Stratification of Gallstones in the Gallbladder

A clinical approach to the diagnosis of congenital cardiac malformations is described which the authors have found effective in exposing the important signs and their significance. Each available diagnostic method is evaluated separately before all data are correlated.

Clinical diagnosis based on history, physical examination, roentgenography and electrocardiography was 94 per cent accurate in a series of cases seen in office consultation and 90 per cent accurate in a series of hospital cases reviewed. The significance of the various signs and symptoms that are routinely searched for in the physical examination is discussed.

The salient points in the clinical diagnosis of the common entities are presented.     

FOXP3 positive regulatory T-cells in cutaneous and systemic CD30 positive T-cell lymphoproliferations

The CD30-positive lymphoproliferations encompass a spectrum of disorders that share histological and phenotypic similarities but differ markedly in clinical behaviour. The basis for this diversity is not known, but it has been proposed that immune suppression by cytokines and/or regulatory T-cells (Tregs) may be implicated. In this study, skin biopsies from lymphomatoid papulosis (LyP) (n = 14), primary cutaneous anaplastic large cells lymphoma (C-ALCL) (n = 13) and systemic anaplastic large cells lymphoma (S-ALCL) with (n = 9) or without (n = 6) ALK expression were examined by immunohistology for FOXP3 expression in tumour cells and tumour infiltrating Tregs. Labelling of a majority of the neoplastic cells was seen in one case of C-ALCL. Another three cases (one LyP and two C-ALCL) displayed weak labelling of very occasional atypical T-cells. In the remaining 38 cases the atypical lymphoid infiltrate was FOXP3 negative. By contrast, all biopsies contained tumour infiltrating FOXP3-positive Tregs. Significant higher numbers were recorded in ALK negative S-ALCL and LyP than in C-ALCL and S-ALCL positive for ALK. In conclusion, it is shown that FOXP3 expression in cutaneous and systemic CD30-positive lymphoproliferations is generally confined to tumour infiltrating Tregs. These cells may have influence upon the clinical behaviour, possibly depending upon the net degree of Treg mediated immune suppression of tumour cells relative to tumour infiltrating, cytotoxic effector cells, thereby implicating the more favourable outcome of LyP compared to C-ALCL.     

Investigational therapies targeting lymphocyte antigens for the treatment of non-Hodgkin’s lymphoma

Introduction: The advent of the anti-CD20 mAb rituximab has opened a new era in the treatment of non-Hodgkin’s lymphomas (NHL), markedly altering standard treatment strategies. Moreover, the proof-of-concept that targeting a specific lymphocyte surface antigen may induce a highly effective and safe targeted killing of malignant cells has opened the door to the development of a plethora of novel mAbs directed towards different B- and T-cell-specific antigens.

Areas covered: This review discusses the recent available clinical data about new-generation anti-CD20 mAbs characterized by increased antibody- (obinutuzumab) or complement-dependent cyotoxicity (ofatumumab) as well as novel investigational agents targeting other lymphocyte antigens (e.g., CD19, CD22, CD30, CD40, CD52, CCR4), which are currently under investigation for B- and T-cell NHL treatment. In addition, antibody–drug conjugates (inotuzumab ozogamicin, brentuximab vedotin, polatuzumab vedotin), bispecific T-cell engagers (blinatumomab) and a new class of antibodies targeting cytotoxic T-lymphocyte-associated antigen 4, programmed death 1 or programmed death ligand 1 (immune checkpoint inhibitors) are specifically considered.

Expert opinion: Among the novel mAbs challenging rituximab, obinutuzumab seems to be in the most advanced phase, with the results of randomized trials awaited shortly. Brentuximab vedotin is increasing its role in T-cell NHL. Furthermore, immune checkpoint inhibitors have the potential to acquire a great relevance in NHL therapy.     

Is 30-Day Mortality after Admission for Heart Failure an Appropriate Metric for Quality?

Background

The Centers for Medicare and Medicaid Services (CMS) model for publicly reporting national 30-day-risk-adjusted mortality rates for patients admitted with heart failure fails to include clinical variables known to impact total mortality or take into consideration the culture of end-of-life care. We sought to determine if those variables were related to the 30-day mortality of heart failure patients at Geisinger Medical Center.

皱瘤海鞘乙醇提取物对HSV-2基因复制的影响

目的：研究皱瘤海鞘乙醇提取物对HSV-2 DNA复制的影响;方法：以Vero细胞为模型,应用CPE法,MTT法、real-time PCR与反向PCR检测皱瘤海鞘乙醇提取物对HSV-2DNA合成的抑制作用。结果：皱瘤海鞘乙醇提取物显著抑制HSV-2所致的CPE;皱瘤海鞘乙醇提取物在HSV-2生物合成早期(-2,0,2小时)时干预,对HSV-2的生物合成抑制效果较好,病毒抑制率达65%以上;皱瘤海鞘乙醇提取物能够显著抑制HSV-2 DNA拷贝数,与病毒对照组比较具有显著差异(P＜0.01),并能下调HSV-2DNA聚合酶UL30基因的表达。结论：皱瘤海鞘对HSV-2DNA复制具有抑制作用,其作用靶点之一是HSV-2DNA聚合酶UL30基因。     

CTP-MELD评分联合血清M30和M65预测乙型肝炎相关慢加急性肝衰竭短期预后的价值

目的探讨肝功能评分(CTP)-终末期肝病模型(MELD)联合血清M30和M65对乙型肝炎相关慢加急性肝衰竭(HBV-ACLF)患者短期预后的预测价值。方法选择2017年1月至2020年1月南京市第二医院接受治疗的HBV-ACLF患者106例,根据90 d预后分为生存组51例与死亡组55例。比较两组患者一般情况、实验室指标、血清M30和M65水平,受试者特征曲线分析下面积CTP-MELD评分联合血清M30和M65与HBV-ACLF短期预后的关系。结果死亡组患者的CTP、MELD评分分别为(23.02±5.18)分和(31.18±5.89)分,高于存活组的(10.49±1.05)分和(13.21±1.34)分(t=16.949、21.276,均P<0.01);死亡组的血清M30、M65水平分别为(1685.12±413.32)U/L和(2799.41±712.05)U/L,均高于存活组的(1001.40±316.49)U/L和(1808.85±669.43)U/L(t=9.507、8.608,均P<0.01)。CTP、MELD、M30、M65单独预测90 d病死的AUC分别为0.624(95%CI:0.525~0.716)、0.804(95%CI:0.716~0.875)、0.750(95%CI:0.656~0.829)、0.887(95%CI:0.810~0.940),4项联合的AUC为0.919(95%CI:0.850~0.963),明显优于CTP、MELD、M30单项评价(P<0.05),高于M65单项评价但差异无统计学意义(P>0.05)。结论CTP、MELD评分和血清M30、M65能够较好地预测HBV-ACLF患者短期预后,且4项联合检测具有更高的预测价值。     

CD30-positive lymphoma in human T-cell leukaemia virus type 1 carrier without monoclonal integration of HTLV-1

Summary. CD30, Ki-1 antigen, an activated T-cell antigen, is a member of the nerve growth factor receptor family. This antigen is expressed on the lymphoma cells of some adult T-cell leukaemia/lymphoma (ATL/L) patients and some patients with Epstein-Barr virus infection. CD30-positive large cell cutaneous T-cell lymphomas occasionally integrate a defective HTLV-1 provirus. We describe here an HTLV-1 carrier who developed Ki-1 lymphoma with no evidence of monoclonal integration of the HTLV-1 proviral sequence.