Magnetization Transfer and T2 Relaxation Components in Tissue

T₂ relaxation makes an important contribution to tissue contrast in magnetic resonance (MR) imaging. Many tissues are known to exhibit multicomponent T₂ relaxation that suggests some compartmental segregation of mobile protons on a T₂ timescale. Magnetization transfer (MT) is another relaxation mechanism that can be used to produce tissue contrast in MR imaging. The MT process depends strongly on water-macromolecular interactions. To investigate the relationship between multicomponent T₂ relaxation and the MT process, multiecho T₂ measurements have been combined with MT measurements for freshly excised samples of cardiac muscle, striated muscle, and white matter. For muscle, short T₂ components show greater MT than long T₂ components, consistent with the belief that they represent distinct water environments. For white matter, quantitative MT measurements were identical for the two major T₂ components, apparently because of exchange between the T₂ compartments on a timescale characteristic of the MT experiment. Implications for accurate modeling of MT in tissue and the use of MT for MR image contrast are discussed.     

Diadenosine polyphosphate (ApxA) as new neurotransmitters

The presence of diadenosine polyphosphates (Ap_xA), diadenosine tetraphosphate (Ap₄A), diadenosine pentaphosphate (Ap₆A), and diadenosine hexaphosphate (Ap₆A), has been described in secretory granules of chromaffin cells, Torpedo synaptic vesicles, and rat brain synaptosomes. The release of these compounds by the action of secretagogues and depolarizing agents, in the presence of calcium, increases their importance as active neurotransmitters. Two high affinity receptors have been described in the three neural models, with Kd values ranging from 0.08 to 0.40 nM for the first binding site and from 5.6 to 18nM for the second lower affinity binding site. Both binding sites exhibit a P_2y-like profile in chromaffin cells and Torpedo synaptic terminals and a different pattern in rat brain synaptosomes, suggesting the presence of a novel P₂-purinoceptor tentatively named P_2d. Studies about the second messenger linked to this receptor, in chromaffin cells, demonstrate the mobilization of calcium from internal stores. Ap_xA receptors at the extracellular milieu are responsible for the inhibition of catecholamine release stimulated by secretagogues. Finally, all diadenosine polyphosphates are destroyed by the action of an ecto-phosphodiesterase which, in chromaffin cells, shows Km values ranging from 1 to 4 μM. © 1993 Wiley-Liss, Inc.     

光照疗法对新生儿红细胞谷胱甘肽还原酶活性的影响

作者对光照疗法（光疗）前及光疗后于口服维生素Ｂ＿２（４３例）和不予口服维生素Ｂ＿２（１７例）的黄疸新生儿的红细胞谷胱甘肽还原酶（ＧＲ）的活性进行了动态观察。结果显示，接受短期光疗的黄疸新生儿其红细胞ＧＲ活性较光疗前的ＧＲ活性有显著下降，光疗后予口服维生素Ｂ＿２可使下降的红细胞ＧＲ活性回升，而不予补充维生素Ｂ＿２者的红细胞ＧＲ活性继续下降。光疗的时间越长，红细胞ＧＲ活性的下降越明显，补充维生素Ｂ＿２使红细胞ＧＲ活性回复到正常水平所需的时间也越长。短期光疗也可引起体内维生素Ｂ＿２的降解，导致红细胞ＧＲ活性的下降，为避免因红细胞ＧＲ活性下降引起的红细胞额外破坏，对接受光疗的黄疸新生儿常规补充维生素Ｂ＿２的是必要的。     

Secretogranin I (chromogranin B) mRNA accumulation is hormonally regulated in GH3B6 rat pituitary tumor cells

Secretogranin I (SgI; chromogranin B) belongs to a class of acidic tyrosine-sulfated secretory proteins believed to play a role in the secretory process of endocrine cells. Our aim here was to compare the levels of SgI mRNA to that of prolactin (PRL) and growth hormone (GH), using rat pituitary cell lines. As far as the constitutive expression is concerned, we found a positive correlation between SgI mRNA and PRL mRNA levels. However, the neuropeptide TRH (50 nM) inhibited the accumulation of SgI mRNA in GH3B6 cells whereas, as expected, it induced a rapid and sustained increase in PRL mRNA accumulation. By contrast, 17β-estradiol (1 nM) stimulated the accumulation of both SgI and PRL mRNAs, with the same EC₅₀ (18–59 pM). Reciprocally, treatment with dexamethasone (100 nM) reduced the level of SgI and PRL mRNAs to 23% and 29% of control, respectively, but led to a 2.1-fold increase in the GH mRNA level. Altogether, the present work shows that SgI gene expression is subject to multiple hormonal regulations and occasionally parallels the regulation of the PRL gene but never that of the GH gene, under the conditions tested.     

Interactions between epidermal growth factor-mediated autocrine regulation and linoleic acid-stimulated growth of a human prostate cancer cell line.

Human prostate cancer (PC) cell lines possess epidermal growth factor (EGF) receptors and secrete EGF-related polypeptides. We used an EGF receptor-blocking antibody (anti-EGF.R) to demonstrate a functional autocrine loop, as well as the interaction between this and the effects of linoleic acid (LA), an omega-6 fatty acid, on PC cell growth. The anti-EGF.R competed effectively with [125I]EGF for receptors on DU145 PC cells, and on a high-passage DU145 variant (DU145M); when added to the culture medium, it suppressed both DU145 and DU145M cell growth in a dose-dependent manner. LA, a precursor for eicosanoid synthesis, had little effect on DU145 cell growth rate but stimulated DU145M growth in a concentration-related manner over a range of 0.25-2.0 micrograms/ml. anti-EGF.R (10(-9) M) caused suppression of LA-stimulated growth of DU145M cells in serum-free medium, which was prevented by the addition of 2 nM EGF. We conclude that an EGF.R-mediated autocrine loop is involved in PC cell growth regulation and that at least one site of action may be the synthesis of eicosanoids from their LA precursor.     

Characterization and phenotypic analysis of differentiating CD34+human bone marrow cells in liquid culture

Abstract: Our current understanding of human haematopoietic stem cell biology is based in part on the characterization of human CD34⁺ bone marrow cell differentiation in vitro. CD34 is highly expressed on early stem cells and haematopoietic progenitor cells with clonogenic potential and is gradually lost during differentiation and commitment. However, CD71 (transferrin receptor) is expressed at low levels on early stem cells and generally increases during haematopoietic progenitor cell proliferation. We reasoned that the combination of these surface markers would provide a useful framework for the simultaneous analysis of multiple lineage differentiation of CD34⁺ haematopoietic progenitor cells in liquid culture. In this report, we identify the phenotype of distinct subpopulations of myeloid, erythroid and lymphoid cells in liquid suspension culture using differential expression of CD34 vs. CD71 in combination with specific lineage markers. Freshly isolated human CD34⁺ bone marrow cells were introduced into suspension culture and monitored over a 6-d period using 3-colour flow cytometry. This is the first demonstration that differential expression of CD34 vs. CD71 can be used to simultaneously monitor differentiation of multiple haematopoietic cell lineages in liquid suspension culture, facilitating the study of cytokine-, drug- or chemical-induced alterations in haematopoietic progenitor cell differentiation in vitro.     

In vivo and in vitro anti-tumour response of selenium-protein polysaccharide extracted from rich selenium Agaricus blazei

In this study, the anti-tumour activity of selenium-protein polysaccharide (SPP), a water extract of the rich selenium Agaricus blazei, was tested both in vivo and in vitro. The results of in vivo experiments show that SPP at doses of 50 and 100 mg/kg inhibits proliferation of implanted Sarcoma 180 by 22 and 37.69%, respectively, and promotes lymphocyte transformation and natural killer (NK) cells activity in tumour bearing mice. During the in vitro experiment, we treated the tumour and non-tumour bearing mice with SPP, and prepared serum treated with SPP (Serum_SPP). The results show that Serum_SPP, whether from tumour or non-tumour bearing mice, significantly inhibits K562 cells proliferation and induces their apoptosis, and also significantly increases caspase-3 activity of K562 cells. However, the difference in anti-tumour activity of Serum_SPP between tumour and non-tumour bearing mice is significantly different (p<0.01). The results, according to the studies both in vivo and in vitro, imply that SPP extracted from rich selenium A. blazei can inhibit growth of implanted Sarcoma 180 and promote lymphocyte transformation and NK cells activity in vivo. Additionally, Serum_SPP can inhibit proliferation and cause apoptotic morphological changes and the fragmentation of internucleosomal DNA, and increase caspase-3 activity of K562 cells in vitro, which indicates that apoptosis of K562 cells induced by Serum_SPP may be related to up-regulation of caspase-3.     

江西省528例非何杰金氏恶性淋巴瘤回顾性病理分析

本文收集了我省十年(1974—1983)来诊断为恶性淋巴瘤的病例,按免疫功能分类复查了全部切片,最后确诊为非何杰金氏恶性淋巴瘤(NHL)528例,进行了分析。本组NHL在首发部位、类型分布等方面与国内外有所不同。本组NHL首发于淋巴结外的占64.02％,明显高于国内其它省、市,而滤泡型淋巴瘤则低于国内多数地区。T细胞淋巴瘤占14.84％,较国内、外均低。并提出提高制片质量和广泛开展及应用免疫学技术的重要性。     

Comparison of iodine-123 low-density lipoprotein (LDL) and indium-111 LDL binding to mononuclear cells of healthy normolipaemic controls and patients with heterozygous familial hypercholesterolaemia

The binding of radiolabelled lipoproteins, iodine-123-labelled low-density. lipoprotein (LDL) and indium-111-labelled LDL, to peripheral blood mononuclear cells (MNCs) was compared in normolipaemic subjects and in patients with heterozygous familial hypercholesterolaemia (FH). ¹²³I-LDL and ¹¹¹In-LDL binding to MNCs exhibited high-affinity, highly specific, time- and temperature-dependent binding reaching saturation at concentrations above 50 nM. The number of LDL binding sites (B_max) was significantly (P<0.01) lower in FH patients (P<0.001; ¹²³I-LDL: B_max 279±44 ng protein/10⁸MNCs; ¹¹¹In-LDL: B_max 309±43 ng protein/10⁸MNCs) as compared with controls (¹²³I-LDL: B_max 2874±246 ng protein/10⁸ MNCs; ¹¹¹In-LDL: B_max 3145±339 ng protein/10⁸ MNCs). The corresponding dissociation constants (K _d) were 16±8 nM for ¹²³I-LDL and 12±6 nM for ¹²³In-LDL in healthy volunteers (¹²³In-LDL vs ¹¹¹In-LDL, P<0.05). In FH patients, the K _d values were 20±8 nM for ¹²³I-LDL and 16±6 nM for ¹²³In-LDL (P<0.05 vs controls for both ¹²³I-LDL and ¹¹¹In-LDL). ¹¹¹In-LDL binding to MNCs was inhibited (IC₅₀) by 30±8 nM in healthy controls and 38±12 nM in FH patients (P<0.05). ¹²³In-LDL binding to MNCs was inhibited (IC₅₀) by 34±8 nM in healthy controls and 46±10 nM in FH patients (P<0.05). Taken together, these results suggest a reduced number of LDL receptors expressed on MNCs from FH patients. We conclude that ¹¹¹In-LDL and ¹²³I-LDL are equally well suited as a probe of receptor-mediated binding and uptake of LDL.