A NEW ANALYTICAL METHOD FOR O_2 AND CO_2 TRANSFER IN SHELL-AND-TUBE(INTRA-LUMINALFLOW)OXYGEN AT ORS

ＡＮＥＷＡＮＡＬＹＴＩＣＡＬＭＥＴＨＯＤＦＯＲＯ２ＡＮＤＣＯ２ＴＲＡＮＳＦＥＲＩＮＳＨＥＬＬ－ＡＮＤ－ＴＵＢＥ（ＩＮＴＲＡ－ＬＵＭＩＮＡＬＦＬＯＷ）ＯＸＹＧＥＮＡＴＯＲＳＡＮＥＷＡＮＡＬＹＴＩＣＡＬＭＥＴＨＯＤＦＯＲＯ２ＡＮＤＣＯ２ＴＲＡＮＳＦＥＲＩ...     

DEVELOPMENT OF A VERSATILE SENSING MEMBRANE FOR IMMUBILIZATION OF PROTEIN AND A NEW IMMOBILIZATION METHOD

ＤＥＶＥＬＯＰＭＥＮＴＯＦＡＶＥＲＳＡＴＩＬＥＳＥＮＳＩＮＧＭＥＭＢＲＡＮＥＦＯＲＩＭＭＵＢＩＬＩＺＡＴＩＯＮＯＦＰＲＯＴＥＩＮＡＮＤＡＮＥＷＩＭＭＯＢＩＬＩＺＡＴＩＯＮＭＥＴＨＯＤＹ．Ｋ．Ｚｈｏｕ，Ｊ．Ｗ．Ｙｕａｎ，Ｓ．Ｑ．Ｘｕ，Ｂ．Ｈ．Ｓｈｕ（Ｄ...     

转染反义Fas阻断T细胞凋亡及对肿瘤的治疗意义

目的 通过阻断Ｔ细胞的Ｆａｓ信号传递途径,探讨消除肿瘤对Ｔ细胞的攻击及其对肿瘤的治疗意义。方法 流式细胞术、ＲＴ－ＰＣＲ方法检测卵巢癌细胞表达Ｆａｓ和ＦａｓＬ。构建ｐｃＤＮＡ３－反义Ｆａｓ真核表达载体,经脂质体转染Ｊｕｒｋａｔ细胞,流式细胞仪检测Ｆａｓ表达变化。以Ａｎｎｅｘｉｎ－Ｖ和ＭＴＴ法检测转染反义Ｆａｓ基因对Ｊｕｒｋａｔ细胞凋亡的影响。采用ＭＴＴ体外杀伤实验观察３ＡＯ对Ｊｕｒｋａｔ细胞杀伤变化。结果 ６种卵巢癌细胞均表达Ｆａｓ和ＦａｓＬ。ｐｃＤＮＡ３－反义Ｆａｓ基因可以使Ｊｕｒｋａｔ细胞表达Ｆａｓ量下降并部分阻断Ｆａｓ单抗诱导的Ｊｕｒｋａｔ细胞凋亡,３ＡＯ对其杀伤减弱。结论 卵巢癌细胞表达ＦａｓＬ可能是其逃逸免疫监视并产生对淋巴细胞攻击的原因之一;应用反义技术阻断Ｆａｓ表达,可部分阻断Ｆａｓ单抗诱导Ｊｕｒ     

OKT3＋rhIL－2激活胎儿脾细胞的研究

观察了１８～２８周龄胎儿脾单个核细胞（ＦＳＭＣ）在体外对ＯＫＴ３＋ｒｈＩＬ－２联合刺激的反应性，结果发现：ＯＫＴ３单独能活化ＦＳＭＣ，最适浓度ＯＫＴ３与ｒｈＩＬ－２联合对ＦＳＭＣ有强协同刺激作用。ＯＫＴ３刺激ＦＳＭＣ后明显促进ＩＬ－２Ｒ表达，表明ＯＫＴ３对ＦＳＭＣ的括化作用与ＩＬ－２／ＩＬ－２Ｒ途径相关。ＯＫＴ３＋ｒｈＩＬ－２协同诱导的ＦＳＭｃ能产生ＮＫ和ＬＡＫ活性，且ＬＭ活住较单用ｒｈＩＬ－２诱导者强，间接免疫荧光染色ＦＡＣＳ分析显示，ＯＫＴ３＋ｒｈｌＬ－２协同激活的ＦＳＭＣ主要是ＣＤ８￣＋Ｔ细胞。结果表明ＦＳＭＣ与成人ＰＢＭＣ－样能被ＯＫＴ３活化。     

LIGHT SCATTERING PROPERTY OF HUMAN BLOOD AT THE WAVELENGTH OF 810NM

ＬＩＧＨＴＳＣＡＴＴＥＲＩＮＧＰＲＯＰＥＲＴＹＯＦＨＵＭＡＮＢＬＯＯＤＡＴＴＨＥＷＡＶＥＬＥＮＧＴＨＯＦ８１０ＮＭＬＩＧＨＴＳＣＡＴＴＥＲＩＮＧＰＲＯＰＥＲＴＹＯＦＨＵＭＡＮＢＬＯＯＤＡＴＴＨＥＷＡＶＥＬＥＮＧＴＨＯＦ８１０ＮＭＪｉａｎＺｈｏｎｇ；Ｄ...     

端粒酶反义腺病毒载体对乳腺癌细胞MCF-7端粒酶的抑制作用

端粒酶ＲＮＡ的反义地人乳腺癌细胞系ＭＣＦ－７细胞端粒酶活性的影响。方法用重组腺病毒转移并表达端粒酶ＲＮＡ的反义ｃＤＮＡ,采用基因重组腺脂质体共转当闰酶反义重组病毒,用Ｓｏｕｔｈｅｒｎ杂交鉴定病毒的整合功能,用ＴＲＡＰ－ 染法检测端粒酶活性。结果ＭＣＦ－７细胞是恶性乳腺癌的典型细胞系。对对照组ＭＣＦ－７、ＭＣＦ－７、ｖＡｄ－ＡＡＶ细胞相比,反义病毒感染后的细胞是恶性乳腺癌的典型细胞系。与对照组ＭＣＦ     

胸腺基质细胞的抗原提呈作用

目的 研究胸腺基质细胞的抗原提呈能力。方法 应用ＯＶＡ－特异的、受Ｉ－Ａ＾ｄ分子识别限制的辅助Ｔ细胞杂交瘤（３ＤＯ．１８．３）识别提呈的ＯＶＡ的ＣＮＢｒ水解片段而被活化后产生ＩＬ－２,测定ＩＬ－２活性来分析胸腺基质细胞的抗原提呈作用。结果ＩＦＮ－γ能促进ＭＴＥＣＩ和ＭＴＳＣ４表达Ｉ－Ａ＾ｄ分子,并促进ＭＴＳＣ４表达Ｂ７－１分子。经ＩＦＮ－γ作用后,ＭＴＥＣ１和ＭＴＳＣ４均有抗原提呈能力,ＭＴＳＣ     

THE INFLUENCES OF SMALL MOLECULES ON FIBRINOGEN COAGULABILITY

ＴＨＥＩＮＦＬＵＥＮＣＥＳＯＦＳＭＡＬＬＭＯＬＥＣＵＬＥＳＯＮＦＩＢＲＩＮＯＧＥＮＣＯＡＧＵＬＡＢＩＬＩＴＹＴＨＥＩＮＦＬＵＥＮＣＥＳＯＦＳＭＡＬＬＭＯＬＥＣＵＬＥＳＯＮＦＩＢＲＩＮＯＧＥＮＣＯＡＧＵＬＡＢＩＬＩＴＹＷａｎｇＣｈｕｎｒｅｎ；ＹａｎｇＺ...     

ER阳性和ER阴性人乳腺癌细胞株p53,mdm—2及p21^WAF1蛋白表达…

目的 研究ＥＲ阳性和ＥＲ阴性人乳腺癌细胞株ｐ５３、ｍｄｍ－２和ｐ２１＾ＷＡＦ１蛋白的表达及其与细胞生物学特性的关系。方法 应用细胞培养、基因转染和免疫组化染色ＬＳＡＢ法等技术，检测ＥＲ阳性、表达野生型ｐ５３（ｗｔｐ５３）蛋白的ＭＣＦ－７细胞和ＥＲ阴性、表达突变型ｐ５３（ｍｔｐ５３）和ＭＤＡ－ＭＢ－２３１细胞以及ＥＲ转染阳性ＭＤＡ－ＭＢ－２３１细胞中ｐ５３、ｍｎｍ－２和ｐ２１＾ＷＡＦ１蛋白的表达水平     

硫代反义寡核苷酸体外对HDV的抑制作用

观察硫代反义寡核苷酸（Ｓ－ＡＳＯＤＮ）体外对ＨＤＶ的抑制作用。方法在ＨＤＶ／ＨＢＶ感染人胎肝细胞中加入不同浓度的针对ＨＤＶ ＳｔｅｍⅠ区６８４－６９８位核苷酸的１５聚Ｓ－ＡＳＯＤＮ,分别采用ＥＬＩＳＡ和斑点杂交法检测上清液中ＨＤＡｇ和细胞中ＨＤＶ ＲＮＡ。结果ＨＢｓＡｇ、ＨＤＡｇ在感染后第２天至第１６天均可测出,以第４天至第１２天达高峰,加入Ｓ－ＡＳＯＮＤ（２、４、６μＭＯＬ／ｌ）ＲＧ ２ＧＤ ,     

Intrathyroidal Dendritic Cells, Epitheloid Cells, and Giant Cells in Iodine Deficient Goiter

Immunohistochemistry and immunofluorescence were performed on thyroid sections of 44 consecutive patients undergoing thyroid surgery for goiter due to iodine deficiency. Sections were compared with specimens from ten individuals without goiters from the same endemic area, with specimens from ten sporadic nontoxic goiter patients, and with specimens from an area with sufficient iodine supply from nine healthy subjects. Cells were characterized using monoclonal antibodies to the CR3 receptor (CD11b) and the p150/95 antigen (CD11c) present on macrophages, to HLA-DR, to antigen presenting cells (RFD1), to T helper (CD4) and to T suppressor/cytotoxic cells (CD8), and with a polyclonal antibody to human cytokeratin. In iodine deficient goiters, focal aggregates were found of RFD1-positive dendritic cells. Furthermore, RFD1-positive epitheloid cells were seen. In 27% of cases, these epitheloid cells completely filled the thyroid follicles. Within the epitheloid cell clusters, multinucleated giant cells could be detected that carried the macrophage markers. Dendritic cells, epitheloid cells, and giant cells were strongly HLA-DR positive. In nongoitrous thyroids from the endemic area such aggregates could also be seen but they were more sparse and were RFD1 negative. Giant cells were absent there. In normal thyroids with sufficient iodine supply, only a few isolated dendritic cells were seen. All except RFD1, which was negative, showed the same marker pattern. In sporadic nontoxic goiters from an area with sufficient iodine supply, dendritic cells occurred in much higher numbers than in the normal thyroids from that area, and they were RFD1 positive. They never aggregated as in iodine deficiency, and giant cells were not observed. These observations on iodine deficient goiter strongly suggest involvement of active antigen-presenting cells in this disorder. However, the immunohistologic difference between this disease and sporadic goiter suggests different underlying mechanisms.     

Stem Cells and Cancer Stem-Like Cells in Endocrine Tissues

Cancer stem-like cells are a subpopulation of self-renewing cells that are more resistant to chemotherapy and radiation therapy than the other surrounding cancer cells. The cancer stem cell model predicts that only a subset of cancer cells possess the ability to self-renew and produce progenitor cells that can reconstitute and sustain tumor growth. Evidence supporting the existence of cancer stem-like cells in the thyroid, pituitary, and in other endocrine tissues is rapidly accumulating. These cells have been studied using specific biomarkers including: CD133, CD44, Nestin, Nanog, and aldehyde dehydrogenase enzyme. Putative cancer stem-like cells can be studied in vitro using serum-free media supplemented with basic fibroblast growth factor and epidermal growth factor grown in low attachment plates or in extracellular matrix leading to sphere formation in vitro. Cancer stem-like cells can also be separated by fluorescent cell sorting and used for in vitro or in vivo studies. Injection of enriched populations of cancer stem-like cells (also referred to as tumor initiating cells) into immunodeficient mice results in growth of xenografts which express cancer stem-like biomarkers. Human cancer stem-like cells have been identified in thyroid cancer cell lines, in primary thyroid cancers, in normal pituitary, and in pituitary tumors. Other recent studies suggest the existence of stem cells and cancer stem-like cells in endocrine tumors of the gastrointestinal tract, pancreas, lungs, adrenal, parathyroid, and skin. New discoveries in this field may lead to more effective therapies for highly aggressive and lethal endocrine cancers.     

Regulatory T Cells in Autoimmune Diseases: Anti-Ergotypic T Cells

T regulatory cells play an important role in regulating T-cell responses to self-antigens and control autoimmunity and autoimmune disease. Anti-ergotypic T cells are a subset of such regulatory T cells that respond to activation markers, ergotopes, expressed on other activated T cells. Anti-ergotypic T cells do not respond to nonactivated T cells. Ergotopes include the α-chain of the IL-2 receptor (CD25). Anti-ergotypic T cells were found to downregulate experimental diseases such as experimental autoimmune encephalomyelitis (EAE) and adjuvant arthritis (AA). Anti-ergotypic T cells are present in humans and are activated after T-cell vaccination. Here we review anti-ergotypic T cells in animal models and in humans and contrast anti-ergotypic T cells with other regulatory T-cell subsets.     

Dendritic Cells and Monocytes as Accessory Cells in T-Cell Responses in Man

The main antigen-presenting cells (APC) of human blood are reported to be the dendritic cells (DC), whereas monocytes (Mo) are only weakly or not at all capable of inducing T-cell immune responses to the soluble antigen purified protein derivative (PPD). In contrast, we found Mo to have a suppressive effect on the APC function of DC in vitro. Removal of Mo by adherence resulted in an increased APC activity, even though Mo produce more interleukin 1 (Il-1) than DC. Furthermore, addition of the prostaglandin synthesis inhibitor indomethacin gave rise to increased Il-1 production, HLA-class II expression, and a stronger antigen-specific T-cell response to PPD. Taken together, our studies indicate that the superior accessory cell function of DC compared with Mo in in vitro cultures may, at least partly, be attributed to the prostaglandin E2 production by Mo and more stable expression of HLA-class II molecules on DC.     

Plaque-Forming Cells in Man

The influence of acetylsalicylic acid (ASA) and steroid (ST) on the number of plaque-forming cells (PFC) developed in pokeweed mitogen-activated cultures of peripheral blood lymphocytes (PBL) was investigated. Cultures of 10(6) PBL were established from blood samples of 16 healthy volunteers before and after intake of 2 g of ASA, and parallel cultures were supplemented with ST in vitro. The immunoglobulin secretion was monitored with a protein A assay. Our results show that pharmacological doses of ASA in vivo decrease the number of PFC by 41%, whereas the distribution of the subpopulations was unaltered. In cultures of PBL obtained before the intake of ASA and supplemented with 10, 50 or 100 micrograms/ml of dexamethasone the number of PFC was decreased by 50%, 41% and 44%, respectively. In cultures of PBL obtained after the intake of ASA and supplemented with 10, 50 or 100 micrograms of ST, the number of PFC was further decreased by 22%, 32% and 38%. The effects of ASA in vivo and ST in vitro were additive. The ratio of IgM, IgG and IgA PFC was unaffected by ASA and ST. It is suggested that the modulation of the PFC response induced by ASA and ST is mediated by the prostaglandin system.     

Plaque-Forming Cells in Man

When the immunoglobulin secretion of 172 normal healthy individuals was investigated with the protein-A plaque assay, 12 persons (7%) did not develop any plaque-forming cells (PFC) in cultures of pokeweed mitogen (PWM)-activated unfractionated peripheral blood lymphocytes (PBL), incubated for 6 days. The effect of irradiation on normal PFC responders and non-responders was also investigated; 2000-rad-irradiated non-responder T lymphocytes co-cultured with autologous untreated B lymphocytes restored the PFC response to normal levels. The evidence of a high level of suppressor activity in non-responder T lymphocytes was further demonstrated by the decreased PFC response of normal B lymphocytes co-cultured with untreated non-responder T lymphocytes.     

Dendritic Cells and Monocytes as Accessory Cells in T-Cell Responses in Man

A method is described for simple and rapid preparation of human dendritic cells (DC) and monocytes (Mo) from peripheral blood. The phenotype of enriched DC and Mo was determined and compared by means of a panel of monoclonal antibodies (Mab's). The distribution and quantitative expression of HLA class II molecules encoded by the subloci DP, DQ, and DR were the same on the two cell types. During in vitro culture a rapid decrease of class II antigens on Mo was observed, whereas the expression of class II antigens on DC was relatively stable. The absence of monocyte markers on DC may indicate that this cell type does not belong to the monocyte/macrophage cell lineage. The phenotypic analysis shows that peripheral blood DC also lack differentiation antigens expressed by epidermal Langerhans cells (OKT6) and lymph node follicular dendritic reticulum cells (DRC-1). The relationship between peripheral blood DC and tissue-localized DC thus remains unsolved. With relatively high numbers of DC now available, production of DC lineage-specific Mab's may be approached.     

Plaque-Forming Cells in Man

This paper describes the results obtained using an indirect protein A plaque-forming cell (PFC) assay applied to human peripheral blood lymphocytes (PBL) activated with pokeweed mitogen (PWM). A maximal response was obtained after 6 days of culture with regard to the three major classes of immunoglobulin (Ig) investigated. No difference was found between females and males. T and B lymphocytes mixed in ratios varying from 1:8 to 8:1 and unfractionated cells were investigated. A maximal PFC response of isolated lymphocytes was found in cultures of 1:4 T/B reconstituted suspensions of untreated cells, whereas the maximal response of untreated B and 2000-rad-irradiated T lymphocytes was found in cultures with a 4:1 T/B ratio. The number of plaques developed in cultures of unfractionated cells exceeded the response of 4:1 T/B reconstituted untreated lymphocytes but was far below the number of PFC developed in cultures of untreated B and 2000-rad-irradiated T lymphocytes. Normal donors developed approximately 70 X 10(3) PFC/10(6) cells. The viability was 85% after the incubation period. No difference was found in the PFC response of cultures of separated, reconstituted T/B lymphocytes set up in autologous and allogeneic combinations.