基于超声影像组学特征列线图模型术前鉴别早期与中晚期宫颈鳞癌

目的 观察基于经阴道超声影像组学特征建立的列线图模型术前鉴别早期与中晚期宫颈鳞癌的价值。方法 回顾性收集经术后病理证实的227例宫颈鳞癌患者,利用3D-Slicer软件于术前经阴道声像图中勾画ROI,提取并经冗余性分析、最小绝对收缩和选择算子(LASSO)和10折交叉验证筛选影像组学特征,构建影像组学模型并得到Radscore评分;利用多因素logistic回归纳入Radscore及临床资料构建列线图模型。比较2个模型术前鉴别早期与中晚期宫颈鳞癌的受试者工作特征曲线下面积(AUC);评估列线图模型的校准度及临床收益。结果 最终纳入18个超声影像组学特征;以之构建术前鉴别早期与中晚期宫颈鳞癌的影像组学模型在训练集和验证集的AUC分别为0.839和0.744;联合年龄、流产次数及Radscore评分构建的列线图模型在训练集和验证集的AUC分别为0.882和0.773。DeLong检验结果显示,上述2模型在训练集的AUC差异有统计学意义(P＜0.05)。Hosmer-Lemeshow检验显示,列线图模型在训练集和验证集的校准度均佳(χ²=5.053、7.063,P均＞0.05);决策曲线分析(DCA)显示其在0.01~1.00阈值区间净收益相对较大。结论 基于经阴道超声影像组学特征的列线图模型可于术前较好地鉴别早期与中晚期宫颈鳞癌。     

自动乳腺全容积扫描影像组学联合临床和超声特征列线图鉴别良、恶性乳腺导管内病变

目的 观察自动乳腺全容积扫描(ABVS)影像组学联合临床及超声特征列线图鉴别良、恶性乳腺导管内病变的价值。方法 回顾性分析144例经病理证实乳腺导管内病变女性患者的临床及超声资料;按照2 ∶ 1比例将其随机分为训练集(n=96)及验证集(n=48)。基于ABVS图像提取并筛选最优影像组学特征,构建影像组学模型,计算影像组学评分(Radscore);将临床、超声特征及Radscore纳入单因素和多因素logistic回归分析,筛选鉴别良、恶性乳腺导管内病变的独立影响因素,构建临床-超声模型,并联合影像组学模型构建列线图模型;以受试者工作特征(ROC)曲线评估各模型鉴别良、恶性乳腺导管内病变的效能。结果 患者年龄 、病变边缘 、微小钙化灶 及Radscore 均为良、恶性乳腺导管内病变的独立影响因素。影像组学模型、临床-超声模型及列线图模型鉴别良、恶性乳腺导管内病变的曲线下面积(AUC)在训练集分别为0.766、0.866及0.901,在验证集分别为0.770、0.765及0.854。结论 ABVS影像组学联合临床及超声特征列线图鉴别良、恶性乳腺导管内病变效能良好。     

基于非小细胞肺癌双能CT表现及影像组学列线图模型预测其血管生成拟态

目的 基于非小细胞肺癌(NSCLC)双能CT (DECT)表现及影像组学构建联合列线图模型,分析其预测NSCLC血管生成拟态(VM)的价值。方法 回顾性分析137例经手术病理证实的单发NSCLC患者,以7 ∶ 3比例将其分为训练集和验证集。基于肺窗CT提取及筛选最优影像组学特征,计算影像组学评分。以单因素分析及多因素logistic回归分析筛选NSCLC表达VM的独立预测因素,分别以之构建临床、能谱及影像组学模型;基于独立预测因素构建联合列线图模型。采用受试者工作特征曲线评估各模型预测NSCLC VM的效能,以校准曲线分析模型的拟合度,以决策曲线分析评估模型的临床获益。结果 最终筛选出6个最优影像组学特征。病灶最大径、毛刺征、CT_{140 keV}及影像组学评分为NSCLC VM的独立预测因素(OR=2.25、9.69、0.99、-14.44,P均＜0.05)。临床、能谱及影像组学模型预测验证集NSCLC VM的曲线下面积(AUC)分别为0.83、0.85、0.87,均低于联合列线图模型(AUC=0.95,Z=2.14、2.10、2.07,P均＜0.05)。联合列线图模型预测结果与实际结果的一致性较好,且其临床获益较高。结论 基于DECT及影像组学构建的联合列线图模型能可有效预测NSCLC VM。     

CT影像组学列线图评估肺腺癌脏层胸膜侵犯

目的 建立CT影像组学列线图模型,观察其评估肺腺癌脏层胸膜侵犯(VPI)的价值。方法 回顾性分析183例经术后病理证实的肺腺癌患者,以7 ∶ 3比例将其随机分为训练集(n=128)及验证集(n=55);根据有无VPI进一步分为浸润组和非浸润组。基于肺CT图像提取影像组学特征,构建影像组学评分(Rad-score)。以多因素logistic回归分析筛选训练集内组间差异具有统计学意义的影像学表现,构建常规模型,并结合Rad-score绘制列线图,对比观察其判断肺腺癌伴VPI的效能,以及列线图模型判断腺癌伴VPI结果与实际结果的一致性及其差异。结果 最终以8个影像组学特征构建Rad-score。多因素logistic回归分析显示,病灶存在分叶征、瘤内坏死、胸膜牵拉及Rad-score是判断肺腺癌伴VPI的独立因素(P均＜0.05)。以同时存在分叶征、瘤内坏死及胸膜牵拉为常规模型,结合Rad-score所绘制的列线图模型判断训练集与验证集肺腺癌伴VPI的AUC分别为0.875、0.865,优于常规模型在训练集的0.779、验证集的0.805,以及Rad-score模型在训练集的0.810和验证组的0.803,差异具有统计学意义(P均＜0.05)。校准曲线及Hosmer-Lemeshow检验结果均显示,列线图模型判断训练集及验证集肺腺癌患者伴VPI与实际结果的一致性良好(P均＞0.05)。结论 CT影像组学列线图模型判断肺腺癌伴VPI应用价值良好。     

增强动脉期CT影像组学特征联合临床术前预测胃癌脉管浸润

目的 观察增强动脉期CT影像组学特征联合临床术前预测胃癌脉管浸润(LVI)的价值。方法 回顾性纳入298例胃癌患者,根据是否伴LVI将其分为阳性组(n=155)及阴性组(n=143),并按7 ∶ 3比例分为训练集(n=208)及测试集(n=90)。基于增强动脉期CT图提取病灶影像组学特征,采用logistic回归分析筛选胃癌LVI的临床影响因素;分别采用支持向量机(SVM)、逻辑回归(LR)、随机森林(RF)及极端梯度提升树(XGBoost)建立影像组学模型、临床模型及临床-影像组学模型,评估各模型预测胃癌LVI的效能。结果 以SVM、LR、RF及XGBoost建立的影像组学模型预测训练集胃癌LVI的曲线下面积(AUC)分别为0.896、0.821、1.000及1.000,其在测试集的AUC分别为0.744、0.801、0.740及0.747。基于4种机器学习建立的临床模型在训练集的AUC均为0.810,在测试集均为0.840。基于SVM、LR、RF及XGBoost建立的临床-影像组学模型预测训练集胃癌LVI的AUC分别为0.920、0.900、1.000及1.000,其在测试集的AUC分别为0.900、0.890、0.840及0.790。测试集中,基于SVM、LR及RF的临床-影像组学模型的AUC均大于影像组学模型和临床模型(P均＜0.05)。结论 增强动脉期CT影像组学联合临床有助于术前预测胃癌LVI。     

联合临床、MR T2WI及表观弥散系数图影像组学特征列线图预测初发前列腺癌骨转移

目的 评估基于临床、MR T2WI及表观弥散系数(ADC)图影像组学特征构建的联合模型列线图预测初发前列腺癌骨转移的价值。方法 回顾性分析110例接受前列腺MR检查且经病理证实的初发前列腺癌患者,根据⁹⁹Tc^m亚甲基二磷酸盐(⁹⁹Tc^m-MDP)全身骨显像分为骨转移组(n=50)和无骨转移组(n=60)。基于T2WI及ADC图各提取851个、共1 702个影像组学特征,筛选最佳特征,计算影像组学评分并建立影像组学模型。应用单因素和多因素logistic回归分析筛选初发前列腺癌骨转移的临床相关独立危险因素,建立临床模型,并构建临床独立危险因素联合影像组学评分联合模型,绘制列线图将之可视化。以受试者工作特征(ROC)曲线评估各模型预测初发前列腺癌骨转移的效能,以决策曲线分析(DCA)评价联合模型的价值。结果 最终选出11个最佳影像组学特征,以之建立的影像组学模型预测初发前列腺癌骨转移的曲线下面积(AUC)为0.82。总前列腺特异性抗原、碱性磷酸酶和N分期是初发前列腺癌骨转移的临床独立危险因素(P均＜0.05),以之构建的临床模型的AUC为0.93。联合模型的AUC(0.96)高于临床模型(Z=－2.066,P=0.039)和影像组学模型(Z=－3.451,P＜0.001)。联合模型在阈值概率0~0.98时的临床净获益大于临床模型。结论 基于临床联合T2WI及ADC图影像组学特征的列线图可有效预测初发前列腺癌骨转移。     

基于临床病理及常规和功能MRI影像组学模型预测乳腺癌腋窝淋巴结转移

目的 评估基于临床病理及常规和功能MRI（fMRI）影像组学模型预测乳腺癌腋窝淋巴结（ALN）转移的价值。方法 回顾性分析140例浸润性乳腺癌,按7∶3比例将其分为训练集（n=99）和验证集（n=41）。采用多因素Logistic回归分析分别建立基于临床病理及MRI特征的临床模型及各序列图像影像组学、联合序列影像组学以及临床病理及常规和fMRI影像组学的个体化模型,以受试者工作特征（ROC）曲线评价其诊断效能;比较个体化模型与临床模型曲线下面积（AUC）的差异,应用决策曲线分析（DCA）评估模型的临床获益。结果 临床模型预测训练集和验证集ALN转移的AUC分别为0.95和0.88;T2WI、DWI、DCE-MRI模型及联合序列模型在验证集中的AUC分别为0.67、0.71、0.72及0.76。个体化模型在训练集和验证集中的AUC为0.98和0.93,与临床模型差异均无统计学意义（Z=1.56、1.34,P=0.12、0.18）。DCA结果显示阈值>0.25时,个体化模型的净受益高于临床模型。结论 基于临床病理及常规和功能MRI的个体化模型预测乳腺癌ALN转移的效能与临床模型相当,其净受益高于后者,且均优于单一序列模型。     

临床、CT影像组学及融合模型预测肝细胞癌分化程度

目的 评价临床、CT影像组学及融合模型预测肝细胞癌（HCC）分化程度的可行性。方法 纳入330例HCC患者,根据病理所见分化程度分为高分化组（n=85）、中分化组（n=161）及低分化组（n=84）,比较组间临床资料及CT征象差异。按3∶1比例随机将各组分为训练集及测试集。提取训练集CT影像组学特征,构建临床模型、影像组学模型及融合模型。绘制受试者工作特征（ROC）曲线,计算曲线下面积（AUC）,评估各模型鉴别不同分化程度HCC的效能。结果 共纳入352个CT影像组学特征,109个来自高、中分化HCC,84个来自中、低分化HCC,159个来自高、低分化HCC。临床模型鉴别高、低分化HCC的AUC为0.85;CT影像组学模型鉴别高分化与中、低分化HCC的AUC分别为0.80及0.79;融合模型鉴别高、低分化HCC的AUC为0.88。结论 临床、CT影像组学及融合模型预测高、低分化HCC的效能均较高。CT影像组学模型可较好地预测高、中分化HCC。     

联合含瘤周肿瘤全体积CT影像组学特征及临床相关独立预测因子列线图预测肺腺癌淋巴血管侵犯

目的 观察基于含瘤周的肿瘤全体积(GPTV) CT影像组学特征及临床相关独立预测因子构建的联合模型列线图预测肺腺癌淋巴血管侵犯(LVI)的价值。方法 回顾性分析142例经病理证实的肺腺癌患者,以7 ∶ 3比例将其随机分为训练集(n=100,40例LVI阳性、60例LVI阴性)和验证集(n=42,17例LVI阳性、25例LVI阴性)。以单因素分析及多因素logistic回归分析筛选肺腺癌LVI的临床相关独立预测因子,以之构建临床模型。分别基于肿瘤全体积(GTV)及含瘤周3 mm、6 mm、9 mm的GPTV (GPTV₃、GPTV₆和GPTV₉)的增强动脉期CT图提取并筛选最佳影像组学特征,构建影像组学模型,即GTV、GPTV₃、GPTV₆和GPTV₉模型并筛选最佳者;基于后者的影像组学评分和临床相关独立预测因子构建联合模型,绘制列线图进行可视化。以受试者工作特征(ROC)曲线评估各模型预测肺腺癌LVI的效能,以决策曲线分析(DCA)评价联合模型列线图的价值。结果 性别、吸烟和毛刺征均为肺腺癌LVI的临床相关独立预测因子(P均＜0.05)。分别基于GTV、GPTV₃、GPTV₆及GPTV₉筛选出7、16、10及8个最佳影像组学特征,用于构建GTV、GPTV₃、GPTV₆及GPTV₉模型。GPTV₃模型预测训练集、验证集肺腺癌LVI的曲线下面积(AUC)分别为0.82、0.77,均高于GTV (0.79、0.72,Z=3.74、2.62,P均＜0.01)、GPTV₆(0.80、0.72,Z=2.40、2.06,P均＜0.05)及GPTV₉(0.77,0.72,Z=3.03、2.59,P均＜0.01),为最佳影像组学模型。联合模型列线图(0.86、0.73,Z=2.66、2.31,P均＜0.05)及GPTV₃模型(0.82、0.77,Z=2.23、2.54,P均＜0.05)于训练集和验证集的AUC均高于临床模型(0.73、0.61),而联合模型列线图与GPTV₃模型的AUC差异均无统计学意义(Z=1.57、0.88,P均＞0.05)。阈值取0.20~0.50时,联合模型列线图与GPTV₃模型的净获益相当,且均大于临床模型。结论 基于GPTV₃影像组学特征及临床相关独立预测因子的列线图可有效预测肺腺癌LVI。     

多时相CT影像组学模型预测胸腺瘤风险分类

目的 观察多时相CT影像组学模型预测胸腺瘤风险分类的价值。方法 纳入86例经病理确诊的单发胸腺瘤患者,包括32例高风险及54例低风险胸腺瘤,按照7∶3比例将其分为训练集(n=59)和验证集(n=27);采用单因素及多因素logistic回归分析训练集临床及CT特征,筛选胸腺瘤风险分类的独立预测因素,构建临床-CT模型。分别基于平扫、动脉期(AP)、静脉期(VP)、平扫+AP、平扫+VP、AP+VP及平扫+AP+VP提取并筛选最优影像组学特征,计算影像组学评分(Rad-score);采用受试者工作特征(ROC)曲线选取最佳影像组学模型,以之联合临床-CT特征构建联合模型。绘制ROC曲线,计算曲线下面积(AUC),评估各模型预测胸腺瘤风险分类的效能。结果 周围脂肪浸润是胸腺瘤风险分类的独立预测因素(OR=0.029,P=0.004)。ROC曲线显示,模型_AP+VP为最佳影像组学模型,其与联合模型预测训练集胸腺瘤风险分类的AUC分别为0.860及0.877,均高于临床-CT模型的0.736(Z=1.925、-2.464,P均＜0.05),预测验证集的AUC分别为0.835及0.847,亦高于临床-CT模型的0.641(Z=1.840、-2.137,P均＜0.05);模型_AP+VP与联合模型在训练集和验证集的AUC差异均无统计学意义(Z=-1.180、0.291,P均＞0.05)。结论 多时相CT影像组学模型可有效预测胸腺瘤风险分类。     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

Physician and Nurse Practitioner Teamwork and Job Satisfaction: Gender and Profession

Designing interprofessional primary care teams composed of physicians and nurse practitioners (NPs) is a national priority. We assessed how profession and gender affect teamwork and job satisfaction among primary care physicians and NPs by using survey data from 186 physicians and 398 NPs practicing in New York State. Our regression models show profession (NP vs physician) moderates the associations of gender with teamwork and job satisfaction. Among NPs, men had higher job satisfaction than women. Among physicians, women had higher job satisfaction than men. Our results can benefit interprofessional primary care teams to optimize their professional and gender mix.     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.