肺腺癌内皮抑素表达与微淋巴管密度及淋巴转移的关系

目的研究内皮抑素在肺腺癌中的表达及其与淋巴管生成和淋巴转移的关系。方法免疫组化法检测60例肺腺癌内皮抑素蛋白的表达及肺腺癌组织微淋巴管密度（MLVD）,分析内皮抑素表达与MLVD及淋巴结转移的关系。结果肺腺癌组织内皮抑素蛋白阳性率[61.7%（37/60）]高于癌旁正常组织[23.3%（14/60）]（P〈0.01）;其表达与肿瘤分期、淋巴结转移有关。内皮抑素阳性组MLVD（7.68±1.89）低于阴性组（9.17±1.95）（P〈0.01）,随内皮抑素表达程度加强,MLVD值减小。结论内皮抑素在抑制肺腺癌淋巴管生成及淋巴转移中可能起一定作用。     

肺腺癌VEGF-C的表达与MVD、MLVD及淋巴转移的关系

目的 探讨肺腺癌血管内皮生长因子-C(VEGF-C)表达与微淋巴管密度(MLVD)、微血管密度(MVD)及淋巴转移之间的关系.方法 RT-PCR法检测36例肺腺癌组织中VEGF-C mRNA的表达,并以免疫组化法检测肺癌组织VEGF-C蛋白的表达、MLVD及MVD.结果 VEGF-C mRNA在肺腺癌组织中的表达比正常肺组织相对较高(P<0.01).VEGF-C蛋白表达在肿瘤周边部位显著高于肿瘤中心部位(P=0.015);其表达与肿瘤分化程度无关,与肿瘤的TNM分期有关,Ⅲ～Ⅳ期显著高于Ⅰ～Ⅱ期(P=0.026).在VEGF-C蛋白阳性组,MVD高于阴性组(P=0.020),MLVD显著高于阴性组(P=0.008),淋巴结转移增多(P=0.039).结论 VEGF- C mRNA在肺腺癌组织中高表达,VEGF-C蛋白表达与肺腺癌血管生成及淋巴管生成和淋巴结转移关系密切.     

肺腺癌组织中VEGF-D的表达变化及意义

目的观察肺腺癌组织中血管内皮生长因子D（VEGF—D）的表达,探讨其意义。方法分别采用RT-PCR法、免疫组化法检测48例肺腺癌组织中的VEGF—D mRNA和VEGF—D、微淋巴管密度（MLVD）、微血管密度（MVD）。结果VEGF—D mRNA在肺腺癌组织中的表达高于正常肺组织（P〈0．01）,VEGF—D蛋白阳性率肿瘤周边显著高于肿瘤中心（P〈0．01）;其表达与肿瘤分化、MVD无关,与TNM分期、MLVD、淋巴结转移有关（P均〈0．05）。结论肺腺癌组织中VEGF—D高表达,与淋巴管的生成及转移有关。     

非小细胞肺癌VEGF-C的表达及LYVE-1标记的微血管密度与淋巴结转移的关系

目的探讨非小细胞肺癌(NSCLC)血管内皮生长因子(VEGF)-C的表达与内皮透明质酸受体-1(LYVE-1)标记的微淋巴管密度(MLVD)与淋巴结转移的关系及意义。方法采用免疫组织化学染色法检测56例NSCLC、10例肺良性病变组织中VEGF-C的表达水平,采用淋巴管特异性标志物LYVE-1检测MLVD,并做相关统计学分析。结果 VEGF-C蛋白在NSCLC组织中的阳性率明显高于肺良性病变组织(P<0.05)。NSCLC组织中LYVE-1标记的MLVD明显高于肺良性病变组织(P<0.05)。VEGF-C表达阳性的组织中MLVD显著高于阴性组织(P<0.05)。VEGF-C蛋白的表达与NSCLC患者淋巴结转移、PTNM分期有关。结论淋巴管生成因子VEGF-C在NSCLC中表达明显升高,其促进了淋巴血管内皮细胞的大量增殖以及淋巴血管的生成,对肿瘤生长和转移起到了促进作用。     

早期胃癌组织MMP-9、MLVD表达及临床意义

目的 探讨基质金属蛋白溶解酶-9(MMP-9)和淋巴管特异性抗体D2-40标记的微淋巴管密度(MLVD)在胃癌发生、发展中的作用.方法 免疫组化法检测74例早期胃癌组织及相应癌旁正常胃黏膜组织中MMP-9表达和D2-40标记的MLVD,分析两者与胃癌临床病理参数的关系及两者的相关性.结果 胃癌组织中MMP-9阳性表达率及MLVD均明显高于正常胃黏膜组织(P均＜0.01);胃癌组织中MMP-9阳性者的MLVD明显高于MM-9阴性者(P＜0.05).MMP-9阳性表达率及MLVD与胃癌的分化程度(P＜0.01)、淋巴结转移密切相关(P＜0.05);MMP-9的表达程度与MLVD呈正相关(P＜0.01).结论 MMP-9及MLVD在早期胃癌中高与其分化程度、淋巴结转移有关,两者联合检测可以作为早期胃癌的预后与转移的重要指标.     

VEGF-C、VEGFR-3在老年肺鳞状细胞癌组织中的表达及意义

目的 探讨血管内皮生长因子C(VEGF-C)、血管内皮生长因子受体3(VEGFR-3)蛋白表达与老年肺鳞状细胞癌(简称肺鳞癌)淋巴管生成以及淋巴结转移的相互关系及老年肺鳞癌淋巴结转移的分子机制.方法 应用免疫组化检测53例老年人肺鳞癌组织、26例癌旁肺组织、20例正常肺组织中VEGF-C蛋白表达情况和VEGFR-3阳性微淋巴管数.结果 VEGF-C蛋白在老年肺鳞癌组织细胞浆中高表达(表达率62.3%),其表达率比癌旁肺组织和正常肺组织高(P≤0.05);老年肺鳞癌组织VEGFR-3阳性微淋巴管数(11.08±4.39)个,比癌旁肺组织和正常肺组织高(P≤0.05);VEGF-C蛋白表达与老年肺鳞癌淋巴结转移情况(P≤0.05)及TNM分期(P≤0.05)密切相关;VEGFR-3阳性微淋巴管数与老年肺鳞癌淋巴结转移情况(P(0.05)及TNM分期(P≤0.05)密切相关;老年肺鳞癌组织中VEGF-C阳性表达与VEGFR-3阳性微淋巴管数呈明显正相关(P≤0.05.r=0.530).结论 VEGF-C和VEGFR-3在老年肺鳞癌的淋巴结转移过程中发挥重要作用;VEGF-C蛋白表达协同VEGFR-3阳性微淋巴管数可用于指导老年肺鳞癌的早发现、早诊断和早治疗.     

连接蛋白43在肺腺癌中表达的意义

目的检测肺腺癌组织及正常肺组织中缝隙连接蛋白43(Connexin 43)的表达。方法应用免疫组织化学法和原位杂交方法检测146例肺腺癌组织及20例正常肺组织中Connexin 43蛋白及mRNA的表达,并分析其表达与肺腺癌转移的关系。结果正常肺组织和肺腺癌组织中Connexin 43蛋白阳性表达率分别为95%(19/20)和39.9%(59/148);mRNA的阳性表达率分别为90%(18/20)和54.7%(81/148)。肺腺癌组织中Connexin 43蛋白及mRNA阳性表达率均低于正常肺组织(P0.05)。在高/中分化和低/未分化的肺腺癌组织中阳性表达率分别为48.7%和30.0%(P0.05);Cx43在无淋巴结转移和有淋巴结转移的肺腺癌组织中阳性表达率分别为56.3%和34.5%(P0.05);Connexin43在Ⅰ、Ⅱ期和Ⅲ、Ⅳ期肺腺癌组织中的阳性表达率分别为51.5%和34.0%(P0.05)。结论 Connexin 43蛋白和mRNA低表达与肺腺癌发生、发展及浸润、转移有关。     

环氧合酶-2和血管内皮生长因子-C的表达与胃癌淋巴结转移的关系

目的 探讨胃癌组织中环氧合酶-2(COX-2)和血管内皮生长因子-C(VEGF-C)的表达及其与淋巴管生成和淋巴结转移之间的关系.方法 采用免疫组化S-P法检测85例胃癌组织和20例正常胃组织中的COX-2、VEGF-C及微淋巴管密度(MLD),并结合临床病理特征进行分析.结果 COX-2、VEGF-C在胃癌组织中的阳性表达率为77.6%、72.9%,COX-2在胃癌组织中的表达与VEGF-C、临床分期、MLD、淋巴结转移有关,差异有统计学意义(P＜0.05),COX-2、VEGF-C与胃癌组织学分型、肿瘤大小、患者性别及年龄均无明显关系(P＞0.05).结论 COX-2、VEGF-C在胃癌组织中高表达,COX-2与VEGF-C、MLD及淋巴结转移呈正相关,COX-2可能通过上调VEGF-C表达参与胃癌微淋巴管生成而发生淋巴结转移.     

LKB1和VEGFR2评价肺腺癌预后的意义

目的探讨LKB1、VEGFR2在肺腺癌中的表达情况,分析其预后意义。方法应用免疫组化方法检测46例肺腺癌中LKB1、VEGFR2的表达情况。结果 LKB1在癌旁正常肺组织、淋巴结转移阴性组肺腺癌、Ⅰ～Ⅱ期肺腺癌中的表达阳性率明显高于肺腺癌组织、淋巴结转移阳性组肺腺癌和ⅢA期肺腺癌(82.61%vs 63.04%、75.00%vs 44.44%、75.00%vs35.71%),差异有统计学意义(P<0.05)。VEGFR2在癌旁正常肺组织、淋巴结转移阴性组肺腺癌、Ⅰ～Ⅱ期肺腺癌中的表达阳性率则明显低于肺腺癌组织、淋巴结转移阳性组肺腺癌和ⅢA期肺腺癌(34.78%vs 58.70%、46.43%vs 77.78%、46.88%vs85.71%),差异有统计学意义(P<0.05)。结论 LKB1、VEGFR2在肺腺癌中的表达情况可能与肺腺癌患者的预后有关,LKB1低表达、VEGFR2高表达可能提示预后不良。     

VEGF-C和Podoplanin在食管癌中的表达及意义

目的 探讨食管鳞癌中VEGF-C和Podoplanin的表达及其与食管癌淋巴管生成和淋巴结转移的关系.方法 应用免疫组织化学SP法检测74例食管鳞癌标本及8例癌旁正常黏膜组织中VEGF-C和Podoplanin的表达,并对两指标表达与临床病理参数之间进行相关分析.结果 ①VEGF-C阳性率和Podoplanin阳性淋巴管密度(LVD)显著高于正常组织(P＜0.05);②VEGF-C阳性率和LVD值在淋巴结转移组明显高于无淋巴结转移组(P＜0.05);③VEGF-C阳性表达的食管癌组织中LVD与阴性表达的LVD比较差异显著(P=0.001).结论 VEGF-C和LVD是食管癌淋巴结转移和淋巴管生成的重要指标,且VEGF-C和LVD明显相关.     

Ligaments of the larynx and the adjacent pharynx and esophagus

Two ligament systems of the larynx are demonstrated by dissection. The suspensory ligament of the esophagus is attached to the posterior aspect of the cricoid cartilage and is also a part of the fascial sheath which is common to the hyoid, thyroid, and cricoid. The ligaments at the inner margins of the vocal, ventricular, and aryepiglottic folds are distinctive in site and, inferentially, in function. The aryepiglottic ligaments join at the incisura between the arytenoid cartilages and are continued as the corniculopharyngeal ligament which splays into the flexible tissues in the anterior wall of the hypopharynx, posterior to the suspensory ligament of the esophagus. These ligament systems are involved in two different actions in swallow. The gross superior and anterior motions of the larynx are transmitted to the esophagus by the suspensory ligament, so that the esophagus is elevated in relation to the bolus and is also opened. These esophageal displacements resemble, in effect, the swallow displacements of the pharyngoesophageal segment and of the constrictor wall of the hypopharynx. The marginal ligaments of the laryngeal folds help to implement the constriction and closure of the larynx during swallow. By anatomical inference, the corniculopharyngeal ligament effects vertical traction within the flexible tissues of the anterior wall of the hypopharynx.     

表观扩散系数值与肝细胞癌分级的相关性以及相关性与肿瘤大小关系的分析

[摘要]　目的　探讨表观扩散系数（apparent diffusion coefficient, ADC）值与肝细胞癌（hepatocellular carcinoma, HCC）组织学分级的相关性以及不同直径肿瘤的ADC值与HCC的相关性。方法?回顾性分析2017年—2020年180例病理证实为HCC的病例资料,按肿瘤直径大小分为＜2 cm、≥2 cm且＜3 cm、≥3 cm且＜5 cm、≥5 cm 4组,标为I、II、III、IV组。分析ADC值与HCC组织学分级的相关性,并分析在不同直径肿瘤ADC值与HCC的相关性。结果?高、中和低分化HCC的ADC值分别为（1.159±0.302）×10-3、（0.951±0.213）×10-3和（0.811±0.239）×10-3 mm2/s,逐级降低（P＜0.05）。ADC值与总体HCC的组织学分级呈负相关（r=-0.474）,与I～III组HCC的组织学分级均呈负相关（r值分别为-0.663、-0.527、-0.364）,而与IV组HCC的组织学分级无相关性。结论?ADC值可以作为非侵入性预测HCC组织学分级的指标,预测结果受肿瘤大小影响,更适用于小肝细胞癌。     

The charity and the care: the origin and the evolution of hospitals

BackgroundThe hospital is considered as one of the founding elements of modern medicine. Such an institution, originally born to be a center for housing the sick and the poor, has provided with a place to improve the medical knowledge and to educate new generations of nurses and physicians. This paper wants to remind the meaning and the development of the hospital institution in the western world.MethodsThe first part of this work analyzed the evolution of hospital, using a classical historiographical approach. In the second part, the history of the “Ospedale Maggiore” in Milan was used as a paradigm to describe the evolution of hospital from the Renaissance to nowadays through a “microhistorical approach”.ResultsThe origins of the public hospital are evidenced in early Christian age, when the Christian message led people to assist the sick and the poor and to establish centers for such interventions, initially in the house of the bishop, then in monasteries and, finally, in autonomous buildings (the hospitals). These institutions were economically supported by the donations of wealthy philanthropists. Since the nineteenth century the hospitals have changed their organization and functions, but have continued to associate the charity and the care.ConclusionChristian charity and the lay culture originated from it may be rightly credited not only as the founding element of ancient hospitals, but also as the virtue which has made possible for the development of medicine, as we know it.     

Diabetes and the survival and recovery of the anoxic myocardium.

In studies with the isolated perfused working hearts from rats with experimentally induced diabetes, the ability of the hearts to survive during, and recovery from, 30 min of anoxia has been studied. In contrast with hearts obtained from normal rats, which gave good and sustained recoveries, the hearts from diabetic animals after an initial period of recovery (approx. 2 min), exhibited cardiac failure for periods of up to 4 min. After this period the hearts entered a second phase of recovery but did not recover to the same extent as the hearts from normal animals. Hearts of diabetic animals therefore appear to be more vulnerable to anoxic damage than do those from normal rats.Using metabolic inhibitors the biochemical basis of this transient post-anoxic failure in diabetic hearts was investigated. It was discovered that the immediate post-anoxic recovery of the hearts was supported in part by endogenous supplies of pre-formed high energy phosphates and in part from energy derived from the glycolysis of endogenous glycogen. During the initial recovery period of approx. 2 min there was little dependence upon the oxidative metabolism of either endogenous or exogenous substrates. In normal hearts the role of major energy provider was rapidly assumed by oxidative processes utilizing exogenous substrate. In the insulin deficient diabetic hearts the impaired transport of glucose into the cell and consequent energy shortage led to the transient cardiac failure and accounted for the delayed secondary recovery. This condition could be completely overcome either by the provision of exogenous insulin or by the provision of substrates such as pyruvate, acetate, citrate or hydroxybutyrate, whose efficient utilization was not impaired by an insulin deficiency.The relevance of these findings in the diabetic rat heart is discussed in relation to the known insulin deficiency occurring in the human during heart failure and the proposed importance of glucose metabolism in the support of the failing myocardium. In addition, these findings are considered in relation to the possible role of insulin both in the genesis and the treatment of heart failure with particular reference to heart failure in humans with diabetes mellitus.