LHRH受体在喉癌组织中的表达及其在喉癌HEp-2细胞膜表面与LHRH-PE40的亲和力

目的探讨人促黄体激素释放激素(luteinizing hormone releasing hormone,LHRH)受体在喉癌组织中的表达及其在喉癌HEp-2细胞膜表面与LHRH-PE40的亲和力。方法取外科手术收集的50份喉鳞癌及20份癌旁组织标本,采用Western blot法检测LHRH受体的表达,免疫荧光分析法检测LHRH受体的亚细胞定位,ELISA法检测HEp-2细胞膜表面LHRH受体与LHRH-PE40的亲和力。结果 LHRH受体在喉癌组织中的表达量明显高于癌旁组织(P0.001);LHRH受体在喉癌组织中定位于细胞膜和细胞质,而在癌旁组织中定位于整个腺体周边;LHRH受体在HEp-2细胞膜表面与LHRH-PE40的结合显示出线性和饱和性,且可被LHRH直接特异性抑制。结论 LHRH受体在喉癌组织中的过度表达及其在喉癌细胞表面与LHRH-PE40的高亲和力表明,其可能是LHRH-PE40的一个潜在的治疗靶点。     

常压下环己烷密度与温度的相关性

以空气和去离子水为标准样,利用振动管密度计测定了常压下环己烷在20~60℃时,几乎每相间1℃密度数据。其中系统温度的控制精度在0.01℃,密度的测量精度为0.000 1 g/cm3。利用3种不同的函数关系,将测量密度与对应温度的数据进行非线性最小二乘法拟合,给出了密度函数的对应参数。对比得出密度与温度间的最优函数关系,用最优函数计算密度的标准误差为0.000 1 g/cm3,符合密度测量精度要求。     

不明原发灶的颈部淋巴结转移癌的治疗探讨(附25例报告)

目的探讨不明原发灶的颈部转移癌的治疗方式。方法回顾分析我院2003～2009年收治的25例不明原发灶的颈部淋巴结转移癌的病例资料,采用治疗方法为手术(S)、放疗(R)、化疗(C)、手术加放疗(S+R)、手术加化疗(S+C)、放化疗(R+C),手术加放化疗(S+R+C)。结果全组5年总生存率为48%,其中转移性低分化癌的治疗方式为以手术+放疗为主,转移性鳞癌则以手术+化疗为主,转移性腺癌以手术+化疗为主,其中的乳头状腺癌采用甲状腺癌联合根治术式,锁骨上区转移癌以化疗及放疗为主。结论对原发灶不明的颈部转移癌的治疗,应根据淋巴结转移的部位、N分期、病理类型及患者的身体状况等多种因素决定,应选择综合治疗。     

常压下二乙二醇丁醚密度与温度的相关性

以空气和去离子水为标准样,利用Anton Paar DMA60 DMA602振动管密度计测定了常压下二乙二醇丁醚在20-60 ℃间几乎每相间1 ℃密度数据.其中系统温度的控制精度在0.01 ℃,密度的测量精度为0.000 1 g·cm-3.同时,利用不同的函数关系,将测量密度与对应温度的数据进行非线性最小二乘法拟合,给出了密度函数的对应参数.对比得出密度与温度间的最优线性函数关系,并且线性函数计算密度的标准误差为0.000 1 g·cm-3,符合密度测量精度要求.     

煤焦油中含水量与密度之间的关联研究

以中煤九鑫焦化有限公司煤焦油为样品,探讨了不同温度下煤焦油水分与其密度之间的关联关系。结果表明,在不同温度下,含水质量分数4%焦油的密度随温度升高而不断降低;同一温度下,焦油密度随含水量升高而降低。实际生产中,可利用密度推算出一定温度下的焦油含水量,从而及时调整小氨水澄清槽焦油水分离以及焦油产品储槽自动控制水分脱除程度(≤4%),以减少脱水消耗蒸汽量。     

超临界水中氢键特性及其空间分布的密度相关性

为了分析超临界水的密度不均匀性,对不同温度(666、700和800 K)的超临界水体系进行分子动力学模拟,研究了在较大的密度范围内(0.4ρ_c～2ρ_c,ρ_c为水的临界密度)超临界水中氢键的数量、键能与空间分布规律。采用经典的TIP4P/2005水分子模型在正则系综下对1 000个水分子进行模拟。结果表明:随着超临界水密度的增大,氢键的数量、平均键能以及氢键空间分布的均匀性均增大。由于密度较低时水分子形成局部团聚,导致氢键在空间上也存在局部团聚现象。在较高的温度下,氢键的数量与平均键能均较低,但其键能大小在空间上分布得较为均匀。对超临界水中氢键特性及其空间分布的密度相关性的定量分析有助于深入理解超临界水密度不均匀性的微观机制。     

超临界流体中反应速率常数与密度的相互关系

A new method,which correlates rate constants of chemical reactions and density or pressure in supercritical fluids,was developed.Based on the transition state theory and thermodynamic principles, the rate constant can be reasonably correlated with the density of the supercritical fluid,and a correlation equation was obtained. Coupled with the equation of state (EOS) of a supercritical solvent,the effect of pressure on reaction rate constant could be represented.Two typical systems were used to test this method.The result indicates that this method is suitable for dilute supercritical fluid solutions.     

密度法测定盐水中硫酸根滴度

目前,在黏胶纤维生产过程中,通常对盐水中硫酸根滴度的测定采用络合滴定法,但该方法操作繁琐、测定时间长且终点颜色不易辨别,不便于过程分析使用。通过试验发现,盐水中主要组分为硫酸钠和氯化钠,可采用密度法计算出硫酸根滴度,此方法相比其他方法操作简便,测定时间短,而且准确可靠。     

PVC注塑件的密度与收缩

分析了PVC注塑件的密度特征和收缩特征,结果表明:PVC注塑件的密度及其分布与PVC注塑件的收缩相互影响。     

灰度值与立体织物密度关系研究

采用了一种新型立体织物密度检测方法——参比密度样品法,制作不同密度的参比密度样品,测得其对应的灰度值,研究了灰度值与立体织物密度的关系,建立了密度与灰度值的关系曲线线性回归方程,从而对被测样品的各区域密度进行定量检测。     

凋亡抑制因子survivin在喉鳞癌中表达及其临床意义

目的　探讨凋亡抑制因子survivin在喉鳞癌中的表达及临床意义。方法　应用免疫组化SABC方法检测 5 4例喉鳞癌手术切除标本石蜡切片组织中survivin的表达 ,并以 10例声带息肉组织为对照。结果　survivin在声带息肉中不表达 ;在 5 4例喉鳞癌中 ,38例 ( 70 .4 % )表达阳性 ;survivin阳性表达率与喉癌患者的年龄、性别、肿瘤大小、临床分型无相关性 (P >0 .0 5 ) ,与喉癌临床分期、组织学分级、淋巴结转移呈正相关 (P <0 .0 5 )。结论　凋亡抑制因子survivin的异常表达所引起的凋亡抑制与喉鳞癌的发生发展相关 ,可作为肿瘤诊断、预后和治疗的一个新指标。     

A Novel Protein Is Lower Expressed in Renal Cell Carcinoma

Engrailed-2 (EN2) has been identified as a candidate oncogene in breast cancer and prostate cancer. It is usually recognized as a mainly nuclear staining in the cells. However, recent studies showed a cytoplasmic staining occurred in prostate cancer, bladder cancer and clear cell renal cell carcinoma. The inconsistency makes us confused. To clarify the localization and expression of EN2 in renal cell carcinoma, anti-EN2 antibody (ab28731) and anti-EN2 antibody (MAB2600) were used for immunohistochemistry (IHC) respectively. Interestingly, we found that EN2 detected by ab28731 was mainly presented in cytoplasm while EN2 detected by MAB2600 was mainly presented in nucleus. To further investigate the different patterns observed above, lysates from full-length EN2 over expression in HEK293T cells were used to identify which antibody the EN2 molecule bound by western blot. Results showed ab28731 did not react with the lysates. For this reason, the novel specific protein detected by ab28731 was not the EN2 molecule and was named nonEN2. Then using the renal carcinoma tissue microarray and renal tissues, we found that the protein expression levels of nonEN2 in kidney tumor tissues was significantly lower than that in kidney normal tissues (p < 0.05), so was in renal cell lines. Taken together, nonEN2 is lower expressed and may play an important role in renal cell carcinoma.     

Fibrinogen-Like Protein 1 Modulates Sorafenib Resistance in Human Hepatocellular Carcinoma Cells

Despite liver cancer being the second-leading cause of cancer-related death worldwide, few systemic drugs have been approved. Sorafenib, the first FDA-approved systemic drug for unresectable hepatocellular carcinoma (HCC), is limited by resistance. However, the precise mechanisms underlying this phenomenon are unknown. Since fibrinogen-like 1 (FGL1) is involved in HCC progression and upregulated after anticancer therapy, we investigated its role in regulating sorafenib resistance in HCC. FGL1 expression was assessed in six HCC cell lines (HepG2, Huh7, Hep3B, SNU387, SNU449, and SNU475) using western blotting. Correlations between FGL1 expression and sorafenib resistance were examined by cell viability, colony formation, and flow cytometry assays. FGL1 was knocked-down to confirm its effects on sorafenib resistance. FGL1 expression was higher in HepG2, Huh7, and Hep3B cells than in SNU387, SNU449, and SNU475 cells; high FGL1-expressing HCC cells showed a lower IC₅₀ and higher sensitivity to sorafenib. In Huh7 and Hep3B cells, FGL1 knockdown significantly increased colony formation by 61% (p = 0.0013) and 99% (p = 0.0002), respectively, compared to that in controls and abolished sorafenib-induced suppression of colony formation, possibly by modulating ERK and autophagy signals. Our findings demonstrate that sorafenib resistance mediated by FGL1 in HCC cells, suggesting FGL1 as a potential sorafenib-resistance biomarker and target for HCC therapy.     

彩色多普勒检测子宫内膜癌阻力指数(RI)与术后检测微血管密度(MVD)关系的临床研究

目的 探讨彩色多普勒检测子宫内膜癌血流阻力指数(RI)与术后CD105标记的微血管密度(MVD)的关系,以积累经验,指导临床工作。方法 收集130例子宫内膜癌患者,术前应用经阴道彩色多普勒超声检查,计算阻力指数,术后采用免疫组织化学技术,检测CD105标记的微血管密度,探讨RI与MVD在不同临床特征中的意义及RI与MVD表达的关系。结果 子宫内膜癌中RI与MVD的表达与肌层浸润深度及淋巴结转移密切相关,而且RI与MVD的表达在子宫内膜癌中呈负相关。结论 应用彩色多普勒检测RI可以反应子宫内膜癌的血管形成情况,且术前检测RI可能对于判断肿瘤的预后具有一定价值。     

Tumor-Stroma Ratio and Programmed Cell Death Ligand 1 Expression in Preoperative Biopsy and Matched Laryngeal Carcinoma Surgical Specimen

Programmed cell death ligand 1 (PD-L1) seems to rely on close relations between neoplastic and immune cells in the tumor microenvironment. Tumor to stroma ratio (TSR) has been associated with prognosis in different malignancies. The aims of this exploratory investigation were to analyze for the first time the: (i) association between TSR, PD-L1 expression and other clinical–pathological features in laryngeal squamous cell carcinoma (LSCC) biopsies and paired surgical specimens; (ii) prognostic and predictive role of TSR and PD-L1. TSR, PD-L1 expression (in terms of combined positive score [CPS]), and other clinical–pathological features were analyzed in biopsies and surgical specimens of 43 consecutive LSCC cases. A CPS < 1 evaluated on surgical specimens was associated with a low TSR (stroma rich) on both biopsies and surgical specimens (p = 0.0143 and p = 0.0063). Low TSR showed a significant negative prognostic value when evaluated on both biopsies and surgical specimens (HR = 8.808, p = 0.0003 and HR = 11.207, p = 0.0002). CPS ≥ 1 appeared to be a favorable prognostic factor (HR = 0.100, p = 0.0265). The association between bioptic and surgical specimen TSR and PD-L1 expression should be further investigated for a potential impact on targeted treatments, also with regard to immunotherapeutic protocols.     

Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice

Intracellular superoxide dismutases (SODs) maintain tissue homeostasis via superoxide metabolism. We previously reported that intracellular reactive oxygen species (ROS), including superoxide accumulation caused by cytoplasmic SOD (SOD1) or mitochondrial SOD (SOD2) insufficiency, induced p53 activation in cells. SOD1 loss also induced several age-related pathological changes associated with increased oxidative molecules in mice. To evaluate the contribution of p53 activation for SOD1 knockout (KO) (Sod1^−/−) mice, we generated SOD1 and p53 KO (double-knockout (DKO)) mice. DKO fibroblasts showed increased cell viability with decreased apoptosis compared with Sod1^−/− fibroblasts. In vivo experiments revealed that p53 insufficiency was not a great contributor to aging-like tissue changes but accelerated tumorigenesis in Sod1^−/− mice. Furthermore, p53 loss failed to improve dilated cardiomyopathy or the survival in heart-specific SOD2 conditional KO mice. These data indicated that p53 regulated ROS-mediated apoptotic cell death and tumorigenesis but not ROS-mediated tissue degeneration in SOD-deficient models.     

对IRR与A／P关系的探讨

分析并给出了A/P的定义，用数学推导的方法验证了IRR与A/P之间的关系，并给出了当生产经营期为15年时计算精度在0.03%以内的IRR与A/P的线性关系式。     

Preferential Expression of Programmed Death Ligand 1 Protein in Tumor-Associated Macrophages and Its Potential Role in Immunotherapy for Hepatocellular Carcinoma

A predictive biomarker of immune checkpoint inhibitor (ICI)-based treatments in hepatocellular carcinoma (HCC) has not been clearly demonstrated. In this study, we focused on the infiltration and programmed death ligand 1 (PD-L1) expression of tumor-associated macrophages (TAMs) in the tumor microenvironment of HCC. Immunohistochemistry demonstrated that PD-L1 was preferentially expressed on CD68⁺ macrophages in the tumor microenvironment of HCC, suggestive of its expression in TAMs rather than in T cells or tumor cells (P < 0.05). A co-culture experiment using activated T cells and M2 macrophages confirmed a significant increase in T cell functionality after the pretreatment of M2 macrophages with anti-PD-L1. Syngeneic mouse model experiments demonstrated that TAMs expressed PD-L1 and tumors treated with anti-PD-L1 showed smaller diameters than those treated with IgG. In these mice, anti-PD-L1 treatment increased activation markers in intratumoral CD8⁺ T cells and reduced the size of the TAM population. Regarding nivolumab-treated patients, three of eight patients responded to the anti-PD-1 treatment. The percentage of Ki-67-positive CD4⁺ and CD8⁺ T cells was higher in responders than non-responders after nivolumab. Overall, PD-L1 expression on TAMs may be targeted by immune-based HCC treatment, and ICI treatment results in the reinvigoration of exhausted CD8⁺ T cells in HCC.     

EGF +61基因多态性与乙型肝炎肝细胞癌的相关性

目的探讨表皮生长因子(EGF)G61A位点(EGF +61)多态性与慢性乙型肝炎肝细胞癌的相关性。方法运用多聚酶链式反应-限制性片段长度多态性(PCR-RFLP)技术,检测中国人群中215例慢性乙型肝炎肝细胞癌患者和104例正常对照者EGF+61位点的基因型,分析基因型及等位基因的分布频率。结果EGF +61位点基因型及等位基因在乙型肝炎肝细胞癌患者及对照者的分布频率差异均无统计学意义。TNMⅠ、Ⅱ及TNMⅢ、Ⅳ两组的基因型及等位基因的分布频率差异也无统计学意义。结论在中国人群中,EGF +61位点的基因多态性与乙型肝炎肝细胞癌的发生和进展程度无密切关系。