Cutaneous intravascular NK-cell lymphoma: report of a rare variant associated with Epstein-Barr virus

Intravascular lymphoma (IVL) is a rare variant of non-Hodgkin lymphoma with a predilection for skin and brain. Except a few cases of T-cell lineage, most of the reported cases were large B-cell lymphomas. We encountered a case of cutaneous IVL in a 71-year-old woman presenting with multiple erythematous patches and nodules on her trunk and extremities. The intravascular large cells showed an immunophenotype of CD3epsilon(+);, CD5(-), CD20(-), CD30(-), CD56(+), and TIA-1(+). The lymphoma cells were also positive for Epstein-Barr virus by Epstein-Barr virus-encoded RNA in situ hybridization test and the T-cell receptor gene was germline. This IVL differs from nasal type NK/T-cell lymphoma only by its intravascular nature. Only 3 cases of intravascular NK-cell lymphoma have been reported before. Because this variant is extremely rare, our case is documented and compared with the 3 previously reported cases.     

灸感法与红外法检测心气虚患者内关穴热敏态的对比研究

目的:探讨腧穴热敏态红外客观显示的可能性。方法:共纳入心气虚患者74例。在自然状态下采用热断层扫描成像系统(TTM)拍摄双前臂内侧红外热像图,图像采集完毕,接受灸感法热敏检测(艾条悬灸内关穴10min)。悬灸结束后记录患者内关穴产生扩热、透热的例数,然后再进行第2次红外辐射测量,记录艾灸后前臂内侧红外图像变化,比较两种检测法对心气虚患者内关穴热敏态的检测差异。结果:艾灸前患者内关穴区红外辐射强度多数显示高温特征,与患者灸感比较,其敏感性为66.7%,特异性为76.9%,准确性为70.3%。艾灸内关穴区后,发生热敏化的内关穴区产生明显的沿前臂内侧纵向扩散的红外辐射增强区域,与患者灸感比较,其敏感性为87.5%,特异性为92.3%,准确性为89.2%。结论:(1)心气虚患者内关穴区热敏态在一定程度上可被红外成像客观显示。(2)艾灸热敏腧穴产生的腧穴扩热、传热的热敏现象,受试者的主观感觉与红外成像有明显的相关。     

新疆生产建设兵团某师中小学生视力不良现状及影响因素分析

目的:了解新疆生产建设兵团某师中小学生的视力不良现状,分析主要的影响因素,为视力不良防控提供科学依据。方法:采用分层整群随机抽样的方法,于2020-08/10抽取新疆生产建设兵团某师城区和团场共12所学校,共计2 982名中小学生,进行视力检查和问卷调查,对视力不良影响因素进行Logistic回归分析。结果:新疆生产建设兵团某师2 982名中小学生视力不良率为65.66%,且以重度视力不良为主。视力不良率女生(70.17%)高于男生(61.47%)(χ²=4.993,P<0.001),城区(70.03%)高于团场(58.96%)(χ²=38.680,P<0.001),汉族(66.83%)高于维吾尔族(52.82%)(χ²=19.772,P<0.001)。随着年龄段增加,视力不良率呈上升走向(χ²_趋势=300.144,P<0.001),到≥18岁年龄段,视力不良率已达80.47%。多因素分析结果显示,女性、年龄≥13岁、每天读写时间≥2h、周末上补习班以及...     

Transketolase counteracts oxidative stress to drive cancer development

Cancer cells experience an increase in oxidative stress. The pentose phosphate pathway (PPP) is a major biochemical pathway that generates antioxidant NADPH. Here, we show that transketolase (TKT), an enzyme in the PPP, is required for cancer growth because of its ability to affect the production of NAPDH to counteract oxidative stress. We show that TKT expression is tightly regulated by the Nuclear Factor, Erythroid 2-Like 2 (NRF2)/Kelch-Like ECH-Associated Protein 1 (KEAP1)/BTB and CNC Homolog 1 (BACH1) oxidative stress sensor pathway in cancers. Disturbing the redox homeostasis of cancer cells by genetic knockdown or pharmacologic inhibition of TKT sensitizes cancer cells to existing targeted therapy (Sorafenib). Our study strengthens the notion that antioxidants are beneficial to cancer growth and highlights the therapeutic benefits of targeting pathways that generate antioxidants.Metabolic reprogramming has recently been recognized as a hallmark of cancer (1). Cancer cells preferentially use glycolysis instead of oxidative phosphorylation to generate energy even in the presence of oxygen (O₂). This metabolic shift, named the Warburg Effect, channels glucose intermediates for macromolecule and antioxidant synthesis. A very important metabolic pathway that connects with glycolysis is the pentose phosphate pathway (PPP). The major goal of the PPP is the production of ribose-5-phosphate (R5P) and NADPH. R5P is the major backbone of RNA and is critical to nucleotide synthesis. NADPH is the major antioxidant that maintains the two major redox molecules, glutathione and thioredoxin, in the reduced state. NADPH therefore counteracts reactive oxygen species (ROS), enabling cancer cells to survive oxidative stress.The PPP is composed of the oxidative and nonoxidative arms. The oxidative arm of the PPP produces NADPH and ribose by three irreversible steps. First, glucose-6-phosphate dehydrogenase (G6PD) converts glucose-6-phosphate (G6P) to 6-phospho-gluconolactone and NAPDH. Second, phosphogluconolactonase converts 6-phospho-gluconolactone to 6-phosphogluconate. Third, 6-phosphogluconate dehydrogenase converts 6-phosphogluconate to ribulose-5-phosphate (Ru5P) and NAPDH. Ru5P then enters the nonoxidative arm of the PPP. Ru5P is converted to xylulose-5-phosphate (X5P) and Ru5P by epimerase and isomerase, respectively. The transketolase (TKT) family [transketolase-like 1 (TKTL1) and TKTL2] transfers two-carbon groups from X5P to R5P to generate sedoheptulose-7-phosphate (S7P) to glyceraldehyde-3-phosphate (G3P). Transaldolase (TALDO) transfers three-carbon groups from S7P to G3P to generate erythrose-4-phosphate (E4P) and fructose-6-phosphate (F6P). Finally, TKT transfers two-carbon groups from X5P to E4P to generate G3P and F6P, which reenter glycolysis. All enzymes in the nonoxidative arm of the PPP are reversible, allowing cells to adapt to the dynamic metabolic demands. When cells experience high oxidative stress, metabolites from the nonoxidative arm are rechanneled into glycolysis to refill the oxidative arm for the synthesis of NAPDH. When cells are in need of nucleotides, the PPP produces ribose through the oxidative arm from G6P and the nonoxidative arm from F6P and G3P.Although the PPP and glycolysis are equally important in the metabolism of cells, attention has been mostly drawn to the mechanisms by which glycolysis benefits tumor growth. Knowledge regarding the roles of the PPP in cancer cells is relatively scarce. Among all of the enzymes in the PPP, only the roles of G6PD and TKTL1 were briefly revealed in cancer. G6PD and TKTL1 were reported to be activated or overexpressed in cervical, lung, gastric, colorectal, and endometrial cancers (2–7). Suppressing TKTL1 in colorectal tumor cells reduced glucose uptake and lactate accumulation and enhanced sensitivity to oxidative stress (8).Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. It is the fifth most common cancer and the second leading cause of cancer deaths. The 5-y survival rate of HCC patients is less than 10% (9). Its high mortality rate is attributable to late symptom presentation and lack of promising curative therapy. Liver transplantation and tumor resection are so far the most effective HCC treatment. However, most HCC patients are not amenable to surgical treatments due to poor liver function or the presence of metastasis. Sorafenib, an oral multikinase inhibitor, is the only FDA-approved drug and extends the median survival of advanced HCC patients for about 3 mo. It is well known that HCC is one of the most rapidly growing solid cancers. Furthermore, the liver is known to be a metabolic hub that is responsible for major metabolic events in the body such as blood glucose homeostasis and glycogen metabolism. Nonetheless, the detailed metabolic alterations in HCC and the molecular mechanisms driving the metabolic adaptation in HCC remain largely unknown. Better understanding of the metabolic machineries of HCC will be beneficial for the development of therapeutic treatment. Here, using HCC as a cancer model, we demonstrate the imperative roles of the PPP in cancer development and illustrate an example that blocking a critical enzyme that connects glycolysis and the PPP, TKT, would be sufficient to impede HCC development and improve the efficiency of Sorafenib treatment in HCC.     

An immunonanogold resonance scattering spectral probe for rapid assay of human chorionic gonadotrophin

BACKGROUND: Several assays for human chorionic gonadotrophin (hCG) such as radioimmunoassay and fluorescence immunoassays were reported. So far, there was no report about the immunonanogold resonance scattering spectral (ING-RSS) assay based on the immunoreaction and resonance scattering (RS) effect. METHODS: Three ING-RSS probes for hCG were prepared, using nanogold in size of 8, 10, 13 nm to label rabbit hCG antiserum (anti-hCG). RESULTS: In citric acid-Na(2)HPO(4) buffer solution and in the presence of polyethylene glycol (PEG)6000, the immunoreaction between hCG and nanogold-labeled anti-hCG took place, the immunonanogold-complex was formed and deposited. The decreased intensity DeltaI(RS) for the nanogold in sizes of 8, 10, 13 nm was proportional to hCG concentration in the ranges of 40-10000, 40-10000 and 40-8000 mIU/ml, with the detection limits of 19.4, 15.1 and 13.6 mIU/ml, respectively. The hCG in urine samples were assayed by the ING-RSS assay, and by immunospectrophotometry. The results of both assays showed a close correlation. CONCLUSION: This assay has simplicity, sensitivity and good selectivity for quantitative determination of hCG.     

Nano-cerium-element-doped titanium dioxide induces apoptosis of Bel 7402 human hepatoma cells in the presence of visible light

AIM： To investigate the apoptotic effect of photoexcited titanium dioxide （TiO2） nanoparticles in the presence of visible light on human hepatoma cell line （Bel 7402） and to study the underlying mechanism.
METHODS： Cerium-element-doped titanium dioxide nanoparticles were prepared by impregnation method. Bel 7402 human hepatoma cells were cultured in RPMI 1640 medium in a humidified incubator with 50 mL/L COL at 37℃. A 15 W fluorescent lamp with continuous wavelength light was used as light source in the photocatalytic test. Fluorescence morphology and agarose gel eletrophoresis pattern were performed to analyze apoptotic cells.
RESULTS： The Ce （Ⅳ）-doped TiO2 nanoparticles displayed their superiority. The adsorption edge shifted to the 400-450 nm region. With visible light illuminated for 10 min, 10 μg/cm^3 Ce （lV）-doped TiO2 induced micronuclei and significant apoptosis in 4 and 24 h, respectively. Hochest 33 258 staining of the fixed cells revealed typical apoptotic structures （apoptotic bodies）, agarose gel electrophoresis showed typical DNA ladder pattern in treated cells but not in untreated ones.
CONCLUSION： Ce （Ⅳ） doped TiO2 nanoparticles can induce apoptosis of Bel 7402 human hepatoma cells in the presence of visible light.     

肢体残疾职业成功者的个人经历特点

我国目前有残疾人8296万人,其中肢体残疾者2412万人,占29.07%,在各类残疾人中居第一位[1].本文对肢体残疾职业成功者的个人经历进行了初步研究,为国家有关部门制定和调整针对残疾人的相关政策提供依据.     

抑郁症患者内隐自尊及其稳定性研究

目的:探讨抑郁症患者内隐自尊及其稳定性状况。方法:采用内隐联想测验和自尊量表测量抑郁症患者(n=30)的内隐自尊和外显自尊,使用失败反馈任务,以2×2完全随机双因素析因设计,探讨抑郁症患者内隐自尊的稳定性。结果:(1)抑郁症患者的内隐自尊水平与正常人差异不显著(270.2±103.7/283.3±172.1,t′=0.35,P=0.72);(2)抑郁症患者内隐联想测验标准分高于Rosenberg自尊量表标准分(-0.05±0.74/-0.62±0.86,Z=2.38,P<0.05),正常对照组Rosenberg自尊量表评分的标准分低于内隐联想测验评分的标准分(0.05±1.22/0.62±0.71,Z=2.21,P<0.05);(3)抑郁症患者不同反馈类型的内隐联想测验评分差异显著(F(1,55)=13.38,P=0.001),失败反馈组的内隐联想测验评分显著低于对照组(81.31±140.53/239.70±185.69),正常人不同反馈类型的内隐联想测验评分差异不显著(F (1,55)=0.36,P=0.549)。结论:抑郁症患者的内隐自尊水平与正常人差异不显著,但其内隐自尊高于外显自尊的倾向和不稳定的自尊特征可能是抑郁症发作的重要原因。     

PI3K p55PIK调节亚单位N末端抑制胃癌细胞株MGC803生长及其机制

背景与目的:p55PIK是磷脂酰肌醇3-激酶(PI3K)的调节亚单位之一。p55PIK依赖于其N末端独特的24个氨基酸结合Rb,这24个氨基酸的表达能抑制细胞周期的进程。本研究目的在于观察p55PIKN末端24个氨基酸的表达对胃癌细胞增殖和生长的影响,并初步探讨其可能的作用机制。方法:通过Lipofectamine介导,用pEGFP-N24表达质粒转染MGC803细胞,用Westernblot鉴定融合蛋白GFP-N24在MGC803细胞中的瞬时表达;MTT法检测转染细胞的生长情况;克隆形成实验观察N24p55PIK过表达对细胞克隆形成能力的影响;动物实验观察表达N24p55PIK的细胞在裸鼠体内的成瘤能力;Westernblot法分析N24p55PIK表达对细胞周期蛋白CyclinD1表达的影响。结果:N24p55PIK在MGC803细胞中能够有效表达,但其表达量明显低于对照组。与对照组细胞相比,N24p55PIK的表达使细胞生长速度减慢,细胞倍增时间明显延长;表达N24p55PIK的细胞在克隆形成的数量上与对照组相比差异无显著性,但在克隆体积上明显小于对照组。表达N24p55PIK的MGC803细胞在裸鼠中的成瘤能力有所下降,其所形成肿瘤的重量和体积分别为(0.398±0.244)g和(408±268)mm3,而空载体对照组分别为(0.763±0.193)g和(829±271)mm3,两组相比差异有显著性(P<0.05)。N24p55PIK在MGC803细胞中的表达抑制CyclinD1的表达。结论:p55PIK调节亚单位N末端24个氨基酸的表达在体外和体内均能抑制肿瘤细胞的生长;减少CyclinD1的表达可能是其发挥作用的主要机制;来源于PI3K调节亚单位p55PIK的N24肽在肿瘤的治疗上可能具有潜在的应用前景。