基于腹腔镜超声的纹理分析鉴别诊断肾透明细胞癌和非透明细胞癌的价值初探

目的 探讨基于腹腔镜超声图像的纹理分析在鉴别诊断肾透明细胞癌与非透明细胞癌中的价值.方法 回顾性分析我院经病理证实的83例肾细胞癌患者的腹腔镜超声检查资料,其中肾透明细胞癌66例,非透明细胞癌17例.在腹腔镜二维超声图像上通过ITK-SNAP软件手工勾画感兴趣区,采用Pyradiomics工具包提取纹理特征.使用组内相关系数选择具有良好稳定性和可重复性的特征;使用最大相关最小冗余(mRMR)和最小绝对收缩和选择算子(LASSO)回归进行特征选择并构建预测模型;绘制受试者工作特征(ROC)曲线分析该预测模型的诊断效能.结果 基于6个纹理特征构建的预测模型为:Y=-1.452+0.329×wavelet.LL glszm SmallAreaLowGrayLevelEmphasis-0.187×wavelet.LH firstorder Mean-0.209×wavelet.HH glszm SmallAreaLowGrayLevelEmphasis-0.107×original gldm DependenceVariance+0.351×wavelet.LH glrlm RunEntropy+0.058×wavelet.HH glszm ZonePercentage.该模型鉴别肾透明细胞癌与非透明细胞癌的ROC曲线下面积、敏感性、特异性和准确率及其对应的95例可信区间分别为0.860(0.771～0.945)、0.765(0.529～0.941)、0.864(0.788～0.939)、0.843(0.747～0.914).结论 基于腹腔镜超声图像的纹理分析可以准确鉴别肾透明细胞癌与非透明细胞癌.     

Cell microarrays

In the postgenomic era, DNA and protein arrays are increasing the speed at which knowledge is gathered on gene expression in cells and tissues. At the same time, researchers realize that a miniaturized and parallelized analysis of whole cells may equally expedite the acquisition of data describing cellular properties and function. Researchers are starting to explore means of generating and using cell microarrays to investigate cells at higher throughput. In this initial phase of exploration, cell microarrays are being developed for various cellular analyses including the effects of gene expression, cellular reactions to the biomolecular environment, and profiling of cell surface molecules. This article will provide an overview of different types of eukaryotic cell microarrays described to date, how they are generated, and their fields of application.     

肿瘤细胞生物治疗中单个核细胞采集的影响因素分析

目的:探讨在肿瘤细胞生物治疗单个核细胞采集中,影响终产品单个核细胞计数(mononuclear cell,MNC)和采集效率(collection efficiency,CE)的因素。方法:对共计142例肿瘤患者和健康供者的采集数据进行分析,包括年龄、性别、身高、体重、身体质量指数(body mass index,BMI)、全身血容量、诊断类别、血管通路、操作者、终产品量、ACD抗凝剂用量、流速、循环次数、采前血红蛋白(Hb)、红细胞计数(RBC)、血小板计数(Plt)、白细胞计数(WBC)、淋巴细胞计数、单核细胞计数、中性粒细胞计数、去掉抗凝剂的循环血量、终产品单个核细胞计数和单个核细胞的采集效率。其中单个核细胞CE(%)=终产品MNC×100/(采前MNC×去掉抗凝剂的循环血量)。采用T检验和多元线性回归分析研究影响终产品MNC和CE的因素。结果:肿瘤患者的CE高于健康供者(24.41±1.91,20.01±0.99,P=0.043),不同操作者之间CE不同(P=0.01,H=18.59)。终产品MNC与终产品容量、ACD抗凝剂用量、采前淋巴细胞计数呈正相关(P=0.00,P=0.01,P=0.00,r=0.811);MNC的CE与流速、采前RBC计数呈负相关,与操作者工作年限、ACD抗凝剂用量呈正相关(P=0.01,P=0.04,P=0.03,P=0.00,r=0.495)。结论:采前淋巴细胞计数越高、ACD抗凝剂用量和终产品容量越多,终产品MNC越多;ACD抗凝剂用量越多,操作者资历越高单个核细胞CE越高;采前RBC越高、采集流速越快,单个核细胞CE越低。     

土贝母制剂诱导Jurkat细胞凋亡及其对细胞周期的影响

目的探讨土贝母制剂对Jurkat(人T细胞白血病细胞株)细胞增殖抑制率及对细胞凋亡,细胞周期各时相的变化。方法应用MTT比色法和流式细胞仪检测经士贝母制剂对Jurkat细胞增殖抑制率的时间效应和浓度效应及凋亡率的变化。结果土贝母制剂对Jurkat细胞有明显的抑制作用,且呈剂量依赖性,流式细胞仪分析,G1期细胞增高,S期细胞减少,G2/M期细胞增多,凋亡率上升。结论土贝母制剂能够抑制Jurkat细胞增殖,抑制G1期细胞向S期转化的进程,促进Jurkat细胞凋亡。     

芒果甙诱导慢性髓系白血病K562细胞凋亡

本研究目的是探讨芒果甙对慢性髓系白血病细胞系K562细胞的作用及其作用机制。用噻唑蓝(MTT)法观察芒果甙时K562细胞生长的影响；应用细胞形态、DNA凝胶电泳和流式细胞术等观察芒果甙时K562细胞凋亡的诱导作用；用RT-PCR方法观察芒果甙作用K562细胞后ber／abl融合基因在转录水平的改变。结果发现。25—200μmol／L浓度的芒果甙均能显著抑制K562细胞的增殖，呈剂量和时间依赖性。并能诱导K562细胞凋亡。随着药物作用浓度的增加，ber/abl融合基因的转录下调。结论：芒果甙可抑制K562细胞的增殖。并可能通过抑制bcr／abl融合基因的表达诱导K562细胞凋亡。     

Giant Cell Arteritis

Giant cell arteritis (GCA) is a medium and large‐vessel vasculitis, which is an important cause of secondary headache in older adults. While GCA has a classic presentation occurring after the age of 50, atypical presentations (eg, fever of unknown origin, cough, low or normal erythrocyte sedimentation rate) may lead to a delay in diagnosis. The topography of vascular involvement has implications for disease‐related complications, which can result in neurologic disease at multiple levels of the nervous system. The most feared complication, vision loss, fortunately becomes uncommon after initiation of corticosteroids. Corticosteroid treatment should not be withheld while waiting the results of a temporal artery biopsy (TAB), which remains the gold standard for GCA diagnosis. Newer diagnostic modalities, including ultrasound, magnetic resonance imaging, and positron emission tomography can play an important role in directing treatment in cases with negative TAB. After successful control of the disorder, patients should be gradually tapered off corticosteroids, with careful monitoring using both clinical and laboratory parameters to assess for relapse. Corticosteroid‐related treatment complications are not uncommon in GCA. There is mixed evidence for use of adjunct corticosteroid‐sparing agents (eg, methotrexate), although these should be initiated in the setting of corticosteroid‐related morbidity and/or cases with frequent relapse.     

T-淋巴瘤细胞的超微结构

为了研究T细胞淋巴瘤患者骨髓中恶性T细胞（malignant T cell，MTC）的超微结构，用流式细胞术分析13例T细胞淋巴瘤患者骨髓浸润MTC抗原表达，电子显微镜观察MTC的形态结构。结果发现：所有患者MTC大小不等，6／13例细胞大小轻度不均，7例显著不均，直径范围在12-28μm之间。所有患者MTC核异染色质少于正常淋巴细胞，核仁范围在2-8μm之间；10／13例细胞核不规则。8／13例MTC胞浆丰富；7／13例细胞表面有丰富的突起或伪足。5／13例Golgi体、分泌泡、致密颗粒和微丝较丰富；8／13例MTC线粒体肿胀明显。结论：骨髓MTC体积普遍不均匀增大；细胞核折叠、切迹、扭曲与核旁微丝增加相关。患者MTC表面突彤绒毛与胞浆Golgi体、分泌泡、致密颗粒及中间微丝呈明显同步发育，大部分患者MTC线粒体明显水肿。     

Diabetes Impairs Stem Cell and Proangiogenic Cell Mobilization in Humans

OBJECTIVE

Diabetes mellitus (DM) increases cardiovascular risk, at least in part, through shortage of vascular regenerative cells derived from the bone marrow (BM). In experimental models, DM causes morphological and functional BM alterations, but information on BM function in human DM is missing. Herein, we sought to assay mobilization of stem and proangiogenic cells in subjects with and without DM.

RESEARCH DESIGN AND METHODS

In a prospective trial ({"type":"clinical-trial","attrs":{"text":"NCT01102699","term_id":"NCT01102699"}}NCT01102699), we tested BM responsiveness to 5 μg/kg human recombinant granulocyte colony–stimulating factor (hrG-CSF) in 24 individuals with DM (10 type 1 and 14 type 2) and 14 individuals without DM. Before and 24 h after hrG-CSF, we quantified circulating stem/progenitor cells and total and differential white blood cell counts. We also evaluated in vivo the proangiogenic capacity of peripheral blood mononuclear cells using the Matrigel plug assay.

RESULTS

In response to hrG-CSF, levels of CD34⁺ cells and other progenitor cell phenotypes increased in subjects without DM. Patients with DM had significantly impaired mobilization of CD34⁺, CD133⁺, and CD34⁺CD133⁺ hematopoietic stem cells and CD133⁺KDR⁺ endothelial progenitors, independently of potential confounders. The in vivo angiogenic capacity of peripheral blood mononuclear cells significantly increased after hrG-CSF in control subjects without DM, but not in patients with DM. DM was also associated with the inability to upregulate CD26/DPP-4 on CD34⁺ cells, which is required for the mobilizing effect of granulocyte colony–stimulating factor.

CONCLUSIONS

Stem and proangiogenic cell mobilization in response to hrG-CSF is impaired in DM, possibly because of maladaptive CD26/DPP-4 regulation. These alterations may hamper tissue repair and favor the development of cardiovascular complications.Diabetes mellitus (DM) increases cardiovascular disease, and this is attributed, at least in part, to shortage of vascular regenerative cells derived from the bone marrow (BM) (1). DM is associated with reduced levels of several circulating progenitor cell phenotypes (2). We have previously shown that DM prevents postischemic progenitor cell mobilization in rats, which translates into impaired vascular recovery after ischemia (3). Recent data from experimental models of type 1 DM and type 2 DM highlight BM pathologies that include microangiopathy (4), neuropathy (5), altered gene expression (6), and niche dysfunction (7). These changes may account for an impaired mobilizing capacity in DM compared with control animals (8). Data on BM function in human DM are scant, whereas there is no information on BM structure. In a retrospective case series of patients undergoing BM autotransplantation, DM was statistically associated with poor mobilization in response to chemotherapy plus human recombinant granulocyte colony–stimulating factor (hrG-CSF) (7). Moreover, in support of the existence of a BM defect in human DM, we have shown a reduction in BM CD34⁺ cells, compared with nondiabetic subjects (9).The mechanism of action of the mobilizing factor granulocyte colony–stimulating factor (G-CSF) is complex and involves cleavage of stromal-derived factor (SDF)-1α through release of proteases, elastases, and matrix metalloprotease-9, suppression of osteoblastic function, and modulation of integrins (10). The mechanism whereby DM impairs stem cell mobilization may depend on altered local concentrations of the chemokine SDF-1α. It is noteworthy that SDF-1α is a natural substrate of the protease CD26/DPP-4, the activity of which is dysregulated in DM (11). The impaired stem cell mobilization in DM has important implications for the care of patients in the hematology clinic. Furthermore, because the BM harbors a variety of regenerative nonhematopoietic progenitors, including endothelial progenitor cells (EPCs), BM dysfunction may contribute to the onset of chronic DM complications (12). Unfortunately, exploration of BM structure and function in humans is limited by the intrinsic low availability of BM samples from nonhematologic patients. Therefore, to confirm the diabetic stem cell “mobilopathy” in humans, we devised a pharmacologic test of BM reserve in a prospective trial of BM stimulation with a single subcutaneous injection of hrG-CSF in individuals with DM and without DM.     

外周血干细胞移植物中残存肿瘤细胞的检测

高剂量化疗联合自体外周血干细胞移植已经越来越多的应用于恶性肿瘤的治疗,干细胞移植物中肿瘤细胞的污染是导致疾病复发的主要原因之一,准确及时的检测出干细胞移植物中的肿瘤细胞具有重要的临床意义,其能更有利地掌握动员效果,有效地指导临床治疗,进一步提高造血干细胞移植的成功率,降低肿瘤的复发等。目前,PCR、免疫细胞化学和免疫磁珠等技术已经成为检测肿瘤患者外周血中微转移肿瘤细胞的主要方法,本文主要就这些方法做一综述．     

Sickle Cell Anemia

For general practitioners, as well as specialists, this department offers the latest, proved methods of treatment of conditions encountered in an average practice. It is not, of course, intended to present these discussions as the only acceptable therapeutic procedures to be used, but rather to offer simple regimens and recommendations based on the extensive experience of the physicians who prepares these summaries.