the protein expression of IRS-1 and GLUT4 (P＜0.05).Conclusions TCF2 overexpression ameliorates insulin resistance of HepG2 cells.

Objective To investigate the expression and clinical significance of miR-126 and vascular endothelial growth factor (VEGF) in proliferative diabetic retinopathy (PDR).Methods 226 cases of diabetic retinopathy (DR) patients admitted in our hospital were studied,including 110 cases of PDR (group PDR),116 non proliferative diabetic retinopathy (NPDR) (group NPDR).80 patients with diabetes mellitus without retinopathy (NDR) were enrolled in DR group at the same period,another 80 healthy subjects (control group) were selected as control group.The plasma miR-126 level of all subjects was detected by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR).The enzyme linked immunosorbent assay (ELISA) method was used to detect plasma VEGF level.The clinical diagnostic value of miR-126 and VEGF in PDR patients was further analyzed.Results Plasma levels of miR-126 in PDR group,NPDR group and NDR group were lower than those in control group (P ＜ 0.05),PDR group was lower than NPDR group and NDR group (P ＜ 0.05);plasma levels of VEGF in PDR group,NPDR group and NDR group were higher than those in control group (P ＜ 0.05),PDR group was higher than NPDR group and NDR group (P ＜ 0.05).Total cholesterol (TC),triglyceride (TG) and glycated hemoglobin (HbAlc) in PDR group were higher than those in NPDR group and NDR group (P ＜0.05),low density lipoprotein cholesterol (LDL-C) in PDR group,NPDR group and NDR group were higher than those in control group (P ＜ 0.05),and LDL-C in PDR group was higher than that in NPDR group and NDR group (P ＜0.05).High density lipoprotein cholesterol (HDL-C) in PDR group and NDR group was lower than that in control group (P ＜ 0.05),C-reactive protein (CRP) in PDR group,NPDR group and NDR group was higher than that in control group (P ＜ 0.05);plasma miR-126 levels in PDR group were negatively correlated with TC,LDL-C,CRP and HbA1c (P ＜ 0.05),but positively correlated with HDL-C (P ＜ 0.05),and no correlation with TG;the plasma levels of VEGF in PDR patients were positively correlated with TC,TG,LDL-C,CRP and HbAlc (P ＜0.05),but negatively correlated with the expressions of miR126 (r =-0.573,P =0.000);the AUC of miR-126 was 0.861,and when the cut-off value was ＜0.64,the diagnostic sensitivity and specificity were 82.50％,83.64％;the area under curve (AUC) of VEGF was 0.889,and when the cut-off value was ＜ 7.000,the sensitivity and specificity of diagnosis were 82.73％,86.25％;0.847 for the AUC of HbA1c,and the sensitivity and specificity 81.82％,87.50％ respectively.Conclusions Plasma miR-126 is low-expressed and VEGF is high-expressed in PDR patients,there is a negative correlation between the two indexes.They may be involved in the course of PDR through abnormal lipid metabolism and inflammatory reaction and may be a potential biomarker for early diagnosis of PDR.

本研究探讨3D影像重建技术结合PBL教学方法在老年呼吸系统疾病教学中的应用.采集层厚为1 mm的正常胸部CT图像,对其进行三维重建,将重建的模型应用于本科生的老年呼吸系统疾病PBL教学,可直观地再现胸部的三维结构并从不同角度进行观察.该教学法可提高本科生的学习积极性,培养学生的循证医学和创新思维,提高临床知识的运用能力.

Objective To analyze the clinical significance of peripheral blood CD4 +CD25 +Foxp3 +regulatory T cells and T calcium mu-cin detection in thyroid papillary carcinoma patients. Methods 40 cases of PTC patients(observation group)and 40 cases of thyroid adenoma patients(control group)were selected retrospectively. The ratio of CD4 +CD25 +Foxp3 +Treg cells and the level of T calcium mucin in peripheral blood were compared between the two groups,and the difference of CD4 +CD25 +Foxp3 +Treg cell ratio and the level of T calcium mucin between different pathological characteristics were compared. Results CD4 +CD25 +Foxp3 +Treg cells and T calcium mucin levels in PTC patients were significantly higher than those of control group(P <0.05),CD4 +CD25 +Foxp3 +Treg cells and T calcium mucin levels in TNMⅢ,Ⅳperiod patients with cervical lymph node metastasis were significantly higher(P <0.05). Conclusion CD4 +CD25 +Foxp3 +Treg cells with calcium sticky protein can serve as markers of PTC,and at the same time,and these are closely related to clinical stages and lymph node metastasis.

目的:探讨老年慢性阻塞性肺病对骨质疏松的影响,为预防老年骨质疏松引发的骨折提供理论依据.方法:选择老年男性慢性阻塞性肺病患者159例,依据GO LD分级,观察年龄、体重指数(BM I)、吸烟及使用糖皮质激素情况,测定肺活量(VC)、第1秒用力呼气量(FEV1)、用力肺活量(FVC)、FEV1/FVC%,以及双能X线吸收骨密度测定仪测定胸椎、腰椎、股骨颈和大转子的骨密度(BMD),并进行相关分析.结果:GOLD4期较其GOLD 1~3级患者有明显的骨质疏松(P<0.05),应用糖皮质激素的患者比不用患者骨质疏松发生率高(P<0.05、P<0.01),低体重指数骨质疏松的发生率高于正常体重指数患者(P<0.05).结论:对于老年患者缺氧、应用糖皮质激素、低体重指数是导致CO PD合并骨质疏松发生率升高的重要因素.

目的:探讨奥氮平和齐拉西酮对精神分裂症患者治疗8周后对于患者代谢指标的影响,并评估两种药物的安全性和疗效.方法:选择精神分裂症患者110例,将其分为对照组和观察组各55例.对照组服用奥氮平,观察组服用齐拉西酮,比较两组治疗8周后血糖、血脂代谢情况,治疗后体重指数、腹围及腰围,治疗过程中发生的不良反应,并统计两组治疗后的整体临床效果.结果:观察组患者治疗后空腹血糖、餐后2h血糖、总胆固醇及甘油三酯均低于对照组(P<0.05),观察组发生头晕嗜睡、口干乏力、体重增加的比例显著低于对照组(P<0.05),治疗后观察组阳性与阴性症状量表(PANSS)总分和对照组比较差异不明显(P>0.05).结论:齐拉西酮治疗精神分裂症患者,能有效调控其血糖、血脂代谢,不导致体重、腰围及腹围增加,且治疗不良反应较少,临床疗效和奥氮平相当.

Objective To investigate the relationship between troponinⅠ( TnI) and creatinine, glomerular filtration rate, C-reactive protein and other related factors in elderly patients with type 2 diabetes mellitus complicated with chronic renal failure. Methods Sixty elderly male patients were selected, with an average age of 73 ± 11 years old, and the rate of glomerular filtration was 44. 73 ± 10. 56 ml/(min·1. 73 m2). The patients were divided into stage 3 group and stage 4 group according to the renal function. The level of TnⅠ, glomerular filtration rate, blood lipids, left ventricular mass, hemoglobin and other indicators were detected and compared between the two groups. Results There were significant differences in age, weight, urea nitrogen, creatinine, triglyceride, C-reactive protein, glomerular filtration rate, hemoglobin, left ventricular mass index and renal resistance index between stage 3 group and stage 4 group. Furthermore, the patients were divided into increased group and normal group according to the levels of TnⅠ. Single factor analysis showed that the levels of total&nbsp;cholesterol, hemoglobin, C-reactive protein, renal resistance index, uric acid, and left ventricular mass index were of significant differences between increased group and normal group both in stage 3 or stage 4. TnⅠ increased with the increasing level of creatinine, C-reactive protein and uric acid. Conclusions TnⅠ is not only a marker of myocardial injury in patients with type 2 diabetic nephropathy complicated with chronic renal failure, but also an indicator of residual renal function and chronic renal failure.

目的分析2型糖尿病合并毛霉菌病的临床特点和预后并结合国内外相关文献报道,进一步加深对疾病的认识并提高早期诊断水平。方法回顾性分析6例2型糖尿病合并毛霉菌病患者的临床资料。结果 6例患者中,分别为随机血糖＞13mmol/L（6/6）、发热（6/6）、酮症（6/6）、白细胞升高（6/6）、酸中毒（5/6）,头颅核磁共振（MRI）和胸部计算机断层扫描（CT）无特征性表现,真菌涂片阳性（3/6）,病理活检阳性（5/6）,早期应用两性霉素B配合局部清创、手术治疗治愈率（5/6）。结论 2型糖尿病合并毛霉菌病的诊断要点为随机血糖＞13mmol/L、糖化血红蛋白＞10%、酸中毒、白细胞升高及进行局部组织病理活检。早期足量应用两性霉素B和进行局部病变的手术治疗是治愈的关键。

Atherosclerosis is a disease of the large- and medium-size arteries that is characterized by the formation of atherosclerotic plaques, in which foam cells are the characteristic pathological cells. However, the key underlying pathomechanisms are still not fully elucidated. In this study, we investigated the role of lipoprotein-associated phospholipase A2 (Lp-PLA2) in ox-LDL-induced oxidative stress and cell apoptosis, and further, elucidated the potential machanisms in human THP1 macrophages. Flow cytometry and western blot analyses showed that both cell apoptosis and Lp-PLA2 expression were dose-dependently elevated after ox-LDL treatment for 24 h and also time-dependently increased after 50 mg/L ox-LDL incubation in THP1 macrophages. In addition, Lp-PLA2 silencing decreased ox-LDL-induced Lp-PLA2 and CD36 expression in THP1 macrophages. We also found that the levels of oil red O-staining, triglyceride (TG) and total cholesterol (TC) were significantly upregulated in ox-LDL-treated THP1 cells, but inhibited by Lp-PLA2 silencing. Furthermore, ox-LDL treatment resulted in significant increases of ROS and MDA but a marked decrease of SOD, effects that were reversed by Lp-PLA2 silencing in THP1 cells. Lp-PLA2 silencing reduced ox-LDL-induced cell apoptosis and caspase-3 expression in THP1 cells. Moreover, Lp-PLA2 siRNA transfection dramatically lowered the elevated levels of p-Akt and p-mTOR proteins in ox-LDL-treated THP1 cells. Both PI3K inhibitor LY294002 and mTOR inhibitor rapamycin decreased the augmented caspase-3 expression and TC content induced by ox-LDL, respectively. Taken together, these results revealed that Lp-PLA2 silencing protected against ox-LDL-induced oxidative stress and cell apoptosis via Akt/mTOR signaling pathway in human THP1 macrophages.

The prevalence of type 2 diabetes mellitus (T2D) is increasing worldwide. Melatonin possesses various beneficial metabolic actions, decreased levels of which may accelerate T2D. Endoplasmic reticulum stress (ERS) has been linked to insulin resistance in multiple tissues, but the role of melatonin on ERS and insulin resistance in skeletal muscle has not yet been investigated. In this study, the results showed that tunicamycin decreased insulin-stimulated Akt phosphorylation, but promoted the phosphorylation of protein kinase R-like ER protein kinase (PERK) time-dependently in C2C12 cells. Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Interestingly, melatonin pretreatment reversed the elevated PERK phosphorylation, as well as the activation of Bip expression and XBP-1 splicing, and prevented the inhibitory effect of tunicamycin on Akt phosphorylation. In addition, the insulin-provoked glucose transport was reduced by tunicamycin, and then promoted by melatonin pretreatment. A strong phosphorylation of inositol-requiring enzyme 1 (IRE-1), c-JUN NH2-terminal kinase (JNK), and insulin receptor substrate 1 (IRS-1) serine, and simultaneously, a dramatic decrease of IRS-1 tyrosine phosphorylation were observed in the presence of tunicamycin, leading to a blockade of insulin signaling, which was reversed by melatonin pretreatment. Furthermore, luzindole pretreatment acted inversely with melatonin action on glucose uptake and insulin signaling. Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells.

目的：：探讨将胚胎切割方法尽早应用于临床。方法：应用显微切割刀和酶消化透明带显微玻璃针分割两种方法：对2、4、8细胞期和桑椹期的胚胎分割为二分胚；将2、4、8细胞期的胚胎切割成卵裂球；同时将2细胞期的胚胎连续2次分割培养；切割的二分胚和卵裂球在 M16溶液中行胚胎体外培养，观察其发育情况，达囊胚期植入子宫。结果：小鼠2、4、8细胞期的切割成功率分别为98.0%、86.6%、77.2%、66.1%，发育率为61.5%、80%、84.8%、89.3%；小鼠2、4、8细胞期切成的卵裂球发育至桑椹胚的成功率随着细胞数的增多而减少。小鼠2细胞期卵裂球的全能性优于4、8细胞期卵裂球。各细胞期半胚的发育率明显好于卵裂球的发育率。连续有两次切割2细胞期的胚胎发育到桑椹胚为15%。发育到囊胚的8细胞期和桑椹胚期的半胚移入假孕母鼠体内妊娠率分别为33.3%和60%。结论：显微玻璃针在切割成功率及后期的细胞成活率上优于纤维切割刀的切割方法。

Urotensin II (UII) is a vasoactive peptide composed of 11 amino acids that has been implicated to contribute to the development of cardiovascular disease. The purpose of this study was to investigate whether UII affects the development of atherosclerosis in cholesterol-fed rabbits. UII was infused for 16 weeks through an osmotic mini-pump into male Japanese White rabbits fed on a high-cholesterol diet. Plasma lipids and body weight were measured every 4 weeks. Aortic atherosclerotic lesions along with cellular components, collagen fibers, matrix metalloproteinase-1 and -9 were examined. Moreover, vulnerability index of atherosclerotic plaques was evaluated. UII infusion significantly increased atherosclerotic lesions within the entire aorta by 21% over the control (P = 0.013). Atherosclerotic lesions were increased by 24% in the aortic arch (P = 0.005), 11% in the thoracic aorta (P = 0.054) and 18% in the abdominal aorta (P = 0.035). These increases occurred without changes in plasma levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides or body weight. Immunohistochemical staining revealed that macrophages and matrix metalloproteinase-9 were significantly enhanced by 2.2-fold and 1.6-fold in UII group. In vitro studies demonstrated that UII up-regulated the expression of vascular cell adhesion protein-1 and intercellular adhesion molecule-1 in human umbilical vein endothelial cells, which was inhibited by the UII receptor antagonist urantide. In conclusion, our results showed that UII promotes the development of atherosclerotic lesions and destabilizes atherosclerotic plaques in cholesterol-fed rabbits.

Glycoprotein nonmetastatic melanoma B (GPNMB) is a type I transmembrane glycoprotein which is overexpressed in many tumors and seems to play a critical role in metastasis of malignant tumors. The purpose of this study was to determine GPNMB expression in small cell lung cancer (SCLC) and analyze the prognostic value in patients with SCLC. A total of 132 cases of SCLCs were analyzed immunohistochemically on tissue microarrays (TMAs). Patients were divided into weak-positive and strong-positive GPNMB groups. In addition, serum GPNMB was evaluated by enzyme-linked immunosorbent assay (ELISA). The average serum GPNMB concentration was 1054.15 ± 363.71 pg/mL in the weak-positive group, 2611.52 ± 457.57 pg/mL in the strong-positive group, and 427.61 ± 273.9 pg/mL in the control. The strong-positive group showed significantly higher serum GPNMB levels than the weak-positive group and healthy control (p < 0.01). Overall survival in the weak-positive GPNMB group was significantly longer than in the strong-positive group (27 months vs 15 months, p < 0.01). These results suggest that the expression of GPNMB may be useful as a prognostic indicator in patients with SCLC.